| By Author | [ A B C D E F G H I J K L M N O P Q R S T U V W X Y Z | Other Symbols ] |
| By Title | [ A B C D E F G H I J K L M N O P Q R S T U V W X Y Z | Other Symbols ] |
| By Language |
|
Download this book: [ ASCII | HTML | PDF ] Look for this book on Amazon Tweet |
Title: A System of Practical Medicine by American Authors, Vol. I - Volume 1: Pathology and General Diseases
Author: Various
Language: English
As this book started as an ASCII text book there are no pictures available.
*** Start of this LibraryBlog Digital Book "A System of Practical Medicine by American Authors, Vol. I - Volume 1: Pathology and General Diseases" ***
Libraries)
A SYSTEM OF PRACTICAL MEDICINE.
BY AMERICAN AUTHORS.
EDITED BY
WILLIAM PEPPER, M.D., LL.D.,
PROVOST AND PROFESSOR OF THE THEORY AND PRACTICE OF MEDICINE AND OF
CLINICAL MEDICINE IN THE UNIVERSITY OF PENNSYLVANIA.
ASSISTED BY
LOUIS STARR, M.D.,
CLINICAL PROFESSOR OF DISEASES OF CHILDREN IN THE HOSPITAL OF THE
UNIVERSITY OF PENNSYLVANIA.
VOLUME I. PATHOLOGY AND GENERAL DISEASES.
PHILADELPHIA:
LEA BROTHERS & CO.
1885.
Entered according to Act of Congress, in the year 1885, by LEA
BROTHERS & CO., in the Office of the Librarian of Congress. All rights
reserved.
WESTCOTT & THOMSON, _Stereotypers and Electrotypers, Philada._
WILLIAM J. DORNAN, _Printer, Philada._
PREFACE.
The present work has been undertaken in the belief that by obtaining
the co-operation of a considerable number of physicians of
acknowledged authority, who should treat subjects selected by
themselves, there could be secured an amount of practical information
and teaching not otherwise accessible. It was determined to restrict
the selection of authors to those of this country--including
Canada--not from any want of recognition of the importance of the
studies of certain special subjects by European investigators, but
because it was felt that the proper time had arrived for the
presentation of the whole field of medicine as it is actually taught
and practised by its best representatives in America.
It is a matter of importance also that a comprehensive study shall be
made of the various forms of disease as occurring among our highly
composite population and under our varied and peculiar climatic
influences. Of course, in the present work comparative studies of this
kind must occupy a subordinate position; yet it cannot fail to enhance
both its interest and its value to have the various forms of disease
as they occur in this country discussed by those among us who are
confessedly the most competent and experienced.
The force of these observations must have been felt by the
distinguished men to whom I made application, for with scarcely an
exception they joined cordially in the laborious undertaking. I take
the greatest pleasure in testifying to the courtesy which has marked
all our relations, and which has lessened materially the labor and
strain inevitable in the production of such a work.
To ensure greater accuracy in the revision of the large amount of
proof-sheets, as well as to relieve me of some of the details
connected with the editorial work, I associated with myself Dr. THOMAS
HOLMES CATHCART, and, after sudden illness had cut short his very
promising career, I was fortunate in securing the assistance of Dr.
LOUIS STARR for the same purpose.
In order to render the work as valuable as possible to the general
practitioner, its scope has been made as comprehensive as could be
done without exceeding the limits prescribed by the nature of the
undertaking. This will be particularly noted in the section on
Gynaecology, where is presented a series of articles by eminent
specialists upon the subjects of chief importance to the general
practitioner, written with special reference to their constitutional
relations and their bearings on associated morbid conditions, while,
among the general diseases, a full article on puerperal fever has
properly been included. Important articles will also be found on
Tracheotomy, the Diseases of the Rectum and the Anus, and those of the
Bladder and the male sexual organs. Comprehensive sections have
further been provided, from the pens of distinguished specialists,
upon medical ophthalmology, medical otology, and on skin diseases,
presenting these large and complicated subjects in a clear and
practical light and with special reference to their relations to
general medical practice. In the presentation of such subjects as
hydrophobia, glanders, and anthrax care has been taken to ensure the
full discussion of these affections, not only as occurring in man, but
also in the lower animals, since it is highly important to provide the
physician with authoritative information on at least such points of
Veterinary Science as have a direct practical bearing on morbid
processes in man.
In view of the intimate relations of all questions of hygiene to the
causation and prevention of disease, in regard to which medical men
are constantly consulted, and are, indeed, often obliged to assume
weighty responsibilities, interesting articles on Drainage and Hygiene
have been provided.
In order to avoid repetition and confusion, and at the same time to
secure a comprehensive presentation of the subjects of General
Pathology and of General Etiology, Symptomatology, and Diagnosis,
considerable space has been devoted to their full discussion. The
chapter on General Morbid Processes will be found to convey distinct
and conservative teaching on all points included under that
comprehensive title, and will thus supply a solid basis for the
subsequent discussions of special morbid conditions. In any work on
General Medicine at the present day frequent allusion must be made to
the relations of various low organisms to morbid processes. This
question--or rather the series of questions which arise in connection
with this subject, and which at present form the most fruitful topic
of discussion and of investigation--will be found treated by different
authors in various places and from various standpoints. No attempt has
been made to secure uniformity of views upon a matter which is still
_sub judice_, and which demands much more skilful and critical
investigation before its true scientific position has been finally
determined. It has even been felt to be desirable to allow a certain
amount of repetition, which has naturally resulted from the
introduction of this discussion, not only in the chapter on General
Etiology, but in connection with the causation of scarlatina,
diphtheria, hydrophobia, pyaemia, puerperal fever, and phthisis.
Throughout the work the chief purpose of the editor and of his
collaborators, to furnish a concise and thoroughly practical system of
medicine, has compelled the omission of bibliographical lists, of
numerous references, and of extended discussions of theoretical views
or of controverted questions, in order that more space might be
devoted to clear descriptions of disease and to a full presentation of
the subjects of diagnosis and treatment. If it should seem, in
consequence, that inadequate recognition has been made of the labors
of others, it must be borne in mind that ample quotations and numerous
references were inadmissible in such a work as the present.
* * * * *
The classification and nomenclature which have been adopted are those
recommended by the Royal College of Physicians of England and by the
American Medical Association. Charts and tables have been inserted
wherever they were needed to elucidate the text, but after mature
reflection it was felt necessary to omit all illustrations that were
not imperatively required, although many original drawings and
paintings of high value were offered with the articles.
THE EDITOR.
OCTOBER, 1884.
CONTENTS OF VOL. I.
PAGE
PREFACE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
GENERAL PATHOLOGY AND SANITARY SCIENCE.
GENERAL MORBID PROCESSES. By REGINALD H. FITZ, M.D. . . . . . . . 35
GENERAL ETIOLOGY, MEDICAL DIAGNOSIS, AND PROGNOSIS. By HENRY
HARTSHORNE, M.D., LL.D. . . . . . . . . . . . . . . . . . . . . 125
HYGIENE. By JOHN S. BILLINGS, A.M., M.D., LL.D. (Edin.) . . . . . 173
DRAINAGE AND SEWERAGE IN THEIR HYGIENIC RELATIONS. By GEORGE E.
WARING, JR., M. Inst. C.E. . . . . . . . . . . . . . . . . . . 213
GENERAL DISEASES.
SIMPLE CONTINUED FEVER. By JAMES H. HUTCHINSON, M.D. . . . . . . 231
TYPHOID FEVER. By JAMES H. HUTCHINSON, M.D. . . . . . . . . . . . 237
TYPHUS FEVER. By JAMES H. HUTCHINSON, M.D. . . . . . . . . . . . 338
RELAPSING FEVER. By WILLIAM PEPPER, M.D., LL.D. . . . . . . . . . 369
VARIOLA. By JAMES NEVINS HYDE, M.D. . . . . . . . . . . . . . . . 434
VACCINIA. By FRANK P. FOSTER, M.D. . . . . . . . . . . . . . . . 455
VARICELLA. By JAMES NEVINS HYDE, M.D. . . . . . . . . . . . . . . 481
SCARLET FEVER. By J. LEWIS SMITH, M.D. . . . . . . . . . . . . . 486
RUBEOLA. By W. A. HARDAWAY, A.M., M.D. . . . . . . . . . . . . . 557
ROTHELN. By W. A. HARDAWAY, A.M., M.D. . . . . . . . . . . . . . 582
MALARIAL FEVERS. By SAMUEL M. BEMISS, M.D. . . . . . . . . . . . 589
PAROTITIS. By JOHN M. KEATING, M.D. . . . . . . . . . . . . . . . 620
ERYSIPELAS. By JAMES NEVINS HYDE, M.D. . . . . . . . . . . . . . 629
YELLOW FEVER. By SAMUEL M. BEMISS, M.D. . . . . . . . . . . . . . 640
DIPHTHERIA. By ABRAHAM JACOBI, M.D. . . . . . . . . . . . . . . . 656
CHOLERA. By ALFRED STILLE, M.D., LL.D. . . . . . . . . . . . . . 715
PLAGUE. By JAMES C. WILSON, A.M., M.D. . . . . . . . . . . . . . 771
LEPROSY. By JAMES C. WHITE, M.D. . . . . . . . . . . . . . . . . 785
EPIDEMIC CEREBRO-SPINAL MENINGITIS. By A. STILLE, M.D., LL.D. . . 795
PERTUSSIS. By JOHN M. KEATING, M.D. . . . . . . . . . . . . . . . 836
INFLUENZA. By JAMES C. WILSON, A.M., M.D. . . . . . . . . . . . . 851
DENGUE. By H. D. SCHMIDT, M.D. . . . . . . . . . . . . . . . . . 879
RABIES AND HYDROPHOBIA. By JAMES LAW, F.R.C.V.S. . . . . . . . . 886
GLANDERS AND FARCY. By JAMES LAW, F.R.C.V.S. . . . . . . . . . . 909
ANTHRAX (MALIGNANT PUSTULE). By JAMES LAW, F.R.C.V.S. . . . . . . 926
PYAEMIA AND SEPTICAEMIA. By B. A. WATSON, A.M., M.D. . . . . . . 945
PUERPERAL FEVER. By WILLIAM T. LUSK, M.D. . . . . . . . . . . . . 984
BERIBERI. By DUANE B. SIMMONS, M.D. . . . . . . . . . . . . . . . 1038
INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1045
CONTRIBUTORS TO VOL. I.
BEMISS, SAMUEL M., M.D.,
Professor of Theory and Practice of Medicine and Clinical Medicine
in the University of Louisiana, New Orleans.
BILLINGS, JOHN S., A.M., M.D., LL.D. (Edin.),
Surgeon U.S. Army, Washington.
FITZ, REGINALD H., M.D.,
Shattuck Professor of Pathological Anatomy in Harvard University,
Boston.
FOSTER, FRANK P., M.D.,
New York.
HARDAWAY, W. A., A.M., M.D.,
Professor of Diseases of the Skin in the St. Louis Post-Graduate
School of Medicine and in the Missouri Medical College, St.
Louis; President of the American Dermatological Association.
HARTSHORNE, HENRY, M.D., LL.D.,
Late Professor of Hygiene in the University of Pennsylvania,
Philadelphia.
HUTCHINSON, JAMES H., M.D.,
Physician to the Pennsylvania Hospital and to the Children's
Hospital, Philadelphia.
HYDE, JAMES NEVINS, M.D.,
Professor of Skin and Venereal Diseases in the Rush Medical
College, Chicago.
JACOBI, ABRAHAM, M.D.,
Clinical Professor of Diseases of Children in the College of
Physicians and Surgeons, New York, etc.
KEATING, JOHN M., M.D.,
Visiting Obstetrician and Lecturer on Diseases of Women and
Children to the Philadelphia (Blockley) Hospital; Surgeon to the
Maternity Hospital; Physician to St. Joseph's Hospital,
Philadelphia.
LAW, JAMES, F.R.C.V.S.,
Professor of Veterinary Science in Cornell University, Ithaca,
N.Y.
LUSK, WILLIAM T., M.D.,
Professor of Obstetrics and Diseases of Women and Children in the
Bellevue Hospital Medical College, New York.
PEPPER, WILLIAM, M.D., LL.D.,
Provost and Professor of the Theory and Practice of Medicine and
of Clinical Medicine in the University of Pennsylvania,
Philadelphia.
SCHMIDT, H. D., M.D.,
Pathologist to the Charity Hospital, New Orleans.
SIMMONS, DUANE B., M.D., Yokohama, Japan,
Late Director, Physician, and Surgeon-in-Chief of the Government
Hospital, also Consulting Surgeon to Prison and Police Hospitals
at Yokohama, Japan.
SMITH, J. LEWIS, M.D.,
Clinical Professor of Diseases of Children in the Bellevue
Hospital Medical College, New York.
STILLE, ALFRED, M.D., LL.D.,
Emeritus Professor of Theory and Practice of Medicine in the
University of Pennsylvania, Philadelphia.
WARING, GEORGE E., JR., M. Inst. C.E.,
Engineer of Sanitary Drainage, Newport, R.I.
WATSON, B. A., A.M., M.D.,
Surgeon to the Jersey City Charity, St. Francis, and Christ
Hospitals, Jersey City, N.J.
WHITE, JAMES C., M.D.,
Professor of Dermatology in Harvard University, Boston.
WILSON, JAMES C., A.M., M.D.,
Physician to the Jefferson Medical College Hospital and to the
Philadelphia Hospital, Philadelphia.
ILLUSTRATIONS.
FIGURE PAGE
1. MICROCOCCI . . . . . . . . . . . . . . . . . . . . . . . . . 142
2. BACTERIA . . . . . . . . . . . . . . . . . . . . . . . . . . 142
3. BACILLUS MALARIAE . . . . . . . . . . . . . . . . . . . . . . 143
4. BACTERIA FROM GELATIN SOLUTION . . . . . . . . . . . . . . . 143
5. VIBRIOS IN GELATIN CULTURE-FLUID . . . . . . . . . . . . . . 144
6. PROTOCOCCUS FROM SLIDES EXPOSED OVER SWAMP-MUD . . . . . . . 144
7. BACILLI FROM SWAMP-MUD . . . . . . . . . . . . . . . . . . . 145
8. BACILLI FROM SEPTICAEMIC RABBIT . . . . . . . . . . . . . . . 145
9. BACILLI FROM HUMAN SALIVA . . . . . . . . . . . . . . . . . . 146
10. BACILLUS ANTHRACIS . . . . . . . . . . . . . . . . . . . . . 146
11. BACILLUS TUBERCULOSIS . . . . . . . . . . . . . . . . . . . . 147
12. CHART OF TYPICAL RANGE OF TEMPERATURE IN TYPHOID FEVER, AFTER
WUNDERLICH . . . . . . . . . . . . . . . . . . . . . . . . 282
13. CHART SHOWING RECRUDESCENCE OF FEVER FROM INDISCRETION OF
DIET. . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
14. CHART SHOWING FALL OF TEMPERATURE FROM INTESTINAL HEMORRHAGE
IN TYPHOID FEVER . . . . . . . . . . . . . . . . . . . . . 284
15. PULSE-TRACING IN RELAPSES OF TYPHOID FEVER . . . . . . . . . 304
16. CHART OF TEMPERATURE IN TYPHOID FEVER WITH RELAPSE.--ORIGINAL
ATTACK . . . . . . . . . . . . . . . . . . . . . . . . . . 306
17. CHART OF TEMPERATURE IN TYPHOID FEVER WITH RELAPSE.--RELAPSE 306
18. TEMPERATURE CHART OF TYPHOID FEVER.--ABORTIVE ATTACK,
FOLLOWED BY TYPICAL ATTACK . . . . . . . . . . . . . . . . 308
19. SPIRILLUM FROM THE BLOOD IN A CASE OF RELAPSING FEVER . . . . 374
20. TEMPERATURE CHART OF TYPICAL CASE OF RELAPSING FEVER, WITH
THREE RELAPSES TERMINATING IN RECOVERY . . . . . . . . . . 379
21. TEMPERATURE CHART OF TYPICAL CASE OF RELAPSING FEVER,
TERMINATING IN RECOVERY . . . . . . . . . . . . . . . . . . 380
22. TEMPERATURE CHART FROM A CASE OF THE BILIOUS TYPHOID OR GRAVE
SUBINTRANT FORM OF RELAPSING FEVER . . . . . . . . . . . . 397
23. TEMPERATURE CHART SHOWING THE LAPSE OF A REMITTENT FEVER INTO
AN INTERMITTENT . . . . . . . . . . . . . . . . . . . . . . 600
24. CHARTS SHOWING THE TEMPERATURE CURVE IN TYPHO-MALARIAL FEVER:
PART I., SHOWING PREDOMINANCE OF TYPHOIDAL ELEMENT;
PART II., SHOWING PREDOMINANCE OF MALARIAL ELEMENT . . . . 617
GENERAL PATHOLOGY.
GENERAL MORBID PROCESSES.
GENERAL ETIOLOGY.
HYGIENE AND QUARANTINE.
DRAINAGE AND SEWERAGE IN RELATION TO THE PREVENTION OF DISEASE.
{35}
GENERAL MORBID PROCESSES.[1]
INFLAMMATION; THROMBOSIS AND EMBOLISM; EFFUSIONS; DEGENERATIONS;
TUBERCULOSIS; MORBID GROWTHS.
BY REGINALD H. FITZ, M.D.
[Footnote 1: In the preparation of this subject full and free use has
been made of the following works: _Die Cellular Pathologie_, Virchow,
4te Auflage, Berlin, 1871; _Handbuch der Allgemeinen Pathologie_, Uhle
und Wagner, 7te Auflage, Leipzig, 1876; _Handbuch der Allgemeinen
Pathologie als Pathologische Physiologie_, Samuel, Stuttgart, 1879;
_Vorlesungen uber Allgemeine Pathologie_, Cohnheim, 2te Auflage,
Berlin, 1882; _Lehrbuch der Pathologischen Anatomie_,
Birch-Hirschfeld, 2te Auflage, 1er Band, Leipzig, 1882; _Lehrbuch der
Allgemeinen und Speciellen Pathologischen Anatomie_, Ziegler, 1er und
2er Theil, Jena, 1882 and 1883.]
GENERAL MORBID PROCESSES.
Disease is to be regarded as representing the result of a series of
processes called morbid or pathological, from the fact that they are
manifested by disturbances in the organism.
The processes concerned are the same in kind as those essential to
health, but they are modified in time, place, or quantity.
Morbid processes, therefore, are to be considered as modified
physiological processes tending to cause disease.
All physiological processes are subject to certain variations which
tend to produce disturbances in the functions of the body. In the
healthy organism this tendency is checked by the automatic regulators
of the functional activity of the various organs, to the importance of
which Virchow[2] long ago called attention. By their action the
influence of external agents is controlled within certain limits. The
lids close and prevent injury to the eye. Sneezing, coughing, and
vomiting bring about the expulsion of noxious irritants. Sweating aids
in neutralizing the injurious effects of exposure to high
temperatures. Rapid respiration permits a sufficient cleansing of the
blood in rarefied atmospheres. When the limits, within which the
regulation of physiological processes is possible, are exceeded, such
processes become pathological and disease begins. A morbid process,
therefore, is usually incapable of recognition till disease is
present. It may exist and disease be unsuspected and denied. A
diminished blood-supply may be one link in the process which
eventually leads to the production of disturbances. {36} Another link
is to be found in the fatty degeneration resulting from this lack of
blood.
[Footnote 2: _Handbuch der Speciellen Pathologie und Therapie_,
Virchow, 1er Band, p. 15, Erlangen, 1854.]
Such a degeneration may have long existed in the walls of a
blood-vessel, and yet the individual appear in the best of health. The
sudden rupture of the weakened wall results in death or disease. With
the manifestation of the disturbances which render the condition of
the vessel obvious the individual is said to be diseased.
In most instances, however, the morbid process makes itself early
apparent. Disturbances of nutrition, formation, or function soon
become sufficient in quantity to attract attention from the resulting
discomfort, and the presence of disease is then recognized. The latter
is thus essentially a conventional term, and begins when the morbid
processes occasion a sufficient degree of inconvenience.
The process is never at a standstill. It either tends toward a return
to the physiological conditions, or its course is in the direction of
their destruction. As physiological processes are absolutely dependent
upon the vitality of the elements of the tissues, so those which have
become pathological cease to exist with the death of such elements. In
the dead body there is no disease, although its results remain, and
furnish the most efficient means of identifying the processes which
occasioned them.
In the study of morbid processes, therefore, one must appreciate the
normal conditions and manifestations of life in the individual.
Physiological laws govern pathological phenomena, and the latter must
always be submitted to the tests furnished by the former.
Just as little, however, as the study of anatomy familiarizes the
student with the anatomical changes resulting from diseased processes,
does the study of physiology accustom the student to the features of
disease. Pathological processes must be studied by themselves and for
themselves, although the means which are employed may be the same as
those used in physiological research.
It is evident that the exactness of method which is the demand of the
physiological investigator cannot be secured by the pathologist. The
material of the latter lies farther, beyond his control. Nevertheless,
much of the ground to be gone over is common, and the object sought
for is essentially the same--the knowledge of the conditions necessary
to maintain life.
In an introduction to the study of disease there are certain processes
which deserve early recognition. They are both the cause and the
result of disease, and may occur in various diseases, either limited
to one organ or present in a series of organs. Their treatment at
present obviates the necessity of repetition, and prepares the reader
for the special consideration of their occurrence in the various
structures and systems of the body.
These processes are named in virtue of some prominent characteristic,
and each is made up of a complex series of conditions and
disturbances. In part, they represent modifications in the circulation
of blood and lymph; in part, they consist of nutritive derangements,
whose consequences appear as the various degenerations, or as the
additions to the body, the new formations.
The processes and groups of processes in question are those included
under the following heads: inflammation; thrombosis and embolism;
effusions; degenerations; tuberculosis; and morbid growths.
{37} Inflammation.
Inflammation is characterized now, as in the time of Galen, by the
presence of redness, heat, swelling, and pain. The disturbance of
function, added to modern definitions, is to be regarded either as a
result or a cause, or both, of the variously modified physiological
processes whose sum is the inflammation.
The redness of inflammation is obviously dependent upon the presence
of an increased quantity of blood. This is readily apparent in the
direct observation of the blood-vessels of an inflamed, transparent
part of the body, as the mesentery of the frog or rabbit, or the
tongue and webbed foot of the former animal. The redness of
inflammation consequently demands the presence of blood-vessels in the
affected region, and becomes all the greater the more vascular the
part--_i.e._ the richer it is in such vessels.
Redness does not suffice for the existence of inflammation, for it may
be found in the absence of other evidence of the latter. The diffused
redness, often extensive, of birth-marks, that from venous obstruction
or temporary congestions, from vaso-motor disturbances--the section of
the sympathetic furnishing a well-known instance--are examples of
non-inflammatory redness. Inflammation may even be present without
redness, as may be constantly observed in the occurrence of
parenchymatous inflammation and of the chronic interstitial varieties.
The heat of inflammation is one of the most important clinical
features, yet not indispensable, as appears from its absence in
chronic interstitial forms of inflammation. In the acute varieties of
inflammation an elevated temperature is constant, and its observation
and record furnish a most valuable means of determining the beginning
and progress of an inflammation, which, for a time, may furnish but
little additional evidence.
The heat of inflammation is the prominent characteristic of
inflammatory fever, and it is the study of this variety of fever of
late years which has resulted in an intelligible and relatively
satisfactory theory concerning fevers in general. Information of much
value is to be found in the recent work of Wood,[3] which contains
abundant historical information, as well as extensive original
observations and conclusions.
[Footnote 3: _Fever: A Study in Morbid and Normal Physiology_, H. C.
Wood, A.M., M.D., Philadelphia, 1880. (Reprint from the _Smithsonian
Contributions to Knowledge_, No. 357.)]
Inflammatory fevers are distinguished from idiopathic forms. The
latter variety includes the occurrence of fever as an attribute of the
disease concerned, the more characteristic symptoms of which follow
the febrile outbreak. Local inflammatory processes may take place
during the progress of the disease with its fever, but such processes
are co-effects of the cause of the latter, rather than its cause. Most
of those diseases in which fever occurs as one of the joint effects of
the cause of the disease, are included among the infective or zymotic
classes.
The inflammatory fevers are those attending an acute inflammatory
process, and are secondary to, and occasioned by, the latter. The type
of this variety is seen in the fever occurring during the progress of
a wound, whether its course is toward healing or extension. Such {38}
traumatic fevers are characterized as septic or aseptic; the former
including the conditions of septicaemia and pyaemia. The aseptic
traumatic fevers, as described by Volkmann,[4] are those which pursue
their course with an elevated temperature, but without most of the
other febrile phenomena.
[Footnote 4: _Beitrage zur Chirurgie_, Leipzig, 1875, p. 24; _Sammlung
Klinischer Vortrage_, No. 121, Genzmer und Volkmann.]
Fever in general is characterized by a combination of disturbances in
the physiological processes of the body. Such processes are those
concerned in the production and dissipation of heat, in respiration
and circulation, digestion and secretion, and in mental, motor, and
other sensorial action. Such disturbances are manifested by a
persistent elevation of temperature, an increased destruction of
tissue, a quickened and modified pulse, accelerated breathing,
increased thirst, diminished appetite, and diminished quantity and
altered quality of the secretions. The sensorial disturbances include
wakefulness and stupor, headache, delirium, twitchings, cramps, and
other symptoms indicative of functional impairment of the nervous
system.
Of all these manifold evidences of fever, the elevation of temperature
is the one whose cause, range, and results have been most carefully
and critically investigated. No record of a case in which fever is
present is regarded as complete without the chart of the daily
variations in temperature, respiration, and circulation. The practical
value of such records is thus admitted, and in the experiments
relating to the origin of animal heat the observations of temperature
are as essential as the chemical analyses, each of which supplements
the other.
The more accurate determination of the heat produced in the body is
obtained either by the use of the calorimeter (an apparatus for
measuring the collected heat liberated from the body) or by estimating
the quantity of heat produced in the destruction of the constituents
of the body from quantitative analyses of the discharged carbonic acid
and urea. The results of such investigations are regarded by
Rosenthal[5] as possessing only a relative value, but justify the
conclusion that most of the heat produced in the organism results from
the oxidation of its constituents.
[Footnote 5: _Hermann's Handbuch der Physiologie_, Leipzig, 1882, iv.
2, 375.]
For the preservation of health it is essential that this heat should
be removed from the body in such quantity that the temperature of the
latter shall not vary to any considerable extent, for any considerable
time, from 37.2 degrees C. (98.4 degrees F.). The removal of the heat
is mainly accomplished by its radiation or conduction into a
surrounding cooler medium, and by the evaporation of moisture from the
surface of the body. Too great a removal of heat results in death from
freezing, while too great an accumulation of heat terminates fatally
from the effects of an unduly elevated temperature. To ensure the
normal range of temperature, constantly changing relations must exist
between the production of heat and its dissipation. The cooler the
surroundings, the more must heat be produced, or the less must heat be
evolved from the body.
An increased production of heat is obvious under conditions of climate
demanding prolonged exposure to low temperature. An abundantly fatty
diet promotes the formation of heat, while suitable clothing checks
its dissipation. Although it is claimed by Liebermeister that sudden
exposure to cold stimulates heat-production, Rosenthal[6] disputes
this {39} statement, and maintains that it is still to be regarded as
doubtful whether the production of heat can be varied to suit the
demands of sudden and temporary changes of temperature. With the
admission of this doubt, the regulation of the temperature of the
body, under the circumstances just referred to, is mainly accomplished
through the influence of agencies favoring or checking the loss of
heat. Since heat is largely brought to the surfaces of the body by the
circulating blood, modifications in the fulness and rapidity of this
superficial current produce corresponding differences in the amount of
heat and moisture presented. Such variations are considered to be
accomplished through the action of the vaso-motor nervous system,
whose differing effects are apparent in the pale, cool skin and the
flushed, warm surface.
[Footnote 6: _Op. cit._, 413.]
The search for the regulation of such vaso-motor action has led to the
view that the production of heat, as well as its dissipation, may be
influenced from a nervous centre. Wood[7] claims that the result of
experiments made by him proves the existence of such a heat-centre in
or above the pons. Although admitting the possibility of its being a
muscular vaso-motor centre, he regards it rather as an inhibitory
heat-centre, which acts, as suggested by Tscheschichin, by repressing
the chemical changes in the constituents of the body through which
heat is produced.
[Footnote 7: _Op. cit._, 254.]
This view is objected to by Rosenthal,[8] on the ground that the facts
are not universally agreed upon, and their interpretation is somewhat
vague. Even the increased production of heat as determined by Wood, if
admitted, may be regarded as the result of a modified circulation.
[Footnote 8: _Op. cit._, 442.]
The preservation of a normal range of temperature in general is to be
recognized as the result of variations in the relation of
heat-production to heat-dissipation. The causes which influence this
relation may act from without or from within, and are regarded as
producing their effect by means of the vaso-motor nervous system. The
causes which act from within are those concerned in the febrile
elevation of temperature. Whether the latter is associated with, or
independent of, inflammatory processes, the question of first
importance relates to the modification of physiological conditions.
The causes of the physiological production of heat and its dissipation
have already been referred to, and the same elements demand
consideration in the pathological range of temperature so striking in
fever.
Relatively accurate inductions with regard to the origin of febrile
heat were first rendered possible by the experiments of Billroth and
Weber. These observers found that the introduction of putrid material
into the circulation of animals produced fever. It was afterward shown
that various substances, not necessarily of a putrid character, might
produce the same result.
From measurements with the calorimeter of the heat produced, it was
concluded by Wood[9] that in the fever of pyaemic dogs more heat was
produced than in healthy, fasting dogs, although less than in
high-fed, healthy dogs. An increased production of heat in the fevered
animal is thus obvious, as his capacity to receive and assimilate food
is considerably less than that of a high-fed, healthy dog. The
calculations of Sanderson, referred to by Wood,[10] based upon the
analyses of eliminated carbonic {40} acid and urea, show that the
febrile human subject produces very much more heat than the fasting,
though less than the fully-fed, healthy, man.
[Footnote 9: _Op. cit._, 236.]
[Footnote 10: _Op. cit._, 239.]
An increased production of heat in fever is generally admitted,
although it alone is not to be regarded as the essential feature in
the elevated range of the temperature. The fasting man or animal under
ordinary circumstances is not febrile, and an increased production of
heat from full feeding in health, equal to that observed in fever, not
being associated with fever, it is apparent that the retention of the
produced heat is of importance for the existence of fever. Although it
has been shown by various observers that more heat is dissipated
during fever than in health, this increased loss is not in proportion
to the increased production of heat. A persistent elevation of
temperature is the necessary result. This elevation is subject to
daily and hourly differences, as is the temperature of the healthy
individual. These variations in the range of the febrile temperature
are apparently due to an agency like that which dominates the course
of normal temperatures--viz. a varying action of the vaso-motor
nervous apparatus, as well as of that controlling the secretion of
sweat, now permitting, now checking, the dissipation of the produced
heat.
For the existence of the elevated temperature of fever, therefore,
there is demanded the presence of an agent within the body which, as
stated by Wood,[11] shall act "upon the nervous system which regulates
the production and dissipation of animal heat--a system composed of
diverse parts so accustomed to act continually in unison in health
that they become, as it were, one system and suffer in disease
together." It may be that there exists, as claimed by Wood and
Tscheschichin, a heat-centre independent of the vaso-motor and other
centres, through which heat is dissipated, or it may be, as maintained
by Rosenthal, that the vaso-motor system alone is concerned in the
regulation of temperature. Such action may be inhibitory or excitant,
according to the views of the one or the other author, without
affecting the main question as above stated.
[Footnote 11: _Op. cit._, 255.]
The elevation of temperature suffices to explain for the most part
certain of the other phenomena of fever, as thirst, digestive
disturbances, increased respiration, and emaciation. A coincident
affection of various cerebro-spinal centres is demanded to explain the
altered action of the heart and the numerous nervous symptoms which
are to be found in fever. The agent producing such manifold effects is
obviously no unit. It may be introduced from without or it may arise
within the body, and its transfer to the nervous centres is
undoubtedly accomplished through the circulation.
Among those agents which act from without are to be included the
specific causes of infective diseases. It is probable that these
produce the fever, as they occasion other symptoms of the disease, and
their action may be regarded as direct, or indirect through the
secondary products of their own vital changes. In the light of the
existing facts the products of minute organisms developed outside the
human body may give rise to fever when introduced, without the
organism, into the body. The history of septicaemia contains numerous
illustrations of the pyrogenetic properties of material produced in
connection with wounded surfaces of the body exposed to the action of
minute organisms. The introduction of blood of the same, or of a
different animal, into the {41} circulation of a given animal is
followed by fever, as is the injection of considerable quantities of
water into the blood-vessels. The same is true of various chemical
substances.
It is further obvious that the agents producing fever may arise within
the body. The fever resulting from the deprivation of water, and from
the destruction of tissues, are instances of the probable origin of
pyrogenetic substances from the rapid metamorphosis of tissues.
It is suggested by Samuel[12] that under given circumstances the fever
may be sanatory. This view is based upon the probability that certain
parasitic organisms are destroyed at such temperatures as may be
produced within the body. The growth of the bacillus of malignant
pustule takes place most vigorously at a temperature of 30.5 degrees
C. (95 degrees F.), while its development is feeble at 40 degrees C.
(104 degrees F.). The bacillus of tuberculosis, as shown by Koch,
thrives at temperatures between 37 degrees C. (98.6 degrees F.) and 38
degrees C. (100.4 degrees F.), but its growth ceases at temperatures
above 41 degrees C. (105.8 degrees F.). The spiral fibre of relapsing
fever, which is present in the blood in great abundance at the
beginning of the febrile onset, disappears at the close, the
temperature being 42 degrees C. (107.6 degrees F.). It is not to be
found in the intervals between the febrile paroxysms, but reappears a
few hours before the recurrence of the fever. The history of
intermittent fever suggests a similar relation between its cause and
the febrile periods.
[Footnote 12: _Op. cit._, 155.]
The value of pain as evidence of inflammation is merely relative. Its
existence depends upon the presence of sensitive nerves, and those
inflammations are the least painful which occur in parts where such
nerves are fewest.
The pain of inflammation is attributable to the pressure upon the
nerves of that product of the inflammation known as the exudation.
This pressure becomes all the greater the more abundant the exudation,
or the greater the obstruction offered to its diffusion throughout the
inflamed part. The intense pain resulting from inflammation of the
fascia or of the periosteum is thus explained, while an inflammation
of the loose connective tissue may be diffused over a wide area with
little or no pain. In the chronic varieties of inflammation, where the
exudation is but scanty, and its accumulation extended over a long
period of time, there may be no pain during the entire course of the
inflammation.
Swelling remains for consideration as the most important of the four
cardinal symptoms. Like the others, its presence is not absolutely
essential. It may exist at one time in the course of the inflammation,
and may be absent at another. Even a diminution in the size of an
organ may suggest the existence of an inflammation, for the yellow and
cirrhotic atrophies of the liver give evidence, respectively, of an
acute and chronic inflammation of this organ.
The swelling of an inflamed part is due to the presence of an
increased quantity of blood, and lymph, and to the exudation. These
constituents of the swelling are not of equal importance. Although the
quantity of blood in the part is increased, no considerable swelling
is produced, provided the flow of blood and lymph from the part be
unobstructed. The current of lymph through the larger lymphatics may
be greatly increased, yet a decided swelling be absent, unless there
is an obstruction to the passage of lymph from the inflamed region.
{42} The exudation is the most essential element of the swelling, and
our knowledge of its origin and fate includes the most important
features of the general pathology of the processes concerned.
The inflammatory exudation is represented by the accumulation, outside
the blood-vessels, of material previously within them. The prevailing
views concerning the manner of origin of this exudation, and its
relation to inflammatory processes, are essentially due to the
rediscovery by Cohnheim of the forgotten observation of Addison, that
white blood-corpuscles pass through the apparently intact walls of the
blood-vessels.
In the observation of the mesentery or other transparent part of a
suitable animal, the changes taking place in inflammation are, at the
outset, limited to the blood-vessels and their immediate vicinity. The
vessels become dilated and the rapidity of the flow within them is
soon diminished. In the veins particularly the white blood-corpuscles
separate in considerable numbers from the general current and line the
wall in constantly-increasing numbers, while the red corpuscles are
borne along the middle of the stream. The white corpuscles stagnate,
stick to the wall for a longer or shorter time, and often change their
place, while the red corpuscles are in constant and progressive
motion. In the capillaries a considerable number of white corpuscles
are found in contact with the wall, but numbers of red corpuscles are
associated with them. The formation of the exudation now begins by the
passage of white corpuscles through the apparently intact wall of the
veins and capillaries, especially of the former. Limited numbers,
under ordinary circumstances, of red corpuscles also make their way
through the walls of the capillaries. This is the phenomenon of
emigration, and is associated with the amoeboid movements of the white
corpuscles.
With the passage outward of the white and red corpuscles there is also
the effusion of liquid material. Both the liquid and solid
constituents continually escape and spread in all directions beyond
the wall, following the course of the least resistance. It is probable
that this course is defined by the pre-existing spaces within the
tissues of the part, the lymph-spaces. The exudation is more abundant
in parts richly provided with blood-vessels and in those containing
the larger spaces; it is diminished where the vessels are less
numerous or the surrounding parts more resistant, with smaller and
fewer lymph-spaces. The resulting swelling is the less when ready
opportunities for the diffusion and removal of the exudation by
lymphatics and veins are presented, and when the material appears upon
surfaces over which it may flow away.
The liquid portion of the exudation represents something more than the
transuded blood-serum, and a certain practical importance results from
the distinction drawn between an exudation and a transudation. Such a
distinction is especially called for when the inflammatory or
non-inflammatory origin of considerable quantities of fluid in the
larger cavities of the body is concerned. From a recent contribution
to our knowledge of this subject by Reuss[13] the following
information is derived: The percentage of albumen is always greater in
exudations than in transudations, and is more constant in the former
than in the latter. It increases with the severity of the
inflammation, being highest in the ichorous forms, less in the
purulent, and least in the serous exudations. When an {43}
inflammatory exudation is found to contain less albumen than usual,
the existence of a transudation with secondary inflammation is
suggested, or the exudation may have taken place in a hydraemic
individual. A sufficient number of exceptions are met with, however,
to interfere with the absolute nature of this test.
[Footnote 13: _Deutsches Archiv fur Klinische Medicin_, 1879, xxiv.
583.]
The coagulation of an inflammatory exudation apparently depends upon
the contained white blood-corpuscles; the more numerous (within
certain limits) these are in a serous exudation, the more abundant is
the formation of fibrin. The cellular element likewise is that which
in abundant liquid exudations characterizes them as purulent. Although
it is generally agreed that most of the corpuscles of pus are
emigrated white blood-corpuscles, it is not necessary to admit that
all are of this nature. The cells present in an inflamed part include
those pre-existing, as well as those which escape from the vessels.
The former are the wandering cells of the connective tissues, as well
as the fixed variety, the epithelial cells of the surface of a mucous
membrane in addition to the subjacent connective-tissue cells.
Amoeboid cells outside the blood-vessels have been seen to divide, and
it is possible that such duplication may serve as the method of
formation of a certain number of pus-corpuscles. The statements
concerning the proliferation of the fixed connective-tissue cells and
of epithelium are derived from appearances, and are interpretations of
these appearances, not observations of a process.
The changes taking place along the walls of the blood-vessels being
the feature of prime importance in the observation of the progress of
an inflammation, numerous investigators have directed their attention
to the determination of the nature of the changes in the vessel wall
by means of which the escape of the corpuscles is permitted. Arnold
represents the most strenuous advocates of the stomata theory,
according to which the leucocytes pass through canals normally
existing in the wall. By means of the silver method of staining, and
by injections of various insoluble pigments into the blood-current,
certain results are met with, which give color to the view that pores
and canals are present upon and in the walls of the vessels, analogous
to those found in the diaphragm. As the latter have been shown to be
in direct communication with the lymphatic system of tubes and spaces,
so the walls of the blood-vessels have been assumed to present similar
channels of communication.
The prevailing views at the present time are in favor of the
artificial nature of the stomata and pores in the walls of the
blood-vessels. An increased porosity of the vascular wall in
inflammation is necessary for the occurrence of the exudation, but
such porosity is regarded rather as a physical condition permitting an
observable filtration, and a filtration of solids as well as liquids.
In this connection reference should be made to the observation of
Winiwarter, who has demonstrated that colloid material, a solution of
gelatin, passes through the vascular wall in inflammation more
readily--_i.e._ under less pressure--than through the normal wall of
the blood-vessel.
The causes of inflammation are to be regarded as those which produce
an increased porosity of the vessel wall without causing its death,
for no exudation escapes from a dead vessel, its contents becoming
clotted.
These causes may act from without or from within, primarily affecting
{44} the tissues outside the vessels, or exerting their action, at the
outset, upon the wall itself. The usual histological relation of
vessels and surrounding tissues is such that both are simultaneously
affected. The occurrence of an inflammation in non-vascular parts,
however, as the cornea, from irritation of its centre, the part
farthest removed from the surrounding blood-vessels, shows that the
affection of the vessels may be indirect as well as direct. This
indirect action is to be regarded as taking place through the agency
of nerves or through that of the nutritive currents. That nervous
influence alone does not suffice to transmit the effect of an applied
cause is apparent from the absence of inflammation of the cornea which
has become anaesthetized by section of the trigeminus nerve. With the
protection of the cornea from external irritation there is an absence
of inflammation.
The consideration of the final symptom of inflammation, the
disturbance of function, which has been added in recent times, belongs
to special rather than general pathology. It varies according to the
seat of the inflammation, the disturbed function of the brain or heart
differing from that of the liver or kidney. The clinical importance of
this symptom of inflammation is greater than of all the rest, as it is
the one whose presence is constant and indispensable.
An inflammation may exist, as already stated, without heat, redness,
or pain. The swelling may escape observation from the limited quantity
of the exudation and other causative agents, or from the
inaccessibility of the inflamed part to physical examination. The
disturbance of function, however, becomes early apparent, and is
present throughout the course of the inflammation. A knowledge of its
nature enables the seat of the latter to be recognized, and its
variations furnish a desired test of the efficiency of therapeutic
agents.
* * * * *
The causes of inflammation may be divided into the traumatic, toxic,
parasitic, infectious, dyscrasic or constitutional, and trophic.
The traumatic causes are those which act mechanically, producing an
injury to tissues by pressure, crushing, tearing, stretching, and the
like. Others represent modifications in temperature, thermic agencies,
and include extremes of cold as well as of heat. The chemicals whose
action is direct, as caustic, include a third variety of the traumatic
causes. Such chemicals are applied to surfaces, cutaneous or mucous,
and comprise the active element producing the perforating ulcer of the
stomach and duodenum, as well as such substances as potash or
sulphuric acid which may have been swallowed intentionally or
accidentally.
The toxic group of causes is closely allied to the chemical variety of
the traumatic agencies. It includes chemicals whose action is
indirect, through absorption in a diluted form rather than from direct
application in a concentrated condition. Such chemicals are derived
from without, as arsenic, phosphorus, and antimony; or may be formed
within the body, and the latter include the chemical products of
putrefactive changes--in the urine, for instance--and, with
considerable probability, certain of the active agents of
blood-poisoning in septic diseases. It is not unlikely that some of
the inflammatory affections met with among the so-called
constitutional diseases, as rheumatism and gout, may owe their origin
to the production of chemical substances within the body, excessive in
quantity if not changed in quality.
{45} The parasitic causes of inflammation are both animal and
vegetable, and act upon the surfaces of the body or within its
deeply-seated parts. Some of the animal parasites act locally at their
place of entrance, while others produce but slight disturbances in
this region, their effects usually resulting from the transfer of
their offspring to remote parts of the body. The vegetable parasites
are for the most part the various fungi, which act locally upon the
skin or on those transitional surfaces lying between skin and mucous
membrane. The resulting parasitic inflammations are known as favus,
sycosis, ringworm, thrush, etc. The border-line between such parasitic
diseases and those included among the infective diseases is somewhat
arbitrarily drawn. Parasites in the limited sense act chiefly as
foreign bodies, while the effect of minute vegetable organisms is
rather that of ferments, in virtue of their products. Such a
distinction is of relative value merely, as the micrococci and
bacteria are capable of acting in other ways than by the production of
septic material.
The infectious causes of inflammation are for the most part parasitic
in their nature, although the discovery and identification of the
parasite are in most of these inflammations assumed rather than
demonstrated. The relation of the anthrax bacillus to malignant
pustule no longer admits of a doubt, mainly in consequence of the
researches of Koch. This investigator has been enabled to establish a
definite etiological relation between the septicaemia of certain
animals and accompanying minute vegetable organisms. His recent
discovery of the bacillus of tuberculosis definitely removes the
tubercular process from the group of dyscrasic or constitutional
affections to that of the infective diseases. The constant presence of
minute organisms in relapsing fever, leprosy, malaria, typhoid fever,
diphtheria, erysipelas, and numerous other affections associated with,
if not characterized by, inflammatory conditions, renders extremely
probable the closest pathological relation between such diseases and a
microscopic organism. That an inflammatory process may be regarded of
infectious origin, it is necessary, according to Koch,[14] that a
characteristic organism should be found in all cases of the disease,
and in such numbers and distribution as to account for all the
phenomena of the disease in question.
[Footnote 14: _Untersuchungen uber die Aetiologie der
Wundinfectionskrankheiten_, 1878, 27.]
These organisms may act in virtue of their growth and the consequent
demand for oxygen, as seems probable in certain cases of malignant
pustule, where the affected individual dies with symptoms of asphyxia.
Their operation may also be like that of ferments, which produce
chemical material whose effect may be remote from the immediate
presence of the minute organism. They may likewise, in connection with
their colonization in various parts of the body, act more immediately
upon the walls of the blood-vessels, and produce that increased
porosity which is so essential a factor in inflammation.
The discovery of the immediate cause of the various infective
diseases, as measles, scarlatina, variola, cholera, dysentery, mumps,
whooping cough, cerebro-spinal meningitis, and numerous other epidemic
and endemic affections, still remains a question for the future. The
constant association of microbia with any or all of such diseases is
but one fact in connection with them, and such a discovery is to be
regarded merely as a step forward, to be followed by others, each of
which represents not only an advance, but confirms the position
attained.
{46} The dyscrasic or constitutional causes of inflammation are those
which, though long established, appear less demanded as our knowledge
advances. Regarded as the result of an alteration in the composition
of the blood, it is obvious that such changes may arise from the
introduction, from without, of wholly foreign material. The dyscrasia
may also represent modifications in the relative proportion of the
normal constituents of the blood. In the former series are included
what, for the most part, have already been referred to under the toxic
and infectious causes of inflammation. The dyscrasiae from lead,
alcohol, and the like belong to this series. Still more important are
the poisons, the virus of tuberculosis and scrofula, of leprosy and
syphilis. The dyscrasiae known as anaemia, leucaemia, uraemia,
icterus, and diabetes are to be regarded less as inflammatory causes
than as predisposing conditions which favor the action of other groups
of causes.
The trophic causes of inflammation are those whose action is supposed
to take place through the influence of nerves. Although, as has
already been stated, a faulty innervation of tissues is an important
element in favoring the action of various inflammatory causes, there
remain certain forms of inflammation where the disturbance of nervous
action seems to be the essential feature. The occurrence of an acute
peripheral gangrene soon after certain traumatic or inflammatory
lesions of the brain or spinal cord, of articular inflammation
following chronic affections of the cerebro-spinal axis, are instances
in point. The origin and distribution of herpes zoster, the occurrence
of sympathetic ophthalmia and symmetrical gangrene, suggest a
predominant disturbance of innervation as the exciting cause. At the
same time, it is desirable to call attention to the recent
observations of MacGillavray, Leber, and others,[15] which suggest
that a sympathetic ophthalmia is due to the extension of a septic
choroiditis along the lymph-spaces of the optic nerve. It is further
apparent that in certain so-called trophic inflammations, as the
pneumonia after section of the pneumogastric, and the inflammation of
the eye following paralysis of the trigeminus, the paralysis of the
nerve is a remote, rather than an immediate cause, of the
inflammation. There still remain, however, a number of localized
inflammations whose origin is so intimately connected with nervous
disturbances as to demand, for the present at least, a corresponding
classification.
[Footnote 15: Wadsworth's "Report of Recent Progress in
Ophthalmology," _Boston Medical and Surgical Journal_, 1882, cvi.
517.]
The course of an inflammation is often indicated by the predominance
of certain symptoms, which, for the most part, indicate a condition of
the individual acted upon rather than a peculiarity of the cause. The
sthenic inflammations take place in robust individuals with powerful
hearts and an abundant supply of blood. In such persons a strong
pulse, high fever, and an injection of the superficial blood-vessels
suggested, in former times, the necessity of bloodletting as the
essential therapeutic agent. The sthenic form of inflammation was most
commonly associated with pneumonia, where the obstruction to the
passage of blood through the lungs was an important cause of the
superficial injection of the blood-vessels.
The asthenic inflammations, on the contrary, are those occurring in
feeble individuals, debilitated in consequence of pre-existing
disease, exposure, or habits. A weak heart, low febrile temperature,
and {47} superficial pallor, characterize the asthenic inflammations,
which show a frequent tendency to become localized in the more
dependent parts of the body, the force of the circulation being too
feeble to overcome the effect of gravitation.
In the typhoidal inflammations are associated those symptoms which are
so prominent in the severe varieties of typhoid fever. These are the
predominant symptoms: hebetude or low, muttering delirium, picking at
the bed-clothes, involuntary evacuations, stertor, and the like. The
nervous disturbances are associated with a feeble pulse and a dusky
hue of the skin.
The constituents of an inflammatory exudation are frequently used as a
basis of classification, and characterize the inflammation from the
anatomical point of view. As the exudation is complex in its
composition, the predominant element is made use of to designate the
variety, and in doubtful cases a combined adjective indicates the
presence of the two most abundant constituents. As the exudation is
directly derived from the blood and contains serum in addition to
white and red corpuscles, the serous, purulent, and hemorrhagic
varieties of exudation naturally arise. The fibrinous and diphtheritic
inflammations relate to the presence of membranes or false membranes.
Finally, there are the productive inflammations, resulting in the new
formation of tissue, and the destructive inflammations, where losses
of substance occur.
Serous inflammations are most frequent in those parts of the body
where the structure contains the largest lymph-spaces. The so-called
serous cavities of the body offer the most favorable opportunities for
the accumulation, as well as for the exudation, of the inflammatory
product; then follow the regions of the larger lymph-spaces, according
to the size and number of the latter.
The serous inflammations may also arise from the epithelial coverings
of the body, as the cutaneous, alimentary, and respiratory surfaces.
The serous exudations of the skin are those present in vesicles,
blisters, or bullae, which owe their limitation to the resistance
offered to the spreading of the liquid inflammatory product by the
coherent epidermis. Serous inflammations of the alimentary canal may
assume a vesicular character, although, from the structure of its
mucous membrane and the macerating influence of its contents, the
vesicles are apt to be of an extremely transitory character.
The more important serous inflammations of the intestines are those
manifested by profuse watery evacuations, the extreme form of which is
to be found in cholera.
Serous inflammation of the lungs accompanies the more severe forms,
and usually represents but a limited and circumscribed affection,
associated with more abundant cellular and fibrinous products.
Serous inflammations of the peritoneum, pleura, pericardium, tunica
vaginalis, and central ventricles often give rise to the presence of
enormous quantities of fluid, whose partial removal from many of the
cavities concerned by operative measures frequently represents a most
beneficial result of treatment.
The smaller lymph-spaces of the connective tissue in various parts of
the body are the frequent seat of the inflammatory oedema, so called,
whose presence is an important indication of the direction assumed by
a {48} spreading inflammation, as well as a suggestion of the frequent
virulence of its cause.
In general, the serous inflammations are to be regarded as less severe
than other varieties, or as representing an early stage of what later
may be otherwise characterized by a change in the nature of the
products.
The purulent variety of inflammation is present when the exudation is
abundantly cellular. As has already been stated, such cells are, for
the most part, white blood-corpuscles. The purulent exudation, like
the serous variety, may appear either on surfaces, when the term
secretion is applied, or within the lymph-spaces of the connective
tissue over a considerable space, when the pus is said to be
infiltrated. When the infiltration is more circumscribed and the walls
of the affected lymph-spaces are destroyed, so that adjoining cavities
are thrown into larger holes, an abscess is present, from whose wall
pus is constantly derived, while the inflammation is progressive.
The attention of the surgeon, in particular, has been directed to the
isolation of the immediate cause of suppurative inflammation, and the
modern, antiseptic, treatment of wounds is essentially based upon the
view of the infectious origin of pus. The frequent presence of
microbia in purulent exudation where no precautions are taken to
exclude their admission, and their frequent absence or presence in
minute quantities where such precautions are taken, have suggested
that through their influence an inflammatory exudation is likely, if
not actually compelled, to become purulent.
Whether the microbia or their products are the cause of most
suppurative inflammations may be regarded as an open question. It is
generally admitted, however, that, as a rule, an inflammation becomes
purulent in consequence of the presence of an infective agent; in
other words, that most pus is of an infectious origin and possesses
infectious attributes. The labors of Lister in insisting upon the
exclusion of all possible putrefactive agencies in the treatment of
wounds have met with universal approval, and the basis of his
treatment remains fixed, although different methods have been devised
for its enforcement. His researches, and those stimulated by his work,
have resulted in the establishment of principles which affect the
whole field of theoretical as well as practical medicine.
Although most pus may be considered as due to the action of a virus
introduced from without, and capable of indefinite progressive
increase within the body, all pus is not to be regarded as of
infectious origin. There are pyrogenetic agencies, like petroleum,
turpentine, and croton oil, which, introduced into the body, produce
suppurative inflammation without the association of microbia.
A bland pus is usually in a state of beginning putrescence, so that it
is only relatively bland, and acquires extreme virulence when long
exposed to putrefactive agencies. It is possible that those agencies
producing an ichorous pus are the same or different from those present
in bland pus. The ichorous exudation contains less corpuscles than
bland pus, is more fluid, less opaque, strongly alkaline, of a
greenish color, and of offensive odor.
In hemorrhagic inflammation the exudation contains large numbers of
red blood-corpuscles. The occurrence of this form is sometimes
associated {49} with peculiarities of the cause, as is obvious from
the epidemics of hemorrhagic small-pox, measles, scarlatina, and
cerebro-spinal meningitis. It is also associated with peculiarities of
the individual, as in such epidemics all cases are not equally
hemorrhagic, and in scurvy the hemorrhages are attributable to the
abnormal conditions to which the sufferers are exposed. Hemorrhagic
exudations are also met with in those inflammations of serous surfaces
accompanying the outcropping of tubercular and cancerous or
sarcomatous growths. In all cases a hemorrhagic exudation represents a
grave complication, and when found in serous cavities has a certain
diagnostic, as well as prognostic, importance.
Fibrinous inflammations are characterized by the presence in the
exudation of considerable quantities of fibrin. As the prevailing
theory of the formation of fibrin demands fibrino-plastic as well as
fibrinogenous material, both are to be sought for in the exudation.
The latter is present in the liquid portion of the exudation; the
existence of the former, as well as that of the ferment, is dependent
upon the presence of the white blood-corpuscles. The more numerous
these, within certain limits, the more abundant the formation of
fibrin. As their death appears essential for the fibrinous
coagulation, the latter is most constantly met with in those parts of
the body where the white blood-corpuscles are quickest separated from
influences favoring their life. The farther removed they are from the
blood-vessels, the more likely is their early death. Fibrinous
exudations are therefore frequent and abundant in cellular and serous
(sero-cellular) inflammation of the great serous cavities of the body.
The clotted fibrin appears as false membrane lying upon the serous
surface, either smooth or rough, tripe-like, or as villosities
projecting above the surface, and again as bands, fibrinous adhesions,
stretching across the cavity and uniting opposed surfaces.
The frequent occurrence of fibrinous exudations on the mucous
membranes of the larynx and trachea, accompanied by the suffocative
symptoms known as croup, has led to the use of the term croupous
inflammation as synonymous with fibrinous inflammation, and its
application to various parts of the body where croupous--_i.e._
suffocative--symptoms are not in question. Croupous inflammation, when
used, is to be considered as an anatomical term, indicating merely the
production of fibrin, and, for the avoidance of confusion, it is
preferable to substitute fibrinous for croupous when such
inflammations are described.
The disease, croup, it is well known, may exist without a
croupous--that is, fibrinous--inflammation, as is familiarly
recognized in the constant use of the terms spasmodic, membranous, and
diphtheritic croup.
Fibrinous inflammation of the mucous membrane of the larger
air-passages is much more frequently met with than that of mucous
membranes elsewhere, as of the intestines, uterus, and bladder. The
pseudo-membranous inflammations of the latter tracts are more commonly
the result of the catarrhal and diphtheritic varieties than of the
fibrinous form. Fibrinous exudations on mucous surfaces, according to
Weigert, can only take place when the epithelium is destroyed. Hence
those causes which give rise to the destruction or detachment of the
epithelium are alone capable of producing a fibrinous inflammation of
mucous membranes, and a fibrinous laryngitis, trachitis, and
bronchitis may result from {50} the local application of such
irritants as steam or ammonia, as well as occur in the diseases croup
and diphtheria.
Fibrinous exudations may also be present within tissues, especially in
those whose meshes are wide, provided the essential elements of
coagulation are present. The coagulative necrosis of various organs,
to be more fully mentioned hereafter, is closely allied to fibrinous
clotting, the fibrino-plastic element being derived from the death of
the parenchymatous cells of the part.
In the existence of a fibrinous pneumonia the conditions are somewhat
analogous to those present in the fibrinous inflammation of serous
surfaces and of the areolar connective tissue. There is present an
abundantly cellular exudation, held in the place of its origin, the
cells undergoing rapid death and surrounded by a wall whose
superficial cells resemble in structure, if not in origin, the
endothelial cells lining the smaller lymph-spaces of connective
tissue, as well as the larger cavities within the same, known as
serous cavities.
The diphtheritic inflammation is no more to be confounded with the
disease diphtheria than is the fibrinous inflammation with the disease
croup. Although diphtheria owes its name to the frequent presence of
an apparent membrane, it may be said that the latter is not essential
to the existence of the former. Diphtheria, like croup, is an
affection in which various exudations may be present, and the
anatomical product alone does not suffice in all instances for the
recognition of the disease. In croup there may be a swollen mucous
membrane, with a slight superficial mucous exudation, or a more
abundant exudation of desquamated epithelium and mucus, as well as a
fibrinous false membrane. In diphtheria the same varieties of
exudation may occur, and in addition the diphtheritic exudation may
also be present. The latter, however, is not limited to the disease
diphtheria, for its presence is apparent in other mucous membranes
than that of the air-passages, and in the pharyngeal mucous membrane
in other diseases than diphtheria. A diphtheritic conjunctivitis,
enteritis, cystitis, and endometritis are recognized. The cutaneous
surfaces of the body may also furnish a diphtheritic exudation. The
diphtheritic inflammations of wounds and of variolous eruptions are
instances in point.
The characteristics of a diphtheritic inflammation are the presence
within the tissues of a clotted exudation, which is associated with a
defined swelling and death of the part. The exudation contains not
only dead leucocytes and interlacing fibres, but is also provided with
abundant granular material, much of which presents the well-known
peculiarities of microscopic organisms. The apparent false membrane is
thus dead, infiltrated tissue, which may be torn away from the
continuous unaffected tissue, leaving a raw, rough surface, but not
peeled from a comparatively smooth surface, as in other forms of
pseudo-membranous inflammation.
The frequent association of a superficial false membrane,
corresponding in area with that of the deeper-seated changes, in which
cells and fibres may be present, is to be recognized. The diphtheritic
process, however, is localized within, and not upon, the tissues
affected. The diphtheritic exudation represents a local death, a
necrosis, of the part concerned, and the result has frequently been
compared with the death consequent upon the action of a caustic.
{51} The immediate cause of a diphtheritic inflammation is now
generally attributed to the action of microbia which enter the tissue
from without, and in their growth beneath the surface produce not only
the local, but also the remote, constitutional disturbances which are
associated with a diphtheritic inflammation. The investigations of
Wood and Formad[16] point to ordinary putrefactive organisms as a
sufficient cause for the diphtheritic inflammation of diphtheria,
while other observers demand a specific organism as the exciting
cause. The occurrence of diphtheritic inflammations in various parts
of the body, in regions, as the intestine, where putrefactive
processes are constantly present, and in the bladder and uterus, where
the phenomena of putrefaction are often associated with diphtheritic
inflammation, suggest the efficacy of ordinary putrefactive agencies
in producing the latter. As all microbia found in putrefaction are not
alike, and as the properties of certain, differ from those of others,
and as our knowledge of the effects of all is but fragmentary, the
characteristics of specific germs for a diphtheritic inflammation of
one part of the body, or of all parts of the same, must still be
regarded as not proven.
[Footnote 16: _Research on Diphtheria for the National Board of
Health_, 1880, Supplement No. 7.]
Productive inflammations are those which result in the new formation
of tissues. One of the frequent products of inflammation is fibrous
tissue, which, at first abundantly cellular, later becomes more
vascular, and is finally transformed into a tissue whose fibres
predominate over its cells. This formation of a cicatricial tissue
demands further recognition when the termination of inflammation is
considered.
In a more limited sense certain inflammations are called productive
when multiple circumscribed new formations, as cancer, sarcoma,
tubercle, and the like, arise in connection with the ordinary products
of inflammation. Such new formations are of frequent occurrence in
serous membranes, and a tuberculous pericarditis or a cancerous
peritonitis, indicates that a growth of tubercles or cancerous nodules
has taken place, in addition to a more or less abundant exudation with
various proportions of serum fibrin and cells. This association of
ordinary and transitory inflammatory products with the formation of
more permanent tissues may be found within organs as well as upon
surfaces. A tubercular arachnitis or lepto-meningitis presents the
various products of an inflammation of the pia mater with an abundant
formation of tubercles. In like manner, a tubercular pneumonia, or a
tubercular nephritis suggests an association of neoplastic growth and
inflammation, in the lung and kidney. Such a relation offers a basis
for the theory in favor of the inflammatory origin of tumors, and is,
in part at least, a cause for the frequent consideration of tubercles
as mere inflammatory products, wholly cellular or cellular and
fibrous, subject to the same modifications as take place during the
course of ordinary inflammations.
Even if tuberculous and scrofulous inflammations are regarded as
inflammatory processes, modified by a specific cause and by
peculiarities of the individual, the cancerous and sarcomatous
inflammations are still to be considered as representing an
association of inflammatory disturbances and specific new formations,
the cause of the latter not being the cause of the former. As ordinary
inflammations of the regions concerned may take place in the absence
of the neoplasms, so may the {52} specific growth appear in the same
regions without anatomical or clinical evidence of inflammation.
The classification of inflammation as to its products is supplemented
by distinctions drawn with reference to the seat. The exudations may
be superficial or deep-seated; they may lie within the cells,
parenchyma, of an organ, or within the interstitial tissue of the
same.
The product of superficial inflammations may lie on the surface, as in
the case of inflamed mucous membranes, or immediately below the
surface, as in numerous cutaneous inflammations, of which erysipelas
may serve as the type. The term catarrhal, applied to superficial
inflammations, carries with it the idea of displacement, flowing, of
the exudation. The product of a catarrhal inflammation must be largely
liquid, that such a displacement may readily take place, and the
catarrhal exudation is chiefly composed of an excess of those elements
which are present in the normal, physiological secretion from the
membrane concerned. Mucus therefore represents a frequent constituent
of the catarrhal exudation, and mucous as well as muco-purulent
catarrhs of the gastro-intestinal, bronchial, genito-urinary, and
other mucous membranes are recognized. The catarrhal inflammation of
the respective membranes usually represents the mildest form, as it
demands an intact epithelium, and a ready removal of the inflammatory
product.
As the cause of a catarrhal inflammation may occasion a destruction of
the epithelium or a necrosis of the mucous membrane, the frequent
association of catarrhal with fibrinous or diphtheritic inflammations
is obvious. In such cases the clinical importance of the latter
varieties gives them the precedence in the designation of the
inflammation. The retention of the catarrhal products is the frequent
cause of permanent disturbances of a more or less serious nature.
These result in part from the mechanical obstruction offered to the
function of parts beyond the seat of obstruction, as pulmonary
atelectasis; and in part from the changes taking place in the retained
product. Purulent otitis media with its dangerous or fatal results,
and gangrene of the lung terminating in septic pleurisy, are not
infrequent instances of severe disturbances from putrefaction of the
retained products of a primarily catarrhal inflammation. A cheesy
degeneration of the catarrhal cells leads to a surrounding fibrous, or
destructive, inflammation, with a corresponding diminution in the
function of the organ affected.
Of the deep-seated varieties of inflammation, that requiring special
mention is the phlegmonous form. This runs its course within the less
dense fibrous tissue known as the areolar or cellular tissue. The term
cellulitis is usually employed by English writers to indicate the seat
and nature of the process, and although the use of the term cellular
tissue is rapidly becoming obsolete, the convenience of cellulitis
favors the retention of the latter name.
The exudation lies within the larger lymph-spaces, and is therefore
sometimes designated as the result of a lymphangitis, the deep-seated,
wider lymph-spaces being concerned rather than those more superficial.
Certain forms of phlegmonous inflammation are of decidedly infectious
origin, and, when seated subcutaneously, are known as phlegmonous
erysipelas, being thus distinguished from the simple erysipelas, whose
seat is defined by the small superficial lymph-spaces of the skin.
{53} Infective forms of cellulitis are also frequently met with in the
loose, sub-peritoneal tissue of the pelvis. The infectious element
usually proceeds from the uterus, and excites the malignant oedema of
the broad ligament, the septic parametritis, or the pelvic cellulitis,
according as the lymph-spaces inflamed lie nearer the fundus or
cervix, and as the direction of the current is upward toward the
spine, or outward toward the sub-peritoneal lymphatics of the pelvic
wall.
Parenchymatous inflammation is present when the exudation is taken
into the cells of an organ, or when the changes dependent upon
inflammation of an organ take place within its functionally important
cells. Virchow originally used the term parenchymatous inflammation in
contradistinction to secretory inflammation, the changes in the former
occurring within the elements of the tissues, while in the latter the
exudation made its appearance on the surface of the organ.
Parenchymatous inflammation is manifested by a degeneration of the
cells affected. This may terminate in their destruction through the
conversion of their protoplasm into fat-drops, fatty degeneration;
although more frequently a simple accumulation of albuminoid granules
(granular degeneration) occurs. The latter represents a transitory
condition, from which a return to the normal state readily takes
place. This form of inflammation is met with in those organs which
present a sharply-defined contrast between the functionally important
cells and the connective tissue which surrounds them. The liver,
kidneys, heart, spleen, pancreas, and glands in general, are
consequently the most frequent seat of parenchymatous inflammation.
Opposed to this variety is the interstitial inflammation. The
exudation of the latter remains within the connective-tissue framework
of the organ. It is essentially cellular in character, and the number
of cells is comparatively small. With their presence and the
possibility of their nutrition a permanent increase in the quantity of
the fibrous tissue of the organ is permitted. This becomes relatively
greater in the course of time, and the parenchymatous cells become
degenerated and absorbed. Interstitial inflammations are likely to
become chronic in character, and, from the outset, are usually
associated with parenchymatous changes.
An important clinical distinction is drawn with reference to the
duration of an inflammation. Acute inflammations are those whose
course is rapid, whose progress is associated with graver disturbances
of function, and with a greater prominence of the cardinal symptoms.
The chronic forms occupy more time in their progress, the functional
disturbances, though severe, are injurious more from their protracted
persistence, than their temporary violence, while redness, swelling,
heat, and pain are symptoms of trifling prominence.
The exudation in acute inflammation, if recovery takes place, is
rapidly removed from the place of its origin, while in the chronic
variety it tends to become a part of the region in which it lies, or,
if removed, slowly disappears, and may be constantly replaced. Acute
inflammations may become chronic, and the chronic variety is liable to
acute exacerbations.
The distinction between acute and chronic inflammations is essentially
one of convenience, and, when considered from the anatomical point of
view, relates rather to the persistence of the results. These may be
{54} present as a variously modified exudation or as a degenerated
condition of the parenchyma of the organ or tissue affected.
Inflammation terminates in resolution, production, or destruction.
For resolution to occur it is necessary that the causes of
inflammation cease to act, either by their removal or their isolation,
and that their results be removed. With the removal of the results
there is often associated the removal of the cause. That such may take
place it is necessary that the function of the vessel walls be so
restored that the exudation ceases to escape. Inflammatory products
already outside the vessels, if present on surfaces with external
outlets, are carried along in the course of the excretions. If they
lie within the cavities of the body not opening externally, their
removal is accomplished through the medium of the circulating lymph
and blood, by absorption. The liquid portion of the exudation becomes
a part of the circulating fluids of the body. The fibrin is converted
into a granular detritus, which eventually disappears from the place
of its formation. The leucocytes may return to the blood-vessels or
enter the lymphatics; the latter course probably being the one taken
by the larger number of the corpuscles. Many undergo a fatty
degeneration, and as they lie in lymph-spaces their conversion into an
emulsion permits a removal of the mechanical obstruction to the flow
of lymph through the spaces in which they were accumulated. The red
blood-corpuscles are destroyed, their pigment being dissolved by the
surrounding fluid and removed in the course of the circulation and
excretions, or it becomes transformed into granules or crystals, which
may remain in the place of their formation, or be transferred, within
amoeboid cells, to remote parts of the body.
When the exudation is abundant, as in the great lymph-sacs of the
body--the several serous cavities--and especially when the openings in
the walls of these sacs are obstructed or the currents within them are
feeble, absorption takes place with great difficulty, and demands a
long interval of time. The fibrinous and cellular portion of such an
exudation frequently becomes converted into a caseous mass, from a
partial fatty degeneration and inspissation. This mass becomes
isolated from the cavity in which it lies, usually at the most
dependent portion, by the formation of a capsule of connective tissue.
It may subsequently become infiltrated with lime salts, calcified, and
thus remain comparatively inert throughout the life of the individual.
The productive termination of inflammation is manifested by the new
formation of connective tissue. This tissue is variously designated,
as the inflammatory process is limited to the surfaces of the body
exposed to the air, or the surfaces of cavities and organs, or as it
lies within organs or the deep-seated parts of the body. In numerous
instances it becomes a permanent constituent of the body, and, as time
is usually essential for its formation, its occurrence is indicative
of a chronic, rather than an acute inflammation. Certain chronic
inflammations are progressive in character, the production of
connective tissue being continuous, with perhaps occasional
intermissions, as in the chronic interstitial inflammations of organs
and tissues. The new-formed tissue, which at the outset is rich in
cells, becomes in time more fibrous, and associated with this change
in structure is a physical modification, manifested by its shrinkage.
This new formation may fill a gap resulting from the destruction of
tissue in {55} the progress of an inflammation, when it is present as
cicatricial tissue--the scar which is usually met with upon the
surfaces of the body or of certain of its organs. When opposed
surfaces are united by the new-formed tissue, the term adhesion is
applied; the adhesions being present as fibrous bands, cords, or
membranes. The pericardial milk-spots and thickenings, the tendinous
or semi-cartilaginous, indurated patches of serous membranes and of
the intima of arteries, are all regarded as manifestations of a
chronic inflammation of these tissues. With the localization of the
inflammation in the outer walls of the bronchi and blood-vessels a
thickening of the external sheath results, called a peri-bronchitis,
arteritis, or phlebitis, as the case may be.
The new formation of blood-vessels is essential for the production and
preservation of this connective tissue, and both arise from
pre-existing tissues. Pus-corpuscles represent the simple cellular
product of an inflammation, and their existence is but transitory.
With the new formation of blood-vessels imbedded in abundant cells
there exists a granulation-tissue, likewise transitory, but out of
which arises the permanent fibrous tissue. The question is still
mooted as to the part played by exuded white blood-corpuscles in the
production of the permanent results of inflammation. It is generally
conceded, especially since the observations of Ziegler, that they are
capable of transformation into lasting constituents of tissue, into
blood-vessels as well as into cells and fibres. Whether all the
resulting permanent products of inflammation are dependent upon their
activity, or whether the pre-existing fixed elements participate, is
still to be considered undecided.
What, at present, appears most probable is, that from exuded
leucocytes there arise, in the course of several days, larger
cells--epithelioid or endothelioid--which are eventually associated
with still larger cells, more irregular in shape, and provided with
projecting filaments, giant-cells. Both varieties may result from the
enlargement of leucocytes by fusion or by the assimilation of
nutriment. The epithelioid cells eventually become fusiform or
stellate, and their projections, as well as those of many of the
giant-cells, become fibrillated. The fibrils of adjoining cells,
becoming united, are thus transformed into a meshwork of fibrous
bundles enclosing irregular spaces, while the nuclei of the cells,
with the immediately surrounding protoplasm, remain upon these bundles
as the permanent cells of the new-formed tissue. The blood-vessels
arise from pre-existing vessels, chiefly capillaries, and probably are
also formed from the cells present in the exudation. The former method
is indicated by the projection of solid sprouts from the wall of a
capillary, which may unite, forming arches, and communicate with
sprouts from neighboring capillaries, thus forming bridges. Both
arches and bridges then become hollowed and admit the circulating
blood. Ziegler maintains that the projections of the larger
epithelioid cells and giant-cells become elongated, and eventually
fused with capillaries, or the projections from capillaries. When this
fusion is accomplished the cells become hollowed, their cavities
communicating with those of the blood-vessels. These epithelioid
cells, whose formation and transformation are of such importance in
the history of productive inflammation, are designated by Ziegler as
formative cells, and are frequently derived from the exuded white
blood-corpuscles, though not identical with them.
{56} The inflammations not terminating in resolution or production,
end in the destruction of the part. This result occurs when the
nutrition of the inflamed territory is so diminished, by the changes
in and around the vessels, as to become insufficient for its
preservation. As the nutriment is derived through the blood-vessels,
the more complete and the more permanent the stagnation in them the
more likely is death to result. This event also depends upon the
quantity and quality of the exudation. The more abundantly cellular
the latter, the more likely is an abscess or ulcer to result.
As most abundantly cellular exudations are considered to be dependent
upon the presence of putrefactive agencies, those inflammations of a
predominant putrid character (gangrenous inflammations) are those
terminating in destruction. The dead product is present as a slough or
sequestrum, when dead soft or hard tissues are detached, entire or in
part, from the living; or as a granular detritus contained in a more
or less abundant liquid. The inflammatory process producing the slough
and sequestrum is characterized as a gangrenous inflammation of soft
parts or a caries of bone, while the process resulting in the
formation of the granular detritus, and which has no necessary
connection with putrefactive agencies, is called a softening, from the
physical condition of its result.
Thrombosis and Embolism.
A blood-clot formed within a blood-vessel during life is called a
thrombus. The entire process of which the thrombus is the essential
element is designated thrombosis.
These terms were introduced by Virchow[17] to avoid the confusion
which resulted from regarding the process and result as synonymous
with inflammation of the vessel. All writers, even at present, do not
adhere to this strictness of meaning. For a thrombus of the vulva
indicates a clot of extravasated blood within the connective tissue of
the labium; in like manner, a vaginal thrombus is the effused and
clotted blood in the loose connective tissue surrounding the vagina.
These exceptions are gradually disappearing, and the word haematoma,
tumor composed of clotted blood, is being substituted in both
instances. A cancerous thrombus represents a mass of cancerous tissue
whose growth is extended along the course of a vessel, its wall having
been penetrated. In general, however, the term thrombus, unless
otherwise qualified, is used as first stated.
[Footnote 17: _Handbuch der Speciellen Pathologie und Therapie_,
Erlangen, 1854, i. 159.]
Although thrombosis is commonly a morbid process, it is not uniformly
so. Its physiological significance is illustrated by the part it takes
in the closure of the umbilical and uterine vessels, after childbirth.
The surgeon makes use of it in his efforts to overcome certain of the
ill effects of amputation, and to accomplish a cure of such local
diseases as aneurism, where it is deemed important to diminish the
supply of blood.
The thrombus being a blood-clot, it is composed, like the latter, of
fibrin and blood-corpuscles. It is presumable that the fibrinous part
of a thrombus owes its origin to the same conditions which determine
the presence of fibrin in blood removed from the vessels during life
or in that within the vessels after death.
{57} According to A. Schmidt,[18] the blood and other fluids, in which
clotted fibrin makes its appearance, contain two generators, called
fibrino-plastic and fibrinogenous. The former is considered to be
paraglobulin, a substance contained mainly in the white
blood-corpuscles, while the fibrinogenous generator is held in
solution in the plasma of the blood. When these materials are acted
upon by a third, the fibrin ferment, clotting takes place and fibrin
is formed. It is thought that the ferment is intimately connected with
the white blood-corpuscles, for with the microscope coagulation is
seen to advance as these become destroyed, and where the leucocytes
are most abundant, there coagulation advances most rapidly. The
elements of clotted fibrin are always present in circulating blood,
but Brucke has shown that blood remains fluid, under ordinary
circumstances, because of its constant contact with the normal
vascular wall.
[Footnote 18: Rollett, _Hermann's Handbuch der Physiologie_, Leipzig,
1880, iv. 1, 114.]
The general causes of thrombosis are those which produce an abnormal
condition of the endothelium, a rapid destruction of the white
blood-corpuscles, or a stagnation of the blood. With the presence of
one of these causes there is often conjoined another, and the
conditions under which they are present are conveniently used in the
classification of thrombi.
Although stagnation of the blood is often an important immediate cause
of its coagulation, it is apparent, from the investigations of
Durante[19] and others, that stagnant blood clots in the living
vessels only when their endothelium is in an abnormal condition. With
the co-existence of abnormal endothelium and stagnant blood, thrombi
form with greater frequency and become more voluminous in a given
interval of time.
[Footnote 19: _Wiener Medizinische Jahrbucher_, 1871, 321.]
The importance of the death of white blood-corpuscles in the formation
of thrombi is generally admitted, and is especially insisted upon by
Weigert. According to the observations of Zahn, the nucleus of certain
thrombi is the result of the death of these leucocytes and their
accumulation upon an altered intima. The experiments of Naunyn,
Kohler, and others show that a thrombus may be rapidly produced by the
injection into the blood of fibrino-plastic substances, and of those
through which free haemoglobin is admitted into the circulation. The
former may be expressed from a fresh blood-clot; the latter may be
obtained by thawing frozen blood, or by injecting such material
(bile-acids, for instance) into the circulating blood as rapidly
destroys the red blood-corpuscles. Although Weigert lays special
stress upon the destruction of white blood-corpuscles in the formation
of the thrombus, it appears, from the experiments above referred to,
that indirectly the destruction of the red corpuscles is also of
importance.
Although largely made up of fibrin, a thrombus also contains
blood-corpuscles, both red and white, and the appearance of the mass
is modified according to the variations in the relative proportions of
these constituents.
Zahn[20] divides thrombi, according to their color, into red, white or
colorless, and mixed varieties. The red owes its color to a large
number of red blood-corpuscles, while the white and mixed forms
contain various proportions of white blood-corpuscles and fibrin and a
diminished number {58} of red corpuscles. The cause of this difference
in the color of thrombi is to be sought for in their method of origin.
When blood clots slowly in a dish, the heavier red corpuscles settle
to the bottom, and the lighter white corpuscles form a superficial
layer. Stagnant blood clotting rapidly furnishes a uniformly red mass.
The red thrombus, like the red clot, is the result of the rapid
coagulation of stagnant blood. The white thrombus, on the contrary,
largely composed of white blood-corpuscles, represents a constantly
increasing deposition of these from flowing blood. The mixed thrombi
arise from a combination of both conditions, and are usually white at
the outset. Thrombi formed in the heart and larger arteries are
usually white, those in the auricular appendages and on venous valves
are mixed, while red thrombi are more common in arteries and veins,
since the conditions favoring their origin are more frequently met in
such vessels.
[Footnote 20: _Virchow's Archiv_, 1875, lxxii. 85.]
Thrombi are frequently stratified, in consequence of the successive
deposition of new layers of blood-corpuscles and fibrin upon a
pre-existing thrombus. Circulating blood is therefore necessary for
the stratification, and such thrombi are likely to be mixed in color.
Unstratified thrombi are usually white or red, the former largely
composed of agglomerated white blood-corpuscles so moulded and
situated as to prevent a stagnation of blood in their vicinity, while
the red thrombus is rarely stratified, since its formation demands a
stoppage of the blood-current. Stratification is intimately connected
with the enlargement or growth of the thrombus, which takes place from
the surface exposed to the flowing blood, and which is greater or less
according to the seat of the thrombus.
Thrombi are usually divided into those from compression, dilatation,
traumatism, and marasmus; in all of which groups an abnormal condition
of the endothelium is to be met with.
Thrombi from compression are frequently formed in veins, in the
vicinity of growing tumors. Their presence is most constant when the
vein is compressed between a resistant surface, especially bone, and
the tumor. A compression of the smaller blood-vessels within an organ,
as the liver or kidney, may take place in consequence of chronic
interstitial inflammation, or the growth of cancerous or other
malignant tumors in such organs. The production of this form of
thrombus is sought for in the treatment of certain aneurisms by direct
pressure, the resulting stagnation of blood being followed by a
coagulation within the aneurismal sac.
Thrombi from dilatation are met with both in dilated arteries and
veins. In aneurism and varix a slowing of the blood-current is
present, and the intima of the diseased region is frequently in such
an abnormal condition that a clotting of the blood readily takes
place. The shape and situation of the dilatation are of importance in
promoting the formation of the thrombus; the more pedunculate and the
more voluminous the sac the more certain is the thrombosis.
Traumatic thrombi result from a direct injury to the vessel. This may
be mechanical, as in the application of ligatures for the obliteration
of vessels, the tearing of the veins during childbirth, and the
infliction of wounds of every variety. The injury may likewise be
chemical, from the action of caustics; somewhat analogous to which,
are the effects of heat and cold. Allied to the traumatic thrombi are
those which arise {59} from acute inflammation of the intima extending
from wounds or inflammatory processes in the vicinity of
blood-vessels.
Marantic thrombi are those whose origin is attributable to that
enfeebled condition of the body known as marasmus. This represents a
weakening of the several functions, especially the circulation,
respiration, and locomotion. Such may take place in disease or old
age; and it is important to bear in mind those diseases in which
marasmus is likely to arise, as thrombosis often proves a complication
of such affections. Protracted fevers, as typhus and typhoid,
puerperal diseases, the disturbances following surgical operations,
chronic wasting diseases, as the tuberculous and scrofulous
affections, are all likely to be accompanied by thrombosis. Stagnation
of the blood, as well as alterations of the intima, is an important
local condition in this variety of thrombosis, which is usually
valvular or parietal at the outset, and may be both arterial and
venous. Such thrombi are likely to become continued and to serve as a
frequent source of embolism.
Thrombi are also divided into primitive, or autochthonous, and
secondary varieties. The primitive thrombus is one which owes its
local origin to conditions existing at the place of its formation and
attachment. The secondary variety demands for its existence a
primitive thrombus, whose place of development is remote in time and
seat, and from which a part has been transferred to serve as the
nucleus for the secondary formation.
The continued thrombus is often confounded with the secondary variety.
Continuance is rather a quality of all thrombi, and is essentially
growth, whether by lamellation or agglomeration. Such continued
thrombi are extended in the course of the circulation, usually by a
conical end, which is pointed toward the heart in the case of venous
thrombi, but away from this organ when the thrombi are arterial.
Parietal and obstructing thrombi form another subdivision. The former
arise from a limited part of the wall of the heart or blood-vessel,
and project into its cavity. They are always in contact with flowing
blood, and are white or mixed in color and primitive. They may attain
a considerable size, and may eventually become obstructing thrombi.
The latter are so called when they are of sufficient size to cause a
considerable or total obstruction to the current of blood. In the last
case the vascular canal is wholly filled by the thrombus. The shape of
the older parietal forms is usually globular or pedunculate, owing to
the growth in all directions except at the place of attachment; the
obstructing thrombi are elongated.
Thrombi are also characterized by consistency and relative absence of
moisture. A thrombus is brittle and dry as compared with a clot. In
distinguishing between the two, difficulty arises only in the case of
a thrombus which may have formed within a few hours before death.
Post-mortem clots are moist, elastic, readily withdrawn from
blood-vessels, and have a smooth and lustrous surface. Their color is
either red, gray, grayish-yellow, or yellow, and is very often mixed.
The lighter colors are due to causes which favor the precipitation of
red blood-corpuscles before actual clotting takes place, or which
occasion an increase of the white blood-corpuscles in fibrin. The
thrombus becomes adherent to the vessel wall within a few hours, after
its formation, in the case of the red thrombus, and at once, in the
case of the white variety. A clot is never adherent, although it may
seem so from its entanglement between the trabeculae and {60} tendons
of the heart and the cavernous framework of venous sinuses. Such
apparent adhesions are easily recognized by the smooth, shining,
intact intima which is disclosed after the removal of a clot.
The thrombus not only tends to become enlarged by further depositions
of material from the blood, but it also tends to become diminished in
size from the contractile properties of its fibrinous constituent.
Moisture is forced from the thrombus in consequence of this shrinkage,
and its dryness is increased by subsequent absorption through the wall
to which it adheres.
The changes eventually taking place in the thrombus are known as
organization, calcification, and softening.
Organization is the transformation of the thrombus into a mass of
fibrous tissue. This is accomplished, according to the researches of
Baumgarten,[21] by an outgrowth of endothelium from the intima of the
vessel, the thrombus being absorbed as the growth of tissue advances.
In the case of a thrombus due to the ligation of a vessel, a
granulation-tissue also makes its way into the thrombus between the
ruptured coats, and the new-formed fibrous tissue which replaces the
thrombus becomes vascularized through this granulation-tissue. The
vascularization of thrombi surrounded by unbroken walls is most likely
to result from the extension into the thickened intima of new-formed
branches of the vasa vasorum. Cohnheim claims that the organization of
the thrombus may take place solely through the entrance of migratory
cells, without any active participation of elements of the vascular
wall. The canal is thus obstructed or obliterated by a fibrous tissue,
which is pigmented or not, as the pre-existing thrombus contained red
blood-corpuscles or not. These, when present, become transformed into
granular or crystalline haematoidin, which may remain as a permanent
constituent of the new-formed tissue.
[Footnote 21: _Die sogenannte Organisation der Thrombus_, Leipzig,
1877.]
Even when the thrombus is completely obstructing at the outset, it is
not necessary that a total obliteration of the vessel should result
from its organization. It not rarely happens, either before or after
the thrombus has yielded to the fibrous growth, in consequence of the
shrinkage of the fibrin of the thrombus or of the contraction of the
fibrous tissue replacing it, that gaps arise which become
communicating canals. Through these the blood flows, and the vessel
thus becomes only obstructed, not obliterated. The sieve-like tissue
thus formed is spoken of as the result of a cavernous or sinus-like
transformation of the thrombus. The length of time necessary for the
removal of the thrombus and its replacement by fibrous tissue varies
considerably. A vascularized granulation-tissue may be present within
a week, and in the course of a month the thrombus may have been wholly
removed, or a period of months may elapse and the thrombus and
granulation-tissue still be present side by side.
The calcification of a thrombus takes place when the latter becomes
impregnated with salts of calcium and magnesium. The condition may be
present in thrombi which are exposed to a rapidly-flowing arterial
stream, as well as in those which lie in venous pockets outside the
course of the direct current of blood. The well-known phlebolites are
examples of the latter variety. A calcified thrombus may be intimately
united to the vascular wall, the results of calcification and
organization being associated. Calcification and, in particular,
organization represent favorable {61} events in the history of
thrombosis, as through their occurrence the process comes to an end,
and disturbances, either local or remote, are prevented.
The softening of the thrombus, on the contrary, is always a source of
danger. This is partly due to the nature of the products of the
softening, whether bland or septic, and partly to the mechanical
disturbances produced by the transfer of portions of the softened
thrombus to remote parts of the body. All thrombi may become softened.
When the process of organization advances normally, the softened parts
are absorbed as rapidly as the formation of vascularized fibrous
tissue progresses. If this formation is checked or stopped, the
process of disintegration still continues. White corpuscles undergo
fatty degeneration; red corpuscles give up their coloring matter and
become converted, like the fibrin, into granules, and there results a
granular detritus. This is present as a viscid, semi-fluid material,
either red, gray, or yellow, according to the color of the thrombus.
This simple softening is to be regarded as essentially chemical in
character, and begins at the oldest portion of the thrombus and
advances toward the periphery. Its products are capable of absorption
without the production of serious disturbances, and are usually
prevented from direct entrance into the blood-vessel containing the
thrombus by the continuation of the latter from new coagulation or
deposition upon its surface. The thrombus is thus extended as the
softening progresses.
When the thrombus is comparatively free from red blood-corpuscles, the
softened product, in consequence of its yellowish color, opacity, and
viscidity, resembles pus. The so-called encysted abscesses projecting
into the cavity of the heart, from its wall, are parietal and globular
thrombi, in the interior of which softening has occurred. This form of
softening is called simple or bland, as it is free from any evidence
of local suppuration, inflammation, or general constitutional
disturbance attributable to an absorption of poisonous material.
Septic softening is accompanied by general evidences of a
blood-poisoning, and by the local phenomena of purulent inflammation.
A suppurative thrombo-phlebitis or arteritis, occurs; that is, an
acute inflammation of the wall of the vessel, corresponding in its
origin to the seat of the thrombus, and characterized by the formation
of pus. In the earliest stage the softened thrombus need not present
products differing in appearance from those occurring in simple
softening, but their effect is manifested by a rapidly-advancing
inflammation of the vascular wall and by the evidence of septicaemia.
Inoculation with such material produces a group of symptoms classified
under the head of blood-poisoning.
Cohnheim lays special stress upon the presence of micrococci in the
softened material, and it is generally agreed that the virulence of
septic softening is connected with, if not due to, the presence of
microbia. A septic softening may be induced by besmearing, with septic
material, the outside of a blood-vessel containing a thrombus, and
this form of softening is usually associated with those conditions
favoring this relation. Such are the gangrenous wounds following
surgical operations, the putrid inflammatory processes affecting the
uterine wall after childbirth, the offensive inflammations of the
middle ear, and the like. It is possible for a septic softening to
occur independently of such contiguous or continuous relations with
the surfaces of the body. It is considered, {62} however, that the
micrococci present in a softened thrombus must have obtained admission
from without through one of the surfaces of the body, mucous or
cutaneous, or through undiscovered abrasions of even intact surfaces
of peculiar structure, as the alveolar wall or the intestinal mucous
membrane. The thrombus is regarded as affording a favorable soil for
the growth and activity of the organism.
The mechanical effect of a thrombus varies according to the venous or
arterial seat of the same. Venous thrombi, as they are continued
toward the heart, tend to become completely obstructing thrombi. In
most parts of the body the venous anastomoses are so numerous that the
obstruction of a vein is readily compensated for through the
collateral venous circulation. When such a compensation is prevented
by an extension of the thrombus from branch to branch, and finally to
the trunk, an accumulation of blood in the peripheral veins must
result. The remote parts become swollen, from the distension of the
vessels with blood and the transudation of liquid, and eventually
solid material from the blood. Venous thrombosis thus leads to oedema,
and even hemorrhage. The more rapidly the obstructing thrombus
extends, the earlier and more extreme is the oedema likely to become,
while the slower the advance of the thrombus, the more favorable is
the opportunity for an enlargement of the collateral vessels through
which a sufficient flow of blood is permitted to check oedema and
preserve nutrition.
Local mechanical disturbances from arterial thrombi are scarcely
perceptible till obstruction is produced, and the results of arterial
obstruction will be mentioned in detail in connection with the
phenomena of embolism. Cardiac thrombi may occasion local disturbances
from interfering with the action of the valves of the heart. Those
thrombi which are attached to the valves, especially when calcified,
may produce inflammation and aneurism of the opposed wall of the
heart, by friction. The most frequent mechanical disturbance from the
non-obstructing parietal thrombi of the heart and arteries results
from the detachment of fragments and their transfer as emboli to
remote parts of the body.
An embolus is a foreign body in a blood-vessel, usually too large to
pass through the smallest capillaries, and the disturbances resulting
from its presence are included under the term embolism. Although most
emboli are detached portions of thrombi, any foreign body of suitable
size may become an embolus. Such are tissues, as the pulmonary elastic
fibres, fragments of diseased valves of the heart and of the intima of
arteries, or portions of tumors growing into vascular canals. Others
are globules of oil entering the torn veins when fat-tissue becomes
crushed, or air-bubbles admitted through veins either wounded by
instruments or opened after parturition by the dislodgment of their
obstructing thrombi. Still others are granules of pigment derived from
the coloring-matter of the blood, as in melanaemia, or introduced from
without, as india-ink and cinnabar. The echinococcus has been found as
an embolus, and it is highly probable that the cysticercus, the
trichina, and other animal parasites may be disseminated as emboli
over the body.
Vegetable parasites, like the bacterium and aspergillus, have also
been included in the list, although the disturbances resulting from
their presence are less due to mechanical obstruction than to
colonization and growth. The experimenter uses the most various
objects as emboli--bits {63} of wood, rubber, and glass, globules of
mercury, fragments of tissue, etc. Emboli are to be regarded as of
arterial or venous origin. The arterial emboli are carried toward the
capillaries, while venous emboli are carried toward the heart. The
effect of both is partly or wholly mechanical, and partly due to the
specific properties of the constituents.
The mechanical effect of an embolus is manifested by the obstruction
it offers to the circulation, and the degree of the obstruction
depends upon the size, shape, and density of the embolus and the
nature and size of the vessel obstructed. An embolus may be so large
as to be unable to pass through the valvular orifices of the heart. A
long and narrow embolus might pass through a vessel which would not
admit one which was short and thick. A jagged and dense embolus, by
repeated blows or prolonged and forcible contact, might cause a
weakening or rupture of the wall of a vessel, and thus produce an
aneurism. Certain vessels (the terminal arteries of Cohnheim) furnish
the sole supply of arterial blood to a district, and when they are
obstructed, the results, to be mentioned later, differ widely from
those taking place where free vascular anastomoses exist. When a trunk
bifurcates, the larger branch usually receives the embolus.
Venous emboli are those which approach the heart by the peripheral
veins of the body or the pulmonary veins, and the liver by the
radicles of the portal vein. Emboli from the veins of the body are
carried through the right side of the heart, if not so large as to be
stopped at the tricuspid or pulmonary opening. As they enter the
latter, they are carried along its course under the influence of
gravity and the direction and force of the current, which are
determined by the direction and relative size of the bifurcations of
the artery, the right primary branch being larger than the left.
Eventually, a point of the artery is reached whose diameter is less
than that of the embolus, and the latter is stopped. This point
usually corresponds with a place of bifurcation, and the embolus
frequently rides the wall separating the branches.
Emboli from the radicles of the portal vein owe their most frequent
origin to thrombi associated with inflammatory processes in the
intestine, especially of the caecum and vermiform appendage, to
inflammatory processes in the spleen and obstruction to the flow of
blood through the splenic artery, or to inflammatory changes
proceeding from the kidneys. Such venous emboli are carried toward the
heart, but are stopped on the way by the intrahepatic branches of the
portal vein.
Arterial emboli are those which enter the left side of the heart from
the lungs, which arise in the left ventricle or auricle, which may
pass through an open foramen ovale from the right auricle, or which
arise from the arterial wall. They are carried along the course of the
arterial circulation, and are distributed over the different regions
and organs of the body. Usually following the more direct course of
the circulation, they are more likely to enter the abdominal aorta
than to be carried toward the brain or upper extremities. Embolism of
the carotids, especially of the left carotid, is more likely to ensue
than embolism of the subclavians. Embolism of the coronary arteries is
rare, while embolism of the splenic artery, the left renal and left
iliac arteries, is comparatively common, and in the order mentioned.
When an embolus is found, or embolism suspected, the source is always
{64} to be searched for in those regions from which the affected part
receives its blood. The source of arterial and portal emboli is
usually found with ease, while the pulmonary embolus may come from so
wide a region, the body-veins, that much time may be spent before its
place of origin is discovered. An appreciation of the laws of the
transfer of emboli renders such a discovery almost certain.
When the embolus reaches a point beyond which it cannot pass, the
resulting disturbance depends essentially, as shown by Cohnheim, upon
the presence or absence of arterial anastomoses beyond the place of
obstruction. He gives the name terminal arteries to those which have
no anastomosing arterial branches. These are met with in the spleen,
kidneys, lungs, brain, and retina. If the obstructed artery is not
terminal, the embolus may produce no further disturbance, the
collateral supply of blood through the anastomoses sufficing for the
nutrition and function of the part. If, however, the vessel is a
terminal artery, and the embolus is completely obstructing, the supply
of arterial blood must be wholly cut off from the region beyond the
seat of obstruction.
If the embolus does not completely obstruct at once, it soon becomes
sufficiently large for this result to ensue in consequence of a
secondary coagulation. The rider assumes legs extending into the
arterial branches beyond the place of obstruction, and a body which
extends backward in the course of the circulation to the nearest
branch. The result of the total obstruction of the vessel is to cut
off the admission of arterial blood, producing a local anaemia. The
contraction of the elastic tissues of the part propels toward the
capillaries a certain quantity of the blood in the vessels beyond the
point of obstruction, till this force becomes neutralized by the
blood-pressure in the vessels surrounding the obstructed region. The
anaemic part may subsequently become engorged with blood; it may die,
a region of anaemic necrosis resulting, or the dead portion may become
softened.
The engorgement of the obstructed territory has received the name of
hemorrhagic infarction. A solid, wedge-shaped mass of a reddish-brown
color is present, whose shape is due to the arborescent branching of
the terminal arteries. According to Cohnheim, the engorgement of the
region with blood takes place from venous regurgitation into the
obstructed part, till the intravenous pressure is overcome by the
resistance of the tissues in the region affected. The capillaries and
larger vessels thus become distended, and an escape of liquid and
solid constituents of the blood takes place. If the veins are provided
with valves, or the venous regurgitant current is opposed by gravity,
the hemorrhagic infarction is prevented or greatly impeded.
Litten,[22] on the contrary, who has furnished a recent contribution
to this subject, claims that the hemorrhagic results of embolism are
not accomplished through venous regurgitation, unless increased venous
tension is produced by coughing, vomiting, and like efforts. His
experiments lead him to maintain that arterial blood from surrounding
tissues is supplied to the obstructed region through the anastomosing
capillaries. The force is not sufficient to drive the blood through
the capillaries into the veins beyond, but an accumulation takes place
in the capillaries, which become dilated and distended. The escape of
blood-corpuscles and {65} serum then takes place, the more freely, as
Weigert[23] suggests, the larger and more numerous are the
pre-existing spaces in the organ. Hence the infarction becomes the
most characteristically developed in such organs as the lungs and
spleen. Causes which obstruct the venous flow, as well as those which
increase the arterial tension, promote the hemorrhagic infarction.
[Footnote 22: _Untersuchungen uber den hemorrhagischen Infarct.,
etc._, Berlin, 1879.]
[Footnote 23: _Virchow's Archiv_, 1878, lxxii. 250.]
A necrosis of the part whose direct arterial supply is cut off takes
place when the structure of the organ affected is such that the
admission of arterial blood is wholly interfered with. This is the
case in the heart and kidneys, and to a less extent in the spleen. The
opportunity is presented for the diffusion of a fibrinogenous fluid,
lymph or blood-serum, through the cells of the organ which contains
the other essentials for coagulation, and the dead part presents the
characteristics attributed by Weigert[24] to death from clotting of
the protoplasm, coagulative or ischaemic necrosis.
[Footnote 24: _Ibid._, 1880, lxxix. 87.]
Embolism of the cerebral arteries produces softening of the brain, not
a hemorrhagic infarction or a yellowish necrosis. Weigert attributes
this result, on the one hand, to the absence in the brain of abundant
cells from which are to be had the ferment and fibrino-plastic
material necessary for coagulation, and, on the other, to the closure
of the spaces into which blood might collect by the rapid swelling of
the tissues from the exuded lymph.
The hemorrhagic results of embolism are also met with in obstruction
of branches of the mesenteric artery, which is considered by Litten,
at least from its function and in connection with its sluggish
current, to correspond with a terminal artery.
If the patient outlives these more mechanical results of embolism, the
local changes taking place are those tending to remove the
extravasated blood or the dead tissues. The embolus has become an
obstructing thrombus, and its removal is accomplished in the manner
already stated in connection with the subject of thrombosis. The
wedge-shaped nodule of hemorrhagic infarction becomes decolorized
through the absorption, in part, of the blood-pigment. That portion
which is not absorbed remains at the site of the original lesion as
granular or crystalline blood-pigment. A granulation-tissue is formed
at the periphery, which extends into the infarcted region, very much
as the endothelial and vascularized growth extends into a thrombus.
Eventually, a patch of cicatricial tissue remains as the sole
indication of the previous disturbance. This termination is rather
suggested for the hemorrhagic infarctions of the lungs. The results
are more apparent and more easily demonstrated in the case of the
anaemic necroses, and the somewhat irregular depressions with
wedge-shaped scars, seen upon the surface of the spleen or kidneys,
call attention to the probable nature of the process giving rise to
these results. A source of embolism must also be associated, that
these scars may be regarded as of embolic origin. The embolic
softenings of the brain are likewise represented in after years by
losses of substance. The superficial, yellow patches or localized
oedematous blebs, with corresponding atrophy of the convolutions
beneath, call attention to a nutritive disturbance, as do cyst-like
cavities in the deeper parts of the brain. Here, too, a source of
embolism must be found, that {66} the local destruction of tissue may
be attributed to embolic obstruction of vascular territories.
When the embolus arises from a septic thrombus, the results differ
from those above described. The embolus then carries not only
mechanical possibilities, but also a virulent action. The latter is
manifested by the rapid production of local inflammatory disturbances,
as circumscribed abscesses and gangrenous destruction of tissue. Since
emboli are frequently lodged near the surfaces of organs, a septic
pleurisy, pericarditis, or peritonitis is the usual result of the
dissemination of the virus contained in the embolus. This virus is
similar in character to that found in septic softening of the
thrombus, and, like it, is intimately connected with the presence of
microbia. Whether the latter are specific in character, as maintained
by Klebs and others, or whether they are to be included among those
associated with putrefactive processes, still remains an open
question.
The symptoms of thrombosis obviously depend upon the resulting
obstruction to the circulation of blood, and in the case of primitive
thrombi are gradual in their occurrence. The degree of mechanical
obstruction is determined by the nature of the thrombus, whether
parietal or obstructing, and by that of the vessel, whether provided
with anastomoses sufficient to permit a compensatory collateral
circulation or not. In the former case, if the thrombus is small and
deep-seated, there may be no symptoms to indicate its presence. When
the collateral circulation is insufficient to remove the blood from a
region whose efferent venous trunk is completely filled with a
thrombus, the phenomena of stagnation are produced. The part becomes
oedematous, and red blood-corpuscles escape from the distended vessel.
If the obstructed vein is superficial, the seat of the thrombus is
indicated by the resistance and sensitiveness of the part.
Characteristic disturbances of function are associated with thrombosis
of the various organs of the body. If the cerebral sinuses are
affected, mental disturbances arise; if a cardiac thrombosis is
present, it is frequently accompanied by irregularity and feebleness
of the heart. When the portal and renal veins are obstructed,
functional disturbances arise in the parts from which they receive
their blood.
The symptoms of embolism, like those of arterial thrombosis, are
primarily due to anaemia. Suddenness is their characteristic in
embolism, while they are gradual and progressive in the case of
thrombosis. An embolic anaemia is complete or incomplete according to
the terminal or anastomosing character of the obstructed vessel. The
effect of the anaemia is to stop or check the function of the part,
and varies according to the size and situation of the vessel.
Hemiplegia, or perhaps aphasia or other evidence of localized
disturbance, follows central embolism; angina pectoris, with a
disturbed cardiac action, results from embolism of the coronary
artery. Sudden suffocative symptoms, with open air-passages, suggest
embolism of the larger branches of the pulmonary artery. A
considerable haematuria often excites suspicion of an embolism of the
renal artery, the hemorrhage coming from the vessels in the
neighborhood of the obstructed region. Embolism of a large artery of
an extremity is often localized by the sensation of a blow at the
part, to be followed by absent pulsation, pallor, and coldness of the
region beyond the place of obstruction.
{67} The symptoms of the subsequent effects of thrombosis and embolism
are to be inferred from what has already been stated with regard to
the nature of the possible lesions. To enter into their detailed
consideration would demand more space than is permitted, and would
modify an established sequence or necessitate a repetition, which is
undesirable in a systematic treatise.
Effusions.
The various fluids of the body are derived from without, and admitted
into the blood-vessels. The physiological transudation through the
walls of these vessels, in the main modified serum, becomes lymph as
it appears in the several lymph-spaces. From the latter the transuded
fluid either returns through the lymph-vessels to the blood-current or
makes its appearance upon surfaces as secretions. These are variously
modified as they pass through the specific cells of glands or as they
are met with in the several closed cavities of the body.
The transudations thus occurring may vary in quantity within certain
limits, the latter being somewhat indefinite, owing to the
difficulties in the way of exactly measuring the fluid transuded. The
greater part of this transudation is represented by the quantity of
lymph flowing through the main lymph-trunk, and of the secretion from
the glandular surfaces of a given region of the body; but that
transuded fluid is not included which may return to the blood-vessels
without being carried into the general lymph-current or secreted from
a gland. Such a direct return may be considered to take place whenever
the pressure upon the outside of the vessel wall is greater than that
within the latter, or when the chemical composition of the fluids on
the two sides of the filter permits endosmosis as well as exosmosis.
This varying relation in the direction of the current through the
vessel wall is likely to be of frequent, if not constant, occurrence
in connection with the physiological processes taking place throughout
the body.
The undue accumulation of the transudation in the various closed
cavities of the body is known as dropsy, and the fluid present is
regarded as an effusion or an exudation. These terms are often applied
somewhat vaguely, now being used as synonymous, again as representing
different conditions of the transudation, which are attributed to the
varying conditions of its accumulation.
Exudation is more generally used when an inflammatory process is the
cause of the increased transudation, while effusion is more strictly
associated with causes other than inflammatory. In the present
consideration this etiological distinction will be maintained.
To appreciate the conditions under which pathological accumulations of
fluid, whether effusions or exudations, may arise, it is desirable to
bear in mind the essential conditions which prevail in the occurrence
of transudation, since the former are likewise chiefly derived from
the blood and are transuded through the walls of its vessels. These
conditions are largely dependent upon the laws governing the diffusion
of substances through an animal membrane, the vascular wall
representing the filter. As a living membrane its relation is
dependent upon vital as well as {68} physical conditions, and the
former produce certain important modifications in the physical process
of filtration.
The transudation through the vessels takes place chiefly through those
with the thinnest walls, the capillaries, although it is probable that
a certain degree of transudation may also occur through the walls of
the smallest veins. The causes which are instrumental in promoting the
circulation of the blood--viz. the contraction and dilatation of the
heart, the contraction of the arteries, the inspiratory action of the
thorax, and muscular movements throughout the body--are also essential
in producing the flow of lymph; and the existence of pressure upon the
haemic side of the filter is the first feature of importance in
occasioning the transudation. The constant removal of the transudation
from the outer side results from the pressure being less in this
position.
At the same time, an increase in the quantity of blood in the vessels
is not necessarily productive of any considerable increase in the
fluid transuded. Cohnheim calls attention to the experiments of Worm
Muller, which show that a plethoric condition may readily be produced
by the injection of quantities of blood into the circulation of
animals, the amount of which cannot exceed twice the volume of the
animal's blood without producing death. Although a temporary increase
of the blood-pressure results, a return to the normal quickly follows.
This is permitted by the propulsion of the excess of blood into the
capillaries and veins, which become consequently distended, especially
those of the abdominal organs. There is no increased transudation
corresponding with the quantity of fluid introduced, nor is there any
considerable distension of the blood-vessels of the skin, subcutaneous
or intermuscular connective tissue. Such experiments show no permanent
increase in the blood-pressure within the large veins if there is no
obstruction to the admission of venous blood into the heart,
presumably owing to their capacity for considerable distension.
Although experiments show that a simple plethora with great distension
of the capillaries of the abdominal organs occasions no considerable
increase of transudation, a different result follows a hydraemic
plethora[25] induced by the injection of immense quantities of salt
water into the blood-current--often six times as much liquid as the
animal had blood. Here, too, the arterial blood-pressure shows no
permanent increase, nor does that within the large veins become
perceptibly increased till enormous quantities of fluid are injected.
The blood flows through the vessels with increased rapidity in
consequence of the diminished friction of the diluted blood, and an
increased transudation begins at once. The various glands, salivary
and gastro-intestinal, kidneys and liver, secrete more copiously, and
the flow of a dilute lymph from the thoracic duct becomes greatly
increased, while that from the cervical lymphatics becomes moderately
accelerated. The lymph from the extremities, however, is no greater in
quantity than that flowing from an animal in a perfectly normal
condition. The localization of the increased transudation from the
blood-vessels is further characterized by the abundant accumulation of
watery fluid in all the abdominal organs and abdominal cavity, in the
salivary glands and surrounding connective tissue, while elsewhere in
the body the organs and tissues are almost invariably in the same
condition with {69} regard to moisture as are those of a healthy
animal under normal circumstances.
[Footnote 25: Cohnheim and Lichtheim, _Virchow's Archiv_, 1877, lxix.
106.]
The importance of these experiments with reference to the causes of
the transudation of fluid from the blood is obvious. The pressure upon
the walls of the blood-vessels cannot become sufficiently increased to
be accompanied with augmented transudation until limits are reached
which are beyond the possibilities of occurrence in the human body.
When such limits are attained in animals, the increased pressure,
however great it may be, does not suffice to produce a general
transudation, but one limited to the vessels of those parts of the
body whose normal function is connected with too abundant transudation
of fluid. A simple hydraemic condition of brief duration has been
proven, by experiment, insufficient to give rise to increased
transudation, neither increased secretion nor increased flow of lymph
taking place. The inference from these experiments is that an
increased transudation is more dependent upon conditions of the filter
than upon those of blood-pressure. The absence of any observable
changes in the filter leads to the assumption of an increased
permeability, of physiological occurrence in certain parts of the
body, as the chief feature in the occurrence of increased
transudations.
Dropsy arises when the transudation is accumulated. As dropsical
accumulations are transudations from the blood, essentially
blood-serum with a diminished percentage of albumen, and as such
blood-serum is practically lymph from its presence in the
lymph-vessels, dropsical effusions are to be regarded as stagnant
lymph. Such stagnations may be present in the small lymph-spaces
within the connective tissue, or in the larger lymph-sacs, as the
peritoneal, pleural, pericardial, and scrotal cavities. In like
manner, the stagnation may take place in the cavities of joints and in
those of the brain and cord, although the latter represent functional
rather than structural lymph-canals.
The term oedema is applied to the accumulation in the
connective-tissue lymph-spaces in general, while the term anasarca is
confined to those cases where the subcutaneous lymph-spaces are
concerned. The accumulation in the great lymph-cavities is known as
ascites when peritoneal, hydrothorax when pleural, hydropericardium
when pericardial, hydrocele when in the cavity of the tunica
vaginalis, hydrocephalus if within the ventricles of the brain, and
hydromyelocele when within the central canal of the spinal cord.
The accumulation of dropsical effusions may be considered as possibly
resulting from an obstruction to the channels through which the
transudation should flow, or from insufficient force to overcome
normal obstructions, or from an abnormally increased transudation.
Lymph-channels are frequently obstructed, but no appreciable diffused
retention of lymph results unless the thoracic duct is obstructed.
This rare affection is followed by enormous distension of the thoracic
and abdominal portions of the parts beyond the stenosis. Ascites and
hydrothorax may follow, but not necessarily any considerable oedema of
the peripheral parts of the body. As a result of the distension of the
thoracic duct, rupture is not unlikely to take place, and the effused
fluid contains chyle.[26]
[Footnote 26: Quincke, _Deutsches Archiv fur Klin. Med._, 1875, xvi.
121.]
{70} That the obstruction is not followed by oedema is attributable to
the innumerable anastomoses between the lymph-spaces, and also to the
probability that a part of the transuded fluid returns to the
blood-vessels when the obstruction is impassable.
The forces necessary to promote the flow of lymph have already been
mentioned, and their entire removal is inconsistent with life. A
diminution of their activity is more likely to result in a diminished
flow of lymph than its accumulation, although a slowing of the
lymph-current may represent a favoring element in the accumulation of
an increased transudation.
The occurrence of dropsy with unobstructed lymph-channels, and in the
presence of efficient agencies in promoting the flow of lymph,
indicates the importance of an increased transudation as the chief
element in the occurrence of a dropsical accumulation. An increased
transudation, with resulting oedema, is readily produced by preventing
the flow of blood from a part, and may be directly observed with the
microscope. Cohnheim states that after a sudden venous obstruction, in
case an efficient collateral circulation does not interfere, the
capillaries and small veins become distended with stagnant blood and
appear as masses of red blood-corpuscles. This distension results from
the continuance of the arterial flow into the capillaries of the
obstructed region under a pressure which is only neutralized by the
resistance of the tissues and the transudation from the capillaries.
Sotnitschewsky[27] shows that a concurrent paralysis of the vaso-motor
nerves, as claimed by Ranvier, is unnecessary. The transudation
through the capillary wall is increased, the flow of lymph from the
part is accelerated, and oedema arises when the transudation is so
much augmented that the calibre of the lymph-vessels is insufficient
for its removal; and the greater this insufficiency the greater is the
oedema. With the continuance of the arterial flow and intravenous
resistance, red blood-corpuscles are forced through the filter, and
form an important constituent of the effusion from venous stagnation.
[Footnote 27: _Virchow's Archiv_, 1879, lxxvii. 85.]
Although the existence of an increased pressure upon the capillary
wall is obvious from the experiment referred to, there is no increased
arterial pressure--rather a diminution--and the important element in
occasioning the increased permeability of the capillary wall is the
obstruction to the outflow of venous blood from the oedematous region.
In consequence of the latter the arterial flow is followed by
increased transudation.
Dropsies resulting from venous obstruction, as well as those following
an obstruction of the thoracic duct or its branches, or of the several
lymphatics of a part, are classified as mechanical dropsies. That from
venous obstruction is the most frequent, and its seat may lie in the
course of venous trunks or in the heart, lungs, or liver. The venous
obstruction must be so situated that the stagnant blood is unable to
find a ready escape through collateral branches. The more sudden and
complete it is, the more likely is the effusion to contain
considerable numbers of red blood-corpuscles.
In addition to the element of venous stagnation in producing increased
transudation, the condition of the filter is of importance. The
occurrence of oedema in chronic diseases, especially of the kidneys,
and in those attended with protracted suppuration, continued
hemorrhage, and the {71} rapid growth of tumors, has usually been
attributed to the watery condition of the blood, with a diminution of
the albumen. Cohnheim, however, suggests that the condition of the
vessel wall is of more importance than the contents as the immediate
cause of the increased transudation. The more or less protracted
action of various agents--temperature, insufficient oxygen, and
diminished albumen--is likely to so modify the condition of the
endothelium as to favor an increased permeability of the wall.
Experiments show that a simple acute hydraemia produces no increased
transudation, and that a chronic hydraemia, if connected with dropsy,
is likely to be influential by increasing the permeability of the
wall. Even in those cases where a hydraemia and an oedema co-exist,
the localization of the latter is favored by obvious disturbances of
the function of the capillary walls, as in case of the cutaneous
oedema after scarlatina. In like manner, a feeble heart, favoring
venous stagnation, and gravitation are of importance, as general
causes, in promoting dropsy in hydraemic conditions.
The possibility of the occurrence of oedema through nervous influence
is not to be denied. The localized and fleeting oedema of urticaria
and erythema, the swollen lip and tongue in connection with digestive
disturbances, are not to be explained by the two main factors of
oedema--viz. venous stagnation and increased permeability of the
vascular walls. Cohnheim refers to the rapid occurrence of oedema of
the tongue as a result of irritation of the lingual nerve, and oedema
is known to occur rapidly in cases of acute myelitis. A similar result
follows the experimental destruction of the spinal cord, although the
mechanism of its production is not apparent.
Dropsies are subdivided, as regards their distribution, into general
and local forms. The causes producing the two varieties are
essentially those already described. The causes of all local dropsies
are not always to be regarded as the same. Regions which are the seat
of mechanical dropsies are often affected by inflammation, with
abundant serous exudation--the so-called inflammatory dropsy. The
properties of the effusion and exudation are quite different, the
former having a small percentage of albumen, but few leucocytes, with
a corresponding absence of fibrin, and few or many red
blood-corpuscles. The exudation, on the contrary, is highly
albuminous, though less so than the blood-plasma; it contains numerous
leucocytes and much fibrin; under ordinary circumstances there are but
few red blood-corpuscles.
The local dropsies are often characterized by special terms. Hydrops
ex vacuo is applied to the collections of fluid found in closed
cavities with unyielding walls, as the cranium and thorax, or to the
recurrence of fluid in cavities from which the same has been rapidly
removed, in the absence of inflammatory disturbances. Collateral
oedema is usually applied to the association of oedema with
inflammatory disturbances, and represents an extension of the
inflammatory process to the region concerned. Oedema of the glottis
and circumscribed oedema of the lung are instances. The term
hypostatic oedema is often used to designate the association of oedema
and inflammation, the former caused by the latter, and to indicate the
effect of gravitation in the localization of oedema from the general
causes already mentioned.
Another localized oedema of interest, from its frequent occurrence and
{72} importance, is oedema of the lungs, often taking place toward the
end of life, at times quite suddenly. This form has usually been
attributed to increased transudation from arterial congestion or
venous stagnation. The former view is directly refuted by the
experiments of Welch,[28] who offers the explanation now accepted.
With the obliteration of three-fourths of the arterial supply to the
lungs of the animals experimented upon, no oedema resulted from the
assumed collateral fluxion into the branches of the pulmonary artery
which were left open. The obliteration of the same area of venous
distribution was necessary before the occurrence of oedema. Oedema of
the lungs was further found to result from a ligature of the aorta
near the heart. The comparative frequency of oedema of the lungs in
man, and the rarity of such extreme mechanical disturbances as those
produced experimentally, led Welch to paralyze the left ventricle. The
conditions as regards the pulmonary circulation then corresponded with
those mentioned as causes for oedema from venous obstruction. The
continued action of the right ventricle forced blood into the
pulmonary capillaries, where it was compelled to accumulate in
consequence of the inability of the left ventricle to receive and
expel it. Welch consequently regards the immediate cause of this form
of pulmonary oedema as a predominant weakness of the left ventricle. A
weak heart does not suffice for the production of the oedema, since
this condition is not found when both ventricles are alike enfeebled.
[Footnote 28: _Virchow's Archiv_, 1878, lxxii. 375.]
Degenerations.
The degenerations represent disturbances in the nutrition of the
tissues of the body, in consequence of which their functions become
impaired, if not destroyed. The latter result obviously attends the
death of cells, which may occur in the course of the degeneration. The
processes concerned are called necrobiotic by Virchow, as they
represent vital processes leading to death. Although in many of them
the cell is decaying during their continuance, its recovery is
possible with the disappearance of the conditions which have
transformed physiological into pathological processes. The
degenerations affect intercellular substance as well as cells, and are
called metamorphoses, infiltrations, or degenerations, as a
transformation of normal into abnormal material, or the addition of
extraneous substances, or the functional impairment of the part
assumes the greatest prominence.
_Cloudy Swelling, Albuminoid Infiltration, Granular Degeneration,
Parenchymatous Degeneration._
Of the various modifications in the appearance of cells under
pathological conditions, there is none, perhaps, more commonly met
with than that known by the above terms. A granular appearance may be
regarded as an essential characteristic of protoplasm, and is an
attribute of cells of epithelial origin as well as of those which
belong to other groups of tissues. The abundance of granules present
in a normal cell depends largely upon its shape, size, and situation.
These granules present various {73} relations to chemical agents, some
being soluble in alcohol and ether, others in acids and alkalies, and
many of them, especially those met with in the form of degeneration
now being considered, show from the various reactions that they are of
the nature of albumen. Since their exact composition, in all
instances, is undetermined, they are called albuminoid, and when in
excess the cell is considered to be infiltrated with these granules,
and the organ presents the appearances regarded as characteristic of
an albuminoid infiltration. A granular cell becomes much more granular
when it is thus infiltrated, and it is therefore a matter of
difficulty to recognize from the appearance of certain single cells,
as those of the liver or kidney, whether or not the number of granules
present is abnormally increased. When, however, a large number of
cells of any given organ contain more than the normal quantity of
these albuminoid granules, the appearance of the organ becomes
modified. In extreme cases the latter is swollen, doughy in
consistency, with ill-defined structural details, and in all instances
presents an opaque appearance. The term cloudy swelling is thus purely
descriptive, and was applied by Virchow to designate the optical
appearances of the condition in question. The granules, which
disappear on the addition of acids and alkalies, are apparently either
added to the cell or result from a precipitation within the same.
Frequently associated with these albuminoid granules are others,
distinctly recognizable as globules of fat. An apparent increase of
nuclei is often observed, and in certain organs, as the kidneys, the
cells seem less coherent than is normally the case. The study of this
condition in the kidneys is further of interest as indicating that the
border-line between a parenchymatous degeneration and a parenchymatous
inflammation is purely arbitrary. From similar exciting causes there
may be associated, with the described alterations of the epithelial
lining of the tubes, the exudation of albumen, the formation of casts,
the desquamation of epithelium, and the presence of leucocytes within
the tubules.
When the macroscopic changes are of moderate degree, and the
disturbance of function relatively slight, while the concurrent
alterations elsewhere, from the simultaneous action of the same cause,
are predominant and characteristic of the disease, the condition is
conveniently regarded as a degeneration occurring in the course of the
latter, rather than an inflammation. The latter term, on the contrary,
is to be applied when the granular infiltration of the cells is
associated with other evidences of an inflammatory exudation, and when
the pathological disturbances are to be directly attributed to the
parenchymatous changes.
It is customary to speak of cloudy swelling as a nutritive change, and
the condition may be induced by those causes which interfere with the
nutrition of parts or of the whole of an organ. Many authorities
regard this granular or parenchymatous degeneration as closely allied
to fatty degeneration, since many of the causes which produce the one
occasion the other. The former is often spoken of as an earlier stage
of the latter, from the frequent association of the albuminoid
granules with numerous globules of fat as a result of the more
prolonged or more intense action of a given cause.
Organs which give evidence of a granular degeneration contain, as a
rule, a diminished quantity of blood. This feature is usually
attributed to the pressure of the swollen cells upon capillary
blood-vessels. The {74} anaemic organ obviously becomes still more
cloudy, gray, and opaque in appearance from the diminished quantity or
impoverished quality of the blood.
The granular degenerations of the heart, liver, and kidneys, as a
whole, usually occur simultaneously, and afford a most important means
for the post-mortem recognition of the infective diseases. The
condition is therefore to be looked for in the exanthemata, especially
in small-pox and scarlet fever, also in erysipelas, septicaemia in its
manifold forms, diphtheria, typhoid and typhus fevers, cerebro-spinal
meningitis, etc. A common feature in all these cases is the occurrence
of fever, and it has been claimed that this element is the cause of
the degeneration. In opposition to this view is the well-known fact of
its presence in afebrile cases of poisoning from carbonic oxide, and
its absence in certain cases of pneumonia and exposure to high
temperatures.
The universal occurrence of cloudy swelling in fatal cases of the
affections above mentioned leads to the inference of its presence in
those instances terminating in recovery without obvious permanent
impairment of the organs and tissues concerned. It is therefore agreed
that the process may terminate in resolution--_i.e._ in a
disappearance of the excess of granular material. On the other hand,
its association, under circumstances, with fatty degeneration suggests
as extremely probable that the latter condition may represent a result
of the albuminoid infiltration. Even if this more serious issue
exists, the possibilities are still at hand for an absorption of the
degenerated material and a restitution of the destroyed protoplasm.
The effect upon the individual is evidently determined by the
persistence and dissemination of the condition, which, in turn, are
controlled by the immediate cause and the peculiarities of the
individual acted upon.
_Fatty Metamorphosis, Fatty Degeneration, and Fatty Infiltration._
The fat which is present within the body under physiological
conditions owes its origin primarily to the food taken. A diet which
is abundantly fatty furnishes a direct source for much of the fat
which appears accumulated in the various organs and tissues. Although
it may now appear that such a statement needs but little confirmation,
it is not long since the opinion prevailed that nearly all the fat in
the body came from the hydrocarbons of the food. This seemed all the
more plausible as the herbivora readily accumulated fat, although
their diet might contain this element in very small quantities.
Hofmann[29] made a decisive experiment with reference to the origin of
fat from fatty food by feeding a dog, made lean by starvation, with
bacon in abundance, but with little meat. In the course of a few days
the greater part of the fat introduced was deposited within the
tissues of the animal. Other experimenters have arrived at a similar
result, and it can no longer be questioned that fat, accumulated
within the body, owes its origin chiefly to the absorption of fat from
the food taken.
[Footnote 29: _Zeitschrift fur Biologie_, 1872, viii. 153.]
Another source for the fat of the body has long been
suggested--namely, the albuminates of the food. In the admirable
article on the formation of fat by Voit,[30] from which most of the
information herein {75} presented is derived, it is claimed that he
and Pettenkofer were the first to prove the origin of fat in the body,
under normal conditions, from albumen. This proof was an inference,
however, although presenting a high degree of probability. Valuable
evidence in the same direction was furnished by Kemmerich, who found
that the milk of a cow during a certain period held more fat than was
contained in the food; Subbotin and Voit have shown that more milk is
secreted the richer the diet in albumen. Still other observers have
furnished more decisive proof that fat is formed from albuminates.
[Footnote 30: _Hermann's Handbuch der Physiologie_, 1881, vi. 1, 235.]
Two sources for fat in the body under physiological conditions are
thus recognized: 1, the free fat in the food; 2, the fat derived from
the decomposition of the albuminates of the food.
Voit admits the possibility of the hydrocarbons serving as a third
source, although this possibility is unnecessary in most cases. Should
instances arise, however, where other sources for fat are found
insufficient, the hydrocarbons must be regarded as filling the gap.
Fat which is taken into the body is considered to be either consumed
or stored. That which is stored is chiefly accumulated in the great
reservoirs--viz. the subcutaneous and perinephritic fat tissue, the
mesentery, omentum, and bone-marrow--although it may be found
elsewhere, in the fluids and tissues of the body. This accumulation
serves as a source to be drawn from in case of need, and is called
upon where the easily-decomposed soluble albumen is disposed of by the
functional activity of the cells. An acting muscle demands food for
its work, and consumes first the soluble albumen, then the fat. An
excessive waste of fat is delayed by the decomposition of
hydrocarbons, but the demands may become so great that albumen, fat,
and hydrocarbons are consumed more rapidly and constantly than they
can be supplied. It being, therefore, admitted that fat is formed from
the albuminates, as well as from the fat of the food, the question
readily presents itself whether fat may not be formed from the fixed
albuminates of the body, especially from those contained within its
cells.
It is well known that in the secretion of sebum the superficial cells
of the sebaceous follicles contain fat in great quantity, while the
deeper layers are comparatively free from any appearances indicative
of the presence of fat. It is further admitted that when pus is
retained for a time the individual corpuscles contain fat-drops in
quantity and become transformed into fatty granular corpuscles.
Eventually, the pus is transformed into a detritus in which fat-drops
are found in great number.
Similar appearances may be present in the protoplasm of muscular
tissue, the cells of the liver, kidneys, and gastric glands, when
poisonous doses of phosphorus or arsenic are given. The occurrence of
an acute fatty metamorphosis of the cells of various organs in
new-born children has repeatedly been observed. The presence of fat in
various organs of the body in pernicious anaemia, and in the heart in
connection with stenosis of the coronary artery, is universally
recognized. The abuse of alcohol, long-continued obstruction to the
flow of venous blood, exposure to high temperatures, are all known to
be conditions in connection with which fat-drops are found in the
various cells of the body. The effects of poisoning with phosphorus
and arsenic are of special importance, as showing that the abundance
of fat present in the cells represents a result of the degeneration of
these cells, {76} since it takes place when the animal is deprived of
food. Although there is an evident destruction of albumen, there is
also a diminished elimination of carbonic acid and admission of
oxygen. These facts are explicable on the ground that the fat present
is not consumed, and the accumulation in the cells is evidence of this
lack of consumption. The fat is not simply stored, as none is taken
in, nor is any food received from which fat might be formed. Its
presence, therefore, must be regarded as due to degeneration.
Since fat may be formed in the body as a result of the metamorphosis
of cell-protoplasm, it is desirable to ascertain whether there are any
means by which stored fat may be distinguished from that present as
the result of a degeneration of the cell. The term fatty infiltration
has been used to indicate the presence of stored fat, the latter being
regarded as simply taken into the cell and retained for a longer or
shorter time, without any necessary interference with other functions
possessed by the cell.
In fatty degeneration, on the contrary, it is considered that the
quantity of fat present indicates a corresponding diminution in the
albuminates of the cell, and is connected with a diminution in the
function of the latter, all the greater the more abundant the fat.
It is found that in fatty infiltration, as a rule, the fat is present
in large drops, the size of the cell being increased in proportion to
the quantity of fat present. Although there may be several drops
present, they tend to run together, as is suggested by their different
size, varying proximity, and the constant presence of a considerable
quantity of protoplasm. In organs, on the contrary, whose function is
seriously, even fatally, impaired, the fat, as a rule, assumes rather
a granular form. Many minute fat-drops are present, and the cell is
not particularly, if at all, increased in size. The more abundant the
fat the less the protoplasm. Appearances are met with indicating a
transition between cells with few fat-granules and those with many.
If the morphological appearances of fatty infiltration and of fatty
degeneration were constant, there would obviously be little or no
difficulty in determining the nature of the process manifested by the
presence of fat. The exceptions occur both in fatty infiltration and
fatty degeneration. In the cells of the liver of an animal poisoned
with phosphorus fat makes its appearance in large drops, while in the
heart and kidneys of the same animal the fat is present in a granular
form.
During absorption from the intestine in the process of digestion fat
is present in the epithelium in a finely granular form. When digestion
is completed fat is no longer met with in these cells. The presence of
large or small drops, therefore, cannot be regarded as a sufficient
test of the origin of the fat. It is of equal, if not greater,
importance to bear in mind the organ concerned.
In the heart, liver, kidneys, and gastric glands, as well as
elsewhere, with the exception, perhaps, of the mammary gland, the
presence of many small fat-drops in the cells indicates a degeneration
of its protoplasm. The presence of large fat-drops, on the contrary,
in the organs and tissues, with the exception of the liver, indicates
an infiltration. Large fat-drops, then, may be present in the cells of
the liver as the result of an infiltration or of a degeneration. In
order to form a satisfactory opinion of the {77} nature of the
appearances in the liver in doubtful cases, it is important to note
the condition of those organs which may be simultaneously in a state
of fatty degeneration.
The accumulation of fat under physiological conditions is obviously
brought about, on the one hand, by those causes which permit a free
introduction, absorption, and deposition, and, on the other, by those
which check its oxidation or elimination with the secretions of the
body, as the bile, in which it may be present to a considerable
extent. A diet rich in fat, or in albuminates readily converted into
fat, offers a favorable element for the absorption of fat by the
healthy individual. If the organism demands but little of this fat for
oxidation, as in the case of the sedentary person, an accumulation is
likely to occur. This may become so considerable that obesity results.
Tissues in which normally but little fat is accumulated may become
infiltrated to a large extent. The intermuscular fibrous tissue thus
becomes loaded, and the activity, as well as the nutrition, of the
muscles is impaired. This accumulation may be manifested not only in
the voluntary muscles, but in the heart as well, which may present
abundant sub-pericardial and sub-endocardial fat, the myocardium also
being interlarded with streaks of fat, the so-called fatty
infiltration of the heart. The abdominal walls may become thickened to
the extent of a couple of inches, and the mesentery, omentum,
perinephritic tissue, and liver may become enormously increased in
weight from the mass of accumulated fat.
This infiltration of fat may take place under pathological as well as
physiological conditions. It is apparent that those causes which check
oxidation are likely also to prevent the consumption of fat, and it is
well known that the destructive processes in the lung, grouped under
the term pulmonary consumption, accomplish this result. Something
more, however, is necessary than the obliteration of pulmonary
blood-vessels and the destruction of an aerating surface. There may
be, as in emphysema of the lung, a diminished respiratory and vascular
surface, yet evidences of fatty infiltration, particularly of the
liver, are wanting. It seems probable that the constant anaemia, with
the loss of the blood-corpuscles, of pulmonary phthisis is an
important additional factor in checking oxidation in this disease.
This factor, it is needless to say, is not a necessary occurrence in
pulmonary emphysema.
Litten[31] has shown that when certain animals are exposed to high
temperatures the appearances of fatty infiltration and degeneration
are present in various organs of the body. He attributes the fatty
degeneration to a direct poisoning of the red blood-corpuscles and a
resulting diminution of the oxidizing processes.
[Footnote 31: _Virchow's Archiv_, 1877, lxx. 10.]
It is universally admitted that in chronic alcoholism a fatty liver is
frequently met with, even in the absence of those chronic interstitial
tissue-changes usually characterized under the name cirrhosis. Alcohol
is known to check the reception of oxygen and the elimination of
carbonic acid, and, whatever other disturbance of cell-activity it may
produce, its effect in favoring the accumulation of fat is directly
attributable, in part at least, to this disturbance of oxidation.
In those conditions known as cachexiae, the constant accompaniment of
progressive and wasting diseases, as cancer, leucaemia, chronic
dysentery, {78} etc., a fatty infiltration, particularly of the liver,
is a frequent accompaniment. A cachexia is dependent upon a complex
series of processes, many of which tend to check oxidation, and in
this respect is to be grouped with the conditions previously
mentioned. That the associated fatty infiltration is intimately
connected with the deficient oxidation is not to be doubted, although
the agents producing this deficiency may vary in detail.
The causes which favor fatty degeneration are numerous, and the result
represents one of the most serious conditions which can affect an
organ. As oxidation represents the chief means of normally disposing
of fat, so, pathologically, deficient oxidation favors the retention
of fat due to degeneration. Were a constant renewal of protoplasm to
take place, the degenerated fat might be displaced into the
circulation or retained within the cell. If the latter event should
occur, the result would be apparent as an infiltration, owing to the
increased size of the cell, although the condition giving rise to the
presence of the fat is a degenerative process. The importance of
impairment of nutrition as the chief cause for fatty degeneration is
thus obvious. It may readily be produced, experimentally, by measures
which check the flow of blood to a part. The same measures necessarily
prevent the presence of abundant oxygen, as fewer red blood-corpuscles
are presented.
Fatty degeneration resulting from impaired nutrition is apparent in
the heart in consequence of stenosis of its coronary arteries, in the
kidneys as a result of interstitial processes obstructing the
capillary circulation, in the brain from obliterative processes in the
arteries at the base or within the organ, and in blood-vessels from
the effect of age.
The cause of fatty degeneration may be general as well as local. In
poisoning from phosphorus and arsenic the appearances in most of the
organs indicate an actual destruction of protoplasm. Analysis of the
secretions confirms this inference, as the production of urea is
largely increased. Furthermore, there is less oxygen taken in and less
carbonic acid eliminated. As has been previously stated, these
conditions may be present in the starving animal. The fatty
degeneration is thus easily explained as a metamorphosis of
cell-protoplasm, and the deficient oxidation of the fat calls direct
attention to its accumulation rather than elimination.
In acute yellow atrophy of the liver and in cases of severe jaundice
fatty degenerations are constantly met with. That the origin and
accumulation of fat in these affections is also due to rapid
tissue-metamorphosis and checked oxidation is highly probable.
Although the elimination of urea diminishes rather than increases, as
shown by Schultzen and Riess, there are other links in the chain of
retrograde changes, as the appearance of leucin and tyrosin,
indicative of the extensive destruction of albuminates.
It is unnecessary in a work of the present character to call attention
to all the possible circumstances under which fat is present in the
body as the result of degeneration. Mention may be made of the acute
parenchymatous (fatty) degeneration of new-born children, of the
results of excessive bleeding, and of pernicious anaemia otherwise
occasioned. The fatty degeneration of the uterus after parturition, of
paralyzed muscles, and of tumors, the atrophic fatty degeneration of
the liver in chronic {79} passive congestion (nutmeg liver), are all
well-known examples. To these may be added the fatty degenerations
associated with amyloid and interstitial processes. It is apparent
that in most of these instances the common features of rapid
tissue-metamorphosis and deficient oxidation are present, and, being
present, offer a ready explanation for the appearance of the fat.
The clinical importance of fatty metamorphosis requires consideration
in connection with the description of the diseases in which its
occurrence is a constant feature. As the presence of fat in cells is
not necessarily pathological, so an interference with the function of
the cell is not invariably implied by its presence. When its existence
is suggestive of a local destruction of albuminates, a diminution of
cell-activity is a necessary consequence. Such diminished activity
must produce different results as the cells are those of muscles, of
vessels, or of glandular organs.
Even if fat is found in cells under conditions favoring such a
suggestion, it does not follow that the destruction of the cell must
result. Not only is it possible that the fat may be reserved for
eventual oxidation, and its place in the protoplasm be filled by
normal constituents, but it is also possible that the fat may be
eliminated, as such, from the body. The latter event is made apparent
by the experiments of numerous observers referred to by Cohnheim, who
have found free fat in the urine after its introduction into the
venous current.
_Cheesy Metamorphosis, Cheesy Degeneration, Caseation._
Virchow introduced the term cheesy metamorphosis, tyrosis, to
designate the process resulting in the incomplete absorption of pus
and the production of apparently similar changes in certain other
occasional constituents of the body. The characteristic cheesy
appearances were regarded as due to the inspissation of the material
concerned, in consequence of the absorption of its fluid. With this
inspissation there was frequently associated a partial fatty
degeneration, and the cheesy matter represented dead material, which
might undergo further changes, of which softening and calcification
were the more important.
Inflammatory products, as pus and fibrin, were especially prone to
become thus transformed, as well as other relatively transitory
materials of new formation--viz. tubercle and parts of various tumors.
The type of the cheesy metamorphosis was found in the enlarged
lymphatic glands, commonly called scrofulous.
The importance of a clear understanding of the cheesy metamorphosis is
now a matter of history. It is merely necessary to allude to the fact
that these cheesy products were formerly regarded as indicative of the
presence of tubercle, and were the tubercles. Tuberculization and the
cheesy condition were synonymous terms, and their indiscriminate use
led to much confusion with reference to the nature of tubercle.
Quite recently Weigert[32] has called attention to the conditions
present in necrosis resulting from the intermediate stoppage of the
blood-current in a part. The effect is manifested, under favoring
circumstances, by a cheesy appearance of the affected region, to which
the terms decolorized hemorrhagic infarction, anaemic or ischaemic
necrosis, have been applied. {80} Weigert lays stress upon the
existence of a coagulation of the protoplasm of the cells, with an
early disappearance of the nuclei, as the essential feature of this
form of necrosis, the conditions present being regarded as analogous
to those met with in the coagulation of the blood. The term
coagulative necrosis has consequently been introduced by Cohnheim to
represent the process first fully described in detail by Weigert. The
optical and physical properties of the ischaemic or coagulative
necroses of tissue are often manifested as cheesy appearances,
although the term coagulative necrosis includes conditions which do
not present a suggestion of cheese. It is thus apparent that cheesy
appearances may result in two ways: 1, by the inspissation of material
in a state of partial fatty degeneration; 2, by a coagulation of the
constituents of cells whose blood-supply is suddenly and completely
cut off. In the more restricted sense these caseous appearances are
regarded as indicative of a cheesy metamorphosis which arises by the
former of these methods. Cheesy appearances, on the contrary,
dependent upon the sudden death of a part, indicate an ischaemic or
coagulative necrosis.
[Footnote 32: _Virchow's Archiv_, 1880, lxxix. 87.]
Whatever may be the origin of the cheesy condition, the material
presenting this appearance is liable to further changes, known as
softening and calcification. The former event results from the soaking
of the dead part with liquid, in consequence of which a detritus
results. The softening usually begins at the oldest part of the cheesy
mass, and advances toward the periphery. The sanatory evacuation of
the emulsive detritus is permitted when a surface continuous with that
of the external surface of the body is reached, as instanced by the
escape of softened cheesy material from the lungs through a bronchus.
The possibility of the complete removal of the dead mass is thus at
hand, and an eventual obliteration of the resulting cavity may take
place by an adhesive inflammation of its walls.
The complete absorption of the cheesy material of an ischaemic
necrosis may occur by the extension into the latter of a
granulation-tissue from the periphery. Whenever cheesy appearances are
found on surfaces, as the degenerated tubercles of mucous membranes or
the circumscribed necroses in diphtheritic inflammation or in typhoid
fever, healing may be accomplished by their detachment as sloughs, a
clean ulcer being left. Cheesy material is frequently
encapsulated--_i.e._ imbedded in a layer of dense connective tissue, a
condition which indicates a local cessation of the process through
which the cheesy appearances arose. The same may be said of the
infiltration of the cheesy mass with earthy salts--calcification--an
event which will again be referred to in connection with the
consideration of the general subject.
_Hyaline Degeneration, Fibrinous Degeneration, Croupous
Metamorphosis._
Certain of the conditions now regarded as indicative of a coagulative
necrosis or a hyaline degeneration were previously described by Wagner
as the result of a croupous or fibrinous metamorphosis. According to
this observer, the cell-contents were transformed, under certain
circumstances, into a substance resembling externally clotted fibrin.
The formation of croupous and diphtheritic membranes, especially of
the larynx, pharynx, and trachea, was thus explained, also the hyaline
casts of the kidney.
{81} The results of this metamorphosis presented a hyaline appearance
under the microscope, and the term hyaline degeneration is now applied
more especially to indicate the production of microscopic changes,
while the hyaline appearances visible to the eye are rather included
under mucous, colloid, or amyloid metamorphoses.
The limitations in the use of the term hyaline degeneration are but
ill defined. On the one hand, there is included the transformation of
muscular tissue, first discovered by Zenker; on the other, the various
changes described by Recklinghausen and others, among which are
embraced the results of Wagner's croupous metamorphosis. As the
hyaline appearances are a frequent result of coagulative necrosis,
these terms are frequently used to indicate the same condition,
according as the optical or etiological features are uppermost in the
mind of the observer.
The hyaline or waxy degeneration of muscular fibre described by Zenker
represents a metamorphosis of the protoplasm of striated muscle in
particular, although the fusiform cells of the muscular coat of the
stomach and intestine may present a similar transformation.
The microscopic appearances are more characteristic than those visible
to the naked eye. To the latter the muscle appears paler, more
translucent, and homogeneous, and proves to be more brittle than
normal. The muscular fibres are found with the microscope to be
swollen, irregular in outline, the myosin transformed into flaky,
glistening masses, without evidence of the normal transverse
striation. These appearances have given rise to the term waxy
degeneration, which suggests a possibility of confusion with the
earlier recognized waxy degeneration of organs, due to the presence of
amyloid material. The waxy transformation of muscular fibre, however,
does not present the reaction with iodine characteristic of amyloid
substance. The degeneration of the muscle is usually regarded as the
result of a coagulation of the myosin, and it is claimed by Cohnheim
that the latter takes place only in dead muscle, either during the
life of the individual or as a post-mortem appearance.
The hyaline degeneration of muscular fibre is found in certain febrile
diseases, as typhoid and typhus fevers, scarlatina, variola, and
cerebro-spinal meningitis. It may also be met with when a muscle has
been exposed to violence, as in the insane who have been placed under
mechanical restraint. It has further been found in the vicinity of
tumors, especially where muscles have been invaded by their growth.
Cohnheim and Weil describe a similar condition in the tongue of frogs
after ligature of the lingual artery.
The pathological importance of the above-mentioned degeneration of
muscle is most prominent in cases of typhoid fever. The occurrence in
this disease of the haematoma or blood-tumor of the rectus abdominis
is thus explained, the degenerated muscle and its contained
blood-vessels being ruptured. The muscles of the thigh and the
diaphragm frequently undergo this degeneration; the change is more
rarely met with in other muscles of the body.
Recklinghausen regards a hyaline substance, hyalin, as a normal
constituent of cell-protoplasm which escapes in drops when the cell
dies. Its presence indicates a diminution in the vitality of the cell
from various causes. Under the microscope it appears as a sharply
defined, highly refractive meshwork, enclosing spaces of irregular
shape and size, in {82} which are frequently found nuclei, more rarely
cells or granules. Langhans has described this appearance as
channelled fibrin. It has been met with in the placenta, diphtheritic
membranes, blood-vessels, tubercles, and gummata.
The latest contribution to the history and nature of this form of
degeneration has been furnished by Vallat,[33] from whose article many
of the above data have been obtained.
[Footnote 33: _Virchow's Archiv_, 1882, lxxxix. 193.]
_Mucous Degeneration, Mucous Metamorphosis, Mucous Softening._
Of the various degenerations presenting a colloid--_i.e._
gelatinous--condition, the mucous variety is one of the most striking.
Its gross appearances may not differ materially from those to be
described under the head of colloid degeneration, but the diagnostic
characteristic of the change is to be found in the presence of mucin.
The presence of this substance is readily detected by the addition of
acetic acid to mucus, the effect being a fibrillated appearance of the
latter, the fibres presenting a more or less parallel distribution.
This fibrillation of mucus is regarded as the result of a coagulation
of its mucin, previously held in solution by an alkali. Mucin is thus
present in the body as a normal constituent, and, in the secretions
from mucous membranes, owes its origin to the existence of epithelial
cells, whether these represent gland-cells, as in the case of the
muciparous glands of the bronchial mucous membranes, or whether they
are superficial cells, as those of the gastric and intestinal mucous
membranes.
In the origin of mucus as a secretion from glands Heidenhain[34]
claims that a destruction of gland-cells accompanies the continuance
of the secretion. At the outset, however, the mucin escapes from the
cells, the latter remaining relatively intact. With the persistence of
the secretion there results a destruction and a new formation of the
muciparous cells. In the pathological production of mucus from mucous
membranes, as in catarrh, there is no reason to doubt that the
persistence of an irritation is the cause of abundant mucus, and that
the latter is dependent upon the rapid formation and destruction of
epithelial cells.
[Footnote 34: _Hermann's Handbuch der Physiologie_, 1880, v. 64.]
The origin of mucus from epithelial cells under physiological and
pathological conditions being apparent, it readily follows that the
epithelioid cells of tumors might be supposed to be liable to a
similar metamorphosis. It is well known that cancerous tumors,
especially those of the stomach and large intestine, are frequently
met with, which present an abundant gelatinous material, more or less
completely filling the spongy, fibrous meshwork. These are the
alveolar, gelatinous, or colloid cancers.
The gelatinous or colloid material often gives the reaction of mucin,
and the microscopic appearances of the tumor show that the jelly-like
substance lies in that part of the tumor which corresponds with the
position of the epithelioid cells. The latter are found in various
stages of degeneration, the appearances being similar to those
observed in the mucous degeneration of true epithelium.
The prevailing theory of the origin of cancer from epithelial
structures {83} readily suggests an explanation for the frequency of
the mucous variety of cancer in connection with those parts from which
mucus normally arises from the degeneration of the epithelium.
The mucous metamorphosis affects connective tissues as well as
epithelium. The Whartonian jelly of the umbilical cord and the
vitreous humor of the eye are known, through the investigations of
Virchow, to owe their gelatinous condition to the presence of mucin.
The latter lies in the intercellular substance; that is, between the
cells. The appearance of these indicates no degenerative process, but
the presence of mucin is obviously an essential constituent of the
tissue. Whether this mucin represents a transformation of the gelatin
of the intercellular substance, or a secretion from the fixed cells,
or a metamorphosis of the migratory cells of the tissue, is not known.
In mucous tissue, however, there is present mucin, wholly independent
of any epithelial degeneration. Mucous tissue is present in the eye as
a normal constituent of the adult, and in the umbilical cord as a
normal constituent of the infant at full term. It is also abundantly
met with in the subcutaneous and intermuscular tissues of the foetus.
Its pathological occurrence in the adult as a circumscribed tumor, the
myxoma, may also be mentioned.
A gelatinous substance containing mucin is found in the adult
independent of the mucous tissue, but obviously arising from a
transformation of intercellular substance. The most striking example
of this occurrence is the cystoid softening of cartilage, especially
of the costal cartilages of old people, the basis substance being
transformed into a fluid containing mucin. A similar metamorphosis is
of frequent occurrence in the intervertebral disks and in the
destruction of cartilage in acute and chronic inflammations of the
joints. The intercellular substance of cartilaginous tumors also
becomes softened and converted into a liquid containing mucin.
In osteomalacia and in the absorption of bone the mucous degeneration
of the bone-cartilage plays an important part. The lime salts are
first set free, and the cartilage then undergoes a mucous
degeneration; the product is either absorbed or remains as a liquid
within cavities of large or small size. The mucous metamorphoses of
fibrous and fat-tissues, likewise of bone-marrow, are well recognized
instances of the occurrence of a mucous transformation of the
intercellular substance of connective tissues. Finally, clotted
fibrin, so often met with as the product of the inflammation of serous
surfaces, may undergo a mucous metamorphosis, and, thus transformed,
offer a suitable material for absorption.
_Colloid Degeneration, Colloid Metamorphosis._
Laennec used the term colloid in a descriptive sense to indicate a
gelatinous appearance, and for a long time its use was thus
restricted. As the colloid appearances were found to differ in their
chemical reaction, their distribution, and their pathological
importance, and as the term was further extended to include
appearances seen with the microscope, it obviously became necessary to
subdivide the colloid series of changes according to the observed
differences. Its use is now limited to those gelatinous conditions or
appearances due to the presence of a fixed albuminate, homogeneous or
finely granular, translucent, colorless or pale {84} yellow, of
varying consistency, which does not become fibrillated on the addition
of acetic acid, and which does not change in color when acted upon by
iodine. This albuminate is considered in most instances to represent
the result of a transformation, a metamorphosis of cells, and is
associated with an impairment of their function--a degeneration which
is progressive, and leads, sometimes, to the destruction of the organ,
as occurs in certain instances of colloid degeneration of the thyroid
body. Usually, the process is limited, affecting particular parts
rather than the whole of an organ. The reaction presented by a
solution of sodium albuminate in the presence of neutral salts leads
to the view that colloid material may represent a coagulation of an
albuminous substance or substances under favoring conditions. The
presence of colloid masses in the kidney thus meets with a plausible
explanation.
The place of its typical occurrence is the thyroid body in certain
cases of goitre, and it is early met with as a homogeneous substance
replacing the granular cell-protoplasm. With its increase the latter
disappears, and the entire cell is transformed into a homogeneous
sphere. At times the colloid substance may be seen to project from the
surface of the cell as a pale rounded clump. The aggregation of these
clumps results in the presence of masses of various size, in which may
be found granules of fat or pigment and crystals of cholesterin, which
are accidental, not essential. Colloid masses are sometimes met
with--in lymphatic glands, for instance--as concretions, mulberry-like
aggregations of stratified colloid bodies, which may be infiltrated
with earthy salts. Colloid material may eventually become liquefied,
transformed into a sodium albuminate; and the presence of cysts in
certain varieties of goitre is thus explained. The coexistence in the
kidney of colloid accumulations and watery cysts has led to the view
that the latter may, under certain circumstances, result from the
former through the liquefaction of the colloid material. The same view
is held with regard to the origin of cysts frequently met with in the
choroid plexuses.
The colloid metamorphosis of cells is also to be found in the
epithelium of mucous membranes and their glands, in the prostate,
suprarenal capsule, sebaceous glands of the skin, and in the cells of
certain tumors.
_Amyloid Degeneration, Amyloid Infiltration, Waxy Degeneration,
Lardaceous Degeneration._
The colloid appearances due to the amyloid degeneration of cells are
of the greatest clinical importance from their frequent occurrence and
the gravity of the symptoms connected with their presence. In amyloid
degeneration there is the transformation of the cell-protoplasm into
an albuminous material different from other albuminates found in the
body. This transformation is at the expense of the functional activity
of the cell, and the latter becomes inert. Amyloid degeneration
represents no mere substitution, but an addition, since the affected
tissue is increased in volume. The albuminate was called amyloid by
Virchow in consequence of its color-reaction with iodine. Its method
of origin is wholly unknown, never being found in the circulating
fluids nor in articles of food. It is met with chiefly in the cell,
although its presence in the intercellular substance of old people is
recognized, and its occurrence in {85} the midst of the thrombotic
deposition on inflamed valves and in the results of inflammatory
processes is also recorded.
At present the question is under discussion whether the amyloid
degeneration may affect cells of the most varied character, or whether
it is limited to those of connective tissues. Eberth[35] maintains
that in all cases the amyloid disturbance is seated in the connective
tissue. Kyber,[36] the latest investigator, in opposition to this view
maintains that this affection is not limited to the connective tissue,
but may also be seated in the parenchymatous cells of organs. Whether
the one of these views is to exclude the other, or whether both are
not correct, remains for future investigation to decide.
[Footnote 35: _Virchow's Archiv_, 1880, lxxx. 138; 1881, lxxxiv.]
[Footnote 36: _Ibid._, 1880, lxxxi. 7, 111.]
Wherever the amyloid material may be situated, the result is a
transformation of the cells into a homogeneous, glistening, colorless
material, which occupies more space than the original cell, and, when
abundant, is accompanied with a loss of the primitive details of the
cell-structure. This material is recognized by the color it presents
when acted upon by iodine alone, by iodine and sulphuric acid, or by
methyl-aniline. The first produces a reddish-brown color, the second a
blue, and the last a violet or purple color. These reactions are all
characteristic, and the first is of special value in the macroscopic
recognition of the process, while the last two are of special
importance in the microscopic recognition of the earlier stages of the
affection.
With the advance of the degeneration and its dissemination, the organ
affected presents, in the diseased portions, pale-gray, glistening,
translucent patches, and becomes increased in size and density in
proportion to the quantity of amyloid material present. The change
appears primarily in the vessel wall or outside the same, and there
results a diminution in the calibre of the vessels, with a lessened
quantity of blood in the organ.
From the homogeneous and translucent appearance of the surface and the
increased density of the tissues the resemblance to bacon or wax is
suggested, and the terms lardaceous, bacony, or waxy degeneration have
been applied. Notable differences in degree and seat occur in
connection with the organs diseased. In the spleen, for example, the
change may be limited to the arteries of the Malpighian bodies and
their immediate surroundings. To this condition the term sago spleen
is applied, the enlarged, rounded, translucent, and projecting bodies
suggesting granules of boiled sago. The appearances of the diseased
part are further affected by the association of other conditions, as
the presence of fat or pigment. When fat is present, it is often to be
regarded as a result of the gradual and progressive increase in the
obstruction to the circulation of blood in the organ.
Although so little is known of the immediate cause of amyloid
degeneration, its distribution in the various organs of the body is
fully ascertained, as well as certain of the conditions which are
likely to be followed by its presence. It is known to occur as a
localized process in cartilage, in the conjunctiva, in certain tumors,
cardiac thrombi, scars, retained inflammatory products, and renal
casts. The causes of this localized appearance are wholly obscure, and
little or no general inconvenience results. Its presence, however, on
a large scale and in various parts of {86} the body at the same time,
is met with under such circumstances as indicate a distinct
etiological relation. An appreciation of these circumstances is of
importance, since their existence demands an investigation as to the
probable presence of the degeneration. The organs thus affected are
the spleen, liver, kidneys, and intestine. It is to their disturbance
of function that the pathological importance of amyloid degeneration
is to be especially attributed.
Other organs which may sometimes be affected are the lymphatic glands,
pancreas, suprarenal capsules, omentum, uterus, bladder, prostate
gland, heart, and thyroid body. In the case of a general diffused
infiltration these organs are variously degenerated, now some, and
again others, showing a more extensive alteration, while few or many
may be simultaneously diseased. The longer the process has continued,
the greater the degree of the disturbance and the larger the number of
the organs infiltrated. Although, in general, a period of months and
years may be demanded for these extensive changes, very serious
disturbances may arise within a short time, and Cohnheim[37] records
several cases which suggest that widely diffused amyloid degeneration
may occur within a few months--in one instance in less than four
months.
[Footnote 37: _Virchow's Archiv_, 1872, liv. 271.]
All that is at present known with regard to the etiology of this
process applies to certain general diseases with which in the course
of time it is likely to be associated. These have one element in
common, that of chronicity, and are likewise the occasion of a
progressive wasting of the body. Of these affections, that which holds
the first place is chronic pulmonary consumption, especially that form
in which extensive destruction of the lungs and ulcers of the
intestine are present. Another disease whose effects are in like
manner to be regarded as general is syphilis, and in the later stages
of this disease amyloid degeneration is likely to occur, and often to
represent by its resulting disturbances the immediate cause of death.
Again, chronic suppurative processes, especially those due to disease
of the bones and joints, are a frequent antecedent of amyloid
degeneration. Finally, the process has been found in connection with
leucaemia, chronic intermittent fever, rickets, gout, and certain
malignant tumors. This last group, however, is one in whose sequence
the degeneration is to be regarded as exceptional.
The clinical importance of this process is due to the resulting
disturbances in the function of such important organs as the liver and
intestines, the spleen and lymphatic glands, and the kidneys. The
nature of these disturbances obviously demands detailed consideration
in connection with the description of the diseases of the respective
organs. It may be mentioned here that the infiltration of the walls
leads to a narrowing of the calibre of blood-vessels, and thus a
diminution in the supply of blood to the part or organ. The resulting
impairment of nutrition becomes enhanced from the condition of the
blood, which is impoverished from the simultaneous infiltration of the
blood-making organs. The nutrition of the individual thus suffers as
well as that of the immediately diseased organ. Fatty degeneration and
atrophy of the parenchymatous cells of organs like the liver and
kidneys is the constant result of long-continued and extensive
infiltration of these glands.
Mention is intentionally omitted of the so-called amyloid bodies, {87}
corpora amylacea, considered in connection with amyloid degeneration
in most text-books on pathology and pathological anatomy. They usually
present a different reaction with iodine, their origin has but little
in common, their distribution is for the most part unlike, and little
or no clinical importance is to be attached to their presence.
_Calcification, Ossification, Petrifaction._
When salts previously held in solution are precipitated under abnormal
circumstances in the tissues of the body, the part is said to be
calcified, ossified, or petrified. Although these terms are often used
as equivalent, the last is to be regarded as more general than its
predecessors, since it includes the deposition of other than the
calcareous salts.
In the pathological ossification, as well as its physiological
prototype, the carbonates and phosphates of calcium and magnesium are
present in a specially formed tissue of the nature of bone-cartilage,
whereas calcification occurs independently of such a new-formed
tissue. The deposition of the calcareous salts takes place either in
the cells or intercellular substance of living or dead tissues, when
the terms calcification or ossification are applied, or as
accumulations of various size in tissues or canals, which are known as
concretions and calculi.
The immediate causes of the physiological deposition in the formation
of bone are so obscure that only more or less probable explanatory
theories are advanced, to all of which obvious objections arise. The
causes of a pathological precipitation may be regarded as equally
hidden. It is apparent, however, that old age usually furnishes the
necessary factors. This in part may be due to the feeble nutrition
associated with impairment of function in advancing years. In part it
may be the result of the numerous opportunities offered in a long life
for the occurrence of inflammation, the products of which are
frequently infiltrated with calcareous salts. The latter are
apparently kept in solution by the action of living cells, for, though
presented to all in the fluids of the body, they are precipitated most
constantly in dead parts or in the vicinity of those cells whose
function is presumably lessened from disease or age. The solvent
action of living cells is further demonstrated by the effect of the
giant-cells in removing calcium salts from living or dead bone.
The causes of calcification are therefore to be regarded as local,
depending upon a destruction or weakening of the cells of a
part--conditions which are directly attributable to an interference
with nutrition. The deposition of calcium salts thus represents a
disorder of nutrition, and may be experimentally produced by agencies
which occasion a necrosis of tissues.
Although the immediate causes of the precipitation of the calcium
salts must be expressed somewhat vaguely, the places and effects of
their accumulation are sufficiently well known, as are the resulting
appearances. The presence of these salts in sufficient quantity
produces a homogeneous, granular, strongly refractive appearance of
the cell or intercellular substance, in addition to a greatly
increased resistance to pressure. When muriatic acid is added to the
affected part, the salts are dissolved, with the escape of abundant
bubbles of gas when a carbonate is present, and with a rapid fading of
the glistening appearance, without effervescence, {88} when the salt
is a phosphate. After the removal, the cell or intercellular substance
is readily recognized, with such modifications in its appearance as
may be due to the action of the strong acid. The parts in which this
deposition or infiltration has taken place are either relatively
normal in appearance or variously altered from disease, and the
calcium salts are to be regarded as absorbed from the constituents of
the food and deposited, or as taken up and transferred from the bones
of the body. That both sources are drawn upon is obvious from the
abnormal presence of calcareous material in the soft parts, in
connection with increased density of the bones, as well as with a
diminution in the density of the latter. The term calcification is
more correctly applied to the presence of the salts in normal tissues
other than bone, or in the products of disease not simulating
bone-cartilage in structure. A pathological ossification is to be
considered present when an actual new formation of bone has taken
place so limited and so situated as not to suggest a tumor of bone, or
when the calcium salts are deposited in a new-formed tissue whose
structure stimulates that of bone-cartilage.
Tissues which may become calcified are, in the first instance, the
connective tissues, and of these fibrous tissue and cartilage are
especially liable. Epithelial, muscle--in particular the unstriped
variety--and ganglion-cells may also become calcified. The frequency
with which blood-vessels, especially arteries, are affected is such
that it is regarded as almost normal in advancing years that
calcareous material should be deposited within the vascular walls. A
distinction is drawn between an ossification and a calcification of
the blood-vessels. The former term should be limited to the osteoid
plates so often found as circumscribed thickenings of the aortic
intima, and which are obviously new-formed patches of fibrous tissue
in which the calcium salts are accumulated. A calcified artery, on the
contrary, is one usually of a size varying between that of the common
iliac and the temporal arteries, whose wall has become rigid and
unyielding, suggestive of a pipe-stem, from the presence of calcareous
deposits in the muscular middle coat.
From the frequency with which the osseous plates of the aorta are
associated with the fatty and fibrous changes in chronic inflammation
of the intima, the so-called atheromatous degeneration of the same, it
is customary to speak of the calcified artery at the wrist or temple
as an atheromatous artery or as evincing an atheromatous degeneration.
The common feature in the aortic changes and in the calcified muscular
coat is the element of age. They are frequently, though not
necessarily, associated. The one is the result of an inflammatory
process productive of a new, fibrous, tissue in which the calcium
salts are infiltrated; while the other is due to a deposition of the
latter in the normal, pre-existing, muscular elements of the vessel.
Calcification and ossification of blood-vessels are frequent when the
latter become dilated, as in aneurisms, whether these occur as
circumscribed tumors or as a serpentine elongation and widening of the
affected vessel.
Cartilage is also a tissue which presents a double relation to
calcareous deposition. On the one hand, there may exist an
ossification resulting from the extension of a growth of bone from the
perichondrium into the cartilage. The structure of this bone presents
all the details found in {89} normal bone--lacunae, lamellae, and
marrow-spaces. On the other hand, a section of the cartilage,
especially the costal cartilages, may contain opaque, gray, or
grayish-yellow patches, grating under the knife, which are wholly due
to the presence of calcium salts in the hyaline intercellular
substance of the cartilage. This calcification of the cartilage, which
may also involve the capsules of the cells, is frequently associated
with an ossification, although this relation is in no way essential.
Calcification of the placenta, of the fibrous framework of the lungs,
of the mucous membrane of the stomach, or of the atrophied glomeruli
of the kidney, are well-recognized instances of the infiltration of
calcareous material in normal or atrophied tissues. On the contrary,
ossification of the fibrous inflammatory products of the pleura,
pericardium, and peritoneum are instances of a pathological
bone-formation, analogous in its nature to that met with in the intima
of the aorta. The fibrinous and fibrino-cellular products of the
inflammation of serous surfaces are favorable positions for the
deposition of calcium salts, as are thrombi arising from the walls of
blood-vessels. The latter are rather instances of the calcification of
dead parts, analogous to the members of the group which includes the
formation of calculi and concretions, the calcification of the dead
foetus in abdominal parturition, of cheesy lymphatic glands, and of
cheesy material in the lungs and elsewhere. Finally, there remains the
calcification of tumors of the most varied nature, the salts being
present either in living or dead parts of the tumor.
Instances of the deposition in the tissues of other than calcareous
salts are abundantly met with in gout. In this disease cartilage,
ligaments, and tendons, bone-marrow, muscle, the endocardium and
aorta, the membranes of the brain and spinal cord, the skin and
kidneys, may contain deposits of acicular crystals and amorphous
granules. Although these deposits are largely composed of sodium
urate, calcium urate may be present with other salts, as sodium
chloride and calcareous compounds. According to Ebstein,[38] the
earthy salts in gout are deposited in necrotic patches of previously
diseased tissue. The local conditions are therefore analogous to those
concerned in the formation of chalky concretions.
[Footnote 38: _Die Natur und Behandlung der Gicht_, Wiesbaden, 1882,
45.]
Concretions and calculi are collections of earthy salts, the former
lying within tissues, the latter being present in canals opening
externally. Both represent the results of a deposition in and upon
organic material, which is often an inflammatory product, at times
surrounding a foreign body acting as the exciting cause of the
inflammation.
The earthy matter of which the concretion is composed consists mainly
of carbonate and phosphate of calcium, while the chemical properties
of the calculi often vary in accordance with the nature of the
secretion which flows by them. The salivary, pancreatic, intestinal,
lachrymal, and prostatic calculi are chiefly formed of calcareous
salts. These salts also are an important, if not the chief,
constituent of biliary and urinary calculi. In the former pigment,
bile acids, and cholesterin may also be present. Urinary calculi are
of still more varied composition, containing not only the calcium
salts, as the oxalate, phosphate, and carbonate, but also uric acid
and the urates of sodium and ammonium, in addition to the
ammoniaco-magnesian phosphate.
The infiltration with calcium salts may prove beneficial as well as
{90} injurious--beneficial under those circumstances where further
changes might prove harmful, as in the softening of cheesy material or
the maceration of a dead foetus in the abdominal cavity. The
calcification of certain tumors, as the fibro-myoma of the uterus, is
equally sanatory, the further growth of the calcified parts being thus
checked. The calcification of an aneurismal sac may prove beneficial
in strengthening a weakened blood-vessel.
The injurious effects are seen more particularly in case of the
calcareous infiltration of the middle coat of arteries. Such vessels
become converted into rigid and unyielding tubes at various parts of
their course, and the nutrition of peripheral parts becomes
correspondingly lessened. Hence, in great measure, the liability of
old people to serious inflammatory processes from trivial irritation
of peripheral portions of the body, such inflammations often
terminating in gangrene.
The calcification and ossification of the cardiac valves and the
calcification of attached thrombi, furnish frequent and constant
occasion for disturbances in the functions of the heart, resulting in
dilatation and hypertrophy, with the sequence of symptoms of chronic
valvular endocarditis.
The great clinical importance of the presence of calcium salts in the
circulatory apparatus is such that further reference in this place to
its results is unnecessary, as its special relations are more
important than its general features.
Calculi act as local causes of inflammation, and their presence is
likely to be followed by ulceration, abscess, and stenosis, perhaps
obliteration, of the smaller canals in which they may lie.
_Pigmentation._
The pathological pigmentation of the body results, presumably, from
the metamorphosis of the coloring matter of the blood or from the
introduction from without of pigments insoluble in the fluids of the
body. The former of these methods has recently been studied by
Langhans[39] and Cordua,[40] and the present views of this subject are
chiefly due to their observations, as well as to the earlier
investigations of Virchow and others.
[Footnote 39: _Virchow's Archiv_, 1870, xlix. 66.]
[Footnote 40: _Ueber Resorptionsmechanismus von Blutergussen_, Berlin,
1877.]
The haemoglobin contained in red blood-corpuscles is considered to be
composed of a coloring matter, haematin, combined with an albuminate,
globulin. When blood is removed from the body the haemoglobin is
readily separated from the corpuscles by various agents, and is then
dissolved in the plasma, which becomes lac-colored. This solubility of
the haemoglobin is of importance in connection with the absorption of
extravasated blood. During the time necessary for this process to take
place, observable changes are apparent in the color of the affected
part when its seat is superficial, especially cutaneous. These changes
in color are largely dependent upon the modifications undergone by the
haemoglobin.
It is well known that a yellowish discoloration of the general surface
frequently takes place when extensive internal hemorrhages have
occurred, constituting a form of jaundice (haematogenous) attributed
to the presence of the coloring matter of the blood. As yet there has
been no satisfactory chemical analysis of this diffused pigment, which
if not haematin must be regarded as its derivative, although a
coexistent increase of the urobilin in the urine has been observed.
The association of the stained skin and urine, {91} in the absence of
causes favoring an absorption of bile-pigment, leads to the inference
that the abnormal discoloration is due to the absorption into the
circulating fluids of the body of a pigment dissolved out of the
extravasated red blood-corpuscles. This view is confirmed by the
microscopic examination of the latter, which discloses the presence of
pale, shadowy, round outlines enclosing faintly granular material,
which are regarded as decolorized red corpuscles. In the course of a
few days glistening crystals and granules of a yellowish-red color
make their appearance in the midst of the unabsorbed blood. The
crystals are usually oblique rhombic prisms, varying in size from the
larger symmetrical shapes to the more minute, apparently granular,
forms. Acicular crystals are also to be met with, more yellow than red
in color, and are sometimes present in great abundance, although they
may be wholly absent. Virchow has applied the term haematoidin to
these crystals. Owing to the resemblance in the chemical reactions of
solutions of haematoidin and of the biliary coloring matter,
bilirubin, and to the similar crystalline forms of the latter, it has
been maintained that the two are identical. Late investigations
indicate that solutions of crystals with the appearances of
haematoidin are not invariably alike in their reaction. A solution of
these in chloroform may become decolorized when acted upon by a dilute
alkali, or it may not be thus altered. Bilirubin presents the former
relation, while chloroform solutions of the coloring matter of the
yelk of egg and of the corpus luteum, called lutein or haemolutein,
are not decolorized by an alkali. Although the crystalline forms of
haematoidin and bilirubin are not to be distinguished, it is not to be
conceded that the two substances are identical. As Maly,[41] the
latest writer on this subject, states, the term haematoidin is merely
indicative of a microscopical picture. Although the identity of the
coloring matter of the blood and of the bile is not admitted, the
intimate relation of the two is not only suggested by the similarity
of crystalline form, but by the relation determined between urobilin,
bilirubin, and haemoglobin. Urobilin is the coloring matter extracted
from the urine in fever by Jaffe, and it has since been obtained from
bilirubin by Maly,[42] who has given it the name of hydrobilirubin.
This hydrobilirubin has also been derived from haemoglobin. According
to Maly, this genetic relation between the coloring matter of the
blood and bile, shown in the production of hydrobilirubin, is the only
chemical evidence of the connection of the two pigments.
[Footnote 41: _Hermann's Handbuch der Physiologie_, 1880, vii. 155.]
[Footnote 42: _Op. cit._, 161.]
Haematoidin is to be regarded not only as directly derived from
solutions of haemoglobin, but as originating through the medium of
indifferent cells. Langhans claims that this pigment is formed within
movable cells which accumulate in great numbers in the vicinity of the
blood-clot, and, in virtue of their amoeboid properties, take into
themselves the extravasated corpuscles, entire or in fragments. The
indifferent cell may become enlarged into a giant-cell, and then
contain numbers of whole or disintegrated red corpuscles. In time
these colored corpuscles and fragments become smaller, more
glistening, and darker-colored, and eventually are transformed into
granular or crystalline haematoidin. These granules may be set free by
the fatty degeneration of the cell, or may be transferred within the
cell to distant parts.
{92} The diffusion and absorption of a solution of haemoglobin, and
the formation of crystals of haematoidin from the same or through the
medium of cells, are supplemented by an apparent inspissation and
condensation of the haemoglobin. The resulting dark-brown pigment may
remain at the seat of the hemorrhage indefinitely, and may be
accompanied with reddish-brown flakes, which, as shown by Kunkel,[43]
are composed of hydrated ferric oxide.
[Footnote 43: _Virchow's Archiv_, 1880, lxxxi. 381.]
Another feature in the absorption of extravasated blood is to be found
on examination of the nearest chain of lymphatic glands. These may be
seen swollen, of a dark-red color, and homogeneous surface. In density
and color, as well as shape, they suggest the small supplementary
spleens so frequently met with. These glands owe their change in
appearance to the presence of large numbers of unaltered red
blood-corpuscles which have entered the lymphatics traversing the
region of hemorrhage. Within the lymph-glands they undergo a
metamorphosis similar to that taking place at the part from which they
were transferred. In the course of weeks or months there remains in
the place of extravasation simply pigment, either as crystals or
granules. Such pigment may remain for years imbedded within the
tissues, or it may become absorbed, no trace of the original
disturbance remaining. Its removal may take place presumably through a
local solution of the pigment or the transfer of the granules or
crystals by means of wandering cells to the nearest lymphatic glands
or to the more remote parts of the body. An eventual elimination may
occur through the secretions, especially the urine or bile, or there
may result a deposition and permanent retention of the granules.
The investigations of Langhans are especially interesting, as
suggesting efficient means for the production of pigment by cells
whose function is intimately connected with pigmentation, as the cells
of the rete Malpighii, of the choroid, and of certain tumors. The
observations of Gussenbauer,[44] however, lead to the conclusion
earlier advanced by Virchow, that pigment may be produced by the
diffusion into cells, outside the vessels, of a solution of the
pigment of the blood in the plasma of the latter. A precipitation of
this dissolved pigment into granules is considered as eventually
taking place.
[Footnote 44: _Ibid._, 1875, lxiii. 322.]
The method of origin of pigment thus described applies only to those
discolorations which are unquestionably due to the metamorphosis of
the coloring matter of the blood. Examples are furnished not only by
the extravasation of blood on a large scale, but also by the escape of
red blood-corpuscles in small numbers. Such an escape takes place from
the pulmonary vessels in chronic obstruction to the admission of blood
into the left side of the heart. The resulting brown induration of the
lungs owes its color to the metamorphosed blood-pigment which is
present as haematoidin in the interstitial tissue of the lungs, as
well as contained within amoeboid cells in the alveolar and bronchial
cavities.
It is probable that a similar transformation of haemoglobin takes
place in the spleen and elsewhere in melanaemia. In this condition the
black granules of pigment, although differing in color and form from
haematoidin, contain iron, and have received the name melanin. These
granules are either free in the blood or are contained within the
white {93} blood-corpuscles. Their origin in the spleen is directly
suggested by their frequent presence, often in considerable numbers,
in the large, so-called splenic, corpuscles of the blood in the
hepatic capillaries. Eventually, the pigment is found at more remote
points in the circulation, and becomes fixed in the interstitial
tissue of the various organs of the body.
The black pigment of the cells of melanotic tumors, also called
melanin, is not to be directly traced to the haemoglobin. Virchow[45]
early called attention to the absence of iron in such pigment.
Ferrated and non-ferrated varieties of melanin are thus to be
recognized, the term being used in the same way as haematoidin,
indicative of a microscopical appearance. A still further complication
in the composition of melanin is suggested by Kunkel,[46] who has
isolated a ferrated pigment from melanotic tumors. It shows, however,
with the spectroscope, no relation to haematin, bilirubin, or
hydrobilirubin. That its nature is similar to the normal pigment of
the skin and choroid is suggested by the customary origin of the
melanotic tumors in such pigmented tissues, and by the resemblance in
appearance and reactions.
[Footnote 45: _Virchow's Archiv_, 1847, i. 378.]
[Footnote 46: Ziegler, _op. cit._, 100.]
That pigment of the most varied sort may be introduced into the body
from without, and may remain indefinitely in the organism, is
sufficiently well known from the results of tattooing. What is
essential in such cases is, that the pigment shall be finely divided
and insoluble in the fluids of the body. The most important of such
pigmentations are those taking place through inhalation into the
lungs. The reception by this channel of particles of soot is so common
that it is most exceptional for the lungs of an adult to be free from
the bluish-black discoloration due to this agent. Particles of
coal-dust presenting the details of vegetable structure are met with
in the lungs of individuals exposed to an atmosphere charged with this
material. The worker compelled to inhale the dust of iron eventually
accumulates a store of this substance, the quantity of which is
essentially dependent upon the length of exposure, the degree of
impregnation of the atmosphere, and the insufficient nature of the
protectives employed.
Although a large part of the pigmentation under such circumstances is
due to the direct presence of the foreign body, the appearances are
also partly the result of consequent minute hemorrhages. The coal-dust
and the iron-filings are often sharp and jagged fragments, which
penetrate the delicate tissues, and the escaping red blood-corpuscles
are acted upon by the amoeboid cells in the air-passages, with the
consequent formation of haematin or haematoidin, as are the
blood-corpuscles in larger hemorrhages. The inhaled pigment finds its
way, either directly or by the agency of amoeboid cells, into the
lymphatics and fibrous tissue of the lungs, and remains indefinitely
either in the bronchial and pulmonary lymphatic glands or in the
interstitial tissue of the lungs.
Attention may be here called to that pigmentation of the skin and
deeper-seated parts of the body, especially of the kidneys, known by
the term argyria. The long continued internal use of nitrate of
silver, in former years so extensively employed, especially in
diseases of the nervous system, results in the reduction of the silver
and its deposition as minute particles in the tissues. Whether the
silver is first reduced in the {94} intestine and then absorbed, or
whether it is absorbed as an albuminate and subsequently reduced,
still remains an open question.
Although the pathological pigmentations form an extended series of
alterations, the clinical importance of the condition may be regarded
in many instances as trivial. The pigments resulting from
extravasation produce no disturbance of function. The presence of
bile-pigment does not account for the symptoms of jaundice. The
clinical importance of melanaemia has perhaps been overrated. The
earlier observations led directly to the inference that mechanical
obstruction to the circulation in various organs might take place. The
particles of pigment and the cells containing them were so numerous
that this inference seemed quite probable. The evidence is still
lacking, however, which proves the existence of definite symptoms and
characteristic lesions as the result of the melanaemic condition.
The inhaled foreign bodies, as coal and iron, are productive of
greater disturbances, and are well known as efficient causes in the
production of chronic pulmonary consumption. The coal-miner's and
scissors-grinder's phthises usually have, as an anatomical basis,
catarrhal conditions of the aerating surfaces and interstitial
inflammations of the pulmonary connective tissue. Mechanical
obstruction to the aeration of the blood may also be present from the
extreme quantity of the foreign material in the lungs.
Tuberculosis.
Until the investigations and discoveries of the past few years, the
presence of tubercles in the various organs and tissues of the body
had been regarded as the essential element of tuberculosis. The
evidence to be presented in the following pages will show that the
immediate cause of tubercles may produce other lesions as well, and
that the presence of a specific virus as the efficient cause of
whatever may be the lesion, rather than the existence of tubercles, is
to be regarded as the characteristic feature of the disease
tuberculosis.
The tendency of the present is to regard the latter term as including
the various morbid processes connected with the origin, presence, and
growth of a specific, organized virus, their dissemination,
metamorphoses, and effects. Whether all those processes in connection
with which the virus is found are due to the latter, or whether some
may not arise and exist independently of the same, are among the
questions whose answer is remote rather than at hand.
As the presence of the cause of tuberculosis is the test demanded by
some authorities for the existence of the process, so the anatomical
classification has depended upon the existence of the tubercle. The
substitution of tubercle for organized virus in the general definition
of tuberculosis represents the distinction between the anatomical and
the etiological classification of this affection.
A tubercle was originally a small rounded body, a little tuberosity,
and at the close of the last century the specific tubercle was
distinguished from other rounded nodules.
Till the discovery of Villemin, the recognition of the tubercle was
{95} essentially based upon its anatomical characteristics. Previous
to the studies of Reinhardt and Virchow these related to appearances,
which were attributed to a deposition of material, scrofulous or
tuberculous, from the blood or lymph. The idea was eventually
maintained that this material formed the basis of a growth or new
formation, and Virchow showed that the tubercle was composed of a
tissue, of cells and intercellular substance, growing within and from
pre-existing tissues. He classified the tubercles among the tumors as
circumscribed new formations whose structure resembled that of
granulation-tissue. The specific tubercle was, at the outset, minute,
smaller than a millet-seed, submiliary, although indefinite numbers of
these minute tubercles might be grouped together and form closely
massed aggregations. From this agglomeration of single tubercles, and
their frequent association with inflammatory products, both of which
were prone to early death and transformation into a cheese-like mass,
the extensive tubercular infiltrations of organs arose. The latter
were regarded as a frequent cause of the wasting disease phthisis,
which was either pulmonary, intestinal, or renal according as the
lungs, intestine and mesenteric glands, or kidneys were the
predominant seat of the tubercular growth.
The histological features of the tubercle were further investigated by
Wagner,[47] who described the resemblances and differences of the
structure of the tubercle and the lymphatic gland. Schuppel[48] soon
after published his monograph, essentially confirming the statements
of Wagner. According to these observers, the typical tubercle, as
found in lymphatic glands, presents essentially the same peculiarities
of structure when seen elsewhere in the body. This structure consists
of a non-vascularized network of fibres, in the meshes of which cells
are imbedded. The fibrous network resembles the reticulum of a
lymphatic gland, and nuclei are often found at those points where the
fibres are united. This appearance has suggested that the network is
formed of branching and anastomosing cells. Within the meshes are
three sorts of cells--viz. giant-cells, epithelioid (endothelioid)
cells, and small, round, indifferent cells. One or several
giant-cells, each with its abundant nuclei, lie near the centre of the
tubercle or are diffused throughout the same. These are usually
immediately surrounded by the large epithelioid cells, with one or
more nuclei, which are often so numerous as to compose the greater
part of the tubercle. The indifferent cells, resembling
lymph-corpuscles, occur singly or in groups, distributed throughout
the tubercle more abundantly at the periphery, between the cells
previously described, and with them completely fill the spaces of the
fibrous network.
[Footnote 47: "Das tuberkelahnliche Lymphadenom," _Archiv der
Heilkunde_, 1870, xi. 6; xii. 1.]
[Footnote 48: _Untersuchungen uber Lymphdrusen-Tuberkulose_, 1871.]
Although the typical tubercle is thus constituted, the structural
features depend somewhat upon its age. It is generally admitted that
the freshest tubercles, as found in the external coat of the smaller
arteries of the pia mater, are composed of little else than a
circumscribed accumulation of small, round cells, without a distinct
reticulum. The giant-cells, the epithelioid cells, and the
well-characterized reticulum appear as the tubercle increases in age.
It is thought probable that the giant-cells represent the
agglomeration of the small, round cells in pre-existing cavities,
lymphatics, blood-vessels, or secretory canals. The epithelioid cells
in like {96} manner are considered to result from the enlargement or
fusion of the smaller cells, while the reticulum represents either a
secretion from, or a transformation of, the cellular elements of which
the tubercle is composed.
The subsequent history of the tubercle is dependent upon its
metamorphoses. These are known as cheesy degeneration, calcification,
and fibrous transformation.
The absence of blood-vessels, already stated, and the abundantly
cellular nature of the growth, with the possible action of
micro-organisms, result in a tendency to the early death of the cells
and a necrosis of the tubercle. This is the cheesy degeneration, and
is regarded as a form of coagulative necrosis, which begins at the
centre, advances toward the periphery, and results in the
transformation of the gray into a yellow tubercle. This termination in
cheesy degeneration likewise affects inflammatory products surrounding
the tubercle, and even relatively normal tissues in which numerous
tubercles may lie. This cheesy material either softens or becomes
infiltrated with lime salts, calcified. The softening of the tubercle
results in the formation of a material capable of removal as a
discharge from the surfaces of the body or by absorption through the
lymphatics and blood-vessels. In the former event ulcers arise upon,
and cavities communicate with, the surfaces of the body opening
externally.
The cheesy material frequently becomes calcified, thus remaining as a
comparatively inert mass. The earthy salts may be diffused throughout
a uniformly cheesy basis, or they may be deposited in a partially
softened, cheesy menstruum, when a mortar-like material results.
The tubercle becomes fibrous with the diminution in the number of its
cells and the increase in the thickness of the reticulum, with the
transformation of the latter into a homogeneous hyaline substance. The
cornified, horn-like tubercle is one whose size is diminished from the
shrinkage of its cells into glistening flakes, without an evident
associated cheesy or fatty degeneration.
The intimate relation of scrofula to tuberculosis has been variously
expressed from time to time in accordance with the amount and accuracy
of the existing knowledge. At the outset the enlargement of the
lymphatic glands, especially of the neck, characterized the scrofulous
affection. As the enlargements of the glands were found to present
intrinsic differences connected with differing clinical histories,
only those glands were regarded as scrofulous which presented the
cheesy appearances. With the recognition of the cheesy condition of
tubercles the latter were identified with the scrofulous gland, from
the cheesy condition common to both.
This identification of scrofula and tubercle prevailed till Virchow
showed that cheesy material might have a different origin, and
maintained that there were cheesy lymphatic glands without tubercle,
as well as tuberculous lymphatic glands which might become cheesy. A
distinction was thus drawn between scrofula and tuberculosis. The
former term was applied to that condition of the individual which
favored the retention and cheesy degeneration of inflammatory
products, not only in the lymphatic glands, but elsewhere in the body.
Tuberculosis, on the contrary, was characterized by the production of
tubercles which were often accompanied by retained inflammatory
products, both of which were prone to undergo cheesy degeneration.
{97} The frequent association of well-defined tubercles with what were
regarded as antecedent scrofulous disturbances also suggested an
intimacy of relation between scrofula and tuberculosis. Virchow[49]
had always maintained the possibility of regarding tuberculosis as a
heteroplastic or metastatic scrofula. The occurrence of cases of
tuberculosis without evidence of an antecedent scrofula prevented him
from making a more absolute statement of the above relation.
[Footnote 49: _Die Krankhaften Geschwulste_, 1864-65, ii. 629.]
The views with regard to the connection between scrofula and
tuberculosis have become essentially modified of late years as a
result of the investigations concerning the etiology of tuberculosis.
In 1856, Buhl[50] first published his view, although he had for
several years been impressed with the idea, that miliary tuberculosis
was an infective disease resulting from the absorption of a specific
virus. He based his theory upon the almost constant coexistence of one
or several cheesy collections and miliary tubercles. The former were
recognized as the remains of previous inflammatory processes, and the
tubercles were looked upon as the immediate result of the absorption
of this cheesy material. The individual thus infected himself.
Buhl[51] claimed that the simultaneous occurrence of tubercles and
inflammatory products was the co-effect of the same cause, and that
the acute miliary tuberculosis, as a localized process, was merely an
inflammation with the development of tubercles. He restricted the term
tuberculous inflammation, however, to those forms which necessarily
and from the beginning, produced tubercles whose presence was limited
to the tissue inflamed. The tuberculous inflammation was regarded as a
primary condition, while the acute miliary tuberculosis was a
secondary process resulting from infection.
[Footnote 50: _Lungenentzundung, Tuberkulose und Schwindsucht_, 1872,
iii.]
[Footnote 51: _Op. cit._, 123.]
The tuberculous inflammation of this author was largely characterized
by those features which, with the exception of the constant presence
of tubercles, were recognized by others as attributes of a scrofulous
inflammation. At the same time, he objected to the latter term as a
substitute, since its use would imply that no other cheesy product
than that from a tuberculous inflammation would serve as the origin of
tubercles. Buhl strictly maintained that the absorption of any cheesy
material, whatsoever its source, might give rise to a general growth
of tubercle in the body.
The views of this author were popularized mainly through the teachings
of Niemeyer[52] concerning pulmonary consumption. The latter adhered
to Virchow's views relating to scrofulous inflammation, but maintained
that most consumptives were in imminent danger of becoming tuberculous
in accordance with the doctrines of Buhl.
[Footnote 52: _Klinische Vortrage uber die Lungenschwindsucht_, 1867.]
The theory of an infectious origin of tuberculosis, advanced from time
to time by others, but most forcibly presented and maintained by Buhl,
was first demonstrated by Villemin[53] in 1865. This observer showed
that certain animals, especially rabbits and guinea-pigs, might be
successfully inoculated, beneath the skin, with fragments of gray
tubercle, cheesy products, sputum, and blood from cases of phthisis.
The development of tubercles took place within three weeks after the
{98} inoculation, and became general within four weeks. He also
demonstrated that rabbits became tuberculous when inoculated with bits
of the tumors occurring in the pearly distemper of cattle.
[Footnote 53: _Etudes sur la Tuberculose_, Paris, 1868, 528.]
Villemin's observations have been repeatedly confirmed and extended;
although subjected to the severest criticism and control, their
results are so constant that the law of the inoculability of tubercle
is almost universally regarded as fixed. Its value as a test is
evident from the statement of Cohnheim,[54] who regards as tuberculous
only that which produces tuberculosis when transferred to suitable
animals. The transfer may be made in various ways. Chauveau and others
were successful in producing an intestinal tuberculosis by the
introduction of tuberculous material into the intestinal canal of
animals, especially the Herbivora. Tappeiner[55] succeeded in
producing pulmonary tuberculosis, with or without general
tuberculosis, in dogs, by compelling them to breathe air in which were
contained minute particles of sputa from tuberculous pulmonary
cavities.
[Footnote 54: _Die Tuberkulose vom Standpunkte der Infections-Lehre_,
1880, 13.]
[Footnote 55: _Virchow's Archiv_, 1878, lxxiv. 393.]
The production of a tuberculosis of the iris, as well as of remote
organs, by the inoculation of tuberculous material into the anterior
chamber of the eye, was an ingenious method devised by Cohnheim and
Salomonsen.[56] It permitted the direct observation of the several
steps in the process of absorption of the inoculated material and
development of the tubercles.
[Footnote 56: Cohnheim's _Vorlesungen uber Allgemeine Pathologie_, 2te
Auflage, 1882, i. 707.]
The objections to the various experiments above alluded to are based
upon the assumption that the results of the inoculation are not
tubercles, but inflammatory products resembling tubercles. It is
further advocated that the inoculation of indifferent material, as
bits of glass or hairs, as well as other foreign substances, will
produce the so-called artificial tuberculosis, especially in rabbits
and guinea-pigs. It is admitted that these animals readily become
tuberculous when exposed to simple inflammatory irritants, the local
action of which frequently results in the production of cheesy
material. This termination is now regarded as due to faults in the
method of experimentation, the animals not being thoroughly protected
from the influence of the virus of tuberculosis.
The objection on the ground of structure loses its force in connection
with the well known differences in the structure of miliary tubercles
in the human body, already mentioned. The tubercles resulting from
inoculation often resemble in structure the meningeal tubercles of the
brain rather than the type presented by tubercles in lymphatic glands.
The development of tubercles in the iris may take place without any
permanent inflammatory reaction. The association of evidences of
inflammation with the development of the tubercle is therefore
unnecessary.
The experiments of Villemin have not only demonstrated the infectious
nature of tuberculosis, but have also led to a more accurate knowledge
of the relation between tuberculosis and its allied affections,
scrofula and pearly distemper.
The anatomical characteristics of scrofula have obviously proved
insufficient in determining the relation presented by this affection
to tuberculosis. The tendency to cheesy degeneration of its
inflammatory {99} products was the feature of chief importance.
Villemin showed that portions of a scrofulous (cheesy) gland when
inoculated were followed by tuberculosis, and that the inoculation of
cheesy material from non-tuberculous or non-scrofulous sources was not
followed by this result. The assumption of Buhl, that the absorption
of cheesy material, as such, was the cause of tuberculosis, was thus
disproved. The frequency with which the inoculation of cheesy
material, from what were regarded as scrofulous sources, was followed
by tuberculosis, led to more exact studies concerning the anatomical
peculiarities of scrofulous inflammation. Koster[57] called attention
to the regularity of the occurrence of miliary tubercles in the
fungous granulations of the inflamed joints of scrofulous and
tuberculous individuals. Wagner[58] and Schuppel[59] discovered that
scrofulous glands, in most if not in all instances, were tuberculous
glands. The regularity of the presence of tubercles in scrofulous
abscesses and ulcers of the skin and in scrofulous caries was shown by
Friedlander.[60] This observer likewise called attention to the
presence of agglomerated tubercles as the chief constituent of the new
formation of lupus. These anatomical discoveries resulted in uniting
more closely the affections scrofula and tuberculosis from the
histological standpoint, and the union has become more firmly cemented
from the etiological investigations.
[Footnote 57: _Virchow's Archiv_, 1869, xlviii. 95.]
[Footnote 58: _Loc. cit._]
[Footnote 59: _Op. cit._]
[Footnote 60: _Volksmann's klinische Vortrage_, 1873, lxiv.]
Schuller[61] has shown that the introduction of finely divided
material from a scrofulous joint--that is, from one containing
tubercles--into the lungs of rabbits was followed by a tuberculosis of
the tracheal wound, the lungs, and liver. Similar experiments with
reference to the introduction of lupus-tissue produced results
suggestive of tubercle, if not actually tuberculous.
[Footnote 61: _Untersuchungen uber die Enstehung und Ursachen der
Skrophulosen und Tuberkulosen Gelenkleiden_, 1880.]
The intimacy of relation between tuberculosis and pearly distemper is
a necessary result of Villemin's[62] experiment, in which the rabbit
became tuberculous after inoculation with fragments of the pearly
tumor. Gerlach,[63] and especially Schuppel,[64] showed that the
structure of the nodules of the pearly distemper is the same as that
of the tubercles of man, and that the two diseases are identical from
the histological point of view.
[Footnote 62: _Op. cit._, 537.]
[Footnote 63: _Virchow's Archiv_, 1870, li. 290.]
[Footnote 64: _Ibid._, 1872, lvi. 38.]
From the anatomical identification and the etiological connection, as
shown by Villemin, Gerlach, and Aufrecht, the pearly distemper became
designated as a bovine tuberculosis.
The experiments of Villemin were further productive in leading to the
discovery by Koch of the bacillus tuberculosis. It was early obvious
that certain cheesy material and gray tubercles possessed the
infectious qualities, and Villemin[65] maintained that the immediate
cause of the latter was a germ introduced from without, which
propagated and perpetuated itself in man and certain animals. This
view acquired prominence through the investigations of Klebs, who in
1877 claimed to have isolated the micrococci which produced tubercles
when injected into animals. Three years later Schuller[66] confirmed
the statements of Klebs, and asserted that he had been enabled to
obtain infective micrococci by cultivation from {100} miliary
tubercles, scrofulous glands and joints, and from the tissue of lupus.
Aufrecht[67] found micrococci, single and in chains, and short
glistening rods, within tubercles resulting from inoculation with
material from pearly tumors. The same organisms were found in
tubercles produced by the inoculation of tubercles from man, and he
regarded these rod-shaped bodies as the specific element productive of
miliary tuberculosis.
[Footnote 65: _Op. cit._, 620.]
[Footnote 66: _Op. cit._, 55.]
[Footnote 67: _Pathologische Mittheilungen_, 1881, p. 43.]
The isolation of the virus of tubercle was thus regarded as an open
question till the announcement by Koch[68] of the constant presence of
a hitherto unknown, characteristic, well defined organism in all
tuberculous affections, which, when isolated and introduced into
animals, produced tuberculosis, the resulting tubercles likewise
containing the organism.
[Footnote 68: _Berliner klinische Wochenschrift_, 1882, p. 15.]
The latter, the bacillus tuberculosis, was to be seen in preparations
methodically treated and carefully stained with aniline colors, by all
of which, excepting the browns, the bacillus was tinged. It was found
in miliary tubercles of the lung, cerebral and intestinal tubercle,
cheesy bronchitis and pneumonia, phthisical sputa, scrofulous glands,
and fungous inflammation of the joints. It was also seen in the
nodules of pearly distemper and in the cheesy masses from the lungs of
cattle. It was furthermore met with in the cheesy lymphatic glands of
swine, in the tubercular nodules of a fowl, and in the tubercles of
guinea-pigs, rabbits, and monkeys. The bacilli were likewise found in
the tubercles resulting from the inoculation of animals with
tubercular virus from its various sources.
The microphytes were described as very slender rods, varying in length
from one-fourth the diameter of a red blood-corpuscle to its entire
diameter, and spores were occasionally seen within the rods. In shape
and size they resembled the bacilli of leprosy, but the latter were
narrower and pointed at the ends. They were found in greatest
abundance when the tuberculous process was recent and rapidly
advancing, and were present within, as well as between, cells. The
younger giant-cells contained them in larger numbers than the older
forms. They were present at the periphery of cheesy nodules rather
than at the centre.
The bacilli were cultivated through successive generations and
required a temperature of between 30 degrees C. and 41 degrees C. (86
degrees F.-105.8 degrees F.) for their development, one of 37 degrees
C. or 38 degrees C. (98.6 degrees F. or 100.4 degrees F.) being the
most favorable. The crop first became apparent on the tenth day after
sowing, and the growth extended through a period of three to four
weeks, forming a compact scale. The cultivated bacilli, even
propagated through several generations, when inoculated, produced the
same positive results as follow the inoculation of fragments of
tuberculous material, although animals might be used which are not
easily infected with tuberculosis.
Koch's publication was immediately followed by a statement from
Baumgarten[69] of his discovery of rod-like bacteria in the tubercles
of rabbits resulting from the inoculation with pearly masses, and in
the pleural and pericardial tubercles of man. They were made evident
by treating the sections for microscopic examination with very dilute
solutions of soda or potash.
[Footnote 69: _Centralblatt fur die med. Wissenschaften_, 1882, xv.
257.]
{101} The discoveries of Koch thus show that the production of
tuberculosis is dependent upon the presence of distinctive bacilli,
and that these bacilli are present not only in miliary tubercles, but
in scrofulous glands and joints, in cheesy inflammation of the lungs,
and in the pearly distemper of animals. The identification of
tuberculosis with the pearly distemper and certain scrofulous
affections is thus established from the etiological as well as the
histological point of view.
As the bacilli are to be regarded as the virus of tuberculosis, so
their introduction into the human body is necessary for the production
of this disease in man. It is obvious, however, that other factors
than the virus are necessary, for not every one exposed to the
reception of tubercular bacilli becomes tuberculous. It may well be
that scrofula is still to be regarded as that condition of the solids
and liquids of the body which offers favorable opportunities for the
retention and growth of the bacilli, and thus for the production of
tuberculosis. Formad[70] claims that he has discovered structural
peculiarities of tissue as a cause for the scrofulous habit, which he
regards as synonymous with a predisposition to tuberculosis. These
peculiarities are manifested by a narrowness of the lymph-spaces and
their partial obliteration by cellular elements. He also maintains
that these features are not only of congenital origin, but may be
acquired through malnutrition and confinement.
[Footnote 70: _Studies from the Pathological Lab. of the Univ. of
Penna._, reprint, 1882, xi. 3.]
The occurrence of a local, circumscribed tuberculosis in extreme old
age, without antecedent or other concurrent evidence of scrofulous
disturbances, suggests that favorable opportunities for the
development of the tubercular bacillus may arise in advancing years.
In like manner, the frequent termination in phthisis of cases of
diabetes suggests the likelihood of tuberculous inflammation arising
in the absence of any evidence of previous scrofulous or tuberculous
disease. The scrofulous condition or constitution, as indicated by
vulnerable tissues, with a protracted course of inflammations, and a
persistence of their products, with a tendency to cheesy degeneration,
may still exist without a sign of tuberculosis. Those who claim that
scrofula and tuberculosis are identical must, in the light of Koch's
discovery, demonstrate the presence of the bacillus in all scrofulous
inflammations, and deny the existence of scrofula apart from
indisputable manifestations of the activity of the bacilli of
tuberculosis. It may be that such evidence will be presented; until it
is collected scrofula and tuberculosis are to be regarded as distinct
though often coexistent. The scrofulous person is frequently
tuberculous, the tuberculous person is usually scrofulous; the
non-scrofulous person, however, may die of tuberculosis, while the
individual may be scrofulous without containing tubercle.
The actual inheritance of tuberculosis is very unlikely, although this
disease is frequently found in successive generations of a single
family. The various members of the family are rather to be regarded as
furnishing a suitable soil for the growth of the tubercular bacillus,
and their exposure to its seed is favored by the existence of
tuberculosis in one or more members of the household. The scrofulous
condition is still to be regarded as hereditary as well as acquired,
and the scrofulous remain as the class to be especially protected from
the reception and effects of the bacilli of tuberculosis.
{102} It is obviously a matter of importance to determine in any given
case of phthisis whether bacilli are present or absent. A ready means
of ascertaining this fact is offered by the examination of the sputum
in cases of pulmonary phthisis, the feces in intestinal phthisis, the
urine in renal phthisis, and the aspirated pus in cases of supposed
tuberculosis of the joints. Koch has found in examining the sputa from
numerous cases of phthisis that the bacilli were present in one-half
the number, and that they were absent from the sputa of individuals
who were not phthisical. Balmer and Fraentzel[71] have found bacilli
in the sputum from one hundred and twenty cases of phthisis, and
concluded that the progress of a case of pulmonary tuberculosis might
be readily determined from the number and degree of development of the
typical bacilli present in the sputum. The more numerous and
well-developed bacilli, with distinct and constant spores, were found
in the graver cases, which advanced more rapidly. The sputum of the
protracted cases contained few, small, and thin bacilli with scanty
spores. The presence of fever was associated with numerous bacilli,
while its absence was noted in those cases where but few were present.
[Footnote 71: _Berliner klinische Wochenschrift_, 1882, xlv. 679.]
The bacilli are readily detected by means of the staining method
devised by Koch. Various modifications have been presented from time
to time, of which that of Ehrlich[72] has proved the most
satisfactory. The essential features are to obtain a dry, thin layer
of a selected portion of the suspected sputum, which is then to be
deeply stained with fuchsin or methyl-violet; the excess of color is
to be removed with nitric acid, and the preparation is then ready for
examination with the microscope. A power of four or five hundred
diameters is sufficient for the recognition, and the object should be
illuminated with a flood of light through a large diaphragm or an
achromatic condenser. The bacillus retains the color notwithstanding
its exposure to the acid, and the violet colors are more strongly
presented if the preparation is tinted yellow after the action of the
acid. If the bacilli are stained red with fuchsin, the background
should be made blue. It is important that the reagents should be
freshly prepared and filtered, that other bacteria may not obscure the
picture, and that all the apparatus employed should be thoroughly
clean.
[Footnote 72: _Allg. med. Centr. Zeitung_, 1882, xxxvii. 458.]
A fragment of thick, opaque sputum is to be taken in forceps, placed
on a cover-glass, and spread into a thin layer by means of a second
cover-glass. The prepared slide is then to be passed slowly through an
alcoholic flame, or that of a Bunsen burner, till the layer of sputum
is dried. A saturated alcoholic solution of methyl-violet or fuchsin
is made and filtered, and added, drop by drop, to a filtered,
saturated solution of aniline oil shaken in water. The color is to be
added with stirring till an opalescent film forms on the surface of
the mixture. The slide containing the dried sputum is to be placed in
or on this staining fluid, and allowed to remain for half an hour or
less, the application of warmth hastening the process, when it is
removed, and the specimen is decolorized in a solution of one part of
nitric acid and two parts of water. The preparation is then washed in
water, and may be examined directly in water, glycerin, or, after
dehydration in alcohol, in oil of cloves. The tinted bacilli are made
more prominent by a secondary staining, for a minute or two, of the
red (fuchsin) preparation {103} in a concentrated solution of
methyl-blue, the violet preparation being secondarily stained in a
like solution of aniline-brown. If the preparation is to be
permanently preserved, it should be dehydrated in strong alcohol after
washing with water, and it may then be treated with oil of cloves and
mounted in Canada balsam.
After the observer has become thoroughly familiar with the tubercle
bacilli by means of the method of Ehrlich, much time may be saved by
following that of Baumgarten.[73] The cover-glass bearing the dried
sputum is placed in a very dilute solution of caustic potash (two
drops of a 33 per cent. solution in a watch-glass of distilled water)
till the layer of sputum becomes transparent. The cover is then placed
on a slide moistened with a drop of water, tapped slightly, and
examined with the microscope. The bacilli are readily seen, and may be
differentiated from other varieties of bacteria, if necessary, by
again drying the object and examining it in a drop of a dilute watery
solution of aniline-violet or of other preparations of aniline used
for staining nuclei. The tubercle bacilli remain unstained, while
putrefactive bacteria are tinted.
[Footnote 73: _Centralblatt fur die med. Wissenschaften_, 1882, xxv.
433.]
The tubercular products of the invasion of the body by the bacillus
tuberculosis are regarded as primary or secondary, according as they
are present at that part of the body which directly receives the
organisms or as they are dependent upon the transfer of the latter to
parts remote from the region of their admission and immediate effects.
This differing relation is also expressed by the terms local and
general tuberculosis. In the former the bacilli excite the growth of
tubercle only at a given part of the body. Their apparent effects may
be wholly limited to this region, and it not rarely happens that the
same is quite distant from the channels through which the bacilli are
admitted. A general tuberculosis occurs when the latter are
disseminated over the body, and their effects, especially the
production of numerous tubercles, are found at various parts. The
dissemination may take place at the time of entrance, or, as is more
commonly the case, apparently occurs at some subsequent period, the
immediate disturbances being localized at a given portion of the body.
The necessary conditions being here offered for the propagation of the
bacilli, their sudden distribution in great numbers is afterward
permitted when favorable opportunities arise for their absorption.
Such conditions are present when the local tubercular growths extend
into lymphatics or blood-vessels. The frequency with which scrofulous
glands are tuberculous--that is, contain miliary tubercles--is already
fully recognized, and a tuberculosis of the lymphatic glands is
essentially regional. These glands become affected in consequence of
disturbances, the local effects of which may have wholly disappeared,
in the region from which they receive their lymph. The cervical glands
become permanently enlarged, perhaps tuberculous, in connection with
persistent or recurrent inflammatory processes in the tonsils and
pharynx, the bronchial glands from similar bronchial or pulmonary
affections, and the mesenteric glands from like intestinal
disturbances. In such instances, the direct reception of the bacilli
into the lymph-current is assumed rather than demonstrated from a
knowledge of the possibilities of absorption and an appreciation of
the conditions in the glands.
That an actual growth of tubercles from the wall of the intestinal
{104} lymphatics may take place has long been known, and Ponfick has
recently discovered that tubercles may be found growing from the wall
of the thoracic duct. The possibility of the direct admission into the
lymph-current of the infective element in tuberculosis is thus
apparent, and its indirect entrance into the blood-current is equally
obvious. That the bacillus of tubercle may be directly received into
the blood-current is likewise evident from the observations of
Weigert, who found tubercles growing from the walls of the pulmonary
blood-vessels, venous as well as arterial. This discovery of a
tuberculosis of the blood-vessels was confirmed by Klebs, who had
found a tuberculosis of the azygos veins. The occurrence of multiple
miliary tubercles of the pulmonary veins, especially near the place of
entrance of smaller branches, has been asserted by Mugge,[74] although
appearances similar to those described by him may be met with, due
simply to the agglomeration of white blood-corpuscles and their
necrosis. Such a condition simulates very closely the miliary
tubercle, but is usually analogous to the appearances figured by
Virchow,[75] and described by him as one of the phenomena of
coagulation. In his observation the white bodies were adherent to the
red clots, and were with them drawn from the pulmonary artery.
[Footnote 74: _Virchow's Archiv_, 1879, lxxvi. 243.]
[Footnote 75: _Die Cellular Pathologie_, 4te Auflage, 1871, 184.]
With the admission into the body, and the colonization of the
tubercular bacilli, their effects may either be progressive until the
death of the individual is occasioned, or, with the cessation of the
growth of the bacilli or a possible modification of their noxious
properties, recovery may ensue. The history of scrofulous glands, as
well as that of circumscribed pulmonary inflammation in scrofulous
persons, both presumably of a tuberculous nature, show that the
effects of an invasion of the parasites may be overcome.
The regions of the body which are usually the seat of a primary
tuberculosis are unquestionably the respiratory and intestinal tracts.
With regard to the first of these regions, the one most frequently
affected, there can be no doubt that in most instances the inhaled air
carries the bacilli or their spores, or both. Their constant presence
in the sputum of the frequent cases of tuberculous phthisis suggests a
ready means for their escape into the atmosphere. The well recognized
infective qualities of the sputum, as demonstrated by the various
experiments before the bacillus was discovered, demand the thorough
disinfection of phthisical sputa, since these are in all probability
the chief source of the dissemination of the disease.
The tuberculosis of the intestine in like manner is to be regarded in
the main as the result of an absorption from its surface of the
specific agent. An obvious direct means of the approach of the bacilli
is offered in the sputum, which, when swallowed, is likely to retain
its virulent properties. The frequent coexistence of chronic pulmonary
and intestinal tuberculosis is thus most readily explained. To what
extent the presence of the bacilli in the pearly distemper of cattle
and in the tuberculosis of other edible domesticated animals, as fowls
and swine, may lead to an infection of the intestinal wall, still
remains an unsolved problem. It is not yet determined at what
temperatures the bacilli are destroyed, although their growth takes
place only between 30 degrees C. (86 degrees F.) and {105} 41 degrees
C. (105.8 degrees F.). The inoculation of pearly masses produces
tuberculosis in certain animals, yet the effect of cooking in
destroying the bacilli and their spores is likely to prove of great
importance. Aufrecht's[76] attempts at inoculating rabbits with cooked
pearly masses proved unsuccessful. Schottelius[77] publishes an
interesting series of observations relating to the prolonged use of
meat from cattle affected with the pearly distemper, and shows that
after a period of years no disease of the nature of tuberculosis
occurred among the one hundred and thirty individuals included in the
families concerned. Whatever may be the value of this negative
testimony, there is, as yet, no evidence on the other side which
satisfactorily determines the point in question--viz. that the flesh
of animals affected with pearly distemper produces tuberculosis in the
human consumer.
[Footnote 76: _Op. cit._, 51.]
[Footnote 77: _Virchow's Archiv_, 1883, xci. 129.]
The milk from cows thus diseased has likewise been regarded with
suspicion, and the frequency of intestinal tuberculosis among children
has been attributed to this source. Although the theoretical
possibility of the escape of the bacilli into the milk of cows
affected with pearly distemper is obvious, their presence in such milk
is first to be demonstrated under conditions which necessitate their
origin from the animal. If boiling the infective material for three
minutes destroys its virulence, as claimed by Aufrecht, a ready means
is offered of destroying the tubercle bacilli which may be present,
not only in the milk from animals affected with pearly distemper, but
in all milk which has been exposed for a certain time to an atmosphere
which may contain the bacilli of tuberculosis. In the light of our
present knowledge extreme hygienic precautions are only demanded in
those cases where such a congenital or acquired basis (constitution)
is present as facilitates the development of tuberculosis.
Morbid Growths.
In a system of practical medicine it is obviously important to include
under the head of Morbid Growths not only what is spoken of by the
surgeon as a tumor, but also those new formations of tissue which, in
virtue of their nature, seat, manner of growth, and retrograde
changes, produce an important series of disturbances in the
physiological processes of the individual. The surgeon deals
essentially with the swelling, which, producing irregularities in the
outline of the accessible surfaces of the body, is regarded as an
excrescence or outgrowth. It is important for him to realize the
nature of this swelling, that he may follow a different treatment for
the abscess, the wen, the watery accumulation, or the fleshy mass. The
last is the tumor in the limited sense; it is the growth which, though
called morbid, becomes so only in consequence of its presence being
associated with symptoms whose existence and persistence interfere
with the well-being of the possessor.
The physician, on the contrary, is more concerned with the tumor as a
growth than as a swelling. The latter element in deeply-seated
portions of the body may not be brought to his attention. The growth
takes place in such a manner as to be productive of certain symptoms
more or less serious, among which swelling is least obvious. The
morbid {106} growth to him becomes prominent as it displaces or
replaces normal tissues by those newly formed, which may or may not be
normal to the part in which the growth is situated. His tumor is
therefore a morbid growth, a new formation, a neoplasm or pseudoplasm,
rather than a swelling, a bunch, or an excrescence.
In a consideration of the general pathology of morbid growths the
first question which suggests itself relates to the method of origin
of the tumor. The tendency of the present seeks for a local cause, and
the most recent theory, that of Cohnheim, demands an accumulation of
dormant embryonal cells as such a cause. Cohnheim supports this view
by the experiments of Zahn and Leopold, which show that foetal
cartilage transplanted into the tissues of a mature animal may grow so
rapidly as to present the characteristics of a cartilaginous tumor,
while tissues transferred from the animal after birth do not increase
in size, but are usually absorbed.
As the active elements of the growth are cells, and all cells
admissibly arise from pre-existing cells, it follows that the
primitive cells of a tumor are derived from those resulting from the
segmentation of the ovum or are introduced from without. Numerous
experiments have been made with a view to the inoculation of tumors,
the transplantation of living fragments of the latter to the living
tissues of a healthy individual, for the sake of producing a tumor,
but hitherto almost invariably without success. The alternative
remains that the embryonal cells are those whose derivatives are
present in, and form the essential element of, the morbid growth. All
tumors may thus be said to have an embryonal origin. As the
segmentation of the ovum eventually results in the production of
normal tissues and groups of tissues whose structure and function are
wholly different, so the possibility of the production of abnormal
groupings of tissue with corresponding irregular manifestations of
function is obvious.
The cells of the part from which a tumor arises may be regarded as
indifferent, those whose limitations of growth, like the early
embryonal cells, are only determined by the changes they undergo, or
their limits of growth may be already defined in kind, and their like
be produced in the formation of the tumor. The origin of a tumor thus
presupposes the existence of such indifferent cells, or the presence
of those whose limit of transformation has already been reached. The
leucocytes of the body, whether found as white blood-corpuscles or
lymph-corpuscles, or as the wandering cells of connective tissue, are,
as Virchow has indicated, such indifferent cells. Always present and
apparently transitory, what they are to become can only be determined
from their condition and surroundings at the time of observation.
Although their actual transformation into the various cells of a more
permanent type is merely a matter of inference in the growth of
tumors, the evidence presented by Ziegler[78] leads directly to the
conclusion that their presence is necessary to the new formation of
tissues whose growth is the result of an inflammatory process. These
tissues may occur under such restrictions as permit them to be
classified as tumors, and the granulomata, or tumors whose tissue
resembles that of the granulations upon the surface of a wound,
represent a well defined group in structure as well as method of
origin.
[Footnote 78: _Op. cit._, 150.]
{107} The production of the cells of a tumor from indifferent cells is
at present an assumption, based upon the frequent presence of the
latter within tumors and in their vicinity; and the obvious objection
arises that even if the presence of these cells is admitted as
indispensable, it by no means follows that they are directly
transformed into the more characteristic cells of the tumor. That they
may serve for the nourishment of the amoeboid cells of certain tumors
is suggested by the existence of both in morbid growths, and the
well-known property of amoeboid corpuscles to take in formed material,
even cells, from without.
The origin of tumors from cells whose limits of growth are already
defined is rendered probable from the absence, entire or in great
part, of indifferent cells from certain tumors, and the direct
continuity of the latter with a similar normal tissue of the body.
Various tumors show such an intimate relation, and there is no sharply
defined border-line between the normal tissue and that which
represents the tumor. The occasional presence of islets of well
characterized tissue at points more or less remote from the normal
position of such tissue at the time of their discovery suggests a
feasible source for an eventual tumor. Virchow long ago called
attention to isolated nodules of cartilage within bones in the
vicinity of epiphyseal cartilages, probably detached from the latter,
which might serve as the origin of a cartilaginous tumor in this
region. This inclusion of tissue is also suggested by the frequency of
certain tumors in certain regions where the developmental conditions
are favorable. Lucke[79] mentions the frequency of dermoid cysts near
the median line of the head, the vicinity of the eye, and the side of
the neck. Such regions are those where fissures exist during foetal
life, with normal involutions of the outer germinal layer; which
involutions may become irregular, and eventually included or shut in,
as the fissures become closed. A similar explanation is offered for
the frequent occurrence of cartilaginous tumors at the angle of the
jaw, it being thought probable that bits of embryonal cartilage,
during the formation of the ear, become included in the salivary
glands.
[Footnote 79: _Volkmann's Sammlung klinischer Vortrage_, xcvii. 819.]
In like manner, Cohnheim explains the frequent occurrence of certain
epithelial tumors at the orifices of the body--the cervix uteri and
the vicinity of the tracheal bifurcation--not through the exposure of
these parts to injury, but because they are regions in which embryonal
irregularities of development are likely to arise.
That congenital, local peculiarities are an important element in the
origin of tumors has already been strongly advocated by Virchow. Not
only are children born with tumors, but instances of growths
eventually arising from birth-marks, and the occurrence of certain
tumors in the same locality in successive generations of the same
family, are sufficiently familiar.
Although certain tumors are admitted to be due to congenital
peculiarities of tissue, and even to represent atypical growths from
embryonal tissue, the theory of such an embryonal origin for all
tumors seems unnecessary. The resemblance in symptoms as well as in
appearance, and even in structure, of certain tumors to inflammatory
products, and their frequent association with these, has led to the
suggestion of an irritant as an exciting cause for the tumor, even in
the absence of local peculiarities of tissue. {108} It is obvious that
were the embryonal theory of origin, as extended by Cohnheim,
universally applicable, the growth demands something more than a focus
of embryonal cells. An immediate cause for their growth after a
dormant period, extending even into old age, is required. Cohnheim
finds such in a sufficient supply of blood. He attributes the
development or rapid growth of the tumor to this feature, and supports
his view by the usual appearance of exostoses when the skeleton is at
its period of most vigorous growth, and of dermoid cysts at a time
when the formation of the beard indicates active developmental
conditions in the outer germinal layer.
The growth of ovarian cystomata at and after puberty, and of these and
mammary tumors during pregnancy, are also explained on the ground of a
more abundant supply of blood at such periods. He and others find in
physiological conditions a source for the abundant blood-supply--that
is, the efficient nutrition for the growth of a tumor. The necessity
of sufficient nutrition in the development of tumors is universally
admitted, and its source may be looked for in pathological as well as
physiological conditions.
The existence of an irritant of some sort often seems probable, and,
although its absence is more frequently determined than its presence,
it is obvious that when present it may be overlooked. Although
traumatic irritants of considerable mechanical severity exist in but a
small percentage of tumors, their occasional influence in the
production of morbid growths is not to be denied. Their action may be
explained as producing a congestion or as enfeebling the opposition of
physiological tissues to pathological growths. The importance of an
irritant as the exciting cause, however its action may take place, is
supported not only by the sequence of injuries and tumors, but also by
the frequent occurrence of tumors in parts exposed to injury and
irritation. Such exposure may result from position, structure, or
function. The orifices and prominences of the body, the retained
testis in the inguinal canal, are notoriously liable seats of tumors.
Soft, friable, and slightly resistant structures, like mucous
membranes, are not only the frequent place of origin of tumors, but
the most exposed parts of such structures are oftenest affected. The
exposure resulting from function is manifest by the relation presented
by the periods of greatest functional activity of the growth of tumors
in such organs as the mammary gland, uterus, and ovaries.
The importance of an irritant is still further suggested by the
association of tumors with inflammation. The growth of tubercles and
cancer from serous membranes is frequently accompanied by an acute
inflammation of the latter; fibrous tumors and chronic interstitial
inflammations often coexist, while elephantiasis is usually preceded
by recurrent, erysipelatous inflammation of the skin.
The recent discovery of infective organisms as an exciting cause for
many of the members of an entire group of tumors, the granulomata, has
resulted in making prominent the etiological rather than the
structural features of the tumors concerned.
Local peculiarities of tissue, whether congenital or acquired, are
thus regarded as representing the beginnings of the growth. With the
multiplication of the cells their transformation may take place or a
change in their grouping may arise. The essential condition in the
production {109} of the morbid growth is that the formation of the
cells should take place at an abnormal time or place and should
progress in a normal or abnormal manner.
The growth takes place with greater or less rapidity in one or another
direction according to the nature of the tumor and its seat. The more
closely the tumor resembles the normal structures of the body, the
slower is its growth; the more it differs in composition, the more
rapid is its progress. This difference may arise from a predominance
of cells over intercellular substance, as in the case of the sarcoma,
or it may result from an atypical combination of tissues, as seen in
the development of epithelium and connective tissue in cancer.
The seat of the tumor is of importance mainly on account of the
vascular supply of a part and the more spongy or yielding nature of
certain regions. That the more abundant the nutrition of certain
regions of the body, the more favorable the opportunities for growth,
may be admitted without question. The spongy nature of tissues implies
a predominance of cavities over solid constituents. These cavities are
lined by surfaces which represent, on the one hand, the walls of
lymph-spaces, on the other the free surfaces of the body exposed to
the air, as the mucous or cutaneous surfaces and the pulmonary
surface. The rapidity of growth in the direction of the least
resistance is amply shown in the projection of tumors above the
surface of serous membranes and the frequent presence of fungoid
excrescences in various parts of the body.
The growth of tumors extends in all directions, but a distinction has
long been drawn between the concentric or interstitial manner of
growth and the excentric or infiltrating form. This distinction is
based upon the presence of a sharply defined limitation of
pathological and normal tissues or upon the absence of such a
limitation. Such a distinction is merely of relative importance, as
certain tumors may grow in both ways. This is best observed in those
bulging superficial tumors whose base is irregularly extended into the
continuous healthy tissues.
The concentric variety of growth includes those tumors which have
commonly been described as encapsulated, and which are capable of
ready enucleation from their surroundings in virtue of a thin layer of
loose connective tissue lying between the tumor and the contiguous
tissue. Such a capsule represents the matrix, the pia mater, in which
lie the blood-vessels going to and coming from the tumor, and is often
nothing else than the distended and hyperplastic fibrous tissue
remaining after the absorption of the muscular fibres or gland-cells
from the tissues surrounding the morbid growth.
The excentric, peripheral, or infiltrating extension of the tumor
takes place when the surrounding parts are invaded by the active
elements of which the tumor is composed. The amoeboid property of the
cells of certain tumors is well known, and the possibility is
admissible that the indifferent cells of the body, so often
accumulated at the periphery of the growth, become impregnated with a
formative function by the constituents of the tumor. Such amoeboid and
wandering cells represent a means through which the growth of the
tumor may become extended in its vicinity as well as in more remote
parts of the body.
The extension in the vicinity may be continuous or the reverse, the
latter through the formation of secondary nodules, which may {110}
eventually become fused with the primary mass. The continuous growth
takes place, as has been more particularly shown by Koster, along the
lymph-channels surrounding the tumor, which may become filled,
distended, and eventually obliterated by projections from the
neoplasm. Both methods of peripheral growth, by secondary nodules and
continuous extension, represent an infection of the surrounding
tissues, especially if it be admitted that the cells through which the
increase is accomplished are direct descendants of the pre-existing
cells of the part. Not only does the extension take place through the
lymphatic vessels about the tumor, but blood-spaces as well as
lymph-spaces may be invaded. Thrombi are then found whose structure is
frequently that of the tumor, and whose connection with the same is
direct through the perforated wall of the vessel. These features in
the growth of tumors lead directly to the consideration of the means
by which multiple tumors appear in remote parts of the body after a
single tumor has appeared in a given locality, and after the removal
of such a primitive growth.
The distinction between primary and secondary tumors is now so obvious
that one is inclined to forget that the presence of numerous tumors at
various parts of the body was at one time regarded as evidence of the
constitutional or dyscrasic nature of the morbid growth. Such a
multiplicity seemed to indicate that the blood was charged with the
constituents of the tumor, which were deposited at various parts of
the body.
Although certain multiple tumors may be present in different
localities without an apparent relation between an antecedent and a
subsequent growth, such tumors are usually limited to certain systems
of the body. Multiple bony tumors are found growing from bones,
fibrous and warty tumors from the skin, and fibro-myomata from the
uterus. Cohnheim's theory of the embryonal origin of tumors may seem
applicable in such cases, but the frequent association of the
osteomata with chronic inflammatory conditions, of cutaneous warts and
fibrous tumors with local irritative processes, makes such a
hypothesis unnecessary.
Those tumors whose multiplicity is of the greatest clinical importance
are the rapidly growing forms terminating fatally. Such are those
which reappear in the scar after the removal of a cancer, or in the
adjoining chain of lymphatic glands or at remote parts of the body.
The most satisfactory explanation of their presence, and of the
generalization, recurrence, or metastasis of tumors, is derived from
what has already been stated with reference to the manner of the
growth of the latter.
It is well known from experiments on animals that various living,
normal tissues when transplanted to remote parts of the same
individual or to other individuals may continue to grow. Cohnheim
claims, as has been previously stated, that a distinction is to be
drawn in this respect between the tissues of the adult and the foetus,
where the genesis of tumors is concerned. This observer, in connection
with Maas,[80] has found that the transplanted material (periosteum),
although growing for a while, disappears at the end of five weeks, and
it is asserted that fragments of tumors, when transferred, suffer a
similar fate. Wile,[81] on the contrary, {111} who has experimented
with reference to the fate of transplanted tissues and portions of
tumors, reports that one hundred days after the transfer of periosteum
the lung was found to contain several centres of ossification. He
regards the latter as proceeding from the fragments of periosteum
introduced into the jugular vein, and his results thus widely differ
from those of Cohnheim.
[Footnote 80: _Virchow's Archiv_, 1877, lxx. 161.]
[Footnote 81: _The Pathogenesis of Secondary Tumors_, reprint from
_Philadelphia Med. Times_, July, Aug., and Sept., 1882.]
Notwithstanding the numerous experiments which have been made in
various parts of the world to excite the growth of transplanted bits
from tumors, most of them have terminated unsuccessfully. Although a
temporary growth of fragments of tumors has taken place after
transplantation, their eventual disappearance has usually occurred.
Cohnheim lays stress upon this fact in connection with his theory of
the origin of tumors. He considers that the fragments of tissue and
tumors disappear in consequence of the inability of the foreign
particles to withstand the metamorphosis of physiological tissues. If
this opposition is neutralized, the existing germs of tumors become
capable of development. Wile, however, found that eight weeks after
the introduction of a bit of cancer into the lung of an animal the
fragment had increased nearly twice in size. He also refers to the
positive experiments of Newinsky,[82] who transplanted a bit of cancer
from a dog to the subcutaneous tissue of another, young dog, and
found, after five months, not only an ulcerating cutaneous cancer at
the place of inoculation, but also a metastatic nodule of the size of
a hazel-nut in an axillary lymphatic gland.
[Footnote 82: _Allgem. medicinische Central-Zeitung_, 1876, lxxi.
875.]
For the present consideration it may be borne in mind that fragments
of normal (foetal) tissues, as shown by the experiments of Zahn and
Leopold, when introduced into the organs of animals, may become
enlarged. It is also certain that bits of tumors, after their
introduction into the tissues and organs of animals, have become
increased in size. What their eventual fate might have been does not
appear; and herein lies the weak point of the experiments with
reference to the production of secondary tumors. For such experiments
to be regarded as crucial it is necessary that a large number of
previously healthy animals, after inoculation with fragments of morbid
growths, should present in various parts of the body well
characterized tumors whose structure should be like that of the
particles introduced.
The experiments above referred to are of value in confirming the views
concerning the generalization of tumors which have been generally
admitted since Virchow's discoveries with regard to the phenomena of
embolism.
Tumors are said to become generalized when they appear not only in
various systems of the body, but in various organs and tissues. They
are found usually in considerable numbers, and with such differences
in size, shape, and appearance as to indicate different ages. Such
tumors are regarded as arising directly or indirectly from a common
source. This source is called the primitive or primary tumor, and its
derivatives the secondary tumors. The latter are usually considered as
the direct descendants of the former, although their relation may be
that of several successive generations.
The primitive tumor in its growth may extend into lymphatics and
blood-vessels, as has already been suggested. Such an extension may be
{112} so little obvious when the tumor is removed by the surgeon that
all diseased tissues are apparently separated from the body. A
recurrence of the tumor is said to take place when the growth returns
in the cicatrix, frequently in a multiple form. The explanation of
such a recurrence is based upon the probable presence, at the time of
the operation, of fragments of the tumor within the tissues forming
the base and edges of the wound. During and after the healing of the
wound their growth is supposed to continue till they become apparent
as small tumors. The progress of these recurrent tumors is at times
extremely rapid, and they may attain a considerable size in the course
of a few weeks. Such nodules are secondary in point of time, although
they were actually a part of the primary growth.
Secondary nodules in descent as well as time are those which appear at
distant parts, often after the discovery of the primary tumor. Such
nodules are regarded as resulting from the transfer of particles of
various size from the primitive growth, either through the
lymph-vessels or blood-vessels. If the invasion of the body takes
place through the former, the fragments may be floated along to the
nearest lymphatic gland, where it remains when too large to pass
through. If it retains the capacity of growth or of stimulating a like
growth, there results a more or less complete transformation of the
gland into a morbid tissue like that from which the fragments came.
Adjoining lymph-glands may become infected from the first, until
eventually an entire series becomes more or less completely
transformed into morbid growths. A like invasion of the lymphatic
glands may take place through a continuous extension along the
lymph-vessels; and it is not rare to find the sub-pleural or
sub-peritoneal lymphatics as an elevated meshwork in consequence of
the neoplastic growth within them. Such a method of extension may take
place when a cancer of the stomach or liver is associated with a
cancer of the pleura, the intervening lymphatics of the diaphragm
offering a direct and continuous communication.
With the outcropping of a tumor upon a serous surface the possibility
of the detachment of particles is at hand. These may become
transplanted to the opposed serous surface or may be transferred to
the most dependent parts, and there serve as seed for subsequent
growth.
The probability of the embolic nature of many secondary tumors was
early suggested in the history of embolism. Rapidly growing tumors
were known to be capable of perforating the walls of adjacent
blood-vessels, especially veins, and to continue growing along the
course of such vessels. The possibility of the detachment of portions
of these tumors and their transfer along the course of the circulation
was an inevitable inference from the results of experimentation with
foreign bodies. Cancerous emboli were thus recognized as a possible
variety, and their distribution was subject to the same laws as those
governing emboli otherwise constituted. Multiple nodules were
frequently found in the lungs in connection with tumors growing into
the inferior vena cava, while multiple nodules in the liver were
usually associated with tumors of the gastro-intestinal canal or other
regions whose vessels formed a part of the portal circulation. The
readiness with which portions may be detached after death from the
soft masses projecting into the interior of veins suggests the ease
with which particles may be {113} separated during life. The
experiments already referred to show that isolated fragments of tissue
serving as emboli may grow in the place of their reception, and it is
presumable that the resulting growth takes place under the same
conditions as those prevailing at the place from which the embolus
started. The question whether the secondary tumor arises from the
reproduction of elements transferred from the primitive disease, or
whether these excite a characteristic, specific growth of the cells in
the place of their retention, may still be regarded as open. The
experiments favor the former view, and they alone are capable of
satisfactorily determining the point in question.
The secondary nodules, whatever may be their method of origin, present
the peculiarities of the primitive growth. If the cells of the latter
are pigmented, those of the former show the same peculiarity. If the
structure of the primitive tumor contains bone, cartilage, or squamous
epithelium, the secondary growths show like characters, though they
may be present in the heart or other organs where such tissues are not
present as normal constituents. So constant and characteristic is this
feature that the structure of the tumor is usually as well displayed
in the examination of the secondary as of the primitive nodule.
Indeed, the structural peculiarities of the growth may be more
characteristically shown in the former in those instances where the
primitive tumor has undergone degenerative changes obscuring its
histological features.
The tissues of the tumor are subject to the various changes which take
place in the normal tissues of the body. Their growth is attended with
a multiplication of cells and a formation of intercellular substance.
Tumors whose growth is the most rapid are those whose blood-vessels
are the most numerous and whose relation to the cells is most
intimate. The slower the advance of the tumor, the more permanent is
it likely to become, while the more rapid the progress, the more
transitory are its elements. The growth may continue, and yet the
actual size of the tumor may diminish through the absorption of its
degenerated parts. The cells of the neoplasm may undergo fatty
degeneration, or they may become cornified. They may undergo the
mucous metamorphosis or the amyloid and colloid degenerations. They
may take up pigment or they may produce the same. The intercellular
substance varies in its character as does that of normal tissues. It
may be slimy, homogeneous, or fibrillated. It may contain mucin,
chondrin, or gelatin, and may be infiltrated with calcareous salts.
Limited necroses with characteristic cheesy appearances are of
frequent occurrence.
Tumors may become the seat of inflammatory processes, indicated by
suppuration and fever, which may result in abscess or gangrene, or
their progress may terminate in the production of scars. Ulceration
may occur in consequence of the extension of an inflammatory process
to the surface, or it may result in the course of the degenerative
softening of a tumor. In both cases the cutaneous or mucous surface is
involved and destroyed, and the interior of the tumor being exposed
putrefactive processes, with fistulae and sinuses, arise, the latter
favoring the retention of the product and the persistence of the
inflammatory process.
Tumors are always pathological, but the resulting disturbances vary
within wide limits and are often of a complex character. The familiar
distinction between benignant and malignant tumors is based chiefly
{114} upon this variance in the nature of the disturbances. Those are
benignant which closely resemble the normal structures of the body,
increase but slowly, and, if they attain a large size, produce mainly
mechanical disturbances. They may prove serious, even fatal, if so
seated as to interfere with the function of important parts of the
body. Very large and heavy tumors may prove burdensome solely on
account of their weight, while others of similar character, elsewhere
seated, may interfere with respiration or circulation, and eventually
with nutrition. Tumors in exposed situations may become important only
in virtue of their liability to injury, while others impede the
function of a part or an organ by pressure upon its nerves and vessels
or by obstructing its ducts.
The malignant tumors, on the contrary, differ in their structure from
the normal tissues of the body. Their growth is rapid and infiltrating
rather than slow and concentric. Such tumors usually have a
predominance of cells and thin walled blood-vessels. The former may be
little else than nuclei enveloped in an easily destructible
protoplasm, or they may be composed of multi-nucleated masses of
protoplasm, and are then known as giant-cells. The most malignant
tumors are those which tend to become generalized as well as to spread
locally. They recur locally, and appear in the nearest lymph-glands
and at remote parts of the body. The disturbances produced by the
malignant tumors depend less upon their mechanical relations than upon
their tendency to destroy tissues and disturb functions. With their
presence and progress in vital organs there is associated, from their
manner of growth, a destruction of the cells of such organs, as the
kidneys and liver, the lungs and heart. When they are seated in the
spleen and lymphatic glands, a disturbance in the blood-making process
must be associated. Their occurrence in the alimentary canal opposes
the admission, digestion, and expulsion of its contents, and produces
disturbances varying as to the seat and peculiarities of the tumor.
The progress of the malignant tumor is often associated with
ulceration, watery discharges, and hemorrhage. The frequent
coexistence of emaciation, weakness, anaemia, and a yellowish
discoloration of the skin forms a group of disturbances which,
included under the name "cachexia," have long been prominent as
significant of malignant tumors. At the present day this cachexia is
regarded rather as the result than the cause of the tumor, whereas
formerly the reverse was the case.
The modern classification of tumors is based chiefly on their
structure, in part upon their method of origin, and in part upon their
cause.
With the observation of the similarity of appearances in the flesh of
which the external and internal neoplasms are composed, the suggestion
readily presented itself to regard the external tumors and the
internal growths as similar in character. External forms, physical
characteristics, clinical peculiarities, all proved insufficient as a
means of identifying the two, and the step was a short one which led
to the minute study of the flesh of the tumor and a comparison of its
resemblances and differences. This comparison obviously included a
knowledge of the structure and peculiarities of normal tissues. As
histological studies advanced, so did the pursuit of pathological
histology, and the tumors which were once designated as encephaloid,
mastoid, pancreatoid, or nephroid, from real {115} or fancied
resemblances to certain organs of the body, became analyzed into their
microscopic rather than macroscopic characteristics.
It is unnecessary to say that the modern classification of morbid
growths owes its foundation and a large part of its superstructure to
Virchow, whose classic work, _Die Krankhaften Geschwulste_, showed the
direction which future investigators were to pursue and the nature of
the discoveries likely to result.
The tumor represents the result of the growth of a tissue or tissues
which are like or resemble those which form the normal constituents of
the body. Although a new formation is present, it is composed of
tissues lying within the possibilities of the individual. A new
formation of feathers, as Virchow suggests, is beyond the productive
powers of human tissues, though within those of feathered animals. A
goose can produce a tumor containing feathers, not one in which hairs
are found; in the human species tumors containing hairs may occur, not
those, however, in which feathers are present. Although the cells of
the tumors of man may deviate in their appearances from the cells of
normal tissues, this deviation is never so extreme that their analogue
cannot be met with in some part of the body.
As the normal tissues originate from pre-existing tissues, so the
pathological tissues of the tumor grow only from the antecedent
tissues. The matrix from which the tumor arises is a normal tissue.
There is produced from it, as a neoplasm, either a tissue which
follows the type of the maternal tissue, a homologous tumor, or one
which deviates in type from that of the matrix, a heterologous growth.
Although the latter differs in its composition from that of the
matrix, it does not vary essentially from a like tissue to be found
elsewhere in the body. It occurs where it does not belong either in
place, time, or quantity. The homologous tumor appears rather as a
hypertrophy of the tissue from which it arises, and the line between
this variety of growth and a simple hypertrophy is often purely
arbitrary.
Although tumors, in the more limited sense, are solid, fleshy masses,
the new formation of tissues may result in the presence of a tumor
within which is a cavity with various contents. Such a cavity is not a
mere hole, but has a distinct wall of connective tissue lined with
epithelium or endothelium. A distinction is thus drawn between cysts
and growths--one which is of daily importance in the practice of
medicine--and Virchow's oncology includes the consideration of the two
varieties of tumors.
Cystic tumors are subdivided according to the nature of their contents
and the method of their origin. One group is composed of clotted blood
within cavities resulting from the laceration of tissues or in
preformed spaces. If the cyst primarily is merely a rent, the wall
becomes thickened in time from a growth of the limiting tissues, and
the blood-clot, of which the tumor was chiefly composed, may remain or
become absorbed. If the latter event occurs, its place of deposit may
become obliterated by a fusion of the walls of the cyst, or may
persist from the subsequent addition of serum.
The cystic tumor whose contents are extravasated blood is the
haematoma, familiar instances of which are met with in the haematoma
of the dura mater, of muscle, of the vulva, and the polypoid haematoma
of {116} the uterus. The latter is the long retained and constantly
enlarging blood-clot, due to the adherence of portions of the placenta
after childbirth.
The second group of cystic tumors has for its contents a more watery
fluid, and to this the term hygroma is applied. This watery fluid
lies, for the most part, within preformed cavities, and its
accumulation is connected with a dilatation of these cavities.
Instances are met with in the tumors resulting from the accumulation
of fluid in the membranes of the brain or spinal cord, and in the
ventricles of the former or in the central canal of the latter. These
lead to the congenital cystic tumors of the cranium or spine, with
watery contents. The ganglion, the house-maid's knee, as also the
hydrocele of the tunica vaginalis, are regarded as hygromata. The
hydrocele of the neck and elsewhere in the subcutaneous or
intermuscular connective tissue is now removed from the hygromata to
the tumors which arise from lymph-vessels. A like transfer of other
hygromata might be made in accordance with the prevailing views
concerning the cavities in which the watery fluid is accumulated.
A third group of cysts contains material which represents essentially
a production from the wall, with a difference of composition dependent
upon the nature of the wall. Such cysts give rise to tumors through
the retention of their contents, and they are called retention-cysts
or retention-tumors. In the wall of the cysts is a gland-tissue, which
may line the surface or lie beneath. The glandular structures may be
cutaneous, mucous, or represent a part of the great glands of the
body, as the liver and kidneys. The atheromatous cyst of the skin, the
mucous cysts of the gastro-intestinal mucous membrane, and the ovula
Nabothi of the uterus are examples of the retention of secretion
within glands. The dropsical dilatations of the antrum, the vermiform
appendage, the uterus, the biliary and renal canals furnish instances
of tumors resulting from the retention of secretion on a large scale.
In the subsequent history of these retention-cysts the secretion may
be modified chemically and physically; the cells upon the walls may be
transformed from columnar forms into flattened and scale-like
varieties. In time, the original secretion frequently becomes a watery
fluid, resembling the contents of the hygroma previously mentioned.
This grouping of cysts in contradistinction to fleshy tumors omits the
consideration of a series of cystic tumors of enormous size, the
multilocular tumors of the ovary. This class represents a more complex
form of cystic growth--one whose tendency is toward the reproduction
of cysts, to which the term cystoma is applied. The cystoma is the
result of an active new formation of epithelium and connective tissue,
and is classified as a variety of the epithelial group of tumors.
Morbid growths, as distinguished from cysts, are divided by Virchow
into the simple and complex forms. The former consist of a single
tissue, the histoid tumors; the latter of several tissues suggesting
an organ, the organoid tumors; while still others, in which the number
and grouping of tissues is so complex as to simulate systems of the
body, even monstrosities, have received the term systematoid or
teratoid tumors.
Virchow claimed that the growth of most tumors took place from the
connective tissues, and that most of the organoid tumors, especially
cancer, arose from the formative action of the connective tissue in
the part where {117} it first made its appearance. The structure of
cancer suggested an organ, as it consisted of collections of cells
resembling epithelium, within spaces or alveoli whose walls were
formed of connective tissue. The epithelioid cells of the cancer, as
well as the connective-tissue corpuscles, were considered to arise
from pre-existing cells of connective tissue.
The first, most important, modification of Virchow's views, which has
led to a more rational appreciation of the relation of the various
tumors, especially of the epithelial group, to each other, arose in
consequence of the investigations of Thiersch and others with regard
to the origin of certain cancers. This observer[83] claimed that the
epithelioid element of cutaneous cancers arose in all instances from
pre-existing epithelium, either of the rete mucosum or cutaneous
glands. Similar views were suggested, with various degrees of
precision, by other authors concerning certain cancerous tumors
elsewhere, but were first applied to all cancers with a more exact
formulation by Waldeyer,[84] to whom the prevailing views with regard
to the histogenesis of morbid growths are due. According to him, the
essential (epithelioid) element of all primitive cancers arises from
pre-existing epithelium; consequently, no cancer-cell can arise except
in organs where epithelium is normally present.
[Footnote 83: _Der Epithelial Krebs, namentlich der Haut, etc._,
1865.]
[Footnote 84: _Virchow's Archiv_, 1867, xli. 470; 1872, lv. 67;
_Volkmann's Sammlung klinischer Vortrage_, 1871, xxxiii.]
This comprehensive statement was rendered possible by the
embryological researches of Remak at the outset, and afterward by
those of His and Waldeyer. Remak showed that after differentiation of
the cells of the ovum into the several germinal layers, those from one
layer could not serve to originate the cells belonging to another
layer. The development of normal tissues takes place within the limits
defined by this differentiation. Epithelium thus is not derived from
connective tissue, nerves, or muscles, nor was the reverse known to
occur. To His is due the exact appreciation of the superficial cells
of serous membranes, which had been previously called epithelium, and
had thus been confounded with the epithelial cells of mucous or
cutaneous membranes and of secretory glands. He showed that these
cells had a wholly different origin from epithelium, and were simply
scale-like cells of fibrous tissue, to which he applied the name
endothelium. The latter is now used as the term for the thin, squamous
cells of fibrous tissue, whether they are found lining the walls of
the great serous cavities or the smaller lymph-spaces, the
endocardium, or the inner coat of blood-vessels and lymphatics.
The importance of this distinction is obvious when the occurrence of
tumors, called cancers, is observed in parts which contain no
epithelium. Aside from the vagueness of the term cancer, as applied
clinically, tumors are sometimes met with, even in parts where
epithelium normally does not exist, whose structure resembles more or
less closely that of cancer as usually recognized. Such tumors are to
be regarded as of an endothelial rather than epithelial character, and
as such their histogenesis falls under the general laws of the
development of tissues.
Waldeyer[85] has suggested that the primitive basis for the
development of the genito-urinary tract contains cells which are
equivalent in their possibilities of ultimate development to the
epithelium of the limiting germinal layers--a suggestion which is of
importance in permitting the {118} epithelial tumors of the ovary to
be brought under the general embryological laws of development.
[Footnote 85: _Eierstock und Ei_, 1870.]
As the growth of embryonal tissues is so defined that descendants are
like their ancestors in all respects, so the development of tissues in
the adult is regarded as defined with equal precision. Eberth and
Wadsworth[86] have shown that the regeneration of corneal epithelium
takes place from pre-existing epithelium. E. Neumann and others claim
in like manner the development of muscular tissue from antecedent
muscular cells.
[Footnote 86: _Virchow's Archiv_, 1870, li. 361.]
The relation of cancer to epithelial tumors is regarded as similar to
that borne by sarcoma to tumors composed of connective tissues. The
growth of the epithelial elements into the neighboring parts is
through paths determined by pre-existing or new-formed connective
tissue. The active element of the cancer lies more especially in its
epithelioid cells, and its growth takes place in an atypical rather
than a typical manner. Of the various epithelial tumors, there are
those like the cutaneous horn or corn, the adenoma or cystoma, whose
epithelial growth takes place in accordance with normal methods of
production. The epithelioid constituent of the cancer, on the
contrary, grows often with great luxuriance and with but little
tendency to carry out the normal mutual relations of the epithelium
and connective tissue of the part from which it proceeds. The
epithelioid masses or sprouts are composed of cells whose relation to
each other resembles that of normal epithelium in the absence of an
intercellular substance, while the shapes of the cells correspond more
or less closely with that of the epithelium in the region from which
the tumor arises. The epithelioid cells of cutaneous cancers resemble
those of the surface, the rete, or the glands of the skin. Cancers of
the stomach or uterus contain epithelioid cells whose shape simulates
the varieties in the stomach and uterus. Such resemblances are carried
out in the degenerations which the cells of cancer undergo. The
horn-like, keratoid, transformation of epidermoid cells in cutaneous
cancers, the mucous degeneration of the epithelioid cells of cancers
of mucous membranes, are sufficiently familiar. Notwithstanding these
resemblances, which are also present in secondary tumors at remote
parts of the body, the epithelioid growth advances without limit and
without reproducing the normal type. Cancer is therefore defined as an
atypical, epithelial new formation.
Sarcoma, on the other hand, whose clinical features correspond so
closely with those of cancer, simulates, as shown by Virchow, the
connective tissues. It is composed of cells and intercellular
substance, both of which may be as varied as are those of the
connective tissues. The shape of the cells is as diverse and their
contents as various, while their possibilities of degeneration are
alike. The cells of the sarcoma are not simply cemented together, as
are epithelial cells, but they are separated from each other by an
intercellular substance, which corresponds in its appearance and
chemical properties with that of mucous, fibrous, cartilaginous, or
osseous tissue. The structure of the sarcoma differs from that of
these tissues in presenting a predominance of cells over intercellular
substance, while the reverse is the characteristic of most varieties
of connective tissue. In this predominant cell-formation lies its
absence of type, {119} whereas the atypical character of the cancerous
growth is manifested rather by the irregular grouping of the cellular
masses than by an abundance of cells.
As the original cancer is considered as possible only in parts where
epithelium is a normal constituent, so the primitive sarcoma is
possible only in parts where connective tissue is present. The
apparent great frequency of sarcoma in recent times is thus obviously
explained. With an agreement as to its histological characteristics,
its possible place of origin is any of the connective tissues of the
body, and their presence is universal. In the manner of its growth,
its recurrence, and generalization it is subject to the same laws
which determine similar events in the history of cancer. Its
degenerations are often the same, and its symptoms are due to the
action of like causes.
The importance of distinguishing between these atypical tumors is
real, in that it is only through the association of causes, symptoms,
and results with defined and constant characteristics that a practical
knowledge of tumors is to arise. The time-honored distinction between
malignant or semi-malignant and benignant growths is always to be
sought for, and can only be fully possessed when the natural history
of the new formations is known. With an exact appreciation of the
structure of a tumor it becomes possible to study its special
pathology. From a knowledge of the latter are to be derived those
features of importance in determining the relation of morbid growths
to other deviations from normal and physiological processes. An
immediately practical benefit arises from the Thiersch-Waldeyer
modification of Virchow's theory of the origin of tumors, in that it
permits with greater ease a more accurate clinical diagnosis.
Lucke[87] has been prominent in calling attention to the suggestions
thus presented.
[Footnote 87: _Volkmann's Sammlung klinischer Vortrage_, 1876, xcvii.]
The diagnostic value of the theory above-mentioned is rather negative
than positive. With rare exceptions, a tumor cannot be epithelial in
character if its origin is from an organ or a part in which epithelium
is absent. The possible exceptions admit theoretical explanations
which present considerable degrees of probability, and are also based
upon the existing views of the development of tissues.
A tumor whose origin from the connective tissues is determined
partakes of the characteristics of its matrix, and is a
connective-tissue tumor. Its development from fibrous tissue is more
likely to result in a fibroma; from fat tissue, a lipoma, or a myxoma;
from cartilage or bone, a chondroma or osteoma.
Tumors developing at certain periods of life in certain parts of the
body are more likely to belong to one than another of the histogenetic
groups. Tumors of the connective-tissue series are stated by Lucke as
more prevalent before the age of thirty-five years, while those of the
epithelial group are more likely to occur after this age, and cancer
of the lip is of special frequency in old age. The fibro-myoma is of
most frequent occurrence in the uterus, and rarely attains a large
size till the approach of the climacteric.
The rapidity of growth of tumors is also associated with their
genesis. It has previously been stated that the more rapidly growing
tumors are those whose cells are most abundant and in the closest and
most {120} intimate relation to blood-vessels. The type of such tumors
is the sarcoma with its scanty intercellular substance, while the
other (histoid) tumors in the same series, as the fibroma, lipoma,
chondroma, etc., are of relatively slow growth. Tumors of the
epithelial series are of slow growth, from the constantly increasing
distance of the new-formed cells from the vascular connective tissue
which provides their nourishment. When, however, the growth of the
epithelium advances into the connective tissue, pushing out in all
directions and coming in contact with new series of vessels, the
opportunities for nutrition are favorable. In like manner, when the
new formation concerns the connective-tissue stroma, as well as the
epithelial sprouts, vascularization proceeds with the development of
the tumor, and favorable conditions for rapid growth are presented.
Large epithelial tumors may thus arise within organs, but, as the
surfaces are reached, the sources of nourishment become farther
removed and the degeneration of the epithelium favors its detachment
and the formation of ulcers. Hence the tumors whose advance is
associated with ulceration belong rather to the epithelial than the
connective-tissue group.
The tendency of the cancerous tumors to become generalized through the
lymphatics, and that of sarcomatous growths through the blood-vessels,
is admitted as an important feature in the differential diagnosis.
Although there are numerous exceptions, the rule is available. Its
explanation is based upon the assumed inability of the larger
epithelial cells of the cancer to pass through the lymph-glands; being
detained, they serve as new centres of growth. The smaller cells of
the sarcoma, on the contrary, are permitted a passage through the
gland. The numerous and thin walled blood-vessels present in the
rapidly growing sarcoma permit an extension of the latter into their
interior, and thus a ready opportunity is offered for the formation of
emboli.
Another important modification in the classification of tumors has
resulted from the recent discoveries regarding the nature and effects
of infective agencies. Virchow grouped together under the term
granulomata certain growths composed of granulation-tissue occurring
in syphilis, lupus, leprosy, and glanders. Their relation to
inflammatory processes was very intimate, yet they were recognizable
as tumors from their possession of many of the characteristics
generally admitted as belonging to such morbid growths. Although at
times their presence might be regarded as evidence of an inflammatory
disturbance, their frequent appearance independently of general
symptoms of the latter was apparent. These tumors, furthermore, were
so frequently accompanied by inflammatory products as to suggest a
like cause for both. Virchow stated that the recognition of the
etiology of these tumors was indispensable to their separate
consideration, and laid stress upon the presence of a specific virus,
contagious and infectious, in the case of syphilis. His views
concerning the etiology of leprosy, though more guarded, yet carried
the suggestion of the importance of exact investigation concerning the
assumed contagious character of this disease. The contagiousness of
glanders was not only admitted, but the similarity of its manner of
origin and propagation to the invasion of syphilis was also stated.
Not only were the resemblances between glanders and syphilis
recognized, but lupus, leprosy, tubercle, and scrofula were also
admitted as presenting a similar relation.
{121} The importance of recognizing the etiology of these tumors
rather than their anatomy as a basis of classification was strongly
urged by Klebs,[88] who proposed the term infective tumors for the
group of granulomata, including syphilis, lupus, leprosy, and
glanders; and for tubercle, scrofula and the pearly distemper of
animals, which Virchow had classified as lymphomata. This group has
been still further extended by the addition of the lymphomata
occurring in typhoid fever, scarlet fever, and diphtheria. Ponfick[89]
has recently added the disease actinomycosis to the series, and
Cohnheim suggests that certain of the lympho-sarcomata may be
similarly classified.
[Footnote 88: _Prager Vierteljahrschrift_, 1875, cxxvi. 116.]
[Footnote 89: _Die Actinomykose des Menschen_, 1882.]
The growths thus included have a common element of structure--the
granulation-tissue, with its possible disappearance through absorption
or its transformation into an abscess or dense fibrous tissue. Such
features are those common to the granulation-tissue resulting from
ordinary inflammation. Their essential characteristic, however, lies
in the etiology of this granulation-tissue, and for many members of
the group the cause has been discovered to be microscopic organisms.
The constant presence of these is determined in sufficient numbers, in
such distribution, and in such relation, as to explain the nature and
occurrence of the tumors.
The evidence recorded is not equally full and exact for all members of
this group. Neisser[90] has discovered the bacillus of leprosy, and
the discovery by Koch[91] of the bacillus of tuberculosis, scrofula,
and pearly distemper has already been referred to. Schutz and
Loffler[92] have lately announced their isolation of the
micro-organism causing glanders, and Bollinger[93] discovered the
fungus whose presence is necessary for the existence of actinomycosis.
[Footnote 90: _Virchow's Archiv_, 1881, lxxxiv. 514.]
[Footnote 91: See page 99.]
[Footnote 92: _Deutsche medicinische Wochenschrift_, 1882, lii. 707.]
[Footnote 93: _Centralblatt fur die med. Wissenschaften_, 1877,
xxvii.]
In the above affections the organisms are to be regarded as the
characteristic active agent in producing the phenomena of the disease
in which they occur. The presence of micro-organisms in syphilis,
typhoid fever, scarlet fever, and diphtheria is admitted, yet their
absolute identification and constant presence as a cause of the
various manifestations of the respective diseases still remains to be
proved.
The classification of tumors herewith presented is essentially that of
Virchow, with such extensions and modifications as have arisen in
consequence of the investigations and discoveries during the twenty
years which have elapsed since the delivery of his memorable series of
lectures. Cysts are mentioned, as well as growths, from the importance
of the former in practical medicine. The frequent simultaneous
occurrence of cysts and growths in the same tumor should be mentioned,
and the cystic feature is usually indicated as a qualification.
CYSTS.
Cavities, either new formed or pre-existing, with various contents.
The latter are blood, liquid other than blood, and gland-secretion or
retained secretion. The wall varies in structure in accordance with
the method of origin of the cavity.
{122} _Haematoma._
A collection of extravasated blood, usually within the tissues.
Examples, haematoma of the pericranium (periosteum), of the external
ear, muscle, dura mater, ovary, broad ligament, vulva, anus, uterus
(from retained placenta), haematocele, dissecting aneurism.
_Hygroma._
A collection of transuded or exuded fluid in pre-existing or
new-formed spaces. Examples, hydrocele, hydromeningocele,
hydromyelocele, hydrencephalocele, ganglion, inflamed bursa.
_Retention-Cyst._
An accumulation of retained secretion in follicles or canals from
obstruction to its escape. Examples, atheroma and comedo of the skin,
mucous cysts of the gastro-intestinal mucous membrane, ovula Nabothi,
and cystic polypus of the uterus; retention-cyst of the antrum,
vermiform appendage, gall-bladder, and bile-ducts; dropsical
dilatation of the ovarian follicles, Fallopian tube, uterus
(hydrometra), parovarium (cyst of the broad ligament); hydronephrosis
and multilocular cystic kidney, spermatocele, ranula, galactocele.
* * * * *
The growths are classified according to the tissues of which they are
chiefly composed and from which they originate, and according to their
etiology. There are consequently the connective-tissue group; that of
tissues of higher function, as muscle, nerve, and vessels; and the
epithelial group, in which the new formation of epithelium is the
essential feature. The teratoid group comprises a more complex massing
of tissues, representing a combination of those derived from all the
germinal layers of the embryo. The infective group includes those
tumors whose structure is closely allied to that of the products of
inflammation, but whose origin is the direct result of the
introduction from without of a microphyte.
CONNECTIVE-TISSUE GROUP.
Each member mainly composed of a more or less typical growth of a
connective tissue:
Myxoma,
Lipoma,
Glioma,
Chondroma,
Fibroma (including papilloma and melanoma),
Osteoma.
To these are added tumors composed of an atypical growth of a
connective tissue, chiefly manifested by a predominance of cells:
Endothelioma,
Sarcoma.
The sarcoma includes as many varieties as there are tissues in this
group, hence,
Myxosarcoma,
Liposarcoma,
Gliosarcoma,
Chondrosarcoma,
Fibrosarcoma, melanosarcoma,
Osteosarcoma.
{123} GROUP OF TISSUES OF HIGHER FUNCTION.
Myoma, of striped (rhabdomyoma) and smooth (leiomyoma) muscular
tissue,
Neuroma, of nerve tissue,
Angioma, of blood-vessels,
Lymphangioma, of lymphatics,
Lymphoma (?), of lymph-gland tissue.
EPITHELIAL GROUP.
Epidermis:
Callus,
Corn,
Keratosis,
Horn,
Onychoma.
Epithelium of mucous membranes or glands:
Struma (?),
Adenoma,
Cystoma.
In the above varieties the growth of epithelium is more or less
typical, a simple hyperplasia, either alone or combined with the new
formation of fibrous tissue. Only the last three members of the series
are tumors in the limited sense.
CANCER.
Cancer remains as an epithelial tumor, representing the atypical
growth of cells resembling epidermis or the epithelium of glands and
mucous membranes, extending into parts where epithelium is not found
as a normal constituent. A new formation of connective tissue is
usually associated with that of the epithelial cells.
Numerous varieties of cancer are described, according to the physical
and structural peculiarities of the tumor. The scirrhus and
encephaloid of the earlier writers are now transformed into fibrous
and medullary cancer. This change in name is due to the stress laid
upon the predominance of the fibrous stroma as the usual cause for the
hard, dense, scirrhous cancer, while an abundance of epithelioid cells
in relatively large alveoli is present in the encephaloid,
marrow-like, medullary variety.
When the growth takes place from the skin or mucous membranes, the
surface frequently presents numerous and usually arborescent papillae
or villi. The papillary cancers of the skin and the villous cancers of
mucous membranes are thus distinguished.
Cancerous growths of the skin and transitional membranes, often called
epithelioma or cancroid, usually contain epithelioid cells resembling
epidermis, and are therefore designated as epidermoid or
pavement-celled cancer. The alveolar contents of certain cutaneous
cancers are cells resembling those of the deeper layers of the rete
mucosum, while those of other cancers of the skin resemble rather the
epithelium of sweat-glands. Growths of the former character extend
laterally, ulcerate early, and are known as superficial cutaneous
cancer. They form one of the varieties of the so-called rodent ulcer.
Cutaneous cancers, simulating in their structure a reproduction of the
epithelium of sweat-glands, represent a variety of glandular cancer.
The latter term is applied to cancerous growths which arise in
glandular organs, with suggested resemblances of their cells to the
gland-cells of the respective organ. {124} Cylindrical-celled cancer
is frequently met with in those parts of which a cylindrical
epithelium is a normal constituent.
The degenerations of the epithelioid cells and stroma suggest
qualifying terms. The mucous and colloid cancers are those whose
alveolar contents or stroma have undergone a mucous or colloid
degeneration. The keratoid cancer is one which presents the horn-like
transformation of its epidermoid cells. The melanotic cancer contains
abundant pigment, melanin, within its cells.
These differences in the structure and appearance of the tumor are
frequently associated with certain modifications of growth and
clinical properties. The epidermoid cancers are less likely to recur
after early removal; the medullary cancers are of rapid growth and
prone to ulceration; while the fibrous or scirrhous forms are of
extreme slowness of growth. In general, however, the pathological
importance of cancerous tumors is essentially the same wherever the
seat and whatever the peculiarities of structure.
TERATOID GROUP.
Includes those tumors, usually of congenital origin and apparent at
birth, composed of connective tissue, epithelium, nerves, muscle, and
vessels. These tissues are often so grouped together as to suggest
systems of the body and parts of an individual. Cysts are often
present which simulate cavities found in the body, whether of normal
or pathological origin.
In this group are the dermoid cysts with their various contents,
epidermis, sebum, hair, teeth, and bone. The solid teratomata, with
all varieties of connective tissue, as fibrous tissue, fat tissue,
cartilage, bone, neuroglia, in addition to nerves, muscle, and
vessels. Squamous, cylindrical, and ciliated epithelium may be present
and line cavities, at times tubular, whose walls are formed of skin or
mucous membrane. Other tumors of this group are commonly included
under monstrosities, and comprise the varieties of duplication of
parts of the body, of which the extreme instances are such double
monstrosities as the Siamese Twins, Ritta and Christina, the Spanish
Cavalier, and the like.
INFECTIVE GROUP.
The chief characteristic is the cause, micro-organisms, which,
introduced into the body, produce, through their dissemination and
development, multiple growths of tissue like those resulting from
persistent inflammation. As their structure corresponds with the
productive results of inflammation, and their cause is analogous to
the infective causes of inflammation, these morbid growths are closely
allied to inflammatory disturbances. Their classification among tumors
is desirable, as they represent circumscribed growths whose
appearance, persistence, and effects closely resemble those
characteristics of the morbid growths, in the limited sense, in which
the new formation of tissue occupies a wider range:
_Granuloma_ of tuberculosis, scrofula, leprosy, glanders,
actinomycosis, syphilis, lupus.
_Lymphoma_ of diphtheria, scarlet fever, typhoid fever.
{125}
GENERAL ETIOLOGY, MEDICAL DIAGNOSIS, AND PROGNOSIS.
BY HENRY HARTSHORNE, M.D.
ETIOLOGY.
Recognizing pathology as simply morbid physiology--that is, the study
of the body and its functions in states of disorder from morbid
conditions--how these morbid conditions are produced is the complex
question to be answered by Etiology.
Nor is this question (or series of questions) by any means only of
speculative or theoretical importance. It is, indeed, eminently
practical. What a difference, for example, there must be in the
diagnosis, prognosis, and treatment of an attack of inflammation of
the eye, in accordance with its causation by ordinary conditional
influences (taking cold), by a particle of steel imbedded in the
cornea, or by syphilis! How great the difference between the wound
made by the teeth of an animal, in one case with, and in another
without, the presence of rabies in its system! Take the instance of
what we call fever: at a certain stage it is almost the same in half a
dozen diseases. By the causation, when known, of this common congeries
of symptoms we judge of the essential nature of the malady, and so of
its proper treatment.
It is a maxim in philosophy that every event or effect must have at
least two causes. In medical etiology we often find many causes
conspiring to produce one effect. These may be, and commonly have
been, grouped together under two heads; as, 1, predisposing, and 2,
exciting, causes. But under each of these may come a number of
agencies contributing toward the production or modification of
disease. Thus, of predisposing causes we may enumerate inherited
constitution, habits of life, previous attacks of disease, atmosphere,
and other immediate surroundings. Exciting causes--say, of an attack
of apoplexy--may be, in the same case, mental shock, a stooping
posture, an over-heated room, etc. One disease is very often the next
preceding cause of another. So we speak of the great class of sequelae
of acute or subacute disorders; as, ophthalmia after measles, deafness
following scarlet fever, or blindness small-pox, abscesses following
typhoid fever, paralysis diphtheria, etc. But this kind of causation
is extremely common also in chronic affections. What a train of
organic troubles, of kidneys, heart, arteries, brain, and other parts,
attend the affection to which we give the name of Bright's disease!
How complex the sequence often of valvular disease of the heart,
itself in many instances the effect of rheumatic fever, with {126}
endocarditis as a local manifestation of that disorder! Hardly any
discovery in pathology (or pathogeny, the generation of diseases) of
the last half century has been more remarkable and fruitful than that
of thrombosis and embolism, with their serious and not rarely fatal
consequences, through obstruction of the blood-supply to different
organs.
Previous diseases constitute an often overlooked class of factors in
predisposing to new attacks, and also in determining their course and
results. Of some affections one attack prepares the way for another,
as is the case with intermittent fever, convulsions, delirium tremens,
and insanity. Just the reverse is true of yellow fever and of all the
exanthemata, as scarlet fever, measles, small-pox; likewise of the
analogous disorders, mumps and whooping cough. The moot question in
this regard concerning syphilis may be left for discussion elsewhere.
Our classification of the causes of disease may be set forth in simple
form, thus:
1. Pre-natal causation--viz. hereditary transmission of a proclivity
to certain disorders, and also the influence of circumstances acting
on either parent at the time of conception or on the mother during
gestation.
2. Conditional causation--_i.e._ that belonging to variations of
temperature, humidity, etc., affecting individuals.
3. Functional causation--that which is connected with excessive,
deficient, or abnormal exercise of any of the functions of the
economy.
4. Ingestive causation--_e.g._ bad diet, intemperance, poisoning.
5. Enthetic causation--viz. that of all contagious, endemic, and
epidemic diseases. Closely allied to this is epithelic morbid
influence--namely, that of the parasites producing certain affections
of the skin, as itch, favus, etc.
6. Mechanical causation. The effects of this belong chiefly, though
not exclusively, to the domain of surgery.
Pre-natal causation is of immense consequence, and its study takes in
the whole scope of the influences of species, race, family, and
individual parentage. Darwin's observations and speculations, and
those of other evolutionists, have not ignored the field of human life
in considering the struggle for existence and the survival of the
fittest. If we are obliged to admit that such a struggle and survival
do exist for men as well as for animals and for plants, it is
nevertheless obvious that either man's reason and will introduce
exceptions to the ordinary laws of development and selection in
nature, or else a very peculiar standard of fitness must be recognized
in the survivals of humanity. Many feeble, inert, deformed, and
diseased forms survive and perpetuate offspring through a long series
of generations, while strong and admirable ones perish, often even
destroying each other.
Leaving this theme, upon which biological science has not yet
pronounced its last word, we may inquire, What diseases are reasonably
ascribed to hereditary transmission? First, it must be remarked that
seldom is a disease actually received directly from a parent. Putting
aside a few asserted instances of variola and allied or analogous
affections in utero, congenital constitutional syphilis and (more
rarely) scrofulosis seem to afford almost the only examples of this.
Nearly always it is a predisposition merely that is inherited. This,
however, may be very strongly marked. Its seat is evidently in that
(as yet) occult law or {127} process of individual organic development
to whose manifestation we give the name of the constitution. In some
families all the men grow bald before forty; in others, scarcely so at
eighty. Some may expect deafness in middle life, others blindness in
old age, and others, again, have a probability of death from disease
of the heart at about fifty or apoplexy at about sixty years of age.
Such considerations enter into every examination for life insurance,
and they are no less important in our prognostications of the results
of diseases in practice.
Speaking more definitely, gout is undoubtedly often hereditary. That
is, a healthy childhood may be followed by liability to gout in adult
or middle age, even in the absence of direct provocatives to that
disorder, but much more frequently when they are present. Gout affords
an example of the general fact that inherited proclivity to special
diseases shows itself at nearly the same time of life in each
generation--scrofula in childhood, phthisis in adolescence or early
maturity, gout from thirty to forty, apoplexy after sixty, etc. But
exceptions to such rules are not at all rare. Gout also exemplifies
another important fact--viz. the occasional modification of the
transmitted morbid tendency or "diathesis." Parents who have regular
gout--_i.e._ painful attacks of acute inflammation of the smaller
joints, followed by deposits of urates, carbonates, etc.--not
unfrequently have children who are subject to neuralgia or dyspepsia
or modified rheumatic attacks (not sufficiently recognized in
practical treatises), to which the name "gouty rheumatism" is most
applicable. Again, in one generation there may be a marked tendency to
insanity; in the next, to paralysis; in a third, to tubercular
meningitis during infancy.[1] Or some of these successions may occur
in a reverse order.
[Footnote 1: For example, in one family known to me the grandmother
had paralysis, the mother died insane, and her three children all died
of tubercular meningitis.]
Constitutional syphilis is undoubtedly often conveyed by inheritance
from either parent. Sometimes the impression of this diathesis is so
intense as to devitalize the foetus in utero, causing still-birth. Or
the manifestations of the disease occur early in infancy, with
symptoms like those of the secondary or tertiary affection in the
original subject of it. Not often, indeed, is the exhibition, in some
manner, of inherited constitutional syphilis delayed beyond the time
of childhood.
Scrofulosis is well known to follow in the same family through
successive generations, in a manner apparently demonstrative of
hereditary derivation. It is true that here we have a problem not
without complication. Certain circumstances, as poverty of living,
dampness of locality, want of fresh air in houses, etc., promote
scrofula in children. Now, are we sure that it is from its parents
that each child, exposed to these morbific surroundings, has obtained
its disposition to strumous disorders? or may it not be that every
time the diathesis is thus originated de novo? It is to be answered
that decisive evidence in favor of inheritance is present in a number
of cases where the affection occurs so early in infancy as to be
almost or quite congenital in its beginnings; and in other instances
where removal of the parents into improved localities, and with better
living altogether, has not prevented the manifestation of the same
tendency in their offspring for two or three generations. The inquiry
does not differ very greatly in its nature from that concerning cases
of enthetic diseases--_e.g._ cholera, yellow fever, typhoid fever; as
to which the {128} succession of cases may be such as to allow
hypothetical explanation, either by transmission from one individual
to another or by the subjection of all to a common local infection or
epidemic influence. But in both sorts of cases crucial instances may,
with care, be found which determine at least the general etiological
law for each malady.
Pulmonary phthisis has been always considered to be, in a marked
degree, a hereditary disease, until, latterly, the hypothesis of a
tubercular virus has threatened to displace old views about it. If,
however, we accept the classification of cases of pulmonary
consumption approved by several leading pathologists, in which a
position is provided for non-tubercular phthisis, we may at least
place hereditary vulnerability, or proclivity to consumption, in this
category, while awaiting the final decision of science upon the real
nature and origin of tubercle. My own conviction continues to be
positive, that tubercular phthisis is often transmitted by
inheritance, in the same sense as other diseases are generally
so--namely, by the bestowal upon offspring of a constitution
especially liable to the occurrence of the disorder at the time of
life when it is generally most apt to appear. The investigations of
Villemin, Cohnheim, Schuller, Koch, Baumgarten, and others have given
(1882) much prominence to the idea of the possibility of the
transplantation of tubercle from one human or animal body to another.
Koch's elaborate experiments especially are asserted to have shown the
existence of a bacillus tuberculosis, a true, minute vegetative
organism, which can be cultivated outside of the body, in a suitable
material, at a temperature like that of living blood, and which, when
inoculated, produces tubercular disease. The discussion of this
subject will occur on a later page as a part of the general topic of
the causation of enthetic diseases.
Rickets occupies a much less prominent place in the experience of
American practitioners than in that of some countries abroad, and it
is therefore less easy here to obtain materials for the study of its
etiology. Among those who have had large opportunities for its
observation, opinion is divided very much in the manner above referred
to. Thus, Wiltshire and Herring assert it to be certainly hereditary;
Jenner denies this altogether, while Aitken adopts the ground that
predisposing causes are derived from the parents or the nurse, which
are so capable of influencing the health of the child as to lead in
course of time to the establishment of the disease.
Goitre is manifestly a family disorder to a large extent in certain
regions, most familiarly in Alpine valleys in Switzerland. But this
local feature takes us back to the same kind of question: Is it the
transmission of a specially modified constitution from parents, or the
direct action of morbid local influences on the children themselves,
that produces bronchocele and its frequent attendant, cretinism?
Undoubtedly, goitre often occurs in children of healthy parents
brought from another locality into one where the disease is common;
and, per contra, goitrous subjects not infrequently recover from the
affection when removed for a length of time from the place where it
was developed in them. We are, apparently, at least safe in taking
here a position like that of Aitken concerning rickets: viz. that
predisposing causes are derived from parentage, whereby, more easily
than in those of different descent, certain influences will develop
goitre or cretinism, or both together.
{129} As to leprosy, there seems no more room for doubt that it is
often--nay, generally--hereditary. The obscurity attending its
history, however (more than one cutaneous affection having been from
time to time classed under the same name), will justify our referring
the reader for the particular discussion of its etiology to another
part of this work. (See DISEASES OF THE CUTANEOUS SYSTEM.)
Haemophilia is clearly hereditary in certain families. Immermann
asserts it to be even a race-liability in the Jews. "Bleeders" upon
occasion of very small wounds of the skin, gums, etc. have been known
in several successive generations, including (Borner; Kehrer) women at
the time of parturition, who then are apt to have dangerous
hemorrhages.
Cancer presents as unmistakable examples of inheritance as any other
disease. Paget asserts this to be traceable in one case out of three;
Sibley, in one of nine; and Bryant, one of ten cases. De Morgan and
others have shown the same thing to be true of non-malignant morbid
growths. But, as Paget has remarked, when other local disease or
deformity is inherited, it usually involves in the offspring the same
tissue, often the same part of the body, as in the parent, but the
transmitted cancerous tendency may show itself anywhere: "Cancer of
the breast in the parent is marked as cancer of the lip in the
offspring. The cancer of the cheek in the parent becomes cancer of the
bone in the child. There is in these cases absolutely no relation at
all of place or texture."
Cataract is believed by good authorities to be promoted by hereditary
tendency. It is of the nature of a degeneration. Possibly, in a
greatly-prolonged decay of all the organs with age, all eyes tend to
become cataractous from structural alteration of the crystalline lens.
Under observation a quite different rate of degenerative change takes
place among the organs of the body in different individuals and
families. Thus, the lens becomes opaque in some at an age when the
hearing continues good and the muscles retain considerable vigor,
while in members of other families the eyes remain in a sound
condition at a time when other organs and powers have failed.
Congenital cataract appears to be altogether independent of any
proclivity transmitted from parents in the nature of an inheritance.
Affections of the nervous system very often show hereditary descent.
Neuralgia prevails strongly in certain families. Particularly, that
form of cephalalgia called sick headache is apt to appear, in the
periodical form, through several generations. Apoplexy and paralysis
are prone to occur at nearly the same time of life under the
transmission of like constitutions by parentage. Still more often this
has been observed of epilepsy and hysteria, and, most of all the
neuroses, in insanity. Monomania and melancholia have been in a great
number of instances traced to generative succession--sometimes,
especially suicidal monomania, through four or five generations.
Predisposition to intemperance, methomania, is also a terrible
inheritance in some families. Although the production of this malady
requires the provocative of indulgence in the use of alcohol for its
development, yet the facility with which this result occurs under the
same circumstances in different families is too marked to leave room
for doubt of its hereditary nature.
Less certainly, but with much probability, we may assign parental
endowment as one of the factors in the causation of organic disease of
{130} the heart, arteries, liver, and kidneys, as well as of angina
pectoris, asthma, croup, dyspepsia, and hemorrhoids.
Is a special proclivity to any of the group of enthetic febrile
diseases ever inherited? Dr. George B. Wood believed this to be the
case with enteric or typhoid fever. Few others have shared this
opinion, but it is not impossible that it has a basis of truth.
Reference has been made already to the difference between periodical
malarial fevers (intermittent, etc.) and yellow fever, in that an
attack of the latter does, and one of the former does not, protect the
individual, usually, from liability to the disease on exposure to its
cause. Does this protection extend to offspring of parents who have
been "acclimatized" to yellow fever? Facts on this point are not easy
to obtain. While, however, there appears to be no proof that a single
generation can ever suffice to outgrow (so to speak) liability to this
disease, it is well known that creoles in Louisiana and the West
Indies are less susceptible to it than recent white residents, and
that the negroes are much less so, as a race, than the whites.
Furthermore, negroes whose ancestors have long been domesticated in
our Southern States appear to re-acquire susceptibility to yellow
fever in a degree more nearly like that of white people than is
observed in natives of Western Africa imported within one or two
generations.
As to autumnal malarial fevers (remittent, intermittent), the black
race exhibits a sort of race-acclimatization, giving negroes, both in
Africa and in America, a much less degree of liability than is common
to all races of European descent.
How far any similar modification may occur in the course of
generations in regard to susceptibility to small-pox and allied
diseases remains at present a matter of speculation. Some authors
insist that there must be at least a kind of natural selection,
according to which a great epidemic of variola, destroying the lives
of many of those most predisposed to suffer from it, will leave the
remaining population less likely to be attacked by it. The endeavor
has even been made to explain away in this manner much of the
diminution of mortality from small-pox commonly credited to
vaccination. But the statistics of the ravages of variola in different
countries before and after the introduction of vaccination show that,
while we cannot deny that some alternation (of generations
respectively more and less susceptible) may occur, no such law can
compare in influence with that of vaccination in the protection of
individuals subjected to it. Indeed, the argument may be inverted;
thus: if in the days before Jenner small-pox itself weeded out the
persons most liable to it, or in some way prepared a partial family-
or race-protection, such a protection ought to be gradually conferred
upon a whole population through universal and persistent vaccination
carried on for several generations.
Is it possible for one hereditary constitution or diathesis to become,
in transmission, not only modified, but transmuted, into another? Some
of the older pathologists imagined this to be the case with syphilis,
to whose past influence upon parents and ancestors they traced the
origin of scrofula. But no sufficient ground for such a pathogeny can
be ascertained. All that appears to be left after scrutiny of the
facts is, that syphilis is a depressing and perverting agency, and so
may join with {131} other depressing causes in preparing the way for
the engendering of scrofulosis.
A few points still remain to be briefly mentioned in connection with
the hereditary conveyance of proclivity to disease. One or several
members of a family will often pass through life without any
manifestation of such transmission, while others, their brothers or
sisters, give marked evidence of it. Sometimes a whole generation may
be passed over, and yet the predisposition may be abundantly shown in
that next following. This is closely similar to atavism, as it is
called in zoology and general biology, according to which traits
occurring under admixture or variation of animal or vegetable stocks
may be absent in the immediate offspring of a couple, but reappear in
their next succeeding descendants, or even a still later reversion may
take place. Such instances are not rare, and they need to be
considered in the proper study of the influence of parentage,
intermarriage, etc. upon health and disease.
A practical question of much importance (belonging, however, rather to
sanitary than to medical science) is, how far confirmation or
modification of hereditary proclivities may occur through the effect
of the conditions of marriage upon offspring. Consanguineous marriages
have been, time out of mind, held to be very objectionable. The
question has been much discussed whether the ground of sanitary
objection is properly against such marriages as per se injurious to
offspring, or whether the bad effect consists merely in reduplicating
and intensifying family constitutional taints. It would not be in
place here to go into this controversy. My own conclusion is, that a
natural law of sexual polarity or affinity exists, according to which,
in all the higher organisms, reproduction is most normal and gives the
best results when a considerable genetic difference (within the limits
of species) exists between parents. While, however, this is probable,
but difficult to demonstrate, it appears to be certain that when a
father and mother both possess morbid constitutional predispositions
(say, to phthisis, insanity, or gout), their children will be at least
twice as likely to suffer from the same as if only one parent were so
endowed. Whether or not, then, the marriage of two perfectly healthy
first-cousins may be expected (as several statisticians aver to have
been shown) to be attended by defects of health in their progeny, the
union of such relations when their common progenitors were in marked
degree consumptive, or scrofulous, or liable to insanity, epilepsy,
etc., has attached to it so unfavorable a prognosis for offspring as
to be rightly forbidden. Moreover, so few families possess an
absolutely faultless health-record that the chances of increasing
existing morbid traits by intermarriages are quite sufficient to
justify the commonly held objection against them.
We must allude very briefly to the influence of conditions affecting
conception and gestation upon the health of offspring. Intemperance in
parents has, in many instances, been known to promote convulsions,
infantile or epileptic, and other cerebral or nervous disorders in
children, besides a general feebleness of constitution. Even
intoxication at the time of procreation has been asserted to mark a
similar difference between one child and another of the same parents.
All are familiar with the (no doubt often quite imaginary) accounts of
the effect on infants in utero of powerful sensory or mental
impressions upon the mother during gestation. Abortion has,
unquestionably, been {132} often produced by violent nervous shocks.
Without deciding the question whether "monsters" are ever developed in
correspondence with particular experiences of the mother, we may hold
it to be clear that all depressing and disturbing agencies may
interfere with the process of nutrition of the foetus, and thus
develop mental anomalies, and that constitutional impairments may thus
be greatly promoted.
All inherited predispositions, it is important to remember, are
aggravated, and each proclivity changed to actuality, by those
influences which in individuals tend to like effects upon health. Such
become exciting causes of various diseases. If these be constantly
avoided, and all the surroundings and the mode of life of the
individual be maintained in a manner most favorable to health, the
hereditary tendency may remain inert through a long lifetime. Every
physician must have seen this in scores of instances. The application
of the principle through special precepts belongs to personal hygiene.
But no physician can rightly ignore the study of this subject, or omit
the utilization of his acquaintance with it by preventive advice to
members of the families under his professional care.
Our last remark in connection with pre-natal causation must be upon
the effects of circumstances and modes of living on masses of men,
especially in large cities and populous countries. Something has been
said already of race-acclimatization by which there may be acquired a
lessened susceptibility to certain endemic fevers.[2] Almost a reverse
action is exhibited in the gradual lowering of vital energy under what
has been called the "great-town system." While those having all the
comforts of life and avoiding excesses may manifest but little of this
deterioration, it is very observable in that mass of men, women, and
children who become the subjects of medical charities. Closeness and
uncleanliness of living, with more or less exposure to dampness and
extremes either of heat or cold, with intemperance and syphilis, are
the main causes of this general constitutional impairment. So
important is it that it should never be forgotten, not only in our
estimate of the causation of diseases, but in our anticipation of
their results, and also in our adaptation of measures of treatment,
medical and surgical, to different classes of patients. All that it is
allowable here to suggest in this regard may be summed up (although
very imperfectly) in the word hospitalism.
[Footnote 2: It is important (but not before remarked in this article)
that cholera does not appear to allow of any such diminution of
liability to it among the natives of the country in which it is
endemic.]
Conditional causation has been, to a certain extent, included under
what has been above said, as it is the action, in part at least, of
surrounding conditions, that establishes a family- or race-proclivity
and inheritance. But we must say something more about the direct
action of conditions upon individuals.
Man, although organized with great delicacy of structure, is capable,
by the use of his intelligence, of adapting himself to a wider variety
of external conditions than any other animal. He is the only truly
cosmopolitan being on the earth. From the remote Arctic regions to the
hottest tropical climates there are tribes whose ancestors have dwelt
for centuries in the same localities. Not that no unfavorable
influence attends these extremes. The Esquimaux are stunted, the
Southern Hindoo and {133} Central African are enfeebled and
degenerate, partly from climate. But with man's numerous protective
devices, great cold and great heat only exceptionally affect
individual health. Freezing to death follows unusual exposures; the
loss of an extremity by sphacelus from congelation is more often met
with; heat-stroke also is tolerably frequent; and the influence of
heat in producing cholera infantum in some large cities is very
important; but much the most common kind of conditional morbid
causation is produced either by sudden changes of temperature or by
diversity of exposure of different parts of the body. These are the
two usual modes of "taking cold." When dampness accompanies a
relatively low temperature, such an effect is much more apt to follow
than in a cold dry atmosphere.
Actual cold-stroke, the analogue of heat-stroke, may sometimes happen.
I once saw such a case in a previously healthy boy twelve years of
age, who, after standing for an hour in his night-shirt on a cold
winter night, became almost immediately ill, fell into a comatose
state, and died in about thirty-six hours.
A simple rationale may be discerned for the phenomena of catching
cold. When, for example, a draught of air blows for a time upon the
back of a person at rest (especially one who has just before used
active exertion), the local refrigerant impression induces
constriction of the superficial blood-vessels. Hence follow two
effects: one, the repulsion of blood in undue amount toward interior
organs; the other, diminution, perhaps arrest, of excretion from the
skin of the exposed portion of the body, and consequent retention of
some effete material, promoting esotoxaemia.[3] If, then, there be in
the body any weak organ--that is, one whose circulation is partially
impeded or whose nutritive and functional activity is low--it suffers
first and most from the impulsion of blood from the surface.
Congestion, irritation, and inflammation may follow, and we have an
attack of pneumonia, pleurisy, bronchitis, or some phlegmasia.
[Footnote 3: That is, blood-poisoning, originating within the body
itself; exotoxaemia being that which is enthetic--_i.e._ resulting
from a poison derived from without.]
Excessive heat with dryness, as under the blasts of the Simoon or the
Harmattan of Arabia or Northern Africa (apart from insolation,
sunstroke, or heat-stroke), may sometimes parch the body even to a
fatal degree. Much more common is the combination of high temperature
with humidity. This has a relaxing effect, promoting indolence of
temperament and predisposing to disorders of a catarrhal nature,
especially of the digestive organs, such as were called fluxes by the
older writers.
Cold climates are well known to present the greatest number of cases
of acute and chronic affections of organs of the respiratory system;
warm and hot climates, those of the stomach, liver, spleen, and
bowels. But we must recollect what various complications belong to
climate. Two important factors, especially, must be kept in view in
comparing the causation of diseases in colder and warmer
countries--namely, the difference in the articles of food partaken of
in each, and the external sources of enthetic disorders; _e.g._
endemic and epidemic fevers, etc.
With humidity must be considered variations in atmospheric pressure.
Physicists have long known that while watery vapor, by itself, is
heavier than air which is perfectly dry, moist air is lighter than air
containing {134} little or no moisture. Hence the barometer falls as
the quantity of atmospheric moisture approaches saturation. Other
causes, however, also affect barometric pressure. With the same degree
of humidity, cold air is denser and heavier than warm air, and by its
contraction lowering the "column" of atmosphere--the temperature of
which is reduced--a flow toward the upper part of the column increases
the actual mass of air pressing upon a particular place. Elevation of
a locality above the general level of the earth reduces atmospheric
pressure, sensibly as well as measurably. So "the difficult air of the
iced mountain-top" has become proverbial.
These variations are familiar, though all their effects upon human
health have been by no means, as yet, fully studied. Most difficult to
determine and analyze are the influences of changes of pressure,
chiefly hygrometric, upon the course of diseases and upon the result
of severe surgical operations. Among the few important series of
observations bearing on this topic have been those of Dr. S. Weir
Mitchell on neuralgia,[4] and Dr. Addinell Hewson on the prognosis of
major operations,[5] in connection with the state of the weather. The
former ascertained a marked relation between the approach of a wave of
low barometric pressure and attacks of irregularly periodic neuralgia;
the latter proved, by the statistics of the Pennsylvania Hospital for
a number of years, that the most favorable time for amputations or
other capital operations is when the barometer is high, or at least on
the ascent.
[Footnote 4: _American Journal of Medical Sciences_, April, 1877, p.
305.]
[Footnote 5: _Pennsylvania Hospital Reports_, 1868.]
Electrical atmospheric states and vicissitudes have, quite probably, a
practical consequence beyond what is usually ascribed to them in
connection with health and disease. But their effects are so difficult
to disentangle from those of other meteorological causes that we must
be content at present without attempting their exact specification.
The same observation may be made with reference to ozone.
Elevation of site has importance, not only in regard to climatic
hygiene, but also to its therapeutic use, particularly in the
treatment of phthisis, goitre, and some affections of the nervous
system. But in our brief and general survey of Etiology this topic
must be left without discussion, since no disorder appears to be
traceable to elevation alone, beyond the temporary prostration on
exertion, with hemorrhages from the nose, lungs, etc., often produced
in those who climb to great mountain-heights or ascend rapidly in
balloons. It has been shown by ample experience that considerable
populations may live in ordinary health through long periods at
altitudes more than 10,000 feet above the level of the ocean.
Depression below the surface of the earth has never become a part of
human experience beyond the limit of a few hundred feet. Miners living
underground in a few places in Europe have been found to exhibit
comparatively feeble health, but the privation of sunlight, the
confined atmosphere, and the dampness of such unnatural abodes will
suffice to account for these effects.
Under functional causation of disease we may include all excessive,
deficient, or abnormal exercise of any of the organs of the body. To
simple excess may be ascribed the scrivener's or bank-officer's
paralysis of the muscles of the hand used in continuous writing; brain
{135} exhaustion from mental labor or anxiety, unrelieved by
sufficient sleep; and sexual impotence, temporary or lasting (or
sometimes even general paralysis), from inordinate sexual or sensual
indulgence.
Deficiency of functional exercise is observed to produce disability,
as when the muscles of a limb, for instance, are for a long time
restrained from use. Surgeons meet with this inconvenience (unless
assiduously guarded against) when a fractured limb is kept long at
rest in a fixed position. Atrophy of the mammae in single women of
retired lives is common; atrophy of the testicles in unmarried men
much less so. These changes, however, are physiological, not
pathological; upon alteration of conditions--_e.g._ marriage--the
atrophy will disappear altogether.
Abnormal functional action as a cause of morbid results is seen when
the eyes are injured by reading, writing, or doing any delicate work
in a bad light; for instance, late twilight. Also, in a secondary or
accessory manner, when a near-sighted person, having the action of the
muscles of convergence in excess of his accommodation, or a
long-sighted (hyperopic) person, whose accommodation is in excess of
convergence, suffers from asthenopia, perhaps with headache, distress,
nausea, etc. Another example of abnormal functional exercise and its
effects is that of self-abuse, where the unnatural mechanical
imitation of the physiological act of sexual coition induces
disturbances of the nervous and circulatory systems, besides debility
from excess.
Ingestive causation is a sufficiently fit designation for all errors
of diet, as well as misuse of medicines, and poisoning. Starvation or
inanition belongs to the same category by negation. Gluttony and
intemperance are major members in the ingestive series, while haste in
taking food, without mastication, and the use of heavy bread, unripe
fruit, and other indigestible articles, account for many cases of
dyspepsia and some of colic, cholera morbus, diarrhoea, etc. With
young children, especially, no more frequently acting cause of
disorder exists than dietetic mismanagement, most of all during the
period of dentition, and earlier, when, from absence or insufficiency
of mother's milk, they have to be artificially fed. Then the supply of
good fresh cow's, goat's, or ass's milk may carry them well through
infancy, while a regimen of arrowroot or gum-arabic and water, or
stale, half sour milk, may either starve or sicken them to death. On
the subject of poisons and of misuse of medicines we have no occasion
here to make special remark. Only it may be mentioned that the
possibility of either is always to be remembered by the physician in
making up his mind in regard to the origin of symptoms observed.
Enthetic causation is a large subject, including all origination of
disease by the introduction of morbid materials from without the
body.[6] Medical opinion has generally accepted, and facts fully
sustain, the recognition of three groups of enthetic disorders, viz.:
those which are personally contagious; such as are locally epidemic;
and epidemic diseases. Of the first group it will suffice to mention,
as an example, syphilis; of the second, intermittent fever; of the
third, influenza.
[Footnote 6: Simon has proposed the term exopathic to indicate the
origin of such maladies; autopathic disorders being those which
originate within the body itself.]
Were all maladies whose causation is evidently of external origin
capable of the same clear discrimination as these, we should have no
difficulty with the present topic. But, in fact, no subject connected
with {136} the history of disease has become surrounded by more
intricate controversy. Many times the same facts are, or appear to be,
explicable in two or three different ways. What some hold to be proofs
of contagion from person to person, others are ready to account for by
the subjection of a number of persons or of a whole community to
either a common local or a widespread migrating (epidemic) influence.
It is sometimes impossible, in the nature of things, to obtain an
absolute demonstration of the truth of one or another of these
theories without such experiments upon human beings as are
impracticable.
While endeavoring to ascertain the limits of our present knowledge
upon these questions, let us first notice what are the most positive
facts concerning them, some of which are common to the whole group or
class of what have been, since Liebig, often called zymotic,[7] but
latterly more often enthetic, diseases.
[Footnote 7: The term zymotic has, with many authors, fallen into
disrepute, chiefly because Liebig's hypothesis concerning the
chemico-physical action of ferments, as well as of contagia, has lost
ground in comparison with the vital or disease-germ theory. Yet the
analogy between fermentation, putrefaction, and the action of a virus
on an animal organism persists; whatever may be the theory of their
explanation, something appears to be common or similar in all these
processes.]
These diseases may be enumerated as follows:
1. _Only produced by contact or inoculation_.
Primary Syphilis,
Gonorrhoea,
Vaccinia,
Hydrophobia.
2. _Contagious also by atmospheric transmission through short
distances_.
Variola,
Varioloid,
Varicella,
Measles,
Diphtheria,
Scarlatina,
Rotheln,
Mumps,
Whooping Cough,
Typhus,
Relapsing Fever.
3. _Endemic, occasionally epidemic_.
Malarial Fevers (Intermittent, Remittent, and Pernicious Fever),
Dengue,
Yellow Fever.
4. _Other zymotic or enthetic diseases_.
Influenza,
Cerebro-spinal Fever,
Erysipelas,
Puerperal Fever,
Tropical Dysentery,
Typhoid Fever,
Cholera,
Plague.
As all observers are agreed in regard to the personal transmission of
the first named of these series (variola, etc.), we need to give
attention here only to the other groups; except merely to say that the
easily demonstrable existence of a morbid material (virus) in the
instances of primary syphilis, gonorrhoea, variola, and vaccinia
presents a very cogent analogical argument for the presumption that
all clearly contagious (even {137} though non-eruptive) maladies, such
as mumps and whooping cough, must also have a morbid material as their
essential cause; and also in favor of the supposition that a morbid
material may probably be the "causa sine qua non" of each of the other
maladies which are known to be endemic or epidemic. A few theorists
only have argued in favor of any other view than this. Sir James
Murray and Dr. Craig of Scotland, and Dr. S. Littell of Philadelphia,
have sustained an electrical hypothesis, and Oldham and others have
advocated one connected with changes of bodily temperature, or ozone,
etc., for the origination of certain endemic and epidemic diseases.
But all the facts point toward the existence of material causes,
specific for each of these disorders, and many observations and much
ingenuity of reasoning have been brought to bear upon the question as
to their intimate nature.
Are these materiae morborum merely inorganic elements or compounds
entering human bodies and acting there as chemical poisons? Against
such a supposition we have, as almost decisive objections, not only
the absence, under the most searching analysis, of any chemical
peculiarity in the air of malarious or otherwise infected regions, but
also the clinging of many endemic and epidemic causes (as known by
their effects) to particular localities, notwithstanding the
recognized law of the diffusion of gases which must antagonize such
concentration. Therefore, we may rule out, as highly improbable at
least, the hypothesis of the inorganic gaseous nature of malaria, as
well as of the essential causes of yellow fever, cholera, plague, and
the other analogous diseases.
By the once general use of the term zymotic, there is suggested a line
of thought which has been quite prevalent since the prominence of
Liebig's teachings in chemical physiology, until recently. That great
chemist did not imagine that a true zymosis or fermentation occurs
under the action of a virus upon the human economy. His thought was
more clearly expressed, in the phraseology of the late Dr. Snow of
London, as the theory of continuous molecular change. Its most
striking physical instance or analogue is the extension of flame from
a burning body to combustible matter within its reach. Sugar formation
from starch by diastase, and the change of albumen into peptone by
pepsin, are familiar examples, in organic materials, of the
propagation of molecular movement in special directions and with
characteristic results.[8] It does not seem to be more than a short
step from these to the processes which we study in fermentation,
putrefaction, septicaemia, and the multiplication of small-pox
contagion, from the smallest inoculation, in the human body.[9]
[Footnote 8: In anticipation of the argument concerning the necessity
of the action of minute living organisms to produce fermentation,
putrefaction, and specific diseases, emphasis may be here laid upon
the fact that the above named changes, and many others like them, are
produced, in the absence of such organisms, by chemical agents formed
in the body, or even (as when sulphuric acid changes starch to sugar)
by inorganic substances. Pasteur considers that the yeast-cell
secretes a sort of diastase which changes starch or cane-sugar into
glucose, on which the cell then lives, decomposing the glucose into
alcohol, carbonic acid, etc. Koch and others now assert that a
bacillus produces the souring of milk, and another the butyric acid
fermentation.]
[Footnote 9: The assertion of some advocates of the "germ theory of
disease," that only living organisms reproduce their kind, loses
weight as an argument in view of the natural history of small-pox and
analogous diseases; unless it be proved that every particle of
contagious matter is (at one time at least) a living organism.]
But here comes in a new hypothetical factor, introduced by the aid of
{138} the microscope, although anticipated conjecturally before actual
discoveries in this field were made certain. So prominent is this
subject in the discussions of the present time, under the expression
"the germ theory of disease," that we are justified in giving
attention to it here somewhat at length.
Stahl proposed a purely chemical theory of fermentation early in the
seventeenth century. Not much later Hauptmann suggested the probable
causation of epidemic diseases by minute living organisms.
Linnaeus[10] revived this hypothesis in the eighteenth century. These
two topics of inquiry, with the intermediate one of putrefaction, then
received much attention, at first apart, but afterward with
recognition of their analogies. When Fabroni, Cagniard de la Tour,
Schwann, and Kutzing had, with the aid of the microscope, made
familiar the life-history of the yeast-fungus[11] (Saccharomyces
cerevisiae), more close consideration still was given to these
remarkable changes in organic materials and forms, dead and living.
[Footnote 10: Linnaeus accepted the asserted observation by Rolander
of acari in the stools in dysentery. The great naturalist deviated
somewhat here from his usual carefulness and accuracy, as that
observation was not afterward verified.]
[Footnote 11: Leuwenhoek, however, had observed and described it in
1680.]
Starting from the physical basis of inorganic chemistry, Liebig
followed the series up from the so-called catalytic[12] action by
which the presence of a substance, itself apparently unchanged,
induces reaction between two or more other bodies, to those which
occur within plants and animals, as examples of vital chemistry. Such
is the influence of diastase or invertin, which in the seeds of plants
brings on the conversion of starch into sugar and of cane-sugar into
glucose and levulose. Such is the agency of ptyalin in the saliva, of
pepsin in the gastric juice, and of pancreatin or trypsin in the
secretion of the pancreas, in the processes of digestion. From these
it appears to be an easy transition to those changes which occur in
organic matter no longer living, as in the fermentation of vegetable
juices and the putrefaction of animal tissues.[13] Liebig endeavored
to explain these also in the same manner as the chemico-vital
processes; and he then went farther to apply the same generalization
to the propagation of disease, by what is called virus, in the
instances of contagious, endemic, and epidemic maladies.
[Footnote 12: The idea expressed by this term was especially favored
by Berzelius and Mitscherlich.]
[Footnote 13: It is noticeable, however, although generally forgotten,
that the one set of changes and assimilations (namely, those of
digestion) are formative actions of life, and the others destructive,
in the direction of, or subsequent to, death.]
But, meanwhile, observation and speculation gave almost equal
prominence to the importance of minute living organisms in the
apparent instigation of all these evidently analogous changes of
fermentation, putrefaction, suppuration, septicaemia (Piorry, 1835),
infection, and contagion.
Upon this side the leading investigator for many years has been
Pasteur. As long ago, however, as 1813 Astier, and in 1840 Henle of
Berlin, and near the same time Sir Henry Holland of London and Dr. J.
K. Mitchell of Philadelphia, gave expression to opinions of a similar
kind, based upon many important facts before very much overlooked. By
exact experimentation, moreover, Schwann, Helmholtz, Schroeder, and
Dusch ascertained that the agent or agents causative of fermentation
and putrefaction can be detained by heated tubes, by animal membranes,
{139} and by cotton wool, anticipating the later observations of
Pasteur,[14] Tyndall, Chauveau, and others to the same or similar
effect. These results of experiments are commonly understood to prove
the particulate character of the agents so studied. What may be called
an era in the practical application of etiological inquiry dates from
the introduction by Lister (about 1860) of the principles of
antiseptic surgery, based upon the theory that disease-germs, derived
from the atmosphere or other external sources, are the essential
causes of suppuration, septicaemia, pyaemia, gangrene, etc. following
injuries or operations.
[Footnote 14: Pasteur's experiments with long-drawn bent tubes had
especial significance.]
So far from this inquiry being yet terminated, while experiments and
observations have become more and more numerous and elaborate,
opinions continue to differ; and we must yet await the time when, by
successively excluding, one after another, all the sources of error, a
truly scientific conclusion may be obtained.
Roughly speaking, it may be said that parties in the debate are
chiefly ranged upon two sides--those who favor the probability that
only chemical, not vital, action is to be traced in fermentation,
putrefaction, suppuration, infection, and contagion; and those who
regard minute organisms, discovered or undiscovered, as causative of,
and indispensable to, all these processes.
Without intention of injustice to other able investigators, the
principal names so far associated with the former of these views may
be thus mentioned: Panum (1856), Robin, Bergmann, Liebig, Colin,
Lebert, Vulpian, Onimus, B. W. Richardson,[15] Beale,[16] Senator,
Rosenberger, Hiller, Naegeli, Schottelius, Harley, Jacobi, Curtis, and
Satterthwaite. Of those maintaining, in some form and with more or
less positiveness, the disease-germ theory, the most conspicuous,
especially as observers, have been Tuchs (1848), Royer (1850),
Davaine, Branell, Pollender, Pasteur, Tyndall, Lister, Mayrhofer,
Ortel, Letzerich, Nassiloff, Hueter, Toussaint, Hansen, Salisbury,
Klob, Hallier, Basch, Virchow, Neisser, Eberth, Tommasi Crudeli,
Klebs, Talamon, Schuller, Tappeiner, Cohnheim, Koch, Baumgarten,
Buchner, Aufrecht, Birch-Hirschfeld, Greenfield, and Ogston. Besides
these the elaborate studies of microphytes by Cohn, and those of Coze
and Feltz, Waldeyer, Recklinghausen, and others upon septic poisoning,
have been of acknowledged importance; and the experimental labors of
Burdon Sanderson in England, and Sternberg,[17] H. C. Wood, and Formad
in the United States (under the auspices of the National Board of
Health), possess great value. But the scientific caution of these last
inquirers, like that of Magnin, has prevented them from formulating,
as yet, positive and final opinions upon the subject. It is not saying
too much to assert nearly the same of {140} several of those mentioned
above, as inclining to one or the other side of the controversy.[18]
[Footnote 15: Dr. Richardson has long contended for the doctrine first
proposed by Panum, that a peculiar chemical agent, (called by Bergmann
_sepsin_) is the cause of blood-poisoning from virulent absorption or
inoculation. Latterly, attention has been called by Selmi and other
observers to the existence of complex compounds called _ptomaines_ in
decomposing animal substances--_e.g._ the human body after
death--these having considerable resemblance in their toxic action to
the poisonous vegetable alkaloids.]
[Footnote 16: Opposed at least to the ordinary form of the germ theory
of disease.]
[Footnote 17: Sternberg's observations and experiments (following
those of Pasteur) with the inoculation of animals with saliva, proving
that even when taken from perfectly healthy men this may be fatally
poisonous to animals, possess remarkable interest. They do not seem,
however, to be decisive either way in regard to the germ theory of
infection.]
[Footnote 18: Billroth and Cohnheim are among those who have changed
their opinions on this subject after prolonged investigation.]
It would appear, then, that the data for a final conclusion have not
yet been made certain. Several hypotheses are conceivable, and
capable, each, of plausible support:
1. The purely chemical theory of Liebig, Gerhardt, Bergmann, Snow of
London, and B. W. Richardson.
2. The bioplastic hypothesis of Beale, according to which germinal
matter may be detached from a living body and planted, while yet
retaining vitality, upon another, and there may undergo changes more
or less morbid, and destructive of the body by which it has been
received. This theory of migrating or transplanted bioplasts has
received very little support besides that of its distinguished author.
3. That the minute organisms discovered so constantly upon diseased
parts of plants and animals (_e.g._ ergot of rye, _Peronospora
infestans_ of potato-rot, _Botrytis Bassiana_ of silk-worm muscardine,
_Panhistophyton_ of silk-worm pebrine, _Empusa muscae_ of the fly,
_Achorion_, _Tricophyton_, _Oidium_, and _Leptothrix_ of human
affections of the skin and mucous membranes) are incidental or
accidental only[19]--acting, as R. Owen observes, {141} most commonly
as natural scavengers in the consumption of effete organic material;
but that they may become noxious under two sorts of
circumstances--viz. when their numbers are enormously increased, as is
known to be the case with trichinae in the human body, and also when
they are brought in considerable number into contact with bodies
already diseased, or at least suffering under depression of vital
energy.
[Footnote 19: This possibility has not been as yet altogether ruled
out in regard to Koch's _Bacillus tuberculosis_; concerning which
active discussion has been going on during the past year or two
(1882-83). A very large number of observers confirm the statement that
the bacilli are found in most specimens of tubercle. Several, also,
have repeated with success Koch's inoculation experiments, in which
tubercle appeared to be propagated by carefully isolated bacilli. But
many facts still stand in the way of the conclusion that the bacillus
is the causa sine qua non of tuberculosis. First, examples of the
production of phthisis by apparent contagion or infection are few.
Although Dr. C. T. Williams found bacilli in the air of the wards of
the Hospital for Consumptives at Brompton, yet of the experience of
that hospital Dr. Vincent Edwards, for seventeen years its resident
medical officer, reports as follows: "Of fifty-nine resident medical
assistants who lived in the hospital an average of six months each,
only two are dead, and these not from phthisis. Three of the living
are said to have phthisis. The chaplain and the matron had each lived
there for over sixteen years. Very many nurses had been in residence
for periods varying from months to several years. The head-nurses,"
says the writer, "sleep each in a room containing fifty patients. Two
head-nurses only are known to have died--one from apoplexy; the other
head-nurse was here seven months, was unhappily married, and some time
afterward died of phthisis. Of the nurses now in residence, one has
been here twenty-four years, two twelve years, one eight years, one
seven years, one six and a half years, and one five years. No
under-nurse, as far as I am aware, has died of phthisis. All the
physicians who have attended the in-and-out patients during the past
seventeen years are living, except two, who did not die from
phthisis."
Against the inoculation and inhalation experiments of Villemin,
Tappeiner, Koch, Wilson Fox, and others, by which the specific
character of tubercle has been said to be proved, must be placed those
of Sanderson, Foulis, Papillon, Lebert, Waldenburg, Schottelius, Wood
and Formad, Robinson, and others, by which tubercles have been induced
by the injection, inoculation, or inhalation of various non-tubercular
materials. In answer to the argument from these, it is asserted by
Koch and his supporters that "there is no anatomical or morphological
characteristic of tubercle," its only sufficient test being its
inoculability. This is almost begging the question; at all events, it
leaves it, for the present, unsettled. Moreover, tubercular deposits
do not always contain bacilli, as has been shown by Spina, Sternberg,
Formad, Prudden (_N.Y. Medical Record_, April 14 and June 16, 1883).
The last named made, in one well marked case, six hundred and
ninety-five sections from ninety-nine tubercles in different portions
of a tuberculous pleura, all of Koch's precautions being observed in
the examination. Belfield (_Lectures on Micro-Organisms and Disease_)
admits the possibility that tuberculosis may be produced by either of
several causes. It has, at least, not yet been demonstrated that the
tubercular tissue is more than a nidus or favorable "culture-ground"
for the bacilli, or that, in the presence of a constitutional
predisposition, they may not merely promote a more rapid destruction
of the invaded organs or tissues.]
4. That such organisms are the essential and direct causes of enthetic
maladies by invading the human and other living bodies as parasites,
consuming and disorganizing their tissues, blood corpuscles,[20] etc.
Pasteur considers the abstraction of oxygen an important part of their
action.
[Footnote 20: Against this view stands especially the objection that,
as Cohn, Burdon Sanderson, and others have fully shown, bacteria and
other Schizomycetae obtain their nitrogen, not from organized tissues,
but from ammonia, and their carbon and hydrogen from the results of
decomposition in organic tissues. (See B. Sanderson, in _Brit. Med.
Journal_, Jan. 16, 1875.) Pasteur has regarded the relation of these
organisms to oxygen as important; some of them requiring it for their
existence (aerobic), and others not (anaerobic). He has defined
fermentation as "life without free oxygen."]
5. That these microbes, microphytes, or mycrozymes act not as
parasites, but as poison-producers, secreting a sort of ferment which
is the specific morbid material (Virchow); or, when multiplying in
excess of their food-material, they may die, and their dead bodies,
like other decaying organic matter, may become poisonous. This
possibility, although not distinctly suggested (so far as I know)
hitherto, appears to me to be not unworthy of consideration. That the
numbers of micro-organisms present have some important relation to
morbid conditions has long since been inferred from familiar facts.
6. That they are not generators, but carriers, of disease-producing
poisons; their vitality giving to the latter a continuance of
existence and capacity of accumulation and transportation not
otherwise possible.
Briefly, the following is a summary of the most generally accepted
classification of those microscopic organisms[21] whose role in the
causation of diseases is now under discussion; chiefly following Cohn
and Klebs:
_Orders_: Hyphomycetae, Algae, Schizomycetae.
Hyphomycetae, _genera_: Achorion, Tricophyton, Oidium.
Algae, _genera_: Sarcina, Leptothrix.
Schizomycetae, or Bacteria, _genera_: Micrococcus, Rod-bacterium,
Bacillus, Spirillum.[22]
[Footnote 21: For further details concerning these the reader is
referred to the works of Magnin, Belfield, and Gradle on _The
Bacteria_, and on the _Germ Theory of Disease_.]
[Footnote 22: Cohn also separates vibrio and spirochaete as genera
distinct from spirillum. They may, however, be regarded rather as
species of that genus. Some recent authors included bacterium and
bacillus under one genus, bacillus; against which simplification there
seems to be no valid objection.]
Micrococci (Sphaerobacteria of Cohn) are asserted (under certain
conditions) by Letzerich, Wood, and Formad[23] to be causative of
diphtheria; Ogston has found them in ordinary pus; Rindfleisch,
Recklinghausen, Waldeyer, Birch-Hirschfeld, and others report them to
be always present in the abscesses of pyaemia; Buhl, Waldeyer, and
Wagner state their occurrence in intestinal mycosis; Eberth, Koster,
Maier, Burkhardt, and Osler, in ulcerative endocarditis; Orth,
Lukomsky, Fehleisen, and Loeffler, in erysipelas; Coats and Stephen in
pyelo-nephritis; Friedlander, in pneumonia; Eklund (_Plax scindens_)
in scarlet fever; Keating[24] and {142} Le Bel, in measles; Leyden and
Gaudier, in cerebro-spinal meningitis; Carmona del Valle, in yellow
fever; Prior, in dysentery; Gaffky, Leistikow, Bokai, and Bockhardt,
in gonorrhoea;[25] besides other similar observations by numerous
writers.
[Footnote 23: _Bulletin of National Board of Health_, Supplement No.
17, Jan. 21, 1882.]
[Footnote 24: _The Medical News_, Philadelphia, July 29, 1882.]
[Footnote 25: Sternberg's careful experimentation seems to show the
identity of Neisser's gonococcus with the Micrococcus ureae, commonly
found in decomposing urine.]
Bacterium termo is regarded by leading authorities as the special
ferment or causative agent of putrefaction[26] (Billroth, Cohn).
[Footnote 26: Others have referred putrefaction to vibriones, less
precisely described.]
Bacillus includes, hypothetically at least, several species; as
Bacillus subtilis, the innocent hay-fungus; Bacillus anthracis, the
microbe of malignant pustule (anthrax, milzbrand, charbon) and the
splenic fever of sheep; Bacillus typhosus (Klebs, Eberth, Meyer) of
typhoid fever; Bacillus leprae (Hansen, Neisser, Cornil, Koebner) of
leprosy;[27] Bacillus malariae, reported as having been
demonstrated[28] by Klebs and Tommasi Crudeli, Marchand, Ceri, and
Ziehl; Bacillus tuberculosis (Koch, Baumgarten, 1882); the bacillus of
malignant oedema (Gaffky, Brieger, Ehrlich); that of syphilis
(Aufrecht, Birch-Hirschfeld,[29] Morrison); of glanders (Loeffler,
Schuetz, Israel, Bouchard); of pertussis (Burger); besides the
Actinomycosis of Israel, Ponfick,[30] Bollinger, and others. Koch has
very recently (1883) been reported to have discovered in Egypt the
bacillus of cholera.
[Footnote 27: Dr. H. D. Schmidt of New Orleans, an experienced
pathologist, reported (_Chicago Medical Journal and Examiner_, April,
1882) that critical examination of numerous specimens of tissues from
three cases of leprosy under his care failed to verify the existence
of bacilli as characteristic of that disease.]
[Footnote 28: Not certainly, however, as shown by Sternberg (_Bulletin
of Nat. Board of Health_, Supplement No. 14, July 23, 1881). Dr.
Salisbury of Ohio in 1866 made a series of observations, on the basis
of which he asserted the discovery of a genus of malarial microphytes,
which he referred to the family of _Palmellae_.
The oval and spherical organisms described by Richard and Laveran as
found in the blood of malarial patients resembled micrococci rather
than bacilli.]
[Footnote 29: More recently described by him as micrococci.]
[Footnote 30: _Die Actinomykose_, 1881.]
[Illustration: FIG. 1. Micrococci: _a_, zoogloea form; _b_,
micrococcus from urine, in rosary chain; _c_, rosary chain from
spoiled solution of sugar of milk (Cohn).]
[Illustration: FIG. 2. Bacteria: _a_, zoogloea of _Bacterium termo_;
_b_, pellicle of bacteria from surface of beer; _c_, _Bacterium
lineola_, free; _d_, zoogloea form of _B. lineola_.]
[Illustration: FIG. 3. _Bacillus malariae_ of Klebs and Tommasi
Crudeli.]
[Illustration: FIG. 4. Bacteria from gelatin solution, inoculated from
swamp-mud, X 1500 (Sternberg).]
[Illustration: FIG. 5. Vibrios in gelatin culture-fluid, X 1000
(Sternberg).]
[Illustration: FIG. 6. Protococcus from slides exposed over swamp-mud,
X 400 (Sternberg).]
[Illustration: FIG. 7. Bacilli from swamp-mud, X 1000 (Sternberg).]
[Illustration: FIG. 8. Bacilli from septicaemic rabbit, X 1000
(Sternberg).]
[Illustration: FIG. 9. Bacilli from human saliva, X 1000 (Sternberg).]
[Illustration: FIG. 10. _Bacillus anthracis_ (Sternberg).]
[Illustration: FIG. 11. _Bacillus tuberculosis_, within and outside of
pus-corpuscles (Sternberg).]
Spirillum (Spirochaeta of Ehrenberg) has its best ascertained example
in the minute forms first observed by Obermeier, and afterward by many
other observers, in the blood of patients suffering with relapsing
fever. They have been found present in the blood only during the
febrile paroxysm, disappearing in the intermission and through
convalescence.
Hastening to close our consideration of this subject, we may note,
without much argument, a few of the points of difficulty needing yet
to be more fully illuminated by {143} careful observation before any
form of the germ theory can take its place as an established doctrine
in etiology:
1. The absence of the characters belonging to definite organisms[31]
in the easily-studied virus of small-pox and vaccinia stands, a
priori, against the probability of such organisms being essential to
the causation of other enthetic diseases.
[Footnote 31: The particulate character of variolous and vaccine virus
has been already alluded to, as asserted to have been shown by
Chauveau and others. Yet it is not absolutely demonstrated that
filtration may not produce an important chemical alteration in some
kinds of highly unstable organic material subjected to it. Cohn
figures a Micrococcus vacciniae in his article on Bacteria
(_Microscopical Journal_, vol. xiii., N. S., pl. v., Fig. 2). Beale
denies (_Microscope in Medicine_, 4th ed.) the existence of any
organisms in vaccine virus. Lugginbuhl, Weigert, Klebs, Pohl-Pincus,
and others have asserted their existence, but, especially in the
absence of any successful culture experiments, it does not seem to be
proved.]
2. Analogy in nature, showing the commonly beneficial action of
nutritive processes in re-appropriating the products of organic decay
on a large or on a small scale, makes the scavenger theory of the
general function of minute cryptogamic organisms more probable, per
se, than that which holds many of them to be destructive parasites or
poison-producers in the bodies which they may inhabit. Few well known
parasites are capable of causing death in higher animals or in man.
3. These microbes are among the minutest objects which can be studied
under the microscope. Bacteria average about 1/9000 of an inch in
their longest diameter; micrococci and spores (Dauersporen, Billroth)
are yet smaller. Much care, therefore, as well as skill, must be
exercised in making observations upon them.[32] Huxley asserted a few
{144} years ago that a distinguished English pathologist had mistaken
for movements of minute living organisms the "Brownian movements" seen
in the particles of many not living substances under a high magnifying
power. One observer, at least,[33] considers that the forms designated
as bacteria and micrococci, etc. are either forms of coagulated fibrin
or granules from morbidly-altered blood-corpuscles (zoogloea of
Billroth, Wood, Formad, and others). Koch denies the validity of the
observation of organisms in tubercle by Klebs and Schuller, while
insisting upon his own demonstration of a bacillus tuberculosis.
Authorities must, by mutual confirmation or correction, remove these
obscurities.
[Footnote 32: A very interesting discovery was made by Tyndall, to the
effect that while one boiling of a liquid would sterilize it for the
time by destroying all the bacteria present, their spores might still
retain vitality and be afterward developed. By repeated exposure to a
boiling temperature, taking these spores in their developing stage,
they were destroyed, and complete sterilization was effected.]
[Footnote 33: R. Gregg, _N.Y. Med. Record_, Feb. 11, 1882. Sternberg,
however, has replied to him (_N.Y. Med. Record_, April 8, 1882, p.
368). The latter admits a doubt as to whether the granules seen within
the leucocytes by Wood and Formad in diphtheritic material, and
believed by them to be micrococci, are such, or are merely granules
formed or set free by disorganization of protoplasm within the
leucocytes. This uncertainty well illustrates the difficulty of these
investigations.
A chemical test much relied upon is, that bacteria resist the action
of acids and alkalies, which destroy granular material of animal
origin; also, that all these organisms are deeply stained by aniline
dyes and by haematoxylin. The most decisive test, however, is
cultivation in a liquid sterilized by heat. Koch prefers a process of
dry culture for the bacillus of tubercle.
Gradle (_Lectures on the Germ Theory of Disease_, Chicago, 1883, p.
28) says that the absolute criterion of the life of bacteria is their
power of multiplication.]
4. Bacteria and micrococci have been abundantly discovered (Kolaczck;
J. G. Richardson) in healthy bodies upon the various mucous membranes
and in the blood. The correctness of such observations has been
denied, but, so far at least as the mucous membranes are concerned, it
has been well established by Nothnagel, Sternberg, and others.
Bacteria have sometimes been found in countless numbers in fecal
discharges.
5. Bacteria become most numerous in materials of a septic or
infectious character after their period of toxic intensity has passed
by.
6. Suppuration can be produced (Uskoff, Orthmann) without the presence
of minute organisms of any kind. Bacteria have been found {145} under
Lister's antiseptic dressings without suppuration following. Paul Bert
destroyed all the microbes in a septic liquid, and yet found it to
retain its poisonous quality. Rosenberger (1881) has made similar
observations.
Panum, Coze, and Seltz, Bergmann and Schmiedeberg, Hiller, Vulpian,
Rosenberger, Clementi, Thin, and Dreyer have, by various elaborate
investigations, proved that fatal septic poisoning can be produced in
animals by the products of organic decomposition, without the presence
of living organisms. Zweifel's experiments seem to have shown that
normal blood, when deprived of oxygen, in the absence of
micro-organisms, may acquire septic properties.
As stated by Belfield,[34] many experiments by Schmidt, Edelberg,
Kohler, Nencki, and others, have shown that septicaemia may be induced
by the injection into the blood of free fibrin ferment and other
substances, in the absence of minute organisms. To such an affection
some authors now give the name sapraemia, to distinguish it from
bacterial infective disorders.
[Footnote 34: _Lectures on the Relation of Micro-organisms to
Disease_, 1883.]
Griffini ascertained that mixed saliva, filtered through porous
plates, and thus containing no microbes, will still produce
septicaemia in animals, when subcutaneously injected. Colin (1876) has
denied the conclusiveness of the experiments of Chauveau, which have
been held to prove the particulate nature of variolous and vaccine
virus. Moreover, it is well known that eggs with shells unbroken are
tainted when placed near others which are unsound.
7. While Klebs and Koch maintain the definite specificity of each
minute microphytic organism, Naegeli and Billroth assert their mutual
convertibility. Burdon Sanderson avers[35] that "the influence of
environment on organisms such as bacteria is so great that it seems as
if it were paramount." Buchner, Grawitz, Greenfield, Pasteur, Wernich,
Thorne, Willems, Law, Wood, and Formad report experiments making it
appear that modification by culture is possible with bacilli and
micrococci, converting an innocent into a malignant parasitic
organism, or a death-producing microbe into one capable only of
causing {146} a transitory and not dangerous local affection; which
nevertheless secures to the animal thus treated immunity when
subsequently exposed to the deadly infection. Most interesting have
been the successes with such culture-inoculations obtained by Buchner,
Greenfield, and Pasteur with anthrax in sheep; by Pasteur also in
chicken cholera; and by Willems and Law[36] with the lung-plague of
cattle.
[Footnote 35: _Brit. Med. Journal_, Jan. 16, 1875.]
[Footnote 36: _N.Y. Med. Record_, June 18, 1881, p. 679. Exposure to
the air for a considerable period seems to be the agency chiefly
relied upon for what may be called the dynamic modification of these
microphytes. When cultivated in the depth of a liquid, so that air is
excluded, they are supposed to acquire a habit of obtaining oxygen by
decomposing organic substances, and thus act destructively upon the
cell-elements of living bodies. Analogous differences have long since
been observed in the study of fermentation between surface and
sedimentary yeast.]
In none of these cases is there reported any morphological change
whatever in the bacillus (Grawitz) or micrococcus (Wood and Formad);
the change in the effects noted, and, in the case of the micrococci of
malignant diphtheria, the acquired capacity of reproduction through
several generations, are all.
8. The immunity against subsequent attacks on exposure (similar to the
protection given by vaccination) continues to be without full
explanation upon any theory. But it is especially difficult to
reconcile it with the hypothesis of the infection being caused by, and
dependent upon, the presence of peculiar microphytes. Why should not
these, whether as parasites or as poisons, always produce the same
effects?
9. The view entertained by Thorne, Wood, and Formad, that a common
benignant affection, such as ordinary sore throat, may be converted
into a violent infectious disease--_e.g._ malignant diphtheria--by
modification of innocent micrococci into those with lethal characters,
through local or bodily conditions, is sufficiently contravened by the
great frequency of such conditions compared with the decided relative
rarity of such malignant epidemics or endemics.
10. Throughout all the investigations which have been, and are likely
to be, conducted, there remains the extreme difficulty, if not
impossibility, of total separation between the microbes themselves and
the matter of the vehicle in which they exist--the membrane, urine,
blood, virus, artificial culture-material, or whatever it may be. All
the effects ascribable to the disease germs may be, with no more
difficulty, attributed to the toxic action {147} of a portion, however
minute, of the soil in which they have lived, whose modifications must
be concomitant with those which they undergo. It appears necessary,
therefore, at the present time, to regard this whole question as still
undecided, with a predominance of probability, however, in favor of
the view that these minute organisms, or some of them, have a direct
and important relation of some kind to the causation of specific
endemic, epidemic, and contagious diseases. Altogether, the strongest
arguments are on the side of the view that the micrococci, bacilli,
etc. cause diseases, not as parasites, living upon their victims, but
as poison-producers infecting them.[37] The germ theory continues to
be in the position of a probable hypothesis, not in that of an
established doctrine of etiological science.
[Footnote 37: This comports much the best with the general natural
history of parasites on the one hand, and of venoms, ptomaines, etc.
on the other. Gautier, Ogston, and others have expressed the opinion
that microphytes may produce ptomaines.]
Practically, the result is nearly the same as if it were altogether
settled, since it is admitted on all sides that the presence of
microphytes (bacteria, micrococci, spirilla) coincides with those
conditions under which originate several of the most malignant
diseases. Measures which prevent the appearance or promote the
destruction of these minute organisms are at least often, and to a
great degree, preventive, if not curative, of such disorders; and the
glory of Jenner's discovery, by which the ravages of small-pox have
been made (potentially at least) controllable, seems not unlikely to
be paralleled by the achievements of Pasteur and others in a similar
preventive mastery over other maladies of men and animals. There is,
therefore, no branch of inquiry in connection with medical science
more worthy of being assiduously encouraged and extended. The present
may almost be said to be, in the history of medicine, an era of
myco-pathology.
For an exhaustive study of Etiology attention would now have to be
given to the modifying influences affecting the occurrence and
character of diseases in connection with age, sex, and temperament.
But, as neither of these is ever, per se, causative of any malady, and
they merely determine some modification of the action of morbid causes
when these occur, want of space must be our justification for leaving
them to be considered, in this work, in connection with the special
causation of the different {148} diseases which will be hereafter
described. A larger treatment of our present subject belongs rather to
hygiene than to practical medicine.
MEDICAL DIAGNOSIS.
For the purposes of the medical practitioner all professional studies
unite to the end of furnishing preparation for the diagnosis and
treatment of diseases. At the bedside the cardinal questions are, How
does the present condition of our patient differ from health? and,
What ought we to do to bring about his recovery?
Diagnosis involves three main directions of inquiry: 1, as to the
general bodily state of the patient; 2, morbid changes in particular
organs, tissues, or functions; 3, as to what name properly designates
the disorder, according to accepted nomenclature.
Pathology can never be out of view in connection with either the
theoretical or the practical study of diagnosis. But it is most
closely regarded when the last of these questions is before us, since
the names of diseases generally have a more or less distinct reference
to their pathological nature. Yet clinical observation always suggests
the early use of provisional terms for recognized groupings of morbid
phenomena; and sometimes these clinical designations remain for a long
time in use because of the imperfection of pathology.
We ascertain, in practice, the nature of a given case, first, by
considering its symptoms. These are those obvious evidences of
deviation from health which the patient himself is aware of, or which
the physician readily discerns or elicits by simple inquiry or
examination.
Secondly, taking the clue furnished by symptoms, a closer inspection
is made, with the intent of finding what is the actual state of
important organs, as the heart, lungs, liver, spleen, kidneys, and
alimentary canal.
Lastly, when these means fail to remove all obscurity, or when special
scientific investigation is practicable, instruments of precision are
employed, as the thermometer, sphygmograph, ophthalmoscope,
aesthesiometer, or aspirator; or by the microscope and chemical
analyses still more minute examination is made into the particulars of
the morbid processes present and their results.
We may subdivide diagnosis, then, into: 1, symptomatology; 2,
organoscopy or physical diagnosis; 3, instrumental diagnosis.
Symptomatology.
Semeiology (from [Greek: semeion], a sign) is a term much in use, with
essentially the same meaning as symptomatology, but less conveniently
distinctive, since it does not so well indicate the contrast between
obvious signs, or symptoms, and those more recondite, obtained by the
methods of physical diagnosis.
Signs of disease cannot be recognized as such except by one who is
{149} familiar with the appearances, actions, and manifestations which
belong to health. Nor can they be understood, so as to infer what they
mean, without knowledge of normal physiology on the one hand, and, on
the other, of the natural history of diseases. Physiology constitutes
the etymological grammar, symptomatology the vocabulary, and diagnosis
the syntax of practical medicine. Just as grammatical knowledge will
not enable any one to read or speak a language without acquaintance
with its words, so clinical observation is necessary to the physician
over and above all the knowledge he may have of physiology and
pathology. He must learn to know diseases by sight, or at least by
personal contact and observation.
Every one has, of course, a general familiarity with the state and
actions of his own and other bodies in health, yet a more exact
knowledge of the movements of respiration, circulation, secretion,
etc., as well as the form, size, and relative location of all the
organs of the body, is needed. Physiology and medical anatomy furnish
such information. The more thorough this knowledge is appropriated,
the better fitted the student is for practical diagnosis. For its
application, however, cultivation of all the perceptive powers is very
important. Some men have a genius for quick and clear discernment of
symptoms and for their interpretation, as well as for that of physical
signs. But all can much improve their senses, and their sagacity in
using them, by experience. For this, if for no other reason,
scientific training, in field or laboratory studies, affords the best
introduction to the work of the medical student and physician. The
traits most needed for success in diagnosis are exactness and
comprehensiveness. First, to be sure precisely what each sign is that
comes under observation; next, to overlook no existing symptoms or
physical signs; and, last, so to combine them into a mental map,
diagram, or picture, as to make a coherent and rational whole. This
nosogram may then be compared with the descriptions of standard
authorities, to find its place (if it has one) in technical
classification. First, however, ascertain the thing, the morbid state
or combination of states; afterward the name, or morbid species, when
practicable. It is always to be remembered that complication of
diseases, or at least the existence of some irregular manifestations
along with those which are characteristic, is more common than the
occurrence of purely typical cases. The portraits of most diseases in
the books are averages, like the composite class-photographs of
Douglas Galton. Not nearly every case will correspond with such an
average in all respects. Moreover, so great is the possible variety of
alterations among the different organs of the body that the chances of
two instances of disease being precisely alike in every particular are
hardly greater than those in favor of every move being the same in two
games of chess with the same opening.
In an essay like the present it is not easy to decide upon the best
manner of treating the subject before us. Too much or too little may
be said. With advanced readers the whole history of symptoms and
physical signs might be left to the special discussions occurring in
articles upon different diseases. But it may be taken for granted that
those who consult the present work will do so either at a
comparatively early stage of their studies or when time has made
desirable a renewal of what may have been once known and then
forgotten. Since, then, it is impossible {150} to anticipate what may
be the exact needs of either class, a somewhat elementary statement of
main facts appears justifiable here.
Following the natural method, we may suppose a call to visit a
patient. Arriving in his presence, the first question (mostly left out
of view and rarely expressed) may be, Is it a case of real or only
imaginary indisposition? Army medical officers, more than most others,
can appreciate the possibility of this inquiry sometimes disposing of
the whole case.
Supposing it to be real, is it an illness or an accident or other
injury? Is it severe or of trifling account? Acute or chronic? We
observe the position of the patient, lying quietly in bed, sitting up,
or walking restlessly about the room. Then the countenance is
observed--pale or flushed, tranquil or excited in expression. We feel
the forehead, touch the cheek and hand. Is the skin hot or cold, dry
or moist? The pulse is felt; the breathing also is counted.
Of the patient himself or of another (in serious acute cases better of
his care-taker, in another apartment) we ask questions whose answers
give us the general history of the case. When not before known these
should include his antecedent personal history, even extending to that
of the family, as far as can be learned. What tendencies have they, or
has he or she, shown by previous attacks and their results?
So we come to the present attack: When did it begin, and how? What
have been its prominent symptoms since? Questions are then to be put
concerning the heat of the body, appetite, complaint of pain, sleep,
movement of the bowels, discharge of urine: in the female,
menstruation; if married, pregnancy or parturition, how often and when
occurring last. Thus the practitioner is enabled to get a clue to the
diagnosis, to be followed out through his own observation and closer
examination. If the patient be a child and the attack be acute and
febrile, an early question must be as to its having passed or not
through the different diseases of childhood--viz. the exanthemata,
mumps, and whooping cough, and also what exposure to any of these it
may have been recently subjected to.
Going farther into particulars, let us review some of the possible
developments obtained in the above questioning of symptoms.
When lying in bed the decubitus may be significant, as, upon the back
with the knees drawn up in peritonitis; with the hands pressing the
abdomen in colic; tossing to and fro in the delirium of fever or of
early cerebral inflammation; on one side constantly in acute
inflammation of the liver or in pleurisy. Or the patient may be
obliged to be propped in a sitting posture (orthopnoea) from
heart-disease, asthma, or ascites, or leaning forward upon the back of
a chair or a pillow with aneurism of the aorta. More remarkable still
may be the subsultus tendinum of low fever, the opisthotonos of
tetanus, the respiratory spasms of hydrophobia, or the clonic
movements of epileptic, hysterical, or occasional convulsions.
In the face we see pallor in syncope and in anaemia in any of its
varieties and with varied associations; a general redness in some
cases of apoplexy and in remittent fever; flushing of the forehead and
eyes especially in yellow fever; dusky redness in typhus, and a more
purple hue in typhoid fever; yellowness in jaundice, in some cases of
remittent and in most of yellow fever; sallowness in cancer; a bright
central glow upon each cheek in early pneumonia or the hectic of
phthisis; a blue or ashen appearance in the collapse of cholera, and
blackish-blue in {151} cyanosis or carbonic acid poisoning; bronzed in
Addison's disease; puffy about the eyelids in Bright's disease; the
surface swollen, yet resistant to the touch, in myxoedema. The eyes
(one or both) glare prominently in exophthalmic goitre; squint in
advanced cerebro-meningitis; roll to and fro often in the prostration
of cholera infantum and in convulsions; are clear and bright in
phthisis; yellowish in hepatic disorder; dull and clouded in low
fevers; without expression in imbecility and general paralysis.
Contraction of the pupil is observed in inflammation of the retina or
of the brain, narcotism from opium (until near death) or eserine, or
apoplectic effusion near the pons varolii. Dilatation of the pupil is
seen in most cases of hydrocephalus and of apoplexy; in
nerve-blindness (amaurosis), glaucoma, cataract, and narcotism from
atropia, duboisia, or hydrocyanic acid. Inactivity of the pupil
(Argyll Robertson) under changes of light and darkness is common in
locomotor ataxia. Different states of the two pupils under the same
light show disorder, either ophthalmic or cerebral in site, or may
indicate pressure on the cervical sympathetic ganglia, as from aortic
aneurism.
In elderly persons we ought always to look for the arcus senilis,
which is a sign of a tendency to fatty degeneration. It is a ring, or
part of a ring, with ill-defined edges, best seen by lifting or
depressing an eyelid, at the junction of the cornea and sclerotic coat
of the eye. In some quite healthy old persons there may be seen at the
same junction a clearly-defined circular line of calcareous nature.
This must be distinguished from the true fatty arcus senilis.
Of the face we may also notice the pinched nose, hollow eyes, and
falling jaw of the facies Hippocratica, presaging death; the square
forehead of the rickety child (not common in this country); ulcers on
the forehead, scars at the mouth-corners, or copper-colored eruptions
in syphilis; the full, flabby lips of scrofula. In peritonitis or
gastritis the mouth is apt to be drawn up with a peculiar expression
of suffering and nausea. Very striking is the characteristic one-sided
appearance in facial palsy, from lesion of the seventh nerve. There
may be a smile, a frown, or other expression on the sound side of the
face, while the paralyzed side is quite immovable. As the seventh
nerve (portio dura) supplies the orbicularis muscles, its paralysis
(so often temporary) may cause inability to close the eye upon the
affected side. Ptosis, or inability to open the eye, involving the
levator palpebrae, which is innervated by the third nerve (motor
oculi) is more significant of cerebral lesion.
Even the ears may have language, as when their lobes are full and
glistening red in the gouty diathesis, or wrinkled in prolonged
cachexiae, or when they are running with discharges in the struma
(scrofula) of childhood. The hair becomes dry and lustreless in
phthisis, and falls out during convalescence from many acute diseases.
If we look at the gums in a case of lead-poisoning, we may expect to
find a blue line along their edges. Scurvy is betokened by a swollen,
spongy, and easily-bleeding state of the gums. Many scorbutic cases,
however, lack this so-called pathognomonic feature. It may be
remarked, by the way, that absolutely pathognomonic signs of
particular diseases, never absent and exclusively seen in them, are
very few. Albuminuria, for example, is not always present in Bright's
disease, and is {152} also met with in a number of other affections.
Sugar in the urine may follow inhalation of chloroform or an attack of
cholera, as well as diabetes mellitus. Rice-water discharges may be
absent in the collapse of cholera, and patients may die with yellow
fever without black vomit. Still, these symptoms have great diagnostic
value, and, taken with others associated with them, may often enable
us to attain to a diagnosis of much importance.
Perfect teeth in an adult in this country are rather the exception
than the rule. In the notched incisors of inherited syphilis, however,
there is something quite distinctive. The notches in Hutchinson's
teeth are vertical, not horizontal.
Old as medicine is the examination of the tongue in disease. It may be
protruded with difficulty, as in low fevers, in apoplexy, and in
cerebral paralysis (bulbar sclerosis, glosso-labio-pharyngeal
paralysis) or thrust to one (the paralyzed) side in hemiplegia. It is
pallid in anaemia; yellow in bilious disorder; red in glossitis (then
swollen also), in scarlet fever, and in gastritis; furred in
indigestion, gastro-hepatic catarrh, and the early stage of various
febrile attacks; dry, brown, cracked, or fissured in typhus or typhoid
fevers and in the typhoid state of malarial remittent fever; bare of
epithelium in advancing phthisis and in imperfect convalescence from
severe acute diseases. Coldness of the tongue is one of the worst
signs in the collapse of cholera.
As we examine the throat internally we look for signs of faucial
inflammation in redness and swelling, with or without enlargement of
the tonsils, or relaxation and elongation of the uvula, or ulceration,
or the gray or brown membranous deposit of diphtheria. In the mouth of
a child we may find the little white vesicular patches called aphthae,
the curd-like exudations of thrush, or possibly the much worse grayish
ulcerations of cancrum oris, or the rarer ashen sloughs of gangrene of
the mouth.
Outside of the throat we must remember the significance of glandular
swellings or scars of suppurated glands in children; nor overlook, if
present, stiffness of the muscles, or torticollis, or goitrous
enlargement of the thyroid gland. Observation should be made also of
the site of the carotid artery on each side, and of the jugular veins,
since aortic regurgitation may be indicated by violent action of those
arteries or tricuspid regurgitation by pulsation of the veins in the
neck.
Long before vaso-motor physiology had any place in science the pulse
was known to afford valuable indications in disease. Either of the
accessible arteries will answer instead of the radial; its convenience
merely makes the wrist the common place of comparison. By careful
examination of the pulse something may be learned of several of the
factors concerned in its production. These factors are--1, the
muscular force of the walls of the heart; 2, the state of the cardiac
valves; 3, the muscularity of the arteries; 4, the elasticity of the
arterial coats; 5, the state of the capillary circulation; 6, the
qualities of the blood; 7, the condition of the nervous system as to
excitability or apathy.
A feeble heart must induce a feeble pulse. Moderate debility may be
attended by slowness of the pulse, but usually a weak circulation is
marked by frequent, small beats, like the vibrations of a short
pendulum. A strong heart-beat (other things being equal) is relatively
slow, with a proportionate pause after the second sound.
{153} Valvular lesions produce various effects upon the pulse. Most
notable are the irregularity connected often with mitral insufficiency
and the jerking pulse (Corrigan) of aortic regurgitation.
Believing, as the present writer does, in the existence of a true
arterial systole following and supplementing the ventricular
contraction,[38] it must be urged that a vigorous muscularity in the
arteries promotes strength in the pulse--not by resistance, but by
auxiliary propulsion of the blood. Another condition altogether is
tonic, spasmodic contraction of the arteries. This is not often met
with pure and simple, but a measure of it is seen in the corded or
wiry pulse of acute enteritis or peritonitis.
[Footnote 38: This view, although advocated by Sir Charles Bell,
Legros and Onimus, Hermann of Zurich, and others, is opposed to the
most prevailing vaso-motor physiology. Several complications and some
contradictions in pathological discussion at the present time would be
cleared up by the abandonment of the now commonly-held stopcock theory
of arterial function, which has really nothing whatever to support it
except the misinterpretation of some experiments upon arteries made
many years since.]
Deficient elasticity of the arteries is not easily separated in
observation from muscular relaxation. When arteries undergo
degeneration (atheromatous, fatty, or calcareous), their middle coat
suffers the deterioration of both elastic and muscular tissues, these
being substituted by materials either more or less yielding, and
always less resilient, than the natural fabric of the vessels.
The influence of the condition of the capillary circulation upon that
of the arterial system and the heart is manifest in inflammations. By
reflex excitation the arteries are made to contract actively and impel
the blood more forcibly than in the normal state toward the centre of
impeded nutrition (stasis). This has been abundantly proved by the
comparison of the amount of blood flowing through the arteries of a
sound limb and those of its fellow, when the latter is the seat of a
violent acute inflammation.
Blood-states also affect the pulse by the differences in direct
stimulation to which the heart and arteries are subjected according to
the qualities and composition of the blood. It is probable that the
fever-pulse of typhus, typhoid, the exanthemata, septicaemia, and
pyaemia has its origin in morbid conditions of the blood, acting in a
twofold manner--directly upon the heart and arteries themselves, and
mediately through the vaso-motor ganglia.
Lastly, the nervous system stands in an important relation to the
action of the heart and arteries, and thus to the pulse. In a nervous,
excitable person, changes in the rate of the pulse may take place,
with slight significance, which in a different constitution might be
of serious import.
To understand the language of the pulse care must be taken in several
respects:
1. Both wrists should be felt. Sometimes there is an abnormal
variation in the course of the main radial trunk which may pass over
the thumb. Again, an aneurism may cause a great difference between the
two radial pulses, or, possibly, an embolus may occlude one of the
radial vessels, annulling its pulsation.
2. Other arteries also, especially the carotids, should be
examined--in all obscure cases at least. Visibly beating, distended,
and tortuous temporal arteries are occasionally met with. They are not
pathognomonic of any one malady, although often referred to the gouty
diathesis. They {154} may attend irregular malarial attacks, or may be
connected simply with a hyperaemic state of the brain.
3. The heart's impulse should always be compared with the arterial
pulsation. The former may be strong and regular, while the latter is
small, feeble, or intermittent. Something must then be wrong, either
in the aortic valves or in the arterial system.
5. On account of possible nervous agitation, the pulse should usually
be examined more than once, during each visit to the patient.
6. Sex, age, position of the body, and time of day must all be taken
account of. In men the average rate of the pulse is between 65 and 75
per minute; in women, between 70 and 80. The pulse-rate of early
infancy varies from 100 to 120, and is very easily hurried. That of
old persons is commonly between 60 and 70, until, at a very advanced
age, with debility, its frequency may be increased, especially upon
exertion. Lying down, we find the slowest pulse; sitting, somewhat
more rapid; and most so in the standing position. In health the time
of day makes no constant difference apart from the effects of food and
exercise. In disorders attended by fever there are important changes
to be regularly observed. Excepting the variable paroxysms of
remittent and intermittent, which are a law unto themselves, in
febrile affections the pulse may be expected to be slowest in the
morning and most excited in the early part of the night. A diminution
of this difference is a favorable sign. Sleep generally slows the
pulse decidedly. The ordinary statement is, that the pulse is always
slower during sleep, but I have several times found that in states of
exhaustion without fever it may be considerably more rapid while the
patient is asleep. Nothing is more sure to increase the strength and
rapidity of the pulse than high temperature.
7. Very important is the relation between the pulse and respiration.
Normally, four pulsations occur to each respiratory act. In pulmonary
affections, while the circulation is often disturbed pari passu with
the breathing, it may be quite otherwise. Great acceleration of the
rate of breathing, with little increase in the rapidity of the pulse,
should lead us to suspect disease involving the respiratory organs.
Conversely, a much hurried or otherwise perturbed pulse, with little
or no change in the breathing, points toward the heart as either
functionally or organically the seat of disorder.
Let us further consider, briefly, the kinds of pulse to be met with
and interpreted in practice.
A natural pulse is always, per se, a good sign. Yet in the history of
a disease usually so well marked as yellow fever some fatal cases have
been recorded (walking cases) in which the pulse, almost to the last,
was natural.
Strength of the pulse, to a certain degree, belongs to it normally.
But this is often exaggerated, and we may have the strong, hard, full,
perhaps bounding, pulse of an inflammatory affection (of the brain,
for example, or of the joints in acute rheumatism) in a person of
vigor. A bounding pulse often accompanies mere palpitation of the
heart, whose source may be the sympathetic influence of indigestion or
nervousness. A similar pulse is apt to be constantly present in
hypertrophy of the heart. In this case it is made more forcible as
well as more rapid by {155} active exertion; while palpitation,
without organic trouble, is usually diminished by moderately active
exercise.
A full pulse is not always strong, nor is a small pulse necessarily
weak. Mention has been made already of the tense, corded pulse met
with in acute peritonitis, and sometimes in enteritis. Gastric
inflammation, with nausea, may exhibit a depressed pulse, weak and but
little accelerated. Under still other circumstances we may find a full
pulse which is soft, easily compressible, even gaseous. Most
frequently a feeble pulse is rapid, and a very rapid pulse is weak.
Slowness, in marked degree, attends apoplexy, opium narcotism, and
fracture of the skull compressing the brain. Functional disturbance of
the heart may occasionally exceed in effect these causes of
retardation. I have met, under such circumstances, with a pulse of 20
in the minute; one of 18 has been recorded. A few apparently healthy
persons have habitually a pulse with but 40 or 50 beats in the minute.
Quickness in each beat may occur, while a long interval makes the rate
per minute slow. The jerking pulse of aortic regurgitation is the most
remarkable example of this. Galabin asserts that without imperfection
of the valves of the aorta a decidedly abrupt pulse may attend great
lowering of arterial tension. Something of the same kind may be
noticed in the temporarily excited pulse of very nervous subjects
under agitation.
Dicrotism, or reduplication of the pulse-beat, is not uncommon in
typhus and typhoid fever. Here relaxation of the heart as well as of
the blood-vessels appears to allow a momentary interruption in the
succession of the arterial upon the cardiac systole.[39]
[Footnote 39: An exceptional phenomenon, noticed by a few observers,
is the recurrent pulse; _i.e._ a pulsation felt below the finger,
whose pressure interrupts the flow of blood through an artery. It may
be explained by supposing unusual fulness of the vessels (local, if
not general) with, at the same time, relaxation of their walls;
bearing in mind, also, the manner of anastomosis of the radial and
ulnar branches which favors recurrence.]
Intermittence and irregularity of the pulse are not exactly the same
thing. Occasional intermittence may be merely a nervous symptom or a
muscular twitch of the heart, like the twitches now and then occurring
without significance in voluntary muscles. Persistent intermittence,
with feebleness of the pulsations (these being generally somewhat
rapid), is among the signs of dilatation of the heart.
It is possible for intermittence of the radial pulse to accompany
regularity in the heart-beat. This usually results from narrowing
(stenosis) of the aortic valvular outlet from the left ventricle. Only
a certain number of impulses fairly reach the more distant arteries.
This symptom may result also from fatty degeneration of the heart.
Absence of pulse in one radial vessel, while it is present in the
other, shows the presence of an obstacle to the circulation on one
side, which may be an aneurism, or an embolus plugging the artery.
Irregularity of the pulse, a total derangement of its rhythm, while
not often important in young children, is a serious symptom at other
times of life. In one disease most common in childhood, acute
hydrocephalus, the pulse in the first stage is apt to be hard and
rapid, in the middle stage slow and tolerably full, in the third
rapid, feeble, and often irregular. Mitral disease frequently presents
considerable irregularity of the pulse; and so does dilatation, even
without mitral lesion. Brain trouble, especially late in life, whether
structural or functional, may produce the {156} same symptom. B. W.
Richardson has pointed this out as one of the effects of the excessive
use of tobacco, even in young persons.
The pulse of continued, relapsing, and remittent fevers is, during the
febrile exacerbation, rapid (100 to 120); in the earlier part of the
attack full, but only moderately hard, or even soft and yielding. As
the attack passes its height and critical defervescence occurs, the
pulse grows slower, unless great prostration has supervened; in which
case it increases in rapidity, while it fails more and more in fulness
and resistance.
The pulse of the moribund state is nearly always small, very rapid
(130-150), and thready, without force or fulness. It may become
imperceptible before death. A pulse of 140 beats in the minute is
always alarming; if much beyond that rate the case is desperate. A
pulse of more than 150 beats in the minute is very difficult to count
accurately.
Exophthalmic goitre is attended characteristically by a full, somewhat
rapid, and bounding pulse, the cardiac impulse being also
proportionately violent and extended. Exercise much increases this
hyper-pulsation.
Pulsation of the jugular veins is ordinarily explained by tricuspid
regurgitation, a portion of the blood being sent back to the vena cava
with an impulse reaching to the jugulars. In some instances, however,
as the writer has repeatedly observed, jugular pulsation takes place
without any abnormality in the action or condition of the heart, from
a local inflammation (as tonsillitis) causing a marked exaggeration of
the muscular contractility resident in the larger veins.
Retardation of the flow of blood through the veins is manifest during
the collapse of epidemic cholera. On pressing the blood back in a vein
upon the hand, for example, and then lifting the finger, instead of
the movement being, as in health, too swift to be seen, it is so slow
as to be easily followed.
Capillary movement may be estimated in a similar manner. If it be very
sluggish, pressure upon the cheek, forehead, or hand will cause a
pallor which remains for some seconds, instead of disappearing at once
when the pressure is withdrawn. This is, it may be noticed, entirely
different from the pitting upon pressure, without much if any change
of color, in local oedema or general anasarcous effusion. The tache
meningitique of Trousseau is a pink or rose-red line left for a time
after drawing the finger across the forehead or abdomen in cases of
acute hydrocephalus (tubercular meningitis).
Respiration must be watched carefully in all cases of disease.
Normally, in the adult, while at rest, from 16 to 18 respiratory
movements occur in each minute. The number is somewhat greater in
women, and is considerably increased in children, at birth being about
40 in the minute. Men breathe most by the diaphragm; in women there is
a greater lifting of the ribs. In either sex a disorder attended by
pain in breathing may modify this proportion. If pleurisy, for
example, be present, the ribs will be but slightly lifted, abdominal
breathing taking predominance. When peritonitis makes every movement
of the abdomen painful, costal respiration is maintained almost alone.
Likewise, a unilateral pleurisy or pneumonia will check the
respiration on the affected side, with an increased movement on the
sound side. This difference is less manifest to the eye than to the
ear in auscultation. In all febrile {157} affections respiration is
hurried proportionately with the pulse, unless some complicating local
disorder disturbs the relation.
Dyspnoea may be produced by many different causes, whose possibility
must be remembered in its interpretation as a means of diagnosis. In
asthma violent efforts are made to compel the entrance of air into the
lungs by the intercostal muscles and diaphragm, aided by all the
accessory muscles of respiration, including the sterno-cleido-mastoid
and others of the neck. Expansion of the nostrils may occur in
sympathy with these efforts. Yet the amount of resistance may be shown
by a partial sinking-in of the lower ribs, as well as by the patient's
distress. These last signs are sometimes very marked in the collapse
of one or both lungs now and then occurring in whooping cough.
Croup induces a similar struggle for breath, although the obstruction
is differently located. Early in the croupal attack a hoarse sound may
accompany each inspiration and expiration. Later, when the danger to
life from apnoea becomes more imminent, a hissing or whistling sound
succeeds. This last-mentioned kind of sound results temporarily, also,
from the spasmodic obstruction to breathing in laryngismus stridulus.
Besides the affections of the lungs which impede respiration (as
pneumonia, hydrothorax, etc.), we may have dyspnoea induced by
extra-pulmonary causes, such as dilatation of the heart, aneurism of
the aorta, mediastinal cancer, pleuritic effusion; also by abdominal
dropsy, extreme elephantiasis, etc. Mention need hardly be made here
of respiratory obstruction from defective or injurious qualities of
the air, threatening or producing asphyxia.
Sighing respiration takes place in heart disease not infrequently. A
peculiar modification of the breathing movements has been associated
especially with fatty degeneration of the heart. From the
distinguished authors who first described it this is called the
Cheyne-Stokes respiration. Intervals of suspension of breathing occur,
after which short, shallow inspirations begin, and gradually increase
for a time in depth; then they grow shorter and shallower again, until
apnoea is reached. Such a cycle may occupy from half a minute to a
minute and a half, with from fifteen to thirty increasing and
decreasing respirations in all. It has been shown by several observers
that this type of respiration is not peculiar to fatty degeneration of
the heart. It has been met with in cases of cardiac dilatation, aortic
atheroma, cerebral hemorrhage, tubercular meningitis, and uraemia.
Sometimes a kind of dyspnoea common in advanced disease of the heart,
especially in mitral lesion with dilatation, has been confounded with
this. Here the breathing is constantly labored (orthopnoea); but the
patient from time to time dozes off into an imperfect sleep, in which
the breathing almost entirely ceases. Then he is awakened with a start
of distress, perhaps out of a painful dream. This succession of dozing
apnoea and waking dyspnoea belongs to a late stage of heart disease,
and usually ends in death.
Stertorous respiration is familiar in apoplectic coma, as well as in
that of brain compression from injury or from opium or alcoholic
narcotism. In uraemic coma true stertor is less apt to be observed;
sometimes the respiration in this condition has a hissing sound.
Along with the movements of respiration we may notice that the breath
{158} is hot and has a heavy odor in the early stages of all febrile
disorders. Disagreeable breath is common, however, in persons not ill,
from bad teeth or from indigestion. It is worst of all, putrid, in
gangrene of the lung. Certain cases of chronic or subacute bronchitis
(as well as of ozaena) also have very offensive breath. Coldness of
the breath is a very bad sign; it is observed sometimes before death
in the collapse of cholera.
Hiccough (singultus) is a spasmodic affection of the diaphragm. It is
innocent, though annoying, in most cases, resulting from indigestion
or from nervous disorder; in children, occasionally, from long crying.
When it takes place in cases of general prostration it betokens
threatening depression or exhaustion of vital energy.
The voice is mostly altered by serious disease. It may be feeble and
whispering, from debility; hoarse, from laryngeal inflammation and
tumefaction; thick, from cerebral oppression; lost (aphonia), in some
cases of chronic laryngitis and in paralysis of the vocal muscles. The
manner of articulating words is often changed in disorders of the
nervous system. A marked example of this is the monotonous scanning
speech of cerebro-spinal sclerosis.
Cough is an extremely variable symptom, always to be understood in
connection with the attendant circumstances. Usually, however, the
character of the cough itself is more or less distinctive. A dry, hard
cough may be merely sympathetic or nervous, or it may belong to the
first stage of acute bronchitis. A hacking cough, with little
expectoration, is not infrequently observed for a time in incipient
phthisis. Pneumonia has, if any, a short and rather sharp cough.
Progressing bronchitis is recognized by the deepening and greater or
less loosening of the cough. In advanced phthisis there are
distressing spells of deep, laborious coughing, especially in the
night or in the morning after sleep. Croup is known (whether sporadic
or in the form of laryngeal diphtheria) by the barking cough of the
early stage and its whistling character toward the fatal end. Nearly
the same sort of hissing or whistling sound in breathing has been
mentioned already as occurring in laryngismus stridulus. Paroxysms of
coughing, with or without whooping, are pathognomonic of pertussis.
Expectoration often affords important signs. Briefly, it may suffice
to say here that it is mucous, whitish, or colorless in early
bronchitis; more or less yellowish and muco-purulent in severe and
protracted bronchitis; rusty, from admingling of the coloring matter
of blood, in pneumonia, early and middle stages; bloody and
muco-purulent in early and of heavy roundish (nummular) masses in late
pulmonary phthisis; putrid, rotten, in gangrene of the lung.
Continuing our survey of obvious symptoms, we must now take account of
the conditions of the general surface of the body. Temperature is of
great consequence. Most precisely determinable by the thermometer, the
touch, when educated, will give very useful indications of its
changes. It is difficult, and not commonly desirable, to separate
variations of moisture from those of temperature. Reserving for
another place the special consideration of medical thermometry, it may
be here said that the skin is hot and dry in the typical condition of
fever, whatever its special associations. Heat and moisture of the
skin are more often met with together in the fever of acute articular
rheumatism than in any other {159} affection. As a rule, perspiration
lessens febrile heat. Copious (colliquative) sweating is habitual in
many wasting diseases, notable in pulmonary phthisis. It is then a
sign of great general relaxation of the system.
Coldness of the surface attends prostration, either from temporary
collapse or from positive exhaustion. The skin is perceptibly cold in
the algid stage of cholera. It may be so in very severe cases of
sporadic cholera morbus. In the chill of intermittent, while the
patient has the subjective sensation of coldness, his temperature is
seldom reduced, and is often higher than natural, although lower than
during the febrile exacerbation.
The color of the skin is pallid in anaemia, phthisis, dropsy, etc.,
and in syncope; ashen or livid in cholera collapse and in the cold
stage of pernicious malarial fever; yellow in jaundice, remittent, and
yellow fever; sallow in chlorosis, cancer, and chronic dyspepsia;
purple, almost black (especially the lips and ends of the fingers), in
asphyxia; dark, as if stained with ink, after long use of nitrate of
silver; bronzed in Addison's disease; bright red in scarlet fever,
etc. The eruptions of this and other exanthemata, and of the different
cutaneous diseases, will be best considered in the special articles
treating them of in this work.
Odor is perceptible and peculiar (though not easily described) in some
bad cases of typhus fever and of small-pox; less often in aggravated
chlorosis. Lunatics and paralytics (especially when assembled together
in institutions) often give off a noticeable smell. Most distinct,
however, is the cadaverous odor, sometimes perceptible for hours
before death. Corroborative of this, in summer, is the flocking of
flies around the bed of a dying patient. In a hospital ward this
selection amongst a number of patients may be quite observable.
Emphysema, from the presence of air in the connective tissue under the
skin, is rarely met with except as the consequence of an injury or of
local gangrene.
Oedema is local watery effusion, which may have various causes and
significance. Anasarca must have a general causation, either connected
with the state of the blood or with disorder of the heart, kidneys, or
liver, or of more than one of those organs at once. Pitting on
pressure is the sign of watery effusion. Soft crackling under the
touch distinguishes emphysema. A firm enlargement of the surface of
the face and upper part of the body occurs in myxoedema.
Swellings of all kind must be carefully observed, and their nature
inquired into--whether they be inflammatory or other chronic
enlargements of joints, tumors, fibrous, fatty, or cancerous,
aneurisms, hernial protrusions, or of any other character. In
protracted disease of the liver (cirrhosis) it is not uncommon to find
the superficial abdominal veins dilated and tortuous.
Abdominal enlargement may result from adipose accumulation (obesity),
distension of the bowels with wind (meteorism), ascites, ovarian
cysts, cancerous or other tumors, aneurism of the aorta, abscess,
retention of urine, or pregnancy. By the methods of physical
diagnosis, along with careful inquiry into the history of each case,
we are to make out the distinctions amongst these different
conditions.
Emaciation always marks either defect of nutrition or morbid excess of
tissue-waste. It is counterfeited in the sudden collapse of malignant
{160} cholera, and exaggerated in appearance during the analogous
condition of cholera infantum. On recovery from these states,
especially the latter, roundness and fulness of the face and limbs may
return much too soon for the actual restoration of fat and flesh. A
young child may be plump and chubby to-day, seemingly wasted with
acute illness to-morrow, and, if soon relieved, the next day almost as
rotund as ever.
Continued diarrhoea, phthisis pulmonalis, mesenteric disease, cancer,
and aneurism of the aorta are among the most frequent causes of great
emaciation. Sometimes, as in progressive pernicious anaemia, we are
struck with the comparatively slight degree of wasting of the body
while the disease is advancing toward death.
In myxoedema there is a swelling or general enlargement, especially of
the upper portions of the trunk. This is not anasarcous, but depends
upon a morbid change in the connective tissue throughout the body.
Articular enlargements may be (particularly in the knee in children)
scrofulous, or gouty (in the smaller joints), rheumatic, with
evidences of inflammation, acute or chronic; or, what is not well
named, rheumatoid arthritis. In this last affection there is a gradual
swelling and stiffening, with but little inflammation, of several,
sometimes all, the joints of the extremities. Locomotor ataxia is in
some cases attended by a degenerative alteration in one or more of the
larger joints.
The limbs may furnish to the eye many expressive signs of disease or
disability. In the listlessness of one arm and hand, while the other
can perform various movements, we see reason to suspect hemiplegia. If
the fingers are rigidly contracted, as well as powerless, we have this
diagnosis confirmed, whether the rigidity be early or late in its
stage. We must then look for a similar condition of the lower
extremity on the same side. Paraplegia and general paralysis have
their more extended (bilateral) indications in like manner.
Characteristic also are the wrist-drop, from paralysis of the
extensors of the hand, in lead-palsy; weakness or incapacity of the
flexors and extensors in writer's cramp; the hand fixed helplessly in
the position for writing in paralysis agitans (advanced stage); the
main en griffe, with shrunken muscles and drawn tendons, of
progressive muscular atrophy (wasting palsy). In the legs at first and
chiefly, but in time also in the arms, increase of bulk with loss of
power in the muscles shows the existence of pseudo-hypertrophic
muscular paralysis.
Gouty fingers have their joints not only swollen, but distorted by
deposits of urates and carbonates. Clubbed finger-ends, in the adult,
are seen mostly, with incurvation of the nails, in advancing
consumption. The nails are sometimes striated after attacks of gout,
the lines disappearing gradually during the interval. In many acute
diseases, transverse ridges are noticeable on the nails, marking the
date when their growth was arrested and subsequently resumed. These
are specially remarkable after attacks of relapsing fever.
A tendency to dropsical effusion is generally first shown, besides a
puffiness of the face, in the feet and ankles, the shoe or slipper
marking off the enlargement above its margin. Often this has no other
cause than debility, with a watery condition of the blood. Varicose
veins, with old and resultant ulcers, are also among the possible
things to be found in examination of the legs and feet.
{161} Movements of the hands are incessant and jerking in chorea;
perpetually trembling in delirium tremens, and often in one arm and
hand only, in paralysis agitans; with tremor, seen in voluntary
motions alone, in multiple cerebro-spinal sclerosis. More unusual is
the rhythmical closing and opening of the hand, successively, of
athetosis.
In the walk of patients able to be upon their feet there may be much
significance. A hemiplegic subject will circumduct the feeble limb
after the other; one suffering with paraplegia will shuffle the feet
slowly along the floor; the hysterical paralytic drags the lame limb
behind the other; the patient with spastic spinal paralysis rises on
his toes in walking, with his legs held close together; the shaking
paralytic rather trots forward, with the body bent; and the subject of
locomotor ataxia lifts his feet and kicks out forward or sideways,
then bringing down the heels with a stamp at each step. In progressive
muscular atrophy and advanced pseudo-hypertrophic muscular paralysis a
waddling or rolling gait is seen. Choreic patients are very irregular
in their walk, as in all other movements. Hip disease (coxalgia) shows
itself in a child by its lifting the pelvis and limb of the affected
side and bending the knee, so as to touch only the toes to the ground.
Club-foot and other deformities require no description in this place.
Sensibility of the extremities and of other parts of the surface of
the body needs to be examined into, with all its possible variations
(hyperaesthesia, anaesthesia, analgesiae, etc.), especially when the
nervous apparatus is for any reason supposed to be involved. Motions
of an unusual character must likewise be carefully noticed.
"Westphal's symptom" is regarded as having considerable diagnostic
value. It is otherwise called the tendon-reflex, with its
modifications. When a person in health is seated with one leg crossed
over the other or with the legs dangling over the edge of a high bench
or table, and a sudden blow is struck upon the tendon of the patella,
the leg and foot will be spontaneously jerked forward. In locomotor
ataxia, even from an early period, this tendon-reflex is abolished. In
spastic spinal paralysis (lateral spinal sclerosis) it is exaggerated.
Quite analogous to this is the ankle-clonus. This is obtained by
firmly flexing the foot and then tapping sharply upon the tendo
Achillis. The foot is then involuntarily extended and flexed several
times in succession. There is more doubt in regard to the associations
of this symptom than as to the knee movement, but it has been
clinically shown to be exaggerated in spastic spinal paralysis.
At our first acquaintance with a case of disease, while making inquiry
into its nature, the genital organs must not be forgotten. Not that we
need always make examination of them, but any pointing in symptoms
toward them must be borne in mind, so as to guide us in or toward
further procedures in diagnosis. In making, in obscure cases, a
diagnosis by exclusion, we are sometimes driven to a scrutiny of the
genital system.
We have now, however incompletely, touched upon the greater number of
obvious signs or symptoms which a view of a patient would furnish
without making minute inquiry of himself or others concerning his or
their knowledge of the illness. Such are the objective signs of
disease, which must be still more exactly and extensively discerned
and understood by means of the processes of physical and instrumental
diagnosis. {162} But the subjective symptoms also, and all those
observed and described by the patient and his or her friends, must
receive very careful attention. Much practical skill may be shown by
the kind of questions asked and the use made of the answers given.
First, as to the alimentary apparatus:
Taste is very commonly altered in disease, being sour in indigestion,
bitter in disorders of the liver, saltish in haemoptysis, rotten in
gangrene of the lungs.
Dryness of the mouth is the rule in fevers. Sometimes the saliva is
viscid and adherent. Increased flow or salivation was formerly
frequent in practice under large doses of mercurials. Jaborandi or its
alkaloid pilocarpin will generally produce it. Iodide of potassium
occasionally has the same effect in less degree.
Loss of appetite nearly always attends serious diseases of any kind.
Excessive craving for food (bulimia) is rare. Tapeworm accounts for it
in some instances. Desire for strange articles of food, as
slate-pencils, ashes, etc., is met with in some instances of chlorosis
and of hysteria. A return of natural appetite is one of the best signs
toward the close of any acute attack of illness.
Thirst is seldom absent in fever. It is also usually present in the
state of collapse, as from cholera, pernicious intermittent, or the
shock of severe (especially railroad) injuries.
Dysphagia or difficulty of swallowing may result from simple debility,
as in the moribund state; inflammation of the fauces, tonsils, or
pharynx; stricture of the oesophagus; obstruction by a foreign body or
by a cancerous or aneurismal tumor; retro-pharyngeal abscess;
paralysis of the muscles of the throat, such as sometimes follows
diphtheria. Soreness of the throat is present in some, but not in all
of these examples of dysphagia, being most marked in the inflammatory
condition of pharyngitis, tonsillitis, scarlet fever, and diphtheria.
Ulceration of the throat should always be carefully looked for, and if
present investigated to ascertain whether it is simple, diphtheritic,
or syphilitic. We must be careful not to mistake a mere local
accumulation of mucus, or aphthous vesicle, or the curd-like formation
of thrush or muguet, either for ulceration or pseudo-membranous
deposit. Aphthae and thrush are most frequently met with in children,
though small aphthous ulcers frequently appear toward the close of
wasting, and especially cancerous, affections. If there be a doubt,
pass a moistened hair pencil lightly over the apparent deposit, or
allow the patient to gargle the throat with water, and then re-inspect
it.
Many causes may produce nausea and vomiting, which almost always occur
together; that is, vomiting rarely takes place without previous
nausea, although the latter may exist without the former. In the
manner of vomiting there are some differences more or less
characteristic, as the distressing retching of sea-sickness and of
tartar emetic or other irritant poisoning, and the spasmodic
out-spurting of rice-water fluid in malignant cholera. The matter
vomited is often very important in diagnosis. In mere indigestion the
food taken is apt to come up, and the same may happen in flatulent
colic. When the liver is involved, as in bilious colic, bile also is
ejected. Nothing peculiar exists in the ejecta of morning sickness in
pregnancy. The ejecta contain mucus in gastritis, blood in ulcer and
in cancer of the stomach, stercoraceous {163} material in obstruction
of the bowels, black vomit in bad cases of yellow fever. Hysterical
vomiting sometimes closely imitates the latter in appearance. Other
affections attended by vomiting are cholera morbus, remittent fever,
brain disease, Bright's disease of the kidney, etc.
Spitting blood may be either haematemesis or haemoptysis proper. If
the former, nausea generally precedes the ejection of the blood by
vomiting, and it is apt to be mingled with food partly digested. It is
coughed up, bright red and frothy usually, when coming from the lungs
or bronchial tubes. But blood may proceed from the gums or throat, or
may run back through the posterior nares from the nose, and then it
gives alarm by seeming to proceed from the chest. It is necessary to
inquire very particularly into all such possibilities in every case of
hemorrhage.
Between vomiting of blood from ulcer and from cancer of the stomach we
have mostly these distinctions: in ulcer it follows soon after taking
food, in cancer (this being generally at the pylorus), an hour or more
after eating; ulcer is attended also by tenderness on pressure at a
certain spot over the stomach, without tumor; cancer presents a tumor,
with much less marked tenderness on pressure. By aid of the microscope
in examination of the matter vomited this diagnosis may be completed.
Constipation is an exceedingly frequent symptom under many and diverse
circumstances. Pathologically, we account for it in several ways: 1,
torpor of the muscular coat of the intestinal canal; 2, deficiency of
secretion in the glands of the bowels and in the liver; 3, imperfect
innervation of the abdominal organs; 4, mechanical obstruction, as by
a foreign body, intussusception, strangulated hernia, cancerous or
other tumor, stricture of the rectum, etc. Dyspeptic persons are
ordinarily constipated. So are almost all patients at the beginning of
attacks of measles, scarlet fever, small-pox, and other acute febrile
maladies. Typhoid fever is scarcely an exception to this; although the
bowels in that affection become loose after a few days, they seldom
are so at the very beginning of the attack. Sea-sickness is commonly
accompanied by total or nearly total inaction of the bowels, the
secretion of the intestinal glands being almost null, often for many
days together. Torpor of the brain is sometimes attended by marked
constipation. The latter may be a contributing cause of the former, as
in certain severe cases of scarlet fever, in which threatening coma
may be relieved by active purgation. We must not, however, occupy
space here by attempting to enumerate the many conditions under which
constipation may present itself as a symptom.
Almost as various are the associations of the opposite state of the
bowels, diarrhoea. Excessive or abnormally frequent discharges from
the bowels may be either fecal, bilious, mucous, membranous, purulent,
bloody, fatty, or watery, and they may occur with or without pain and
straining (tenesmus).
If, with frequent disposition to pass something, only small quantities
of bloody mucus escape, with pain and bearing down, we recognize
dysentery. When, instead, a large quantity of colorless fluid, with or
without floating flakes (rice-water), comes from the bowels at short
intervals, with vomiting of the same sort of material, we suspect
epidemic cholera, and must inquire for corroborative or corrective
indications in {164} reference to that suspicion. Very bad cases of
cholera morbus also may, at a late stage, present this symptom. So may
exceptional cases of pernicious malarial fever. The diarrhoea of
typhoid fever exhibits usually liquid stools of a brownish color
(gutter-water passages). Occasionally, hemorrhage from the bowels adds
to the danger of this fever, as well as to that of malarial remittent
fever. In phthisis pulmonalis, at a late stage, colliquative
diarrhoea, like colliquative perspirations, shows the breaking up of
the system by excessive waste. Very foul, offensive discharges from
the bowels may always be understood as showing that in the alimentary
canal, whether originating there or in the blood, morbid changes have
been going on. The indication is to promote the elimination of such
material as soon and as thoroughly as possible.
Clayey stools show absence or deficiency of bile in the intestines,
whether from its non-secretion by the liver or from obstruction to its
entrance by a gall-stone in the common gall-duct. Green stools are not
uncommon in sick children. The cause of the color has been much
disputed. Probably it depends chiefly on a modification of the
bile-pigment, with some admixture of altered blood. When mercurials
have been taken sulphide of mercury may give a green color to the
discharges.
Blood, nearly or quite unmixed, coming from the bowels, may have its
origin in internal hemorrhoids, intestinal ulceration, cancer of the
rectum, intussusception, rupture of an aneurism, typhoid or yellow
fever, or vicarious menstruation.
Pus is discharged per anum in cases of dysenteric or other ulceration
of the bowel; also when an abscess occurring in any part of the
abdomen (most frequently hepatic) opens into the intestine.
Pseudo-membranous discharges, shreds or other fragments of fibrinous
material, appear sometimes in what may be called diphtheritic
dysentery. Tubular casts are occasionally seen (diarrhoea tubularis),
which, however, are most likely to consist of thickened and
accumulated mucus. Fatty discharges from the bowels are rare. Authors
report observation of them in cases of disease of the liver or
pancreas, as well as in phthisis, typhoid fever, diabetes mellitus,
cholera, and tubercular enteritis of children.
Lientery is the term applied when imperfectly changed food appears in
the stools. It shows, of course, great deficiency in the process of
digestion.
Urination affords symptoms often of extreme consequence in disease.
Suppression of urine is one of the most alarming of signs; an
approximation to it only is likely to be met with in cholera, a late
stage of scarlet fever, typhus or typhoid fever, in acute yellow
atrophy of the liver, and in advanced kidney disease. Careful
examination of the abdomen, by inspection, palpation, and percussion,
as well as by inquiry of attendants, is needful in all cases of fever
or other disorders with delirium or stupor, to ascertain the presence
or absence of retention of urine. Dysuria--_i.e._ difficult urination,
strangury--may have several causes. Cantharides, absorbed from a
blister, may produce it temporarily. The more continuous states which
cause it are--stricture of the urethra, enlargement of the prostate
gland, and calculus in the bladder. In stricture, when the patient can
pass water, it is apt to be in a twisted stream. Dribbling often
occurs when the prostate is enlarged. When a stone is present the
{165} stream may flow naturally for a time and then suddenly cease
from obstruction at the outlet of the bladder. Enuresis, incontinence
of urine, is often very troublesome in children; its diagnosis
presents no difficulty.
Diabetes properly means simply excessive flow of urine. It may be
attended by no change in the secretion except dilution of its solids
(diabetes insipidus), as in certain nervous cases or after very large
imbibition of fluids. More serious is diabetes mellitus, in which
large amounts of sugar are found in the urine.
Variations in the quantity and in the composition and solid
ingredients of the urine, as ascertained by aid of chemical analysis
and the microscope, will be fully considered in other portions in this
work.
Menstruation in the female requires scrutiny in every case of
deviation from health. Its abnormities will be elsewhere treated of.
The subject of the signs of pregnancy belongs of course to treatises
on Obstetrics.
Pain is one of the most important of the signs of disease. We must
always examine its character, location, and associations. As to
character, that of pleurisy is sharp and cutting, increased by deep
breathing or coughing. In pneumonia and in myalgia it is dull or
aching. Rheumatic joints or muscles suffer a gnawing, tearing pain. In
neuralgia it is darting, shooting, lancinating; and the last of these
expressions is often applied to the pains of cancer. Griping pains
occur in colic, and bearing-down pains in dysentery, as well as in the
second stage of labor. Besides these varieties we have the pulsating
pain of an acute external inflammation, as of the hand, especially
before suppuration has occurred; the burning and smarting of
erysipelas; and the stinging, nettling sensations (formication) of
urticaria.
Tenderness on pressure is significant either of local inflammation,
whose other signs are then to be discerned, or of non-inflammatory
hyperaesthesia. The origin of the latter may require careful
examination of various organs for its discovery. If pain is relieved
by pressure, we may be sure of the absence of severe acute local
inflammation.
Not infrequently the seat of disease may be at some distance from that
of pain, as in the familiar instances of pain at the top of the head
in uterine derangement; in the glans penis from calculus in the
bladder; in the knee from hip-joint disease; under the shoulder-blade
in liver disorder; about the heart or between the shoulders from
dyspepsia.
Anaesthesia, loss of sensibility, has much value as a symptom in
neurotic affections, as paralysis, etc. Its discussion will find place
in connection with diseases of the Nervous System in other portions of
this work.
As an example of the diversified associations of pain, cephalalgia
(headache) may be mentioned as having at least the following possible
causes: congestion of the brain, neuralgia, rheumatism of the scalp,
uterine irritation, disease of the kidneys, early stage of remittent,
typhoid, or yellow fever, alcoholic intoxication, chronic disease of
the brain.
Abdominal pain may, in like manner, be traced, in different cases, to
many morbid conditions, such as flatulent colic, lead colic, neuralgia
or rheumatism of the bowels, intestinal obstruction, dysentery,
passage of a gall-stone or of a nephritic calculus through one or the
other duct {166} respectively; cancer, aneurism of the aorta, caries
of the spine; in the female, dysmenorrhoea, metralgia or
ovaralgia--_i.e._ neuralgia of the uterus or ovaries.
Similar diversity in the origins of pain might, but for want of space,
be pointed out in morbid states of the contents of the chest and of
other parts of the body.
Subjective symptoms often affect the special senses.
Taste and touch have been already referred to. Of sight we may have
photophobia, connected with exaggerated sensibility of the retina or
of the brain; muscae volitantes, specks, rings, or chains of spots
from floating semi-opaque particles in the vitreous humor; diplopia,
double vision; hemiopia, seeing only half of an object at a time;
amblyopia, indistinctness of vision of all objects.
Hearing is affected, besides all possible degrees of deafness, with
the subjective sensations of ringing, whistling, or roaring
sounds--tinnitus aurium. One form of this (as I conclude from
observation in my own ears) depends upon spasmodic vibration of the
tensor tympani or stapedius muscle. Sometimes the seat of the
sensation is in the auditory nervous apparatus proper. It has, not
seldom, a marked connection with brain-exhaustion. An attack of
Meniere's disease (labyrinthine vertigo) is often preceded by it. No
constant signification, however, can be attached to aural tinnitus.
Large doses of quinine or of salicylic acid will occasion it in many
patients.
Very briefly, deafness may be here disposed of by mentioning that, in
greater or less degree, it may be produced by accumulated wax in the
ear; obstruction of the Eustachian tube; thickness of the membrana
tympani; perforation of that membrane; mucus or pus in the middle ear;
disease of the ossicles of the ear; paralysis of the auditory nerve;
typhus or typhoid fever; excessive doses of quinine or salicylic acid.
Vertigo is chiefly of two kinds, dizziness or giddiness (swimming in
the head), and reeling vertigo, or a disposition to fall or turn to
one side or the other. Giddiness is produced by running or whirling
many times in a circle, or, in some persons, by swinging rapidly or
sailing. Reeling vertigo is mostly observed in connection with
disorder of the brain or of the labyrinth of the ear (Meniere's
disease). Dizziness, with nausea, is common as a symptom of cholaemia
(cholesteraemia of Flint) in what is popularly called a bilious
attack.
Delirium is present in many acute disorders, and not infrequently at a
late stage in pulmonary phthisis. Its special study will be taken up
in connection with the special articles upon these affections.
Coma, or stupor, is met with chiefly in the following morbid states:
severe typhus or typhoid fevers; malignant scarlet fever; small-pox;
rarely in measles; pernicious malarial fever; uraemia; apoplexy;
opiate narcotism, or that from chloral or alcoholic intoxication;
asphyxia from inhaling carbonic acid gas, ether, chloroform, etc.;
fracture of the skull with compression of the brain.
For an account of aphasia and other morbid psychological
manifestations the reader is referred to the articles on Aphasia,
Insanity, Hysteria, etc. in this work.
Physical and Instrumental Diagnosis will be treated in connection with
those diseases in which they have special importance.
{167} PROGNOSIS.
The elements of medical prognosis are essentially involved in
diagnosis. Our ability to anticipate the mode of progress, duration,
termination, and results of any case of illness depends upon our
knowledge--1, of the nature of the malady, with its tendencies toward
death, self-limitation, or indefinite continuance; 2, the soundness or
imperfection of the patient's constitution, with or without special
predispositions or the consequences of previous ailments; 3, the
present state of his system as to the performance of the general
functions, his strength, and vital resistance or persistence; 4, the
probable modifying influences of medical treatment, and also those of
situation, surroundings, and nursing--_i.e._ the care of those
attending to the patient during the absence of the physician and
having the duty of carrying out his directions.
1. As to the nature of the malady. While every sickness must be
supposed to encroach somewhat upon the vital energy of its subject,
very few diseases (leaving aside deadly poisons and surgical injuries)
are, ab initio, certainly fatal. Hydrophobia (rabies canina) has been,
until latterly, regarded as incurable, and always mortal within a few
days or a week or two. A few cases have, during the last few years,
been reported as cured, but the diagnosis of these continues to be
somewhat doubtful.
Cancer exhibits a tendency to extend its destructive malnutrition so
as to render death inevitable unless it can be removed early and
completely, or unless the morbid process can be arrested in some
manner not yet known. Remedies, such as condurango and Chian
turpentine, which furnished hope of such an effect, have, after
prolonged trial, been abandoned as not justifying the confidence of
the profession.
Tubercular phthisis was once considered to be almost necessarily a
fatal disease, although with a very indefinite period of duration.
Under improved hygienic management, with mild palliatives and
recuperative medication, a not inconsiderable minority of cases now
end in recovery. This term may be properly applied when, with
cicatrization of a cavity or cavities in the lungs, no more tubercle
is deposited and lung-substance enough is left for good respiration,
even although the structurally changed portions of pulmonary tissue do
not undergo entire repair.
Tubercular meningitis is a nearly always incurable affection. Yet a
few instances of lasting recovery have been reported where the
diagnosis was as certain as it can be in that disease in the absence
of post-mortem examination. A child attended by myself, in whom the
symptoms had been of the most unfavorable kind, became apparently
quite well, and continued so for a month. Then it was attacked
suddenly with convulsions, which were almost unremitting until it died
within a day or two.
Gangrene of the lung is very seldom recovered from, but, unless the
diagnosis from examination of putrescent sputa has been at fault,
there have been cases in which, with the limited destruction of the
affected lung, it was not fatal.
Pseudo-membranous croup destroys life in the majority, but not in
nearly all the cases of its occurrence. It is most likely to end in
death when distinctly a part of an attack of epidemic or endemic
diphtheria.
{168} Valvular heart lesions were formerly regarded as incurable, in
the sense of restoration of the normal condition and action of the
valves impaired, yet not incompatible with years of life. This
restoration certainly very seldom takes place. But the experience of
many close observers leads to caution in anticipation of necessary and
permanent disability of the heart because of murmurs, or even
functional disturbances, seeming to prove either aortic or mitral
insufficiency or stenosis.
Aneurism of the aorta is very seldom recovered from, but, besides a
variable duration, whose period can almost never be anticipated with
exactness, there appear to have been some cases of disappearance, or
at least prolonged quiescence, of the tumor and of its morbid effects.
Yellow atrophy of the liver is one of the disorders most rarely ending
otherwise than in death.
With a course altogether indefinite in time, there appears to be a
tendency to exhaust vital energy, without self-limitation, in the
different forms of organic degeneration, such as fatty heart,
Addison's disease, chronic Bright's disease, diabetes mellitus,
cirrhosis, and amyloid degeneration of the liver, etc. The same may be
said also of the different forms of cerebral and spinal sclerosis, of
pernicious anaemia, and of myxoedema.
Lastly, it is an exception to a very general rule of fatality when a
case of trichinosis, with well-marked abdominal, muscular, and general
symptoms, ends otherwise than in death within a few weeks.
Self-limitation is familiar in the natural history of typhus and
typhoid fever, relapsing fever, yellow fever, cholera, diphtheria,
whooping cough, mumps, small-pox, varicella, scarlet fever, and
measles. In the sense of a definite duration of each paroxysm
intermittent and remittent fevers are self-limited. Are they so also
in tending toward recovery, without curative treatment within a
certain time? This has been asserted, and in the case of remittent
there is evidence that spontaneous cures do sometimes happen. Some
observers aver that ague tends toward cessation of the chills after
six, eight, or ten weeks. The obstinacy of the attacks in many
instances under anti-periodic medication seems to make it probable
that spontaneous recovery from intermittent hardly belongs to the
typical natural history of the disease.
Whether the term self-limited can or cannot with propriety be applied
to pneumonia and other acute inflammations, as pericarditis, etc., has
been a mooted question. If it be so, it appears to the writer to be
true in a different meaning of the word self-limitation from that in
which it is applied to variola or typhoid fever. Yet some nosologists
deny this distinction, and regard pneumonia as strictly a lung fever.
Some of the facts supporting this view belong to the history of
pneumonia as complicating malarial fever; _e.g._ in the winter fever
of some parts of our Southern States. It must be admitted, however,
that the inflammatory process, though morbid, is generally eliminative
or corrective of a disturbing cause which produced it, and, unless
that cause is continued or repeated in action, a limitation belongs to
the succession of stages, ending either in resolution or in adhesions,
serous accumulation, suppuration, or gangrene.
2. It is not necessary to dwell here upon the significance in
prognosis of the patient's original constitution and hereditary or
acquired {169} predispositions, or on that of results left by previous
attacks of illness. These are all obviously of importance. In a member
of a family predisposed to consumption a bronchial attack following
exposure may be much more dangerous than in others. So also a cause of
mental agitation may produce insanity in a person who inherits a
tendency thereto or who has before had an attack of mental
derangement, while it would be innocuous to another who has no such
proclivity. A second or third attack of delirium tremens is much more
dangerous to life than a first attack. On the other hand, if yellow
fever occurs at all in a patient who has before had it, the course of
the disease is apt to be milder than usual. The most striking example
of the influence of previous disease is seen in the comparative
mildness of varioloid--_i.e._ small-pox modified by the system having
been placed under the action of the vaccine virus.
3. Most important of all data in prognosis are, in most cases, the
indications of the present state of the patient's system as to the
performance of the organic functions, his sum of energy, and vital
resistance and persistence. Especially must these indications be
regarded comparatively; that is, ascertaining whether, in a period of
weeks, days, or, sometimes hours (in malignant cholera even of
minutes), the patient's general condition has been and is gaining or
losing in the evidences of strength and healthy function of the great
organs.
Every student of clinical medicine must become acquainted, as soon as
possible, at the bedside, with these tokens and evidences, which make
almost the alphabet of practice: What is a good, a doubtful, and a bad
pulse? How does a patient breathe when moribund from simple
exhaustion, and how does such respiration differ from the toil and
struggle of asthma or the stertor of narcotism? Why does a glance
suffice to make known to a surgeon the state of collapse after a
railroad accident, or to a physician that of cholera or pernicious
intermittent? What is the impression given to the finger upon the skin
by intense fever, and what by the relaxation which precedes death?
These and many other such questions are to be answered fully to each
student only by the use of his own senses, with such interpretation as
is to be obtained by the careful comparison of cases, with the aid of
books and didactic instruction.
To a well-trained eye and hand a look and a touch will often suffice
to make known the commencement of convalescence or of the precipitous
decline toward death. Yet a wise physician will be very cautious in
acting upon even seemingly obvious prognostications. Changes may be
going on in important organs whose effects have hardly yet begun to
show themselves, and which may after a while materially alter the
aspect of the case. Particularly near the beginning of an attack of
enthetic disease, such as scarlet fever, small-pox, typhus or typhoid
fever, the physician should beware of too confidently forecasting the
progress of the case for better or for worse. In nothing, probably, is
the prudence of a practitioner more often or more severely tested than
in his answers to inquiries made concerning prognosis.
4. Anticipation of the modifying action of remedies is undoubtedly a
proper factor in our estimate of the probable result of any case of
illness. Few diseases, however, are as yet so subject to control by
specific medication as to allow certainty in such expectations. In a
first attack of ague we may look with much confidence toward the
speedy cure of our {170} patient under quinia. In one who has had
chills all winter even this confidence may need qualification. A
sufferer with syphilitic rheumatism may generally be promised relief
under the use of iodide of potassium, or one afflicted with scabies
under the application of sulphur ointment. We seldom have misgivings
about our ability to give relief in colic, constipation, or diarrhoea.
Yet the first two of these may prove to be symptoms of intestinal
obstruction resisting treatment, and the last may depend upon chronic
ulceration of the bowel, giving it unexpected continuance. In all such
instances careful and (when practicable) accurate diagnosis must
precede prognosis; our estimate of the action of remedies becomes then
a secondary, although often a valuable, part of the calculation of the
probabilities of the case.
Prognosis in particular diseases involves the consideration not only
of those signs of the general vital condition to which we have just
been giving attention, but also of such as are more or less peculiar
to each disorder. To a certain extent these signs may be grouped. We
may refer to good and bad signs in pulmonary, cardiac, intestinal,
renal, cerebral, and febrile affections respectively. Still, there
will be for each malady, if it really has a distinctive character,
some tokens which experience shows to be specially indicative of
favorable or unfavorable progress and results.
Let us notice some of these as examples.
In pneumonia the best signs are the lowering of a high temperature,
reduction of the number of respirations to 20 or 25 in the minute,
expectoration of sputa less and less tinged with red or brown, and
gradual reduction of the region of dulness on percussion. Worst, in
the same disease, are an axillary temperature over 106 degrees,
respirations 40 or more per minute, with delirium, and expectoration
becoming more abundant, grayish, and purulent; also with continued
dulness on percussion and abundant mucous rales on auscultation.
In croup the best sign is, after a hoarse, dry, barking cough and
dyspnoea, a soft, liquid rale, heard in the larynx and trachea during
respiration or coughing. Worst, in croup, is a steadily or
paroxysmally increasing difficulty of breathing, with a dry hissing or
whistling sound of respiration and cough succeeding the barking sounds
of the earlier stage.
In phthisis pulmonalis among the best signs are the patient's
increasing in weight, coughing and expectorating less, ceasing to have
hectic and night sweats. These may give renewed hope, even before much
change is discernible in the physical signs. Of bad omen are intense
hectic fever, incessant cough with abundant nummular sputa, copious
perspirations, diarrhoea, breathing growing shorter and shorter, and
extreme emaciation and debility.
In all organic affections of the heart an extremely rapid and
irregular pulse, with orthopnoea and increasing anasarca, and
especially the Cheyne-Stokes respiration (described under DIAGNOSIS),
must cause unfavorable expectations.
In obstruction of the bowels the best of all symptoms is, usually, of
course, a copious fecal evacuation. Yet a few cases have occurred in
which a very large evacuation, delayed by obstruction for a week or
two, has been almost immediately followed by collapse and death. The
worst signs in cases of obstruction are (besides long-unyielding
constipation) {171} stercoraceous vomiting, a small, rapid pulse, and
increasing coldness and clamminess of the surface of the body.
In cholera infantum the best signs are cessation of vomiting and
purging, the discharges growing more nearly natural, the face becoming
less shrunken in aspect, sleep taking the place of coma vigil or
waking apathy, and water or milk, when taken, remaining on the
stomach. Worst, in the same disease, are incessant rejection of
everything swallowed, watery passages from the bowels every half hour
or hour, shrinking of the face and body to skin and bone, with an
apathetic expression of the open or half-open eyes, the latter rolling
often from side to side.
In epidemic cholera good signs are the arrest of vomiting and of
rice-water discharges from the bowels, rapid movement of the blood in
the veins after removal of momentary pressure, return of natural color
and warmth to the skin, with filling up of the pulse at the wrist. Bad
signs in cholera are shrinking of the cheeks and of the flesh upon the
hands, deepening ashiness or blueness of the skin, coldness and
clamminess to the touch, dyspnoea, loss of pulse, incessant vomiting
and purging of rice-water stools, constant cramps of the limbs, and
suppression of urine.
In acute cerebral meningitis good signs are lessened temperature of
the head, quiet sleep without stertor, disappearance of delirium, more
natural pulse, and attention to surrounding objects, without
disquietude. Bad signs in the same disease are deep stupor,
strabismus, convulsions, paralysis, involuntary defecation and
urination.
In typhus fever good signs are the pulse becoming slower and fuller,
the skin less hot, more soft and moist, the tongue moist and clean,
the face losing its dusky flush, and consciousness returning instead
of muttering delirium.[40] Bad, in the same fever, are deepening of
the flush of the countenance, profound stupor, rapid and feeble pulse,
lying on the back and sinking down toward the foot of the bed, with
suppression of urine.
[Footnote 40: Incidentally, it may be mentioned that the return of the
pulse to its normal rate is often considerably delayed in
convalescence from typhus and typhoid fevers and other protracted
diseases. If, then, the temperature is not above 99 degrees F., and is
stable from morning to night, the tongue is clean and moist, and
appetite begins to appear, we need not be alarmed, although the pulse
continues as high as 90 or 100 per minute, in a case attended by
positive debility.]
In typhoid fever many of the good and bad signs are the same as in
typhus, belonging to closely similar general conditions. But in
typhoid fever we observe also as favorable signs the lessening of
tympanites, more nearly natural fecal stools, and the absence of
tenderness in any part of the abdomen. As unfavorable, increase of
tympanites and diarrhoea, sometimes large hemorrhages from the bowels;
worst of all, at a late stage, sudden increase of abdominal
distension, with dulness on percussion, coldness of the skin, great
rapidity and feebleness of the pulse following perforation of the
bowel, resulting usually in fatal peritonitis.
In scarlet fever, measles, and small-pox it is a favorable sign for
the eruption to come out well at the usual time; its sudden recession
threatens malignancy. In small-pox a confluent eruption marks a
dangerous case, and so does the occurrence of distinct pustules in the
throat. Early in scarlet fever stupor is very threatening, though not
necessarily mortal. Late in the same disease bloody urine, or, worse
yet, suppression of urine, may well cause alarm.
In all children's diseases the early occurrence of convulsions shows a
{172} severe but not always a dangerous attack. The late occurrence of
convulsions is commonly much more serious in its significance.[41]
Convulsions are always of vastly less importance, prognostically, in
children than in adolescents or adults. Yet they are always serious
signs. While recovered from in the large majority of cases, they may
at any time be fatal.
[Footnote 41: Yet I saw a case of acute cerebro-meningitis, in a girl
ten years of age, in which a violent convulsion occurred on about the
sixth day of the disease, and was followed by convalescence.]
These enumerations, selected as examples merely, might be much farther
extended but that the special prognosis of each disease will be fully
set forth in the several articles upon them in the body of this work.
Those now given may suffice for the illustration of the method and
general principles by which the physician must be guided in his
anticipation of the progress and result of cases of disease. The
caution may be repeated, to observe great care in forming a conclusion
in regard to prognosis in every instance, and still more in expressing
it, unless in the presence of very clear and positive evidence.
{173}
HYGIENE.
BY JOHN S. BILLINGS, M.D.
The purpose of this paper is to indicate some of the ways in which
hygiene, both private and public, is connected with the duties of the
general practitioner, and to give some information as to modern
methods of investigation and work in preventive medicine.
While the business of the physician is more especially the care of the
sick with reference to the cure of disease, or, where that is beyond
his power, as is too frequently the case, to relieve suffering and
secure temporary ease for his patient, he is nevertheless often called
upon to answer questions as to the causes of disease, and the best
means of avoiding or destroying these causes. Not only does diagnosis
often turn upon considerations of etiology, but a very considerable
part of the treatment of actual disease must be hygienic in the
broader sense of the word. The prescription or the surgical operation
must not only be supplemented by advice as to residence, clothing,
food, exercise, etc., but must, in many cases, be merely supplementary
to such advice, which indicates the really essential method of
treatment; and the giving this advice then becomes the most important
part of the physician's work, although not usually recognized as such
by his patients. The chief value of the prescription is, in fact,
often to methodize the mode of life of the patient and to remind him
at frequently recurring intervals of the regimen which has been
ordered with it.
The physician has also certain duties in relation to the public at
large, as well as to his individual patients, and these duties become
more numerous and important as the density of population increases, so
that in the large cities of most civilized countries he finds himself,
nolens volens, in almost daily contact with legally constituted
authorities in the shape of registrars, health officers, coroners,
etc., and is not infrequently summoned before the courts as a supposed
expert in matters connected with the public health.
Moreover, the physician who has become eminent in his profession is,
in many cases the adviser, and, so far as professional subjects are
concerned, to a great extent the guide, of those who legislate for, or
execute the laws of, not only his own city or county, but his state
and the nation; and he must to a corresponding degree be held
responsible for the position which he takes and the advice which he
gives in regard to public health matters. This is true whether his
attitude on these subjects {174} be active or passive, for his silence
will be taken to mean that there is no necessity for action or change.
The limits of this paper do not permit the presentation of proofs and
illustrations of these somewhat dogmatic assertions, but it is
believed that they will meet with general assent from medical men
without formal and detailed argument, and that it is unnecessary here
to urge the interest or importance of practical hygiene upon the
medical profession, or to enlarge upon the desirability that the
practitioner, as well as the professional sanitarian, should be
familiar with the conclusions of modern science and technology with
regard to it.
In the minds of many intelligent and thoughtful physicians there is,
no doubt, a feeling of unformulated distrust as to the real
possibilities or probabilities of improving the health and diminishing
the mortality of the community at large; and this feeling is in part
due to the exaggerated claims and emotional exhortations of some
advocates of hygiene. A careful and unprejudiced survey of what has
been accomplished by sanitary measures will, however, largely
dissipate this distrust.
The natural term of the life of man is fixed by the physiologist at
about one hundred years, which is nearly in accordance with the law
indicated by Flourens, that the period of life of an animal is about
five times that required to perfect the development of its skeleton
and unite the epiphyses with the shafts of the long bones. The actual
average duration of human life is less than half this, but there is
satisfactory evidence that it has increased in civilized countries.
The ancient estimate is expressed in David's declaration, that "the
days of a man are threescore years and ten, and if by reason of
strength they be fourscore years, yet is their strength labor and
sorrow." Kolb, a cautious and learned statistician, concluded, from
his studies, that while the maximum age reached by man has not
materially changed for many centuries, the number of persons who now
survive infancy and of those who reach a ripe old age has decidedly
increased; and this opinion is sustained by Mr. Lewis, the secretary
of the Chamber of Life Insurance of New York, who points out that
while civilization largely interferes with the laws of evolution by
survivorship, it aids by economizing the waste which occurs in its
absence. "Under natural selection, when variations in capacity arise,
thousands of them are wasted where one is secured, fixed, and
transmitted. But human society economizes much of this waste, fastens
upon and improves an immensely larger proportion of the capacities
lavishly produced by Nature, and thus concentrates forces which would
otherwise spread their operation over countless ages."[1]
[Footnote 1: "Influence of Civilization on the Duration of Life,"
_Reports Am. Pub. Health Ass'n_, N.Y., 1877, vol. iii. p. 173.]
We have, however, no record of the duration of life in ancient Greece
and Rome, and it is quite possible that it was greater than in Western
Europe during the Middle Ages, which formed a period of retrogression
in a sanitary point of view. The Jew, the Greek, and the Roman, prior
to the Christian era, were probably cleaner in person and in dwellings
than the people of the time when dirt became the odor of sanctity.
In the absence of reliable data for this country, it is impossible to
speak with certainty of the results of attempts made here to prevent
disease and death. Each sex, race, and age has its own rate of
mortality, {175} and until this rate is determined we can only guess
as to whether good work is being done or not.
We can never hope to diminish the total number of deaths which will
occur in long periods, say two hundred years, but we may rationally
try to prolong the average duration of life, to diminish infant
mortality, and to secure greater comfort and better health for
individuals and for the community at large.
The reader must remember that only a mere outline of the subject can
be presented here; the details would require several volumes, and the
tendency to specialization in this, as in other branches, is so great
that it is hardly to be expected that any one man shall have either
the theoretical or the practical knowledge necessary for covering the
entire field. There are certain things in relation to hygiene which
every physician should know; there are many other things with regard
to which it is sufficient if he knows where to find full and reliable
information when he needs it. With this preface we will pass at once
to our subject, which may be conveniently divided as follows:
I. Causes of disease, means of discovery, and prevention.
II. Personal hygiene in its relations to the practice of medicine.
III. Public hygiene in its relations to physicians.
I. Causes of Disease, Means of Discovery, and Prevention.
Although the origin of disease has from the earliest times been the
subject of study by medical men, the physician has not heretofore,
usually, been called upon to investigate the causes of disease in
particular localities, until the occurrence of sickness in that
locality has called attention to the matter. The education of the
public as to the importance of sanitary work has, however, recently
made great progress, and it is now not unusual to ask the opinion of
the family physician as to the healthfulness of a given locality or
house. The question may be presented in three different ways: First.
In a given case of disease, what is the probable cause? Second. Given
the presence of a known or suspected cause of disease, what are the
best means of avoiding or destroying it? Third. In the absence of
cases of disease, to determine whether causes of disease are probably
present, and if so, what causes.
The word "cause" is here used in its widest sense, including not only
what are commonly called predisposing and exciting causes, but also
those conditions which aggravate or continue the disease. These causes
may be roughly classed as follows: Heredity; impure air; impure water;
climate; habitations; occupation; food; intemperance of various kinds;
clothing; errors in exercise; sexual errors; parasites; contagia;
expectant attention and other mental causes, including worry, etc. In
most cases two or more of these classes of causes are combined in
action for the production of a given case or outbreak of disease, and
when we refer any disease to a single factor, what is meant usually
is, not that this is the sole and exclusive cause, but that it is the
most prominent one.
Bearing this in mind, let us consider briefly some of the causes above
mentioned.
I. HEREDITY.--That the child inherits from its parents its physical
{176} type, including color, stature, physiognomy, temperament, and
certain peculiarities of structure or arrangement of internal organs,
is well known. This hereditary influence is stronger from the
immediate than from the remote ancestry, although the curious
phenomena of atavism sometimes form exceptions to this rule. The
hereditary causes of disease can be guarded against when known.
Theoretically, by preventing generation on the part of persons who are
unfit to produce offspring; practically, to a certain extent, by
taking special precautions against these causes and their effects in
the individual, particularly at those ages in which these influences
seem to have their greatest force. The most important of these
hereditary diseases are syphilis, consumption, scrofula, cancer, gout,
certain skin diseases, insanity, and criminal tendencies of various
kinds.
The physician's advice is rarely asked with regard to the propriety,
from a sanitary point of view, of a proposed marriage, nor is it often
taken when given, unless, indeed, it happens to correspond with the
wishes of the recipient; nevertheless, he is occasionally in a
position to exert influence in such a matter, and when this is the
case the following general rules may be borne in mind: 1. No marriage
should occur between persons having the same hereditary tendency to
disease; and this is especially important in marriages between
relatives. 2. A girl should not marry under the age of twenty. 3. A
person affected with hereditary or well-marked constitutional
syphilis, or having a strong consumptive taint, or tendency to mental
unsoundness, should not marry at all.
The precautions to be taken in individual cases in which there is a
known hereditary predisposition to certain diseases will probably be
indicated in the articles upon those special diseases. The most
important of these, from the sanitary point of view, are consumption
and gout, partly because of their frequency, partly because of the
undoubted power which a proper regimen, applied in time, has in
controlling them. The pain in gout has often an excellent sanitary
effect; it is an inducement to temperance much stronger than any
amount of good advice.
The influence of heredity in producing abnormities of refraction and
accommodation of the eye, and the importance of detecting these early
and giving them proper treatment, have not hitherto received, from the
general practitioner, the attention which they deserve. Children of
parents affected with astigmatism, ametropia, etc. should be carefully
examined before being placed at school, and if necessary fitted with
proper glasses.
The heredity of idiosyncrasies as to certain articles of food or
certain drugs must also be borne in mind by the physician, for,
although implicit confidence is not always to be placed in the
statement of a patient that he cannot take a certain medicine, yet a
knowledge of the facts will occasionally save the prescriber from some
awkward mistakes.
The importance of bearing in mind the family peculiarities is best
appreciated by the old family doctor who has had two or three
generations pass under his hands: he knows, for example, that in one
family he may expect brain complications, in another lung troubles,
and that what would be grave symptoms in one house are of
comparatively small import in another. Unfortunately, the greater part
of this kind of knowledge has not yet been formulated, and each
physician has to acquire it for himself; but he will find the process
of acquisition greatly facilitated if in all cases in a new family he
makes it a rule to learn something of the medical {177} history of the
parents, and he will find intelligent laymen quick to appreciate his
inquiries in this direction.
The importance of taking into account hereditary influences is well
illustrated by the care which is taken to obtain information with
regard to them in well-conducted life insurance companies. The medical
examiners of such companies have their attention specially called to
this matter, and the following extract from a manual of instructions
shows how it is regarded from a business point of view: "If
consumption is found to have occurred in the family of the applicant,
he is to be regarded not insurable under the following circumstances,
viz.:
YEARS OF AGE.
If in both parents, not insurable until . . . . . . . . . 40
If in one parent, not insurable until . . . . . . . . . . 30
(Except for ten-year endowments, then 20 years.)
If in two members (not parents) . . . . . . . . . . . . . 35
If in one member (brother or sister) . . . . . . . . . . 20
(Except for ten-year endowments, when peculiarly favorable.)"
If apoplexy, paralysis, or heart disease is found to have occurred in
any two members of the applicant's family, he is to be regarded as
insurable only upon the endowment plan, the term of insurance to
expire prior to his reaching the age of fifty years. If insanity shall
have so occurred (in two members), a provisionary clause is essential,
and is attached to the policy by the company.
II. IMPURE AIR.--The dangers of impure air, water, and food depend
largely upon the fact that through these media may be introduced into
the body particles of organic matter, living or dead, which tend to
produce disease in the recipient. The parasites are types of this mode
of disease-production, and these blend with the contagia of the
specific diseases in such a way that it is not easy to draw the
distinction in all cases. There are also certain poisonous gases and
inorganic compounds which may occasionally be present in air or water
to such an extent as to produce disease; but as a rule the gaseous
impurities of the air are offensive to the smell rather than
dangerous, as will be seen when we come to consider the effluvium
nuisances.
The subject of ventilation, for the purpose of procuring an adequate
supply of pure air, is one of so much importance, and one upon which
the physician is so liable to be called for practical advice, that it
seems proper to state briefly the general principles which should
govern investigations into, or recommendations upon, this subject.
The impurities of air which are to be disposed of by ventilation are
for the most part derived from the human body, chiefly from
respiration, and these only will be considered here. In some cases it
is necessary to make special provision for the products of combustion
from gas, etc., but as a rule this is rather for the purpose of
regulation of temperature than anything else. The impurities of air
due to the presence of human beings consist mainly of carbonic acid,
ammonia, sulphuretted hydrogen, and sulphide of ammonium, and of
various organic compounds, mostly in the form of minute particles of
organic matter of uncertain structure, but extremely prone to
decomposition. It is usual to estimate the degree of impurity by the
amount of carbonic acid present, and this leads many persons to
suppose that the carbonic acid is in itself the chief and most
dangerous impurity. This gas is, however, not perceptible to the
senses, {178} nor is it injurious to health, unless present in much
greater proportion than that in which it will be found in the most
crowded habitations or assembly-rooms. Its importance in questions of
ventilation depends upon the fact that its increase in a room beyond
the amount present in the outer air may usually be taken to be in
direct proportion to the amount of the really dangerous and offensive
impurities present, and that the amount of carbonic acid can be
ascertained by chemical tests with comparative ease and rapidity;
which is not the case with regard to the organic matter. The carbonic
acid is therefore taken as the measure of the impurity, although it is
not itself the impurity of which we are most anxious to be free.
To decide as to whether a room is well ventilated or not, some
standard of permissible impurity must be fixed, and this standard is
now usually taken to be, in a room occupied by human beings, that
condition of air which produces in a person having a normal sense of
smell, and who enters from the fresh air, a faint sensation of an odor
very slightly musty and unpleasant. Upon testing the air of such a
room, it will be found that the amount of carbonic acid impurity
present--that is, the excess of this acid over the amount in the
external air--will be between 2 and 3 parts in 10,000.
As the amount of carbonic acid in normal air varies from 2 to 5 parts
in 10,000 in different places, and in the same place at different
times, it is better to look to the carbonic acid impurity as above
defined rather than to the total amount of the acid found present, if
strict accuracy is desired; but usually the statement of Dr. Parkes is
correct, that the organic impurity of the air is not perceptible to
the senses until the total carbonic acid rises to the proportion of 6
parts in 10,000 volumes. When the carbonic acid reaches 9 parts in
10,000 the air is close, and when it exceeds 1 part in 1000 the air is
usually decidedly unpleasant. If we take 2 parts in 10,000 as the
permissible maximum of carbonic acid impurity, it follows that the
amount of fresh air which must be supplied and thoroughly distributed
for each person per hour is 3000 cubic feet. If 3 parts per 10,000 be
taken as the permissible maximum (which is the standard of
Pettenkofer), the amount of air per head per hour must be 2000 cubic
feet. While it is impossible, as Dr. Parkes remarks, to show by direct
evidence that the impurity indicated by 7, 8, or even 10, parts of
carbonic acid per 10,000 is injurious to health, it is advisable to
accept his standard, because it is a simple one, and can be
practically applied without special apparatus or technical skill, and
because there is evidence of the injury to health which continued
exposure to air impure, by this standard, ultimately produces.
Keeping this standard in view, the physician may be called on for an
opinion as to whether the ventilation of a given building is
satisfactory or as to the merits of a proposed plan for ventilation.
The first is a question of fact: What are the effects produced upon
the inmates? Are there unpleasant odors in the building or not? What
percentage of carbonic impurity is present? What is the number of
cubic feet of air per head that is introduced and removed per hour?
And what is the character of the fresh-air supply as to purity? Does
it come from the cellar, or from other rooms, or from a foul area?
Air-currents can usually be best investigated by the fumes of nascent
muriate of ammonia produced by {179} exposing a cylinder of common
blotting-paper, moistened with dilute hydrochloric acid, to the vapors
coming from a crumpled fragment of the same paper moistened with
common aqua ammonia and placed within the cylinder. The process for
carbonic acid determination is simple, and can be learned in three
hours in a laboratory under a skilful teacher. It does not seem worth
while to describe it here. The determination of the amount of air
passing through a given register, flue, or chimney in a given time is
to be made by the use of an anemometer, an instrument which registers
the velocity of the current of air passing through it.
In judging of the merits of a plan of ventilation the following points
should be remembered: The defect in most plans for ventilation is in
the air-supply. Many people suppose that they have made all necessary
provision for ventilation if they have put in tubes or openings for
the escape of foul air, forgetting that these outlets will have no
effect if corresponding inlets are not provided. Examine, first of
all, therefore, the ducts, flues, and openings proposed for the
fresh-air supply, with reference to their size and position and the
amount of air to be furnished by them. These will almost invariably be
found to be too small. The proper size of flues and registers for a
given room is ascertained by dividing the number of cubic feet of air
to be supplied per second by the velocity in feet per second which the
air is to have in the flue or opening, bearing in mind that it is much
better that these flues and registers shall be too large than too
small, since it is easy to reduce their capacity, but, in most cases,
impossible to increase it. When the fresh-air register is so situated
that the current of air from it is liable to strike upon the person of
an occupant of the room, the velocity of this current should not
exceed 1-1/2 feet per second if unpleasant draughts are to be avoided;
and it will usually be found best that the velocity of the air in the
flue shall not exceed 6 feet per second, except in the case of very
large flues, where the element of friction becomes of comparatively
small importance. In the great majority of cases the amount of air to
be supplied depends upon the number of persons, and not on the cubic
space; but in exceptional instances, where the amount of cubic space
is very large in proportion to the number of persons, and the heating
is effected by warm air, it may require more air to keep the room at a
comfortable temperature than is necessary for the supply of the
occupants. The cubic space is also relatively much more important in
rooms which are to be occupied but a short time continuously, and can
then be thoroughly aired, than it is in rooms constantly occupied.
The methods of calculation can be best illustrated by one or two
examples. What should be the number and size of flues and registers
for fresh-air supply for a hospital ward to contain 24 beds, the ward
being a rectangular pavilion with windows on opposite sides? In this
case the room is constantly occupied, and the supply of air should be
1 cubic foot per head per second, or, in all, 24 cubic feet per
second. The velocity of current at the registers should not exceed 3
feet per second--better only 2. This will require from 8 to 12 square
feet of clear opening in the registers. If we allow four on each side
of the room, each register must have at least 1 square foot of clear
opening. The velocity of the air in the flues supplying these
registers should not exceed 4 feet per second, and therefore the area
of each flue should be about 9 by 12 {180} inches. Suppose the same
question be asked with regard to a school-room to contain 48 pupils.
In this case the room will not be occupied more than two hours at a
time. The air-supply desirable may be put down at 35 cubic feet per
head per minute, or 28 cubic feet per second for the whole. The
velocity in the flues may be put, as before, at 4 feet per second;
hence we need 7 square feet area of flue, or seven flues, each having
1 square foot of area. It is safe to say that there are not twenty
school-houses in the United States which have fresh-air flues of
sufficient area; the deficiency is made up, for the most part, by
leakage of the outer air through cracks around windows and directly
through the wall, and also by the passage of air from the central hall
into the room, this last air coming from the cellar or basement.
The velocity of the air at the foul-air registers and in the foul-air
ducts may be greater than in the fresh-air flues, since there is no
danger of its causing draughts, and hence there is no truth in the
common notion that the outlets should be larger than the inlets to
allow for the expansion of heated air. It is important that the
velocity of the current in the outlet shaft or chimney should be at
least 8 feet per second at the point where it escapes into the outer
air; and if the outlets be too large for the inlets, the result may be
that some of the foul-air flues will work backward and become inlets.
The plan of making everything a little larger than is necessary is not
a safe one as regards chimney-flues and outlet shafts.
The merits of a plan of ventilation depend not only on the amount of
air introduced, but on its distribution. The test for distribution is
chemical analysis of samples taken in different parts of the room and
at different levels. A very good idea of the direction taken by the
incoming air can also be obtained by the use of fumes of nascent
muriate of ammonia, as above described. In considering the
distribution which will probably take place in a given plan, care
should be taken not to fall into the common error of supposing that
because pure carbonic acid gas is heavier than air, therefore the
carbonic acid derived from respiration sinks to the floor, and that
special provision should be made to remove it at that point. The law
of the diffusion of gases effectually prevents this separation and
sinking of the carbonic acid from the mixture of gases expired, and it
will be found to be present in about equal proportions in all parts of
an inhabited room.
The methods of introducing and distributing fresh air depend to a
great extent upon the methods of heating employed; and it is necessary
to remember that while good ventilation is a very desirable thing,
satisfactory heating is, in cold weather, still more desirable, and
must be attained even if the ventilation is interfered with for that
purpose. The principal difficulty in the way of securing good
ventilation is its cost. In a cold climate satisfactory heating, good
ventilation, and cheapness are not compatible; it is comparatively
easy to obtain any two of them, but impossible to have the three
together. This fact should be fully understood and realized by the
physician, for its comprehension will save much time in considering
the merits of various patent ventilators and ventilating appliances,
which, according to their inventors, produce good ventilation at no
expense beyond that of the original cost of the apparatus; which is
practically about the same as a claim to have discovered perpetual
motion. Patent ventilators are usually cowls to be placed upon the top
of outlet {181} flues. I know of none which are superior to the common
Emerson Ventilator, on which there is now no patent. In cold weather
the air must be warmed to secure comfort; it must be changed to secure
ventilation. The changing of the air carries off heat, the loss of
which must be supplied by fuel, which fuel costs money. The greater
the ventilation, the more rapid the change and the more heat required.
It is therefore quite possible to judge somewhat of the merits of a
heating and ventilating apparatus--for example, of a
school-house--from the amount of fuel consumed; but the conclusion
will be precisely the reverse of that drawn by the average trustee,
since it will be, that within certain limits the less fuel required
the less satisfactory the apparatus.
The evil effects of insufficient ventilation, although very certain
and very serious, are not immediate, or such as to attract attention
at first, except in very aggravated cases with excessive
over-crowding. The power of the organism to adjust itself to
surrounding circumstances is very great, and perhaps as great in
regard to the endurance of foul air as anything else. Yet this power
is greater in seeming than in reality, for at last such air produces
disease and shortens life. Its effects are manifested in diseases of
the respiratory organs, acute and chronic, and it is now generally
admitted that the undue prevalence of phthisis in troops is due to the
foul air of the barrack-rooms.
Some persons are much more susceptible than others to the effects of
impure air, and will suffer from headache, languor, loss of appetite,
etc. where others would experience little inconvenience. Children thus
susceptible dread the school-room as ordinarily constructed and
ventilated, and their discomfort should be taken into account and
guarded against.
Thus far, reference has been made only to those impurities of air due
to respiration and lights; in other words, the necessary impurities
found in human habitations. The impurities due to sewer gases will be
referred to hereafter; they should be prevented absolutely, and not
provided for by ventilation. One of the most difficult problems
presented to the physician is to determine whether the effluvia from a
given locality are injurious to health, and if so, to what extent.
These effluvia may be due to certain occupations or manufactures, or
they may result from the disposal of excreta, from obstructed drainage
giving rise to swamps and the collection of decaying organic matter,
and in other ways. The best definition of the term "injurious to
health" in this connection is perhaps that suggested by Dr.
Ballard--_i.e._ that exposure to the offensive effluvia causes bodily
discomfort or other functional disturbance, continuing or recurring as
the exposure continues or recurs, and tending by continuance or
repetition to create an appreciable impairment of general health and
strength, to render those exposed more liable than others to attacks
of disease, and more apt to suffer severely when attacked, and, in the
more serious forms, to the direct production of the disease and the
shortening of life.
The group of symptoms due to offensive effluvia is, as Dr. Ballard
remarks, a tolerably constant one, and consists of loss of appetite,
nausea, headache, giddiness, faintness, and a general sense of
depression, with, in some cases, vomiting and diarrhoea. But it is
usually impossible to prove by statistics that these phenomena are due
to a given effluvium complained of, for those who suffer from it are
usually exposed to other causes of ill-health, such as poverty,
overcrowding, collection of filth, etc.; and, on the {182} other hand,
many of those exposed to the effluvium seem to suffer very little, if
at all, from their surroundings. And so true is this, that in the
carefully prepared report upon effluvium nuisances recently issued by
Dr. Ballard,[2] it will be found that as a rule no attempt is made to
prove that the effluvia from any particular branch of industry are
injurious to health; the test practically applied is that they produce
offensive odors.
[Footnote 2: _Report in respect of the Inquiry as to Effluvium
Nuisances arising in connection with various Manufacturing and other
branches of Industry_. By Dr. Ballard, London. Her Majesty's
Stationery Office, 1882, 8vo.]
The legal view of this subject is given in the various decisions as to
what should be considered a nuisance, the essence of which is the use
of one's own property in such a way as to inflict damage upon, and
injure the rights of, another. If a man collects on his own premises,
for his own use, any material, such as water or filth, he is bound to
retain it within his own premises or to let none of it escape in such
a way as to damage others; and this holds good as regards gases,
vapors, and odors. The decision of Mansfield, in the case of Rex _vs._
White, is often quoted approvingly by jurists, viz.: "It is not
necessary that the smell be unwholesome; it is enough if it renders
the enjoyment of life uncomfortable." But, practically, the question
as to whether the discomfort produced is sufficient to produce
ill-health will be the one upon which the physician is called to give
evidence, and the one also upon which he will find it most difficult
to obtain data sufficient to enable him to form a positive opinion.
III. IMPURE WATER.--Of all the various preventable or removable causes
of disease to which the attention of the physician engaged in practice
in the small towns and rural districts is directed, it will usually be
found that the water-supply is the most important, because it is in
these localities that it is most liable to become contaminated in such
a way as to produce sickness.
All water used for drinking purposes is impure in the chemical sense,
since it contains some inorganic matters or salts, and in most cases
organic matter also. It is difficult to define precisely what should
be considered an impure water in a sanitary sense, and the best we can
do is to indicate probabilities in the absence of positive evidence of
the production of disease by the suspected water. So far as inorganic
impurities are concerned, the most important, from the sanitary point
of view, are the salts of lead, magnesia, and lime, but in this
country these are so rarely the cause of disease that they hardly
require special notice. The physician should, however, bear in mind
possibilities of lead-poisoning in some obscure cases which he will
meet.
The diseases due to impure water are certain specific fevers,
diarrhoeal diseases, and some affections due to parasites which find
entrance to the body through this medium. The water-supply is to be
suspected in case of prevalence of diarrhoeal disease in a community,
and especially if the outbreak be sudden and affect a number of
persons and families. Sudden outbreaks of cholera, typhoid fever, or
malarial fever, confined to a limited locality, should lead to careful
examination of the water-supply. The impurity in water which causes
these diseases is supposed to be either organic or the product of
organic life, and at present the prevailing opinion is that the really
dangerous impurities consist of minute living organisms or {183}
germs. It is usual to estimate the impurity of water by the amount of
organic matter present, but it is evident that this alone can give no
positive information, since by this standard milk and soup would be
very dangerous. Much depends upon the character of the organic matter,
whether it is derived from the animal or vegetable kingdom--whether it
is in a state of fermentation or putrefaction, etc. etc.; but the
presence of specific germs in it is the most important part of all,
and at the same time the most difficult to ascertain. Nitrogenous
organic matter in a state of decomposition is dangerous, yet it does
not always produce disease, even when ingested in comparatively large
quantity, as in case of "high" game or tainted meat; and it is easy to
find instances where water strongly polluted with sewage has been used
for a considerable period without producing marked ill effects. It is,
however, so extremely probable as to be for practical purposes
certain, that water contaminated with the discharges from persons
suffering from certain diseases will produce similar diseases in those
who drink it, and there is also enough evidence that water containing
filth of various kinds either produces or promotes disease to warrant
much more attention to this subject than has heretofore been bestowed
upon it.
The chemical examination of a suspected water is by no means a simple
process, and in most cases had better be referred to an expert in such
matters. It is highly desirable, however, that the physician should
have sufficient technical knowledge to be able to make a rough
analysis at least, if for no other reason than that he may be able to
appreciate the results reported by the chemist. As a rule, when a
water is so polluted with decomposing organic matter as to be
positively dangerous it will have an unpleasant odor, which is best
developed by half filling a quart bottle with the water to be examined
and shaking it thoroughly. The so-called simple and ready methods
which are from time to time advocated in the newspapers, such as the
addition of sugar to the suspected water and allowing fermentation to
take place, the use of tannin as a precipitant, or the decolorization
of a solution of potassium permanganate, are really of very little
value and should not be relied upon. In the hands of an expert the
best simple method of determining the quality of a water is by
evaporation of a known quantity and the ignition of the solid residue.
From the amount of the total residue, the quantity left after
ignition, the amount of blackening produced, and the odor, a very fair
opinion can be formed as to the amount of organic matter present, and
whether it is of animal or vegetable origin.
It is not within the province of this paper to describe the methods
used by chemists in water analysis, of which the principal are known
as the Franklin and Armstrong, the Wanklyn, and the permanganate
methods. A careful examination of these methods has recently been made
under the direction of the National Board of Health, and a preliminary
note of the results, prepared by Professor Mallet, has been published
in the _Bulletin_. From this it appears that the chief value of
chemical analysis is, first, the verification of gross pollution,
which will usually be detected by the appearance and smell of the
water; and, second, in periodical examination of a water-supply to
detect changes from the normal or usual character of the water, which
may be taken to have a certain local standard of purity. Special
importance is attached to the careful determination of {184} nitrates
and nitrites in water to be used for drinking, these being the results
of oxidation of organic matters, and therefore giving evidence of
previous contamination.
Prof. Mallet concludes that "there are no sound grounds on which to
establish such general standards of purity as have been proposed,
looking to exact amounts of organic carbon or nitrogen, albuminoid
ammonia, oxygen of permanganate consumed, etc., as permissible or not.
Distinctions drawn by the application of such standards are arbitrary
and may be misleading." While this is perfectly true, considered from
the standpoint of scientific precision, it does not sufficiently take
into account the value of probabilities in these matters, considered
as motives to action. It is perfectly true that there can be no fixed
standard--that a water which the chemist would report as relatively
pure might be much more apt to produce disease than one which he would
pronounce impure--but it is nevertheless true that from the results of
chemical analysis, taken in connection with evidence as to the source
and history of the water, an opinion can be formed as to the danger
from its use which is sufficiently reliable to be acted upon in the
absence of positive evidence, such as the production of disease.
In many cases the matter must be doubtful, and Prof. Mallet truly says
that it will not do in all such cases to forbid the use of the water,
for it often happens that this should not be done unless it is
absolutely necessary; but there are many other cases in which there is
very little doubt, and where action should be governed by the
probabilities.
The microscopical examination of suspected waters sometimes gives
decided indication as to the nature of the impurities; and it may be
that hereafter, in connection with physiological tests, it will become
of even more importance than the chemical. To determine the presence
of organisms in a sample of water the best method known at present is
to kill and coagulate them by means of osmic acid or chloride of
platinum, and allow them to subside. This method is of course
inapplicable if it be desired to use them for either culture- or
inoculation-tests.
Chemists have no uniform system of reporting the results of their
analyses, some using grains per gallon, U.S. or Imperial as may be,
and others parts per hundred thousand or per million of the water. It
is therefore difficult to appreciate the value of the figures as given
by them. The following, in parts per 100,000, will enable the
practitioner to form a general estimate of the character of analytical
reports; but the opinion in individual cases is so modified by the
coincident amounts of chlorine, ammonia, nitrous and nitric acids,
that the experienced sanitarian only is qualified to put on the
results an estimate which shall be in accordance with our present
knowledge of such matter:
_Upland Surface-Waters_.
Allowable. Doubtful. Impure.
Total organic elements to .4 .4 to .6 Over .6
Oxygen required to .3 .3 to .4 " .4
Albuminoid ammonia to .015 .015 to .025 " .025
_All Other Waters_.
Total organic elements to .2 .2 to .4 Over .4
Oxygen required to .15 .15 to .2 " .2
Albuminoid ammonia to .010 .010 to .015 " .015
{185} In connection with impure water should be mentioned impure ice.
Ice is purer than the water from which it forms, but if cut on a foul
pond it will itself be foul, and the vitality of some microscopic
organisms is not destroyed by their being frozen, as is shown by the
fact that samples from the centre of blocks of ice will inoculate
sterilized infusions with the germs of putrefaction, precisely as the
water of which the ice is composed would have done before it was
frozen. Disease has been traced to impure ice, and it may be that it
is more frequently due to this cause than has heretofore been
supposed; at all events, it is well to bear the possibility in mind.
The subject of impure water will be further considered in speaking of
habitations.
IV. CLIMATE.--The literature of the effects of different climates upon
the human body is very extensive, following the general rule that the
less positive or precise knowledge there is upon a given subject the
more will be written about it. Of all animals, man seems to adapt
himself most readily to the extremes of climate; and, although it is
commonly supposed that a tropical climate is injurious to those coming
from cooler regions, yet it has been found that where he takes the
same precautions to ensure cleanliness, pure water and air, and proper
food, the European does not have a higher rate of mortality in Algeria
or in the East or West Indies than he does at home, if the effects of
cholera and yellow fever be excepted.
Dr. Parkes defines the effect of climate upon the human body to be
"the sum of the influences which are connected with the solar
agencies, the soil, the air, or the water of a place;" in other words,
he makes it nearly equivalent to the locality or the environment. By
"climate" we understand, commonly, the sum of meteorological
influences, the most important of which, as regards health, are
temperature, humidity, and wind. The effects of temperature in
producing disease are often confounded with the effects of change of
temperature, which last is perhaps the more important of the two, and
should be specially borne in mind in advising climato-therapy for
chronic or wasting diseases.
The influence of climate in causing disease, although well known for
over two thousand years, has not led to much effort to avoid or
prevent effects which are accepted as inevitable by the great
majority. It is true that in the effort to secure physical comfort by
houses, clothing, artificial heat, and the like, much hygienic work
has been done, and the steadily increasing tendency on the part of all
who can afford it to seek rest and comfort at the seaside or in the
mountains during hot weather is no doubt due, in part, to the fact
that experience has shown that the money expended in thus securing
health and strength is a good investment. It is unfortunate that
"health resorts," so called, do not always prove to be such: they
become fashionable, overcrowded; the arrangements for the disposal of
excreta are cheap makeshifts, leading to soil- and water-pollution,
until finally an epidemic of diarrhoea or typhoid fever occurs, with
the usual results.
The consideration of climate as a therapeutic agent belongs with the
articles relating to the several diseases to which it is applicable.
The great desideratum wherewith to place this subject upon a
scientific and practical basis is a system of reliable returns of the
deaths, and if possible of {186} certain diseases, throughout the
country, and especially at those points most in vogue as health
resorts.
V. HABITATIONS.--That a man's health depends very much on the
character, condition, and location of his dwelling-place is now so
generally admitted that in many cases where a physician is called in
he will be asked whether he thinks the disease has been caused by any
peculiarity about the house or the bedroom of the patient. And a
careful examination will usually discover in one of them several evils
to be remedied, although their connection with the case in hand may be
very doubtful. There are very few homes properly constructed from a
sanitary point of view; and, although we may not agree with Dr.
Wilson, that "the modern prison is in all sanitary essentials the best
existing type of what a healthy dwelling ought to be," it is
nevertheless certain that the health of the inmates is much more
carefully consulted in planning a penitentiary than it usually is in
planning a college, a hotel, or a dwelling-house. Matters are
gradually improving in this respect: the worst of the tenement-house
rookeries and fever-nests in most of our large cities have been
improved or abolished, and our wealthier citizens are beginning to pay
some attention to their house-drainage as well as to the pattern of
their mantelpieces. But the great majority of men are still careless
and negligent as to the sanitary condition of their homes, and
probably two physicians out of three live in houses in which numerous
defects would be pointed out by a sanitary engineer--defects of which
they are themselves more or less aware. The majority of people in our
large cities under existing conditions cannot afford to have healthy
houses, and the great causes of the excessive mortality, and brevity
of life, in all such cities, are poverty and overcrowding, the latter
resulting from the former. The problem as to the best mode of
improving the sanitary condition of the tenement-house population does
not, however, come before the practising physician for special
consideration, and need not be considered here. Nor is the physician
liable to be consulted with regard to the sufficiency, from a sanitary
point of view, of the plan of a house yet to be built, although he
will occasionally be asked as to the healthfulness of a proposed site.
The questions which he will be asked are such as the following: "Is
the cause of this particular case of disease in the house, or
connected with it? and if so, what is it?"--"Do you think this is a
healthy house?"--"Is the location a healthy one?"--"Is it necessary
that I should give up this house to preserve the lives and health of
my children?" While it is, of course, often impossible to answer with
precision such questions as these, an answer of some kind must be
given; and this should not be a mere random guess, but based on a
deliberate estimate of the probabilities in the case. The
healthfulness of a house is to be judged of, in part, from its
history, if it be possible to obtain any; in part, from such facts as
can be discovered by a careful examination of the premises and
vicinity. The sanitary history of a house is the history of the
diseases and deaths which have occurred in it, together with a set of
plans showing the precise location and character of the house-drainage
and of its fresh-air supply. Such a record is in most cases,
unfortunately, not attainable, although to a person proposing to buy
or rent a house it would often be quite as important as a record of
title. In a well-organized health-office it should be possible to
ascertain the number and causes of the deaths which have {187}
occurred in any given house or square in the city, and also the
character and location of its drainage and sewer connections. Such
records are especially valuable in an investigation of an outbreak of
disease in a community.
The sanitary inspection of a house includes the site and the building
itself. The character of the site is mainly determined by its dryness,
by the presence or absence of organic matter in the soil, and by its
porosity taken in connection with the character of the vicinity.
One-third of the volume of some soils consists of air, and all dry
soils and rocks contain a much larger quantity of air than is commonly
supposed. The influence of soil upon health is exerted mainly through
the media of water and air, but it also affects temperature and
vegetation, being an important factor in climate. Residence on a damp
soil has a tendency to produce diseases of the lungs, and especially
phthisis; but how it does this is unknown, though it would be easy to
construct a plausible theory in connection with the supposed causation
of phthisis by a bacillus. The practical point for the physician is,
that the prevalence of phthisis in a locality, even if it be so
limited as to comprise but a single house, should cause suspicion and
investigation as to the character of the soil-drainage. Soil-moisture
is also an important factor in the development of periodical fevers,
and the effect of thorough drainage in diminishing malaria is now
generally understood.
It sometimes becomes an important question as to the influence which a
collection of water, such as a mill-pond or a reservoir, has upon the
health of a community, and the physician may be called on for an
opinion in such cases where large property interests are involved. The
essential points to be borne in mind are--first, that stagnant water
and damp soil do not in themselves produce malaria; there is something
else necessary, which is commonly designated by the word "germ."
Second, that they are in most cases essential conditions for the
production of the disease, so that if removed the disease will
disappear. Third, that the development of malaria may follow either
the rise or fall of the ground water. Fourth, that the condition of
the border of the collection of water as to presence of organic matter
and moisture is of more importance than the pool itself. And, finally,
that each case is a problem by itself, to be determined by the history
of the sickness of the vicinity, and that only probabilities can be
stated in any case, although these probabilities may be so great as to
amount, practically, to certainty. Of the four factors which appear to
be essential to the production of the malarial poison--viz. moisture,
high temperature, organic matter of vegetable origin, and certain
micro-organisms--the first is the one which in any given locality is
most under human control; it is the link in the chain of causation
which is most easily broken.
The influence of the rise and fall of the soil water in typhoid fever,
upon which so much stress is laid by Pettenkofer and others, no doubt
exists, acting in some cases through pollution of the drinking water
by the subsoil water leaking through a polluted soil; in other cases,
perhaps, by air from the soil bearing the unknown germ. The filtering
power of soil as regards air is, however, very great, a few inches of
sand being sufficient to remove the ordinary germs of putrefaction
from air drawn through it, and this for a long period; while, on the
{188} contrary, many feet of the same sand will not remove the germs
from water passed through it. Usually, as Dr. Parkes remarks, in an
examination of soil the immediate local conditions are of more
importance than the general geological formation, yet this last, as
influencing conformation and the movement of water and air over and
through a country, is also important. The practical questions on this
point are, what higher ground than the site in question exists in the
vicinity? what are the character and direction of the strata between
such elevation and the site? and, what sources of soil-pollution exist
on the higher level? As to the site itself, is it on made ground? what
is the height of the foundation above the subsoil water? and, what
precautions have been taken to secure drainage and to cut off
communication between the interior of the house and the ground air?
Probably a trial excavation or boring may be necessary to determine
some of these points.
The level of the subsoil water should be at least five feet below the
foundations, although it is often impossible to obtain this. At all
times when the temperature of the house is higher than that of the
external air--_i.e._ during a large part of the year and nearly every
night--there is a strong and constant aspirating force at work to draw
into the house, through the cellar floor and walls, all gases and
vapors contained in the adjoining soil. If this soil contains a large
proportion of organic matter, as is often the case in filled-in ground
in cities, or if there be a leaky cesspool or sewer or gas-pipe under
or near the house, the ground air passing into the house may be of
such a character as to be positively dangerous to its occupants. For
this reason it is very undesirable to have a sewer or soil-pipe
crossing beneath the site of a house, and when such location is a
necessity, as it often is in cities, the soil-pipe should be laid in a
cement-lined trench covered with a movable flap, so that it can always
be easily inspected and any leaks detected and remedied. Dampness in
the cellar or basement of a house is always a sign of danger. The
exhalation of gases and vapors from the ground into the house can be
to a great extent cut off by a layer of impervious material, such as
concrete covered with asphalt, but this layer must cover the sides of
the cellar as well as the floor to be thoroughly efficient. If a house
have no cellar, the space between the floor and the ground should be
thoroughly ventilated; and for this purpose, as well as to secure
cleanliness, the floor should be sufficiently elevated to permit of
easy access beneath it.
Next to its dryness, the nature and condition of the arrangements for
removing excreta and soiled water from a house are of the greatest
importance in determining its healthfulness; and in cities it is with
regard to the sufficiency of these, including the whole system of
house-plumbing and pipe-fitting, that the inquiries of one wishing to
determine as to the presence or absence of causes of disease will most
frequently be directed. The soil-pipes, etc. of a house are commonly
referred to as constituting the system of house-drainage, but it is
desirable to use another term, for we need the word "drainage" to
describe the removal of surface and subsoil water, and it should be
distinguished from "sewerage," which has a different purpose and
requirements.
In a properly-arranged system of house sewerage all the pipes, traps,
etc. are easily accessible for purposes of inspection, and an
examination of them is a comparatively simple matter. This examination
is to be {189} made with reference to the following points: 1. Are all
the pipes, joints, and connections air-tight? 2. Is the soil-pipe well
ventilated, or has it dead ends? 3. Is the communication between the
soil-pipe and the street sewer uninterrupted? 4. Are the pipes
properly trapped, and is there liability to the removal of water from
any of the traps, either by siphonage or evaporation, to such an
extent as to break the seal? 5. Is the water-supply of each closet
entirely cut off from the main supply to the house by means of a tank
or cistern?
In houses as heretofore constructed it is often very difficult to
obtain satisfactory information upon these points, because a large
part of the soil-pipe and its connections is buried beneath the house
or concealed in the walls or floors; in which case the services of a
skilled mechanic will usually be necessary to obtain access to the
various parts of the system. In a paper of this kind it is of course
impossible to go into details as to methods of inspection, or as to
what is and what is not satisfactory; but the following are the
general principles upon which a judgment as to the merits of a system
should be formed, and these should be so clearly understood by every
physician that he can be neither persuaded nor frightened into
thinking them incorrect by the eloquence of the man with a patent
remedy to dispose of. The principal dangers to health from house
sewerage are due, first, to the passage of air from the general system
of sewers or from a cesspool into the house through the soil-pipe and
its connections; second, to the generation of offensive and dangerous
gases and organisms in the soil-pipe itself, and the passage of these
into the house; third, to leakage of soil-pipe causing contamination
of the water-supply either by improper connections of water-pipes with
water-closets or slop-hoppers, or by contamination of wells, cisterns,
or tanks with sewage or sewer gases.
There is, of course, no such thing as a sewer gas having a definite
and distinctive composition, and the nature of the mixture of gases in
sewers is constantly varying according to season, temperature, etc.
The tendency which sewer air has to cause disease depends in part upon
certain gases, in part on minute particles of solid or semi-solid
matter which are suspended in the air. In rare instances the sewers
also contain illuminating gas, derived from leakage of gas-pipes in
the vicinity. These gases produce debility, headache, loss of
appetite, etc. As found in sewers and soil-pipes, they are so diluted
that they are not absorbed by the water of a trap and given off on the
other side to a sufficient extent to produce an evil effect. The air
in a soil-pipe which is not ventilated is much more impure than that
of the ordinary sewer, since the process of decomposition is
constantly going on in the slimy coat which lines the interior of the
pipes; and it is for this reason that it is so important to secure
thorough ventilation of all the soil-pipes in a building. When this
ventilation is secured, the proportion of dangerous gas in the pipes
becomes very small, and the amount absorbed by the water in traps is
almost inappreciable. The chief danger to life from sewer and
soil-pipe air arises from the presence of minute particles of organic
matter, dead and living, the so-called germs. Danger to life from
these germs cannot be entirely removed by dilution, as can be done
with gases. It has been found by the experiments of Dr. Carmichael and
Dr. Wernick that an ordinary water-trap entirely prevents the passage
of these germs, and that organic putrescible fluid will remain
unchanged when exposed only to the air immediately {190} above such a
trap. A pin-hole or minute sand-crack in the soil-pipe, or a very
slight defect in a joint, is far more dangerous than a trap.
The forms of disease produced by sewer air and its contents are more
especially diphtheria, typhoid fever, and ill-defined disorders of the
throat and digestive organs. It is possible that the germs of other
specific diseases, such as scarlet fever, may be at times transmitted
through sewer air, but such transmission must be very rare. While it
is true that the germs of the specific diseases are very rarely
present in sewer air, the house system of sewerage must be arranged as
if they were always present, in order to obtain security. It must also
be remembered that a system originally well planned and properly
constructed will not always remain so; the pipes will corrode, the
joints will become loosened, the valves will become clogged, and
whenever alterations or repairs are made there is always danger of
injury. Bearing these points in mind, the method of investigating a
system can be readily understood.
The first step is to ascertain whether there is a trap outside the
house disconnecting the sewer from the house system and permitting
inspection. If there is not, the first thing to be done is to make an
excavation and open the drain at the proper point for placing such a
trap. The next step is to set the water flowing in the various closets
and watch the flow at the external trap, or opening, which has been
made to ascertain whether there is any obstruction in the pipe within
the house. If the sewer is properly arranged for inspection, as has
been above suggested, to determine whether there is any leakage from
the sewer under the house will be an easy matter; if, however, it is
buried beneath the cellar floor, as is usually the case, an excavation
should be made along the floor in the line of the pipe, with a view to
having it properly arranged, as well as for the purpose of examining
the soil. It may also be tested by opening the upright soil-pipes at
the farther end of the house-drain at the height of three or four feet
above the floor and pouring water into it, having temporarily stopped
up the drain at the external trap or opening. If the water remain at a
constant level in the upright piece, the sewer is water-tight; if not,
the leakage may be ascertained by the rate at which it sinks. Having
settled this, the next point is to determine whether all the
soil-pipes are air-tight and properly trapped. The test usually
applied for this purpose is the pouring of a small quantity of strong
oil of peppermint, followed by a dash of hot water, into the top of
the soil-pipe, which should always pass through the roof and be freely
opened to the outer air. If the odor of the oil is perceptible in the
house, it indicates a leak, which must be further sought for. Ether
may be used for the same purpose. The smoke test is, however, the
best, but it requires a special apparatus which as yet is little used
in this country. It is applied by a small machine with a fan, by which
the smoke from burning cotton-waste saturated with oil, or of coarse
brown paper impregnated with sulphur, can be blown into the pipes;
this locates leaks with great precision.
It is not, of course, expected that a physician will personally make
the examination necessary to determine whether the plumbing of a house
is in good order, but he should be able to make it, if necessary, if
for no other purpose than to know whether the inspector employed for
the purpose understands his business.
The dangers to health from a properly-constructed system of house
{191} sewerage, such as is now generally agreed upon by sanitary
engineers, are so very small as to practically amount to nothing,
being, in fact, less than those of a well-kept yard privy of a country
house, setting aside altogether the question of water pollution. The
real difficulties in the way are the expense of such a system, which
is considerable, and the finding of skilled and honest workmen to
construct it and keep it in repair. Not every one who chooses to style
himself a sanitary engineer or a sanitary plumber is to be regarded as
such, by any means, but the physician should make it his business to
know who are really reliable in this respect, for he will constantly
be called in for advice on this point by those who have learned that
good plumbing is the only true economy, but who do not feel themselves
competent to distinguish between good and bad work. The main points of
a satisfactory system are the following.[3]
[Footnote 3: For further details consult the following: _American
Sanitary Engineering_, by E. S. Philbrick, N.Y., 1881; _House-Drainage
and Water-Service_, by James C. Bayles, N.Y., 1878; "House-Drainage
and Sanitary Plumbing," by W. P. Gerhard, in _Fourth Annual Report
State Board of Health Rhode Island_, 1882; _The Sanitary Engineer_, a
weekly journal published at 140 William St., New York City.]
1. All soil- and waste-pipes should be extended up to and through the
roof, and be freely open at the top. The extension of the soil-pipe
should be full size--_i.e._ from four to six inches in diameter.
2. There should be a fresh-air inlet in the house sewer just outside
the house, and between this inlet and the main sewer should be a trap
so arranged as to permit of inspection. This prevents the ventilation
of sewers through the soil-pipes. If a perfect system of sewers,
uniformity of house-connections, and uniform height of houses could be
guaranteed, this inlet and trap would not be so necessary, although
even then it would be useful.
3. Every water-closet, wash-bowl, bath-tub, sink, etc. should have a
trap placed as close to it as possible. This trap is desirable,
whether the discharge be into the sewer system or not. For example, a
kitchen sink, the pipe from which passes to the outer air and
discharges there, should be trapped, for this pipe is foul, and if it
be untrapped will act as an air-inlet.
4. The nearer to the soil-pipe that the fixtures can be arranged the
better. It is especially desirable to avoid the necessity for long
horizontal waste-pipes from stationary waste-bowls and from bath-tubs.
5. Bell traps, D traps, bottle traps, and mechanical traps are
objectionable. The S trap is, upon the whole, the best, but it should
be provided with a vent-pipe to prevent siphonage.
6. The best kind of water-closet for general use is probably some form
of what are known as the wash-out closets. They are made in one piece
of earthenware, have no machinery inside them, have a quantity of
water in the basin into which the excreta drop, and do not require a
separate trap beneath them. Each closet must, however, be carefully
tested by itself: a very small warp or twist produced in the baking
may so interfere with the siphonage as to make it practically
worthless, and the basin cannot be altered or repaired. For use in
public places some of the hopper closets are very satisfactory, the
best which I have examined being the Rhoads Hopper and the Hellyer
Hoppers. Where there are no {192} children, and it is certain that the
fixtures will be used with reasonable care, valve closets may be used.
No form of pan closet can be considered as satisfactory, nor have I
found any form of plunger closet that I would specially recommend.
7. Water-closets should always be flushed from a special tank provided
for the purpose, and never direct from the main system of water-pipes.
The flush must be large and rapid, and this requires a large
supply-pipe, and for many forms of closets a flushing rim. Whatever be
the form of closet, it should not be encased in a wooden box or
closet, as is usually done, but it should stand freely exposed to
light and air. Sanitarians commonly advise that water-closets should
be located in outer walls and have an open window for ventilation.
Such a position is usually impossible, and is not specially desirable
in our climate. The open window acts as an inlet quite as often as it
does as an outlet, and the air of the closet is thus swept into the
house. The room should be ventilated in such a way that the tendency
of the air at the door shall always be from the house into it. This is
to be effected by a shaft passing through the room up and through the
roof; and it is well to have this shaft take its air-supply from just
behind the closet or from beneath the seat. It is best made of
galvanized iron, and at a convenient point should be expanded into a
lantern and have a gas-jet placed in it. The air-supply for the closet
is to be taken at the bottom of the door or through a transom or
louvres. Ventilating pipes from a water-closet should never be run
into a brick flue. While it is not so important as many writers seem
to think that a water-closet should be placed on an outer wall, it is
very important that it should be as light as possible, and the placing
it in a dark corner in the basement or under the stairs is very
objectionable.
8. No overflow-pipe from any cistern or tank, except the one used for
flushing water-closets, should be connected with the soil-pipe or
sewer. Trapping such an overflow-pipe does not prevent the danger. The
same rule applies to waste-pipes from refrigerators and to the
waste-pipes from the safes which are commonly placed beneath fixtures.
9. Grease-traps placed inside a house--for instance, beneath the
kitchen sink--are of very doubtful expediency, and if they cannot be
placed outside, they had better not be used at all.
In an unsewered city one of the first things to be considered in a
sanitary inspection is the manner in which the sewage of the premises
is disposed of. The question is, however, by no means superfluous in
many sewered cities, for cesspools and vaults are to be found in most
of them, and not only in yards, but beneath houses, and houses of the
better class. A privy-vault or cesspool beneath a dwelling or near its
cellar walls is always to be considered as very dangerous, for it is
practically impossible to prevent the passage of gases from it into
the interior of the house. A cesspit is a dangerous thing anywhere,
even in the country; but in a city it is so dangerous that its
existence should not be permitted.
If the water-supply of a house is derived from a well, and there is
reason to suspect that this may have been contaminated from a
neighboring privy-vault, the first test to be applied to the water is
that for the detection of chlorides. If none are present, the water is
not polluted. If they are present, the quantity is to be noted, and a
peck or two of common salt is then to be thrown into the suspected
vault. If repeated {193} examinations of the water show a marked
increase in the amount of chlorides present, it may be inferred that
the contents of the privy pass to the well. The fact that the water of
infected wells and springs is usually much liked and sought for is to
a considerable extent due to the presence of these chlorides. Wanklyn
recommends the addition of 50 grains of common salt per gallon to
drinking water to render it palatable. Popularity of a certain well is
therefore a reason for suspecting its purity.
This subject may be dismissed with one caution. Taking the
dwelling-houses of a city or town as they come, it will be found on
examination that over half of them would be described by a competent
inspector as being in a condition which might produce disease. It is
therefore more than an even chance that in any case of disease some
sanitary defect will be found about the premises quite irrespective of
any direct causal connection with the case. Let the physician
therefore be cautious in deciding as to such causal connection, and
not conclude that because a case of diphtheria or typhoid fever and a
leaky soil-pipe occur in the same house, therefore one is the cause of
the other. Such cases occur in houses whose sewerage is perfect and in
houses which have no sewerage, and it is folly to attribute them
exclusively or mainly to sewer gases.
The same caution applies to investigations into the causes of a sudden
outbreak of disease in a community where a number of cases occur
almost simultaneously or in rapid succession. Such an outbreak may be
due to direct contagion, although sometimes very difficult to trace;
as, for example, an explosion of small-pox in a community largely
unprotected by vaccination, and where, owing to circumstances
connected with the first few cases, a large number of persons have
been exposed to the cause about the same time. The same applies to an
apparently sudden development of yellow fever throughout a city.
Another cause of such outbreaks is a polluted water-supply, as in some
epidemics of diarrhoeal disease or of typhoid fever. If the outbreaks
of these diseases are pretty sharply localized, and depend upon the
fouling of a well or wells, it will usually not be very difficult to
trace this cause. If, however, the town has water-supply by means of
pipes from a single source, while the outbreak of disease is limited
to a part of the town or to a single large building, it will probably
be almost impossible to establish any connection between the disease
and the drinking water. The possibility of the contamination of a part
only of a system of general water-supply by means of the drawing of
foul air into the temporarily empty pipes connected directly with a
water-closet flush should never be forgotten, for such a case has
actually occurred, and the account of its discovery is one of the best
pieces of sanitary detective work with which I am acquainted. If the
outbreak of typhoid fever cannot be traced directly to the
water-supply, the next point to be investigated is the milk, and after
that other possible modes of the conveyance of the contagium.
In cases of obscure disease characterized by fever of no definite
type, disorder of the digestive organs, headache, malaise, etc., and
which seem to be connected with residence in a particular house or in
one room in a house, the possibilities of arsenical poisoning from
wall-paper or hangings should be remembered, for much useless
medication and some real danger will be avoided if this cause be
promptly recognized. The effects {194} produced by arsenical dust are
very various, and simulate sometimes some of the specific fevers,
indigestions, or neuroses in a way that is very puzzling if the true
nature of the case is not suspected. The popular notion is that
arsenic is found only in greens (more especially in bright greens in
wall-papers), whereas in fact it is found not only in dull greens, but
in some browns, grays, and dull reds. The test for its presence in
quantity sufficient to be a cause of disease is an easy one, and is
fully given in any manual of chemistry or toxicology.
VI. OCCUPATION.--While the effects of occupation upon health are no
doubt great, they are in many cases so blended with those of condition
in life, including habitation, food, and intemperance, that it is very
difficult to distinguish them. In attempting to investigate these
effects by means of statistics, it is necessary to beware of a fallacy
which not unfrequently vitiates the conclusions drawn from otherwise
carefully prepared tables intended to show for different occupations
either the relative mortality or the average age at death. This
fallacy lies in the fact that the number of persons engaged in each
business is unknown; that, in this country at least, men often change
their occupations; and that certain trades or professions are chiefly
carried on by persons of certain ages. This last is perhaps best
illustrated by the remark of Dr. Farr, that the fact that the average
age at death of second lieutenants is much less than that of
major-generals proves nothing with regard to the comparative
healthfulness of the two grades. Statistics showing merely the number
of a particular class or grade dying in a given time are absolutely
worthless, unless the number of the same class or trade living at the
same time is also given.
It is also necessary to bear in mind the power of habit and the
effects of natural selection, especially when the effects of an
unhealthy occupation are immediate and marked upon those unfitted for
them. For example, young men, when first employed as scavengers or in
sewage-pumping works, usually suffer from disorders of the digestive
organs. A certain number find it necessary for their health and
comfort to soon leave the business; some acquire protection by passing
through an attack of fever; and by this process of selection a class
of men are obtained who seem to thrive in the midst of filth and
remain unaffected by effluvia which will promptly cause illness in
those unaccustomed to them. When men find that, to use a common
phrase, they "cannot stand" a particular kind of work, they are apt to
give it up and try something else, especially if the effects are
prompt and well marked.
Much attention has been given of late years in England, France, and
Germany to the means of protecting both the workmen and the
neighborhood from the ill effects of dangerous and offensive trades,
and the reports of the medical officer of the Privy Council and of the
Local Government Board are a mine of information on this subject. It
may be truthfully asserted that in those trades in which the special
danger is caused by dust of various kinds, or by gases, or by metallic
poisons--and these three include the greater number of the dangerous
occupations--it is almost always possible to so arrange the work as to
make it comparatively healthful and harmless. Overcrowded and
unventilated workrooms are responsible for much disease, and when to
these is added the risk of metallic poisoning, as is the case with
printers, artificial-flower {195} makers, etc., bad results are almost
sure to follow. It is curious that so comparatively little ill effect
seems to be produced by exposure to great heat, as in stokers,
foundry-men, glass-blowers, etc.; but further information is needed on
this point as to the real facts in the case. In some occupations the
chief evils arise from want of out-door exercise, a subject which will
be considered presently. The want of useful or interesting occupation
sometimes becomes indirectly the cause of disease among the wealthier
classes, and the giving a man or woman something to do is in such
cases the best prescription which can be made. This danger is
especially apt to occur in the case of an active, energetic man who
retires from business, intending to spend the rest of his life in
pleasure and in the enjoyment of the fruits of his industry: the
preventive or remedy is obvious.
VII. FOOD.--The comfort, energy, usefulness, and moral character of a
man depend largely upon his digestion, and this in turn depends
largely on what it has to act upon--viz. food. There are, it is true,
many men who boast that they can digest anything, and who are really
comparatively indifferent as to the kind, or mode of preparation, of
the food set before them, so that the quantity be sufficient; but were
it not that habit and heredity--which is the family habit--combine
with natural selection to adapt men to their food, it is probable that
the frying-pan, the pie, and soda-bread would depopulate large
portions of this country. As it is, there can be no doubt that fried
food swimming in grease, leathery, sodden pie-crust, and heavy bread
tend to make life short and the reverse of merry; and when the effect
of these is combined, as it often is, with those of malaria, damp
soil, and a free use of whiskey, the result is plenty of work for the
doctor and very little to pay him with. This state of things is being
gradually improved, but in all classes of society and in almost all
parts of the country the rule is, that while the raw materials of food
are abundant and of excellent quality, the cooking is bad. This is
due, in part, to an idea that it is to a certain extent discreditable
to a person that he should give much attention to his food, at least
so far as its appearance and taste are concerned, and that a man who
can plan a good dinner must be more or less of a sensualist and a
glutton.
Another popular error is, that a large amount of disease is due to
overeating, and that abstemiousness in diet is either certain to
secure health, or is, at all events, indispensable for this purpose.
Upon this point the reader should consult a capital paper by Dr.
Austin Flint on "Food in its relations to personal and public health,"
which will be found in vol. iii. _Reports American Public Health
Association_, N.Y., 1877. After remarking that many of the popular
errors about food and diet are relics of old and abandoned medical
theories, one of which is embodied in the not uncommon advice that one
should always stop eating before the appetite is fully satisfied, and
that food should only be taken at regular fixed periods, no matter how
hungry one may be, he says: "Physiology, experience, and common sense
are alike opposed to these popular notions relating to food.
Conditions for perfect health are, first, a sufficient appetite;
second, the gratification of normal appetite before the want of food
reaches the abnormal degree expressed by hunger; third, the
satisfaction of appetite by an adequate quantity of food. These
conditions of health are fulfilled by compliance with instructive
provisions for {196} alimentation. But, it will be asked, is appetite
infallible as a guide in dietetics? Following it as a guide, is food
never taken beyond the requirements of health? I answer, It is a
reliable guide under normal circumstances. The inevitable
circumstances of life are often not altogether normal, although
producing no distinct morbid affection. Experience teaches, for
example, that in a state of fatigue or exhaustion (which is not a
normal state) inconvenience may arise from the full gratification of
appetite; that if unusual exertions, mental or physical, are to
follow, a hearty meal may occasion disturbance; and other examples
might be added. Irrespective of abnormal or disturbing influences, if
appetite be not infallible, it is, at all events, more reliable than a
rule based on theoretical ideas, popular notions, or on purely
physiological data. Moreover, it was evidently not intended that the
quantity of food should be accurately adjusted to the needs of the
economy. To do this is impossible, and therefore it is necessary to
elect between the risk of taking either more or less food than is
actually required. Which is to be preferred? Undoubtedly, it is vastly
better to incur the risk of taking too much than that of taking too
little. Nature provides for a redundancy, but there is no provision
against a persistent deficiency. Ex nihilo nihil fit. An ample supply
of alimentary principles is indispensable to nutrition; and inasmuch
as the supply cannot be made to contain precisely the needed amount of
the different alimentary principles, we may say that a superabundance
of food is a requirement for health.
"As in appetite we have a guide in respect of the times of taking food
and the quantity to be taken, so taste is a guide in respect of the
kinds of food required. The discrimination of food with reference to
the wants of the system is the evident purpose of the sense of taste,
and the enjoyment connected with this sense was designed to afford a
security, in addition to appetite, for adequate alimentation.
"Among professional men and those who live sedentary lives the mistake
is not uncommon of paying too much attention to the sensations after a
meal, and deciding therefrom whether certain articles of food are
unhealthy or not. If the man who does this is not already dyspeptic,
he will pretty surely become so. The remedies in this case are
exercise and attracting the attention to something else."
A physician ought to understand something of cooking, and a short
course of practical instruction in what might be dignified as the
culinary laboratory would be of more real value to him than some of
the branches which are now considered indispensable in the medical
curriculum. He should know why oysters are the best thing with which
to begin a dinner, and why a cocktail is one of the worst; how to make
a salad, or a cup of good coffee, or a perfect consomme; and a number
of other things pertaining to gastronomy of which most people are
woefully ignorant.
It is not within the scope of this paper to give details with regard
to the diet of either the sick or the well, but it seems proper to
remark with regard to the feeding of infants, more especially in our
large cities in the summer months, that all the various patent
preparations for infants' food are more or less pernicious, and should
be discountenanced by all medical men. The proper food of an infant is
milk--human milk if it can be had, cow's milk if it cannot. If it be
remembered that an infant suffers {197} from thirst as well as hunger,
and care be taken to give it enough pure cool water to quench this
thirst, it will be found that in most cases it will thrive on pure
cow's milk.
With regard to adulterations of food, the only form of such
adulteration found in this country, which has any special interest
from the sanitary point of view, pertains to milk. This adulteration
is in most cases the dilution of the milk by water, and this is very
common in large cities. The danger from the use of such milk is by no
means confined to infants, and it is probable that a larger proportion
of the typhoid fever, diphtheria, scarlet fever, cholera infantum, and
diarrhoeal diseases in our cities is due either directly or indirectly
to the milk-supply than is now even suspected. The possibility of this
mode of origin should always be borne in mind in investigating the
causation of such affections.
A very large amount of food is now furnished preserved in tin cans,
and it is almost invariably of excellent quality. There is a
possibility of the contamination of such food by the salts of lead or
tin, but such contamination to an extent which is injurious to health
must be so extremely rare as to be hardly worth considering. The
danger from the entrance of parasites, such as trichinae, etc., in the
food is also extremely small--in fact, is nothing where the food is
properly cooked.
Milk has so often been the cause of disease, and is so universally
used, that it seems worth while to refer to it again. The special
aptitude of milk for absorption of odors has long been known, and of
late years it has been clearly proven in a number of instances that
milk has been the means of conveying the cause of typhoid fever and of
scarlatina. Diphtheria, yellow fever, and intermittent fever have also
been supposed to be conveyed by milk. The variety of nutritive
principles contained in milk, which makes it so valuable as a food,
also gives it the power of sustaining many different sorts of minute
organisms, and it perhaps comes as near being a universal
culture-fluid as anything yet devised for that purpose. The
possibilities of the contamination of milk are so numerous, and
especially in the case of that furnished from small establishments,
that, in the case of outbreaks of typhoid or diarrhoeal diseases in a
town, investigations into causation should always include the milk- as
well as the water-supply. Milk from diseased animals is no doubt often
used without producing bad results, but its effects in conveying to
man the disease known as milk-sickness are well established, and it
has also been known to produce symptoms of the contagious aphthae, or
foot-and-mouth disease, in man, when derived from an animal affected
with that disease. The only danger in the use of the milk of animals
fed upon sewage-grown grass appears to be in the possible
contamination of the milk, after it is drawn, by particles of dust in
the stable, derived from the food or litter of the animal or from
uncleanliness of the exterior of the udder, etc.
VIII. INTEMPERANCE.--Every one knows that alcoholic drinks are the
cause of a vast amount of disease, crime, and misery in all civilized
countries. No one knows how this is to be prevented, for no one knows
how to make the great mass of the people wise and contented. The
effects produced by excessive use of alcohol are well known to all
physicians, and the remedy is self-evident. I see no use in adding to
the heap of useless rubbish which exists in the shape of the great
mass of existing {198} popular literature on this subject, and
therefore leave the subject to the reader, who is quite sure to know
all that is really important on this subject.
IX. CLOTHING.--The hygiene of clothing is also a subject which may be
treated summarily in this paper. People wear what they can afford,
made according to the prevailing style. Diseases due to insufficient,
excessive, or badly-fitting clothing occur most frequently in women
and children, and the use of such clothing is for the most part due to
poverty or fashion, either of which is beyond the power of the
physician to successfully cope with. Here and there, in individual and
exceptional cases, he may be able to do a little good by advising
against tight lacing, high-heeled shoes, insufficient covering for the
chest or legs, etc., and he will find that a knowledge of the
peculiarities of the various styles of modern under-clothing will
sometimes be very useful. Men are, as a rule, comfortably and sensibly
dressed to suit their business and surroundings, and require no advice
on this subject.
X. EXERCISE.--The ease and completeness with which the functions of an
organ or of an organism are performed depend to a great extent upon
the frequency and regularity with which such functions are exercised.
Hence comes the importance of bodily exercise for the preservation of
health, and every physician meets cases of disease due largely to want
of work.
The term "exercise," or "bodily exercise," is commonly used as if it
referred only to the muscles, and the amount of exercise which a man
should take in a day is stated as equal to a certain number of
foot-pounds. The mere giving work to muscles is not, however, exercise
in the sanitary sense. A better definition is that of Du Bois
Reymond--viz. that "exercise is the frequent repetition of a more or
less complicated action of the body with the co-operation of the mind,
or of an action of the mind alone, for the purpose of being able to
perform such actions better." From this point of view it will be seen
that exercise relates quite as much to the nervous system as to the
muscles. When, for example, a student takes a walk over ground with
which he is familiar, and is at the same time so deeply engaged in
thought as to be practically unconscious of what he is doing, only
being recalled to himself, it may be, by arriving at his own door, the
exercise which he has had is but partial and insufficient. Going to
the extreme, we can, as Du Bois Reymond remarks, conceive of a man
with muscles individually exercised until they were like those of the
Farnese Hercules, and yet who would be unable to walk, much less
execute more complicated movements; for the proper co-operation of the
muscles, which is effected through the nervous system, is quite as
necessary as the force of their contraction.
The amount of exercise which is necessary for health varies with the
individual and with age, season, etc., so that it is difficult to
state any general rule upon this subject; but if stated in terms of
muscular force only, the estimate of Dr. Parkes seems a fair
approximation--viz. that every healthy man ought to take daily an
amount of exercise equivalent to 150 tons lifted 1 foot, or a walk of
about nine miles. The majority of trades and bodily occupations demand
at least this amount of work, but in some of them the greater part of
the exertion is made only by certain groups of muscles, and they are
carried on in crowded and {199} ill-ventilated shops. Such workmen, as
well as all who are engaged in sedentary pursuits, require exercise in
the open air--exercise which will bring into play the unused muscles
and will break the train of thought of the professional man.
One of the most important questions with regard to physical exercise
is the extent to, and manner in, which it should be provided for in a
proper system of education. One of the latest and most instructive
articles on this subject is that by Du Bois Reymond in the "Physiology
of Exercise," a translation of which is given in the _Popular Science
Monthly_ for July and August, 1882. He divides the physical training
which is more and more becoming a part of modern systematic education
into three classes: The first, the turning, or gymnastics of the
Germans; the second, the Swedish system, in which the exercises are
limited to very simple though varied movements; and the English
system, or rather want of system, consisting largely of athletic games
and contests of various kinds. His objection to the Swedish system is
that, while it strengthens the muscles, it does not increase the power
over composite movements; in other words, it does not exercise the
nervous system. Naturally, he prefers the German system to any other,
although admitting that the English meets better the demands arising
from our structure. "Were the end masterhood in running, jumping,
climbing, in dancing, fencing, riding, in swimming, rowing, or
skating, then nothing could be more advisable than to practise equally
the necessary concatenations in the actions of the ganglion cells,
without pausing at the not practically applicable preliminary and
intermediate steps of the German turning."
From a sanitary point of view, the gymnasium, as usually located and
managed, is by no means equivalent to out-of-door sports and contests,
although it is often the best substitute for them. The form of
exercise most used by men whose occupation does not involve bodily
labor is walking, and next to this riding. Whatever mode be selected,
it is very desirable that it should be taken for some other object
than that of the mere making muscular exertion, or otherwise it will
soon come to be looked upon as an unpleasant task, the time spent upon
which is given grudgingly; and it will be partially or wholly
abandoned as soon as the immediate discomfort which induced its use
has ceased.
It is not an uncommon error among men engaged in mental work to
suppose that they can, and ought to, take the same amount of exercise
which gives good results in those whose occupations involve physical
rather than mental effort, or to think that the more exercise they
take the more study or writing they are equal to. This is a grave
mistake. Expenditure of brain-tissue is not to be repaired by muscular
exertion, but by sleep and food, and exercise in the fresh air
sufficient to produce appetite and sufficient weariness to ensure
restful sleep is all that is necessary. For a time it is true that the
student or writer who has a well-developed body can continue to burn
the candle at both ends, and win literary honors while also standing
high as an athlete; but this surely leads to physiological bankruptcy
in the end.
It is to be remembered that good muscular development is not
necessarily synonymous with health, and that strength is not a
guarantee against disease. And, while it is true that in this, as in
most other matters of individual hygiene, each man must to a great
extent be a law to {200} himself, and learn by experience what kind of
exercise and how much of it he requires, yet the physician can often
supply the motive which was wanting, or check undue effort. Exercise
for the sake of health and comfort is not an end, but a means; yet if
this means can be made to secure to the patient an end agreeable and
pleasant in itself, so much the better.
XI. CONTAGION AND DISINFECTION.--By "contagion" we mean the
communication of disease from one person to another, either by direct
contact or through some medium, such as air, water, etc. It therefore
includes "infection," which is now generally used as a synonym for it.
The so-called infective diseases of modern German writers
(Infections-Krankheiten) include, besides what are commonly termed in
English, contagious diseases, the so-called miasmatic diseases.
The characteristic of a contagious disease is its specificity; that
is, the disease transmitted is always the same in its essential
characteristics. It does not, however, follow that all cases of the
disease are equally liable or have the same power to transmit it; in
other words, the degree of virulence of the contagiousness is not an
essential characteristic. That the same disease sometimes spreads
rapidly and is very fatal, and at other times seems hardly to have any
contagious properties and is very mild, has long been noticed, and has
been attributed to an unknown something called the medical
constitution of the place--the constitution medicale of French
writers. The true cause is probably very complex, but in some cases,
at all events, it seems to be due to difference in the contagion
itself. If we suppose this contagion to be a minute organism, it is
easy to form a theory as to the cause of these differences, but there
is much careful experimental work to be done before we shall have
positive knowledge on this point. The results obtained by Pasteur in
attenuating the virus of chicken cholera and splenic fever indicate
one line which these experiments will take, and the researches of Koch
point out another.
The diseases which spread by contagion until they form epidemics are
those which have from the earliest times attracted the most general
attention, and which have given rise to organized efforts for
prevention--_i.e._ to public hygiene.
They are also the diseases which have given rise to the most bitter
controversies among medical men as to the means of their propagation
and the best methods of prevention. Plague, cholera, yellow fever, and
typhus are those with regard to which this difference of opinion has
chiefly occurred--one party considering their chief cause to be
contagion, or specific germs derived directly or indirectly from the
bodies of the sick; the second party declaring that they are due to
filth plus an unknown something, which is variously termed epidemic
constitution, pandemic wave, Providence, or _x_. The great majority of
opinions at present is in favor of the view that they are all
contagious, but not all, or always, contagious from person to
person--that they spread from infected localities, which localities
receive their infection from cases of the disease. The best means of
dealing with them under ordinary circumstances are now tolerably well
understood, and where these means can be commanded--as, for instance,
among troops in time of peace--epidemics of these diseases can be
stopped with great precision and promptness by isolation and
disinfection.
{201} By "isolation" is meant not only the separation of the sick from
the well, but the isolation of the infected locality or water-supply
until it has been rendered harmless.
By "disinfection" is meant the destruction of the specific causes of
disease, and more especially of the infectious or spreading diseases.
A disinfectant is not necessarily an antiseptic or a deodorant, nor
are these last necessarily disinfectants. The best practical
antiseptic for sanitary purposes is cleanliness; the best
disinfectants are heat, bichloride of mercury, sulphate of iron,
chloride of zinc, sulphurous acid, chlorine, sunlight, and pure air,
and, for yellow fever, cold. With our present very imperfect knowledge
of the nature of specific causes of disease which we wish to destroy,
we have no means of determining the presence of these causes in or on
an article of clothing or of furniture, or in a room or other
locality, except by the production of their specific effects on man or
by inductive reasoning; in other words, we can only say that it is
more or less probable that such causes are present. This makes it
necessary, or at least expedient, to employ disinfectants in many
cases where the presence of such causes is doubtful. The practical
difficulties are, first, to bring the disinfecting agent into such
relation with the causes of disease that it can act upon them, and act
upon all of them; second, to avoid unnecessary destruction or injury
of things which should be preserved. The majority of the causes of
disease upon which we wish to act by disinfectants are probably minute
particles of solid or semi-solid matter which are living, and may be
conveniently designated by the word "_germs_." In the presence of
moisture the destruction of the vitality of these germs can be
effected with comparative ease and rapidity, but when they have become
dried, or, as in the case of the bacilli, are in the form of spores,
it is a more difficult matter.
To illustrate the methods to be pursued and the precautions to be
taken, let us suppose the physician to be called on for directions as
to the management of a case of scarlatina, the object being to prevent
its spread. The first thing to be done is to get the patient in a room
by himself, and to leave nothing in this room which is not necessary.
Remove the carpet, curtains, and all stuffed or upholstered furniture.
Let the nursing be done, as far as possible, by one person only, and
do not allow others, and especially children, to enter the room, no
matter if they have had the disease. The danger of contagion depends
upon particles coming from the skin and mucous membranes. All excreta,
and more especially the sputa or discharges from the mouth or nose,
are to be treated as dangerous. The excreta should be received in
vessels containing a solution of sulphate of iron, one and a half
pounds to the gallon. All clothing, towels, bed-linen, handkerchiefs,
napkins, etc. should be placed in a solution composed of four ounces
of sulphate of zinc and two ounces of common salt to the gallon of
water as soon as they are not needed for further use. Especial care
should be taken that none of these articles are removed from the room
while dry, and while they are in the room, and before they have been
moistened, they should not be shaken or disturbed more than is
absolutely necessary. If for any reason the zinc solution above
referred to is not at hand--which should very rarely be the case--the
clothing, etc. should be placed in a bucket, tub, or boiler containing
enough scalding water to entirely cover them, and be removed {202}
from the room in this vessel. All such articles should be boiled at
least one hour.
No sweeping or dusting in the ordinary way is to be done in the room;
dust and dirt are to be removed by damp cloths, which are to be
treated like the bedding and clothing. The great object is to prevent
as far as possible the production of dust in the atmosphere of the
room. The entire body of the patient, including head, face, and limbs,
should be kept thoroughly anointed with camphorated oil, vaseline, or
some similar substance, and especial care should be taken in this
respect during the period of convalescence so long as any roughness or
desquamation of the skin continues. No toys or books which it is
desired to preserve should be allowed to remain in the room, and under
no circumstances should books or toys be borrowed to amuse the child
if they are to be returned. The best way to disinfect such articles is
to burn them in the room.
When the patient is fully convalescent and all desquamation has
ceased, cleanse him thoroughly with a warm bath and soap for four
successive days. If at the end of that time no roughness of the skin
remains, he may be dressed in clean clothes and taken from the room,
for he is no longer a source of danger. The room itself and the
furniture are then to be thoroughly cleansed and disinfected. The
ceiling and walls, if of ordinary hard finish, are to be scraped and
whitewashed. All woodwork should be rubbed with damp cloths and the
floor well scrubbed. Care should be taken to remove all dust from the
ledges over windows and doors. All the cloths used in this cleansing
process are to be burned.
If these directions have been carefully carried out, there is no need
for further disinfection. But if upholstered furniture has been
allowed to remain in the room, or other articles which cannot be
burned or scrubbed or soaked in the zinc solution, it may be desirable
to attempt to disinfect the whole room and its contents by means of
chlorine or sulphurous acid gases. Of these, sulphurous acid gas is
the cheapest, and upon the whole the best, but it must be used in
large quantity, and for a longer time than is customary, if it is to
be relied upon. For this purpose all openings into the room should be
closed, and pillows, mattrasses, upholstered furniture, and articles
which cannot be treated with the zinc solution should be opened, so
that they may be exposed throughout to the fumes. The sulphur should
be burned in an iron pan or pot, placed in a tub containing water or
upon a large surface of sand. About 18 ounces of roll sulphur should
be used to each 1000 cubic feet of space, and after twenty-four hours
12 ounces more should be burned and the room be then closed for
twenty-four hours longer, after which it may be opened and aired. In
case of death the body should at once be wrapped in a sheet thoroughly
soaked with the chloride of zinc solution, and either be placed in an
air-tight coffin at once or be buried without delay. The funeral
should be strictly private, and the sheet referred to should not be
disturbed or the body exposed to view.
The cases most liable to spread the disease are those in which the
attack is very light and the child is not confined to its bed. It is
desirable that children in a house in which there are cases of scarlet
fever should not be allowed to attend school or mingle with other
children who have not had the disease.
With regard to disinfectants, it may be well to note that none of the
{203} various patent disinfectants are superior to bichloride of
mercury, chloride of zinc, sulphate of iron, chlorine, and sulphurous
acid; very few are equal to them, and none cost so little. As a
gaseous disinfectant for rooms, etc. chlorine is superior to
sulphurous acid, but it has the disadvantage of injuring metals, is
not so easily applied, and is more costly. It will destroy the
vitality of the spores of the bacilli more rapidly and certainly than
sulphurous acid, which last, to make sure work, must be exhibited for
a much longer period than is customary. I should not feel confident as
to the thorough disinfection by sulphurous acid of the hold of an
infected ship unless the fumes had been applied for sixty hours.
Carbolic acid as ordinarily used is an antiseptic rather than a
disinfectant. Its vapor in a sick room is absolutely useless. When
applied in strong solution it is effective, for a time at least, but
as thus used it is expensive, its odor is unpleasant to many, and
masks the odors from putrefying substances and excreta, etc., thus
preventing the warning which these odors would give. Its use is in
many cases very much like removing the rattle from the rattlesnake.
The suggestions made above for limiting the spread of scarlatina from
a case to be treated in the residence of the patient apply--with
certain modifications for each form of disease, which will readily
suggest themselves to the physician--to all the affections due to
portable contagia.
Among the poorer classes, however, it will often be found impossible
to obtain the separate room and service and the constant intelligent
care which are necessary to ensure the desired result; and in such a
case the patient should be removed to a hospital, for his own sake as
well as for that of the community. The utility of small hospitals for
infectious diseases is by no means generally understood, and very few
of our small cities and towns are provided with anything of the sort.
If the subject is urged on the authorities of a place, the reply will
be that it is an unnecessary expense, that the people would not go to
it, and that such an institution is in itself a source of danger. The
facts are, that such a hospital costs very little, and is the cheapest
insurance against epidemics which a town can have; if it is kept clean
and comfortable, the people will use it freely, and if properly
managed it does not offer the slightest danger to the vicinity. This
question will be further discussed in the last section of this paper.
The principles of isolation as applied to a single case as indicated
above may also be applied to infected localities in case of epidemics.
When taken in time, all diseases which depend upon particulate
contagia for their origin can be stamped out by isolation and
disinfection. Unfortunately, to effect this promptly and successfully
requires money, labor, and the co-operation of the well in the
vicinity; which last it is usually impossible to obtain voluntarily or
to compel sufficiently to secure the desired results. A question which
sometimes arises in case of epidemics, and with regard to the
necessity for which physicians will be consulted, relates to the
closure of the public schools. It is certain that the assemblage of
children in schools exerts a powerful influence on the spread of such
diseases as scarlet fever, diphtheria, and whooping cough. On the
other hand, the closure of the schools infringes upon the rights of a
large number of the community, and if long continued, as it sometimes
must be to be really efficacious, inflicts upon them {204} a permanent
loss. It is, moreover, a confession on the part of the authorities of
inability to induce or compel what must always be a comparatively
small part of the community to take the proper precautions. It is
never justifiable to close schools on account of small-pox, and where
there is a competent health authority supported by the influence of
the medical profession, it must be a very exceptional set of
circumstances which justifies their closure for diphtheria or
scarlatina.
It is not deemed expedient here to discuss the vexed question of
quarantine. It is more important against yellow fever than any other
disease, because every day of delay of the entrance of the disease
which it secures lessens largely the subsequent mortality, since the
duration of the disease is limited by frost. This is not the case with
cholera, and the mere keeping this disease out of a place for a few
weeks does not diminish its ravages when it has once gained an
entrance. To rely altogether on quarantine, either maritime or inland,
to keep yellow fever, cholera, or any other disease out of this
country is a far greater mistake than to neglect it altogether. The
practical way to isolate and quarantine is to get as close to the
affected spot as possible. Precautions at Havana for yellow fever, or
at Hamburg for cholera, are far more useful to the United States than
the same amount of work at our own ports can possibly be; really good
work in this direction must be not only national, but international.
XII. MENTAL CAUSES OF DISEASE.--A man may give too much attention to
his health and the means for its preservation, and the doing so is
both a sign and a cause of disease--probably oftener the former than
the latter, except in cases of psychological epidemics. The power of
expectant attention, especially if accompanied by belief or fear, to
produce derangement of function in the nervous system, and through
this to affect the circulatory and digestive systems, is well known to
medical men. The effects of an undue amount of brain-work, and
especially of the anxiety and worry which often accompany this when it
is specially directed to the acquiring of wealth, fame, or power, are
also familiar to physicians in our large cities. The analogies between
mental and physical exertion are close in some respects, and
especially as to the effects of over-exertion in a limited time under
the influence of excitement.
The danger from simple mental work, such as study, when there is no
excitement from a contest, is small, and depends mainly on lack of
physical exercise and consequent disorder of the digestive organs. The
risk of producing what Fothergill calls "physiological bankruptcy" is
greatest in the youth studying for a prize, the speculator, the man
who feels responsibility which he knows he probably cannot meet. The
danger of injury from overwork under excitement is a very real one in
many of our schools, and, while the evil results are most apparent in
girls of the middle and upper classes, the boys and the young men also
suffer. The system of pass examinations, in which the standing of the
pupil is to be determined, not from the average results of his daily
recitations, but from a single examination at the end of the year,
produces the greatest risks to health; and this is especially the case
where the ambition and pride of the children are stimulated by
competition for prizes, medals, etc. Such systems of grading by a
single final examination should not be used in ordinary schools, and
for some pupils there will always be a risk to health connected with
them even when they are of age. No doubt the stimulus of {205}
competition is useful with the majority of children as well as of
adults, but with some of them it is pretty sure to go too far.
The symptoms produced by undue mental strain are familiar to all
physicians, and there is usually little difficulty in tracing the
effect to the cause when attention has been directed to the matter; in
fact, the patient himself usually knows very well the cause of his
troubles. The remedy is, of course, rest--but that does not mean
idleness. In speaking of occupation, allusion has been made to the
fact that the physician must at times advise his patient as to the
adoption of some pursuit, and in cases of this kind such advice is
also useful.
The effects of mental strain are often mingled with, and aggravated
by, those of stimulants which have been used to spur the flagging
energies. Alcohol, tobacco, opium, or coffee used in this way finally
increase the very discomforts which at first they relieved.
II. Personal Hygiene in its Relations to the Practice of Medicine.
In the preceding section have been indicated briefly some of the
principal causes of disease and the methods for their investigation or
removal. We have now to consider some of the practical applications
which may be made of the laws of etiology and prevention of disease in
the treatment of the sick. While the removal of the cause of illness
by no means always effects a cure, yet the importance of a knowledge
of this cause as an aid to diagnosis, prognosis, and therapeutics is
so evident as to require no proof.
To discuss with anything like completeness the practical applications
of what would be commonly considered as hygienic rules in the
treatment of disease would be to write a treatise on nursing, and
would also include a large part of the practice of medicine, for
regimen is the more important half of practical therapeutics. The
hygienic requirements peculiar to each disease will be pointed out by
the writers upon special subjects, and I shall only venture upon one
or two general remarks in addition to the hints already given in
speaking of the several causes.
In the acute stages of disease the sensations--or, if the term be
preferred, the instincts--of the patient are usually the best guide to
his regimen so far as they go. In most cases he desires quiet, shade,
but not absolute darkness, and little or no food, although there is
often a craving for drinks, especially of a cooling character. In the
specific fevers which have a tolerably definite period and course it
is important to keep up the nourishment even during the period of
anorexia, in order to provide against the debility which is to follow.
This nourishment is best given in the form of drink, and very
frequently fresh milk is the type of what is required. The old notion
that whatever a sick man desired must be hurtful, and therefore that
the fever patient must be kept hot and refused cool water, has now
almost entirely passed away.
In convalescence from acute disease and in many chronic cases, the
sensations of the patient are not to be trusted as a guide in the
choice of food. In such diseases as yellow fever and typhoid fever to
allow the convalescent to follow the dictates of his appetite is to
run great risk of a fatal result. In other cases the patient really
has no wish in the matter, but it {206} will often be found that one
who can think of nothing which he desires to eat, and who will even
refuse a dish which he has requested and been thinking about, will eat
with enjoyment some unexpected dainty when presented at the right
moment and properly served as a skilled nurse knows how to do. The
manner of serving the food, independent of its cooking, is not a
matter of such small importance that the physician can afford to
overlook it, and he will succeed best as a practitioner who best
appreciates the influence which cracked goblet, a chipped saucer, a
soiled napkin, or, on the other hand, a hot plate or a touch of color
in the shape of a leaf or flower, may have upon the capricious
appetite of the sick. In ordering diet for convalescence it is not an
uncommon error to select only those articles which are agreeable to
the physician himself, forgetting the old proverb, that what is one
man's meat may be another man's poison, and also that it is above all
things desirable to avoid monotony. One doctor always orders chicken,
another eggs, a third a mutton-chop, etc. The practice in this respect
has probably been unduly influenced by the reports of Beaumont of the
results of his observations on Alexis St. Martin, and we still find
that the relative digestibility of various articles of food is
estimated according to the scale laid down in these reports, with no
allowance for individual peculiarities, previous habits, mode of
cooking, etc. The secret of success in the diet of convalescence lies
mainly in the simplicity of the individual dishes, in varying the
different meals, in the manner of serving, and in carefully observing
the effects on the sick person, and being guided by the results.
To promote appetite and digestion, and to secure refreshing sleep, one
of the most important things is fresh air, but in many houses a sick
person will obtain but a very limited allowance of this if the
physician does not give special attention to the matter. Except in
cases of contagious disease, the rules for managing which have been
given in a previous section (p. 201), as soon as a patient is
sufficiently recovered to be moved for a short time into another room
his bedroom should be thoroughly aired and cleansed, and this should
be done morning and evening thereafter.
In treating cases of contagious disease the question often arises as
to means of individual prophylaxis to be used by those who must be
exposed to the effects of the infected locality or of the presence of
the sick. The attempts which have been made to secure this individual
protection in the midst of an epidemic have been numerous and varied,
ranging from the use of the "vinegar of the four thieves" of the
Middle Ages to the employment of the sulphites and chlorates to make
the blood unsuited to the growth and multiplication of the supposed
germs, or of cotton-wool respirators to strain the infected air, or of
supposed specifics for particular diseases, as belladonna for scarlet
fever and vaccination against small-pox. As yet, there is little or no
satisfactory evidence as to the value of individual precautions
against those diseases whose contagion is conveyed through the air,
small-pox alone excepted, but in case of diphtheria in one member of a
family of children it might be well to try the use of chlorate of
potash internally, combined with the local application of the tincture
of the chloride of iron, as suggested by E. M. Hunt. The question is
one to be investigated by careful observation and experiment; and,
though it is improbable that any definite results will be obtained
except in those diseases which are communicable to animals, and
therefore {207} susceptible of direct experiment, still, it is
possible that some advance may be made. In rare and exceptional
cases--as, for instance, in exploring a crowded, filthy, and intensely
infected typhus-fever nest, as a tenement-house, or an infected
yellow-fever ship--it may be worth while for the physician or
inspector who is unprotected by a previous attack of these diseases to
make use of a cotton-wool respirator, which is readily extemporized,
and belongs to that exceedingly valuable and popular class of remedies
which, "if they do no good, can do no harm." In epidemics of typhus,
cholera, or yellow fever one of the most valuable prophylactics is to
have a mind so occupied with other matters that it pays little or no
attention to the danger, while in case of small-pox fear of the
disease is indirectly the best prophylactic, since it leads to careful
vaccination.
This branch of the subject is closed with the remark that it would be
well if physicians, and especially the younger ones, gave more
attention to the preservation of their own health than many of them
do. The possession of a medical diploma does not prevent the evil
effects of irregular and hurried meals, insufficient sleep, exposure
to inclement weather, and lack of systematic and sufficient exercise;
and too much tobacco, sometimes too much alcohol, and in exceptional
cases too much study and literary work, so often combine with anxiety
about individual patients or with pecuniary worries to damage the
digestion and nervous system of the young practitioner that the wonder
is that so many survive the ordeal. And, in fact, the mortality among
physicians under the age of thirty is higher than that of any other
profession during the same period of life.
III. Public Hygiene in its Relations to Physicians.
An important difference between man and animals is found in the extent
to which he will sacrifice a present pleasure or convenience to secure
a future good or to avoid a future evil. The savage will do this to
only a very limited extent--little more, in fact, than the beaver or
the squirrel--and the lesson is learned but slowly and by sad
experience. This is especially the case as regards matters affecting
health. When a man begins to take special precautions as to his diet
or exercise, having in view rather his future health than his present
comfort and tastes, he has in most cases already begun to suffer from
the effects of his imprudence, and does not commence a hygienic course
of life as a perfectly sound and healthy person. The same is true for
a community. It will not usually submit to the burden of taxation
necessary to secure drains and sewers or a proper registration of
vital statistics, nor to the cost and inconvenience of the machinery
necessary to limit the spread of contagious diseases, until the
neglect of these things has resulted in such an amount of disease and
death as to forcibly call attention to the matter. The result is, that
the burden is far heavier than it would have been had the work been
undertaken in proper season, and individuals may find it to their
interest to leave the place and settle elsewhere rather than remain
and meet their proportion of the expense.
When a state or municipality has so far advanced in civilization as to
consider it desirable to take measures to protect the public health by
preventing individuals from polluting the air or water liable to be
used by {208} their neighbors, etc., the services of the medical
profession are always called upon. The foundation of public hygiene is
information as to the occurrence of certain forms of disease, the
cause of which can be referred with more or less precision to a
certain limited locality. This information may be very imperfect,
consisting of little more than rumor and opinions as to the existence
of an undue amount of sickness or mortality in a certain place, or it
may consist of precise reports setting forth the number of deaths from
each cause, the proportion of each of these to the population by age,
sex, occupation, etc., and of the whole to births--constituting what
is commonly called the "vital statistics of a place"--and also of
reports of the occurrence of certain preventable diseases; and between
these two the information may be of various degrees of completeness,
but, whatever there be, it is for the most part obtained either
directly or indirectly from medical men. The reliability and
completeness of the information thus obtained by the state determines
to a great extent the direction and character of the work done in
destroying or preventing the causes of disease, and it is also an
important means of increasing our knowledge with regard to the nature
of these causes.
The character of this information depends largely upon the character
of the physicians who furnish it. In a large part of the country
medicine is legally in the position of any common occupation; that is,
the term "physician" is defined as applied to "any one who publicly
announces himself to be a practitioner of this art, and undertakes to
treat the sick either for or without reward." Under such circumstances
there can be no guarantee that all who call themselves physicians are
properly qualified or competent to furnish reliable information for
registration purposes, and, as a matter of fact, a large number are
not so qualified. It is for this reason that there is such a close
connection between public health authorities, registration of vital
statistics, and the registration of those physicians whose
certificates as to causes of deaths, etc. will be accepted by the
state; and hence the nature of the public health organization of a
state and the personnel of its officials are matters of great
importance to physicians. On the other hand, the efficiency of a
public health service depends very largely upon the relations which it
holds with, and the light in which it is regarded by, the medical
profession. A health officer who is distrusted and disliked by the
physicians of his district cannot effect much unless he can overcome
this feeling, and his tenure of office must always be very insecure.
The official relations of the practitioner with the health authorities
are usually confined to the subjects of registration of vital
statistics and of checking the spread of contagious diseases. The most
marked exception to this rule is furnished by the States of Alabama
and North and South Carolina, in which the State Medical Society is
the State Board of Health, having been given legislative powers and
the right of selecting the health officers. The most complete
organization of this kind is that of the State of Alabama, where by
the act of 1875 the Medical Association of the State was constituted
the State Board of Health, and the county medical societies in
affiliation with the State Society were made county boards of health,
to be under the general direction of the State Board. These county
boards at first had advisory powers only, and were to be conducted
without expense to the State or the county, except that the competent
legal {209} authorities of any county might invest the county board
with such powers and duties for the promotion of the public health as
might be mutually agreed on; but in such case the right to elect or
appoint those employed in sanitary administration is reserved to the
board of health, while all questions relating to salaries,
appropriations, and expenditures shall be reserved to the legal
authorities. It was further provided "that no board of health, or
advisory or executive medical body of any name or kind for the
exercise of public health functions, shall be established by authority
of law in any county-town or city of this State except such as are
contemplated by the provisions of this act, the object of this
prohibition being to secure a uniform system of sanitary supervision
throughout the State." By an act of 1881 the county board is directed
to elect a health officer, who is to keep a register of the births,
deaths, and cases of pestilential or infectious diseases occurring in
the county, and furnish to physicians, free of charge, reliable
vaccine--to obtain information as to the sanitary condition of his
county, etc. etc. It will be seen that this plan of organization is an
attempt to overcome the practical difficulties in the way of obtaining
from physicians the information necessary for the registration of
vital statistics and the work of preventing the spread of infectious
diseases.
While the great majority of physicians are willing to furnish the
information as to the cause of death, etc. which is necessary for a
useful registration, there are always some who either neglect or
refuse to do so; and if the law be made compulsory, it provokes
hostility unless compensation is furnished, while as regards the
requiring physicians to furnish information as to the existence of
contagious diseases, this always rouses opposition on the part of a
certain number of medical men, even if payment for such notification
is provided. And while this opposition is no doubt in many cases due
to improper motives, such as personal hostility to the existing
authorities, party politics, or a desire for notoriety, its strength
nevertheless rests upon the fact that it is unjust for the state to
compel the services of any man or class of men without furnishing
compensation. The advocates of health and registration laws are thus
placed between Scylla and Charybdis: if they propose compensation,
which involves appropriations from the public treasury, the law cannot
be passed; if there is no compensation allowed, complete results
cannot be obtained.
The Alabama law makes compulsory the furnishing by physicians of
information relating to births, deaths, and infectious diseases, and
gives compensation--not in money, but by allowing the medical
profession to have the sole management of the matter and to choose the
health officers to whom they are to report; in other words, they are
allowed to tax themselves. The result in Alabama is yet doubtful. If
competent and faithful health officers and registrars can be obtained
without paying them a fair compensation, it will be contrary to
experience; and if these officers receive a salary, it will be strange
if the positions do not become the reward of partisan political work.
It should be noted that the requiring a physician to report the births
occurring in his practice stands on a very different basis from the
requiring him to report the cause of death, since there is no special
necessity for the former. It requires no expert knowledge to report a
birth, and the duty should obviously devolve on the householder.
{210} In those States in which by law only properly qualified medical
men, as determined by examination, have the right to practice, to hold
medical office, or to furnish medical certificates, the State
certainly is entitled to require of all physicians thus registered and
authoritatively recommended to the people as competent, that they
shall furnish, free of charge, certificates of the cause of death in
those cases where they are cognizant of such cause.
States and municipalities often demand much more than this; as, for
instance, that the medical man shall fill out the whole certificate,
including age, nativity, nativity of parents, etc., and that he shall
furnish the information to the registrar. In some cases it is provided
that any physician having attended a person during his last illness
shall furnish the certificate: this would apply to cases where the
physician may not have seen the case for weeks before death.
While it is most convenient to have the certificate of cause of death
upon the same form which contains the data necessary to identify the
individual, the certificate should be distinct from the latter, and
the duty of making the return to the registrar should devolve on the
householder or undertaker, and not on the physician. On the other
hand, it is easy for the physician to be hypercritical in these
matters: his certificate is to be considered rather as a statement of
opinion than as a statement of facts within his personal knowledge,
precisely as he would certify as to his own age and birthplace.
The compulsory notification of infectious diseases to the health
authorities is a matter presenting much greater difficulties than that
of certificates as to causes of death. The state has no right to
require such notification from the physician without giving some quid
pro quo, and it is not expedient to make it compulsory, even with
payment, except from physicians employed by the state or municipality,
to furnish gratuitous medical attendance to the poor. The state has
the right to require such information from the parent or householder,
and it has also the right to require the physician to notify the
parent or householder as soon as he recognizes the existence of such
infectious disease. It is extremely desirable that the health
authorities of a city should receive promptly, and direct from
physicians, notification of the occurrence of such diseases, and there
will usually be no difficulty in obtaining this if the health officer
has tact and discretion and the city is prepared to do its duty. This
duty is not confined to registering the information or placarding the
house, nor will it be properly performed by merely removing the sick
person to a hospital and disinfecting the premises. If the case occur
in a family which can secure its proper isolation, and the attending
physician certifies that it is so isolated and makes himself
responsible for its management (for which responsibility he should be
paid by the patient or his friends), the health officer should not
interfere nor do more than furnish a competent person to secure
disinfection if required. The employment of a trained nurse known by
the health authorities to be competent and reliable would do away with
most of the difficulties connected with such cases in the upper and
middle classes of society; and such nurses should be registered just
as physicians and midwives are.
Where the case cannot be thus isolated and properly cared for, it
should be removed to a proper hospital. This presupposes that the city
has such a hospital, and if it has not, and is not prepared for such
cases, notification {211} is useless. When the city places a house in
quarantine so as to interfere with business, it should be for the
shortest possible time consistent with securing thorough disinfection
of the premises, and the city should bear not only the cost of such
disinfection, but the cost of caring for the persons in the house in
an isolated place until no further danger is to be apprehended for
them. When the city undertakes to pay all expenses for isolation and
disinfection of such cases, it has the right to require that all such
cases shall be so treated, leaving it to private parties to meet the
cost in case they prefer not to use the buildings and apparatus
provided by the city for that purpose. And when the city does its duty
in this respect, it will be found that physicians and the people will
do theirs, with rare exceptions.
When a city becomes very unhealthy the usual policy is to conceal the
fact as much as possible, and to attribute the mortality to some other
than the real cause. The influence of the mercantile part of the
community is in such a case strongly exerted on the daily press and on
the health authorities to produce such representations of the
condition of things as will tend to allay apprehensions on the part of
their customers. The healthfulness of a place is usually estimated
from its mortality reports, but the reliability of these is by no
means always what it should be. Yellow fever is called typho-malarial
or pernicious fever, typhoid is reported as diarrhoea or malarial
fever, etc. etc., and great stress is laid upon what is called the
sanitary condition of the place, which is declared to be excellent.
Unfortunately, this phrase, "sanitary condition," means different
things at different times. When the mortality is low, sanitary
condition means the healthfulness of a place; when it is high, it
means the cleanliness of a place. To a certain extent physicians are
responsible for the truth of the statistical returns, not so much in
relation to the number as to the causes of deaths; but none save those
who have practised in a city liable to epidemics can realize the
enormous pressure which is brought to bear on medical men to induce
them to aid in or wink at concealing the true state of the case. Of
course, this ostrich-like policy is in the long run an exceedingly
unwise one, but neither the average householder nor community can be
expected at present to pursue any other, except under pressure.
There are many questions as to the best form of public health
organization, and the powers and duties which should be conferred upon
it, which can only be properly answered by taking into consideration
the circumstances in each case. In a large city the health officers
must have great powers if they are to be really efficient. They have
to contend with ignorance, custom, and self-interest, and their action
must in many cases be prompt and unrestricted if it is to be
efficacious. They must sometimes be in conflict with wealthy and
powerful corporations, whose interests are opposed to the reforms
which they urge, and although their business is to protect the most
important interest of the community at large--_i.e._ its
health--against the interests of individuals, yet these last are much
more immediately concerned, and are, naturally, so active that they
are often, although few in number, able to defeat any attempt to
interfere with their occupations.
It not unfrequently happens that a health board may have all the power
{212} necessary, so far as the laws are concerned, and yet may be able
to accomplish little for want of funds to pay the inspectors and other
officials whose services are necessary. For a city, a health officer
usually does better work than a board of health: his responsibility is
more direct, and he has stronger motives to do good work, than a
board. Of course, a poor health officer is less efficient than a good
board of health, but the general rule is as above stated. The problems
of hygiene require special knowledge, and the man who is to deal with
them requires special training. The folly of treating diseases by
their names with popular or patent remedies is not greater than that
of the attempt to make a healthy house or city by men who are not
architects or engineers or physicians, or who have only the
information possessed by the average architect or engineer or
physician. And, of all professional or educated men, the physician
especially should recognize his own ignorance. When he is asked what
one should take for dyspepsia or pneumonia his answer is, "Take the
advice of a physician;" and so when he is asked how the plumbing of a
house should be arranged, how a hospital should be ventilated, how a
city should be sewered, how a marsh should be dealt with or a
water-supply provided, he should reply, "Get expert advice and
supervision, and be prepared to pay the amount necessary to secure
it." It is the special duty of the physician to exert his influence to
secure properly constituted sanitary authorities for his own locality,
his State, and for the nation, and to support these against the
hostility which they must inevitably arouse if they are efficient. And
he should do this, not blindly and as a partisan, but intelligently
and with due consideration of all the important interests involved.
The body of educated physicians in a community forms the tribunal by
which the work of sanitary officials is to be judged, and they cannot
judge wisely unless they appreciate the difficulties with which health
officials have to contend. If a city has an incompetent or dishonest
board of health, the medical profession of that city are to a certain
extent responsible for it; if a competent, energetic, and faithful
sanitary officer is crippled and harassed or forced out of office
because he is on the wrong side of politics, or because in the
legitimate and proper exercise of his functions he has come in
conflict with the interests of powerful and wealthy individuals or
corporations, it is the duty of medical men to support him, and to do
this actively and promptly. And I take great pleasure in being able to
say, as the result of somewhat extended observation, that, as a rule,
the physicians of this country do cheerfully and promptly co-operate
with the sanitary authorities where such exist, and are the first to
try to have them properly organized and given the necessary means and
powers to do effective work.
{213}
DRAINAGE AND SEWERAGE IN THEIR HYGIENIC RELATIONS.
BY GEO. E. WARING, JR.
For reasons, sometimes sound and sometimes fanciful, the drainage
question often presents itself to the medical practitioner as an
annoying if not as a serious one. It is not necessary for the
physician to make himself an adept in the art of sanitary drainage,
but he can properly meet neither the demands of nervous patients nor
the exigencies of sometimes serious situations without having an
intelligent general idea concerning it. Not only to prescribe
improvement, but frequently to allay ill-grounded apprehension, he
should be able to address himself, intelligently and promptly, at
least to the few simple problems presented in connection with ordinary
houses. I use the expression "ill-grounded apprehension," not because
the drainage in and about houses is generally tolerably good, for it
is not, but because the race seems to have so inured itself to certain
grave defects in plumbing-work that one may reasonably hesitate, and
look elsewhere for the occasion of diseases before accusing the
imperfect sanitary appliances of an average house.
Anything like a treatise on the technical details of house-drainage
would be quite out of place here. There are note-books easily
accessible to such physicians as care to make a thorough study of the
subject. It does seem worth while, however, to pass in careful review,
in a work of this character, the various conditions of interior and
exterior drainage upon which a physician is frequently called to pass
judgment.
The perfect drainage of a house, like the perfect drainage of a town,
implies the immediate and complete removal, to a point well beyond its
limits, of all waste matters which are a proper subject of
water-carriage; such a thorough ventilation of the channel which these
matters have traversed as to reduce to a minimum the production of
deleterious gases arising from the decomposition of the film with
which they may have soiled the walls of their conduit; and adequate
provision for the absolute and permanent exclusion from the atmosphere
within the house of the air of the pipe or sewer. This is a brief and
simple statement of the fundamental and absolute requirements of all
good drainage. It is founded on the one grand object which governs all
improvement of this character: the prevention of decomposition of
refuse matters anywhere in house or town.
Practically, it is safe to say that these conditions are never
complete, and that instances of perfect work are so exceptional as to
need no {214} consideration here. We have to assume, substantially in
every case that is presented, that we are dealing with defective work,
ordinarily with work that is very seriously defective. Most houses
have been built by contractors, and the plumbing is perhaps the item
of the whole structure that it is considered easiest and safest to
scamp or to neglect. Even where the motive of economy has had no
controlling influence, the drainage has almost invariably been planned
by a plumber who has learned his trade and conceived his ideas in the
performance of work which was done at a time when no one realized the
serious consequences of its being improperly done. The absence of
interior ventilation, leaky joints, ill-arranged connections between
the various plumbing appliances and the main outlet from the house,
pipes and traps so large that an ordinary current is powerless to keep
them clean, defects of form, defects of material, and defects of
construction, are met with on every hand. This general statement is of
itself sufficient to show how hopeless it is for the average physician
to prescribe the manner in which the drainage of a house should be
constructed or remodelled.
If we view the question solely with reference to its bearing on the
causation of disease, we enter a field where neither the sanitarian
nor the physician is ever sure of his footing. The precise relation
between bad drainage and ill-health no man knows. Certain diseases are
undoubtedly traceable to conditions of air or of drinking-water due to
the improper disposal of organic wastes, but the extent and exact
bearing of these influences are still greatly a matter of conjecture.
It is, however, undoubtedly safe to assume--and the assumption is
supported by ample general observation, if not by precisely
ascertained facts--that whether we are considering serious diseases or
the slighter ailments, every argument leads to the enforcement of the
most strenuous requirements of cleanliness. Through all the ages no
one has disputed, and no one has improved upon, the simple sanitary
formula, "Pure air, pure water, and a pure soil." We may safely wait
until the enthusiastic investigators now engaged with the subject
shall have adduced the testimony of positive facts, if we will in the
mean time adhere strictly to the requirements of Hippocrates'
prescription. The physician will surely not go wrong if he treats all
obvious defects of drainage as positive evils, and insists upon their
complete reformation.
Not to confine ourselves to houses which are provided with the
ordinary modern plumbing-works, but to include all collateral branches
of the subject, we have to consider the following conditions:
I. THE REMOVAL OF HUMAN EXCREMENT:
(_a_) By water-carriage in houses provided with modern plumbing;
(_b_) By some form of dry conservancy;
(_c_) By the fiendish privy-vault which prevails so generally,
save in the larger cities.
II. THE REMOVAL OF LIQUID HOUSEHOLD WASTES:
(_a_) By delivery to public sewers;
(_b_) By irrigation disposal;
(_c_) By delivery into cesspools.
Incidentally to the above there must be considered the influences of
the ultimate disposal of all household waste, whether by the public
sewer or the private house-drain.
{215} I. THE REMOVAL OF HUMAN EXCREMENT.--We are too apt to judge of
the power for mischief of any waste matter by its original
offensiveness, and the world at large regards the solid and liquid
exuviae of the human body as the most dangerous material with which it
has to deal. Doubtless it is so under certain exceptional
circumstances. If impregnated with the infective principle of cholera
or of typhoid fever, for example, its influence for evil may be
widespread and active, but in the absence of such infection these
substances offer a less serious problem, and, as their offensiveness
causes them to be more carefully avoided, their evil influence is
less, and is less widely disseminated, than is that of the
comparatively inoffensive wastes of the kitchen-sink. This is a
consideration important to be borne in mind. Nothing is more common
than the expression of the opinion that the wastes of a population are
offensive and dangerous in proportion to the degree to which
excrementitious matter is allowed to flow away with its general
drainage. The fact is, that the drainage from a house or from a town,
if reasonably diluted with water, is very slightly offensive until it
has passed through a considerable degree of decomposition. The outflow
of a perfectly sewered town, where the whole community uses
water-closets, is less offensive than the neglected back-yard drain of
an average New England farm-house. The trouble begins with the
condition of putridity. Fecal matter and urine are somewhat quicker
than the other wastes of the house to enter into putrefaction, but the
difference is only one of degree, and the latter rapidly overtakes the
former in the foulness of its condition; so that where a house is
provided with two cesspools, one for water-closet matter and the other
for kitchen waste, it is quite impossible to determine from the
character of their contents which is which; therefore examinations of
the drainage of a house should by no means be confined to the manner
in which its excrementitious matters are disposed of. Setting aside,
in this connection, the peculiar liability of these matters to become
the seat of specific infections, it is fair to assume that equally
complete and cleanly arrangements are needed for all else that flows
to waste, as for the discharges of the water-closet. The purpose of
these remarks is of course not to belittle the importance of proper
care in the disposal of human excreta, but to prevent the giving of an
undue importance to this branch of the subject, with too light
treatment of the very serious difficulties presented by the others.
(_a_) Modern conveniences may fairly be said to be the bane of modern
society, or at least of such of its members as have the questionable
good fortune to be housed within the same four walls with every device
that a misguided talent for invention has led the American mechanic to
provide for the comfort and convenience of the occupant. Properly
regulated, there is no element of modern house-building more conducive
to health than such a system of plumbing as brings within reasonable
limits the labor of supplying abundant water at every point in the
house, and obviates the need for exposure and removes the temptation
to neglect and postponement attending the use of out-of-door houses of
convenience. The spigot and the water-closet are the two essential
sanitary agents which the plumber offers to us. The bath may be
replaced by the sponge, the stationary wash-basin may be, and
generally should be, replaced by the bowl and pitcher of our fathers,
but there is no sufficient {216} substitute for an ample supply of
water on each floor of the house and for a cleanly water-closet placed
within doors. The evil that the plumber has inflicted upon the race is
due very largely to his not having held his hand when he had fairly
provided for our reasonable requirements. When he fills our bedrooms
with stationary basins, connects our refrigerators with the sewer,
provides twenty outlets for water which had better reach the drain
through less than half that number, and incidentally underlays all our
floors with pipes, every foot of which is a possible source of danger,
he turns what ought to be a blessing into what is too often an
unmitigated curse.
It will not be easy to convert persons who have become accustomed to
the universal diffusion of plumbing-works throughout the house to a
belief that their best sanitary interest, and, perhaps hardly less,
the best requirements of refinement, point to the abandonment of what
is practically superfluous in the way of wash-bowls, bidets,
foot-baths, sitz-baths, urinals, etc.; but one who has given careful
attention to the subject cannot hesitate to recommend that in a house
which is "strictly first class" it would be the part of wisdom to
reduce by at least three-fourths the openings which lead to the
soil-pipe and drain and sewer, and to concentrate upon the remaining
fourth the flushing effect of wastes which are now so widely
distributed. Strenuous effort is being made, not only by those who
write and talk in the interest of the plumber and manufacturer, but by
many who honestly believe that the good the plumber has to give us
cannot be given with too free a hand, to prove that so long as they
are properly constructed and properly arranged we may use plumbing
appliances at every point in the house with the utmost freedom and
with a minimum of danger. The minimum of danger, and often more than
the minimum, does, however, exist. It exists, perhaps, in a constantly
increasing degree with every extension of the work, and it can only be
the part of wisdom to insist, so far as advice can have influence, on
the reduction of all these appliances to the least requirements of
reasonable comfort and economy of labor. My own advice would be, in
all cases, to permit the use of no wash-bowl or bath or other vessel
at a greater distance than a few feet from a vertical soil-pipe, and
not to permit their use in any case in bedrooms or in closets opening
only into bedrooms.
At the risk of seeming extravagant, I would say that the stationary
wash-bowl as ordinarily used is one of the most uncleanly of modern
household appliances. Long experience in the inspection of houses and
in the examination of waste- and drain-pipes has led me to the belief
that servants, by no means rarely, use these vessels as the most
convenient means of voiding and cleansing chamber utensils. Their
overflow-pipes are coated with soap and with the exuviae of the skin
to a degree which makes them usually the seat of an offensive
decomposition. Their plugs and chains are almost invariably foul, and
those devices which provide for closing the outlets by valves or
plugs, somewhat removed from the strainers at the bottom of the bowl,
bring the water in which the face is washed into an interchanging
communication with a considerable length of foul and uncleanable
waste-pipe--a communication that is made active by the bubbling of the
contained air as the pipe fills with water. The labor of filling
pitchers from a spigot on the same {217} floor, and the labor of
emptying chamber-slops into a water-closet on the same floor, are not
to be considered as compared with the greater cleanliness and the
greater sanitary security that such an arrangement ensures. There is
no serious objection to the placing of wash-basins and baths in the
same apartment with the water-closet, or elsewhere immediately
adjoining the soil-pipe; but it certainly cannot be disputed that the
extension of the drainage system by horizontal lead pipes to remote
points is altogether and wholly to be condemned.
However, the question more immediately at hand is that of the disposal
of human excreta by the use of water-closets; and it is the
water-closet that first attracts the attention of one who is called
upon to examine the sanitary condition of the work. There are several
radical defects in water-closets, which are so widespread and which
have become so familiar to the world at large as to attract less
attention than they deserve. For example, it is a radical defect of a
water-closet to be tightly encased in carpentry. Nearly all the
water-closets now in use have a somewhat complicated mechanism about
their bowls. They consist in part of earthenware and in part of iron,
generally with an unstable connection between the two. More often than
not they overflow or drip or leak, and whatever may escape from them,
whether foul air or foul water, is confined within an unventilated
space, but a space which is still not absolutely excluded from the
atmosphere of the house. The removal of the "riser" or vertical board
under the front of the seat will usually disclose at once a condition
that suggests at least the need for thorough ventilation. It also
discloses in some cases a complication of machinery and pipes and
levers and chains which makes a thorough dusting and cleansing of the
space difficult, even were it accessible. There are water-closets
which are essentially good in their construction and working, which it
is important to protect by a "riser," but this "riser" should never be
of close work. It should at least be freely perforated with large
holes, or, better still, be made with slats or blinds, so that there
may be the freest possible circulation of air under the seat. If there
is an entire absence of machinery, so that the whole space may be left
open, being well finished with tiles or hard wood or other suitable
material, it is better that it should be unenclosed and that the seat
should be hung on hinges, so that it may be turned back, exposing the
whole space to easy cleansing. It is better too, in all cases, that
the ventilation should not even be interfered with by a cover over the
seat, the freest possible exposure to the air being of great
importance.
A very large majority of the water-closets in use throughout the world
are either very imperfectly flushed "hoppers," which are generally
foul and which are often defective in their traps, or that worst of
all forms, known as the "pan" closet, where a slight depth of water is
held in the bowl by a hinged pan closing over its outlet. This pan
swings in an iron chamber under the bowl, which is entirely cut off
from ventilation, which is generally foul with adhering fecal matter,
and which as an abomination has no equal in the whole range of
plumbing appliances. The closet of which it forms a part has
everything to condemn it, and only its cheapness and its apparent
cleanliness, and the habit of the world in its use, to commend it. If
flushed, as it usually is, by a valve on the supply-pipe, it is rarely
flushed adequately, and its use not seldom leads to an indraft {218}
of foul air (or worse) into the main water-supply system of the house.
Such closets may be easily inspected as to their condition by shutting
off the water-supply, opening the pan, and lowering a candle into the
container below. Such an inspection will almost invariably disclose an
extremely and dangerously filthy condition. Yet the worst part of the
container, that which never receives an adequate flush, is even then
concealed from view by the pan being thrown back against it. The nose
will here be a good adjunct to the eye, and the odor escaping from
this filthy interior chamber will generally afford convincing
testimony of the impropriety of allowing such a vessel to remain in
use.
It is a rule almost without exception that closets, except perhaps on
the first floor of the house, which are flushed by valves connected
with the bowls, are to be condemned. However good or however bad the
state of a closet thus supplied with water, its condition will always
be improved by giving it a copious flush from an elevated cistern
delivering never less than two and a half gallons of water at each
use, and delivering it through a pipe so large and so direct as to
secure a thorough cleansing at every discharge.
It would be out of place here to enter into a detailed description of
the various closets which are and which are not to be recommended for
use. So far as the physician's inspection is concerned, it is perhaps
sufficient to say that wherever an odor, however slight, can be
perceived, and wherever a fouling of the interior surfaces of the
closets or of the spaces under the seat can be detected by the eye,
radical reformation is necessary. The only safety with a water-closet,
as with any other vessel connected with the drainage of the house, is
to secure an immediate and complete washing away of all foul matter of
every kind. Where this result is not attained, it should be insisted
upon. This much lies within the province of the medical attendant; the
manner in which it shall be secured is not necessarily for him to
decide.
One other branch of this subject is worthy of attention. The
cleanliness and freedom from offence of the water-closet or of a
waste-pipe or drain is in proportion to the frequency with which it is
used and to the abundance of the discharge of water through it. A
dozen closets used by a dozen persons will be quite likely all to be
offensive. If the dozen persons all used only one closet--not a pan
closet--the frequency with which its trapping water is removed and the
frequency with which its walls are washed would secure its tolerable
condition, even if not of the best construction. In this case, as in
all others, simplicity should be the controlling principle.
(_b_) Dry conservancy next after water-carriage is the best and safest
system for the removal of human excreta. By dry conservancy is meant
the admixture of dry earth, ashes, or similar material with the
matters to be disinfected and absorbed. Theoretically, the effect of
such admixture is entirely satisfactory; under very careful and
intelligent regulation it is practically so. It has been proved,
however, by much experience that under ordinary circumstances--that
is, where no greater care is given than is ordinarily given to a
water-closet or to a common privy--the dry conservancy system is open
to serious objections, though always an improvement on the cruder
privy-vault. The theory of the effect of a sufficient admixture of
earth or ashes with urine and fecal matter is, that by the {219}
admission of air thus secured to every part of the material there is a
complete oxidation of their organic constituents, similar to, though
slower in its operation than, actual combustion in an active fire. In
isolated houses and in hospitals, factories, and other buildings not
provided with sewerage facilities, there is no question that the
earth-closet or the ash-closet affords the best available means for
disposal, if we except a system, to be described hereafter, for the
distribution of water-carried wastes over or under the surface of
suitable ground.
Incidentally--and this is of special interest to the physician--the
use of dry earth or of dry ashes in the close-stool of the sick
chamber effects not only an immediate and complete deodorization, but
without doubt a complete disinfection as well. A quart of dry earth at
the bottom of the vessel to receive the deposits, and rather more than
a quart with which immediately to cover them, constitutes a means of
relief always available and always efficient.
Where the house is provided only with an old-fashioned out-of-door
privy the greatest relief and the most complete security may be given
at little cost by filling the vault, and placing under the seat a
movable box to receive the mixture of fecal matter and of the
absorbent material, which, if it is desired to avoid the simple
patented appliances made for the purpose, may be kept in a box or
barrel in the apartment and thrown down after each use of the closet
with the hand-scoop. The objections to the common privy are so
obvious, so universal, and so well understood that the practical value
of such a means of relief should be appreciated without argument.
(_c_) Privy-vaults are the sole reliance for the disposal of fecal
matter, and often of chamber-slops, of probably 95 per cent. of the
population of this country, and of Europe as well. It is curious, in
examining the recommendations of public health officers and the
requirements of local boards of health, to observe the uniformity with
which this most important subject is passed over with the prescription
that the vault shall be tight, sometimes that it shall be vaulted
over, and sometimes that it shall not be within a certain small number
of feet of a boundary-line or of a drinking-water well. These
prescriptions are most absurd. It is safe to say, that of the millions
of privy-vaults in this country not more than hundreds are really
tight; that a still smaller number are so vaulted over as to prevent
the free exhalation of the gases of decomposition; that those which
are so vaulted over are in all respects of worse sanitary effect than
those which have freer communication with the air, and that their
possibilities of evil reach many times farther than the limits of
distance usually required to intervene between them and the well or
the neighboring property. In view of the universality of their use and
of the completeness with which modern communities are inured to their
presence, it seems almost hopeless to attempt to secure a proper
realization of their great defects. They are always the seat of the
foulest, and even of the most dangerous, decomposition. They taint not
only the air and the soil, but the water of the soil which goes so
often to feed our sources of drinking-water, and their local stench is
of itself sufficient to sicken all who have not by daily and lifelong
habit become accustomed to it. Taking the country at large--farm
houses and village houses as well as the dwellings of cities--it is
not too much to say that the best sanitary service that {220} can be
rendered by those interested in the removal of causes of ill-health
would be in securing the abolition of these barbarous domestic
appliances. In many ways the cesspool is as bad as the vault, but in
some respects the vault is facile princeps as a public and private
nuisance of the most annoying and dangerous character. Wherever a
public or private sewer is available, wherever disposal by irrigation
is possible, and wherever even the crudest attention can be secured
for an automatic or simpler earth-closet, the strongest effort should
be directed to the absolute inhibition of the common privy-vault.
II. THE REMOVAL OF LIQUID HOUSEHOLD WASTES.--As has been stated above,
the liquid household wastes are of much more serious consequence from
a sanitary point of view, as compared with excrementitious matters,
than the public has been wont to suppose. These, owing to the large
amount of water which they contain, are beyond the reach of any system
of dry conservancy. They consist almost invariably of a flood of water
containing but a small percentage of refuse food, urine, soap, filth
of the laundry, grease--everything, in fact, except fecal matter and
the coarser garbage and ashes--constituting the waste of the
household. Where water-closets are used fecal matter is generally
added to the flow, but its relative quantity is small, and its
presence or absence does not seriously affect the problem of disposal.
In a house provided with abundant, generally superabundant, plumbing
appliances, with a large consumption of water, the whole apparatus is
constructed on the theory that all manner of filth is to be taken up
by running water and carried well without the house. Where this
theoretical end is completely attained there exists a condition of
drainage rarely met with and little to be criticised. Unfortunately,
the theoretical excellence is rarely secured. Running water confined
within a narrow channel, and so compelled to move with force
sufficient to give an energetic scouring to the walls of its conduit,
may be trusted to carry with it or to drive before it pretty nearly
all foreign matter that may have been contributed to it, but the
moment this vigorous current is checked, that moment the tendency to
excessive deposit begins. It is checked in practice in various ways:
First. By too great a diameter of the pipe: a volume of discharge
requiring a velocity of 4 feet per second in a pipe 1 inch in diameter
would have a velocity of only 1 foot per second in a channel 2 inches
in diameter, and of less than 6 inches per second in a channel 3
inches in diameter. Ordinarily, except as the deposits are removed by
decomposition (always objectionable), the deposited matters accumulate
and reduce the original bore to the diameter which will secure a
cleansing flow. It is the part of wisdom to provide only this bore at
the outset or not greatly to exceed it, and it is one of the earliest
recommendations of an experienced sanitary engineer to reduce the size
of too large bores where they exist.
Second. By the use of traps larger than the pipes leading to them and
from them, thus increasing the natural tendency of all traps to
stagnation and deposit.
Third. By the use of vertical waste-pipes, which are almost universal,
and which are very often necessary. The velocity of a current measured
along the axis of the pipe is less if the direction is vertical than
if it is laid on {221} a steep slope, because of the tendency of
liquids flowing through vertical pipes, which they do not fill, to
adhere to the walls and to travel with a rotary movement. I have seen
vertical soil-pipes furred with excrement to a thickness of nearly
three-eighths of an inch; I have never seen a corresponding deposit in
a pipe of good slope where the current was direct. This latter point
is rather one of curious interest than of practical value--certainly
from the physician's point of view. Even in original construction it
is rarely possible to give soil-pipes other than a practically
vertical course as they pass from one story to the next. Indeed, the
physician need not trouble himself to consider the question of the
size or of the direction of this main channel. He will often find
occasion to criticise the use of unduly large waste-pipes from single
vessels; as, for example, two-inch pipes leading from bath-tubs; two
and a half-inch pipes leading from laundry-tubs; and three-inch pipes
leading from kitchen-sinks. Where reconstruction is to be undertaken,
he may with advantage exert himself to secure in these lateral
waste-pipes a diameter never exceeding one and a half inches, and from
kitchen- and pantry-sinks, whose outflow is loaded with grease,
preferably not exceeding the diameter of one and a half inches, with
traps of even a little less size. Where several vessels lead into the
same waste-pipe these small diameters may increase the tendency to the
emptying of the traps by siphonage, but if proper mechanical traps are
used for baths, wash-bowls, and laundry-tubs, and if ample flushing
appliances are connected with kitchen- and pantry-sinks, the temporary
removal of the trapping-water by siphonage may generally be
disregarded. It will seldom happen that the removal of water will be
so complete as to prevent the satisfactory closing of the mechanical
valve by capillarity, even if it fails, in itself, to make a perfectly
tight fit.
A favorite recent requirement of theoretical sanitarians, and one
which has perhaps for business reasons been eagerly accepted by the
plumbing trade, is what is called the "back" ventilation of traps;
that is, the carrying of a vent-pipe from every trap in the house to a
point above the roof. In my judgment, there is more to condemn than
there is to commend this practice, for I believe that the more rapid
emptying of traps by evaporation where they are not constantly
supplied by frequent use, the dangers of accident to lead pipe, which
is generally used for ventilating purposes, and the misapplication of
a large outlay which might better be applied in other directions,
constitute convincing arguments against this favorite new method of
preserving the integrity of the water-seal. There are a number of
traps which are closed by floating balls, or by balls bearing upon the
outlet, which seem to be quite satisfactory and efficient. The worst
waste-pipes, by far, are those of kitchen- and pantry-sinks which pass
a large amount of hot grease. This soon cools sufficiently to congeal,
and it attaches itself to the walls of the pipe, where it does congeal
until the bore is reduced to what is barely sufficient to furnish the
necessary limited water-way. Grease-traps of various forms have been
invented with a view to retaining this obstructing material. After
much experience with all of them that have been in general use, I have
become convinced that the only satisfactory way to avoid the
difficulty in question is to retain the outflow of the sink until a
certain considerable quantity has accumulated, and until its grease
has entirely {222} congealed, then to discharge the whole volume
rapidly through a pipe of small calibre. This may be done with
Carson's grease-trap by throwing in a pail of water to start a siphon
action when the vessel has become filled to its overflow-point. It is
more simply accomplished by a device of my own, wherein the whole
outflow is retained by a plug at the bottom of a large vessel working
after the manner of the plug of a wash-basin, until it is filled to
the level of the sink, and then opening the outlet for its sudden
discharge.
Good workmanship is as important as, if not indeed more important
than, good arrangement. It seems a very simple proposition to say that
all waste-pipes, whose office it is to carry foul liquids out of the
house, should be made tight in material and in joint. It is a
remarkable fact, however, that leaky joints in soil-pipes and in
drains are by no means rare. Probably there are few houses, very few,
in which they do not occur. The soil-pipe is put together by inserting
the small end of each section into the bell at the top of the section
below it, practically like putting the outlet of one funnel into the
larger upper portion of another. There may be abundant space for
leakage at every joint from the top to the bottom of the house,
without there being the least show of the leakage of water. The foul
air within the pipe may escape freely through a dozen openings, while
the heavier liquid flow takes its easiest and most direct course
downward from the point of one pipe through the bell of the one below.
When we come to the horizontal run of the soil-pipe in the basement,
if an imperfection of the joint occurs on the lower side there is an
obvious drip, which continues at least until closed by rust. Similar
imperfections in other parts of the joint would not be so manifested.
It has recently been demonstrated that there is no safety in the
construction of soil-pipes short of that absolute assurance which can
be secured only by an efficient test. Plugging all the outlets of the
soil-pipe and filling it with water, the slightest leak will be
exposed.
However defective may be the condition of an iron soil-pipe, vertical
or horizontal, it is perfection itself compared with the usual state
of a drain laid under the cellar floor; and here is a point where the
least experienced inspector of house drainage cannot be mistaken.
Under all circumstances, at least in all work hitherto executed, he
should demand as absolutely necessary that the drains under the cellar
floor be removed, that the earth which has been fouled by the leakage
of its joints and its breaks shall be taken out to the clean untainted
soil below, and refilled with well-rammed pure earth or with concrete,
the drainage being carried through a properly-jointed iron pipe above
the pavement, and preferably with a fall from the ceiling of the
cellar to near the floor at the point of outlet--in full sight for the
whole distance. It sometimes happens that the necessity for using
laundry-tubs or other vessels in the cellar makes the retention of an
underground course imperative. When retained, the drain should be of
heavy cast iron with most securely leaded joints tested under a head
of several feet. When found to be tight and secure, it should not be,
as ordinarily recommended, left in an open channel covered with boards
or flags and surrounded by a vermin-breeding, unventilated and
uninspected space, but closely and completely imbedded in the best
hydraulic cement mortar. Its careful testing before this {223}
enclosure is of course the only condition under which the work can be
permitted.
Tightness of all waste-pipes being secured, the next point in order is
their proper ventilation. A good deal has been said, and little has
been proved, about the different effects on the human system of the
gases of decomposition which have been produced in the absence of a
sufficient circulation of air, and those produced where the
ventilation and dilution are more complete. The probabilities of the
case are, of course, entirely in favor of the latter condition, and it
is accepted by all sanitarians as an axiom that all water-ways and all
vessels in which organic decomposition, even the decomposition of
adhering slime, takes place, should be ventilated as thoroughly as
possible. Until about ten years ago nearly all waste-pipes were
tightly closed at the top, and were shut from the sewer by a trap at
the foot, allowing absolutely no communication between the outer air
and the atmosphere of the pipe except as fresh air might be carried in
through the water-seals of the traps at each end. At about that time
it was becoming the general custom in the better class of work to
carry a small vent-pipe, often only one inch in diameter, rarely more
than two inches in diameter, through the roof of the house, closing it
at the top and perforating it with a few inefficient holes. This had
undoubtedly the effect of relieving the pressure on the atmosphere of
the pipe caused by the filling of unventilated sewers with tide-water
or storm-water, or by a sudden increase of temperature from the
admission of hot water. Later, it was accepted as a universal rule,
and it became a quite general practice, to carry the soil-pipe above
the roof with its full diameter, providing its summit with some form
of ventilating cowl. All this constituted not ventilation, but
venting. Real ventilation was introduced only with the very recent
improvement of admitting fresh air at the foot of the soil-pipe, so as
to make a complete circulation from one end to the other--a
circulation sufficient to produce, by the diffusion of gases, a very
fair ventilation of lateral waste-pipes of moderate length. It is now
coming to be understood that ventilating cowls, of whatever form, are
an obstruction to the movement of air in the absence of wind, and
that, as what is needed is never a vigorous current, but always a
living one, these cowls had better be dispensed with. We have learned,
too, that the most efficient means for increasing the flow of air
through the top is to increase its diameter at the top, enlarging the
highest length of a four-inch pipe, for example, to a diameter of six
inches. With this arrangement, and with a foot-ventilation four inches
in diameter opening at a point where it can never be obstructed by
rubbish or by snow, there will be secured a condition perhaps more
efficient in improving the condition of an imperfectly drained house
than any other one thing that may be done.
I have sketched above, in a very hurried manner, the main outline of a
system of house-drainage which may be accepted or which may be
recommended by a physician with confidence of securing a good result.
To go more into detail in technical matters would be out of place in a
paper of this character. Before leaving this subject, however, it is
important to call attention to the fact that what is recognized in our
houses as sewer gas is in far greater degree the product of
decomposition taking place within the house-drains themselves than the
product {224} of decomposition in the distant sewer forced into the
house through its connecting drain. It is emphatically a case of the
beam in our own eye as compared with the mote in the eye of our
neighbor. It is a rule which has exceptions, but they are few, that
the contained air of the house-pipes is far worse than the contained
air of the sewer; and the conviction is growing that the use of a trap
to the main drain between the house and the public sewer is more often
objectionable than advantageous. Such a trap always tends to check the
flow of the drain and to induce deposits whose decomposition is
objectionable. Wherever the abandonment of the trap is anything like
universal the considerable ventilation of the sewer thereby secured
brings its atmosphere to a condition which makes it not objectionable,
and generally useful, as a source of movement in the air of the
interior drain- and soil-pipe.
(_a_) Public sewers are more or less good or bad entirely according to
their character and condition. As a rule, a well-flushed sewer which
is used for no other purpose than the removal of foul waste, built on
what is called the separate system, and automatically flushed at least
daily, may be considered to be, if well laid and tightly jointed,
absolutely safe. A public sewer of large size and of irregular
construction, receiving not only household wastes, but the wash of
streets as well, may be regarded at least as an object of grave
suspicion. These general statements may be so far qualified by the
character of the sewers of each class as to run very nearly together;
that is to say, separate sewers, with leaky joints, irregular grades,
defective alignment, insufficient flushing, and inadequate restriction
as to the matters they are to receive, will be an intolerable and
dangerous nuisance; on the other hand, a large brick sewer built in
the best manner and of the best material, with sufficient fall and
sufficient supply to maintain itself in a cleanly condition, is free
from the serious drawbacks which usually attach to sewers of this
class.
With sewerage as with house-drainage it is not worth while to attempt
here to give anything like detailed directions for inspection and for
reformation. It will suffice to call attention to this one broad and
general rule: Every sewer or drain having for its object the removal
of putrescible organic matters must be so arranged as to maintain
itself in a condition of practically absolute cleanliness, without, as
in the case of storm-water sewers, waiting for the flushing effect of
storms, which often come only at long intervals, during which the
worst condition of decomposition may be established. Whether the sewer
be intended for drainage only or for both drainage- and storm-water,
if it contains at any time deposits of any kind, it is defective--more
or less so, of course, according to the extent and duration of the
accumulation.
Although it should be rigidly insisted upon in every case that the
sewer should maintain itself free from deposits, there will still be,
unavoidably, a certain amount of foul gas produced by the
decomposition of the matters coating its walls, and in order to dilute
and to remove this, and perhaps in order to modify their original
character, the most thorough ventilation is necessary.
Any sewer or other drain which at any time gives forth the odor of
putrid decomposition is in bad condition and should be at once
rendered inoffensive. So far as I know, there is no exception to this
rule. I have met no conditions in towns of any size where absolute
self-cleansing may {225} not be secured. It is worth while, however,
to repeat here the statement made above, that sewer gas, in so far as
it is a serious factor in connection with the drainage of houses, is
the product of the interior pipes of the house much more frequently
than of the public sewer in the street.
(_b_) The disposal of liquid wastes by irrigation, so far as this
method is applied to the outflow of public sewers, is not of especial
interest here, but an important modification has been made of the
system of irrigation which is of the greatest consequence in
considering the sanitary improvement of isolated country-houses, of
hospitals, prisons, etc., and of houses in towns about which there is
a small amount of available land. The process which has been found
best suited to the purpose is the invention of the Rev. Henry Moule,
the inventor of the earth-closet. He found it a serious drawback to
the dry-earth system that it was incapable of taking care of the
liquid wastes of the house. He devised a method of conducting the
liquid into very shallow drains made with open-jointed agricultural
drain-tiles, so porous in their character as to allow the liquid
carried by them to escape at the joints into the soil, and thus get
the benefit of its purifying qualities without the unsightly and often
offensive process of allowing the liquid to flow over the surface. The
first use made of this system was about 1866. Since that time its use
has extended very considerably both here and in England, and many
improvements have been made in its details, so that it may now be
accepted as entirely satisfactory.
The process in its best development, as applied to the drainage of
single houses, may be thus described, many of the appliances used
being the subject of patents: The outflow from the house is delivered
into a settling-basin or grease-trap of sufficient size to still the
flow, to cause solids to settle to the bottom, and grease and other
light matters to float at the top. The outlet from this basin is
through a pipe having its inlet at some distance below its
overflow-point; that is, at the level of the comparatively clarified
liquid, below the grease and above the sediment. The outflow passes
into another vessel known as a flush-tank, where it accumulates until
it reaches the summit of a self-acting siphon. This height being
reached, any considerable addition to the flow sets the siphon in
action, and the whole contents of the flush-tank are discharged with
rapidity into the drain beyond. The discharge completed, air is
automatically admitted to the siphon, and no further flow can take
place until the flush-tank has again been filled. The drain, of iron
or vitrified pipes tightly joined, is continued to the edge of the
ground prepared for purification. It here delivers into a series of
open-jointed agricultural tiles, laid with their bottoms not more than
ten inches below the surface of the ground. The total length of these
tile-drains is regulated according to the discharging capacity of the
flush-tank, with a view to their becoming entirely filled at each
discharge. Within a short time after the flow has ceased the liquid
has all left the pipes and entered the soil, its impurities being
retained and its filtered water settling away into the porous or
artificially drained ground below. During the interval between the
discharges of the flush-tank, a day or more, the process of
purification (oxidation) of the retained impurities goes on in the
soil, and its thorough aeration prepares it to purify the next
discharge. This method of {226} disposal is now employed in connection
with hundreds of houses, and its use, which has in some cases
continued for a dozen years, is constantly increasing. Its application
implies a certain amount of fall, but this amount need not be great.
The discharging height of the tank need not be more than twelve
inches. The main outlet need not fall more rapidly than at the rate of
1 to 300, and the absorption-drains ought not to fall more rapidly
than at the rate of 1 to 600. If the tank can be built on the top of
the ground, an average surface fall of 1 to 400 can usually be made to
meet all the requirements. Where waste matters are to be removed from
cellars and basements below the level of the ground, a greater fall is
necessary, or the wastes which are there collected must be thrown to
the tank by pumping or otherwise.
Where there is a bit of grass-land a little removed from the house
(and from sight), it answers a perfectly satisfactory purpose to
dispense with the absorption-drains and to deliver the main outlet
directly on to the surface of the ground. The effect in both cases is
entirely different from what it would be were the flow of the drains
not regulated by the use of the flush-tank. The moment we have a
constant slight discharge, either on the surface of the ground or into
the absorption-drains, we establish a condition of constant saturation
which leads to the over-fouling of a small area, which is rarely if
ever purified by aeration. For an intermittent discharge some form of
flush-tank is an absolute necessity. It is often found in practice,
where the flow from the house is considerable, that the discharge of
the house-drains into the settling-basin produces such an agitation of
its contents as to set in motion and to carry into the flush-tank bits
of paper partly macerated, grease, etc. This has been met by a recent
improvement, which consists in building a transverse wall in the
settling-basin, which checks the current from the house-drain and
causes the flow from the house side of the wall to pass over its top
in a thin small current which does not materially agitate the contents
of that part of the basin from which the outflow pipe is fed.
(_c_) The cesspool is still the chief reliance of the world at large.
There is nothing to be said in its favor save what may be based on the
old adage that "what is out of sight is out of mind." There is
everything to be said in its condemnation, whether we regard its
contents as a great mass of putrefying and infecting filth, as the
source of oozings which travel through crevices of rocks, through
layers of gravel, through seams in clay, or through lighter soils into
and under cellars and into drinking-water wells and defectively
constructed cisterns, or as an ever-active gas-retort supplying the
pipes of the house with the foulest products of putrefaction. It is in
all respects and under all circumstances a curse, unless placed far
away from the possibility of tainting the air we breathe or the soil
over which we live, or from which we or others take our
drinking-water, and even then it had better be abandoned.
The simple drainage of the soil involves a question of the greatest
importance. If the ground under the house or about it is at any time,
unless perhaps immediately after heavy rains, saturated with moisture,
we have to apprehend a condition of insalubrity more or less serious
in proportion to the degree of saturation and the degree of foulness
with which this is associated. The drainage requirements of land
outside of the house are less easily determined, but it requires
nothing more than a casual {227} examination of the cellar in
ordinarily wet weather to determine whether or not an improvement of
its soil-water drainage is necessary. If it is at such times wet, or
even persistently damp, thorough drainage is demanded; and it is only
necessary to say that this should be secured by some process which can
under no circumstances bring the air of the cellar into communication
with the air of a sewer or foul drain.
* * * * *
I have purposely abstained in the foregoing remarks from invading the
province of the physician or the physiologist by discussing the
influence of bad drainage on the health of those living subject to it.
It may safely be assumed that physicians who care enough about the
subject to interest themselves in investigating the condition of local
or general drainage have convictions concerning it which could not be
strengthened by the opinion of one belonging to another profession.
The assumption is also confidently made that no intelligent medical
man will hesitate for a moment to accept the dictum that the site of
the house must be dry, and that it and its neighborhood must be
entirely exempt from the influence of foul organic decomposition.
{229}
GENERAL DISEASES.
FROM SPECIAL MORBID AGENTS OPERATING FROM WITHOUT.
SIMPLE CONTINUED FEVER.
TYPHOID FEVER.
TYPHUS FEVER.
RELAPSING FEVER.
VARIOLA.
VACCINIA.
VARICELLA.
SCARLET FEVER.
RUBEOLA.
ROTHELN.
MALARIAL FEVERS.
PAROTITIS.
ERYSIPELAS.
YELLOW FEVER.
DIPHTHERIA.
CHOLERA.
PLAGUE.
LEPROSY.
EPIDEMIC CEREBRO-SPINAL MENINGITIS.
PERTUSSIS.
INFLUENZA.
DENGUE.
RABIES AND HYDROPHOBIA.
GLANDERS AND FARCY.
MALIGNANT PUSTULE.
PYAEMIA AND SEPTICAEMIA.
PUERPERAL FEVER.
BERIBERI.
{231}
SIMPLE CONTINUED FEVER.
BY JAMES H. HUTCHINSON, M.D.
DEFINITION.--A continued, non-contagious fever, varying in duration
from one to twelve days, and in temperate climates almost invariably
ending in recovery. It may arise from any non-specific cause capable
of producing a temporary derangement of one or more of the important
functions of the body, is generally easily distinguished from the
other continued fevers by the absence of the characteristic symptoms
of these diseases, and presents in fatal cases no specific lesions.
SYNONYMS.--Synocha, vel Synochus Simplex, Febricula, Ephemera or
Ephemeral Fever, Irritative Fever, Ardent Continued Fever, Sun Fever.
HISTORY.--Much difference of opinion continues to prevail, even at the
present time, in regard to the existence of a simple continued fever,
which, on the one hand, occurs independently of local inflammations or
traumatic causes, and, on the other, is distinct from typhoid, typhus,
and relapsing fevers; many observers contending that the condition to
which this name is given is only a mild or modified form of one or
other of the graver varieties of continued fever, from which the
characteristic symptoms are absent. Prominently among modern writers,
Dr. Tweedie[1] has taken this view of the subject, for, after
reviewing the arguments for and against the recognition of simple
continued fever as a distinct disease, he asserts that there is not
sufficient evidence to justify us in encumbering our nosology with a
doubtful novelty. If, however, there is room for doubt as to its right
to a place in the list of diseases, there is certainly no good reason
for characterizing it as a novelty, since it has been referred to,
according to Murchison,[2] by many authors from the time of
Hippocrates down to the present day, who not only separate it from the
graver forms of fever, and give a very accurate description of its
symptoms, but seem to have been perfectly familiar with the causes
which give rise to it, and to have had very correct notions as to its
proper management. Thus, Riverius[3] was aware of the existence of two
forms of simple fever--the ephemeral, which lasts, as its name
implies, only a single day, and the Synochus Simplex, arising from the
same causes, but in which the fever continues for from four to seven
days. Strother[4] and Ball[5] also allude to this fever in terms that
leave no doubt upon the mind but that they distinguished it clearly
from other forms of continued fever. {232} Among more recent writers
who have made this distinction may be mentioned Lyons,[6] Jenner,[7]
G. B. Wood,[8] Flint,[9] Murchison,[10] and J. C. Wilson.[11] Indeed,
the weight of authority is decidedly on the side of those who claim
for it a recognition as a distinct and separate disease.
[Footnote 1: _Lectures on the Continued Fevers_.]
[Footnote 2: _A Treatise on the Continued Fevers of Great Britain_,
London, 1873.]
[Footnote 3: _The Practice of Physick, being chiefly a Translation of
the Works of Lazarus Riverius_, London, 1678.]
[Footnote 4: _A Critical Essay on Fever_, 1718.]
[Footnote 5: _A Treatise on Fevers_, London, 1758.]
[Footnote 6: _A Treatise on Fever_, London, 1861.]
[Footnote 7: _Medical Times_, March 22, 1851.]
[Footnote 8: _A Treatise on the Practice of Medicine_, Philadelphia,
1855.]
[Footnote 9: _A Treatise on the Principles and Practice of Medicine_,
Philadelphia, 1868.]
[Footnote 10: _Ibid._]
[Footnote 11: _A Treatise on the Continued Fevers_, New York, 1881.]
Unquestionably, many cases which have been classed under the head of
simple continued fever, are really mild or abortive cases of typhoid
or typhus fever, in which, in consequence of partial protection on the
part of the patient, the characteristic symptoms of these diseases
have not been developed. Such cases are seen in numbers during
epidemics of these diseases. But, making due allowance for this source
of error, there yet remain many cases which cannot be thus explained.
Moreover, the disease occurs at times when no such epidemics exist. It
may, therefore, be safely assumed that there is such a fever, and
that, consequently, it must be accorded full recognition.
CAUSES.--Any non-specific cause which is capable of producing a
profound derangement of one or more of the important functions of the
body may give rise to simple continued fever. It may follow,
therefore, upon excesses of the table, extreme mental or bodily
fatigue, exposure to the direct rays of the sun, or to great heat or
cold, or upon the suppression of a secretion. One of its most frequent
causes is over-exertion in warm weather. James C. Wilson has called
attention to its frequent occurrence as a consequence of the combined
influence of the excitement, the physical exhaustion, and the exposure
to the direct rays of the mid-day sun which are attendant upon
surf-bathing. It is often due in young children to the irritation
involved in the process of teething or to that caused by the presence
of worms in the alimentary canal. Wood taught that it might also
sometimes occur during the prevalence of contagious diseases as an
effect of the epidemic influence in those who were partially protected
by a previous attack of the disease, or from some other cause, but it
is more probable that cases arising under these circumstances are
either mild cases of the prevalent disease or else are attributable to
fatigue from nursing or to over-anxiety. The disease is more common in
the young than in the old, and in children than in adults--probably
from the greater impressionability of the nervous systems of the
latter.
The causes of the ardent continued fever of the tropics, which is
usually recognized as a form of simple continued fever, do not differ
materially, except in degree, from those of the simpler forms of the
disease; but exposure to the direct rays of the sun would seem to be
especially prone to give rise to the disease in those who are
unaccustomed to the heat of a tropical climate. Robust young Europeans
lately arrived in a warm country are, it is said, peculiarly liable to
suffer from it.[12] It is most common in those parts of India which do
not experience much of the benefit of the monsoon rains, and whose hot
season is not tempered by regular breezes from the sea. It is hence
more frequently met with {233} in inland districts in which the
temperature is high, but in which malaria-generating conditions are
absent.
[Footnote 12: Morehead, _Clinical Researches on Diseases in India_,
London, 1856; also Twining, _Clinical Illustrations of the More
Important Diseases of Bengal_, Calcutta, 1835.]
SYMPTOMS AND COURSE.--Simple continued fever occurs in this country
only as a sporadic disease, and almost invariably ends in recovery; in
tropical climates, however, it may prevail epidemically, and sometimes
presents symptoms of a very grave character. In its mildest form it
not infrequently runs its course in a few hours, and is rarely
prolonged much beyond twenty-four, and is hence called ephemera. It
then usually begins somewhat abruptly with a chill, but in a few
instances this is preceded by feelings of languor and weariness.
Febrile reaction is soon established, and is generally well marked;
the pulse is quick and full, the temperature rises rapidly, and the
face is flushed. The tongue is coated with a whitish fur, the urine is
scanty and high-colored, and the bowels are constipated. Other
symptoms are excessive thirst, headache, restlessness, and
sleeplessness, or, on the other hand, a tendency to somnolence.
Vomiting is not common except in those cases which follow upon an
error of diet, but there is generally some nausea and anorexia.
Muscular pains are also occasionally present, and may give rise to a
good deal of distress. The subsidence of these symptoms is often quite
as abrupt as their onset, the crisis being frequently marked by a
copious perspiration.
In other cases, however, the fever is more prolonged, and the
symptoms, although not differing in kind, are apt to be more severe
than those above detailed. The pulse is often full, hard, and
bounding; the headache throbbing or darting in character; the tendency
to somnolence increases, or gives place to delirium; and the pyrexia
is more marked. Frequently an eruption of herpes is observed upon the
lips and upon other parts of the face, from which circumstance the
disease is sometimes called herpetic fever. Davasse[13] also observed
in a few cases pale bluish spots, not elevated above the surface and
not disappearing under pressure, which are identical with the taches
bleuatres sometimes seen in typhoid fever and other diseases, and
therefore have no diagnostic value. In this form the duration of the
disease may be from four to ten or twelve days. The defervescence is
usually less rapid than the rise in temperature, and is generally
accompanied by a free perspiration, diarrhoea, a copious deposit of
urates in the urine, or less frequently by hemorrhage from the uterus
or rectum,[14] or from the nose, mouth, or urethra. This constitutes
the synocha or inflammatory fever of the older writers. In children in
whom there is no reason to suspect malarial poisoning the disease
sometimes assumes a remittent form, and then constitutes a variety of
the infantile remittent fever of authors--a name, however, which, it
must be remembered, has been made to include a great many distinct
diseases.[15]
[Footnote 13: Quoted by Murchison.]
[Footnote 14: Murchison.]
[Footnote 15: Lyons.]
When the disease occurs in individuals who are broken down in health
from any cause[16]--as, for instance, previous illness, deficient
food, long-continued anxiety, or great fatigue--it not infrequently
presents symptoms of an asthenic character. The febrile reaction is
then less intense, and the pulse feebler and more frequent, than in
the variety just described. The duration of the disease in this form
is also generally longer. Murchison has proposed for it the name of
simple asthenic fever.
[Footnote 16: Wood.]
Under the name of ardent continued fever, Indian medical writers have
described a variety of the disease which is frequently met with in
tropical {234} countries, and which is usually much more severe than
the varieties already referred to. In addition to the symptoms
presented by these, Morehead[17] says that there is often intolerance
of light and sound, contracted and subsequently dilated pupils,
ringing noises in the ears, anxious respiration, pains in the limbs
and loins, and a sense of oppression at the epigastrium. The bowels
are sometimes confined; at others vitiated bilious discharges take
place. The tongue is white, often with florid edges, and the urine
scanty and high-colored. At the end of from forty-eight to sixty hours
the febrile phenomena may subside, the skin become cold, and death
take place from exhaustion and sudden collapse. In some cases the
symptoms of cerebral disturbance are greater in degree, and in these
coma may soon supervene upon delirium. Convulsions, epileptiform in
character, with relaxation of the sphincters and suppression of urine,
also frequently occur, and occasionally cerebral hemorrhage. In other
cases the symptoms of gastritis are more prominent, or jaundice may
appear and aggravate the disease.
[Footnote 17: _Clinical Researches on Disease in India_, London, 1856.
See also "Croonian Lectures," by Sir Joseph Fayrer, _Brit. Med.
Jour._, April 29, 1882.]
Symptoms closely resembling those just described are occasionally met
with in this country in patients who have been exposed for some time
to the direct rays of the summer sun, but who have escaped a
sunstroke. Indeed, a few writers have been so much impressed with the
general resemblance which this latter condition bears to the fevers
that they have insisted upon including it in this group, and have
given it the name of thermic or heat fever. This view of the pathology
of sunstroke has, however, never been generally accepted.
One of the most characteristic symptoms of the disease in all its
forms is the rapid rise of temperature, which may in ephemera be as
great as from four to seven degrees in the course of a few hours, and
which may be followed in a few hours more by an equally abrupt
defervescence. When the fever is more prolonged, although the
temperature rises rapidly, it may not attain its greatest elevation
for from forty to sixty hours after the onset of the symptoms, and its
fall will be more gradual than in the preceding variety.
Unfortunately, there are no reliable thermometric records of ardent
continued fever. The urine is usually scanty and high-colored during
the height of the fever, especially in the severer forms of the
disease. Its specific gravity is high, and it contains a large amount
of solids, especially of urea. With the fall of the temperature it
rapidly increases in quantity, and is very apt to let fall a copious
lateritious sediment on cooling. According to Parkes,[18] who closely
observed six cases with the view of determining this question,
albuminuria does not occur at any stage of the disease. Convalescence
is usually rapid, and is not liable to be interrupted by the
occurrence of sequelae.
[Footnote 18: _The Composition of the Urine_, by Edmund A. Parkes,
M.D., London, 1860.]
DIAGNOSIS.--The diagnosis in those cases of simple continued fever in
which the connection between the disease and some one of the
conditions which have been referred to above as capable of exciting it
has been distinctly made out, presents little difficulty. It is
otherwise, however, when this relationship is not apparent. Indeed,
the symptoms of the disease so closely resemble those of an abortive
or mild attack of typhoid or typhus fever, in which the characteristic
eruption is wanting, that the {235} physician may sometimes remain in
doubt as to the nature of the disease he has been called upon to
treat, even after the recovery of the patient. This difficulty will of
course be especially likely to present itself during the epidemic
prevalence of these diseases. Simple continued fever may, however,
generally be distinguished from either of the latter by the much
greater severity of its initial symptoms, and particularly by the
rapid rise of temperature--a rise of from four to seven degrees in the
course of a few hours--which does not take place in these fevers, but
which, it must be remembered, may occur in erysipelas, measles,
pneumonia, and some other diseases. The absence of a characteristic
eruption, although it would not render it certain, would be in favor
of the diagnosis of simple continued fever, as would also the absence
of diarrhoea in cases in which there was difficulty in deciding
between this disease and typhoid fever. On the other hand, Murchison
regards the presence of an herpetic eruption on the lips as almost
pathognomonic of simple continued fever; but in this country such an
eruption is not an infrequent attendant upon fevers of malarial
origin, and many observers attach great importance to it in the
diagnosis of these diseases.
Simple continued fever is not likely to be mistaken for relapsing
fever, except during epidemics of the latter disease. It may be
discriminated from relapsing fever, the first paroxysm of which it
closely resembles, by the absence of severe articular pains, of
tenderness in the epigastric zone, of enlargement of the liver and
spleen, and of jaundice. It may be mistaken for tubercular meningitis,
especially in those cases in which the nervous symptoms are more than
usually prominent, or in which a hereditary predisposition to
tuberculosis exists; but its true nature may generally be recognized
by its more abrupt commencement, and by the absence of the constant
vomiting, screaming fits, strabismus, and paralysis so characteristic
of the latter disease.
It is scarcely necessary to add that a local inflammation or a
traumatic cause may give rise to symptoms simulating those of simple
continued fever, and that the diagnosis of this disease must be
uncertain until these conditions have been positively ascertained to
be absent, or, if present, until they have been proved to be
complications, and not the causes of the disease.
PROGNOSIS.--The prognosis of this disease, as it is met with in this
country, is favorable. Indeed, when uncomplicated it may be said to
end invariably in recovery, except in the aged and feeble, in whom,
when it occurs during the great heat of the summer season, it is apt
to assume the asthenic form, and to be accompanied by symptoms of a
grave character. The ardent continued fever of the tropics, on the
other hand, not infrequently terminates fatally, or may leave the
sufferer from it a chronic invalid for life, which is frequently
shortened by obscure cerebral or meningeal changes, which give rise to
irritability, impaired memory, epilepsy, headache, mania, partial or
complete paraplegia, or blindness.[19]
[Footnote 19: Sir Joseph Fayrer, K.C.S.I., M.D., F.R.S., _Brit. Med.
Jour._, April 29, 1881, p. 607.]
ANATOMICAL LESIONS.--Death so rarely occurs in this latitude from
simple continued fever that the opportunities for making post-mortem
examinations do not often occur. There are, however, a sufficient
number of such examinations on record to show that the disease gives
{236} rise to no specific lesions. According to Murchison and
Martin,[20] inspection in fatal cases of ardent continued fever
usually reveals the presence of great congestion of all the internal
organs and of the sinuses of the brain and pia mater, of an increased
amount of intracranial fluid, and occasionally of an effusion into the
abdominal cavity, and more rarely into the thoracic cavity.
[Footnote 20: _The Influence of Tropical Climates on European
Constitutions_, by James Ranald Martin, F.R.S., London, 1856.]
TREATMENT.--In the milder forms of the disease little or no treatment
is required--a fact which seems to have been recognized and acted upon
long ago, since Strother remarks that the cure of it is so easy that
physicians are seldom consulted about such patients. An emetic when
the attack has been caused by excesses of the table, and there is
reason to believe that there is undigested food in the stomach, a
purgative when constipation exists, and cooling drinks, the
effervescing draught or some other saline diaphoretic, are usually the
only remedies that are called for. In cases in which the febrile
action is more intense and prolonged, in addition to the use of these
remedies an effort should be made to reduce the heat of the skin and
the frequency of the pulse by sponging with cold water and by the
administration of digitalis and aconite. The headache which is often a
distressing symptom may usually be relieved by the application of
evaporating lotions, and restlessness quieted by the bromides.
Subsequently, quinia may be given with advantage. The patient should
be restricted to liquid diet during the continuance of fever.
In the asthenic form quinia and the mineral acids, nutritious food,
and very frequently alcoholic stimulants, must be given from the
beginning. In the treatment of the ardent continued fever of the
tropics the cold affusion or the cold bath, with quinia, would appear
to be indicated, but Morehead and other Indian physicians advise the
use of evacuants with copious and repeated venesections, cupping, and
leeches, aided by tartar emetic, till all local determination and the
chief urgent symptoms are removed; and Murchison expresses the belief,
founded on his own observations, that life is often sacrificed by
adopting less active measures.
{237}
TYPHOID FEVER.
BY JAMES H. HUTCHINSON, M.D.
DEFINITION.--An endemic infectious fever, usually lasting between
three and four weeks, and associated with constant lesions of the
solitary and agminate glands of the ileum, and with enlargement of the
spleen and mesenteric glands. Its invasion is usually gradual and
often insidious. Sometimes the only symptoms present in the beginning
are a feeling of lassitude, some gastric derangement, and a slight
elevation of temperature; at others there are slight rigors or chilly
sensations, headache, epistaxis, diarrhoea, and pain in the abdomen.
The principal symptoms of the fully-formed disease are a febrile
movement possessing certain characters, headache passing into delirium
and stupor, diarrhoea associated with ochrey-yellow stools,
tympanites, pain and gurgling in the right iliac fossa, a red and
furred tongue, which later often becomes dry, brown, and fissured; a
frequent pulse; an eruption of rose-colored spots, occurring about the
seventh or eighth day, slightly elevated above the surface,
disappearing under pressure, and coming out in successive crops, each
spot lasting about three days; prostration not marked in the
beginning, but rapidly increasing; and occasionally deafness, sweats,
and intestinal hemorrhages. When recovery takes place, the
convalescence is usually tedious, and may sometimes be protracted by
the occurrence of one or more relapses.
SYNONYMS.--The following are a few of the many names which have been
given to the disease at different times. Most of them have ceased to
be applied to it, and only three or four of them are at present in
general use: Febris Mesenterica, 1696; Slow Nervous Fever, 1735;
Febricula or Little Fever, 1740; Typhus Nervosus, 1760; Miliary Fever,
1760; Typhus Mitior, 1769; Synochus, 1769; Common Continued Fever,
1816; Gastro-Enterite, 1816; Entero-Mesenteric Fever, 1820; Abdominal
and Darm Typhus, 1820; Typhus Fever of New England, 1824;
Dothienterie, 1826; Enterite-folliculeuse, 1835; Infantile Remittent
Fever, 1836; Enterite Septicemique, 1841; Mucous Fever, 1844; Enteric
Fever, 1846; Intestinal Fever, 1856; Ileo-Typhus, 1857; Pythogenic
Fever, 1858; Mountain Fever, 1870.
NAME.--It has been objected to the name "typhoid fever" as a
designation for this disease that it tends to perpetuate among the
laity the mistaken impression that typhoid fever is only a modified
typhus fever, and also that the word typhoid has been generally
applied to a condition of system which is common to a great many
different diseases, {238} and which is not of necessity present in
this. In spite of these objections, and although it must be admitted
that they are not without force, I prefer to retain the name typhoid
fever, and for the following reasons: 1st. It was the name given to
the disease by Louis, to whom we owe the first full and accurate
description of it. 2d. It is the name by which it is best known to the
profession, not only in this country but abroad. 3d. No other name has
been proposed for it which is not quite as much open to criticism.
Thus the term enteric fever, originally suggested by the late George
B. Wood, and adopted by the London College of Physicians in its
_Nomenclature of Diseases_, is objectionable because it brings into
undue prominence the intestinal lesions and implies that they are the
cause of the fever. The same objection may be urged against the name
"intestinal fever," proposed by Budd. The name "pythogenic fever"
rests upon a theory of the disease which has never been proven, and is
regarded by most observers as untenable. Under these circumstances
even the influence of its distinguished proposer, the late Dr.
Murchison, has been insufficient to secure its adoption by the
profession at large.
HISTORY.--Certain passages in the writings of Hippocrates have been
appealed to by Murchison and other physicians in support of the
opinion that typhoid fever was a disease of at least occasional
occurrence in ancient times; but, although from the nature of its
causes it is probable that it has occurred in all ages and wherever
men have congregated in towns and villages, the descriptions given by
the Father of Medicine in the passages alluded to are not sufficiently
full to render it at all certain that typhoid fever had ever come
under his observation. Indeed, there is no author of an earlier date
than Spigelius[1] whose writings furnish any positive evidence that he
ever met with the disease. Spigelius, however, in spite of the doubt
thrown upon his observation by Hirsch,[2] would seem to have had
opportunities for examining the bodies of those who had died of it,
since he gives an account of several autopsies, in which he says that
the small intestine was inflamed and that that part of it next to the
caecum and colon was frequently sphacelated. Panarolus[3] also says
that the intestines had the appearance of being cauterized
("apparebant tanquam exusta") in some cases observed by him in Rome a
little later in the same century. Willis[4] would certainly appear to
have been familiar with two forms of fever, which, from the
description he gives of them, could have been nothing else but typhoid
and typhus fevers. Sydenham[5] also described a fever in which the
prominent symptoms were diarrhoea, vomiting, delirium, a tendency to
coma, and epistaxis, and which was distinguishable from the febris
pestilens by the absence of a petechial eruption. Baglivi[6] of Rome
in the latter part of the seventeenth century described the
haemitritaeus of previous writers {239} under the title of febris
mesenterica, and maintained that it was always accompanied by and
dependent on inflammation of the intestines and enlargement of the
mesenteric glands. A similar observation was made soon after by
Hoffmann,[7] and by Lancisi[8] in 1718. The latter seems to have fully
recognized the characteristics of the eruption, for he says that it
consisted of "elevated papules which disappeared completely on
pressure." In 1759, Huxham described, under the title "slow, nervous
fever," a disease which there can be no doubt was typhoid fever. He
moreover pointed out very clearly the distinctions between this
disease and another to which he gave the name of "putrid, malignant,
petechial fever," and which was unquestionably typhus. Sir Richard
Manningham[9] also described typhoid fever under the title of
"febricula, or little fever." In the preface of his work he calls
attention to its insidious origin, and to the fact that its gravity
was often underrated at its commencement, "till, at length, more
conspicuous and very terrible symptoms arise, and then the Physician
is sent for in the greatest hurry, and happy for the Patient if the
Symptoms, which are most obvious, do not, at this Time, mislead the
Physician to the Neglect of the little latent Fever, the true Cause of
these violent Symptoms." About the same time Morgagni[10] described
certain post-mortem examinations in which the lesions of the
intestines were evidently those of typhoid fever. Other authors, whose
works bear evidence that they were familiar with the symptoms or
lesions of typhoid fever, are Riedel, Roederer and Wagler, Stoll,
Rutty, Sarcone, Pepe, Fasano, Mayer, Wrenholt, Sutton, Bateman, Muir,
Edmonstone, Prost, Petit and Serres, Cruveilhier, Lerminier, and
Andral.
[Footnote 1: _De Febre Semitertiana_, Frankf., 1624; Op. Om.,
Amsterdam, 1745. Quoted by Murchison.]
[Footnote 2: _Handbuch der Historisch-Geographischen Pathologie_, von
Dr. August Hirsch, Stuttgart, 1881.]
[Footnote 3: _Observat. Med. Pentecostae; Romae_, 1652. Quoted by
Murchison.]
[Footnote 4: _Dr. Willis's Practice of Physick_, translated by Samuel
Pordage, London, 1684.]
[Footnote 5: _The Works of Thomas Sydenham, M.D., on Acute and Chronic
Diseases_, with a Variety of Annotations by George Wallis, M.D.,
London, 1788.]
[Footnote 6: _Opera Omnia Medico-practica et Anatomica_, Paris, 1788.]
[Footnote 7: _Opera Omnia Physico-Medico_, 1699. Quoted by Murchison.]
[Footnote 8: _Opera Omnia_, Geneva, 1718.]
[Footnote 9: _The Symptoms, Nature, etc. of the Febricula or Little
Fever_, London, 1746.]
[Footnote 10: Quoted by Hirsch.]
To Bretonneau[11] of Tours appears to belong the credit of having
first distinctly pointed out the association between certain symptoms
and the lesions of the solitary and agminated glands of the ileum. He
regarded the disease of the intestinal glands as inflammatory, and
therefore gave to it the name "dothienenterie" or "dothienenterite"
(from [Greek: dothien], a tumor, and [Greek: enteron], intestine),
but, unlike Prost, fully recognized the fact that there was no
necessary relation between the extent of the intestinal lesions and
the gravity of the febrile symptoms. Hirsch, however, claims this
honor for Pommer, whose little work on _Sporadic Typhus_ he thinks has
not received the consideration its merits deserve. Louis, to whom for
his careful study of typhoid fever we owe a large debt of gratitude,
was also fully aware of the lesions of the intestinal glands which
occur in this disease.
[Footnote 11: Quoted by Trousseau, _Archives Generales_, 1826.]
The progress in pathology which observers were making was temporarily
impeded about this time by the fact that while typhoid fever was of
frequent occurrence in Paris, typhus fever was comparatively rarely
met with and had not been epidemic there for several years.
Bretonneau, Louis,[12] Chomel, and indeed the greater number of
contemporary French physicians, therefore fell into the error of
supposing that the fever which was then common in England was
identical with that which they were describing, while the English
physicians of the period, with but few {240} exceptions, contended
with equal strenuousness that there was but one form of continued
fever, and that this was very seldom associated with disease of the
intestines. In the second edition of his work Louis abandoned his
former opinion, and admitted that the typhus fever of the English was
a very different disease from that which formed the subject of his
treatise; but the confusion which existed in England in regard to this
disease was not completely dispelled until the appearance in 1849 and
the following two years of several papers on this subject by Sir
William Jenner,[13] in which it was conclusively demonstrated that
typhoid and typhus fevers were separate and distinct diseases. In
Germany, however, the non-identity of these diseases was recognized as
early as 1810. Murchison says that the names by which they are still
generally known in that country, typhus exanthematicus and typhus
abdominalis, were given to them not long after.
[Footnote 12: _Researches Anatomiques, Pathologiques et Therapeutiques
sur la Maladie connue sur les Noms de gastro-entente, etc._, par P. C.
A. Louis, Paris, 1829.]
[Footnote 13: _Med. Chir. Trans._, vol. xxxiii.; _Edinburgh Monthly
Jour. of Med. Sci._, vols. ix. and x., 1849-50; and _Med. Times_,
vols. xx., xxi., xxii., xxxiii., 1849-51.]
The contributions made by American physicians to the knowledge of
typhoid fever have been both numerous and important. In 1824 it was
described by Nathan Smith[14] under the name of typhus fever of New
England, and in 1833, E. Hale, Jr.,[15] of Boston, published in the
_Medical Magazine_ for December an account of three dissections of
persons considered by him to have died of the disease. In reference to
these cases, Bartlett[16] says that if the diagnosis could be looked
upon as certain and positive they would constitute the first published
examples of intestinal lesion in New England. In February, 1835,
William S. Gerhard of Philadelphia, who was then under the impression
that the two diseases were identical, reported two cases under the
name of typhus fever, the symptoms and post-mortem appearances of
which he showed differed in no respect from those he had been
accustomed to see in the cases of typhoid fever he had observed with
Louis during his studies in Paris. The year after Gerhard had,
however, the opportunity of observing an epidemic of true typhus
fever, and was at once struck with the difference between the symptoms
of the cases which then fell under his care and of those he had seen
in Paris. In an admirable paper which appeared in the numbers of the
_American Journal of the Medical Sciences_ for February and August,
1837, he points out very clearly the differential diagnosis between
the two diseases. He particularly insisted on the marked difference
between the petechial eruption of typhus and the rose-colored eruption
of typhoid fever. He showed that the latter disease was invariably
associated with enlargement and ulceration of Peyer's patches and with
enlargement of the mesenteric glands, and that these conditions were
never presented in the former. He also fully recognized the fact that
typhus fever was eminently contagious, while, on the other hand, he
was fully aware that typhoid fever was not contagious under ordinary
circumstances, "although in some epidemics," he says, "we have strong
reason to believe it becomes so." The appearance of this paper marks
an epoch in the history of typhoid fever. Murchison, when speaking of
it, says that to Gerhard, and Pennock (who was associated with Gerhard
in his observations) certainly {241} belongs the credit of first
clearly establishing the most important points of distinction between
this disease and typhus fever, and M. Valleix alludes to it in terms
equally complimentary. It is undoubtedly owing to it, more than to any
other cause, that the differential diagnosis of these two diseases was
perfectly understood by the great body of the profession in this
country long before the question of the relation which they bore to
each other was definitely settled in Great Britain,[17] or even in
France.
[Footnote 14: _Medical and Surgical Memoirs_, Baltimore, 1831.]
[Footnote 15: _Observations on the Typhoid Fever of New England_,
Boston, 1839.]
[Footnote 16: _The History, Diagnosis, and Treatment of the Fevers of
the United States_, 1842.]
[Footnote 17: The honor of having first clearly pointed out the
distinguishing characters of typhoid and typhus fevers has been
recently claimed for Sir William Jenner, but, as we have seen above,
his papers on this subject were not published until thirteen years
after that of Gerhard.]
Bartlett gave in the _Medical Magazine_, June, 1835, a short account
of the entero-mesenteric alterations in five cases of unequivocal
typhoid fever, which alterations, he said, corresponded exactly to
those described by Louis. In the same year, James Jackson, Jr., of
Boston, published an account of the intestinal lesions observed by him
in cases during the years 1830, 1833, and 1834; and again in a _Report
of Typhoid Fever_, communicated to the Massachusetts Medical Society
in June, 1838, says that the alterations of Peyer's patches had been
noticed at the Massachusetts General Hospital previous to 1833 in
cases which were carefully examined. In 1840, Shattuck of Boston
published in the _American Medical Examiner_ an account of some cases
of typhoid and typhus fever which he had observed at the London Fever
Hospital during the previous year. In this paper, which had been
already communicated to the Medical Society of Observation of Paris,
and which had unquestionably exerted a marked influence upon medical
thought there, he pointed out very fully the distinguishing
characteristics of each disease. In 1842, Dr. Bartlett issued the
first edition of his work on _The History, Diagnosis, and Treatment of
the Fevers of the United States_, which contains very full
descriptions of both of these diseases, and of the means by which they
may be distinguished from each other. Since then there have been
numerous additions in this country to the literature of typhoid fever,
among the most important of which may be mentioned the chapter on the
disease in the respective works on _The Practice of Medicine_ by
Professors Wood and Flint, the article on typho-malarial fever in the
_Transactions_ of the International Medical Congress of 1876, and the
article in the work on _The Continued Fevers_, by James C. Wilson.
Abroad, the medical press has been no less active. Within the last
twenty or thirty years Jaccoud and Trousseau in France, Liebermeister
and Hirsch in Germany, and Tweedie and Cayley in England, have all
made important additions to our knowledge of the disease. To the late
Dr. Murchison[18] of London, however, is justly due the honor of
having produced the best treatise on typhoid fever in any language,
and the writer cheerfully acknowledges that he has drawn largely upon
it for the material of the present article.
[Footnote 18: _A Treatise on Continued Fevers_, London, 1873.]
GEOGRAPHICAL DISTRIBUTION.--Although it will be generally admitted
that the conditions of civilization favor the occurrence and extension
of typhoid fever, yet there is abundant evidence that they are not
absolutely necessary to its production, as there is no country,
whether civilized or not, of the diseases of which we have any
knowledge, in which it has not occasionally made its appearance, being
met with in every variety of climate. It is endemic in North America,
attacking alike the inhabitants {242} of Greenland and British America
and those of Mexico. In our own country it prevails from time to time
in every State of the Union, committing its ravages as well among the
rocks and hills of New England as in the more fertile valleys of the
West and South. In many of the newly-settled portions of our country
malarial fevers are, as is well known, exceedingly rife. In
proportion, however, as towns and cities spring up, and as the land is
properly drained, they diminish in frequency, and are gradually
replaced, to a certain extent at least, by typhoid fever; but the
influences which produced them retain for a long time enough of power
to stamp their impress upon all other diseases. In large portions of
the Western and Southern States typhoid fever is therefore rarely
uncomplicated, and is much more likely to assume the form which will
be fully described later as typho-malarial fever.
Typhoid fever has also occurred frequently in Central America and the
West India Islands. It has prevailed from time to time in the states
of South America, and occasionally assumed in some of them--as, for
instance, Brazil and Chili--an epidemic form.
Typhoid fever is endemic in the British Isles, but, according to
Murchison, is most common in England, more common in Ireland than in
Scotland, and in Scotland more common on the west than on the east
coast. It also exists as an endemic disease in every country of the
continent of Europe, from Sweden and Norway on the north to Turkey on
the south, and in some of them--as, for instance, France and
Germany--would seem to be of much more frequent occurrence than in
this country, or even in England. Medical literature is also not
deficient in evidence that it has prevailed at various times in all
the different countries of Asia and Africa and in Australia. Morehead
asserted in the first edition of his _Clinical Researches on Diseases
in India_ that India enjoyed an absolute immunity from typhoid fever,
but in the second edition of this work he acknowledged that a larger
experience had led him to change his opinion on this point. Moreover,
the writings of Annesley, Twining, and other Indian authors furnish
convincing proof that the disease is by no means unknown in that
country. Indeed, even the relative immunity from it which it has been
claimed that tropical and subtropical countries possess has been
found, upon a fuller study of the diseases of these countries, not to
exist to anything like the degree that was formerly supposed.
The occasional occurrence of typhoid fever in islands separated from
the main land by a considerable distance--as, for instance, the island
of Norfolk,[19] which is situated in the Pacific Ocean four hundred
miles west of South America--is an interesting fact, and one which,
with the present limits to our knowledge on the subject, it is
impossible to explain satisfactorily.
[Footnote 19: Metcalfe, _Brit. Med. Jour._, Nov., 1880.]
The ETIOLOGY of typhoid fever may be considered under the heads of--1,
predisposing, 2, exciting causes.
1. PREDISPOSING CAUSES.--All observers agree that the predisposition
to typhoid fever is greater in childhood and early adult life than
after thirty years of age. Thus, Murchison states that during
twenty-three years nearly one-half the admissions to the London Fever
Hospital were of patients between fifteen and twenty-five years of
age, and that in more than a fourth, the patients were under fifteen
years. On the other hand, {243} in less than a seventh were they over
thirty, and in only one in seventy-one did their ages exceed fifty.
Taking these facts in connection with the circumstance that the entire
population of England and Wales in 1861 was 12,481,323 persons under
thirty years of age and 7,584,901 above thirty, it follows, he says,
that persons under thirty are more than four times as liable to
enteric fever as persons over thirty. Jackson found that the average
age of the patients in two hundred and ninety-one cases observed at
the Massachusetts General Hospital was a little over twenty-two years,
the average age in the fatal cases being somewhat greater than in
those in which recovery took place. Liebermeister, from an analysis of
a large number of cases treated at the hospital in Basle, has arrived
at the same conclusion. No age, however, enjoys a complete immunity
from the disease. Manzini[20] has recorded a case in which lesions of
Peyer's patches similar to those of typhoid fever were found in a
seventh-month foetus which died within half an hour after its birth.
Cases are also on record in which death has occurred from this disease
in the first few weeks of life. I have myself observed several cases
in young children at the Children's Hospital in Philadelphia. The
probability is, that it is of even more frequent occurrence in
children than is generally supposed, as this class of patients is not
often admitted into general hospitals, and as from the absence of some
of its characteristic symptoms when it occurs in the very young the
nature of the disease is often unrecognized.
[Footnote 20: Quoted by Murchison.]
On the other hand, the disease occurs not infrequently in advanced
life: 83 cases out of 5911 were observed at the London Fever Hospital
in persons over fifty, 27 in persons over sixty, and in 2 the age was
seventy-five. In a case recorded by D'Arcy the age of the patient was
eighty-six, and in one reported by Hamernyk it was ninety.[21]
Bartlett long ago contended that the disease was not so rare as was
generally supposed among people over forty years of age; and there is
really no good reason to believe that the susceptibility to the causes
of the disease in an unprotected person diminishes with advancing
years, the immunity from this disease which elderly people appear to
enjoy being probably due to the fact that, as the disease is not
uncommon in early life, they are in many instances protected by having
already passed through an attack.
[Footnote 21: Quoted by Murchison.]
The mean age of the male patients treated at the London Fever Hospital
was slightly in excess of that of the female, but in the cases
analyzed by Jackson the reverse of this was observed.
The statistics of all general hospitals, with very few exceptions,
show a greater or less preponderance of males over females among the
typhoid fever patients treated in them. According to Murchison, of
5988 cases admitted into the London Fever Hospital during twenty-three
years, 3001 were males and 2987 were females. Of 891 cases admitted
into the Glasgow Infirmary during twelve years, 527 were males and 364
females. Liebermeister states that 1297 male typhoid patients and 751
female were treated in the hospital at Basle from 1865 to 1870.
Occasionally, the difference is even greater than is indicated by
these figures. Thus, of 138 cases observed by Louis, all but 32
occurred in males. When, however, we consider that the proportion of
men who apply for admission to hospitals when sick is much larger than
that of women, we should hesitate before accepting these statistics as
proof that the former {244} are more liable to be attacked by typhoid
fever than the latter. Indeed, the opinion which Murchison expresses
is generally accepted as correct by authors, that neither sex is more
likely than the other to contract the disease. Liebermeister asserts
that pregnant and puerperal women and those who are nursing infants
enjoy a relative immunity. On the other hand, Nathan Smith says that
while the sexes are equally liable to it, more women are cut off by it
than men, in consequence of its appearance during pregnancy or soon
after parturition.
It was long ago pointed out by certain French observers that newcomers
are much more liable to be attacked by typhoid fever than persons who
have lived for some time in an infected locality. In 129 cases
examined with reference to this point by Louis, the patients in 73 had
not resided in Paris more than ten months, and in 102 not more than
twenty months. Bartlett noticed that during an epidemic in Lowell
which he had the opportunity of observing the disease attacked the
recent residents in much larger proportion than the old. Liebermeister
also calls attention to this peculiarity of the disease. Murchison's
experience in reference to this point has been somewhat similar, for
he found upon examination of the records of the London Fever Hospital
that 21.84 per cent. of the patients admitted there for typhoid fever
had been residents of London for less than two years. Almost all of
these patients came, he says, from the provinces of England, and were
in good health and comfortable circumstances at the date of their
arrival in London and for some time after. Moreover, a large
proportion of them were first attacked within a few weeks after
changing their residence from one part of London to another. He also
refers to instances in which successive visitors at the same house at
intervals of months, or even years, have been seized shortly after
their arrival with typhoid fever or with diarrhoea, from which the
ordinary occupants were exempt. These facts indicate with sufficient
clearness that habitual exposure to the causes of the disease confers,
to a certain extent at least, an immunity from their effects, just as
it does in the various forms of disease arising from malaria. It is
not unlikely, as has been suggested by Wilson,[22] that one of the
causes of the frequency of typhoid fever in the early autumn in our
American cities among well-to-do people is to be formed in the
circumstance that during an absence of two months or more in the
mountains or by the sea they have to some extent lost the immunity
acquired by habitual exposure to sewer emanations, and return to the
atmosphere of the city unprotected.
[Footnote 22: The occurrence of typhoid fever in the early fall among
persons who have spent the summer out of town is, however, susceptible
of another explanation. In many instances they have returned to houses
which have been not only unoccupied, but closed, during several
months, and which, in consequence of the more or less complete
evaporation of the water in the traps of the drain-pipes, have been
thoroughly permeated by sewer gas.]
There is no evidence that any particular occupation acts as a
predisposing cause of typhoid fever. Among the 621 patients treated at
the Pennsylvania Hospital during the last ten years, were
representatives of every branch of industry, and the same fact has
been observed at every general hospital, not only in this country, but
abroad. There is also no reason to believe that the station in life of
itself exerts much influence in predisposing to the disease. The rich
suffer equally with the poor. It would appear, indeed, that since the
recent general introduction of ill-ventilated water-closets and
stationary washstands into the houses of the {245} better classes the
liability of the former to suffer from the disease is greater than
that of the latter.
Persons recovering from an illness or in an infirm condition of health
do not appear to be more liable than others to be attacked by typhoid
fever. Among the many patients who have fallen under my care only a
very few were in ill-health at the time of their seizure. The same
fact has been noticed by Murchison and other observers. Indeed,
Liebermeister goes so far as to say that typhoid fever attacks by
preference strong and healthy persons, while it avoids those suffering
with chronic ailments. That this latter class of patients enjoys no
immunity from the disease when exposed to its causes is shown by a
fact which he himself records. During his service at the hospital at
Basle from 1865 to 1871 several of the patients in the medical and
surgical wards were attacked by typhoid fever, the cases being
especially numerous in two rooms which were situated one directly over
the other. Upon investigation it was found that a wooden pipe which
extended from the sewer to the roof ran by both of these rooms. The
sewer at the point where this pipe ran into it was of faulty
construction, and was turned at a right angle, so that the refuse
matter collected there. Since this source of infection was made known
repeated cleansings, washings, and disinfections have been followed by
satisfactory improvement, and Liebermeister believes that if the sewer
were entirely altered the infection would disappear.
It would seem only natural that intemperance, by diminishing the
powers of resistance in the individual, would increase his liability
to contract typhoid fever, but there is no proof that it does so. Few
of the patients who have come under my care were intemperate, and
still fewer were broken down by this cause. There is also no evidence
that grief, fear, or any other depressing emotion is a predisposing
cause of the disease, and the same may be said of bodily fatigue and
overcrowding. On the other hand, much importance has been attached by
writers to idiosyncrasy as a predisposing cause of typhoid fever. What
the peculiarities of constitution are which increase the liability to
the disease are not definitely known, but there can be no question
that it occurs much more frequently, and is much more fatal, in some
families than in others.
Typhoid fever occurs with the greatest frequency in this country, as
it does with very few exceptions elsewhere, during the latter half of
summer and the early part of autumn. Indeed, its greater prevalence at
this season than at other times has given to it the name of "autumnal"
and "fall fever," by which it is popularly known in many sections of
this country as well as of England. On the other hand, the disease is
usually at its minimum in May and June. The number of cases, however,
does not usually immediately diminish upon the onset of cold weather.
On the contrary, R. D. Cleemann,[23] from a comparison of the
mortality returns of Philadelphia for a period of ten years, observed
that after diminishing in November they not infrequently underwent a
marked increase in December. Of 621 cases treated at the Pennsylvania
Hospital during the last ten years, 89 were admitted during spring,
259 during summer, 182 during autumn, and 91 during winter. Of 5988
cases treated at the London Fever Hospital,[24] 759 were admitted in
the {246} spring, 1490 in summer, 2461 in autumn, and 1278 in winter.
Of the whole number, 27.7 per cent. were admitted in the two months of
October and November, and in April and May only 7.3 per cent.
Hirsch[25] has published statistics which do not differ materially
from these. He also mentions the interesting fact that in Rio Janeiro
the maximum of the disease occurs in the months from March to June,
or, in other words, in the season which in that latitude corresponds
to our autumn. There are, however, some exceptions to the general rule
of the greater prevalence of the disease during the autumn. Bartlett,
who was aware of its greater frequency at that time, refers to an
extensive and fatal epidemic which occurred in the city of Lowell in
Massachusetts during the winter and early spring; and similar
visitations have been observed in other places.
[Footnote 23: _Transactions of the College of Physicians of
Philadelphia_, 3d S. vol. iii.]
[Footnote 24: Murchison.]
[Footnote 25: _Handbuch der Historisch-Geographischen Pathologie_,
Stuttgart, 1881.]
Most authors agree with the statement made by Murchison, that typhoid
fever is unusually prevalent after summers remarkable for their
dryness and high temperature, and that it is unusually rare in summers
and autumns which are wet and cold. Certainly, the severest epidemic
of the disease which has been observed in Philadelphia in several
years occurred in the year 1876, during and after a summer of
exceptionally high temperature, and one characterized by a decidedly
diminished rainfall. Still, there can be no question that the
increased prevalence of the disease at this time was due, in part at
least, to the crowded condition of the city consequent upon the
Centennial Exhibition. In 1872, although the mean of the summer
temperature was slightly higher than that of 1876, the disease did not
prevail in an epidemic form. This may be explained by the fact that
the rainfall of the summer months of this year was decidedly greater
than the average. Hirsch, however, attaches much less importance to
temperature as a factor in the production of typhoid fever than most
other authors. He says that he has found, from a comparison of a large
number of epidemics, that the disease occurs almost as often in cool
as in hot summers, in cold as in warm autumns, and in mild as in
severe winters. Murchison, moreover, admits that mere dryness of the
atmosphere is not conducive to an increase of typhoid fever. On the
contrary, he says, warm, damp weather, when drains are most offensive,
is often followed by an outbreak of the disease.
The relation which temperature and moisture bear to the causation of
typhoid fever is therefore not definitely ascertained. It is certain,
however, that the largest number of cases does not occur at the period
of the greatest heat, but is usually not observed until from six weeks
to two months afterward, and the minimum is not reached until about
the same length of time after that of the most intense cold. This
difference in time Murchison explains by the hypothesis that the cause
of the disease is exaggerated or only called into action by the
protracted heat of summer and autumn, and that it requires the
protracted cold of winter and spring to impair its activity or to
destroy it. On the other hand, Liebermeister, who believes that the
breeding-places of typhoid fever lie deep in the earth, holds that the
time is consumed in the penetration of the changes of temperature to
the place where the typhoid poison is elaborated, in the development
of the poison without the human body, and in the period of incubation.
In some places the maximum of the disease is observed earlier in the
year than in others. In Berlin, for {247} instance, the largest number
of fatal cases occurs in October, while in Munich it does not occur
until February. This depends, he thinks, upon the difference in the
distance beneath the earth's surface of these breeding-places in
different localities, and the deeper they are the longer, he says,
will it be before they are affected by the heat of summer or the cold
of winter, since the changes of the temperature of the air are
followed by corresponding changes in the temperature of the earth more
and more slowly the deeper we go beneath the surface.
Buhl and Pettenkofer have, as the result of a series of observations
carried on in Munich over a number of years, reached the conclusion
that an intimate relation exists between the variations in the degree
of prevalence of typhoid fever and the rise and fall of water in the
soil. When the springs were low they found that there was a marked
increase in the number of cases; when, on the other hand, they were
high, there was just as decided a diminution. Out of this fact they
have evolved the theory that the cause of typhoid fever lies deep in
the soil, and has the power of multiplying itself there, and that this
property is very much increased when the water-level sinks, and the
upper layers of the earth are consequently exposed to the air. It is,
on the contrary, diminished when the water-level rises and the earth
is again saturated with moisture. It is unquestionably true, as has
already been stated, that it is principally after hot and dry weather,
when the springs are of course low, that typhoid fever is most
prevalent, and that it very frequently subsides after the occurrence
of very heavy rains; but it is not necessary to adopt the theory of
Buhl and Pettenkofer to explain these facts. It seems quite as
probable that the increased prevalence of the disease after dry
weather is due, as suggested by Buchanan and Liebermeister, to the
greater amount of solid matter which is then suspended in the water of
the springs. A larger proportion of the germs of the disease, if there
should be any present in the soil, will therefore be contained in any
given quantity of the drinking-water. The theory fails to account, as
pointed out by Murchison, for the connection which is frequently
observed between defective house-drainage and outbreaks of typhoid
fever, occurring irrespectively of any variations in the subsoil
water. And, moreover, outbreaks of the disease have occurred under
precisely opposite circumstances, as the outbreak at Terling in 1867,
recorded by Thorne,[26] which was coincident with a rise in the
subsoil water after drought.
[Footnote 26: Quoted by Murchison.]
It is believed in many parts of our country that there is an
antagonism between typhoid fever and the various forms of malarial
fever, and it is unquestionably true that in many districts in which
the latter were formerly prevalent they have ceased to be frequent,
and have been replaced apparently by the former. In the cultivation of
the soil the causes of malarial fever disappear, or at least become
less potent. On the other hand, the increase of population and the
neglect of all sanitary laws in the building of towns, and the
construction of sewers with their house connections, seem to favor the
occurrence of typhoid fever. But there is no real antagonism between
the diseases. During the recent Civil War typhoid fever was not
infrequently developed in soldiers suffering from malarial disease.
Indeed, so frequent was it to have the manifestations of the two
diseases in the same individual that many observers at that {248} time
supposed they had a new disease to deal with, to which they gave the
name of typho-malarial fever.
2. EXCITING CAUSES.--Much diversity of opinion has existed in times
past and to a certain extent continues to exist, in regard to the
contagiousness of typhoid fever. In the early part of this century
there was quite a number of good observers, including Nathan Smith in
this country, and Bretonneau and Gendron of Chateau du Loir in France,
who held the opinion it was an eminently contagious disease. Indeed,
Smith went so far as to say that its contagiousness was as fully
demonstrated as that of measles, small-pox, or any other disease
universally admitted to be contagious. This was also the opinion of
William Budd, who maintained that the contagious nature of typhoid
fever was the master truth in its history. The late Sir Thomas Watson
was also a warm supporter of the same view. At the present time,
however, the large majority of physicians, whose opportunities for
observation give weight to their opinions, do not regard the disease
as contagious in the strict sense of the word. During the past
twenty-four years I have been almost uninterruptedly connected with
large general hospitals, and during that time have had a large number
of cases of typhoid fever under my care, and a still larger number
more or less under my observation. During all this time I have never
known but one case to originate within a hospital, and that occurred
in a servant whose duties did not bring her in immediate contact with
the sick. Murchison's experience with a much larger number of cases
has been very similar. In twenty-three years, in which 5988 cases were
treated in the London Fever Hospital, only 17 residents contracted the
disease, and most of these had no personal contact with the sick.
Liebermeister asserts that he has never known a case to originate in a
hospital from direct contagion. When such cases appeared to have
occurred, they could generally be traced, he says, to some defective
sanitary condition of the hospital.
There are, nevertheless, many facts on record which, unless duly
weighed, appear to lend a good deal of support to the theory of the
contagiousness of typhoid fever. Among the most important of these are
(1) the occurrence in rapid succession of several cases in the same
house, and (2) the limited epidemics which occasionally follow the
arrival of an infected person into a previously healthy locality.
These facts are, however, susceptible of an entirely different
explanation.
1. In those instances in which several cases of the disease have
occurred in the same house, it not infrequently happens that some
defect in its sanitary conditions is detected, or that the
drinking-water is found to be impure. The same cause which produced
the first case may, therefore, also have produced those which
succeeded it. Indeed, the interval between the cases is sometimes so
short that for this reason alone, if there were no other, they could
scarcely be attributed to contagion. It not infrequently happens that
the seizure of one member of a large family is followed on the next
day by that of another, and on the third or fourth by that of still
another. Now, while it is undoubtedly true that the period of
incubation has appeared in some cases to be very short, we know that
under ordinary circumstances it is usually about two weeks.
2. The explanation of the second fact is not more difficult, but in
order that it may be clear to the reader it will be well to give in
detail a few {249} of the instances on record in which the arrival of
an individual sick with typhoid fever in a previously healthy locality
has been followed by an outbreak of the disease. Nathan Smith refers
to two cases of this character. In both of these the disease appeared
to be communicated to several individuals by patients who had
contracted the disease elsewhere. So little is said in the reports of
these cases of the water-supply of the localities in which they
occurred, or of the manner of disposing of the discharges of the
patients, that they would scarcely now be used as arguments in favor
of the contagiousness of the disease. The report of a local epidemic
by Austin Flint, Sr., is more satisfactory in this respect, and is as
follows: A stranger was detained in a small village near Buffalo by an
illness which proved fatal in the course of a few days, and which was
recognized as typhoid fever by his attending physicians. Up to this
time, it is stated, typhoid fever had never been known in the
neighborhood. In the course of a month more than one-half of the
population, numbering forty-three, was attacked by the disease, and
ten had died. The family of the tavern-keeper at whose house the
stranger lodged was the first to suffer, and of the families
immediately surrounding the tavern but one wholly escaped, that of a
man named Stearns. Upon investigation, it was ascertained that this
family alone, of all these families, did not use the well belonging to
the tavern, but had its own water-supply. The occurrence of the
disease naturally produced great excitement, and Stearns, between whom
and the tavern-keeper a quarrel existed, was suspected of having
poisoned the well; but an examination of the water showed this
suspicion to be unfounded. There can, however, be little doubt that
the water of the well, which was in all probability contaminated by
the discharges of the stranger, was the means of propagating the
disease; for although it is said that the family of Stearns was cut
off by the quarrel from all intercourse with that of the
tavern-keeper--a fact upon which some stress is laid by Flint--it does
not appear that a similar isolation existed as regards the other
families affected.[27]
[Footnote 27: _A Treatise on the Principles and Practice of Medicine_,
by Austin Flint, M.D., Philadelphia, 1868.]
The manner in which the arrival of a sick person may cause the
dissemination of the disease in a previously healthy community is even
better shown by the following histories of local outbreaks:[28]
"The water-supply pipes of the town of Over Darwen were leaky, and the
soil through which they passed was soaked at one spot by the sewage of
a particular house. No harm resulted till a young lady suffering from
typhoid fever was brought to this house from a distant place. Within
three weeks of her arrival the disease broke out and 1500 persons were
attacked. At Nunney a number of houses received their water-supply
from a foul brook contaminated by the leakage of a cesspool of one of
the houses, but no fever showed itself till a man ill with typhoid
came from a distance to this house. In about fourteen days an outbreak
of fever took place in all the houses."
[Footnote 28: Wm. Cayley, M.D., _Brit. Med. Jour._, March 15, 1880.]
There are many other observations which seem to render it certain that
the alvine dejections are a most important medium by which typhoid
fever is communicated to others; and yet there is no evidence that
they possess this power in a fresh condition. They have been
repeatedly examined, and even handled, with impunity, and, as has
already been stated, it {250} is rare for the disease to be imparted
to the immediate attendants upon the sick, or in a well-ventilated
hospital to the other patients in the same ward, provided that the
discharges are disinfected and removed immediately after being passed,
and the bed-linen and clothes of the patient changed whenever they are
soiled. The feces must therefore undergo some changes before they
become possessed of virulent properties. This appears to be shown
conclusively by the following facts: (1) laundresses who wash the
soiled clothes of typhoid fever patients not infrequently contract the
disease; (2) the occupants of houses connected by ill-trapped drains
with sewers into which the discharges of such patients have found
their way often suffer severely from the disease; and (3) the use of
water polluted by such discharges is, as has already been shown,
almost certain to induce the disease in persons not protected by a
previous attack.
The following histories of outbreaks of typhoid fever will show
clearly how the dejections of patients may be the means of propagating
the disease to others:
ILLUSTRATIVE CASES--Lausen[29] is a village lying on the railway
between Basle and Olten shortly before coming to the great Hauenstein
Tunnel. It is situated in the Jura, in the valley of the Ergolz, and
consists of 103 houses with 819 inhabitants. It was remarkably
healthy, and resorted to on that account as a place of summer
residence. With the exception of six houses it is supplied with water
by a spring with two heads which rises above the village at the
southern foot of a mountain called the Stockhalder, composed of
oolite. The water is received into a well built covered reservoir, and
is distributed by wooden pipes to four public fountains, whence it was
drawn by the inhabitants. Six houses had an independent supply--five
from wells, one from the mill-dam of a paper-factory. On August 7,
1872, ten inhabitants of Lausen, living in different houses, were
seized by typhoid fever, and during the next nine days fifty-seven
cases occurred, the only houses escaping being those six which were
not supplied by the public fountains. The disease continued to spread,
and in all 130 persons were attacked, and several children who had
been sent to Lausen for the benefit of the fresh air fell ill after
their return home. A careful investigation was made into the causes of
this epidemic, and a complete explanation was given. Separated from
the valley of the Ergolz, in which Lausen lies, by the Stockhalder,
the mountain at the foot of which the spring supplying Lausen rises,
is a side valley called the Furjust, traversed by a stream, the
Furlenbach, which joins the Ergolz just below Lausen, the Stockhalder
occupying the fork of the valley. The Furlenthal contains six
farm-houses, which were supplied with drinking-water, not from the
Furlenbach, but by a spring rising on the opposite side of the valley
to the Stockhalder. Now, there was reason to believe that under
certain circumstances water from the Furlenbach found its way under
the Stockhalder into one of the heads of the fountain supplying
Lausen. It was noticed that when the meadows on one side of the
Furlenbach were irrigated, which was done periodically, the flow of
water into the Lausen spring was increased, rendering it probable that
the irrigation water percolated through the superficial strata and
found its way under the Stockhalder by subterranean channels in the
limestone rock. Moreover, some years before a {251} hole on one
occasion formed close to the Furlenbach by the sinking in of the
superficial strata, and the stream became diverted into it and
disappeared, while shortly afterward the spring of Lausen began to
flow much more abundantly. The hole was filled up, and the Furlenbach
resumed its usual course. The Furlenbach was unquestionably
contaminated by the privies of the adjacent farm-houses; the soil-pits
communicated with it. Thus, from time immemorial, whenever the meadows
of the Furlenthal were irrigated the contaminated water of the
Furlenbach, after percolation through the superficial strata and a
long underground course, helped to feed one of the two heads of the
fountain supplying Lausen. The natural filtration, however, which it
underwent rendered it perfectly bright and clear, and chemical
examination showed it to be remarkably free from organic impurities,
and Lausen was extremely healthy and free from fever. On June 10th one
of the peasants of the Furlenthal fell ill with typhoid fever, the
source of which was not clearly made out, and passed through a severe
attack with relapses, so that he remained ill all summer; and on July
10th a girl in the same house, and in August a boy, were attacked.
Their dejections were certainly, in part, thrown into the Furlenbach;
and, moreover, the soil-pit of the privy communicated with the brook.
In the middle of July the meadows of the Furlenthal were irrigated as
usual for the hay crop, and within three weeks this was followed by
the outbreak at Lausen.
[Footnote 29: William Cayley, M.D., _British Medical Journal_, Mar.
15, 1880.]
In order to demonstrate the connection between the water-supply of
Lausen and the Furlenbach, the following experiments were performed.
The hole mentioned above as having on one occasion diverted the
Furlenbach into the presumed subterranean channels under the
Stockhalder was cleared out, and 18 cwt. of salt were dissolved in
water and poured in, and the stream again diverted into it. The next
day salt was found in the spring at Lausen. Fifty pounds of wheat
flour were then poured into the hole, and the Furlenbach again
diverted into it, but the spring at Lausen remained clear, and no
reaction of starch could be obtained, showing that the water must have
found its way under the Stockhalder, in part by percolation through
the porous strata, and not by distinct channels.
Volz[30] refers to an epidemic which occurred at Gerlachsheim, a
village of Germany, some years ago, in which, in the course of three
weeks, 52 persons residing on one of the principal streets were
attacked by the disease. It was found, upon investigation, that they
all got their water from a well which was polluted by the stools of
the first patient. A. Pasteur[31] reports an epidemic caused by the
contamination of a well by typhoid dejections, and which ceased when
the use of the water was discontinued. Niericker[32] also reports an
outbreak which was found to be due to a similar pollution of the
drinking-water, and which likewise ceased when the water-supply was
derived from another source.
[Footnote 30: _Schmidt's Jahrbuch_.]
[Footnote 31: _Revue med. de la Suisse_, Mars 15, 1881.]
[Footnote 32: _Schweiz. Corr. Bl._, ix. 1, 1879.]
An outbreak of the disease which occurred in a farm-house situated
about eight miles from the city of Philadelphia came under my own
observation. The first case occurred in a young girl of sixteen, who,
with the exception of an occasional visit to the city, had not been
away from her own home for several months before she was {252} taken
ill. The disease ran in her a severe course, and eventually terminated
fatally. About three weeks afterward four other members of the family
were attacked, one of whom died. Two other persons, living in a house
on the opposite side of the road, but who were in the habit of
drinking water from the same well, also took the disease. There was no
other case of typhoid fever in the immediate vicinity, nor had there
been for some time. The farm-house is situated in a cup-shaped
depression, so that water flowed toward it from all directions. The
cellar was constantly filled with water during the winter, and just
before the outbreak had contained not only an unusually large
quantity, but also a large amount of decaying vegetable matter. The
well from which the family drew their drinking-water is situated
within a few feet of the kitchen door, and at some distance from the
cesspool used by the family, so that there was no reason to believe
that there was any communication between the two. The wall of the well
was found to be very much loosened by the roots of two trees growing
in the immediate vicinity. As the ground was also very much cut up by
the burrows of rats, the water used for the various household
purposes, and which was habitually thrown into a gutter which ran past
the well, found a ready access to it. There would seem to be but
little doubt that the first patient contracted the disease in some way
during her visits to the city, and that the disease in the other
patients arose from their drinking the water of the well which had
been polluted by that used in washing her soiled linen.
Ballard[33] has shown very clearly that milk may also be a medium of
communication of the disease. He found that an epidemic which occurred
in the parish of Islington, London, in 1871 was (1) almost entirely
confined to a district comprised within a circle having a radius of
not more than a quarter of a mile; (2) that out of 62 families living
within this district, who were known to have suffered from typhoid
fever, 54 were constantly supplied with milk from a particular dairy,
and it was satisfactorily proved that at least three of the remaining
eight had occasionally partaken from the same source; and (3) that out
of 142 families, comprising all the customers of this dairy, and
living not only within the district above specified, but in other
parts of the parish, 70, or very nearly one-half, were invaded by
typhoid fever within the ten weeks during which the outbreak lasted.
Upon a visit to the farm from which the milk came it was ascertained
that a member of the dairyman's family had been ill with typhoid
fever, and that the water of the well which supplied the family with
drinking-water had been polluted by his discharges. Although the
dairyman denied that this water had ever been mixed with the milk, he
admitted that it had been used to wash the milk-pans. Murchison was
also able, in an outbreak which occurred in another district of
London, to trace the disease to the same source.
[Footnote 33: _On a Localized Outbreak of Typhoid Fever in Islington_,
London, 1871.]
Typhoid fever may be likewise propagated in consequence of the
contamination of the atmosphere by the typhoid poison. This may be the
result of allowing the undisinfected stools, or linen soiled by them,
to remain for some time exposed to the air, or may arise from
pollution {253} of the soil from the same cause or from defective
sewage. Hermann Schmidt[34] refers to several epidemics breaking out
in garrisons which he believed to be due to pollution of the soil. In
the citadel of Wurzburg typhoid fever occurred through several years,
and persisted in spite of the cutting off of the water-supply, which
was believed to be impure. It was finally found that the ground upon
which it was built was saturated with all kinds of impurities. Volz
refers to outbreaks of the disease from the same cause.
[Footnote 34: _Die Typhus Epidemie in Fusillier Bat. zu Tubingen in
Winter 1876-77, enstanden durch einathmung, giftiger Grundluft_,
Tubingen, 1880.]
But perhaps the most striking example of this mode of propagation of
the disease is that recorded by Budd,[35] and is as follows: Two
adjacent cottages, which for the sake of convenience may be designated
as Nos. 1 and 2, had a privy in common, which was in the form of a
lean-to against the gable end of No. 2. Through this privy there
flowed with very feeble current a small stream which formed the
natural drain for it. Having already performed this office for some
twenty or thirty other houses higher up its course, the stream had
acquired all the character of a common sewer before reaching the
cottages in question. About a quarter of a mile farther on it acted as
a drain for a privy, common as before, for two other cottages, Nos. 3
and 4. Notwithstanding the condition of the stream, which was so foul
that it was said that the stink from it was often enough "to knock a
man down," no evil result appeared to have occurred until a man living
in No. 1 contracted typhoid fever--elsewhere, it was believed. As a
matter of course, all his discharges were thrown into the common
privy. In this way for more than a fortnight the stream which passed
through it was daily fed with the specific excreta from the diseased
intestines of the patient. No further cases occurred until the latter
end of the third week or the beginning of the fourth week, when
several persons were simultaneously attacked by the same fever in all
four cottages. From first to last, the outbreak was confined to these
four cottages, and there was no other case of typhoid fever at this
time in the neighborhood.
[Footnote 35: _Typhoid Fever: Its Nature, Mode of Spreading, and
Prevention_, by William Budd, M.D., F.R.S., London, 1873.]
The mattrass used by typhoid-fever patients, their bed-linen and
clothes, have each been the medium by which the disease has been
communicated to others. This is, as has already been pointed out,
unquestionably due to the fact that these articles are generally
soiled by their discharges, and that time has been allowed for the
latter to acquire infective properties. It seems not improbable that
the few cases in which the disease appears to have been contracted
from the dead body may be explained in the same way. The statistics of
the London Fever Hospital show that laundresses are more liable to
contract typhoid fever than the immediate attendants upon the sick.
This liability is greatest in those cases in which the bed-linen and
clothes of patients are not immediately disinfected after use.
According to Budd, the sputa in cases of typhoid fever where
bronchitis is excessive may sometimes contain the germs of the
disease, and mentioned a case in which he believed they were the means
by which the disease was propagated.
The question naturally arises here, whether this is the only way in
{254} which the disease can originate. This is a subject which has
given rise to a good deal of controversy, and therefore demands some
consideration at our hands. On the one hand, it is argued that typhoid
fever never occurs in the absence of the specific poison or germ of
the disease, and that this is contained principally, if not wholly, in
the alvine dejections. On the other hand, it is contended that it may,
and often does, originate spontaneously, and that all that is
necessary to produce it is the presence of decomposing fecal or other
organic matter, and the consequent contamination of the food, drink,
or atmosphere. Both of these views have found able advocates. Among
the upholders of the latter view is Murchison, who cites the histories
of several outbreaks of typhoid fever which occurred in localities
which had not been visited by it for many years, and which, after a
careful investigation of all the circumstances attending them, he was
forced to conclude had no connection with any previous case of the
disease, and could only be explained by admitting that it might
occasionally have an independent origin. Among the more remarkable of
these outbreaks is the following, which we give in Murchison's own
words:
"In August, 1829, 20 out of 22 boys at a school at Clapham within
three hours were seized with fever, vomiting, purging, and excessive
prostration. One other boy, aged three, had been attacked with similar
symptoms two days before, and had died comatose in twenty-three hours;
another boy, aged five, died in twenty-five hours; all the rest
recovered. Suspicions were entertained that they had been poisoned,
and a rigorous investigation ensued. The only cause which could be
discovered was, that a drain at the back of the house, which had been
choked up for many years, had been opened two days before the first
case of illness, cleared out, and its contents spread over a garden
adjoining the boys' playground. A most offensive effluvium escaped
from the drain, and the boys had watched the workmen cleaning it out.
This was considered to be the cause of the disease by Latham and
Chambers, and by others who investigated the matter, and also by Sir
Thomas Watson. The morbid appearances in the two fatal cases were
described as like those of the common fevers of this country. Peyer's
patches and the solitary glands of the small and large intestines were
enlarged like 'condylomatous elevations,' and in one case the mucous
membrane over them was slightly ulcerated. The mesenteric glands were
enlarged and congested."
"A remarkable instance of a circumscribed outbreak of fever was
recorded by Sir R. Christison in 1846. It occurred in an isolated
farm-house in the thinly-peopled county of Peebles, N.B. Every one of
the fifteen residents was seized with fever, and three died. Many of
the servants who worked during the day at the farm were also affected,
but none communicated the disease to their families who did not visit
the farm. There was no evidence that the disease was imported from
without, and the only explanation of the outbreak was, that the drains
and sewers were found all closed and obstructed with the accumulated
filth proceeding from the privies and farm-yard, the effluvia from
which was very offensive."
"About Easter, 1848, a formidable outbreak of fever occurred in the
Westminster School and the Abbey Cloisters, and for some days there
{255} was a panic in the neighborhood respecting the 'Westminster
fever.' No case of fever had occurred in the Abbey Cloisters for three
years, and there was no evidence of its having been imported. Within
little more than eleven days it affected thirty-six persons, all of
the better class, and in three instances it proved fatal. Shortly
before its first appearance there occurred two or three days of
peculiarly hot weather, and a disagreeable stench, so powerful as to
induce nausea, was complained of in the houses in question. It was
found that the disease followed very exactly in its course the line of
a foul and neglected private sewer or immense cesspool, in which fecal
matter had been accumulating for years without any exit, and into
which the contents of several small cesspools had been pumped
immediately before the outbreak of fever. This elongated cesspool
communicated by direct openings with the drains of all the houses in
which it occurred; the only exception was that of several boys, who
lived in a house at a little distance, but who were in the habit of
playing every day in a yard in which there were several gully-holes
opening into the foul drain."
The following cases would seem, however, to furnish stronger evidence
in favor of the occasional spontaneous origin of typhoid fever than
any of those referred to by Murchison. The first is recorded by P.
Herbert Metcalfe,[36] and occurred in Norfolk Island in the Pacific
Ocean, 400 miles from the nearest inhabited land. The patient was a
gentleman who had come from England four months previously. To
Metcalfe's certain knowledge, there had been no typhoid fever on the
island for fifteen months. Three years previously a man is reported to
have died of it, and in 1868 there had been an epidemic of fever, but
he could not ascertain of what kind. Upon inquiry, he found that his
patient had been drinking water from a well which had the reputation
of being unclean, and that he was the only person who had done so. He
also found that at a distance of seven feet there was an open sewer,
and that just opposite to the well much of the sewage-water became so
stagnant as to form an offensive cesspool. The well was cleaned out,
and at the bottom of it were found four feet of stinking sewage mud,
the skeleton of a duck, a pig's jaw, etc. The well was so situated
that had there been any typhoid fever previously to this case the
water could not have been contaminated by the specific poison, as the
above-named sewer only conveyed water from the kitchen, which is a
building detached from the dwelling-houses of the mission, and is far
from and on a higher level than the open closets in use.
[Footnote 36: _British Medical Journal_, Nov. 6, 1880.]
In the second case, which is reported by R. Bruce Low,[37] Medical
Officer of Health, Helmsley, Yorkshire, occurred in a lad who had not
been away from his home for months. No stranger had visited his house,
and there was no fever in the district, the last case having occurred
eight months previously in a sequestered valley eight miles away. The
patient's habits and those of his family were revoltingly dirty. The
garden privy was in bad repair, the filth level with the seat, and the
smell from it very offensive. Thirty years before there had been five
cases of slow typhus in the house. In his remarks on this case Low
says: "This case did not owe its origin to direct infection, and the
question naturally arises, was this a case originating de novo, or had
the poison {256} been due to infection in some way or another from the
cases which occurred thirty years previously?"
[Footnote 37: _Brit. Med. Jour._, 1880.]
There can be but little doubt that in many of the cases cited by
Murchison as instances of the spontaneous origin of typhoid fever
there was an introduction of the germs of the disease from without. At
all events, the evidence to the contrary is by no means convincing.
For example, in the account of the outbreak at the Westminster School
it is expressly stated that "the contents of several small cesspools
had been pumped before the outbreak of the fever" into the large
cesspool, the emanations from which it was believed had caused the
fever. It does not seem that it was positively ascertained that none
of these small cesspools had been used by a typhoid-fever patient, or
that typhoid stools had not found their way into them in some other
way. Moreover, in diseases generally admitted to be contagious it is
not always possible to ascertain positively the source of infection in
a particular instance. But after the elimination of all doubtful cases
there yet remains a certain number in which it is reasonably certain
that there has been no recent importation of the typhoid-fever germs,
as in the case which is reported by Metcalfe and which occurred on
Norfolk Island, and in that recorded by Low. The assumption does not
seem an unwarranted one that in these cases the poison of the disease,
which had been present before in a latent condition, had been suddenly
called into activity by favoring influences. The following observation
of Von Gietl[38] shows the length of time typhoid-fever stools may
retain their infective properties: "To a village free from typhoid an
inhabitant returned suffering from the disease, which he had acquired
at a distant place. His evacuations were buried in a dunghill. Some
weeks later five persons, who were employed in removing dung from this
heap, were attacked by typhoid fever; their alvine discharges were
again buried deeply in the same heap, and nine months later one of two
men who were employed in the complete removal of the dung was attacked
and died." If we assume--and there is no reason to doubt that this
point was fully investigated by Von Gietl--that the patient in the
latter case had not been otherwise exposed to the causes of the
disease, the observation shows that the stools in typhoid fever retain
their virulence for nine months. If for nine months, why may they not
do so for a much longer period--for as many years, for example? No
probability is violated by this hypothesis. On the contrary, it is in
full accordance with what we know of some of the lower forms of life,
and will serve to explain many outbreaks of the disease which would
otherwise be inexplicable--for example, the outbreak at Clapham
referred to by Murchison. Admitting that the disease in this instance
was really typhoid fever--and this has been denied by some observers,
among whom is Sir Thomas Watson--the assumption does not seem an
unwarrantable one that the germs of typhoid fever had been present in
this choked-up drain long before it was cleared, but that in
consequence of their exclusion from the air their infecting power was
at a minimum. It was, on the contrary, much increased when the
contents of the drain were exposed to the vivifying influence of the
atmosphere.
[Footnote 38: Quoted by Cayley, _Brit. Med. Jour._, Mar. 15, 1880.]
On the other hand, it is alleged that an individual may be exposed to
the direct emanations of sewers or of foul privies, or even drink
water {257} contaminated by leakage from them, without contracting
typhoid fever, so long as they do not contain the specific germ of the
disease. Every physician in large practice, either in the city or
country, can call to mind instances in which the air of houses or the
water-supply has been polluted in this way, and yet no typhoid fever
has occurred. Let, however, the specific cause of the disease be
introduced from without, and this immunity almost invariably
disappears. There is no reason to believe that the contamination of
the water used by the family which suffered in the outbreak of the
disease which has been already referred to as having come under my own
observation last year was of recent origin. On the contrary, there was
evidence to the contrary, and yet no disease occurred until it was
imported by a member of the family who was in the habit of making
frequent visits to the city. Even more strongly corroborative of this
view is the history of the epidemic reported by Ballard, in which milk
was the medium of communication. The water which had been used with
impunity to wash the milk-pans, or perhaps to dilute the milk, became
a source of danger only after the occurrence of the disease in the
family of the dairyman.
Several epidemics of typhoid fever have been recently reported in
which the disease appears to have been caused by the use of the flesh
of diseased animals or of meat in a condition of putrefaction. In some
of these the symptoms were rather those of irritant poisoning than of
typhoid fever, and consisted principally in violent vomiting and
purging coming on very shortly after the ingestion of the unwholesome
food. There yet remains a certain number in which the symptoms cannot
be thus explained.[39] One of the most remarkable of these occurred in
1878 at a festival which was held at Kloten, a place about seven miles
north of Zurich, of which the following is a condensed description:
Out of 690 persons who sat down to the collation, 290 were taken ill;
378 other persons, who did not attend the festival, but who partook of
the meat provided for it, were also affected. In addition these, 49
secondary cases occurred--_i.e._ of persons who subsequently became
affected without having eaten of the meat. All other sources of
infection could be certainly excluded, as Kloten was quite free from
typhoid fever at the time, and as it was clearly shown that the water
was not the cause of the outbreak. All the visitors at the festival
who ate no meat escaped, as did also several persons who drank wine to
excess and subsequently vomited. The period of incubation was short,
as in other epidemics arising from the same cause. Some of the people
were ill on the second day, with loss of appetite, nausea, headache,
pain and swelling of the belly, and slight fever. These cases were
slight, and generally ended in recovery. The greater number were
affected between the fifth and ninth days. The symptoms in these
cases, which usually ran a rapid course, and generally ended in
recovery, were chills, fever, diarrhoea, great prostration, frequently
violent delirium, and also profuse intestinal hemorrhage. The
rose-colored eruption was present in almost all of them, and in a few
the taches bleuatres were detected. On post-mortem {258} examination
the characteristic appearances of typhoid fever were found. With
regard to the meat supplied, the following facts were ascertained:
Forty-two pounds of veal were furnished by a butcher at Seebach, taken
from a calf which appears to have been at the point of death when it
received the coup de grace from the hands of the butcher. All the
flesh of the animal was sent to supply the festival at Kloten, but the
liver was eaten by an inhabitant of Seebach, and he was attacked by
typhoid fever. The brain was sent to the parsonage at Seebach, and all
the household became affected by the same disease. It was also
ascertained that another of the calves was diseased. The veal from
this calf had been kept fourteen days, and was in a decomposed state.
All the meat was placed together in the meat-receptacle of the inn at
which the festival was held. This receptacle was in a horribly filthy
state, and Cayley thinks there can be no doubt that the putrefying
flesh of this last calf, together with the state of the receptacle,
would rapidly excite decomposition in the whole supply.
[Footnote 39: _On Some Points in the Pathology and Treatment of
Typhoid Fever_, by William Cayley, London, 1880; also Prof. Huguenin,
_Schmidt's Jahrbuch_, from _Schweiz. Corr. Bl._, viii. 15, 1878; Carl
Walder, _Schmidt's Jahrbuch_, from _Berl. klin. Wochenschr._, xv. 39,
40, 1878; George R. Shattuck, M.D., Supplement to _Ziemssen's
Cyclopaedia_, New York, 1881.]
Geissler, it is true, doubts whether the epidemic above described was
really typhoid fever, and points out that the symptoms occurred too
soon after the ingestion of the diseased meat, and reached their full
development too rapidly. The cases were also accompanied by more pain
in the abdomen than is generally met with in typhoid fever. The
proportion of recoveries also appears to have been unusually large.
Unquestionably, the patients in the Kloten epidemic were in a large
number of instances simply suffering from the action of an irritant
poison; but the presence of the characteristic lesions of typhoid
fever in some of the fatal cases renders it certain that this disease
also existed in the village at the same time.
In the report of this epidemic it is not stated that either of the
calves which furnished a part of the meat for the entertainment were
suffering from typhoid fever at the time they were slaughtered. It is
now known positively that this animal is liable to be attacked by this
disease, and a certain number of cases are on record in which the
eating of the flesh of such animals has been followed by typhoid
fever.[40] That it does not oftener occur from this cause is probably
due to the fact that a certain time must elapse before the flesh of
such an animal acquires infective properties, and that it is usually
used as food before this has been allowed to pass.
[Footnote 40: _Medical Times and Gazette_, Feb. 8, 1879, p. 149, from
_Berl. klin. Wochenschrift_, No. 39, 1878.]
Ludwig Letzench[41] asserts that he has produced some of the
intestinal appearances of typhoid fever, as well as a high degree of
pyrexia, in rabbits by the subcutaneous injection of the sputa and
stools of typhoid fever patients.
[Footnote 41: _Arch. f. exper. Pathol. u. Pharmak._, 1878 and 1881.]
THE BACILLUS TYPHOSUS.--From what has preceded, it will be seen that
the writer is disposed to range himself with those who hold that the
exciting cause of typhoid fever is an organized germ, or, in other
words, a contagium vivum. Although this view cannot be regarded as
positively proven as yet, it has recently received some support
through the investigations of Klebs, Eberth of Zurich, and others,[42]
who believe that they {259} have found in the bodies of those who have
died of typhoid fever a micro-organism peculiar to that disease.
[Footnote 42: Klebs (_Philadelphia Medical Times_, Dec. 3, 1881, from
_Archiv fur experimentelle Pathologie und Pharmakologie_, Bd. xiii. H.
5 and 6) claims that he has proved "that there exists in typhoid fever
a separate and distinct bacillus--the _Bacillus typhosus_; that it
undergoes certain transformations, consisting at first of little rods
and small fine threads, containing a spore in the centre and often at
the end, which spores divide off and form new bacilli. It later
assumes a larger thread-like form, twisted at the end, and frequently
taking a beautiful spiral shape; that the bacilli are observed first
in the masses of epithelial cells which accumulate in the alimentary
tract or in the air-passages; that they later penetrate the tissues,
and are carried along by the blood-vessels and the lymphatics, and
form a large network among the tissues they invade; that under a
certain procedure, which never causes this same staining in any other
living organism or tissue, they appear of a blue color; that they are
found only in enteric fever, in which disease every part of the human
body is the seat of masses of these bacilli, their quantity
corresponding exactly with the severity of the symptoms; and that they
produce, when carried into the system of animals, exactly the same
disease with the same morbid alterations as in men." He says, further,
that "the Bacillus typhosus enters the system by the respiratory
passages and by the alimentary canal. This is the cause that in some
cases of typhoid fever almost no abdominal symptoms are present, but a
low form of pneumonia, developing from the very beginning, so that the
lung seems alone to bear the brunt of the disease." He has found these
bacilli in greatest numbers in Peyer's patches.
Eberth (_British Medical Journal_, Nov. 26, 1881, from _Virchow's
Archiv_, Bd. lxxxi. and lxxxiii.) has shown that in typhoid fever the
intestinal mucous membrane, the mesenteric glands, and the spleen
contain rod bacteria, differing, as he believes, from organisms found
in the body in other conditions (among others in phthisis with
extensive ulceration of the intestinal mucous membrane). In seventeen
cases of typhoid these bacilli were found in six and wanting in
eleven. In the six cases the number of bacilli were in inverse
proportion to the duration of the disease. They were not found in the
spleen in the cases of the longest duration, and only scantily in the
mesenteric glands. These bacilli appear not to differ in shape and
size from the ordinary rod bacteria, but Eberth believes that they
differ from them in their small capacity for taking on the staining of
haematoxylon, methyl-violet, and Bismarck brown.
Wernich's views (_Vjhrschr. f. Off. Geshpfl._, xiii. 4, p. 513, 1881)
in regard to the nature of the Bacillus typhosus differ from those
held by the two authors just quoted. He regards the specific Bacillus
typhosus as nothing but the ordinary Bacillus subtilis of the large
intestines, which under certain circumstances acquires the power to
accommodate itself to the small intestines, to undergo a higher
development and to become the exciting cause of disease.]
PERIOD OF INCUBATION.--The conditions under which typhoid fever occurs
in large cities render it difficult, if not impossible, to arrive at a
definite conclusion as to its period of incubation. Occasionally,
however, the time which has intervened between the exposure to the
cause and the invasion of the disease may be ascertained with
precision in the outbreaks which occur in small towns or in isolated
country-houses. Under these circumstances it has been found to vary
within very wide limits. In the three cases related by Griesinger the
attack began the day after exposure to the infection, and in the
outbreak at the school at Clapham, referred to by Murchison, twenty
out of twenty-two boys were seized with the disease within four days
of exposure to the causes. Other instances of a similar character are
on record. In cases like the above the rapidity with which the attack
follows upon exposure to the cause is no doubt due to the intensity of
the poison--a view which is to a certain extent at least supported by
the fact that the invasion of the disease under these circumstances is
very apt to be abrupt; the attack being often ushered in with vomiting
and purging or with grave cerebral symptoms. Sometimes, indeed, the
gastro-intestinal symptoms have been so violent as to have given rise
to suspicions of criminal or accidental poisoning. In the majority of
cases, however, the period of incubation is probably very much longer
than in those above referred to. In the outbreak which recently
occurred in a farm-house about seven miles distant from {260}
Philadelphia, the history of which has already been given in detail,
the second case began three weeks after the first, the other six
following in rapid succession. In the celebrated epidemic which
occurred at Lausen in Switzerland in 1872, and which is referred to by
Cayley,[43] the first ten patients were attacked within three weeks of
the time when the contamination of the spring which supplied the
village must have taken place, and these ten cases were followed in
the course of nine days by fifty-seven others. In the town of Over
Darwen 1500 persons were seized with typhoid fever within three weeks
after a patient suffering from this disease was brought to a
particular house, the sewage of which was allowed to soak into the
ground through which the water-supply pipes of the town passed, and at
a point at which they were leaky. Lothholz observed in an epidemic
which occurred in the neighborhood of Jena that the average period of
incubation was three weeks, the shortest period eighteen days, the
longest twenty-eight days. Haegler found in three cases produced by
contaminated water a period of at least three weeks.[44] There are,
however, epidemics on record in which the period of incubation was
under two weeks, as, for instance, that of Basle, referred to by
Liebermeister, in which a few persons were attacked who had only been
in the city from seven to fourteen days. Cayley also refers to
localized outbreaks of the disease, as those of Calne and Nunney, in
which persons were attacked within fourteen days of their exposure to
the cause. C. J. C. Muller of Posen[45] says that the average period
of incubation of the disease is fourteen days; that it may be not more
than ten days, or, on the other hand, as long as from three to four
weeks; and that he has known a case in which it was thirty-four days.
Murchison believed that it was most commonly about two weeks, and
William Budd arrived at the conclusion, from the observation of a
large number of cases, that it varied from ten to fourteen days.
[Footnote 43: _Brit. Med. Jour._, Mar. 15, 1880.]
[Footnote 44: _Ziemssen's Cyclopaedia_, vol. i.]
[Footnote 45: _Neue Beitrage zur Aetologie des Unterleibs-Typhus_,
Posen, 1878.]
From this review of the opinions of various authors the conclusion
would seem to be justifiable that the period of incubation in typhoid
fever is usually between two and three weeks, but that in many cases
it does not exceed ten days, and in rare instances has unquestionably
been very much less. On the other hand, there are authentic cases on
record in which it is said to have reached, or even exceeded,
twenty-eight days. Unfortunately, we do not possess any reliable data
with which to decide the question whether it is shorter or longer when
the poison is imbibed with the ingesta than when it is inhaled. It
would seem, however, that there is a difference in the susceptibility
of different individuals to the poison of this disease, in many
persons a single exposure to the cause being sufficient to induce an
attack, while in others the disease is contracted only after repeated
exposure.
MORBID ANATOMY.--As a thorough knowledge of the morbid anatomy of
typhoid fever is absolutely necessary to a correct understanding of
its pathology, it seems to me better to deviate from the order usually
observed in systematic treatises and to proceed at once to a
description of the former, rather than to defer it, as it is usual to
do, until after the symptomatology of the disease has been discussed.
Rigor mortis is generally more marked and more prolonged than after
{261} typhus. Emaciation is often extreme in cases in which death has
taken place after the third week, especially if they have been
attended by much diarrhoea and fever. No traces of the characteristic
rose-colored eruption are found after death, no matter how profuse it
may have been during life. Sudamina, on the other hand, persist, and
discolorations of the dependent portions from settling of blood are
always present in the dead body.
The lesions of typhoid fever may be divided into two classes. The
first class includes certain changes in the glands of Peyer, the
solitary glands of the intestines, the spleen, and other lymphatic
structures of the body. These changes, which consist essentially in a
medullary infiltration of these glands, will be minutely described
presently. They are peculiar to the disease, and are just as
characteristic of it as the condition of the lungs and their membranes
found in pneumonia and pleurisy are characteristic of those diseases.
They are usually most developed in grave cases, but occasionally they
are slight and but little marked in cases in which the general
symptoms were severe. They therefore cannot be regarded as the sole
cause of the latter. It is more probable that they are themselves the
results of the local action of the typhoid poison, and bear somewhat
of the same relation to typhoid fever that the eruption in small-pox
does to that disease. The second class is made up of lesions which are
met with not only in this disease, but in other diseases accompanied
by high fever, and are therefore unquestionably the result of the
general process. They consist essentially of parenchymatous
degenerations of various organs and tissues, and are generally more
marked in typhoid fever because the pyrexia is not only of high grade,
but also of longer duration than in other diseases.
We shall first consider the lesions peculiar to typhoid fever. Among
the most important of these are the changes which occur in the
agminated and solitary glands of the intestines. These have been
usually described as passing through four stages, as follows: (1) the
stage of medullary infiltration; (2) the stage of softening or
sloughing; (3) the stage of ulceration; (4) the stage of
cicatrization. These stages are said to last almost a week, and
correspond to certain definite periods of the disease, but it is not
uncommon to find in the same intestine glands in two or more of these
stages. Indeed, the same gland may sometimes be found ulcerating at
one side while cicatrization is going on at the other.
In the first stage the agminated glands are enlarged, each patch
preserving its oblong shape, and being flattened on the surface and
elevated from half a line to two lines above the surrounding mucous
membrane, from which it is separated by an abrupt border, and which it
may in a few cases overhang like a fungous growth. The solitary
follicles are also swollen, and may vary in size from a hempseed to a
split pea. In very severe cases all the glands may be more or less
involved, but in mild cases the changes may be limited to three or
four of the patches of Peyer, although the solitary glands rarely
wholly escape. It is uncommon also for the latter to be alone
affected, but a few such cases have been reported. In these the mucous
membrane appears to be studded with pustules, and hence Cruveilhier
designated this variety as the forme pustuleuse. The mucous membrane
covering the affected glands is reddish-green in color, and that in
their immediate vicinity is {262} often injected. The changes above
described occur early in the disease--Murchison has seen them in two
cases in which death took place at the end of the first day--and they
are often well marked at the end of the third or fourth day. They are
usually limited to the glands in the lower part of the ileum, the
agminated glands being often found perfectly healthy four feet above
the ileo-caecal valve. In mild cases, indeed, the lesions may be
confined to those nearest to this valve. So, too, the changes in the
solitary glands may be confined to the last twelve inches of the
smaller intestine, but this is by no means universally the case, for
these glands are not only often found enlarged higher up in the small
intestine, but also occasionally in the caecum. The agminated glands
are sometimes found enlarged in the bodies of those who have died of
measles and of some other diseases, but the degree of enlargement is
rarely as great as in typhoid fever, and the further changes presently
to be described are never found except in the latter disease.
Under the microscope the medullary infiltration upon which the
enlargement of the glands depends is found to be due to proliferation
of the cellular elements. In the case of the agminated glands this
proliferation may be limited to the follicles or it may extend to the
intercellular tissue, and even to the adjacent mucous membrane. In the
former case the patches have a reticulated aspect; they are soft and
but little elevated. These are the plaques molles of Louis and the
plaques reticulees of Chomel. In the latter they are harder, smoother,
and more elevated. To this variety Louis has given the name of plaques
dures, Chomel that of plaques gauffrees. The morbid process is also
very apt to extend from the solitary follicles to the surrounding
mucous membrane.
In a large number of the glands in many cases, and probably in all of
them in the abortive form of the disease, the changes never advance
beyond the first stage, a restoration to their normal condition taking
place by colliquative softening.[46] The morbid material upon which
their enlargement depends breaks down into an oily debris which is
gradually absorbed. This retrograde process takes place faster in the
follicles than in the interfollicular tissue, and, as pigment is very
apt to be deposited in the depressions thus formed, the patches
acquire an appearance which has been compared to that of a recently
shaven beard. This appearance is met with, however, in other diseases,
and is therefore not peculiar to typhoid fever.
[Footnote 46: Rindfleisch, _Pathological Histology_, Sydenham Society
Translation, vol. i. p. 441.]
The description of the changes in these glands in the subsequent
stages of the disease which follows is taken mainly from Rindfleisch's
work on _Pathological Histology_.
In the stage of necrosis small portions of single Peyerian patches,
varying in size from that of a lentil to from three-quarters of an
inch to an inch and a quarter in diameter, assume a yellowish-white,
opaque tint instead of their former reddish and translucent aspect,
gradually become separated from the surrounding tissue by a sharp line
of demarcation, and then pass into a state of cheesy necrosis. Here
and there the same changes are observed to have taken place in the
solitary glands. When once this has occurred, recovery can only take
place by expulsion of the necrosed parts and consequent ulceration.
Necrosis of the glands {263} probably rarely occurs before the
beginning of the second week, but it has occasionally been observed
much earlier. Murchison reports cases in which he saw it as early as
the first and second days. The process usually involves the mucous
membrane only, but it may extend to the muscular and even to the
peritoneal coats.
In the third stage the dead parts are gradually thrown off, the
process of separation usually occupying several days. At first an
increased degree of congestion, followed by suppuration, is observed
at the edges of the sloughs, which before their complete detachment
may often acquire a yellow, green, or brown color from the imbibition
of bile. The ulcers which result correspond in size and form with the
sloughs. They are, therefore, in the case of the agminated glands
elliptical in shape, with their long diameter corresponding to the
axis of the intestine. Their edges are swollen and overhanging, and
their floor is generally formed by the deepest layer of the submucous
connective tissue. They sometimes penetrate much more deeply, and may
even extend to the peritoneal coat, and thus give rise to perforation
of the bowel. The ulcers which result from sloughing of the solitary
glands are, as a rule, small and round. Murchison says that ulceration
may also be produced in the following way: The mucous membrane becomes
softened, and one or more superficial abrasions appear on the surface
of the diseased patch, which extend and unite into one large ulcer,
and this ulcer proceeds to various depths through the coats of the
bowel, and even to completed perforation, but Rindfleisch and other
recent German writers do not allude to this process.
The fourth stage, or that of cicatrization, usually commences with the
beginning of the fourth week. The swelling of the edges of the ulcers
gradually diminishes, and they become adherent to the tissues beneath.
The floor of the ulcers covers itself with delicate granulations,
which in course of time are converted into connective tissue. This is
ultimately coated with epithelium, but neither the villi nor the
glands of the mucous membrane are ever reproduced. The resulting
cicatrices may be recognized by the affected parts of the bowel being
thin and more translucent than in health, and may retain these
characters after the lapse of several years. They never give rise to
contraction of the bowel. The time occupied in the cicatrization of
each ulcer is said to be about two weeks. It occasionally happens that
while cicatrization is taking place at one end of the ulcer the
process of necrosis and ulceration is still going on at the other, so
that two or more ulcers may occasionally run together. This form of
ulcer may often retard recovery, and may sometimes end in perforation
of the bowel, even after convalescence seems to have been established.
The color and consistence of the mucous membrane of the caecum and
colon are in a large proportion of cases normal. In a few the membrane
is paler than in health, and in others it is of an ash-gray color. It
is also sometimes injected and softened. The solitary glands are
frequently enlarged and ulcerated, like those of the ileum. In the
former case the mucous membranes of the large intestine throughout its
whole extent, but especially that of the caecum and of the part of the
colon adjacent to it, is studded with minute elevations about a line
in diameter. When ulceration has occurred the ulcers are generally
round {264} and small, but they may occasionally be oval and of
considerable size. In the latter case their long diameter will
correspond in direction with that of the circular fibres of the
intestine. Murchison has known them to measure fully an inch and a
half in length. The colon is generally found much distended with
flatus.
Enlargement of the mesenteric glands from cellular hyperplasia and
hypertrophy of the connective tissue is constantly associated with the
morbid changes of the intestines just described. This enlargement
varies in different cases. In some the glands are not larger than a
pea or bean; in others they are said to have reached the size of a
hen's egg. It is always more marked in the glands which lie in the
angle between the lower end of the ileum and the caecum, and usually
bears some proportion to the intensity of the local disease; but it is
not to be regarded merely as a result of the local irritation, as it
has been observed in parts of the mesentery corresponding to perfectly
healthy portions of the intestine, and as the meso-colic glands have
been involved in cases in which the colon was free from disease. It
has, moreover, been observed in cases in which death has occurred very
early in the disease, and there can therefore be little doubt that it
is as much the result of the infective process as the infiltration of
Peyer's patches. In addition to being enlarged, if death has taken
place before the end of the second week the glands are hyperaemic and
of a purplish color. Later than this, when the sloughs become detached
from Peyer's patches, the swelling of the glands diminishes; they lose
their color and become pale, and if convalescence ensues they return
finally to their former healthy condition. Still, Murchison has seen
them shrivelled and pale or bluish for some time after convalescence.
In other cases the substance of the glands softens, with the formation
of a puriform liquid. If the softening only involves a small part of
the glandular structure, restoration to health may take place through
the absorption of this liquid. If it is more extensive, the whole of
the glands may break down into this puriform liquid, which, when the
patient recovers, undergoes caseous and finally calcareous
degeneration. Occasionally, a gland in this condition is the cause of
death from rupture and extravasation of its contents into the cavity
of the peritoneum.
The glands in the fissure of the liver, the gastric, lumbar, inguinal
glands, and indeed all the lymphatic glands in the body, have
occasionally been found swollen and congested, but their enlargement
cannot be classed among the specific lesions of the disease, but is
merely the result of a local irritation. Thus, Jenner says that in the
case of extensive ulceration of the oesophagus which came under his
observation there was marked enlargement of the oesophageal glands.
Liebermeister says that the lymphatic follicles which surround the
glands at the root of the tongue and in the tonsils are often affected
in the same way as the glands. In most cases after a time the swelling
disappears, but sometimes softening and rupture take place.
The spleen is almost invariably found to be increased in volume and to
have undergone changes in consistence and color. The degree of
enlargement and the other changes vary of course with the stage of the
disease at which death has occurred. The enlargement occurs with less
frequency in elderly than in young people, and is most marked at the
height {265} of the disease, the organ being then often twice or three
times its normal size, and in some cases, it is said, even larger.
Later, and especially during convalescence, the enlargement has
generally very much diminished. During the first ten days of the
disease the spleen is generally tense and firm, engorged with blood,
and dark red in color. Between the tenth and thirtieth days its
appearance remains the same, but the organ is found to be soft and
friable. During convalescence it becomes paler and firmer again, and
is often so shrunken in size that its capsule is relaxed and wrinkled.
Hemorrhagic infarctions are often met with. These sometimes soften and
break down into a puriform liquid, which may sometimes cause
peritonitis by rupture into the peritoneal cavity. Rupture of the
spleen is also said to have occurred from mechanical violence. These
changes are due in part to variations in the amount of blood, and in
part to a medullary infiltration of Malpighian corpuscles similar to
that which takes place in Peyer's patches and the glands of the
mesentery.
LESIONS WHICH ARE NOT PECULIAR TO TYPHOID FEVER, BUT ARE OF MORE OR
LESS FREQUENT OCCURRENCE.--The mucous membrane of the pharynx and
oesophagus may present a perfectly healthy appearance, but
occasionally it is congested and the seat of ulcerations which are for
the most part superficial. Sometimes, however, they have been found to
extend to the muscular coat, but they have never been known to
penetrate all the coats of these organs. Jenner refers to one case in
which there was extensive ulceration of the oesophagus, but usually
the number of ulcers is not large. In a few cases the mucous membrane
of the pharynx is coated with diphtheritic false membrane, and the
submucous tissue is infiltrated with serum and pus (Murchison).
The stomach and the upper part of the intestinal tract present no
lesions which are at all peculiar to typhoid fever. In a certain
number of cases congestion, softening, and even superficial
ulceration, of the mucous membrane of the stomach, and less frequently
of that of the duodenum, have been found. The mucous membrane of the
jejunum and of the upper part of the ileum is not usually much
reddened, and may be even paler than in health. In cases which have
been protracted it may be of an ashy-gray or slate color. The contents
of this part of the intestinal tract, which is rarely much distended
by flatus, do not differ materially in appearance or consistence from
the matter which generally composes the typhoid stool. The bowels may,
of course, be found filled with blood in cases in which a recent
hemorrhage has taken place. Invaginations of the small intestines,
unaccompanied by any evidences of inflammation, are occasionally met
with in the bodies of those who have died of typhoid fever. They are
produced, there is good reason to believe, during the death agony, but
are not peculiar to this disease, as they occur in many other
diseases.
Enlargement of the liver has been found in only a few cases after
death from typhoid fever. Softening is more common, but even this is
not a frequent result of the disease, for it was absent in 41 out of
73 cases examined with special reference to this point by Louis,
Jenner, and Murchison. The organ is occasionally hyperaemic, and
darker in color than in health, but it is oftener pale or normal in
appearance. Even, however, where it appears to be perfectly healthy to
the unassisted eye, {266} the microscope shows that its cells are very
granular and filled with oil-globules which often render the nucleus
indistinct or completely conceal it. When death has taken place at an
advanced stage of the disease many of the cells are found to be
completely broken down into a granular detritus. These changes are
usually proportional to the degree of pyrexia which has been present
during life. Rarer lesions of the liver are pyaemic deposits,
embolism, abscess, and emphysema.
The mucous membrane of the gall-bladder has been found to be the seat
of ulcers by Jenner and numerous other observers. It also occasionally
presents the evidences of catarrhal or diphtheritic inflammation. The
gall-bladder usually contains a pale watery liquid of a less density
than bile. When, however, inflammation of its lining membrane has
existed, its contents are mixed with pus and shreds of false membrane.
The mucous membrane of the larynx is sometimes found to have been the
seat of catarrhal or diphtheritic inflammation, and sometimes also of
ulceration. Jenner says that in typhoid fever laryngitis independent
of pharyngitis is extremely rare, but the German writers express a
different opinion. Griesinger estimated that laryngeal ulcers were
present in one-fifth of the fatal cases. Hoffmann found them
twenty-eight times in two hundred and fifty autopsies, and that the
ulcers had extended to and involved the cartilages in twenty-two out
of the twenty-eight cases. They are most commonly found in the
posterior wall of the larynx, and may involve the vocal cords. These
are often discovered after death in cases in which their existence was
not suspected during life. They were formerly supposed to be the
result of typhoid infiltration of the laryngeal glands, but careful
investigation has shown that they are the consequence of diphtheritic
inflammation of the mucous membranes. Inflammation and ulceration of
the trachea are comparatively rare. Hypostatic congestion and
infarction of the lungs are not uncommonly found after death from
typhoid fever, and less frequently the lesions of pneumonia. Evidences
of recent pleurisy are also discovered in a few cases. Acute miliary
tuberculosis of the lungs is more often met with as a sequela than as
a complication.
The changes in the brain and its membranes caused by typhoid fever are
few and unimportant, even in cases attended by severe nervous
symptoms. Those most frequently found are adhesions of the dura mater
to the inner surface of the cranium, injection or oedema of the pia
mater, congestive oedema, and sometimes softening of the brain and
effusion at the base of the brain. The microscopic changes do not
appear to have been carefully studied. Liebermeister says that the
gray substance of the cortical portion of the brain and of the
interior is sometimes of a rather yellowish-brown color, and that he
noticed besides diffuse yellow and blackish-brown spots in different
places, particularly in the corpus striatum and thalamus opticus. In
such places, he says, the microscope shows a diffuse yellow
coloration, a deposit of small brown pigment-granules, and also,
especially in the optic thalamus and corpus striatum, the
ganglion-cells thickly crowded with brownish or blackish
pigment-granules in such numbers as to conceal the outlines of many of
the cells. These changes Hoffmann,[47] who has specially studied them,
is inclined to place by the side of the parenchymatous degeneration of
other organs. {267} The ganglion-cells of the sympathetic ganglia are
said by Virchow also to contain an unusual amount of pigment.
[Footnote 47: Quoted by Murchison.]
The muscles are frequently the seat of marked changes in typhoid
fever. Their macroscopic appearances vary with the stage of the
disease at which they are examined. When death takes place in the
first or second week they are usually dark red or reddish-brown in
color, and very dry. If it is delayed until later, they "present a
peculiar fawn or yellow tint permeating the ordinary red in patches
and veins not unlike the appearance of veined marble." Their
consistence is also so much diminished that the finger may be readily
passed through them. Occasionally, pseudo-abscesses and hemorrhages
into the muscular sheath are found, and Dauve and B. Ball[48] report
cases in which, in addition to these changes, rupture of muscles had
occurred. Zenker, who was the first to call attention to them, ranged
the changes seen under the microscope under two heads: (1) granular or
fatty degeneration; (2) waxy degeneration. In the first variety the
transverse striae disappear and the sarcolemma appears filled with
finely granular matter. In the second variety the striated muscles
become, as it were, pervaded by a coagulating material which sets, and
in contracting breaks up the fibres into great numbers of short
waxy-looking lumps, not unlike a certain variety of casts of the
tubuli recti of the kidneys. When recovery takes place the affected
fibre is believed to be regenerated by a cell-growth within the
sarcolemma. These changes occur in most fevers, as typhus, small-pox,
scarlet fever, and are attributed by authors generally to the
hyperpyrexia which is a frequent accompaniment of these diseases.
Hayem, however, asserts that he has found them well marked in cases
not characterized by a high temperature, and that, on the other hand,
they are sometimes absent in cases where this has been present. The
waxy form of degeneration may affect all the striped muscles, but is
oftenest seen in the muscles of the abdominal walls, the adductors of
the thigh, the muscles of the diaphragm, and tongue.
[Footnote 48: _L'Union Medicale_, 1866, quoted by _Biennial Retrospect
of Medicine and Surgery and their Allied Sciences_, for 1865-66.]
The heart, in common with the other muscles of the body, suffers from
both the forms of degeneration above described, but the granular form
appears to be more common than the waxy. In protracted cases it is
usually much softened, and when thrown upon a plate no longer retains
its form. It has usually lost its normal color and acquired the tint
described by the French as feuille morte (faded leaf). Upon minute
examination the degeneration is found to have taken place in patches,
the diseased fibres being found alongside of others which have
scarcely undergone any alteration. These patches are especially common
in the papillary muscles of the mitral valve--a fact which explains
the occasional presence of systolic murmurs in typhoid fever. In
addition to the microscopic appearances of the muscles already
described, Hayem[49] has observed in his examinations of the heart a
cellular infiltration of the connective tissue and a proliferation of
the muscle nuclei. These changes are sufficient in his opinion to
establish the existence of myocarditis. The same observer thinks he
has also found evidences of the frequent occurrence of endoarteritis
in the multiplication of the cellular elements {268} of the internal
coat of the small arteries, which he has discovered under the
microscope.
[Footnote 49: _Lecons cliniques sur les Manifestations cardiaques de
la Fievre typhoide_, Paris, 1875.]
Some discrepancy of opinion exists in regard to the condition of the
blood in typhoid fever. Trousseau, for instance, speaks of it as being
profoundly altered and in a state of dissolution; Liebermeister says
that at the height of the disease the blood is very dark-colored, and
that after coagulation it presents a small and soft clot; and
Murchison, that a dark, liquid condition of the blood is rarer than in
typhus, and that fine white coagula are more common. Harley too has
frequently found firm colorless clots of fibrin in the heart and roots
of the great vessels in subjects dead in the third week of the
disease. Forget concludes from an examination "of one hundred and
twenty-three specimens of blood derived from patients in all stages of
the disease that an appreciable alteration of the blood in the several
periods of enteric fever cannot be accepted as a general fact; that
the blood is rarely altered in the first period; that the alteration
is more marked in proportion as the disease is more advanced; that the
alteration is not always in proportion to the gravity of the
disease."[50] I have myself seen the disorganization of the blood as
complete in severe cases of typhoid fever which have rapidly proved
fatal as in cases of diphtheria or of other malignant diseases. On the
other hand, in protracted cases and during convalescence the blood is
often thin and watery.
[Footnote 50: Quoted by Harley, Reynolds's _System of Medicine_, vol.
i.]
The kidneys are sometimes engorged with blood, sometimes pale and
flabby. Under the microscope the appearances are similar to those just
described as occurring in the liver, and it is therefore unnecessary
to refer to them more fully here. As a rule, the epithelium becomes
granular earlier and to a marked degree in the cortical than in the
tubular portion. The absence of albuminuria must not always be
accepted as proof of a healthy condition of the kidneys, as this
symptom has been wholly wanting in cases in which the organs have been
extensively diseased.
Analogous changes have also been observed in the salivary glands and
pancreas, except that, according to Hoffmann, a cellular proliferation
precedes the degenerative process.
CLINICAL DESCRIPTION.--The invasion of the disease is usually so
gradual that it is often impossible to obtain from patients exact
information as to the time of the beginning of their illness. Among
those who present themselves for treatment at the Pennsylvania
Hospital it is not uncommon to find that many have suffered for
several days, it may be as long as a week, or even longer, before
taking to their beds, from vague feelings of discomfort, from headache
more or less intense, aching pains in the back or limbs, or from
sensations of chilliness alternating with flashes of heat. In other
cases derangements of the digestive system are more prominent, such as
nausea, or even vomiting, diarrhoea, or irritability of the bowels.
Notwithstanding these symptoms, and the indisposition to exertion
engendered by them, they have frequently continued to follow their
usual avocations up to the time of their application at the hospital
for admission. There is generally, however, no difficulty in
recognizing at once the nature of their disease. Upon examination the
pulse is found to be frequent, the respiration accelerated, the tongue
furred, the skin hot and dry, and the abdomen tympanitic.
{269} Among patients whose position in life enables them to pay
greater attention to trifling symptoms than those who are compelled to
seek hospital relief, opportunity is frequently afforded to the
physician to study the disease at a period less remote from its
commencement. The symptoms it presents when seen as early as the
second day are generally of a very indefinite character. There may be
a feeling of malaise, headache with a tendency to giddiness, pain in
the back and limbs, a slightly coated tongue, thirst, and anorexia.
The patient may complain of chilly sensations alternating with flashes
of heat, but it will rarely be found that the attack has commenced
with a decided chill. Diarrhoea may also be present at this time, or
may not supervene until later. Even in cases in which it is absent the
bowels will generally act inordinately after the administration of a
gentle purgative. Occasionally, the attack begins with vomiting, but
this is not, in my experience, a frequent mode of commencement. If the
visit be made in the morning, the febrile symptoms will be little
marked, the pulse being only slightly accelerated and the temperature
being rarely more than from a half to a degree above the normal. In
the evening, however, the thermometer usually indicates a greater
elevation of temperature.
At subsequent visits the same symptoms are presented. It will be
observed, however, that the fever is decidedly remittent in character,
the evening temperature being always from a degree to a degree and a
half higher than that of the morning, while the temperature of each
succeeding day is a little higher than that of the day which preceded
it. The patient is restless and wakeful at night, or sleep, when
obtained, is unrefreshing and disturbed by dreams. He grows dull and
slightly deaf, and although able to answer questions intelligently
when roused, does so with an effort, and soon after lapses into his
former condition. Although obviously growing weaker every day, it is
sometimes difficult to get him to take to his bed. The diarrhoea
continues and increases in severity; the stools become watery in
character and ochrey-yellow in color; they may exceed six, or even
twelve, in the twenty-four hours. Epistaxis either consisting of a few
drops of blood only, or so profuse as to endanger life, may also occur
during the first week. Examination of the abdomen toward the middle or
close of the first week will almost always reveal the existence of
tympany and of tenderness and gurgling in the right iliac fossa, and
very frequently also of slight enlargement of the spleen. The urine at
this stage of the disease is dense, scanty, and of high color. The
tongue too will be observed to be more heavily coated than at first,
and to be dryish, the fur being disposed on the middle of the dorsum
of the organ, while the tip and edges are free from it and abnormally
red in color. Usually, toward the close of the first week, the pulse
will be found to be between 100 and 120 in frequency. It often,
however, does not attain this frequency, and in some cases does not
exceed 50 throughout the whole of the attack. At the same time, the
thermometer generally indicates a temperature of from 102 degrees to
104 degrees, and in bad cases even one much higher than the latter.
These symptoms are not pathognomonic, but Murchison regards their
existence in a young person as warranting the suspicion that he is
suffering from this disease. About this time, however, or, to speak
more accurately, usually from the seventh to the twelfth day, a new
symptom occurs {270} which is more characteristic. This is an eruption
of isolated rose-colored spots, the taches roses lenticulaires of
Louis, occurring principally upon the surface of the abdomen, but not
infrequently seen also upon the chest, back, limbs, and even,
according to some authors, upon the face. They are round in shape,
with a well-defined margin, usually about a line in diameter, but
sometimes considerably larger, slightly elevated above the surface,
and disappearing upon pressure, but returning when the pressure is
removed. They can almost always be found at this stage of the disease
if diligently sought for.
If the disease tends to run a severe course, all the symptoms become
aggravated toward the end of the second week. The tongue grows dry and
brown, the pulse more frequent, feeble, and markedly reduplicated in
character, the diarrhoea still more severe, and the fever higher than
before, with little or no tendency to remit in the morning. The
nervous symptoms also come into prominence. The headache may grow more
violent or may be replaced by increased dulness, which may sometimes
be so decided as to render it difficult to fully rouse the patient. At
other times delirium is a prominent symptom. This may only occur at
night, but not infrequently is observed during the daytime as well. It
is usually more active in character than that which accompanies
typhus. Trembling of the tongue and of the limbs is not uncommon at
this time. The urine becomes more abundant, paler, and less dense than
before. Even in cases characterized by symptoms as severe as those
above detailed some improvement is, however, often observed to take
place between the fourteenth and twenty-first days. The morning
remission becomes more decided, the evening temperature less high than
that of the preceding day; the stools lessen in number, and gradually
assume a more healthy appearance; the pulse diminishes in frequency
and gains in force; the tongue becomes moist, and shows a tendency to
throw off its fur; the trembling grows less marked; the dulness and
delirium lessen; and the patient falls into a refreshing sleep. In
other cases, in many of which recovery eventually takes place, there
is at this time, instead of an improvement, a still further
aggravation of the symptoms. The pulse becomes more feeble and
frequent; the tongue is not only excessively dry and brown, but
shrivelled and fissured; the lips and teeth are encrusted with sordes;
the stools contain shreds of membrane, and often blood; the subsultus
tendinum increases; carphololgia, or picking at the bed-clothes,
occurs. The prostration becomes so extreme that the patient frequently
slips down in bed from sheer weakness. The active delirium of the
previous stage is replaced by the low muttering form, or the patient
lies upon his back with his eyes half closed in a semi-unconscious
condition, from which he is with difficulty aroused, and which may
deepen into coma. Occasionally, however, the active delirium
continues, and is associated with an obstinate wakefulness; the urine
and feces are passed involuntarily, or, with an apparent incontinence
of the former, there may be retention, which is very apt to be
overlooked. If these symptoms continue for any length of time,
bed-sores may form not only over the sacrum, but on other parts
subject to pressure, and the patient, worn out by long-continued
suffering, dies from exhaustion.
Occasionally, in the midst of these symptoms, and sometimes even in
cases in which the condition is not so alarming, prostration
approaching {271} collapse, without obvious cause, suddenly
supervenes. The pulse becomes a mere thread, the surface is bathed in
a clammy sweat, and the temperature is found to have fallen from four
to seven degrees, and in some cases even more. These symptoms almost
always indicate that intestinal hemorrhage has taken place, and are
followed by the discharge of blood either in the course of a few hours
or not until a day or two subsequently. If the hemorrhage be moderate
in amount, and does not recur, reaction usually takes place in a short
time; but if, on the other hand, it is profuse or frequently repeated,
death may occur, either immediately or later, as the result of the
exhaustion it has induced. Very much the same set of symptoms attend
the occurrence of perforation of the bowel, an accident which is also
liable to happen in the course of typhoid fever, but which may
generally be distinguished from intestinal hemorrhage by its being
accompanied by a sharp pain in the abdomen, which is frequently so
severe as to cause the patient to cry out, by its not being attended
with the same reduction of temperature, and by the absence of blood in
the discharges. In a day or two all doubt will be set at rest, if the
case be one of perforation, by the occurrence of general peritonitis.
A fatal termination is by no means the usual result, even in cases in
which the disease has assumed its worst features. Indeed, it may be
said that there is no condition in typhoid fever so grave that
recovery from it is impossible. Many authors would make perforation of
the bowel an exception to this general rule, but there are
observations on record which would seem to show that this accident is
not invariably fatal. Even in cases in which the patient has lain
helplessly on his back in a semi-unconscious or comatose condition,
passing his discharges under him, the physician will often be
gratified to find at one of his visits some evidence of improvement,
trifling as it will probably be. It may be only a slight change of
position, an inconsiderable fall of temperature, or a scarcely
appreciable moistening of the tongue; but these changes, insignificant
as they apparently are, are sufficient to indicate to the practised
eye of the observant physician the approach of convalescence. Next day
there will be a still further reduction of temperature, a more decided
moistening of the tongue, a sensible diminution of the nervous
symptoms, and a reduction in the frequency of pulse. In this
condition, however, as may be readily imagined, convalescence may be
retarded by numerous accidents, and life may hang trembling in the
balance for several days, or even weeks, before it is fully
established. It is not necessary to recount here the various steps by
which a return to health is reached, as they are essentially the same
as those which mark the convalescence of the less severe variety of
the disease, and have already been fully referred to in the
description of that form.
But even after the establishment of convalescence, and after the
patient has been free from fever for several days, febrile attacks
lasting for a day or two, or even longer, may occur as the consequence
of very slight causes, such as undue excitement, or fatigue of any
kind, or the immoderate indulgence of the appetite, which in this
condition frequently needs to be restrained. These attacks are usually
spoken of as recrudescences of fever, and do not differ materially
from attacks of irritative fever occurring under other circumstances.
They usually subside under appropriate treatment with the removal of
their cause, but leave the patient somewhat {272} weaker than they
found him. In other cases, it may be a week or ten days after the fall
of the temperature to the normal, and frequently at a time when all
danger seems to have been passed, a true relapse of the disease
occurs. In this, of course, all the symptoms of the primary attack are
reproduced, including even the eruption of rose-colored spots. The
temperature usually, however, attains the maximum more rapidly, and
the duration of the fever is generally shorter, than that of the
original attack. A second relapse is also not very uncommon, and even
a third may occur. Various complications and sequelae also occur in
the course of typhoid fever, which will be referred to fully
hereafter.
Another form of the disease, which it may be well to allude to briefly
here before closing the general description of the disease, is the
abortive form. In this variety the attack begins and runs its course
up to a certain point, including often even the occurrence of the
eruption, as it does in the majority of cases; but at a period which
varies between the seventh and fourteenth day the symptoms suddenly
subside and the patient rapidly convalesces. In some cases it may be
difficult to distinguish this form from an attack of simple continued
fever, and, in fact, in cases in which the eruption is absent it will
be impossible, unless other cases of typhoid fever have occurred in
the same house or family, or unless the patient has been unmistakably
exposed to the influences under which the disease arises.
In a few cases the disease begins abruptly with a chill, intense
headache, or with gastro-intestinal symptoms, which have in rare
instances been so violent as to have suggested to the mind of the
attending physician the possibility of corrosive poisoning. This,
according to Chomel, is the most frequent mode of commencement, but
his experience on this point is opposed to that of the great majority
of observers.
* * * * *
I shall now proceed to describe in detail some of the most important
of the symptoms presented by the disease.
Even in the beginning of an attack of typhoid fever the face has a
listless and languid expression, although the eyes are usually bright
and the pupils dilated. In mild cases no further alteration of the
physiognomy than this may be noticeable throughout the whole course of
the disease, but in bad cases, when the typhoid condition is fully
developed, the expression becomes dull and heavy. There is, however,
never the general suffusion of the face seen in typhus. On the
contrary, the face is often pallid, or there is at most a
circumscribed flush on one or both cheeks, which is most marked during
the exacerbations of fever or after the administration of food and
stimulants. During convalescence the effects of the long illness are
fully visible in the face.
Prostration, or loss of muscular strength, is present from the
beginning in a large number of cases of typhoid fever, but is
generally not so marked in the early stages as in typhus fever. It is
usually most intense in grave cases, but to this rule there are
numerous exceptions. It is not rare to find patients, in whom the
other symptoms are severe, able to sit up in bed, and even to rise to
stool, throughout the attack. Bartlett records a case in which the
patient did not confine herself to bed until the occurrence of
perforation, and I have had under my care a man who, supposing he was
suffering only from a slight diarrhoea, performed the duties {273} of
a nurse in a military hospital until two days before his death,
although the autopsy showed very extensive ulceration of the
intestine. Several cases have come under my care in the second week in
which patients have walked a considerable distance to make application
for admission to a hospital. Generally, however, the prostration
becomes extreme in the third and fourth weeks of bad cases, the
patient lying helplessly on his back, and frequently slipping down in
bed from sheer weakness.
Epistaxis may occur at any stage of typhoid fever, but is most common
in the forming stage. Observers differ in opinion in regard to its
frequency. Murchison noted it in only 15 of 58 cases, and gives it as
his belief that it is more common in France than in England or this
country. Flint found that it had occurred in 21 only of 73 cases, and
Jenner in 5 of 15 fatal cases. On the other hand, Bartlett says that
it is quite a common symptom, and Wood and Gerhard, from the frequency
with which they had met with it in the beginning of the disease, were
accustomed to regard its presence as of importance in a diagnostic
point of view. Part of this divergence of opinion is probably due to
the fact that it is usually small in amount, and therefore very apt to
be overlooked. I have in many cases, after having been told there had
been no epistaxis, found the evidence of it upon the fingers or
bed-clothes of the patient. It may, however, be so profuse as to
endanger life and render necessary the use of the tampon. Except in
the latter case it is without influence upon the course of the
disease.
The skin may be almost constantly dry as well as warm throughout the
whole course of the fever in a small proportion of severe cases. But,
on the whole, perspiration occurs with greater frequency in typhoid
fever than in any other acute disease, unless it be rheumatism. It
takes place most commonly at night after the evening exacerbation, or
in the morning when the patient awakes from sleep, but it is not very
rare to find the skin clammy at other times. The sweating is usually
general, but in a few cases it is local only. When colliquative, it is
frequently exhausting, and is then a grave symptom. It is sometimes
prolonged into convalescence, when it is not only annoying, but in
consequence of the prostration it induces may sometimes retard the
restoration to health.
I have never been able to satisfy myself that any peculiar odor is
given off by the skin in typhoid fever, and most observers make a
similar statement. Chomel, however, asserted that the perspiration has
a strong acid odor, and Bartlett agreed with Nathan Smith in thinking
that typhoid fever patients exhale a peculiar odor, not pungent and
ammoniacal, like that of typhus, but "of a semi-cadaverous and musty
character," which is especially noticeable during the later stages of
severe and fatal cases.
The eruption is one of the most characteristic symptoms of the
disease. Indeed, in many cases, without it the diagnosis would be
impossible. It is rarely absent in a well-developed case. Murchison
says that it was noted in 4606 cases only out of 5988 admitted into
the London Fever Hospital in twenty-three years, but admits that it
would probably have been found in some of the others if it had been
properly looked for. Wood says that he has seldom met with cases in
which it was absent. It is oftener absent in children than adults--a
circumstance which makes the diagnosis of the disease in the former
often a matter of great difficulty. It consists of isolated
rose-colored spots, slightly elevated above {274} the surface,
circular in form or nearly so, having well-defined margins, usually
about a line in diameter, but sometimes varying from half a line to
two and even three lines in diameter, and disappearing on pressure, to
return when the pressure is removed. They are generally first observed
some time between the seventh and fourteenth days, but cases are on
record, especially in children, in which they are said to have
appeared much earlier, and others in which they could not be
discovered until the twentieth day. In the latter cases, however, it
is not improbable they had really been present at an earlier period,
but had escaped detection. The eruption occurs in crops at intervals
of three or four days, each spot lasting from three to five days, and
the whole duration of the eruption being usually from ten to twenty,
and varying of course with the severity of the attack. It may continue
to appear as late as the twentieth day, and in cases of relapses very
much later. Spots are sometimes seen on the abdomen or elsewhere after
the subsidence of fever, and whenever seen indicate that the diseased
process is not at an end. They are usually scattered over the lower
part of the front of the chest and the abdomen, but are also not
infrequently met with upon the back, and if they are not found upon
the abdomen, the patient should be gently turned upon his side and
this part of his body carefully examined. When very abundant they are
often also seen upon the extremities, and occasionally even upon the
face. Wood has seen them abundant on the upper and inner part of the
thigh, and confined to that place. When tardy in making their
appearance, they may often be brought out by application of a mustard
plaster or by that of heat in any form; and it is probably, therefore,
owing in large measure to the warmth of the bed that they are often so
fully developed upon the back. In number they may vary from two or
three to several hundred. In one case Murchison counted one thousand,
and in three cases which came under my care in the winter of 1881-82
the body was so thickly covered by spots of an unusually large size
that when I first saw the patients I directed them to be isolated
under the fear that the disease would prove to be typhus fever. When
very numerous the edges of two or three of the spots may run together,
giving the eruption an irregular character. No relation between the
copiousness of the eruption and the severity of the disease has ever
been proved to exist. While the prevailing impression, therefore, that
cases in which the eruption is freely developed are apt to be of a
mild character, is true in many instances, it is by no means so in
all. The three cases above referred to all ran a severe course, and
one of them proved fatal. The spots disappear after death, and are
rarely converted into petechiae, but in bad cases I have seen purpura
spots, and even vibices, developed independently of them. Sometimes
the appearance of the eruption is preceded for a day or two by a
delicate scarlet rash, which Tweedie says resembles roseola and has
been mistaken for scarlet fever.
Sudamina, so called from their resemblance to sweat-drops, also occur
not infrequently in this disease. They are minute vesicles, often not
larger than a pin's head, but sometimes two lines in diameter, and
occasionally, in cases in which two or three have coalesced, much
larger. They usually contain at first a clear serum, which may,
however, subsequently become turbid, and when very minute must, in
consequence of {275} their transparency, be viewed obliquely to be
seen. Frequently, when they cannot be distinguished by the eye, they
are readily detected by the touch. They rarely occur before the
twelfth day, and often not before the close of the third week. Their
most usual seat is the neck, the folds of the axillae, and the groin,
but there is no part of the body except the face in which they may not
occur. They are most frequently seen in those cases attended by
profuse sweating, and are by no means peculiar to typhoid fever, but
are met with in other diseases--as, for instance, acute
rheumatism--which are attended by this symptom. They are generally
followed by branny desquamation of the cuticle in the position they
have occupied.
Spots of a delicate blue tint--the "taches bleuatres" of French
writers--are sometimes observed on the skin in cases of enteric fever.
They must be of infrequent occurrence in this country, for, although I
have looked carefully for them in every case that has come under my
care, I have rarely been able to detect them. According to Murchison,
"they are of an irregularly rounded form and from three to eight lines
in diameter. They are not in the least elevated above the skin, nor
affected by pressure, even at their first appearance. They have a
uniform tint throughout their extent, and they never pass through the
successive stages observed in the spots of typhus. Two or three of
them are sometimes confluent. They are most common on the abdomen,
back, and thighs." They are said in some cases to be distributed along
the course of the small cutaneous veins, and to occur most frequently
in cases which are mild. They are met with in other diseases, and
usually precede in appearance the characteristic eruption of typhoid
fever.
The hair is very apt to fall out after an attack of typhoid fever. The
nails suffer in their nutrition in common with other parts of the
body--a fact which may be recognized by the peculiar markings which
are found upon them after recovery, and to which attention has been
particularly drawn by Morris Longstreth in a paper in the
_Transactions_ of the College of Physicians of Philadelphia, vol.
iii., 3d Series.
The circulation is usually accelerated from the beginning of an attack
of typhoid fever. The degree of acceleration is commonly proportioned
to the severity of the other symptoms, and especially to the elevation
of the temperature, and is generally more marked in the evening than
in the morning. It is subject, however, to numerous variations, not
only in different cases, but even in the same case from day to day,
and even from hour to hour. Murchison refers to a case in which the
pulse sank to 37, and never exceeded 56 during the fever, although it
rose to 66 during the convalescence. I have never had the opportunity
myself of observing such an infrequent pulse in the febrile period of
the disease, but have had cases under my care in which the pulse often
fell below 60, and in which it never exceeded 80 until after the
commencement of convalescence. A comparatively infrequent pulse may
coexist with a high temperature. Thus, for example, a pulse of 80 was
noted in one of my cases at the same time that the thermometer showed
that the temperature was 105 degrees, and on another occasion in the
same case the pulse was 82 and the temperature 104-1/2 degrees. As a
rule, the pulse is more frequent in cases which terminate fatally than
in those which end in recovery; but to this rule there are numerous
exceptions. In eight of Louis's cases it never {276} went above 90,
and in some of my own it did not reach 100 on more than one or two
occasions. On the other hand, in mild cases the pulse may be
exceedingly frequent, reaching, and even exceeding in many cases, 120.
When the disease is prolonged and the prostration is extreme, a pulse
of from 140 to 150 is not uncommon. In the majority of cases which
have come under my care the pulse has varied in frequency from 80 to
120. In some cases the range has been between these two figures, in
others it has been very much less.
During convalescence the pulse usually gradually diminishes in
frequency, and may sometimes fall below the normal standard. I have
known it in a few instances to fall to 38, and have often met with
pulses ranging between 40 and 60 at this period. In other cases, on
the contrary, the pulse continues frequent during convalescence, or
readily becomes so after a slight exertion or excitement of any kind.
A slow pulse during convalescence has been in my experience most
frequent in men whose health previous to the attack was good, and a
frequent pulse in women and delicate men. If the convalescence is
retarded by a complication, the pulse will maintain its frequency
until this is removed.
The pulse will of course present other changes than those above
referred to. It is in the beginning firm and full, but after the first
week becomes small and compressible, and acquires the peculiarity
known as reduplication. Sometimes, when this is not well developed, it
will be rendered quite distinct by elevating the patient's arm.
Irregularity or intermission of the pulse, although not commonly
observed in this disease, occasionally occurs. The heart's action will
also be observed to grow feeble in the course of severe cases, and its
first sound indistinct, but neither of these changes is as marked in
typhoid as in typhus fever. Hayem asserts that in a certain number of
cases a systolic bellows murmur, with its point of greatest intensity
at the apex, is heard during the course or at the close of the second
week. This murmur is sometimes soft in the beginning, but becomes
harsh and intense later, or may have these characters from the start
to such a degree as to give the impression that endocarditis exists.
During convalescence an anaemic murmur is not infrequently present.
The respiratory movements are accelerated in typhoid fever, as they
are in all febrile conditions, independently of any disease of the
lungs, and their frequency is generally proportional to that of the
pulse. In looking over my records of cases I find that the former are
less liable to fluctuate from day to day than the pulse, and that when
the latter becomes abnormally infrequent they do not sink below the
standard of health. In several cases of which I have notes the
respiration was from 20 to 28, while the pulse was below 60, and in a
case referred to by Murchison the pulse was 42 at the same time that
the respirations, although no pulmonary lesion could be discovered,
were 48. The respiration is often, as in the case just alluded to,
very much accelerated when the most careful examination of the chest
will not lead to the detection of any disease there. This is sometimes
the consequence of very great tympanites, which, by interfering with
the descent of the diaphragm, gives rise to dyspnoea, but it may also
occur as a purely nervous phenomenon. The air expired by patients has
been examined, and has {277} been found sometimes, in the later stages
of the disease, to contain ammonia.
Bronchitis is so common an accompaniment of typhoid fever that
auscultation rarely fails to reveal its presence in some form or
other. In some cases there may be only slight harshness of the
respiratory murmur at the base of the chest, but in a large number of
cases the auscultatory signs will be sonorous, sibilant, and mucous
rales. The last named may be so numerous that I have known the disease
in the beginning mistaken for acute bronchitis, and even acute
phthisis, by accomplished diagnosticians.
Headache is one of the most constant symptoms of typhoid fever.
Bartlett says that it is rarely absent, Louis found it in all but 7 of
133 cases, and Jackson noted it in nearly all his cases. It is often
the first symptom of which the patient complains, and, when not
present at the beginning of the attack, makes its appearance soon
after. It is almost as common, although less severe, in mild cases as
in grave ones. It sometimes persists throughout the attack, but
oftener subsides at the close of the first week or toward the middle
of the second, or the patient may cease to complain of it in
consequence of the dulness which is very apt to supervene. It is
usually referred to the forehead and temples, but may extend over the
whole head. It is usually dull and heavy, but in a few cases is
throbbing. It is said by authors rarely to be severe, but I have known
it so intense and acute as to cause the disease at its commencement to
be mistaken for meningitis, and Jackson asserted that it is sometimes
so severe that local bloodletting, and even venesection, had to be
employed for its relief. It would appear to be as common in children
as adults.
The headache is sometimes accompanied by vertigo and dizziness, and
even by retraction of the head. Distressing pains in the back and
limbs may also occur, and in rare cases even contraction of the hands
and feet.
In the beginning of an attack of typhoid fever the patient usually
suffers from wakefulness and restlessness at night, and it
occasionally happens that the wakefulness becomes a distressing
symptom. But in a great many cases, sooner or later in the course of
the disease, drowsiness supervenes. In mild cases this symptom is late
in making its appearance, and is generally slight and evanescent, but
in grave cases it may come on as early as the eighth day, and when
once present may gradually become more profound until it deepens at
last into unconsciousness. It usually persists until the occurrence of
death or of convalescence, but may alternate with periods of delirium,
the delirium being more frequent at night and the somnolence by day.
It is as frequent in children as in adults. Occasionally, the
wakefulness of the earlier stage may reappear at the beginning of the
third week, and coexist with muttering delirium, or occasionally with
delirium of a more violent character. It then constitutes a most
unfavorable symptom, the patient frequently passing several days and
nights in incessant agitation, and sinking finally from exhaustion due
to want of sleep.
Some degree of mental hebetude is rarely absent, even in the mildest
cases of typhoid fever, and is usually among its earliest symptoms. It
may, however, be absent occasionally in cases which run a severe
course. It exhibits itself in the beginning in an indisposition to be
disturbed, a slight inability to fix the thoughts, or a loss of
memory. Generally, the {278} patient will be able at first, by an
effort, to rouse himself from this apathy, but the moment he relaxes
this effort will lapse into his former condition. As the disease
progresses the hebetude becomes more profound and is overcome with
greater difficulty. In mild cases it may continue until the occurrence
of convalescence, but in grave cases it is soon lost in delirium. This
is one of the commonest symptoms of the disease. If I should rely
solely upon my own experience, I should say that it was rare for any
but the mildest cases to run their course without its occurring at
some time or other. Louis found, however, that it was absent in 32
cases, 8 of which were fatal, out of 134 cases, and Murchison in 33
cases, 3 of which ended in death, out of 100 cases. In 8 of these
fatal cases death was due to perforation--a fact which would seem to
show, as suggested by James C. Wilson, that this symptom is not
dependent upon the intensity of the local disease alone. The delirium
of course varies with the severity of the other symptoms, and
especially with the intensity of the fever. In its mildest form it
consists of a slight confusion of ideas, which is readily dissipated
by fixing the patient's attention, and is most apt to occur in the
night or when he first wakes up from sleep. In other cases it is much
more marked; occasionally it is violent and noisy; the patient may
talk wildly and incoherently, he may break out into a paroxysm of
screaming, or, possessed with a sudden terror, he may leave his bed
and attempt to rush from the room or to jump from the window. Later in
the course of the disease the active delirium subsides, and low
muttering delirium takes its place. The latter may go on until
convalescence occurs, or the patient may gradually fall into a
comatose condition, which very often ends in death.
The delusions from which the patient suffers are various. I have known
in two instances a perfectly pure young girl call loudly for her baby,
which she accused her mother and sister of keeping from her. Very
frequently patients insist that they are in a strange place, and beg
piteously to be taken to their home and friends; occasionally, in
grave cases, the patient declares that there is nothing the matter
with him. This Louis was accustomed to regard as a bad symptom, having
never known recovery to take place after it. Delirium generally first
makes its appearance some time in the course of the second week, but
occasionally the invasion of the disease is marked by maniacal
excitement. I have known delirium to occur on the second or third day.
Louis records two cases in which it was present during the first
night, and Bristowe[51] one in which it was noted on the fourth night.
It is sometimes so prominent a symptom in the beginning of an attack
that the patient has at first been supposed to be affected with acute
mania. M. Motet[52] indeed refers to a case in which a man was
actually admitted into an insane asylum before the true nature of his
disease became known. On the other hand, delirium may not occur until
much later in the disease--sometimes not before the close of the third
or even the fourth week, when it may suddenly make its appearance when
least expected. I have known it to be present in a marked degree
during a relapse when it had been wholly wanting in the primary
attack.
[Footnote 51: _Trans. Path. Soc. Lond._, vol. xiii.]
[Footnote 52: _Archiv. gen. de Med._, 1868, quoted by Murchison.]
During convalescence, especially in cases in which there has been much
{279} mental disturbance during the febrile period, the intellect may
be weak, and continues so in some cases even after recovery in other
respects is complete; but it is rarely permanently impaired. Insanity
may also occur during the convalescence or after recovery, but it is
usually under these circumstances amenable to treatment. In some cases
the moral sense appears to be weakened after an attack, as in the case
reported by Nathan Smith, in which a young man of previously good
habits developed thieving propensities after his recovery.
Hyperaesthesia of the skin exists, according to Murchison, in about 5
per cent. of the cases, and may occur at any stage of the disease. It
is chiefly observed in the abdomen and lower extremities, and is more
frequently met with in women and children than in adult males. In a
case which was partially under my care during the past summer the
slightest touch made the patient, a boy of fifteen years, cry out with
pain, and the administration of an enema gave him excruciating agony.
Occasionally, the tenderness over the abdomen is so great that it is
sometimes difficult to distinguish it from that due to peritonitis,
except by the coexistence of hyperaesthesia in other parts of the
body. It is very often associated with spinal tenderness, and
sometimes with other spinal symptoms. Murchison does not regard it as
a formidable symptom.
Cutaneous anaesthesia may also occur, but it is certainly less common
in the earlier stages than hyperaesthesia. Rilliet and Barthez look
upon it as of grave diagnostic import when it occurs in children.
Muscular tremor is also a common symptom of typhoid fever. A little
tremulousness of the tongue when protruded may often be detected
before the close of the first week. A little later the hands will be
observed to tremble when held up, and still later twitching of the
tendons at the wrist may be appreciable while the pulse is being felt.
When muttering delirium supervenes this subsultus tendinum becomes
constant, and extends to other parts of the body. The hands of the
patient are frequently then in constant motion, either picking at the
bed-clothes--a very unfavorable symptom--or moving in an objectless
manner through the air. This condition presents many points of
resemblance to that often seen in delirium tremens, and is said to
come on earlier and to be more marked in those who are addicted to the
abuse of alcoholic liquors. Hiccough is occasionally observed toward
the close of grave cases, and is justly regarded as a bad symptom.
Spasmodic contraction of various groups of muscles is occasionally
observed in severe cases, but is less frequent than muscular tremor,
and in my experience is generally met with in the earliest period of
the disease. The muscles of the extremities, especially those of the
legs, are oftenest affected, but I have known the head as rigidly
retracted as in tubercular meningitis, and have seen cases in which
strabismus has been an early symptom. Murchison has had patients under
his care who have suffered from constriction of the pharynx to such an
extent that they could not swallow. He also reports cases in which
trismus and spasm of the glottis have been present. General
convulsions are not common, but occasionally do occur. Although a very
grave symptom, they are not invariably fatal. Recovery took place in
one of two cases which came under my own observation, and in four of
the six recorded by Murchison. They are not always associated with an
albuminous {280} condition of the urine. In neither of my cases was
there albuminuria, and in only one of the four of Murchison's cases in
which the urine was examined was it present. In one of my cases--the
fatal one--the convulsions seemed to have been induced by giving the
patient improper food; in the other no cause could be discovered.
Ringing or buzzing noises in the ears are present in the early stage
of the disease in a large proportion of the cases, and may sometimes
persist until the disease is well advanced. Usually, however, after a
few days they subside and give place to deafness. This is a very
common symptom, and may either affect both ears or be limited to one.
In the former case it is probably generally due to the blunted
perceptions of the patient, although in a few instances it may be
caused, as suggested by Trousseau, by inflammation of the Eustachian
tube. When only one ear is affected the deafness is of more serious
import, as it is then dependent upon the presence of local
inflammation, which may possibly extend to the meninges. It is, as a
rule, most marked in the severest cases. Unless there has been a local
inflammation it is not followed by permanent impairment of the
hearing. It has even been regarded by some observers as a favorable
symptom, but this opinion does not appear to rest upon a more
substantial basis than the observation of Louis, that the most
profound deafness adds nothing to the gravity of the prognosis.
Imperfect or perverted vision occasionally occurs in the course of
typhoid fever. In a case which was recently under my care, and which
has already been referred to in another connection, there was double
vision associated with strabismus. Sometimes haziness of vision, and
sometimes even visual illusions, are observed. Bartlett and Murchison
have often known intolerance of light present in cases characterized
by active febrile excitement. As a general rule, the pupils are widely
dilated and the conjunctiva pearly white--a condition which is in
marked contrast with what is seen in typhus fever. When, however,
stupor supervenes in bad cases, the pupils are frequently as much
contracted and the conjunctivae as much injected as in the latter
disease. In a few cases unequal dilatation of the pupils has been
noticed. Trousseau was accustomed in his clinical lectures to call
attention to the frequency with which sloughing of the cornea occurred
in the condition known as coma vigil, in which the patient lies with
his eyes wide open. He attributed this accident to the fact that the
eye in this condition is not kept constantly moist by the occasional
closure of the eyelids, and hence, as its innervation is also
impaired, is especially prone to take on ulcerative inflammation. In
other cases there is a free secretion of viscid matter, which often
glues the eyelids together.
The sense of taste is often lost or perverted. This is partly due to
impaired innervation of the tongue and palate, and partly to the thick
deposits which usually cover the mucous membrane of these organs.
Frequent observations of the temperature in typhoid fever not merely
give most important information in a diagnostic and prognostic point
of view, but also often furnish valuable indications for treatment.
From a close study of a large number of cases, Wunderlich and other
physicians have discovered that the pyrexia has certain characters
which distinguish it from other fevers, and which, being present in a
case in which the other symptoms are obscure or ill defined, will
often enable us to recognize {281} its true nature. The pyrexia may be
divided into three periods, each having its own peculiarities. It is
usually said that each period lasts about a week, but in severe cases
the second and third periods extend over a longer time than this, and
the occurrence of a complication or of any other disturbing influence
will have its effect in producing either a prolongation of any one or
more of these periods, and especially of the last two, or an unwonted
elevation or fall of temperature. During the first period there is a
progressive rise of temperature, but the rise is never so abrupt as in
typhus or in many of the phlegmasiae. As there are morning remissions,
ranging from a degree to two degrees in extent, corresponding to the
morning fall in the daily variations of temperature, the tracing upon
the temperature chart will be a zigzag line, each evening temperature
being from a degree and a half to two degrees higher than that of the
preceding evening, while the same difference will be observed in the
morning temperature. The temperature ought, therefore, never in an
uncomplicated case to be much over 100 degrees on the first evening or
102 degrees on the second. A temperature of 104 degrees at any time
during the first or second day will consequently exclude typhoid fever
from the diagnosis. From six to eight days are usually occupied before
the maximum is reached. I have seen it attained as early as the fourth
day in mild cases, and, on the other hand, not until much later in
severe ones. It is usually 104 degrees or 105 degrees, but will of
course vary with the gravity of the other symptoms. The temperature
rarely rises higher than 106 degrees at this period. On the other
hand, I have known cases in which it never exceeded 103 degrees during
their whole course. It would therefore be wrong to exclude typhoid
fever from the diagnosis, as Wunderlich does, if this temperature is
not reached by the sixth, or at latest the eighth, day.
[Illustration: FIG. 12. Chart of typical range of temperature in
typhoid fever, after Wunderlich.]
In the next period the temperature usually ceases to rise, but has a
tendency to oscillate about the maximum temperature of the previous
period as a fixed point, occasionally not quite reaching it, at other
times rising a little above it. The morning remissions, too, become
less decided. In other words, the fever now becomes continuous. This
period, although usually lasting about a week, may extend over more
than two weeks, even in the absence of complications, in cases which
run a severe course, and when it is prolonged from this cause the
temperature may again show a tendency to rise, and may even attain an
elevation considerably above that of the preceding period. The
prognosis in all such cases in which the temperature rises after the
middle of the second week is grave. Temperatures of 108 degrees, and
even of 110.3 degrees, have been noted at this time. Death invariably
follows such high temperatures as these, but before death actually
occurs a considerable fall of temperature very often takes place.
Wunderlich has also called attention to the fact that it is not
uncommon for a sudden and temporary remission of temperature to take
place at this stage, varying from one degree to two degrees and a
half, which may last from ten to twelve hours, and which usually has
occurred in his experience from the sixteenth to the eighteenth day.
Toward the close of the second period the morning remissions will be
observed to be more decided, while the evening temperature remains
about the same as before. The beginning of the third period is
indicated by a diminution of the evening exacerbation, while the
morning remissions become still more marked. The diminution is
progressive, but slow, the {282} temperature each evening falling
short by from half a degree to a degree of the point it reached the
preceding evening. The morning remissions, on the other hand, each day
become greater, a fall of three and a half degrees being not uncommon.
The lysis, therefore, occupies usually a longer time than was required
by the pyrexia in reaching its maximum. Toward the close of this
period the morning temperatures may be normal, as even subnormal,
while an elevation of temperature may continue to take place in the
evening. Occasionally, however, an abrupt defervescence takes place.
The duration of this period will be very much prolonged if
complications are present or if the intestinal ulcers are slow in
healing. I have known it to last for more than three weeks. During
convalescence the temperature is frequently subnormal even in the
evening, but the slightest cause is often sufficient to produce a
considerable though temporary elevation of temperature. I have known
the temperature in one case to rise from 99 degrees F. to 105.6
degrees in a few hours in consequence of an indiscretion in diet, and
in another from 100 degrees to 104 degrees from the suffering and
excitement caused by a severe attack of toothache. Indiscretions in
diet are a fruitful source of these recrudescences of fever. The fever
of the third period has all the characters of an irritative fever, and
is probably kept up by the irritation arising from the intestinal
ulcers. On the other hand, that of the first two periods is due to the
action of the specific poison upon the nervous system and the other
tissues of the body, and corresponds exactly with the primary fever of
the eruptive diseases.
{283} [Illustration: FIG. 13. Chart showing recrudescence of fever
from indiscretion of diet.]
The febrile movement, however, rarely follows a perfectly typical
course, and I consequently find, in looking over the temperature
sheets of a large number of cases, very few which bear, except during
the first period, anything more than a general resemblance to the
chart which {284} Wunderlich has prepared as typical. A very slight
cause will exercise, as has already been said, a disturbing influence
upon the course of the fever, and serious complications or accidents
will of course produce a still more marked effect. An intestinal
hemorrhage, for example, will cause a rapid and decided fall of
temperature. I have often known it to fall from 104 degrees to the
normal temperature, or even below it. This depression, unless the
bleeding continues and the case ends fatally in the course of a few
hours, is only temporary, the temperature rising within twenty-four
hours to its former height, and sometimes even beyond it. A free
epistaxis or a copious diarrhoea will in the same way cause a fall of
the temperature, but it is rarely so marked as in the preceding case.
The same effect is produced by the administration of large doses of
quinia or by the application of cold water either in the form of the
bath, the douche, or any other form, to the surface of the body. On
the other hand, the occurrence of a complication will cause a rise of
temperature, often considerably above the maximum of the first period.
[Illustration: FIG. 14. Chart showing fall from intestinal
hemorrhage.]
The thermometer should be used at least twice daily. In this country
it is generally introduced into the axilla, and less frequently into
the mouth, for the purpose of making an observation. In other
countries it is not infrequently inserted into the rectum, and even
into the vagina. The best hours for making the thermometric
observations are eight in the morning and eight in the evening, since
it has been ascertained from {285} frequent observations that the
daily remissions are more marked between the hours of 6 and 8 A.M.,
and that the temperature usually reaches its maximum some time between
those of 7 and 12 P.M.
Loss of appetite is, except in mild cases, one of the earliest
symptoms of the disease, and usually persists as long as the fever
lasts. It is sometimes accompanied by positive loathing for food, but
generally there is no great difficulty in persuading the patient to
take the necessary amount of nourishment. During convalescence the
appetite returns, and is occasionally immoderate, so that it is
frequently necessary to curb it lest harm should be done by over
indulgence.
Thirst, usually proportionate to the degree of fever, is also present
in the beginning of the fever. Later, when the patient sinks into a
semi-unconscious condition and becomes insensible to the wants of the
system, he will cease to call for water, although it is still urgently
needed.
Nausea and vomiting sometimes occur at the beginning of the disease,
but they have not been such frequent symptoms in my experience as they
would appear to have been in that of Murchison, who says that they are
of such common occurrence that the patient is often supposed at first
to be suffering merely from a bilious attack. He does not regard them,
when occurring at this stage, as serious symptoms. Indeed, he
expresses the belief that the subsequent course of the disease is
sometimes favorably modified by them. They may also occur later in the
disease, and are then of grave import, as they are not infrequently
the consequence of peritonitis. Louis regarded vomiting as a grave
symptom, but it is probable it occurred in the cases from which he
makes his deductions late in the course of the disease. It may
sometimes occur during convalescence, and may then interfere very
materially with the proper nutrition of the patient. The matter
vomited usually consists of a greenish bilious fluid, with the food
last taken. In some cases blood has been thrown up.
The tongue at the beginning of an attack of typhoid fever is usually
moist and coated with a thin white fur, and in mild cases may retain
these characters until the close. Even in some cases which terminate
fatally in the course of the second week, the tongue, with the
exception of being less moist than in health, may present no marked
deviation from this appearance. Generally, however, as the disease
progresses, and sometimes as early as the tenth day, it becomes dry
and brownish, and is protruded with a tremulous motion. Still later it
tends to cover itself with a thick brown coating. This coating is
disposed principally along the middle of the organ, leaving uncovered
the edges and tip, which are very apt to be unnaturally red in color.
The bare portion at the tip is often rudely triangular in shape--a
point which is regarded as of some importance in the diagnosis of the
disease by Da Costa. In bad cases, during the course of the third week
the tongue is frequently crossed by cracks and fissures, which are the
cause of much discomfort to the patient, and when deep may bleed and
leave behind them scars which are recognizable during the remainder of
his life. In other cases the tongue is dry, brown, and shrivelled, or
covered with a tenacious, viscid secretion which renders it difficult
to protrude it.
In favorable cases, as convalescence approaches the tongue regains by
degrees its normal appearance. At first the only noticeable change may
{286} be that the organ is a little less dry than before. In a few
days it will be observed to have become moist and to be gradually
throwing off its coating. The process is, however, a slow one, and
one, moreover, subject to frequent interruption. Very often, when it
seems nearly completed it will be suddenly arrested, and the tongue
become dry and brown. Sometimes, instead of cleaning itself gradually,
the tongue throws off its coating in large flakes, leaving the mucous
membrane red and shining, as if deprived of its papillary structure.
Wood was accustomed to teach that if the tongue when thus cleaned
remained moist convalescence might be expected, but would always be
tedious. This is an observation the correctness of which I have had
abundant opportunity to confirm. If anything happens, however, to
interfere with the progress of convalescence, it not infrequently
becomes dry and coats itself over again. When the restoration to
health is retarded by the continuance of diarrhoea or by the
occurrence of any intercurrent affection, the tongue will often become
pale and flabby and be the seat of superficial ulcerations or of
aphthous exudations.
The mucous membrane of the posterior fauces is also often red and dry
and covered with a glutinous secretion, which often materially
interferes with swallowing. The lips and teeth are in bad cases
encrusted with sordes, and the former are dry and cracked, and bleed
readily when picked.
Meteorism or tympanites is observed in the greater number of cases of
typhoid fever, having been noted by Murchison in 79 out of 100 cases,
and by Hale in 130 out of 179 cases, and in only 43 of the remainder
of his cases is it expressly stated to have been absent. My own
experience leads me to believe that it is present in even a larger
proportion of cases; in fact, that it is rarely absent. It is, as a
rule, later in making its appearance than the other abdominal
symptoms, showing itself usually about the end of the first or the
beginning of the second week. It is generally most marked in grave
cases, especially those attended by severe diarrhoea, but I have seen
it highly developed in cases in which the symptom was not present at
all or but little developed. It may vary, moreover, frequently in
degree at different times in the same case, but when once present
generally persists until convalescence is established or death occurs.
When extreme, it may give rise to distressing dyspnoea by preventing
the descent of the diaphragm.
The meteorism is usually preceded and accompanied by gurgling and
tenderness on pressure in the right iliac fossa. The former of these
symptoms is most marked in cases in which diarrhoea exists, and is
caused by the presence of liquid and gas in the lower part of the
ileum. The tenderness is unquestionably due to the presence of ulcers
in the same part of the bowel. There is also occasionally pain in the
region of the umbilicus, but this is a much less frequent symptom.
Enlargement of the spleen was noted by Hale as being present in some
of the cases which he has described. It is a frequent symptom of the
disease, and may be generally demonstrated by percussion in the course
of the second week. It has not, however, often happened to me to be
able to feel the organ enlarged through the abdominal walls, as
Murchison asserts he has been able to do. Indeed, tympanites is
usually present in a sufficient degree to render this difficult. The
enlargement {287} occurs more frequently in persons under thirty years
of age than in those over it.
Diarrhoea is one of the most frequent symptoms of the disease,
especially in severe cases, and there are very few mild cases in which
it does not occur at some period of their course. Louis noted it in
all but three of his fatal cases, Murchison in 93 out of 100, and M.
Barth in 96 out of 101. It varies in different cases in severity, in
duration, and in the time at which it appears. It may be one of the
earliest symptoms, presenting itself frequently on the first day, and
often being the only one which occasions uneasiness to the patient or
his physician. At other times its appearance may be postponed until
the end of the first week, or even until the patient is apparently
entering on convalescence. It may be mild in the beginning and become
more severe as the disease progresses, or after having been at first
acute may cease spontaneously in a few days to occasion any
uneasiness. In degree it may vary from two stools to three or four, or
even twenty, in the course of the twenty-four hours. It is absent in a
few cases, but in many even of these cases the bowels will be found to
act inordinately after a very moderate dose of purgative medicine. I
have known, for instance, the administration of a single teaspoonful
of castor oil to be followed by five or six stools in an adult.
Constipation does, however, actually exist in a certain number of
cases. Murchison has known the bowels in cases in which a relapse has
occurred to be constipated in the primary attack and relaxed in the
relapse. There is no relation between the severity of the diarrhoea
and the extent of the local lesion. Although oftenest met with in mild
cases, constipation has existed in cases in which perforation of the
bowel or intestinal hemorrhage has occurred during life, or very
extensive lesions been found after death.
The stools are fetid and ammoniacal, and are alkaline in reaction,
instead of acid as in health. They are usually liquid and of the color
of yellow ochre. Murchison says that they separate, on standing, into
two layers--a supernatant fluid and a flaky sediment--but that,
occasionally, instead of being watery they are pultaceous, frothy, and
fermenting, and so light as to float in water. I have myself often
seen the appearance which Bartlett compares to that of new cider. They
may contain blood, and when they do, occasionally present the
appearance of coffee-grounds. They are not infrequently, in grave
cases, passed involuntarily.
Intestinal hemorrhage is fortunately not a frequent symptom of typhoid
fever. It may occur as early as the fifth or sixth day, but is more
common after the middle of the second week or in the third or fourth
week. In 60 cases observed by Murchison in which the hemorrhage
exceeded six ounces it began during the second week (mostly toward its
close) in 8; during the third week in 28; during the fourth in 17;
during the fifth in 1; during the sixth in 3; during the seventh in 1;
and during the eighth week in 1; while in one case the date of its
occurrence is not noted. In the cases observed by Liebermeister and
Griesinger, 113 in all, the bleeding took place in a much larger
proportion of cases at an early period of the disease, occurring in as
many as 43 in the second week, and in only 27 during the third. In 7
cases in which I had the opportunity of observing it in patients under
my own care it occurred on the seventeenth day in 1; on the
twenty-third day in 1; during the {288} third week in 2; during the
fifth week in 2; and on the fifth day of a relapse in 1. There may be
a single hemorrhage, or the bleeding may be repeated one or more
times. In 5 of my cases there was a second hemorrhage, and in 2 of
them a third; and in several of Murchison's cases it recurred at
varying intervals after its first appearance.
When the bleeding occurs early in the disease it is usually
insignificant in amount, and is due either to extreme congestion of
the mucous membrane of the intestine, giving rise to rupture of the
capillaries, or to disintegration of the blood, allowing its ready
passage through the walls of the vessels. In the latter case it
usually coexists with petechiae or a hemorrhage from some other part
of the body, as, for instance, epistaxis or hematuria. After the
middle of the second week the hemorrhage is generally the result of
the laying open of a small artery, either by the detachment of a
slough from one of the glands of Peyer or by the involvement of its
walls in the ulcerative process. It is then often profuse, and may
even reach several pints in quantity. Murchison has, however, seen
profuse hemorrhage at such an early stage of the disease that it was
impossible that ulceration could have taken place. The blood is not
always voided immediately after a hemorrhage has taken place; it may
be retained for some days. Indeed, if the amount be large the patient
may die within a few hours of its occurrence without any appearance of
blood externally. This is, however, rare; it is more usual for the
hemorrhage to be repeated before death takes place, but the occurrence
of the bleeding may be suspected in such cases by the abrupt fall of
temperature, sometimes below the normal standard, and by the extreme
prostration and pallor which come on suddenly without other assignable
cause. The depression of the temperature does not continue long. It
generally reaches its former elevation, or even exceeds it, in the
course of twenty-four hours.
There would appear to be a slight difference in the frequency with
which intestinal hemorrhage occurs in different times and at different
places. Murchison noted it in 58 cases of 1564, or 3.77 per cent.;
Louis in 8 cases of 134, or 5.9 per cent.; Liebermeister in 127 cases
of 1743, or 7.3 per cent.; Griesinger in 32 cases of 600, or 5.3 per
cent.; and I have noted it 7 times in 81 cases, or in about 8.5 per
cent. Liebermeister makes it twice as frequent in women as in men. It
seems to be much less common in children than in adults, for in 252
patients under fifteen years of age observed by Taupin, Rilliet, and
Barthez it occurred in 1 only. There is considerable diversity of
opinion among observers in regard to the importance of this symptom.
Murchison lost 32 of his 60 cases. In 11 of the 32 fatal cases the
immediate cause of death was peritonitis; in 14 of the remaining 21
cases the patients died within three days of the bleeding, and in 8 of
the 14 within a few hours. Of Liebermeister's 127 cases 49, and of
Griesinger's 32 cases 10, terminated fatally; 3 of my own cases ended
in death, but none of them until several days had elapsed after the
bleeding. In the face of facts such as these there have not been
wanting authors to assert that the effect of the hemorrhage was
sometimes beneficial. Chief among these are the celebrated Irish
physician Graves and his devoted admirer Trousseau. There may
occasionally be a slight subsidence of the nervous symptoms upon the
occurrence of a hemorrhage, consequent upon the reduction of
temperature {289} which usually accompanies it, but this relief is
only temporary, and procured at too great expense to be really of
service to the patient.
The bleeding is most frequently observed in bad cases. All the cases
which were under my care in which it occurred were of great severity
from the very start. In 18 of Murchison's 60 cases the antecedent
symptoms were mild. In 3 of my cases there was severe diarrhoea. In 2
of the other cases, 1 of which was fatal, the bowels were constipated,
and in another one, also fatal, they were slightly loose. In 8 of
Murchison's cases, 6 of which were fatal, the bowels had been
constipated up to the time of its occurrence. The blood, if voided
immediately after its escape into the intestines, is generally fluid
and bright red in color. When retained for a day or two it is passed
in dark clots, and if retained longer than this it is usually mixed
with fecal matter when discharged from the bowels, and gives the
stools a tarry appearance and consistence, which is not always
recognized by inexperienced attendants as due to blood.
It has been asserted that intestinal hemorrhage has become more
frequent since the introduction of the cold-water treatment, but
Liebermeister shows this to be an error, for he has found that of 861
cases treated before the introduction of this treatment, 72, or 8.4
per cent., had intestinal hemorrhage, but that of 882 cases treated
since its introduction hemorrhage occurred in 55, or in 6.2 per cent.
Other methods of treatment have also been charged with inducing a
tendency to hemorrhage, but probably not upon more substantial grounds
than the above.
The occurrence of perforation may be suspected when the patient is
suddenly seized with acute pain in the abdomen, accompanied by
symptoms of collapse and occasionally by rigors. The fall of
temperature is often considerable. Liebermeister refers to one case in
which it was as much as 5-1/2 degrees, or from 104 degrees to 98-1/2
degrees. Very soon the abdomen becomes tender on pressure, and, if it
were not so before, hard and tympanitic; the pulse grows frequent,
small, and sometimes almost imperceptible; the breathing is thoracic;
the physiognomy expresses great suffering; the features are
contracted, and the face is bathed in profuse perspiration. Nausea and
vomiting come on soon after inflammation has commenced, and rapidly
exhaust the patient. The decubitus is dorsal, and the legs are
generally drawn up so as to relax the abdominal muscles. Prostration
rapidly increases until death puts an end to the patient's sufferings.
Occasionally, the symptoms are more obscure. Pain and rigors may both
be wanting, and nothing but the extreme prostration, the frequent and
feeble pulse, and the distended condition of the abdomen will indicate
the gravity of the danger. This is not infrequently the case in
delirious patients. Death may take place during the collapse, but this
is rare. It more frequently takes place on the second or third day; on
the other hand, it may be postponed until much later. Liebermeister
and Murchison refer to cases in which there was an interval of two or
three weeks between the first symptom of perforation and the fatal
result.
Perforation of the intestine was formerly regarded as an inevitably
fatal accident, but this view is no longer entertained. I have had
under my observation cases in which all the symptoms of this accident
were present, and in which recovery took place. In some of these cases
there {290} may have been an error of diagnosis, but all of them will
not admit of this explanation. Moreover, cases of a similar character
have been reported by physicians whose skill in diagnosis is
universally recognized. Thus, Murchison reports six such cases,
Tweedie two, and Wood one. Liebermeister and Bristowe[53] also both
say that recovery is possible. This view is sustained by the results
of certain autopsies. In one of these, reported by Buhl,[54] a
perforation was found completely closed by adhesions to the mesentery,
and in others reported by Murchison partial adhesion had taken place
between the edges of the perforation and the abdominal walls or to an
adjoining coil of intestine. Occasionally, the inflammation excited by
the perforation may be circumscribed and terminate in an abscess,
which may permit recovery by discharging itself into the bowel or
externally. At other times, however, it ruptures into the peritoneal
cavity, when death speedily ensues.
[Footnote 53: _Transactions of the Pathological Society of London_,
vol. xi. p. 115.]
[Footnote 54: Cited by Murchison.]
Perforation is, fortunately, not a frequent accident in typhoid fever.
It was the cause of death in 20 only of 250 fatal cases collected by
Hoffmann. It occurred, according to Liebermeister, in only 26 cases, 3
of which ended in recovery, in more than 2000 cases observed at the
hospital at Basle. Murchison observed it 48 times in 1580 cases,
Griesinger 14 times in 118 cases, and Flint twice in 73 cases.
Murchison found that in a total of 1721 autopsies, the details of
which were collected from various sources, it was the cause of death
in 196, or 11.38 per cent. It would appear to be rather more common on
the continent of Europe than in England or in this country.
Perforation is much more frequently met with in men than in women. The
patients were men in 15 of 21 of Liebermeister's cases, in 51 of 73 of
Murchison's, and in 72 of 106 cases collected by Nacke. It is rarer in
children than in adults. Rilliet, Barthez, and Taupin met with it only
three times in 232 children under treatment. Murchison has, however,
had a fatal case in a child of five years of age. It is also not
common after forty years of age, but does occasionally occur, although
the contrary has been asserted.
Perforation is most likely to happen during or after the third week of
the disease, but it has been met with as early as the eighth day, as
in a case reported by Peacock. On the other hand, in three cases cited
by Morin[55] it did not occur until the seventy-second, seventy-sixth,
and one hundred and tenth day, respectively. Instances are on record
in which it has taken place after the patient was supposed to be
thoroughly convalescent and had returned to his occupation. When it
occurs early it is due to the separation of a slough. After the middle
or end of the third week it is probably always the result of the
extension of the ulcerative process to the peritoneal coat. In a large
proportion of cases the perforation has been preceded by symptoms of
great gravity, such as severe diarrhoea, great tympany and tenderness
of the abdomen, and intestinal hemorrhage, but in a certain number of
instances the cases in which it has occurred have been of a mild
character, the patient in many of them not considering himself sick
enough to take to his bed or even to abstain from his daily labor.
After death the perforating ulcer has been found to be the only one.
[Footnote 55: Quoted by Murchison.]
The most frequent causes of perforation are the irritation arising
from {291} indigestible and unsuitable food, distension of the bowels
by feces or gas, vomiting, and movements on the part of the patient.
Liebermeister calls attention to the frequency with which ascarides
are found in the intestines of those who die of perforation, and is
inclined to think they may have something to do with causing it.
Morin[56] reports a case in which the perforation appeared to be
caused by the administration of an enema.
[Footnote 56: Quoted by Murchison.]
For our knowledge of the changes in the composition of the urine we
are largely indebted to Parkes and certain German observers. As the
disease generally begins insidiously, the condition of the urine
before the attack and during the first two or three days has not been
ascertained with certainty. During the latter part of the first week
the amount of water is greatly diminished, occasionally falling to
one-fourth or one-sixth of the usual quantity. In the second and third
weeks it increases, and at the end of the fourth week may again be
normal. The amount may, however, vary from day to day, but its
variations do not stand in close relation to those of the febrile
heat; that is, the thermometer may mark one day 104 degrees, and the
next day 100 degrees, while the amount of urine remains the same.
Still, when the temperature begins to fall permanently it increases at
once, or, according to Thierfelder, two or three days after. The
specific gravity is usually high in almost all cases in which the
urine is scanty, and may be as high 1038. With the establishment of
convalescence the specific gravity often diminishes before the water
begins to increase. In other words, the lessening of the solids of the
urine frequently takes place prior to the increase of the water.
The reaction of the urine is very acid in the beginning, but the
acidity is not due to an increased secretion of acid, but simply to
concentration. Later it may become alkaline, and even ammoniacal. The
color of the urine is darker than in health during the early part of
the febrile period. This is due partly to concentration, and partly to
increased disintegration of the blood-corpuscles, which is a
consequence of the fever.
The quantity of urea is augmented during the fever, and especially
during the first week, when the water and chlorides of sodium are most
diminished. As a general rule, the higher the temperature the greater
the amount of urea. It may, however, be very much diminished during
the presence of inflammatory complications. On the other hand, it is
not affected by diarrhoea. Uric acid is uniformly increased, the
amount of increase being relatively greater than that of the urea; it
is often doubled, and sometimes the increase is even more than this.
This increase takes place, according to Zimmer, up to the fourteenth
day. It diminishes after this, and during convalescence may fall below
the normal amount. Copious deposits of urates may occur at any time in
the course of the disease. The chloride of sodium is usually
diminished in amount. This diminution is partly due to a less amount
of this salt being taken with the food, and partly to the fact that
large quantities of it pass away with the stools. As the diminution
cannot always be fully accounted for in this way, it would appear that
it is also stored up in the body during the fever. In cases in which
sweating and purging are absent the sulphuric acid is increased in
amount. The phosphoric acid is at first slightly diminished, but later
undergoes an increase. The hippuric acid is also diminished.
{292} Parkes found albumen in the urine in 7 out of 21 cases. In 5 of
these it was temporary, and entirely disappeared before the patients
left the hospital. Becquerel found it in 8 out of 38 cases, Andral in
only 4 out of 34 cases. Griesinger found it commonly, though it was
usually temporary. He met with only four or five cases in which it was
never present. Kerchensteiner found albumen in a fourth part of the
severe cases. Brattler noticed it in 9 out of 23 cases. I have very
frequently found it myself, but it has always been in my cases a
temporary phenomenon. Desquamative nephritis may occur occasionally in
the course of typhoid fever, and give rise to the appearance of a
large amount of albumen in the urine, and also occasionally of blood.
Renal epithelia and casts are sometimes seen in cases in which there
is albuminuria, but usually soon disappear. Zimmermann asserts that in
all but very slight cases casts may be found even when no albumen can
be detected. The statement is probably too general, but there is no
doubt of the occasional presence of casts under these circumstances.
Bladder epithelia and pus-cells are seen in a few cases in small
quantities, but decided cystitis is rare, unless it has ensued upon
retention of urine. Sugar has not been found except in the urine of
diabetic patients, who may have happened to contract typhoid fever. In
these patients the sugar diminishes, and is sometimes wholly absent
during the continuance of the fever. Leucin and tyrosin have been
found by Frerichs, but at present no observations have been made as to
the frequency or import of their occurrence.
In many cases, when the prostration is extreme, the urine is passed
involuntarily, but in some of these cases the incontinence of the
urine is only apparent, and is really the result of over-distension of
the bladder. This is a condition which is very apt to be overlooked,
and I have known paralysis of the bladder to result in consequence of
this neglect, and to continue sometimes after convalescence has been
established.
COMPLICATIONS AND SEQUELAE.--Although cerebral symptoms are among the
commonest manifestations of the disturbing effects produced in the
economy by the typhoid fever poison, they are almost always
independent of inflammation of the brain and its membranes. In a few
cases, however, the lesions of meningitis have been found after death.
In some of these it has come on without assignable cause, in others it
has been the consequence of pyaemia, of tubercles, or of the extension
of inflammation from the petrous portion of the temporal bone.
Occasionally, during convalescence, some impairment of the intellect
is observed. This may consist in simply some loss of memory or
childishness of manner. At other times delusions of a mild form are
present, or else the patient is liable to attacks of acute mania,
sometimes violent, coming on suddenly and without fever. In a few
instances the moral sense seems to have been perverted, as in the case
reported by Dr. Nathan Smith, already referred to, in which a young
man of previously good character developed a propensity to steal after
his attack. Recovery with the re-establishment of the physical health
almost occurs in these cases. Murchison says he knows of no case in
which this condition has been permanent. On the other hand, Dr. C. M.
Campbell,[57] who had the opportunity of observing an attack of
typhoid fever among some insane patients {293} at the Durham County
Asylum, reports that the mental state was in no case injuriously
affected by the disease, but, on the contrary, underwent a marked
improvement in several of the cases. Indeed, in two of the cases, in
which the prognosis had become very unfavorable, mental recovery began
during the attack of fever.
[Footnote 57: _The Journal of Mental Science_, July, 1882.]
Paralysis, muscular tremors, and chorea are also occasionally observed
after attacks of typhoid fever. According to Murchison, paralysis does
not supervene until several weeks after the commencement of
convalescence. It may last for several weeks or months, but recovery
in the majority of instances eventually takes place. According to
Nothnagel,[58] the most common form is paraplegia, but it may also
take the form of hemiplegia, strabismus, paralysis of the portio dura,
motor paralysis of individual spinal nerves, such as the ulnar or
peroneal, or local anaesthesia. On the other hand, neuralgias and
disturbances of sensation are not common sequelae of typhoid fever.
[Footnote 58: Cited by Murchison. See also article by Paget, _St.
Bartholomew's Hospital Report_, vol. xii.]
Degeneration of the muscular tissue of the heart is probably present
in some degree in every case of typhoid fever, being, of course, most
marked in the severest cases. There would seem, however, to be no
special tendency to disease of its valves or membranes. Arterial
thrombosis or embolism, giving rise to gangrene of the part supplied
by the obstructed artery, is of occasional occurrence. Patry,[59]
Hayem,[60] Trousseau,[61] and others report or refer to several cases
in which gangrene of the leg, hand, or cheek was observed, and among
others a case in which sphacelus depending upon obstruction of the
carotid artery, the result, as Patry thought, of arteritis, commenced
in the left ear, and extended from there to the forehead and
cheek.[62] A. Martin[63] reports the case of a woman who expelled from
the vagina a fetid-smelling structure of cylindrical form, which
proved to be the cervix of the uterus, with the upper part of the
vagina, and in whom menstruation was not re-established until after
the performance of an operation. Spillmann[64] has also called
attention to the occurrence of gangrene of the vagina and vulva in
cases of typhoid fever. {294} This complication is generally met with
toward the end of the febrile period.
[Footnote 59: _Archives generales de Medicine_, 1863, vol. i. pp.
129-549.]
[Footnote 60: _Loc. cit._]
[Footnote 61: _Clinique medicale_.]
[Footnote 62: Since the above was written Barie has called attention
in the _Revue de Medicine_, Jan. and Feb., 1884, to the frequency with
which acute inflammation of the arteries occurs as a sequel of typhoid
fever. The author, whose investigations were limited to the larger
arteries, found that the vessels generally implicated are in the order
of their frequency, the posterior tibial, the femoral, and the dorsal
artery of the foot. The affection is usually unilateral, appears
during convalescence or when the patient leaves his bed, and occurs
just as often after light as after severe cases. He distinguishes two
varieties: 1, acute obliterating arteritis, and, 2, acute parietal
arteritis. The first variety is characterized by embryonal
infiltration of all the tissues, by disappearance of the smoothness of
the intima, which becomes uneven and granular, and by the formation of
a secondary thrombus, and almost invariably terminates in dry
gangrene. The second is merely an inflammation without such a clot,
and always terminates in recovery without gangrene.
The symptoms of obliterating arteritis are--pain, more or less sudden
in its onset, directly over the course of affected vessels, and
increased by pressure, by the erect position, and by walking;
diminution, and then absence, of pulsation; swelling of the limb,
without oedema or redness; and, later, the appearance of bluish
mottling of the surface, and, more rarely, of patches of purpura;
lowering of the temperature, with or without troubles of sensibility,
such as formication, anaesthesia, etc., and the appearance of a hard
and painful cord, due to the formation of the thrombus. In the
parietal form the diminution of the pulsations is sometimes preceded
by a considerable exaggeration of their amplitude, and, while the
temperature on the affected side is usually lowered, it may sometimes
be increased.]
[Footnote 63: _Centralblatt f. Gynakol_, 1881.]
[Footnote 64: _Archives generale_, Mars, 1881.]
Venous thrombosis, the result of weakness of the heart's action, is
more frequently observed. It occurs generally during the convalescence
of cases which have run a severe course, and usually affects the veins
of the lower extremities. I have seen both the femoral veins
obstructed from this cause at the same time. All the cases which have
come under my own observation have ended in recovery, and only 2 of 31
collected by Liebermeister terminated fatally. Death occurred in 3 of
the 17 cases collected by Murchison, but in none of them was this
result attributable to this complication alone. There is, however,
always danger of a portion of the thrombus becoming detached and
producing embolism of the pulmonary artery.
Pyaemia is said by Murchison and other authors to be an occasional
complication, but it is certainly rare in this country. In the milder
cases abscesses form during convalescence beneath the skin in
different parts of the body. In the more severe cases pus is deposited
in the joints or in the internal organs. Albert Robin[65] has reported
two cases in which there was suppurative joint affection. In one of
these the joints of the fingers and toes, with the sheaths of the
corresponding extensor tendons and both knee-joints and one
shoulder-joint, were affected. In the other the left knee was filled
with pus. In both cases the fever soon assumed an adynamic character.
[Footnote 65: _Gazette de Paris_, 1881.]
Laryngitis may sometimes occur in the course of typhoid fever, and
when it assumes the diphtheritic form and runs on to the formation of
ulcers is a very serious complication of typhoid fever, as it is not
infrequently accompanied by oedema of the glottis and gives rise to
the necessity for tracheotomy. It is fortunately, at least in its
worst forms, rare in this country. In Germany, judging from the number
of cases collected by Hoffmann and Griesinger, it is of more common
occurrence. The ulcers are oftener met with in some epidemics than in
others. During the winter of 1860-61, which I passed in Vienna, the
frequency with which they occurred was the subject of remark among
those who were in attendance upon the various clinics.
I have already called attention to the frequency with which bronchitis
in some form or other attends upon typhoid fever. When it invades the
smaller bronchial tubes it occasionally gives rise to lobular
pneumonia or to collapse of some of the lobules of the lung. Lobar
pneumonia may also occur in the course of typhoid fever. It was
observed 52 times in 1420 cases of typhoid fever under treatment at
the Basle hospital from 1865-68. When it comes on late in the disease,
especially if the patient is comatose, or even semi-conscious, it may
be entirely overlooked, unless the lungs are carefully examined, as it
often does not reveal itself to us by any of the ordinary symptoms. It
may, however, occur early, and I have known it so prominent in the
beginning of an attack that the existence of typhoid fever was not
suspected. It sometimes terminates in abscess or gangrene, but is more
usually followed by chronic pneumonia, which may eventually either end
in recovery or lay the foundation for phthisis. Pleurisy with effusion
is also not an uncommon complication. It was observed, according to
Liebermeister, at the hospital at Basle 64 {295} times in 1743 cases
of fever. It is also a serious complication, as 21 of the 64 cases
terminated fatally. Murchison refers to three cases in which it was
followed by empyema. Other morbid conditions of the respiratory organs
which may occur as complications of typhoid fever are oedema,
infarction, hypostatic congestion of the lungs, emphysema, and
pneumothorax. Acute miliary tuberculosis is also an occasional
complication, but is oftener met with as a sequel. According to
Liebermeister, the tendency to pulmonary complications has diminished
since the introduction of the cold-water treatment.
Catarrhal or diphtheritic inflammation of the fauces and pharynx
occurs in a large number of cases, and frequently gives rise to a
great deal of difficulty in swallowing. Indeed, it has been so
frequently observed in some epidemics that a few writers have regarded
it as a symptom rather than a complication of the disease. Either of
the varieties of inflammation may extend through the Eustachian tube
to the middle ear and be the cause of deafness, which usually passes
off as the inflammation subsides. Occasionally, however, the affection
of the middle ear gives rise to perforation of the tympanum or to
caries of the petrous portion of the temporal bone.
Murchison says he has known the symptoms of and lesions of dysentery
to coexist with those of typhoid fever in several cases, and
Liebermeister asserts that diphtheria of the intestinal mucous
membrane is an occasional sequel to severe cases, especially when
other mucous membranes are the seat of diphtheritic inflammation. In a
few instances which have come under his observation it had given rise
to perforation of the bowel or to gangrene of the intestinal mucous
membrane.
Jaundice occasionally occurs in the course of the disease. I have
never happened to see this complication, and am inclined to think it
is rare in this country. Liebermeister, however, met with it 6 times
in 1420 cases, and Griesinger 10 times in 600 cases. Hoffmann found it
in 10 of 250 fatal cases, and Murchison was able to collect 9 cases,
all of which but one terminated in death. Several of Griesinger's
cases, however, ended in recovery. In a few cases the jaundice may be
attributed to catarrh of the biliary ducts, but this solution of the
question will not explain those cases in which the feces remain
colored throughout. In fatal cases marked degeneration of the liver
has been found, which Liebermeister regards as of similar character to
that which occurs in acute yellow atrophy. In two of Murchison's cases
the liver was small and its secreting cells loaded with oil. In most
cases it does not appear until late in the disease, but it has been
observed as early as the fifth day.
Abscess of the liver and diphtheritic inflammation of the mucous
membrane of the gall-bladder are among the rarer sequelae of typhoid
fever.
Peritonitis is the most serious of all the complications of typhoid
fever. Its most common cause is perforation of the bowel, but it may
also be due to the extension of inflammation to the peritoneal
membrane without ulceration. Liebermeister believes that it is
sometimes the result of the typhoid infiltration so frequent in
various tissues of the body taking place in the serous membrane. In
other cases it arises from the rupture of softened mesenteric glands,
of softened {296} infarctions in the spleen, or of the abscesses which
are sometimes the consequence of the circumscribed inflammation by
which perforation is occasionally prevented from proving immediately
fatal. Less frequent causes of it are rupture of the gall-bladder,
with the escape of gall-stones into the cavity of the abdomen,
abscesses of the ovary, and abscesses in the walls of the urinary
bladder. It is said by Murchison to have been in one case the result
of a pseudo-abscess in the sheath of the rectus muscle bursting
inward.
Swelling of the parotid gland occasionally occurs in typhoid fever,
but is much less common than in typhus. It is most frequently met with
in bad cases about the end of the third week or later, and generally
involves one side only. The swelling is hard and firm in the
beginning, and may terminate in resolution or suppuration. I have seen
it three times only, twice in my own practice, and once in that of a
medical friend. One of my cases was fatal, the other ended in
recovery, as did, I believe, the third case. Murchison saw it in only
6 cases, 5 of which were fatal. According to Hoffmann,[66] 16 cases of
suppurative parotitis were found at Basle among about 1600 typhoid
fever patients, 7 of the 16 ending fatally. Parotitis without
suppuration occurred three times. In 15 cases the attack was confined
to one side, 9 times to the right and 6 to the left; in 4 it was
double. Trousseau[67] looks upon these swellings as a very grave
accident, and says that he has scarcely ever seen a case recover in
which it has occurred, either in the course of typhoid fever or any
other disease. Chomel, on the other hand, is said to have regarded
them as critical and auspicious.
[Footnote 66: Quoted by Liebermeister.]
[Footnote 67: _Clinique medicale de l'Hotel Dieu_, t. i. 1861.]
Menstruation occasionally occurs during typhoid fever, and may be
profuse. Bartels,[68] who has investigated the histories of 172
patients in reference to this point, says that the catamenia always
appear if the menstrual period falls within the first five days of the
fever, and that they do so in two-thirds of the cases if they are
expected between the sixth and fourteenth days. On the other hand,
menstruation does not occur if the time for it falls in the third
week. He says also that the catamenia generally appears about the time
they are expected, or later, and very seldom earlier. Liebermeister,
on the contrary, says that they often occur prematurely. Other uterine
hemorrhages seldom occur, and never in those who have ceased to
menstruate or in whom the function has not been established.
[Footnote 68: _Petersb. Med. Wochenschr._, 1881.]
Suppuration of Bartholini's glands is said by Speilman to have taken
place in one case.[69] In the fourth week the patient complained of
violent pains in the right nympha, which, upon examination, was found
to be swollen. A tumor as large as a nut, which was red and painful on
pressure, could also be felt in the vagina.
[Footnote 69: _Arch. generales_, Mars, 1882.]
Pregnancy was formerly thought to confer an entire immunity from
typhoid fever, but recent and accurate investigations have shown that
if this immunity really exists, it is only relative, not absolute.
Gusserow[70] says that the disease is more frequently met with in the
first half than in the latter half of pregnancy. Abortion under these
circumstances commonly occurs. Gusserow says that it takes place in
from 60 {297} to 80 per cent. of the cases. He believes it to be due
to the high temperature, which causes the death of the foetus, which
is then expelled from the uterus. In a few cases, however, the child
is born living. Of Murchison's 14 cases, 10 recovered, and two of the
ten patients carried the child, at the fourth and eighth months
respectively, throughout the attack. All the others miscarried or
aborted, only one of them being delivered of a living child. Out of 18
pregnant women[71] treated in the hospital of Basle for typhoid fever,
between the years 1865 and 1868, 15 miscarried or aborted. In the
three years following the introduction of the anti-pyretic treatment
only five cases of abortion occurred, and but one of these proved
fatal. This accident generally happens during the second or third week
of the fever. It is always a serious complication, and if it occurs in
the first three months of pregnancy it generally gives rise to profuse
hemorrhage, which is usually followed by a fall of temperature as
marked as that observed in hemorrhage from the intestines. Just as in
the latter case, the fall is only temporary, being soon succeeded by a
rapid rise of the temperature to its former height, or even beyond it.
[Footnote 70: _Schmidt's Jahrbuch_, Bd. 193, No. 1, 1880, from _Berl.
klin. Wochenschr._, 1880.]
[Footnote 71: Liebermeister, _loc. cit._]
The danger of bed-sores occurring in typhoid fever is in consequence
of the impaired nutrition of the tissues, the length of time the
disease lasts, and the great emaciation which usually attends
it--greater than in any other acute disease. They constitute a very
serious and troublesome complication, and may occur on any part of the
body subjected to pressure, but are most frequent over the sacrum and
trochanters. Oedema of the lower extremities from feebleness of the
circulation is occasionally observed in the convalescence from
protracted attacks. Lendel has published a series of 7 cases observed
at Rouen, in which the entire body became very oedematous in the
second or third week of the attack or during convalescence. In none of
the cases was the urine albuminous. All the patients recovered except
one, who died of peritonitis. Similar cases have been reported by
other observers. Barthez and Rilliet have seen several cases in
children.
Periostitis is an occasional sequel. I have seen it in one case only.
Sir James Paget,[72] who appears to have met with it in several cases,
says that it never occurs in the continuity of the fever, but always
when the patient is apparently convalescent, when his temperature is
normal and constant, and he is beginning to move about and to grow
stronger and stouter. Its most usual seat is the tibia, but it is also
met with in the femur, ulna, and parietal bone. Except in one case,
Sir James has never seen it in more than one bone in the same person.
It is always circumscribed within a space of from one to three inches
in extent, and usually subsides without necrosis or other abiding
change of structure; but in some cases the patient has remained for
some time subject to repeated attacks of pain and swelling of
periosteum. In the few cases, he says, in which the periostitis is
followed by necrosis the extent of dead bone has always been less than
that of the inflammation over it. Murchison, however, refers to two
cases of necrosis of the tibia, to one of the temporal bone, and to
two in which extensive necrosis of the lower jaw occurred. Gay[73]
also reports a case of extensive necrosis of the thigh-bone in a child
three years old, following an attack of typhoid fever.
[Footnote 72: _St. Bartholomew's Hospital Report_, vol. xxi.]
[Footnote 73: _Path. Trans. Lond._, vol. xx., p. 290.]
{298} Very frequently after an attack of typhoid fever the patient
evinces a tendency to grow stout, which is either continuous or else
is gradually lost after he fully recovers his health. This increase in
flesh is not always accompanied by a corresponding gain in physical
strength, and he may remain for a long time after convalescence is
apparently complete incapacitated for much bodily or mental exertion.
Sometimes, on the other hand, the patient, instead of gaining flesh
and strength, may continue weak and emaciated, even when he is taking
a full amount of nourishment, which he is, however, unable to
assimilate. Cases of this kind may terminate in phthisis, but they
occasionally prove fatal, without any discoverable lesion after death
except an abnormally smooth appearance of the mucous membrane of the
ileum and a shrivelled condition of the mesenteric glands.[74]
[Footnote 74: Murchison.]
Patients suffering from typhoid fever may occasionally contract other
specific diseases. Murchison has notes of eight cases in which the
eruption of this disease coexisted with that of scarlatina, and says
that it was not uncommon in the London Fever Hospital for a patient
suffering from the former disease to contract the latter. Similar
cases are recorded by other observers. Typhoid fever may also be
complicated with rubeola, pertussis, diphtheria, variola, and
vaccinia. I have repeatedly seen children convalescent from typhoid
fever in the hospitals of Paris contract one or other of the eruptive
fevers.
VARIETIES.--A great variety of forms of typhoid fever has been
described by various authors, but as many of them present few points
of difference from the usual form of the disease, it will not be
necessary to discuss them at any length. They derive their names from
some peculiarity of the mode of seizure, from the prominence of some
one symptom or set of symptoms, or from the presence of complications.
They are--(1) The adynamic form, in which prostration is marked in the
beginning and throughout the attack. (2) The ataxic or nervous form,
which is characterized by the predominance of delirium, subsultus
tendinum, and other nervous symptoms. (3) The hemorrhagic form, in
which there is a special tendency to hemorrhage from the different
mucous membranes. (4) The abdominal form, in which the abdominal
symptoms, such as diarrhoea and tympanites, are well developed. (5)
The thoracic form, so called from the presence of some thoracic
complication. (6) The gastric or bilious form, in which the disease is
complicated at its commencement by gastro-intestinal catarrh. La forme
muqueuse of French authors is probably identical with the above. (7)
The acute form, in which the disease begins abruptly and with great
violence, and runs a very rapid course, terminating usually in death
before the end of the first week or early in the second, before
ulceration can have taken place. Delirium is an early and prominent
symptom in this form, so that it has sometimes been mistaken for
meningitis.
Certain forms of the disease deserve a little fuller consideration.
One of the most important of these is the abortive form, in which, as
its names implies, the fever is cut short in its course, and in which
there is every reason to believe that infiltration of Peyer's glands
takes place as usual, but that the subsequent course of the disease is
different, the glands undergoing resolution instead of advancing to
ulceration. The majority {299} of observers agree that in the
beginning there is nothing to distinguish such attacks from those
which follow their usual course. Liebermeister and Jaccoud state,
however, that their commencement is usually more abrupt than in the
ordinary variety, the former asserting that the temperature generally
reaches its maximum earlier, and the same opinion is expressed by
other authors. They are occasionally characterized by severe symptoms,
including a high temperature. In the few cases which have come under
my own observation the symptoms have been mild, but they were
sufficiently developed to leave no doubt on the mind as to the nature
of the disease. In a case which aborted on the twelfth day there were
hebetude, diarrhoea, tympany, and rose-colored spots persisting even
after the subsidence of the fever. Constipation would appear, however,
to be more frequent than diarrhoea in this class of cases. The
subsidence of the fever may occur at any time between the seventh and
fourteenth days; Griesinger has seen it occur as early as the fifth
day. Sometimes the defervescence occurs abruptly, with copious
perspiration; at others it is gradual and similar to that which takes
place in ordinary attacks. Between the abortive form of typhoid fever
and simple continued fever there are, of course, many points of
resemblance, but cases of the former may generally be recognized by
the presence of this rose-colored eruption and enlargement of the
spleen, or, where these are absent, by their occurring in the same
house or under the same circumstances as typical cases of the disease.
Liebermeister has called attention in his article on typhoid fever in
_Ziemssen's Cyclopaedia_ to a class of cases which, he thinks, is also
caused by the typhoid infection, and of which the prominent feature is
the insignificance of the fever or the entire absence of it which
characterizes them. Such cases appear to be of frequent occurrence in
Basle. Many of them, he says, never show during their entire course
any rise of the temperature, or occasionally a slight elevation only,
but an enlargement of the spleen could generally be detected, and
occasionally an unmistakable rose-colored eruption. The action of the
bowels was usually irregular; sometimes there was diarrhoea, and
sometimes, on the other hand, obstinate constipation. The other
symptoms were prostration, pains throughout the body, often headache,
persistent loss of appetite, with more or less swollen and furred
tongue, and markedly diminished frequency of the pulse, which
disappears with convalescence, while its quality is not appreciably
altered. The long duration of an apparently trifling indisposition he
considers as especially characteristic. Cayley also refers to cases,
and even epidemics, of typhoid fever in which the temperature has been
below the normal throughout the whole course of the attack. Strube[75]
had the opportunity of observing such an outbreak during the siege of
Paris by the Germans in 1870. "In many of the cases," he says, "the
temperature throughout was subnormal, and in others never exceeded the
normal point. The roseola was usually profuse; the nerve symptoms were
of marked severity, and were in inverse ratio to the temperature,
consisting of violent delirium alternating with stupor; the duration
of the fever was very short, defervescence usually taking place at the
end of a fortnight. Of the 23 fatal cases, in 20 death took place
during the first fourteen days. The abdominal {300} symptoms were
slight, but the characteristic lesions were found on post-mortem
examination. All the cases were characterized by great prostration.
These cases presented some features which were probably due to this
peculiarity of the temperature; thus, the pulse was but little
accelerated, seldom exceeding a hundred; the tongue did not become dry
and brown; and the enlargement of the spleen was either absent or much
less marked than usual. Strube attributed the peculiar features of
this epidemic to the depressed condition of the troops; they had been
exposed to great hardships on the way to Paris, over-fatigued by
forced marches, and very insufficiently supplied with food."
[Footnote 75: Quoted by Dr. Cayley.]
A mild form of the disease has been described by certain authors, in
which the symptoms, although not severe, are characteristic, and in
which there is therefore, with due care, little danger of making a
mistake in diagnosis. It therefore seems an unnecessary refinement to
set apart such cases under a separate head.
The latent form, or the typhus ambulatorius of the Germans, is of more
importance from the fact that the symptoms are so mild, or that so
many of the ordinary symptoms are wanting or masked by those due to
complications, that there is great danger of regarding the attack as
of little moment. In many cases there is no symptom present but
prostration and fever to indicate that the patient is ill, and these
may be so slight that he may positively refuse to go to his bed, and
may even insist upon pursuing his ordinary avocation, in the midst of
which he is often suddenly seized with alarming symptoms, such as
violent delirium, intestinal hemorrhage, or, what is more common,
those due to perforation of the bowel. Still, even in these cases a
careful examination will often disclose the presence of some symptom
which had failed before to attract attention, and which will often
reveal to us the true nature of the disease. I was myself the subject
of such an attack nearly twenty years ago. Supposing that the
excessive prostration from which I was suffering was due to overwork
at a large army hospital in the neighborhood of Philadelphia, I
determined to seek repose in travel and in change of scene. On the eve
of doing so I fortunately sent for a medical friend, who, after a
thorough investigation of my symptoms, succeeded in finding a few
rose-colored spots upon my abdomen. The attack subsequently ran a mild
but well-marked course. Occasionally, the symptoms due to a
complication so predominate over those arising from the disease itself
that they completely mask it. I have known bronchitis so severe as to
divert in this way the attention of a skilful diagnostician from the
primary disease. When vomiting, together with other symptoms of
hepatic derangement, is especially prominent in the beginning of
typhoid fever, the mistake is not infrequently made of attributing
these symptoms to a "bilious attack."
TYPHO-MALARIAL FEVER.--Under this name, which was originally suggested
by J. J. Woodward, Surgeon U.S.A., early in the summer of 1862, as a
designation for a class of cases in which the symptoms of typhoid
fever are associated with those of remittent, and which was especially
common among the soldiers of the United States Army during the late
Civil War, are probably included at least two distinct conditions:
1st, remittent fever, in which the disease, on account of the
depressing circumstances surrounding the patient, assumes {301} a
typhoid form; and, 2d, typhoid fever, occurring in a patient who has
also been exposed to malarial influence. This association of diseases
is of course not new, or even undescribed before this name was
suggested for it. Woodward thinks that he has found enough in the
description of Roderer and Wagler to justify him in concluding that
the epidemic which occurred at Gottingen in 1762 was really of this
character. There would seem also to be no doubt from the descriptions
of Dawson[76] and Davis[77] that the fever which decimated the British
army in the Walcheren expedition was typhoid fever, modified by the
malarial influence to which the soldiers were subjected. The latter of
these authors says that the ileum and jejunum in the bodies of those
who died of this disease were frequently found interspersed with
tubercles, inflamed and ulcerated in different parts.
[Footnote 76: _Observations on the Walcheren Diseases_, Ipswich, 1810,
by G. P. Dawson.]
[Footnote 77: _A Scientific and Popular View of the Fever of
Walcheren_, J. B. Davis, London, 1810.]
In our own country the occasional association of these two diseases
has also long been recognized. Drake describes it under the name of
remitto-typhoid, and Dickson seems to have been perfectly familiar
with it, for he says that typhoid lesions will sometimes be found in
the bodies of those dead of bilious remittent. Levick recognized the
presence of the symptoms of both diseases in some patients who were
under his care as early as the spring of 1862, and proposed the name
of miasmatic typhoid fever for this class of cases in the following
June.[78] Meredith Clymer has also frequently met with cases in which
the symptoms of the two diseases were coexistent.[79]
[Footnote 78: _Med. and Surg. Reporter_, June 21, 1862.]
[Footnote 79: _The Science and Practice of Medicine_, by William
Aitken, M.D., 3d Amer. ed.; with additions by Meredith Clymer, M.D.,
Philadelphia, 1872.]
As is indicated by the name given to it, the symptoms in this form of
typhoid fever are modified by the presence of malarial poisoning. The
cases always manifest a decided tendency to periodicity, the evening
exacerbations are more decided than in the ordinary form, the
remissions are often ushered in with a profuse sweating, gastric and
hepatic derangements are more marked, and headache is more severe.
There is frequently less mental hebetude or dulness than in ordinary
typhoid fever. In some of the cases observed by Levick[80] the
symptoms were those of pernicious congestive remittent fever, such as
copious serous discharges, not unlike those of Asiatic cholera,
colliquative sweats, and other symptoms of exhaustion.
[Footnote 80: _Amer. Journal of the Med. Sci._, April, 1864.]
TYPHOID FEVER IN CHILDREN.--It was formerly thought that infants and
very young children were not often the subjects of typhoid fever, but,
so far is this opinion from being correct, it is now known that they
are especially liable to suffer from it. The rose-colored eruption is
more often wanting in them than in adults, and the fever more apt to
assume a distinctly remittent type; and hence, no doubt, the
difficulty which is often experienced in diagnosticating this fever
from other forms of fever in children. There is no doubt that many
cases which have been described by authors under the head of infantile
remittent fever are really examples of typhoid fever modified simply
by the age of the patient. It may occur in infants not more than six
months old, and is not infrequent in {302} children of two or three
years of age. Henoch,[81] who has had the opportunity of observing a
large number of cases, says that the rise of temperature is commonly
more abrupt in children than in adults, and that the disease generally
runs its course in a shorter time. The pulse is more frequent, and may
be as high as 144 in cases in which the prognosis is not grave.
Dicrotism is very rare. Slowness and irregularity of the pulse, like
that observed in basillar meningitis, he has never seen. The nervous
symptoms are not so pronounced even when the temperature is high, and
they bear no relation in severity to the height of the temperature.
Diarrhoea in the cases observed by Henoch was often absent during the
whole course of the attack, and the stools were often brownish or
greenish instead of yellow.
[Footnote 81: _Charite Ann._, 1875.]
TYPHOID FEVER OF AGED PERSONS.--The modifications which the disease
undergoes when it occurs in patients advanced in life are precisely
those to be expected from the diminished activity of the processes of
life in them, as compared with those of younger persons. The febrile
movement is generally prolonged, although of low grade, the
temperature rarely rising high, and frequently during convalescence
sinking below the normal. The diarrhoea is commonly not so severe, the
delirium so violent, or the rose-colored eruption so often present. On
the other hand, adynamic symptoms, such as excessive prostration,
tremors, subsultus tendinum, and the like, are frequently prominent
from the beginning of the attack.
Several authors, among whom may be mentioned Arnat,[82]
Hornburger,[83] and Greenhow,[84] have described a renal form of
typhoid fever. In this form the urine is blood red in color or like
dark broth. It often contains albumen during the first week of this
disease, usually hyaline or more or less granular casts, and
occasionally red blood-discs, white cells, epithelia of kidneys and
bladder, and epithelial detritus. The specific gravity is high, and
the quantity is usually diminished. The prominent symptoms are pain in
the region of the kidneys, oedema of face, tense and frequent pulse,
great prostration, profuse epistaxis, violent delirium, and
hyperpyrexia. The temperature may be 105.8 degrees. On the other hand,
the intestinal symptoms are less marked. In fatal cases the lesions of
intestinal nephritis have been found at the autopsy.
[Footnote 82: Thesis, _Sur la Fievre typhoide a forme renale_.]
[Footnote 83: _Berlin klin. Wochenschrift_, 1881.]
[Footnote 84: _Transactions of Clinical Society of London_, 1880.]
RELAPSES.--Much difference of opinion will be found to exist among
authors in regard to the frequency with which relapses occur in
typhoid fever, and this difference does not appear to be due to any
greater frequency of this accident in some countries than in others,
since Liebermeister met with them in 8.6 per cent. of the cases
treated at the hospital at Basle, while, according to other German
observers quoted by him, they occur in 6.3 per cent. (Gerhardt), in 11
per cent. (Baumler), and in 3.3 per cent. (Biermer). Murchison noted
them in 80 of 2591 cases in the London Fever Hospital, or in 3 per
cent., and Maclagan in 13 of 128 cases at Dundee, or in 10 per cent.
about. Immermann[85] of Basle says that they occur in 15 per cent. of
the cases, and that in very unfavorable years the proportion may be as
high as 18 or 19 per cent. Prof. Henoch[86] observed relapses in 16
cases out of 96, or 16.6 per cent. In my own {303} practice they have
not been very numerous. I find that in 80 cases of which I have full
notes they are recorded five times, or in 6.25 per cent., and I
believe this ratio correctly represents the frequency with which they
have happened in all the other cases which have come under my care.
Part of this difference of opinion is unquestionably attributable to
the fact that under the term relapse are sometimes included two
distinct conditions: (1) Mere recrudescences of fever, which occur
during the stage of defervescence or that of convalescence, and which
are provoked by errors of diet, mental or bodily fatigue, or some
other irritating cause. They usually last a day or two, and are
entirely distinct from (2), true relapses, in which all the
characteristic symptoms of the primary attack are reproduced, and
which commonly occur some time after the disease has apparently run
its course. There is occasionally no distinct apyretic interval
between the two attacks, but in by far the greater number of instances
the relapse occurs in the second or third week, or even later, after
the establishment of convalescence. In 20 cases reported by W. M. Ord
and Seymour Taylor[87] the relapse occurred in the third week of the
disease in 1; in the fourth week in 5; in the sixth week in 3; in the
seventh week in 7; in the eighth week in 3; in the ninth week in 1.
James Jackson refers to a case in which the date of the relapse is not
given, but in which he was able to detect the rose-colored eruption in
the sixty-sixth day[88] from the commencement of the disease. In my
five cases the relapse occurred on the seventh, eighth, ninth,
eleventh, and twentieth day after the apparent establishment of
convalescence. In these cases the duration of the relapse was 11, 13,
17, 20, and 13 days respectively. The highest temperature noted in any
of the relapses was 105 degrees, which occurred in two cases. In both
of these this temperature had also occurred in the original attacks.
In one of the others, however, a temperature of over 104 degrees F.
was repeatedly observed in the relapse, while in the primary attack it
had never risen above 102 degrees.
[Footnote 85: _Schweiz. Corr. Bl._, viii. 1878.]
[Footnote 86: _Charite Ann._, ii. 1875.]
[Footnote 87: _St. Thomas's Hospital Report_, vol. ix., London, 1879.]
[Footnote 88: Since the above was written I have had under my care a
case of typhoid fever in which a third relapse occurred nearly four
months after the patient, a woman aged thirty years, was first taken
ill. The following is a brief abstract of the history of this
remarkable case: The original attack began about Sept. 20, 1883, was
of moderate severity, and lasted between three and four weeks.
Convalescence, which seems to have been nearly complete, as the
patient had left her bed, was interrupted on Nov. 1st by a relapse,
during which she was admitted into the Pennsylvania Hospital. This
relapse was severe, and before it had entirely run its course was
itself interrupted, on Nov. 17th, by an intercurrent relapse, which
lasted two weeks. During these two relapses extensive bed-sores formed
upon the nates, occasioning more or less irritation and consequent
febrile reaction. On Jan. 11, 1884, a third relapse occurred. This
relapse was accompanied by diarrhoea, rose-colored spots, tympany, dry
and brown tongue, and other characteristic symptoms of typhoid fever,
the diagnosis being fully concurred in by my colleague, Dr. Morris
Longstreth, who saw the case with me. Convalescence was again
interrupted on Feb. 13th by fever, which continued for two weeks, but
which possessed none of the characters of typhoid fever, and was
clearly due to imprudence on the part of the patient. The patient is
now (April 25, 1884) entirely well, and will shortly be discharged
from the hospital.]
The onset of a relapse is usually much more abrupt than that of the
original attack. It is rarely preceded by prodromata. The temperature
rises more rapidly and attains its maximum earlier, which may be much
greater than in the original attack. In one case under my care it
reached 105 degrees on the evening of the first day, and temperatures
of 103.5 degrees and 104 degrees on the evening of the second day are
not infrequent.
{304} The rose-colored eruption appears earlier. In 38 cases
investigated by Murchison with reference to this point, it appeared on
the third day in 7; on the fourth in 8; on the fifth in 7; on the
sixth in 2; on the seventh in 12; and at a later date in 2. In the
case the history of which is given below it was detected on the second
day. The delirium also comes on sooner. The relapse is usually less
severe, and is of shorter duration, than the primary attack. All my
cases terminated in recovery. Occasionally, however, it is much more
severe. In one case in which the primary attack was so mild that the
patient could scarcely be persuaded to remain in bed, the relapse was
so severe that for many days it was uncertain whether the patient
would recover. In another intestinal hemorrhages to an alarming extent
occurred on two occasions. Moreover, of Murchison's 53 cases, 7 were
fatal; in 2 of the cases death was due to perforation; in 2 to
peritonitis, induced by infarction of the spleen; and in 1 to
abortion; and of Ebstein's 13 cases, 3 were also fatal. Occasionally,
a second, and it is said even a third, relapse is noted. In one of Da
Costa's cases hemorrhage from the bowels took place during a second
relapse.
[Illustration: FIG. 15. Pulse.]
The following histories and temperature charts illustrate the
prominent peculiarities of relapses occurring in typhoid fever:
TYPHOID FEVER (with a relapse).--G---- L----, aet. 20, single, seaman,
Italian, admitted March 6, 1878; April 30, 1878, left in ward. Patient
is unable to speak English. The following history is obtained through
an interpreter: His family history is good, and he is naturally a
healthy man, never having had any serious illness--no venereal
disease, no cough or rheumatism, no intermittent fever, and he has not
been in the habit of drinking to excess. His vessel has been lying off
Gloucester Point, and two seamen have recently been similarly affected
on another vessel anchored near by. For about two weeks he has had
malaise, but not until three days ago was he so ill that he was
obliged to give up work. He was then taken with cough, chills followed
by fever, diarrhoea, headache, and pain in the abdomen. Has had no
epistaxis or vomiting.
Upon admission patient has fever, his face is flushed, his tongue
coated with a brown fur in the centre, dry, fissured, and red and
glossy at the tip and edges. He has hebetude and some delirium, though
not very active; he is deaf. His abdomen is somewhat tense and
tympanitic, and covered with very numerous rose-colored spots, which
disappear momentarily on pressure; they are also distributed over
thighs and chest. There seems to be no tenderness on pressure over
abdomen, and there is no gurgling felt. Has moderate diarrhoea, having
about three stools daily, which are light yellow in color and are
loose and fetid. Urine cloudy orange red, acid, 1021. No albumen.
{305} _3.7_. Ord. Ol. Terebinth. gtt. x; Acid. Muriat. dil. gtt. v
every two hours, with Quinine gr. viij daily, and restricted diet.
_3.8_. Tongue not so dry; is better. Whiskey fl. oz. ij.
_3.9_. Temperature elevated. Ord. to be sponged.
_3.10_. Has had four stools in the last twenty-four hours. Some
sonorous rales over chest posteriorly. Sponging to be repeated when
temperature rises.
_3.11_. There is some subsultus. There are more numerous rales heard
over chest posteriorly.
Ord. whiskey fl. oz. v daily; turpentine stupes to chest. His
diarrhoea is better; considerable hebetude.
_3.12_. Tongue is not so dry, and is cleaner. The spots over his body
are beginning to assume more the appearance of petechiae. They are
found everywhere on his body. Has had but one stool within the last
twenty-four hours.
_3.13_. He is brighter; skin feels better; tongue cleaner; pulse but
80. Fewer rales heard in chest. No change in his treatment.
_3.14_. Spots disappearing. Two stools in last twenty-four hours, not
so loose in character. Pulse dicrotic.
_3.15_. There is no tympany. Had one natural stool yesterday.
Sudaminae over abdomen.
_3.16_. Doing well. Pulse very slow.
_3.17_. Tongue moist and clean; no diarrhoea.
_3.18_. No diarrhoea; spots are still to be seen, but are fading every
day.
_3.20_. Takes a little lemon-juice, as the gums are disposed to be a
little spongy.
Stop turpentine and muriatic acid.
_3.25_. Bowels somewhat constipated.
Ord. enema of castor oil.
_3.26_. Stop quinine; give whiskey fl. oz. iij only. Allowed chicken
and two eggs daily.
Ord. Tr. Cinch. Co. fl. drachms ij s.t.d.
_4.4_. Slight chill, headache, and pain in side. Temp. 101 degrees.
_4.5_. Temp. normal again; as well as before.
_4.8_. Has been up for a week, and steadily gaining in strength,
except the slight attack on the 4th, when to-day, without his having
taken any indigestible food, or indeed any reason to which it could be
assigned, he was seized with a relapse, his temperature rising to 105
degrees, but being reduced a half degree by sponging.
_4.9_. Spots have again appeared in great numbers, and they are very
large. Last evening his temperature reached 104-3/4 degrees, and was
reduced to 101 degrees by sponging.
_4.10_. Doing very well; spots are still making their appearance.
_4.12_. Diarrhoea not at all excessive.
_4.15_. Spots are very numerous.
_4.20_. Temperature nearly normal.
_4.25_. Doing perfectly well; up and about.
_4.30_. Left in ward, upon completion of my term of service.
{306} [Illustration: FIG. 16. Chart of temperature in typhoid fever
with relapse.--Original attack.]
[Illustration: FIG. 17. Chart of temperature in typhoid fever with
relapse.--Relapse.]
ABORTIVE ATTACK, FOLLOWED BY TYPICAL ATTACK.--Thomas Rogers, October
15, born in Philadelphia, assistant nurse. Admitted {307} January 25,
1883; discharged March 26, 1883, cured. Father died of hemorrhage from
the lungs; mother living and healthy. Two years ago he sustained a
compound fracture of the left leg from a bale of cotton falling on
him; otherwise he has always enjoyed good health. For the past three
months he has been assisting the nurse in the receiving ward of this
hospital. Four days before admission, without unusual exposure, he had
a slight chill, and felt cold for several hours. This was followed by
fever and a feeling of weakness. He also had slight headache and the
bowels were constipated; no epistaxis.
Upon admission patient has a good deal of hebetude, face flushed,
temperature 102 degrees, pulse 106, tongue slightly coated, moist. Has
slight pain in right lumbar region, but no distension of abdomen.
Urine negative.
Ord. quinine gr. viij. daily; liq. ammon. acet. fl. drachms ij. q.q.h.
_Jan. 29th_. More hebetude; tongue more coated with brownish fur, red
at tip; bowels continue costive; opened by an enema.
_31st_. Is brighter and better. One doubtful rose-colored spot seen on
abdomen.
_Feb. 4th_. The morning temperatures for the past two days have been
subnormal and the evening rise is very slight. All the symptoms also
indicate the approach of convalescence.
_6th_. More fever; pulse weaker; functional murmur heard over heart;
sudamina out over abdomen. Ord. whiskey fl. oz. ij.
_8th_. Some fulness of abdomen; had three loose yellowish-colored
stools in the last twelve hours.
_9th_. A few doubtful rose spots out over abdomen and back; sudamina
still abundant.
_10th_. More tympany; numerous rose-colored spots out over abdomen and
back; slight epistaxis and bronchitis.
_11th_. Pulse more feeble; still slight diarrhoea. Increase whiskey to
fl. oz. iv.
_15th_. Has a good deal of hebetude, but no headache; fewer spots;
pulse weaker; temperature lower. Increase whiskey to fl. oz. vj.
_17th_. Temperature high again; most of the spots have disappeared;
slight epistaxis and subsultus; no delirium; bowels not open for two
days.
_20th_. Temperature falling; spots disappearing; still fulness of
abdomen.
_25th_. Temperature has been subnormal for several days, and he is
doing well; tongue cleaning. Has emaciated a good deal, and is weak.
_March 1st_. Is convalescent; tongue has lost its redness.
_8th_. Continues to improve; allowed semi-solid food.
_17th_. Is now quite well; has gained a good deal in flesh, and is
stronger.
{308} [Illustration: FIG. 18. Temperature chart of typhoid
fever.--Abortive attack, followed by typical attack.]
The examination of the bodies of those who have died during a relapse
reveals the presence of two sets of lesions in the cicatrizing ulcers
of the primary attack and the recent ulcerations of the relapse. The
latter are usually less extensive, and are found to be situated at a
greater distance from the lower end of the small intestine, than the
former, for the reason that the Peyer's patches most remote from the
ileo-caecal valve are least apt to be affected in the primary attack.
No satisfactory explanation of these relapses has as yet been
discovered. {309} They occur in patients of both sexes and of all ages
with about the same frequency. They have been attributed to errors of
diet, mental and bodily fatigue, and the like, but, while we know that
causes of this character often provoke recrudescences of fever, and
can understand that they may act as exciting causes of a relapse in
cases in which the predisposition exists, it does not seem possible
that they should by themselves be able to bring back all the
characteristic symptoms of a specific disease. It has been maintained
by some authors that a relapse indicates that a new infection has
taken place; but this hypothesis, even if we admit that it accounts
for those cases in which the patient is allowed to remain in the place
in which he has acquired the disease, does not explain those in which
he is removed during the first attack to a hospital where all the
sanitary arrangements are presumably perfect. Griesinger has
endeavored to explain relapses occurring in hospitals by suggesting
that they may possibly be due to a fresh contagion from other patients
with typhoid fever in the same ward; but this explanation is rendered
improbable by the fact that relapses have occurred when cases have
been thoroughly isolated. As I have already said, during a long
connection with the Pennsylvania Hospital I have only known a single
case of typhoid fever to originate within its walls, although relapses
probably occur in its wards with the same frequency as in other
hospitals. To adopt Griesinger's explanation, it would therefore be
necessary to assume that a patient just recovered from an attack of
the disease is more susceptible to the action of its contagion than
patients suffering from other disease; which seems improbable, to say
the least. It has also been maintained that relapses are due to the
inoculation of the previously healthy Peyer's patches by the typhoid
poison which is thrown off with the sloughs from those first affected.
Maclagan alleges that relapses are more frequently met with in cases
in which constipation is present in the primary attack, a condition
which he regards as favorable to absorption; but this is opposed to
the experience of almost every one who has paid any attention to the
subject. In the cases which have come under my own observation it
certainly was not the case, diarrhoea having been present in all of
them. It is more likely, as suggested by Liebermeister, that part of
the poison remains latent somewhere in the body, not developed,
destroyed, nor expelled during the first attack, but brought later
into activity by some exciting cause. Da Costa adopts this view, and
says that relapses of typhoid fever are not unlike the outbreaks of
malarial fever which occur after worry or fatigue and when there has
been no chance for a fresh infection. Different plans of treatment
have at various times been charged with increasing the predisposition
to relapses. This is especially true of the cold-water treatment, and
the records at the hospital at Basle show that the proportion of
relapses and the number of deaths from them are both increased under
the use of cold water. Liebermeister thinks, however, that this does
not necessarily prove that this treatment favors the occurrence of
relapses, since before the introduction of this plan of treatment many
more typhoid fever patients died in the first attack of the disease.
Employing those cases only for statistical purposes in which the
patients have survived the first attack, he finds that the difference
at once disappears, there being 9 per cent. of relapses before the use
of cold water, and 10.3 per cent. after its use.
{310} Gerhardt[89] asserts that in cases in which relapses occur the
enlargement of the spleen does not diminish during the non-febrile
period that intervenes between the original attack and the relapse.
[Footnote 89: _Ziemssen's Cyclopaedia_, vol. i. p. 193.]
Da Costa[90] has shown that the appearance of the white line and
furrow left by the primary attack, to which attention has already been
drawn, may sometimes be of service to us in diagnosis when we see the
patient for the first time during the relapse. In a case which was
recently under my care their appearance certainly rendered the nature
of the previous illness from which the patient had suffered much
clearer than it would otherwise have been.
[Footnote 90: _Transactions of the College of Physicians of
Philadelphia_, 3d S., vol. iii.]
DURATION.--The mode of invasion of typhoid fever is generally so
insidious, and the first symptoms so little pronounced, that the
patient, even if free from mental hebetude and confusion at the time
when he first comes under the care of a physician, is usually unable
to fix with certainty the time of the beginning of his illness. This
inability is of course most marked in what are known as walking cases,
in which, notwithstanding that the disease is far advanced, the
patient continues to pursue his ordinary avocations or at least
refuses to go to bed. In a few cases, however, either in consequence
of the violence of the first symptoms or from some other cause,
opportunity is afforded to the physician of observing the disease from
its onset. In many others the date of commencement may be
approximately ascertained. The average duration of such cases, if
uncomplicated, has been found to be between three and four weeks.
According to Bartlett, the average duration of 255 cases at the
Massachusetts General Hospital between the years 1824 and 1835,
inclusive, was twenty-two days. It was a little less than this in
patients under twenty-one years of age, and a little more in those
over. As these cases occurred before the introduction into use of the
clinical thermometer, and as the commencement of convalescence is
fixed in them at the time when the patients were able to take a little
solid food, it is possible the fever may have continued in them some
time after convalescence was supposed to have been established. Of 200
cases which ended in recovery, and in which Murchison was able to
ascertain with precision the date of commencement, the duration was 10
to 14 days in 7 cases, 15 to 21 days in 49 cases, 22 to 28 days in 111
cases, and 29 to 35 days in 33 cases. The mean duration of these 200
cases was 24.3 days, while that of 112 fatal cases was 27.67 days.
From the same author we learn that the average stay in hospital of 500
cases which recovered was 31.24 days, and of 100 fatal cases was 16.52
days, while the average duration of the illness before admission in
the 600 cases was 10.78 days. During the twenty years from Jan. 1,
1862, to Dec. 31, 1881, 621 cases of typhoid fever, 121 of which were
fatal, were admitted into the Pennsylvania Hospital. No notes of many
of these cases were taken, and of some of the others the notes are
incomplete or inaccessible, so that they cannot, unfortunately, be
used for the purpose of determining the duration of the disease. The
books of the hospital, however, show the length of time each patient
remained in the wards. From these we learn that the average stay of
the 500 patients who recovered was 43.5 days, while that of the 121
patients who died was only 8.75 days, and that of these a large number
(28) died within {311} 48 hours after their admission to the hospital.
As a rule, patients are retained at the Pennsylvania Hospital until
they are fully able to return to work, while at the English and
continental hospitals it is usual to discharge them when they cease to
need active treatment. This circumstance probably explains the much
greater average duration of the cases admitted to the Pennsylvania
Hospital than that of the cases referred to by Murchison. In the
abortive form the duration of the disease may not exceed ten days, and
there are authors who contend that it may occasionally be very much
less.
Death may occur at almost any time in the course of typhoid fever. I
have never seen it myself take place before the seventh day. Murchison
reports two cases in one of which the disease terminated fatally
within twenty-seven hours of its commencement, and in the other on the
second day. Instances are more numerous in which death has occurred on
the fourth, fifth, or sixth day, but still they are comparatively
infrequent, and, as a rule, the fatal termination takes place most
frequently during the course of the third week. On the other hand,
death may sometimes occur at a very much later period. This is, of
course, the case when it occurs during a relapse, but if the fever
continues after the third week the patient may sometimes die from
exhaustion or from the intercurrence of a complication. Death may also
be the result of a sequela long after the disease has run its course.
DIAGNOSIS.--The insidious invasion of typhoid fever, together with the
absence of pathognomonic symptoms in the beginning, always renders the
diagnosis difficult, and sometimes impossible, during the first week.
Still, even at this time the existence of the disease may be suspected
if the frequent use of the thermometer reveals from day to day a
gradual increase of the fever and the existence of evening
exacerbations followed by morning remissions, the temperature rising
each evening from a degree to two degrees higher than it had done the
preceding evening. If in addition to this character of the pyrexia
there are diarrhoea with ochrey-yellow stools or an increased
susceptibility to the action of cathartic medicines, epistaxis,
enlargement of the spleen, slight fulness of the abdomen, with
tenderness and gurgling in the right iliac region, slight hebetude and
some confusion of ideas upon awakening, the diagnosis becomes more
probable. During the next week the symptoms are usually much more
characteristic. The presence of marked abdominal symptoms, together
with the eruption of rose-colored spots, will generally render the
recognition of the disease at this time an easy matter. There are,
however, a few cases in which no rose-colored spots can be found, and
in which the abdominal symptoms, if they exist at all, are so little
marked that they do not arrest attention. Even in these cases the
temperature record, when carefully studied, will often throw a good
deal of light upon the nature of the disease. If the febrile movement
resembles that usual in typhoid fever, if it has continued for more
than a week, if the patient has not been recently exposed to malarial
influences, and presents no symptoms of local disease, the diagnosis
may still be made with at least an approach to certainty.
The following are the diseases which are most likely to be mistaken
for typhoid fever:
Typhus fever has a course which is so essentially different from {312}
that of typhoid that in well-marked cases it would scarcely be
possible to mistake one for the other. Cases, however, do occur which,
in consequence of a very profuse and dark-colored eruption in the
latter, or of the existence of abdominal symptoms in the former,
present at first a good deal of difficulty in diagnosis. The invasion
of the former is more abrupt and its duration shorter than in typhoid
fever. The eruption is usually also much more copious, and appears in
the former as early as the fourth, fifth, or sixth day, while that of
the latter is rarely observed before the seventh day. The fever in the
former is much more nearly continued in type than that of the latter.
Defervescence occurs in the former by crisis; in the latter, by lysis.
The expression of the physiognomy is different in the two diseases. In
typhus there is a uniform dusky hue of the face, with injection of the
conjunctivae and contraction of the pupils. In typhoid fever the
pupils are often widely dilated, the conjunctivae clear, and the face
pallid, with the exception of a circumscribed flush on each cheek.
Diarrhoea is much less frequent in the former than in the latter, and
when it does occur is not accompanied by ochrey-yellow stools.
Epistaxis, tympanites, pain, and gurgling in the right iliac region,
and intestinal hemorrhage, common symptoms in the latter, are very
infrequently met with in the former. On the other hand, petechiae and
vibices, which are of almost constant occurrence in the former, are
rarely met with in the latter. The circumstances also under which the
two diseases are contracted are different. Typhus originates from
overcrowding or is due to direct contagion. The origin of typhoid
fever is often involved in more obscurity, but it can generally be
traced either to a polluted water-supply or to defective drainage.
Relapsing fever, with due care, is not likely to be confounded with
typhoid fever. The abrupt commencement of the former, the high fever,
lasting for from five to seven days only, and terminating by crisis
with a profuse sweat, and the period of complete apyrexia of a week's
duration, followed by the relapse in which the temperature rises even
higher than in the primary paroxysm, and which also terminates by
crisis, form a chain of symptoms which has no counterpart in the
latter. The mind in relapsing fever is usually clear, there being none
of the hebetude and mental confusion commonly observed in typhoid
fever. The rose-colored eruption is, moreover, wanting, and diarrhoea
and tympanites are absent. On the other hand, jaundice and tenderness
in the epigastric zone are more common than in typhoid fever.
Influenza sometimes, Murchison says, when epidemic, closely simulates
typhoid fever, but as the two diseases occur in this country the
resemblance between them is not often sufficiently strong to lead the
careful observer astray. In both there are fever, prostration,
sleeplessness, delirium and sweating, and occasionally deafness,
diarrhoea, epistaxis, and a dry red tongue; but the onset of the
attack in the former is more abrupt, its duration shorter, and
subsequent convalescence more rapid than in typhoid fever. The
prostration, too, is more decided in proportion to the degree of fever
present. Coryza and bronchial catarrh are much more marked symptoms in
the former than in the latter, while hyperaesthesia of the surface,
which is present in almost every case of influenza, is only rarely met
with in typhoid fever.
Remittent and typhoid fevers often prevail together in the malarious
{313} districts of this country, and, as they present many points of
resemblance, they are sometimes with difficulty distinguished from
each other. They both may begin with nausea and vomiting; abdominal
and cerebral symptoms are common to both, and so is enlargement of the
spleen. The typhoid state may supervene in either, and in both the
febrile movement is remittent in character. In remittent fever,
however, the remissions are more marked, and are usually accompanied
with more profuse sweating, than in typhoid fever. Jaundice and other
symptoms of hepatic derangement are also more common, and the pains in
the back and limbs are more frequent and more severe. The effect, too,
of quinine in producing a permanent reduction of the temperature, is
generally more decided. On the other hand, the rose-colored eruption
of typhoid fever is never present in pure remittent fever.
Occasionally, in cases of the variety of typhoid fever known as
typho-malarial fever, the symptoms of the latter may be so prominent
as entirely to mask those of the former. In such cases the discovery
of a few rose-colored spots somewhere on the surface will clearly
reveal the true nature of the disease.
Epidemic cerebro-spinal meningitis differs from typhoid fever by its
more abrupt invasion, by the retraction of the head which rapidly
supervenes, and by the appearance a short time afterward upon
different parts of the body of petechiae, which are not likely, even
at first, to be mistaken for the rose-colored spots of typhoid fever.
The fever has, moreover, no constant character, but is remarkable, on
the contrary, for its great irregularity. The duration of the disease
is in fatal cases much shorter, death taking place not infrequently
within the first week, and occasionally as early as the second or
third day. On the other hand, the duration in cases which recover may
be even longer than in typhoid fever.
Simple continued fever may readily be mistaken in the beginning for
typhoid fever, especially in those cases complicated by diarrhoea,
but, as a general rule, the different character of the febrile
movement, its more abrupt commencement and termination, and its
shorter duration, together with the absence of the rose-colored
eruption, will usually serve to distinguish it.
The eruptive fevers are always readily distinguishable at the period
of invasion from typhoid fever, and the mistake of confounding them
with the latter disease may generally be avoided by a close study of
the character of the pyrexia. In the eruptive fevers the temperature
rises abruptly, frequently attaining its maximum in the course of
twenty-four hours, and sometimes in very much less time. There are
also in all of them early symptoms which indicate pretty clearly their
true nature, as, for instance, the sore throat of scarlatina, the
naso-pulmonary catarrh of measles, and the rachialgia of small-pox.
The uncertainty, moreover, is of short duration, as the characteristic
eruption appears in all of them before the fourth day.
Acute tuberculosis of the lungs is the condition which in my
experience has been the most difficult to distinguish from typhoid
fever. Indeed, in some cases which have come under my observation
physicians of recognized skill as diagnosticians have been unable to
make the discrimination until after the death of the patient. Muscular
prostration, a dry brown tongue, delirium, stupor, bronchitic rales,
dyspnoea, and even cyanosis, are symptoms frequently met with in both
diseases, so that when the {314} rose-colored eruption and enlargement
of the spleen happen to be wanting in typhoid fever, or diarrhoea and
tympany present in acute tuberculosis, as they may be, the distinction
is often impossible. The diagnosis may, however, even in these cases,
be sometimes made after a careful study of the temperature range,
which in acute tuberculosis is irregular and rarely presents any
resemblance to that which is typical of typhoid fever.
Acute tubercular meningitis has also many symptoms in common with
typhoid fever, such as high fever, headache, vomiting, delirium, and
stupor, but in the former disease the rose-colored eruption,
epistaxis, enlargement of the spleen, and intestinal hemorrhage do not
occur. Diarrhoea is also rare, and the abdomen, instead of being
tympanitic, is flat, and in many cases even scaphoid. The headache,
too, is much more acute than in typhoid fever, and is very apt to be
associated with retraction of the head. Here, again, the frequent use
of the thermometer will yield very important results in diagnosis, as
the temperature range in tubercular meningitis is always irregular and
does not present any resemblance to that usually observed in typhoid
fever.
Several of the inflammations, especially when associated with the
typhoid state, have so many symptoms in common with typhoid fever that
they may very readily be mistaken for one another by a careless
observer. I have known, for instance, the general disease to be
entirely overlooked in a case of typhoid fever complicated by
pneumonia, and, on the other hand, it has sometimes been supposed to
be present in a case of pure typhoid pneumonia. Gastro-enteritis is
another disease which is also occasionally confounded with typhoid
fever. The diagnosis in these cases will rest principally upon the
presence or absence of epistaxis, enlargement of the spleen,
tympanites, the rose-colored eruption, and of a temperature range
presenting some similarity to that usual in typhoid fever.
Trichiniasis is not likely to give rise to much difficulty in
diagnosis, for although vomiting, diarrhoea, and the typhoid state
occur in it as well as in typhoid fever, the former disease may
usually be recognized by the severe muscular pains and the local
oedema which are constant accompaniments of it, and by the absence of
the characteristic symptoms of the latter.
PROGNOSIS.--There is no other disease in which the physician should be
more careful in making a positive prognosis than in typhoid fever. On
the one hand, accidents of a fatal character frequently occur in cases
which are apparently progressing favorably, and, on the other,
recovery has often taken place after all hope of it had been
abandoned. But, although it is impossible to foretell with absolute
certainty the result in any particular case, there are certain
symptoms which furnish very important indications for prognosis, and
the proper appreciation of which will generally enable us to arrive at
a correct conclusion as regards the gravity of the disease. Prominent
among these is the character of the pyrexia. A fever characterized by
high temperature should always give occasion for great anxiety. This
is very fully shown by the statistics of the hospital at Basle. Thus
of those patients in whom the temperature did not reach 104 degrees,
only 9.6 per cent. died; of those in which it reached or exceeded 104
degrees, 29.1 per cent. died; and, finally, of those in whose axilla
the temperature rose to or above 105.8 degrees, more than half died.
{315} Wunderlich has arrived at very nearly the same conclusions, for
he says that the prognosis is very unfavorable when the temperature
rises to 106.16 degrees, that the deaths are almost twice as numerous
as the recoveries when it rises to 107.06 degrees, and that recoveries
are rare when it rises to 107.24 degrees. Murchison has, however,
known recovery to follow a temperature of 108 degrees. The highest
temperature recorded in any of my cases was 106 degrees F. In this
case, which proved fatal, the temperature reached 105 degrees F. five
times. In three other cases, in all of which recovery took place, a
temperature of 105.5 degrees F. was observed. In twelve cases the
temperature reached 105 degrees F. on more than one occasion. Six of
these ended fatally; in the others the patients recovered.
The prognosis is more unfavorable in a fever in which the temperature
is continuously high, and in which the morning remissions are slight
or wanting, than in one in which the daily fluctuations are greater,
even though the temperature may reach a higher point during the
evening exacerbations in the latter variety than is attained at any
time in the former. Occasional remissions, even if produced by quinia
or other remedies, are to be regarded as favorable omens, as they
indicate that the fever tends to subside. A high morning temperature
ought, therefore, to give rise to more alarm than a high evening
temperature. The prognosis is grave when the morning temperature rises
to 104 degrees or is persistently above 103 degrees. Murchison says
that recovery is rare after a morning temperature of 105 degrees.
Fiedler[91] saw, with a single exception, all patients die whose
temperature in the morning rose to or exceeded 106.25 degrees, while
of those whose temperature in the morning rose to 105.44 degrees, if
only on one day, more than half died. Any marked deviation from the
usual temperature range in the course of the fever is unfavorable. A
rapid rise of temperature indicates increased danger: it may be due to
the occurrence of a complication or of some other cause acting
unfavorably upon the patient. A sudden and decided fall should excite
even more alarm, as it is generally the consequence of a free
intestinal hemorrhage. A temporary abatement of the fever, with
amelioration of the other symptoms, occurring between the tenth and
twentieth days, and giving rise to the hope that convalescence is
about to commence, but followed by a return of the symptoms in an
aggravated form, is also unfavorable. Such cases, according to Chomel,
Louis, Bartlett, and Murchison, almost invariably terminate fatally.
[Footnote 91: Quoted by Liebermeister.]
The prognosis is bad in cases in which coma or wild or violent
delirium comes on early. A moderate amount of delirium, especially
when it occurs only at night or upon wakening in the morning, and is
readily dissipated by attracting the patient's attention, or stupor
which disappears when he is thoroughly roused, is not unfavorable.
Insomnia, subsultus tendinum, carphologia, slipping down in bed,
incontinence of the urine or feces, and retention of urine, are all
symptoms of bad omen. Rigidity of the limbs is also a bad symptom; Dr.
Jackson reports six cases in which this symptom occurred, only one of
which recovered. Excessive subsultus is especially unfavorable, as it
is generally most marked in cases in which the ulcerations of the
intestines are most extensive. Extreme deafness occurs in mild as well
as severe cases; it is therefore without significance in prognosis.
{316} In estimating the importance, in a prognostic point of view, of
these various nervous symptoms, it is important to bear in mind that a
degree of fever which produces no disturbance of the mental functions
in a phlegmatic person will give rise to active delirium and other
marked cerebral symptoms in a person of an excitable temperament.
A change in the character of the pulse and of the action of the heart
is often the earliest indication of the approach of danger in typhoid
fever, and both pulse and heart should therefore be carefully examined
at every visit. The first change is usually a diminution in the
intensity of the first sound of the heart. This is significant, as it
is frequently the earliest premonition of cardiac failure, to which a
large proportion of the deaths in typhoid fever is due. A pulse of 120
and over, especially if it is at the same time feeble, is also
unfavorable. The important part which the frequency of the pulse plays
in the prognosis is shown by the following observations made by
Liebermeister at the hospital in Basle: Of 63 cases in which the pulse
rose to or above 120, 40 were fatal, or nearly two-thirds. Among these
63 were 37 in which it did not rise to 140; of these, 19 were fatal,
or about one-half; in 26 it rose above 140; of these, 21, or about
four-fifths, were fatal. In 12 patients it rose above 150; of these,
11 died. Of those in which the pulse rose to 160, the only case that
ended in recovery was that of a girl twenty-one years old suffering
from an imperfectly developed typhoid. Intermittence of the pulse is
unfavorable, especially, according to Hayem,[92] when it occurs during
the first week of the disease. In convalescence intermittence is not
to be regarded as an unfavorable symptom. The prognosis is bad also in
those cases in which, with excessive weakness of the pulse, there are
other evidences of cardiac failure, as, for instance, congestion of
the lungs, cyanosis of the surface, coldness of the extremities. A
very frequent pulse is not so unfavorable in a child as in an adult,
or in a person of a nervous temperament as in one of a different
disposition.
[Footnote 92: _Loc. cit._]
Other unfavorable symptoms are a dry, brown tongue, excessive
tympanites with great abdominal tenderness, severe diarrhoea, vomiting
when it occurs late in the disease, intestinal hemorrhage, and
colliquative sweats. The delusion sometimes observed in very severe
cases, in which the patient declares that he is not ill, is a very bad
sign, many authors, and among them Louis, asserting that they have
never known recovery to take place after it has been manifested.
Peritonitis is a very serious complication, whether due to perforation
or to some other cause. Still, it would appear not to be invariably
fatal, since recovery has occurred in cases in which all the symptoms
of this complication were present.
Favorable symptoms, on the other hand, are a gradual decrease of the
temperature with increasing morning remissions, moistening and
cleansing of the tongue, a lessening of the delirium, and other
nervous symptoms, reappearance of an intelligent expression,
recognition by the patient of friends and attendants, and a diminution
of the diarrhoea. A copious eruption is also regarded by many as a
favorable symptom. Cases in which constipation exists generally do
well. Nathan Smith never knew a patient to die whose bowels were
constipated throughout the attack.
The death-rate of typhoid fever is found to vary very considerably in
different years and in the different seasons of the year, as will be
seen {317} from the two following tables. Statistics as to the
mortality of the disease to be reliable must therefore be based upon a
large number of cases extending over a series of years.
The following table shows the number of cases admitted into the
Pennsylvania Hospital during each of the twenty years ending Dec. 31,
1881, and the ratio of mortality among them:
TABLE NO. 1.
-------+------+------+------+------+--------+--------+-------+-------
| | | | | | | |Percen-
| | | | | | | |tage of
| | | | | | | | deaths
| | | | | | | | after
| | | | | | | |deduct-
| | | |Number| | | | ing
| | | | of | | | | cases
| | | |deaths| Average| | | fatal
| | | |within| stay | | | within
| | | | 48 |in cases| | | 48
| |Number|Number| hours| ending | Average| | hours
|Number| of | of | of | in | stay |Percen-| of
| of |recov-| dea- |admis-| recov- |in fatal|tage of| admis-
YEAR. |cases.|eries.| ths. | sion.| ery. | cases. |deaths.| sion.
-------+------+------+------+------+--------+--------+-------+-------
1862 | 89 | 68 | 21 | 7 | 54-1/3 | 8 | 23.6 | 17.7
1863 | 36 | 33 | 3 | 2 | 32-1/5 | 3-1/3 | 8.3 | 2.9
1864 | 43 | 35 | 8 | 1 | 38-1/2 | 8 | 18.6 | 16.3
1865 | 36 | 31 | 5 | 1 | 38-1/2 | 5-1/2 | 13.9 | 11.4
1866 | 23 | 17 | 6 | 0 | 45-2/3 | 9 | 26.0 |
1867 | 24 | 20 | 4 | 0 | 37-1/3 | 6-1/2 | 16.6 |
1868 | 27 | 23 | 4 | 0 | 44-3/4 | 10 | 14.8 |
1869 | 21 | 16 | 5 | 1 | 35-1/2 | 14 | 23.8 | 20.0
1870 | 24 | 19 | 5 | 1 | 47-1/2 | 11 | 20.8 | 17.4
1871 | 32 | 26 | 6 | 1 | 37-3/4 | 13-1/2 | 18.8 | 15.0
1872 | 21 | 16 | 5 | 3 | 37-1/2 | 4-1/2 | 23.8 | 11.1
1873 | 12 | 8 | 4 | 2 | 34 | 9 | 33.3 | 20.0
1874 | 16 | 12 | 4 | 0 | 54-1/2 | 9-3/4 | 25.0 |
1875 | 20 | 18 | 2 | 1 | 48 | 4-1/2 | 10.0 | 5.3
1876 | 30 | 21 | 9 | 2 | 45-1/2 | 11 | 30.0 | 25.0
1877 | 48 | 34 | 14 | 4 | 48-1/2 | 12-1/2 | 29.2 | 22.7
1878 | 8 | 5 | 3 | 0 | 49 | 5-2/3 | 37.5 |
1879 | 17 | 15 | 2 | 0 | 53-1/3 | 8 | 11.8 |
1880 | 40 | 35 | 5 | 2 | 47 | 10-1/2 | 12.5 | 8.0
1881 | 54 | 48 | 6 | 0 | 41-3/4 | 8 | 11.1 |
-------+------+------+------+------+--------+--------+-------+-------
Totals,| 621 | 500 | 121 | 28 | 43-1/2 | 8-3/4 | 19.5 | 15.7
-------+------+------+------+------+--------+--------+-------+-------
Out of the 621 cases admitted, 121 were fatal. This gives a death-rate
of 19.5 per cent.; but if we deduct the 28 cases in which the patients
died within forty-eight hours of their admission, it falls to 15.68
per cent., or about the same ratio as Murchison found to exist among
the cases treated at the London Fever Hospital. Other observers have
obtained slightly different results. Thus, the mortality was 11.16 per
cent. in 197 cases analyzed by Dr. Hale, and 13.5 per cent. in 303
cases collected by Dr. James Jackson. Dr. Cayley[93] found the
death-rate of the several hospitals in London to be 17.8 per cent.,
and Geissler[94] that it was in all the German hospitals 12.8 per
cent. in 1877, and 13.5 per cent. in 1878. Flint had 18 deaths in 73
cases, or 24.4 per cent. According to Liebermeister, the ratio of
mortality at the hospital at Basle during the twenty-two years from
1843 to 1864, or before the introduction of a {318} systematic
anti-pyretic treatment, was 27.3 per cent., and only 8.2 per cent.
during the six years immediately following its adoption. As the
results obtained at the Pennsylvania Hospital are apparently not so
favorable as those reported at some of the continental hospitals, it
is only proper to state that a large proportion of the cases were
severe, that many of them were far advanced in the disease when
admitted, and that very few of the patients were under twenty-one
years of age. These are all circumstances which influence very
decidedly the prognosis in typhoid fever. In no other city are the
laboring classes able to surround themselves with so many comforts as
in Philadelphia. This fact, fortunate as it is in the main, often
operates to the disadvantage of the patient by enabling his family to
indulge for a time the reluctance which it naturally feels to part
with a member when sick. In the case of the young this reluctance is
so hard to overcome that children with acute affections are rarely
brought to hospitals for treatment. There were also special causes for
the large mortality in certain years. This was particularly the case
in 1862, when a large number of soldiers fresh from the battlefields
of Virginia, and suffering from the typho-malarial form of the
disease, were admitted into the hospital. Many of them were moribund
upon admission, and others, exhausted by the fatigue incident to
transportation here and by previous hardships, soon succumbed to the
disease.
[Footnote 93: _Med. Times and Gaz._, 1880.]
[Footnote 94: _Schmidt's Jahrbuch_.]
Table 2 gives the number of cases, with the number of deaths occurring
in each season, at the Pennsylvania Hospital during the last twenty
years:
TABLE NO. 2.
-------------------------+---------+---------+---------+---------
| Spring. | Summer. | Autumn. | Winter.
-------------------------+---------+---------+---------+---------
Number of cases | 89 | 259 | 182 | 91
Recoveries | 73 | 191 | 163 | 73
Deaths | 16 | 68 | 19 | 18
Percentage of mortality | 18.0 | 26.2 | 10.4 | 19.8
-------------------------+---------+---------+---------+---------
It will be seen from this table that the highest death-rate occurred
in the summer and the lowest in autumn, while there was only a slight
difference between the death-rate of spring and that of winter.
Murchison's experience, based on a much larger number of cases, has
led him to conclude that while the disease is a little less fatal in
autumn, the difference in the mortality at different seasons is very
inconsiderable. Chomel believed that the percentage of deaths was
highest in France during the winter months, and Bartlett held the same
opinion as regards America. Epidemics of great severity have
undoubtedly prevailed in winter, as the in Lowell, Mass., referred to
by Bartlett, but there can be little doubt that the death-rate is
highest in this country during the warm months of the year. Dr.
Cleemann[95] found that the monthly average mortality in Philadelphia
for the ten years from 1866 to 1875 was highest in August, and next
highest in September, confessedly the two months of the year when the
heat in this city is most exhausting. I feel very sure I have lost
patients with typhoid fever in these months {319} and in July who
would probably have recovered if the weather had been cooler. With a
temperature often rising above 90 degrees F. at midday, and sometimes
for several days at a time never falling below 80 degrees, all
radiation of heat from the surface of the body is arrested, and death
frequently occurs as the result of hyperpyrexia.
[Footnote 95: _Transactions of the College of Physicians of
Philadelphia_, 3d S., vols. ii. and iii.]
The stage of the disease at which efficient treatment is begun has a
manifest influence upon the result. This is strikingly shown by some
observations of Jackson: 90 cases were admitted into the Massachusetts
General Hospital during the first week--of these 7 died, or 1 in
12.85; 139 cases were admitted in the second week--of these 16 died,
or 1 in 8.68; 46 cases were admitted in the third week--of these 10
died, or 1 in 4.60; and 21 cases were admitted in the fourth week, and
of these 5 died, or 1 in 4.20. Convalescence also occurred much
earlier in those who were admitted early.
Murchison found that in a large number of cases the death-rate varied
at different ages as follows: Under ten years it was 11.36 per cent.;
from ten to fourteen years it was 12.86 per cent.; from fifteen to
nineteen years it was 15.48 per cent.; from twenty to twenty-nine
years it was 20.46 per cent.; from thirty to thirty-nine years it was
25.90 per cent.; from forty to forty-nine years it was 25 per cent.;
and above fifty years it was 34.94 per cent.
According to Liebermeister, among the 1743 patients treated for
typhoid fever in the hospital at Basle from 1865 to 1870, inclusive,
there were 130 who were more than forty years old; of these 39, or 30
per cent., died, while the mortality among the patients under forty
amounted only to 11.8 per cent. Among the cases of typhoid fever in
individuals over forty years of age collected by Uhle, more than half
proved fatal. According to Friedrich,[96] there were, among 16,084
children treated in the Children's Hospital at Dresden, 275 cases of
typhoid fever, of which 31, or not quite 11 per cent., proved fatal.
Age, therefore, exercises a positive influence upon the mortality of
typhoid fever. Its influence is less decided in this disease than in
typhus, in which the death-rate does not reach 4 per cent. until after
the age of twenty, when it rapidly rises from 12.34 per cent. until it
reaches 57.03 per cent. in patients above fifty years of age. The
comparatively slight mortality of typhoid fever among children is
probably due to the fact that the temperature is less often
continuously high in them than in adults, and that while hyperpyrexia
is frequently present, it is generally better borne and less likely to
produce paralysis of the heart. Liebermeister says that the only case
which he has seen recover after the temperature had repeatedly risen
to 107.5 degrees F. was that of a girl fourteen years of age. It is
also said that the intestinal lesions are not so severe, and the
liability to complications and sequelae less marked, in children.
[Footnote 96: Quoted by Liebermeister.]
Typhoid fever appears to be a slightly more fatal disease in women
than in men, for while in some local epidemics the percentage of
deaths is greater among the latter than among the former, the reverse
is found to be the case when the records of a large hospital for a
number of years are carefully examined. According to Murchison, the
mortality at the London Fever Hospital was about 1 per cent. higher
among the female than among the male patients, and about the same
difference in the death-rate {320} of the two sexes has been reported
by continental physicians. A greater disparity even than this has been
observed by Liebermeister at the hospital at Basle, where the
death-rate for women was 14.8 per cent., and only 12 per cent. for
men. Murchison says that this excess of mortality among the former
cannot be accounted for by the influence of child-bearing upon the
course of the fever, since it is much more decided between the ages of
five and fifteen than in the period of child-bearing.
The rich are not only as liable to contract typhoid fever as the poor,
but the disease is also quite as fatal among them. Murchison found
from the statistics of the London Fever Hospital that the mortality is
not greater among the destitute than among the better class of
patients, and expresses the opinion that in private practice enteric
fever is probably more fatal among the upper classes than among the
very poor. Chomel and Forget seem to have reached a similar
conclusion.
All authors agree that the prognosis is unfavorable in corpulent
persons, not only on account of the diminished power of resistance to
disease generally which such persons exhibit, but also because the
febrile movement is often intense in them, and the degenerative
changes of the muscles and organs of the body which it induces are
generally early developed and of high grade. Liebermeister goes so far
as to say that even in the case of ill-nourished, anaemic, or
chlorotic individuals the chances for life are better than in the
corpulent. Murchison has also expressed the opinion that a large,
muscular development is likewise an unfavorable element in prognosis,
having seen the strong and robust succumb to the disease oftener than
the feeble. The mortality from the disease appears to be greater in
certain families than in others. This has been ascribed by some
writers to peculiarities of constitution, but it may be due to other
causes, as, for instance, difference in the intensity of the poison.
The disease is also often very fatal among the intemperate, who
usually bear the disease badly in consequence of the presence of
various degenerations of one or more of the important organs of the
body caused by the excessive indulgence in alcoholic stimulants;
paralysis of the heart being not an infrequent cause of death among
them.
Certain epidemics have been exceedingly fatal, while in others the
percentage of deaths has been very small. There can be no doubt that
in most of these cases there has been a difference in the virulence of
the poison. Recent residence in an infected locality has been shown by
Murchison and other writers to have a decided influence in increasing
the fatality of the disease. Second attacks are, on the other hand,
usually mild. Some diversity of opinion exists among authors in regard
to the effect that pregnancy has upon the course of the disease.
Murchison believes that it is a far less formidable complication than
is usually thought, while Liebermeister, on the contrary, holds a
directly opposite opinion. He also regards the prognosis as
unfavorable when the disease occurs in childbed or a short time
afterward. Individuals with disease of the heart, emphysema, or
bronchial catarrh who contract typhoid fever are said to be more
liable to paralysis of the heart than others, hence the existence of
these diseases materially diminishes their chances of recovery.
TREATMENT.--Inasmuch as the spread and propagation of typhoid fever
may be prevented to a great extent, if not entirely, by the {321}
employment of judicious sanitary measures, it is proper, before
entering upon the discussion of its curative treatment, to devote a
few words to the prophylaxis of the disease.
Whether the physician accepts the theory so ably advocated by
Murchison, that typhoid fever may arise from exposure to the products
of the fermentation of healthy feces, or adopts the view now held by a
large number of investigators, that the disease is never generated in
the absence of the specific germ, he will admit the great importance
of an efficient system of sewerage, with a thorough flushing of the
sewers at regular and frequent intervals, for disposing of the fecal
discharges of the population of all towns, no matter how
inconsiderable in size. No less important is it that the drains of
every dwelling should be well constructed and kept in good order. They
should be trapped just before they empty into the sewer, and should be
provided with the means of thorough ventilation between the trap and
the walls of the house by a free communication with the outer air. The
soil-pipe should be carried up three or four feet above the top of the
house, and every water-closet, bath-tub, stationary washstand, and
sink should have its own separate trap, and none of them should be
placed in rooms unprovided with a window or with some other sufficient
means of ventilation. Physicians should, as sanitarians, urge upon the
authorities of all cities and towns the importance of deriving their
water-supply from a source unpolluted by sewerage or by any other
substances likely to be deleterious to health. They should also see
that when water is stored in a tank inside of a house the overflow
pipe does not communicate directly with the drain, since if this is
allowed to occur the water may very soon become contaminated with
sewer gas, and consequently unfit for internal use.
In the case of isolated country-houses and of small villages some
other means of disposing of the fecal discharges of the inhabitants
than by sewers has to be found. In the great majority of instances no
better way presents itself than by the ordinary cesspool. Care should,
however, be taken that this is so constructed and situated that there
can be no filtration of its contents into wells from which water for
drinking is obtained.
As the alvine dejections of the sick are beyond question the medium by
which typhoid fever is most frequently communicated to others, the
importance of thoroughly disinfecting them before they have acquired
the power of imparting the disease cannot well be overestimated.
Liebermeister recommends that the bottom of the bed-pan should be
strewed, each time before being used, with a layer of sulphate of
iron, and that immediately after a passage crude muriatic acid should
be poured over the fecal mass, as much as one-third or one-half of the
bulk of the latter being used. He also urges, whenever it is
practicable, that the contents of the bed-pan should be emptied into
trenches dug anew every two days and filled up when discarded, care
being of course taken that they are not located anywhere in the
vicinity of wells. Murchison seems to prefer carbolic acid to other
chemical agents as a means of preventing fecal fermentation. For this
purpose the liquid carbolic acid may be diluted with water in the
proportion of 1 to 40 to 1 to 20, or it may be mixed with sand or
sawdust. I have myself employed as a disinfectant with success the
solution of the chlorides sold under the name of Platt's chlorides. As
the discharges must in cities, in the great majority of instances, be
emptied into {322} water-closets, these should be freely flushed with
water after every time they are used; and it is well to impress upon
the attendant on the sick the importance of doing this. The bed-linen
of the patient and his clothes, if they are soiled by his discharges,
should be removed as soon as possible, and subjected to a high degree
of heat (248 degrees F.) or soaked in a solution of the chlorides or
of carbolic acid for several hours before being washed. If these
precautions are observed, cases of typhoid fever may be treated in the
wards of general hospitals without danger to the other patients.
In the doubt and obscurity which generally envelop the diagnosis of
the disease when the physician is first called upon to treat it, it is
impossible to lay down any positive rules for the management of
typhoid fever at its commencement. But even in those cases which begin
insidiously, if the patient is carefully examined enough of the early
symptoms of typhoid fever will be detected to put the physician on his
guard. The thermometer will show the existence of fever, which has a
tendency to increase at night. There will generally be found to be a
little diarrhoea, or at least an increased susceptibility to the
action of purgative medicines; perhaps a little tympany and tenderness
in the right iliac fossa, and moreover a prostration which is out of
all proportion to the other symptoms.
These symptoms, it is true, are not infrequent concomitants of many
diseases besides the one under consideration; but when their presence
cannot be otherwise satisfactorily explained, especially if they have
continued for several days, it is a safe rule in practice to regard
the case as one of typhoid fever, and to regulate the treatment
accordingly. The patient must be put to bed at once, and not allowed
to leave it on any pretext, not even to empty his bladder, after the
first week. This is a rule which should be rigidly enforced in every
case, no matter how mild the symptoms may be. Its non-observance,
either through the neglect of the physician or the ignorance or
wilfulness of the patient, has been the cause of some disastrous
results; in illustration of which it is only necessary to refer to the
frequency with which perforation of the bowel occurs in walking cases
of typhoid fever. Perfect quiet should be maintained in the sick room.
Visitors should be excluded from it, and the attendants limited in
number to those actually necessary to carry out the directions of the
physician. All unnecessary talking is to be avoided, and especially
conversation carried on in a low tone of voice, which is always
annoying to the sick.
There is only one condition under which I should be disposed to break
the rule of absolute quiet and rest laid down above, and that is when
called upon to treat typhoid fever in the built-up portion of our
large cities during the summer season. If the patient were still in
the first week of the disease, if his circumstances were sufficiently
affluent to enable him to surround himself with every comfort, and if
it did not involve a journey of more than a few hours, I should
unhesitatingly send him to the sea-coast. I have so often seen cases
prove fatal in summer in consequence of the great heat of the city--a
heat, too, which is sometimes almost as great at night as in the
day-time--that I should feel that I was giving him an additional
chance of life by sending him where the heat was, at least
occasionally, tempered by cool breezes from the ocean. During the late
war numbers of soldiers were frequently sent in the early stages of
{323} typhoid fever from the camps in the South to their homes or
hospitals in the North, and it is fair to say that they did at least
as well as those who remained behind. But when the journey may be
accomplished by means of Pullman cars and the other appliances of
modern travel the risk, and even discomfort, it involves to the
patient is reduced to the minimum.
As the disease is usually one of long duration, the patient being
rarely able to leave his bed under four weeks, and more frequently
being obliged to keep it for a much longer time, the sick room should,
wherever practicable, be large, airy, and provided with an open
fireplace, which is a much more efficient means of securing thorough
ventilation than an open window, while it is not liable to the
objection sometimes applicable to the latter of causing a direct
draught upon the patient. It is well, however, for the physician to
remember that the danger from this source is very much exaggerated by
the laity, and that patients in the febrile stage of typhoid fever do
not readily take cold. Still, the same end may generally be attained
without the least risk to the patient by opening a window in an
adjoining room. The temperature of the sick room should be steadily
maintained at between 65 degrees and 68 degrees F.
The careful regulation of the diet is also a point of great importance
in the management of typhoid fever; for in this disease there are not
merely the high fever and other exhausting symptoms, speedily inducing
excessive prostration, loss of strength, and emaciation, common to
many fevers, but there is also the peculiar ulceration of the bowels,
which gives rise to danger of its own and demands special
consideration in treatment. The food must therefore be not only
nourishing, but also readily digestible, and not likely to create
irritation in its passage through the intestines. All solid food
should therefore be excluded from the dietary of the patient as long
as the fever lasts. Indeed, it is better to continue this prohibition
even after the subsidence of the fever if rose-colored spots are still
to be seen on the abdomen or elsewhere, or if there exists a tendency
to diarrhoea or any other symptom indicating that the disease has not
fully run its course. Having myself seen some rather disastrous
results from a too early return to solid food, I have been accustomed
in my own practice to interdict its use until at least two weeks after
the beginning of convalescence. Jaccoud also lays much stress upon
this point, saying that the early administration of meat always gives
rise to fever, to which, from its cause, he gives the name of febris
carnis. On the other hand, Flint[97] and Peabody have recently
advocated the giving of solid food immediately after the cessation of
fever, in the belief that recovery is thereby promoted. Milk as an
article of diet is unquestionably to be preferred to all others in
typhoid fever. It is open, it is true, to the objection of
occasionally forming tough curds in the stomach, but this may
generally be prevented by giving the milk in small quantities at a
time, diluted with lime-water or barley-water or mixed with some
farinaceous substance. No positive general rule can be laid down as to
the amount to be given. This will be found to vary not only in
different cases, but also in the same case at different times. Indeed,
in those cases which begin abruptly with symptoms of gastro-intestinal
irritation, if it is forced upon the patient in large quantities it is
not only usually rejected, but also causes an aggravation of the
symptoms, while after {324} this irritation is allayed it will be
digested without difficulty. As a general rule, most adult patients
will be able to take from a quart and a half to two quarts of milk
daily, given in quantities of from four to six ounces every two or
three hours. It should be remembered, however, that if more is taken
than can be assimilated it will act as an irritant and increase the
diarrhoea. If, therefore, the stools contain undigested milk, the
quantity should be diminished. Patients are occasionally met with, but
not in as great number as is often asserted, with whom milk habitually
disagrees. In these cases it must of course be replaced in whole or in
part by some other article of food. Under these circumstances some one
of the liquid preparations of beef may be given with advantage,
although it may be objected to them also that they sometimes occasion
an increase of diarrhoea. Beef-tea or beef-essence, made from the
fresh meat whenever this can be obtained, is to be preferred to all
others; but when it cannot, that made from the preparations of
Johnston or Brand is the best substitute. When the stomach is very
irritable, Valentine's meat-juice, in consequence of the smaller bulk
in which it is given, often answers an admirable purpose.
[Footnote 97: _Medical News_, Mch. 29 and Apl. 5, 1884.]
Various farinaceous substances, such as farina, corn-starch, and
arrowroot, are also occasionally given in typhoid fever, and, although
the last named would seem to be indicated in cases in which diarrhoea
is a prominent symptom, their tendency to cause flatulence is so great
that their use in the acute stage of the fever has not found favor
among physicians generally. In convalescence, on the other hand, they
are generally perfectly well borne.
The subject of the administration of alcoholic stimulants in typhoid
fever may be conveniently considered in this connection. Some
difference of opinion exists in regard to the quantity in which they
should be given, and indeed in regard to the necessity for their use
at all in many cases, as, for instance, in those of young persons
whose health and habits had been good previously to the attack. I have
myself treated several such cases without alcohol, and have not been
able to perceive that their duration was longer and the result less
favorable than in cases in which it was given in the usual amount. It
is, moreover, not necessary to prescribe it always, even in very
severe cases, at the beginning of an attack. When given at this time,
it not infrequently does harm by increasing the fever. It should be
reserved, therefore, until the action of the heart grows feeble and
the first sound becomes indistinct. It is not possible to lay down any
general rule as to the amount to be given, even in severe attacks.
This will vary in different cases, and to a certain extent will be
determined by the effects it produces. If the pulse grows stronger and
the delirium diminishes under its use, it is doing good and should be
continued; if, on the other hand, there is increase of delirium and
restlessness, the quantity should be diminished.
In cases in which only a gentle stimulus is required wine in the form
of wine-whey will often be found to meet the indication fully.
Generally, however, it will be necessary to have recourse to whiskey
or brandy. The choice between these may usually be left to the
patient's fancy; brandy is, however, to be preferred in cases in which
diarrhoea is a prominent symptom. These stimulants should be given in
small quantities frequently repeated. In many cases a dessertspoonful
every two or three hours, {325} either diluted with water or, when the
stomach is irritable, with carbonic acid water or given in the form of
milk punch, will be sufficient. In others a tablespoonful every two
hours, or even at shorter intervals, will be required, but it will
rarely be necessary to exceed eight ounces a day for more than a few
days at a time.
Although the physician will not often be called upon at the present
day to encounter and combat the prejudice so common formerly against
the free administration of water in the febrile condition, he will
frequently find nurses and others not sufficiently alive to the
importance of supplying it when the patient, having fallen into the
typhoid state, ceases to ask for it. The high temperature which is
generally present in this condition, and the rapid combustion of
tissue which it causes, make a full supply of liquid an urgent
necessity which it is dangerous to disregard. Water is the best of all
diuretics, and it is important in this disease, as indeed it is in
many others, that the functions of the kidneys should be kept active,
so that the products of the combustion of the tissues may be
eliminated with their secretion. Care, however, should of course be
taken, as pointed out by Da Costa,[98] that water is not given in such
quantity that the desire for and capability of digesting food is
destroyed by it.
[Footnote 98: Preface to Wilson's _Treatise on the Continued Fevers_.]
In the few cases which begin abruptly with symptoms simulating those
of a so-called bilious attack the practitioner will usually content
himself with the administration of medicines calculated to allay the
irritability of the stomach and bowels. For this purpose I have found
the bicarbonate of potassa in solution, to which lemon-juice is added
at the moment it is taken, so as to produce an extemporaneous
effervescing draught, often an admirable remedy. In other cases I have
used with advantage small doses of calomel or blue mass, followed, if
necessary, by a gentle saline purge. When the symptoms have occurred
soon after a hearty meal, or when there is evidence that the stomach
is overloaded, it will occasionally be necessary to have recourse to
an emetic. Usually, the indications for treatment at the beginning of
an attack are much less definite, and even in the class of cases just
referred to they become so after the subsidence of the
gastro-intestinal symptoms. Indeed, the treatment in the larger number
of cases must be purely symptomatic until the nature of the disease
has fully declared itself. The presence of fever will suggest the use
of the neutral mixture, effervescing draught, or spirit of Mindererus,
combined, if there is decided tendency to evening exacerbations, with
sulphate of quinia in full doses. If there is much diarrhoea, Hope's
camphor mixture or opium in some other form may be given; if delirium
is a prominent symptom, ice or cloths wrung out of cold water should
be kept constantly applied to the head.
But even after all doubt in regard to the diagnosis has been dispelled
and the existence of typhoid fever has been recognized, the treatment
most in favor with physicians is in large measure symptomatic in
character. It is true that various specific treatments, to which
fuller reference will be made hereafter, have been lately proposed,
but the results obtained by them up to the present time where they
have been fairly tested are not so favorable as to induce the body of
the profession to adopt them to the exclusion of all other methods. It
is certain that no remedy or plan of {326} treatment has yet been
discovered which has the power of cutting the disease short, although
this power has been claimed at different times for several. Thus, at
one time quinia in very large doses was believed to possess it, at
another venesection, and at another cold baths. But experience has
shown that these and other perturbating remedies often do harm, and
there is good reason to believe that the apparent good which has
followed their use in a comparatively small number of instances may be
better explained by supposing that an error of diagnosis has been made
than by attributing to them the power of arresting the progress of the
disease. Medicines are, however, by no means useless in the treatment
of typhoid fever. There is no question that the disease is not only
generally conducted to a favorable issue, but that its duration is
often materially shortened, by their judicious use. It is evident,
however, that the treatment must vary with the severity of the attack.
In a few cases it is scarcely necessary to interfere with the course
of the disease by the administration of medicines. In others, on the
contrary, it is necessary to act promptly and energetically in order
to save life.
When called upon to treat typhoid fever, if the case is a mild one
with no bad symptoms, such as excessive diarrhoea, delirium, tremors,
and the like, and especially if the temperature does not rise higher
than 102 degrees F., I am accustomed, after giving minute directions
as to the diet and general care of the patient, to prescribe from two
to three grains of sulphate of quinia four times daily. No great power
in reducing the temperature of the body can, of course, be claimed for
these doses, but experience has shown that the impression which they
make is useful, and they do not interfere with the administration of
the drug in larger quantities should this become necessary. Their
action, too, is tonic, and, as they rarely produce cinchonism, the
objection often made to the use of larger doses does not apply to
them. I am also in the habit of adding to each dose of quinia from ten
to fifteen drops of one of the mineral acids. These acids were
originally prescribed in typhoid fever under the impression that they
neutralized the cause of the disease, which was supposed to be an
alkaline poison. Although the results of recent research, which tend
to show that the cause of the disease is an organized germ, give no
support to this theory, they continue to be used by a large number of
physicians of experience. I do not know that any satisfactory
explanation of their action in typhoid fever has ever been given. They
are certainly tonics, and are therefore indicated, if not in the
beginning of the disease, as soon as the strength begins to fail. If,
as the disease progresses, the tongue becomes dry and fissured, and if
there is much tympany, it will be well to give, in addition to the
quinia, ten drops of the oil of turpentine in mucilage every two
hours. This was a favorite remedy of the late George B. Wood, the
distinguished professor of the Theory and Practice of Medicine in the
University of Pennsylvania, who attributed the improvement in the
symptoms which generally follows its use to a direct influence of this
medicine upon the ulcers in the intestines. Although inclined to
believe that the correct explanation of this improvement is its
stimulating action upon the circulation and secretions, I fully agree
with him in regard to its usefulness in many cases. Under its use I
have often seen the dry, fissured, and shrivelled tongue {327} grow
moist and throw off its coating much earlier than in all probability
it would otherwise have done.
No other than this simple treatment is required in a large number of
cases, but even in mild cases symptoms occasionally arise which render
necessary some modification of it. It will, however, be more
convenient to postpone the discussion of this part of the treatment of
typhoid fever until after the treatment of the more serious forms of
the disease has been considered.
When typhoid fever assumes a severe type, the success of the physician
in the management of the disease will depend largely upon the
readiness with which he detects indications for treatment and the
promptness with which he meets them. Usually, one of the first
symptoms to demand attention is the high temperature. This is not only
an early symptom in many bad cases, but may continue throughout the
attack; or it may suddenly supervene in cases in which the fever has
previously been moderate in degree, and when excessive may be the
direct or indirect cause of death. The reduction of the temperature is
therefore an indication the importance of which cannot well be
overestimated. Fortunately, there are several methods by which this
end may be accomplished. It will, however, be necessary for our
purpose to consider only two of them in detail: 1, the cold-water
treatment; 2, sulphate of quinia in full doses.
The cold-water treatment is not new, since it was practised in the
form of cold effusion in the treatment of fevers as long ago as 1787
by Currie of Liverpool, who may be said to have introduced it, and who
asserted that it had the power not merely of moderating the symptoms
of these diseases, but also, in many cases, of cutting them short. It
enjoyed at first a high degree of popularity, which lasted for from
twenty to thirty years, but finally fell into disuse, probably in
consequence of the exaggerated character of the claims which were made
for it by its advocates. Although resorted to from time to time in
various parts of the world, the merit of having brought it again into
notice seems to be due to Brand of Stettin, who published a work on
_The Hydrotherapy of Typhoid Fever_ in 1861. Still more recently, the
recorded observations of Bartels, Jurgensen, Ziemssen, and
Liebermeister in Germany, and of Wilson Fox and others in England,
have so far restored the treatment to professional favor that there
are few physicians either in this country or abroad who do not
occasionally have recourse to it.
The cold-water treatment may be applied in several different ways: 1,
the cold bath; 2, the graduated bath; 3, cold affusions; 4, the cold
pack; 5, cold sponging; 6, cold compresses; and 7, frictions with ice.
They all act in the same manner, and depend for their efficacy upon
their power of abstracting heat from the body, and are useful just in
proportion as they do this. There is no reason for believing that they
have the power to modify the conditions upon which the production of
heat depends, but there is, on the other hand, no doubt that under
their use distressing and dangerous symptoms, such as coma, stupor,
subsultus, and the like, are often much relieved. They probably act,
therefore, by diminishing the metamorphosis of the tissues, and the
consequent loading of the blood with excrementitious products which
the hyperpyrexia has a tendency to promote.
The cold bath is the most effective of all the methods of applying the
{328} cold-water treatment. Liebermeister recommends that the bath for
an adult should be at the temperature of 68 degrees F., and its
duration should be about ten minutes; if, however, the patient shows
signs of great weakness, it should not exceed seven. After the bath he
should be wrapped up in a dry sheet or light blanket and put back in
bed. If the pulse should then show signs of failing, or if there
should be shivering or any other evidence of weakness, he should be
given a glass of wine or brandy or a dose of some other diffusible
stimulus, and bottles containing hot water should be applied to his
feet. The process of cooling goes on for some time after the patient's
removal from the bath, for while a thermometer placed in the axilla
will show that the external temperature is immediately affected by it,
the same instrument placed in the rectum will indicate a gradual fall,
which will continue in many cases for at least half an hour. Shortly
after this the temperature will be observed to rise, and in many cases
it will not be more than two hours before it has attained its former
height. Liebermeister therefore recommends that the thermometer should
be frequently used, and that the baths should be repeated as often as
the temperature rises to 103 degrees F. or above it. He has himself
given them as often as every two hours, or as many as two hundred
during an entire illness, but usually finds that not more than six or
eight a day are required. It often requires some persuasion to
overcome the repugnance which most patients feel at first for these
baths, and the shock of being suddenly immersed in cold water is
agreeable to very few. Later, this repugnance, he says, entirely
disappears. Intestinal hemorrhage, perforation of the bowel, and great
weakness of the heart's action are all contraindications to the use of
the cold bath. They are especially to be avoided, according to
Liebermeister, when the force of the circulation is so far reduced
that the surface of the body is cold while the interior is very hot.
On the other hand, the advocates of this plan of treatment contend
that the existence of pneumonia or of hypostatic congestion of the
lungs is not a sufficient reason for abandoning it, the congestion
often disappearing under its use.
The graduated bath possesses some advantages over the cold bath, as
its use involves less of a shock to the system. It is therefore more
suitable than the latter for nervous and excitable patients, for
persons of advanced age or of general feebleness of constitution, or
for very young children. In it the temperature of the water, which at
the time of the immersion of the patient should be at or above 95
degrees F., is cooled by the gradual addition of cold water until it
is reduced to 72 degrees, or below this point. These baths, to produce
the same effect as the cold baths, must be of longer duration. They
are contraindicated in the same conditions as the latter, but to a
less degree.
Although fully willing to admit the good effects of the cold bath in
many cases, having been, of course, myself a witness of them, I am
indisposed to have recourse to it except in cases of hyperpyrexia of
such intensity that death seems imminent and only to be averted by
energetic treatment, or in cases in which other antipyretic remedies
have failed to reduce the temperature; and for the following reasons:
1. In the first place, it is generally possible to produce a decided
effect by the other methods of applying the cold-water treatment, with
much less discomfort to the patient. 2. In a private house it is not
always practicable to have {329} a bath brought to the bedside of the
patient, and in a general hospital to do so often would occasion a
good deal of annoyance to the other patients in the same ward, and I
have seen ill result from carrying him some distance to the bathroom.
But even where the bath is brought directly to his bedside, it
involves so much movement, and is sometimes the cause of so much
excitement, that its good effects are more than neutralized by its
bad.
Cold affusions, while not nearly so efficacious in reducing the
temperature of the body as the cold bath, are open to many of the
objections which may be urged against the latter mode of treatment.
They are, therefore, rarely employed at the present time.
Liebermeister, however, thinks that they may sometimes be resorted to
with good effect for their brisk stimulating effect on the psychical
functions or the respiration.
The cold pack possesses the advantage over the cold bath and cold
affusions of involving less movement on the part of the patient and of
being less terrifying to children, and may therefore be resorted to in
cases in which the latter method of applying the cold-water treatment
is contraindicated, as, for instance, in persons of feeble
circulation. It is, however, inferior to either of them in its cooling
effects, and must be longer applied to produce the same effect.
Liebermeister estimates that a course of four consecutive packs, of
from ten to twenty minutes' duration apiece, is about equivalent in
effect to a cold bath of ten minutes.
Cold sponging is assigned a very low place among the methods of
abstracting heat from the body by many writers. It has, however, often
been in my hands of much service, and its easy application and the
comfort which patients derive from it are certainly strong
recommendations in its favor. I have employed it frequently in cases
of intestinal hemorrhage, and even in cases of great debility, and
have never yet had any reason to repent my having done so. The
addition of a little vinegar to the water has seemed to me to increase
the effect of the sponging.
Cold compresses, either in the form of cloths wet with cold water or
bladders filled with ice, can only produce a local fall of
temperature, and therefore, except when applied to the head, can be of
little service.
Frictions with ice are a powerful means of depressing the temperature
of the body, and may therefore be resorted to in cases of intense
hyperpyrexia when for some reason the cold bath cannot be obtained,
and when there are no contraindications to the latter.
Liebermeister classes cold drinks, the internal administration of ice,
and the injection of cold water among the means of cooling the body in
fevers; but it is doubtful if any great reduction of temperature can
be brought about by any of these remedies in the quantities in which
it would be safe to use them. The first two, and to a less extent the
last, meet a very important indication, that of supplying water to the
system. Their free use, therefore, forms a very important part of the
treatment of typhoid fever.
Luton of Rheims[99] extols the Diaeta hydrica in the treatment of
typhoid fever. The patient receives absolutely nothing else to drink
but water, which is given in large quantities, for from four to six
days. No nourishment is given until the beginning of the third week,
and first of all milk. If fever returns, the water is given again.
Medicines such as {330} quinia and eucalyptus are given in adynamic
conditions, which Luton says are rare under this treatment. He
believes that the increase of the typhoid germs is prevented by
absolute diet and abundant supply of water.
[Footnote 99: _Journal de therapie_, Oct., 1880.]
Quinia to produce a decided antipyretic effect must be given in large
quantities. Murchison says that a dose of from fifteen to twenty
grains causes within an hour or two a fall of the temperature, and, to
a less extent, of the pulse, which may last from twelve to eighteen
hours, and that he has never known any other disagreeable symptoms
result from its use than noises in the ears, temporary acceleration
and irregularity of the respiration, and occasional vomiting. This
quantity will often, however, be found to be insufficient to produce a
notable reduction of the fever, and it is therefore necessary
occasionally to increase it. Liebermeister usually gives to adults
from twenty-two to forty-five grains of the sulphate or the muriate of
quinia, and this dose must positively be taken within the space of
half an hour, or, at the most, an hour, as it is useless, he says, to
expect the full benefit of this dose to appear if the dose is divided
and its administration is extended over a longer time. He never
repeats it in less than twenty-four hours, and, as a rule, does not
give it again under two days. Jurgensen has exceeded the dose of
forty-five grains without observing any bad effects from it. When
these large doses are taken the fall of the temperature usually begins
a few hours after the administration of the medicine, the minimum
being reached in from six to twelve hours, and it is usually not until
the second day that the temperature attains its former height. It is
found in practice that the most decided results are obtained when the
medicine is given in the evening, so that the time of its fullest
antipyretic effects will coincide with that of the morning remission.
When these large doses produce vomiting, as they occasionally will,
the quinia must be given by the rectum or hypodermically.
Quinia possesses the great advantage over the cold bath that it may be
given in conditions in which it would be dangerous to resort to the
latter. The existence of great cardiac weakness, of perforation of the
bowel, or of intestinal hemorrhage do not usually constitute
contraindications to its use. In my own practice I have not often
found it necessary to have recourse to much larger doses than those
recommended by Murchison, preferring to repeat them if necessary
rather than to give a single dose of even half a drachm.
It will be well, in this connection, to allude briefly to a few other
remedies which have been given for their antipyretic effect. One of
these is digitalis, which has been administered for this purpose in
very large doses. Thus, Liebermeister recommends that from eleven to
twenty-two grains should be given in the course of thirty-six hours. I
have never used this drug in these doses, and therefore cannot speak
of its effects from personal knowledge of them. I have frequently had
recourse to it, however, in more moderate doses, and I think with
advantage.
Another is sodium salicylate. This remedy has been used largely in
England and Germany, and to a less extent in this country. It has been
claimed for it that it has the power of destroying the germs of
typhoid fever, but Stricker[100] finds it difficult to accord it this
property in the face {331} of the fact that he has had three cases of
typhoid fever under his observation which occurred in patients just
recovered from rheumatism, which had been treated by this drug. My own
experience with it in the treatment of this disease is small, but has
been unsatisfactory. While it is undoubtedly an antipyretic, the pulse
becomes weak and the inspiration less strong under its use. The brain
symptoms do not diminish under its use. Indeed, it is said to produce
narcotism in some cases. Dr. Jahn[101] and Dr. Jh. Platzer[102] speak
more favorably of it, but admit that its administration is
occasionally attended by the inconveniences above referred to. The
verdict of the profession in regard to it, tersely expressed by one
who had given it a fair trial, appears to be that it is a remedy that
brings nothing but disappointment to the physician and disaster to the
patient.
[Footnote 100: _Deutsche Milit.-arztl Zeitsch._, 1877.]
[Footnote 101: _Deutsches Arch. f. klin. Med._, 1877.]
[Footnote 102: _Bayr. Arztl. Intell. Bl._, 1877.]
Eucalyptus, in the form of the tincture, is also a favorite remedy
with many practitioners. Dr. Benj. Bell[103] is in the habit of giving
a teaspoonful every three or four hours in a wineglass of water, and
asserts that it diminishes the tendency to diarrhoea and the duration
of the illness.
[Footnote 103: _Edin. Med. Jour._, Aug., 1881.]
The different varieties of typhoid fever require slight modifications
only of the treatment laid down above. In the typho-malarial form,
especially in those cases in which the malarial element predominates,
and in which there is a marked tendency to remission, the early
administration of quinia in full antiperiodic doses is urgently called
for. In some cases which he had the opportunity of observing in the
army, A. L. Cox[104] found great advantage from the use of arsenious
acid in rather large doses. When the disease attacks elderly people,
an early resort to alcoholic stimulants is usually necessary, in
consequence of the excessive prostration it induces in them. Henoch
and Steffen[105] assert that cold baths are not so well borne in
children as in adults. Their influence is transitory only, and their
use has sometimes been followed by fatal collapse. In the renal form
dry, and in some cases cut, cups should be applied externally and
saline diuretics given internally.
[Footnote 104: _Outlines of the Chief Camp Diseases of the United
States Armies_, by Joseph Janvier Woodward, M.D., Philada., 1863.]
[Footnote 105: _Jahrb. f. Korhde_, 1880.]
SYMPTOMS REQUIRING SPECIAL TREATMENT.--Vomiting, when it occurs early
in the disease, is usually checked by the administration of an emetic
and by the application of sinapisms to the epigastrium. The use of
emetics is no longer advisable when it occurs after the first week. It
is better then to trust to small doses of hydrocyanic or carbolic
acid, aromatic spirit of ammonia, or bismuth. It will often be found
that lime-water and milk will remain upon the stomach when every other
article of food or medicine is rejected. In some severe cases which
have been under my care the symptom was permanently relieved by the
frequent administration of small quantities of brandy in iced
soda-water. When vomiting is a consequence of peritonitis it usually
resists every form of treatment.
Diarrhoea, if the number of the stools does not exceed two or three in
the course of twenty-four hours, does not need special treatment.
When, however, it is more severe, prompt measures should be taken to
check it. Under these circumstances laudanum injections have seemed to
me to be {332} by far the best remedy. It is not necessary that these
injections should always contain a large amount of laudanum or that
they should be repeated frequently. In many cases twenty drops once a
day will be found to be sufficient, and it is rarely necessary to
exceed forty drops twice daily. Opium given by the mouth or in
suppository in equivalent quantity does not act with anything like the
same efficacy. If the laudanum injections fail to restrain the
diarrhoea, it will be well to have recourse, in combination with
opium, to the subnitrate of bismuth or the acetate of lead. Nitrate of
silver was at one time much employed in the treatment of typhoid
fever, especially by the late J. K. Mitchell of this city, but was
afterward suffered to fall into neglect. Its use has been recently, to
a certain extent, revived in consequence of the recommendation of
William Pepper,[106] who claims for it the power of modifying the
course of the disease. I have given it in a number of cases, but have
never been able to satisfy myself that it possessed this power. I have
therefore ceased to prescribe it except in the later stages of the
disease, when the symptoms indicate that the intestinal ulcers are in
an atonic condition. Under these circumstances it has appeared to me
to promote their cicatrization. It is important, however, to remember
that diarrhoea is occasionally caused and kept up by more food being
given to the patient than he can assimilate, and it is therefore a
good rule to examine the stools from time to time to see whether they
contain curds of milk or other undigested food. If such is found to be
the case, the amount of nourishment should be diminished, and it will
be well also to prescribe pepsin either in powder or in solution.
[Footnote 106: _Philadelphia Medical Times_, Feb. 12, 1881.]
Tympanites also occasionally requires treatment, for in addition to
interference with the descent of the diaphragm and other discomfort it
produces, the distended condition of the bowels directly increases the
risk of perforation. It is usually sufficient to employ embrocations
or stupes of equal parts of sweet oil and oil of turpentine, or of
camphor liniment. If the tympanites coexist with constipation,
enemata, either with or without a small quantity of oil of turpentine,
may often be used with advantage. If it is extreme, an intestinal tube
should be introduced very carefully into the rectum and the gas drawn
off. Charcoal has occasionally been administered in this condition
with a view of preventing decomposition of the intestinal contents.
Tympanites occasionally rapidly supervenes upon the occurrence of
perforation, and must then, of course, be treated with due reference
to the latter condition.
Intestinal hemorrhage is a symptom which always demands prompt
attention, no matter how slight it may seem to be, for it is to be
remembered that not only is there a danger of its recurrence, but that
the quantity of blood which appears in the stools is by no means a
reliable measure of that actually lost, as more blood frequently
remains in the intestines than appears externally. In estimating its
severity, it is therefore proper to take into consideration the
gravity of the other symptoms which attend it, such as the fall of
temperature, feebleness of the pulse. In many cases the enforcement of
absolute rest, with the administration of cold drink and a small
amount of opium to diminish peristaltic action, is all that is needed.
In cases in which the symptoms are graver it will be necessary to have
recourse to more energetic {333} measures. Under these circumstances
the hypodermic injection of from three to five grains of ergotin,
repeated if necessary, has seldom in my experience failed to check the
hemorrhage. Dilute sulphuric acid, oil of turpentine, and acetate of
lead have also proved themselves useful remedies in my hands. The
application of ice to the surface of the abdomen has also been said to
be attended with good results, but the objections to the use of this
remedy in the condition of collapse, which is so apt to accompany
profuse intestinal hemorrhage, are so evident that it is unnecessary
to discuss them here. Monsel's solution, tannic acid, and various
other mineral and vegetable astringents have been recommended for
their direct effect upon the bleeding surface, but, even admitting
that they can, when administered by the mouth, reach this unaltered or
in a sufficient state of concentration to be active, it is evident
that they could only do so after the loss of valuable time.
When perforation occurs, it is obvious that the indications for
treatment are to preclude the extravasation of the contents of the
intestine into the cavity of the peritoneum, and to prevent the
peritonitis which is a consequence of this accident from becoming
general. Both of these indications are met by the administration of
opium, which diminishes, and, if pushed, arrests, the peristaltic
action of the intestines. By means of it the bowels may be kept as
free from movement as if "placed in splints." A grain of solid opium
may be given every hour until a decided effect is produced, or if it
is found to disagree with the stomach an equivalent quantity may be
given by the rectum, or it may be substituted by morphia administered
by the mouth or hypodermically. With the same view, food is to be
allowed in small quantities only at a time, and of a character capable
of digestion by the stomach. A light poultice, or, if there is much
evidence of inflammation, ice should be applied to the abdomen. It has
been recommended also, in cases in which the peritonitis has become
general, to apply leeches to the abdomen, but few patients in this
condition will readily bear the loss of much blood. It is very
important not to interfere with the constipation which results from
the above treatment, and which it is one of its objects to promote,
until all inflammatory symptoms have been absent for at least a week,
when a simple enema may be administered. Peritonitis resulting from
other causes than perforation of the intestine does not require any
modification of the above treatment.
Severe abdominal pain, when it occurs independently of inflammation,
is best treated by the application to the abdomen of light poultices,
to which two or three teaspoonfuls of laudanum may be added.
Constipation is an occasional symptom, but it rarely calls for active
interference. When it is present so early in the course of the disease
that the diagnosis is still uncertain, and has continued for several
days, it is best to prescribe a small dose of castor oil; a
dessertspoonful is generally sufficient. The late Dr. Gerhard was in
the habit of giving a tablespoonful of sweet oil in this condition.
The inordinate action which frequently follows the administration of
these mild purgatives will often dispel all uncertainty as to the
nature of the disease we have to do with. When it occurs in a more
advanced stage of the disease it is best met by the administration of
enemata, which may contain, if there is much tympanites present, a
small quantity of oil of turpentine. Under all {334} circumstances it
will be well to remember the advice given by Baglivi two centuries
ago, to avoid the use of active cathartics in this disease.[107]
[Footnote 107: "Fuge purgantia tanquam postem," _Opera Omnia
Medico-Practica et Anatomica_, Georgii Baglivi, 1788.]
The headache which is sometimes a distressing symptom in the beginning
of the disease is usually relieved by the application to the head of
cloths constantly wet with ice-water or by that of a bladder filled
with ice and lard. If it is very severe and does not yield to these
remedies, a few leeches applied to the temples often have a very happy
effect in moderating the pain. Murchison recommends that the cold
affusion should be administered by simply placing the patient's head
over a basin at the edge of the bed and pouring water on it from a
height of two or three feet. He also says that warm fomentations are
to be preferred to cold in aged and infirm persons of feeble
circulation. Sleeplessness will often disappear under the use of
remedies presented for the relief of the headache and other nervous
symptoms. It is occasionally so persistent as to call for special
treatment. If it occur early in the disease, it will generally be
sufficient to prescribe at bedtime ten grains each of potassium
bromide and chloral, repeated once or twice during the night. Later in
the disease this combination ceases to produce any effect, besides
which chloral cannot be administered with safety after the action of
the heart becomes feeble. It is therefore necessary to have recourse
to opium in some form or other. There are, it is true, theoretical
objections to its use in typhoid fever, such as its interference with
digestion and its tendency to lock up the secretions; but these will
hardly weigh in the balance against the fact that the patient will die
of exhaustion if the insomnia is allowed to continue, and that under
certain circumstances opium is the only drug which will procure the
needed sleep. The form in which it is given is not a matter of much
importance. I prefer the deodorized tincture, twenty or thirty drops,
repeated if necessary in an hour or two, but I have seen good results
from the solid opium and from the hypodermic injection of morphia.
When the insomnia is attended by much tremor and muttering delirium,
camphor may be added to the opium, and given throughout the day as
well as in the evening. Violent delirium is sometimes also relieved by
administration of opium and alcoholic stimulants, and by the
application of cold to the head. It is also much lessened by the
cold-water treatment. When the delirium is so violent that restraint
is necessary, it is better that this should be mechanical than that it
should be left wholly in the hands of ignorant and untrained nurses. A
folded sheet passed over the chest of the patient and fastened to the
sides of the bed is frequently all that is needed. Stupor requires
very much the same kind of treatment as that suitable for the other
forms of nervous derangement. If it is extreme, counter-irritants
should be applied to the nape of the neck and cold to the head. The
late Dr. Wood was in the habit of shaving the hair and applying a
blister to the scalp of a patient in this condition, and I have seen
good in more than one instance result from this treatment. The urine
should also be examined, and if the quantity be insufficient diuretics
should be given. If it contain albumen or blood, counter-irritants and
even cut cups should be applied to the loins. It is also important, if
the patient be in this condition, that the physician should not rest
satisfied with the nurse's {335} assurance that the urine is passed
freely, but should from time to time examine the supra-pubic region
himself. It is not infrequently found under these circumstances that
there is really retention, and that the wetting of the bed upon which
the nurse has based her assurances is really the consequence of the
dribbling of urine from an over-distended bladder. I have known of
serious results, such as cystitis, paralysis of the bladder, having
followed the neglect of this very simple precaution. Convulsions when
they occur are to be treated by the application of cold to the head
and counter-irritants to other parts of the body.
Epistaxis is rarely so severe as not to yield to the use of simple
remedies, such as the application of ice to the forehead or back of
the neck, or of styptics locally. In a few cases, however, it is
profuse, and it will then be necessary to have recourse to hypodermic
injections of ergotin, as in the case of hemorrhage from the
intestines, or to plug the nostrils.
TREATMENT OF COMPLICATIONS.--Hypostatic congestion of the lungs, as it
is usually the consequence of feeble action of the heart, is best
treated by frequently changing the position of the patient, and by
remedies calculated to increase the power of the organ, such as
alcoholic stimulants, ammonium carbonate, oil of turpentine, and
digitalis. Recent German authors, however, regard digitalis as a
dangerous remedy when the heart has undergone the granular
degeneration peculiar to fevers. It had, therefore, better not be
given if the congestion occurs late in the disease. I have myself
always found advantage from the application of turpentine stupes to
the chest, and occasionally from the application of dry cups.
Pneumonia when it occurs as a complication does not render necessary a
material modification of the above treatment. It may sometimes be
well, if it occur early in a robust subject, to take blood locally,
but it can rarely be justifiable to do so by venesection.
Bed-sores may generally be prevented by frequently changing the
position of the patient, by scrupulous attention to cleanliness, and
by bathing prominent parts of his body with whiskey and alum. These
parts should also be protected from pressure by the judicious
arrangement of pillows and cushions. When redness or abrasions appear
the part should be covered with soap plaster smoothly spread upon kid.
This application may be continued even after the formation of sloughs.
As soon, however, as these show a tendency to suppurate poultices
should be applied, and the resulting ulcer treated as if occurring
under other circumstances.
Thrombosis of the femoral vein is best treated by elevating the
affected leg and enveloping it with flannel cloths saturated with hot
vinegar and water. Thrombosis of other veins is to be treated on the
same general principles. When an artery becomes obliterated, whether
from embolism or thrombosis, the part which it supplies should be
surrounded with cotton wool and every effort made to favor the
establishment of the collateral circulation. If sphacelus occurs, it
should be treated on general surgical principles.
TREATMENT OF CONVALESCENCE.--The importance of a strict adherence to a
liquid diet in the early part of the convalescence of typhoid fever
has already been alluded to. The ulcers in the intestines often remain
unhealed for some time after the subsidence of the fever, and errors
in diet may therefore readily cause recrudescences of fever, if not
true relapses. {336} These recrudescences are sometimes produced by
very slight causes. I have seen them follow undue mental exercise or
worry, or sitting up too early or too long. It is therefore important
to guard our patients at this stage of the disease from undue fatigue
or excitement of any kind. Medicines calculated to build up the
strength and to improve the nutrition are clearly indicated at this
time. If the diarrhoea should persist, nitrate or oxide of silver,
sulphate of copper, and subnitrate of bismuth in appropriate doses,
given with a little opium, will all be found to be useful remedies.
When, on the contrary, constipation exists, it is still necessary to
avoid the use of drastic cathartics; indeed, even mild laxatives
should be given by the mouth only after enemata have failed to produce
a movement of the bowel.
SPECIFIC TREATMENT.--The search for a specific remedy in typhoid fever
is not new. It is as old as the theory that the disease is generated
by a specific cause. The hypothesis that this is an alkaline poison
led many years ago to the use of the mineral acids, and it was only
after experience had shown that they were without power to cut the
disease short, or even to control many of its symptoms, that they
ceased in a measure to be prescribed. Calomel also, which was
occasionally resorted to formerly for its antiphlogistic effects upon
the intestinal lesions, has been lately recommended in Germany in the
treatment of typhoid fever on account of its supposed antidotal
properties. Seven and a half grains of the drug, and in some cases a
much larger dose, are given four times daily on alternate days as soon
as the nature of the disease is fully recognized. It is claimed for
this treatment that when it is begun early the rate of mortality and
the duration of the disease are much less under it than under any
other. Its advocates admit, however, that the latter is not always the
case--a variety in the action of the medicine which is attributed to a
difference in the way in which the poison of the disease has been
taken into the body. Salivation is rarely produced by the calomel. The
diarrhoea, which is at first increased by it, subsequently diminishes,
and the administration of each dose is followed by a decided although
temporary reduction of temperature.
A diminution in the rate of mortality is also said to have been
obtained by the administration of iodine in typhoid fever, although
the results of its use are on the whole less favorable than those of
calomel. Liebermeister recommends that three or four drops of a
solution of one part of iodine, two parts of iodide of potassium, and
ten parts of water should be given every two hours in a glass of
water.
--------------------------+---------+--------+--------------
| Number | Number | Percentage of
| treated.| died. | mortality.
--------------------------+---------+--------+--------------
Non-specifically treated | 377 | 69 | 18.3
Treated with calomel | 223 | 26 | 11.7
Treated with iodine | 239 | 35 | 14.6
--------------------------+---------+--------+--------------
Total | 839 | 130 | 15.5
--------------------------+---------+--------+--------------
The preceding table, which is taken from Liebermeister's article on
typhoid fever in _Ziemssen's Cyclopaedia_, is based upon the results
of {337} treatment in 839 cases, a part of which were treated with
iodine, a part with calomel, and a part with neither, the rest of the
treatment being exactly alike in all of them, and consisting in the
employment of a partial antipyretic method.
James C. Wilson[108] has recently used with great success in the
treatment of typhoid fever the following prescription, which was
originally suggested by Roberts Bartholow: Rx. Tinct. Iodinii fl.
drachm ij.; Acid. Carbolici liq. fl. drachm j.--M. Of this, one, two,
or even three drops is given in a sherry-glassful of ice-water after
food every two or three hours during the day and night. In addition to
this prescription his patients were given a dose of calomel varying in
amount from seven and a half to ten grains, which was repeated on
every alternate night until three or four doses had been administered
in the course of the first six or eight days. Of sixteen cases so
treated, none proved fatal, although eight of them were severe, the
temperature reaching or exceeding 104 degrees F. Da Costa[109] has
used carbolic acid in this disease, and has found it useful in
controlling the diarrhoea and in lowering the temperature, but
suggests the use of thymol in doses of from half a grain to one grain
as a substitute, on account of its greater acceptability to the
stomach. C. G. Rothe[110] recommends a mixture of carbolic acid,
tincture of digitalis, tincture of aconite, brandy, and tincture of
iodine. Its use causes a decided fall of temperature and diminution in
the frequency of the pulse.
[Footnote 108: _Transactions of the College of Physicians of
Philadelphia_, 3d Series, vol. vi., Philadelphia, 1883, p. 221.]
[Footnote 109: _Ibid._, p. 234.]
[Footnote 110: _Deutsche Med. Wochenschr._, 1880.]
My own experience does not enable me to speak with positiveness of the
value of this plan of treatment. Indeed, it has been used in so few
cases, to the exclusion of all other remedies, that it is difficult to
decide how far the result attained in cases treated by them is due to
them, and how far to the other therapeutic means employed. With the
testimony of such competent observers as those above named it is only
proper that the treatment by iodine and carbolic acid should have a
further trial. More caution, it seems to me, is required in the use of
calomel. While it is probable that in a few cases the intestinal
lesions may be favorably modified by the purgation which it induces,
the indiscriminate use of the drug is, I am sure, calculated to do
more harm than good.
{338}
TYPHUS FEVER.
BY JAMES H. HUTCHINSON, M.D.
DEFINITION.--Typhus fever is an acute contagious disease, usually
occurring epidemically, lasting from ten to twenty days, and
characterized, among other symptoms, by an abrupt commencement, great
prostration, profound derangement of the nervous system, and a
peculiar eruption which appears between the third and eighth days, and
which, disappearing at first under pressure, soon becomes persistent,
and in severe cases may be converted into and be associated with true
petechiae. When it proves fatal, it generally does so at or near the
end of the second week. The lesions found after death are not specific
in character, and consist mainly of a marked alteration of the blood,
congestions of internal organs, softening of the heart, and atrophy of
the brain.
SYNONYMS.--Petechial Typhus, Putrid or Malignant Fever, Camp, Jail,
Ship, or Hospital Fever, Spotted Fever, Irish Ague, Contagious Typhus,
Brain Fever, Adynamic or Ataxic Fever, Ochlotic Fever, Catarrhal
Typhus.
The term typhus was first applied by Sauvages in 1760, and afterward
by Cullen, to certain forms of fever, characterized by marked
prominence of the nervous symptoms, to distinguish them from another
group of cases to which they gave the name synochus, and is derived
from the Greek word [Greek: typhos], which literally means smoke, and
which is employed in the treatise on internal affections attributed to
Hippocrates for a similar purpose. According to Murchison,[1]
Hippocrates used the word to define a "confused state of the
intellect, with a tendency to stupor." The appellation typhus,
therefore, as indicating a very prominent symptom of the disease about
to be described, is perhaps the best that could be given to it. It has
been generally adopted by the physicians in England and in this
country to denote this disease, but on the Continent, and especially
in Germany, it is applied also to typhoid fever, the two fevers being
usually designated there as typhus petechialis and typhus abdominalis,
respectively.
[Footnote 1: _A Treatise on the Continued Fevers of Great Britain_, by
Charles Murchison, M.D., LL.D., F.R.S., etc., second edition, London,
1873.]
HISTORY.--As human want and misery and the evils which follow in the
train of war have never been wholly absent from the world, and as
these are the conditions which are now known to be favorable to the
spread, if not to the generation, of typhus fever, it is highly
probable that this disease was the cause of some of the epidemics to
which allusion is made by the sacred and profane writers of antiquity.
Yet their descriptions are too vague to justify us in assuming that
such was positively the {339} case. The records of the first fifteen
centuries of our own era are similarly wanting in details, for, with
the exception of a brief notice of an outbreak of the disease in the
monastery of La Cava, near Salerno, in the year 1083, by Corradi[2] it
may be said to have been practically undescribed before the year 1546,
when Fracastorius[3] published his work, _De Contagionibus et Morbis
Contagiosis_. From the description which this distinguished physician
gives there of the epidemics which prevailed in Verona in the years
1505 and 1508, there can be no doubt that the disease he had the
opportunity of observing was really typhus fever. Not only are the
principal symptoms succinctly described, but its contagiousness and
tendency to early prostration fully recognized. We learn also, from
the same work, that the disease, although previously unknown in Italy,
was one with which the physicians of Cyprus and the neighboring
islands were perfectly familiar. According to the same authority, it
again made its appearance in 1528 in Italy, and from there extended to
Germany.
[Footnote 2: In _Chron. Cavense Annali_, p. 1, 101, quoted in
_Handbuch der Historish-Geographischen Pathologie_, von Dr. August
Hirsch, Stuttgart, 1881.]
[Footnote 3: Quoted by Murchison.]
During the last half of the sixteenth century epidemics of typhus
fever would seem to have been of more frequent occurrence than before
it, since many of the medical authors of this period not only refer to
it very fully, but also give accurate descriptions of the disease.
There is also abundant evidence of the same kind that it frequently
prevailed epidemically in almost every part of Europe during the
seventeenth and eighteenth centuries, following generally in the wake
of famine and of war, and often attaining a high degree of virulence
in besieged towns. The histories of many of these epidemics are
exceedingly interesting, especially those of the so-called Black
Assizes which occurred at different times in several of the towns of
England, and which derived their name from the fact that the disease
was communicated from the prisoners on trial to the judges and other
persons in attendance upon the court; but to give these in detail
would be beyond the scope of this article. Although many of the
authors of these two centuries boldly advocated copious venesection as
the only rational method of treating the disease, there was a not
inconsiderable number who recognized its essentially typhoid nature,
its tendency to early prostration, and the fact that patients
suffering from it bear bleeding badly, as fully as is done by
physicians of the present day. They were also unquestionably quite
aware of the circumstances under which typhus fever generally arises,
for in 1735, Browne Langrish[4] wrote that it originated from "the
effluvia of human live bodies," and that its principal cause was
overcrowding with deficient ventilation, as a result of which "people
were made to inhale their own steams;" and a similar opinion was
expressed a few years later by Sir John Pringle,[5] J. Carmichael
Smyth,[6] and others.
[Footnote 4: _The Modern Theory and Practice of Physics_, by Browne
Langrish, p. 354, London, 1764.]
[Footnote 5: _Observations in Diseases of the Army_, London.]
[Footnote 6: Quoted by Murchison.]
Epidemics of typhus fever have frequently occurred in various parts of
Europe during the present century, although they have, on the whole,
shown a greater tendency than before to confine themselves to the
place in which they first appeared. The most severe of these began in
1846, and after committing great ravages in Ireland extended to
England, and {340} subsequently to the Continent. The disease proved
much more fatal than the sword in the armies of Napoleon in the towns
besieged by him in the early part of this century, and was the cause
of an immense loss of life in the Russian and French armies in the
Crimea after the fall of Sebastopol.
In our own country typhus fever has appeared several times during the
present century, but the outbreaks have rarely attained the magnitude
of epidemics, such as are seen in Europe, and have usually been
distinctly traceable to importation from abroad. It was first met
with, according to Wood,[7] in New England in 1807 and in Philadelphia
in 1812, continuing to lurk, this author says, in the lanes and alleys
of that city until the winter of 1820-21, when, as a student of
medicine, he had an opportunity of studying it. Another outbreak of
the disease occurred in the same city in 1836, and is the subject of
an admirable paper by the late Wm. S. Gerhard.[8] Since then epidemics
of moderate severity have repeatedly occurred at different times in
several of the American cities, and have been described, among others,
by Flint, Da Costa,[9] and Loomis. A large number of cases of typhus
fever (1723), with 572 deaths, were reported to the Surgeon-General's
office during the late Civil War, but doubt has been thrown upon the
correctness of the diagnosis of many of these cases by Clymer[10] and
Woodward,[11] and by other army surgeons, who, as the result of their
investigations of this subject, have reached the conclusion that
typhus did not prevail as an epidemic, however limited, among our
soldiers at depots for returned prisoners of war. A like immunity from
this scourge may be assumed to have been enjoyed by the Confederate
forces, since Joseph Jones,[12] one of the most eminent of their
medical officers, has stated positively that no case of true typhus
fever came under his observation during the war in any army, in any
field hospital, general hospital, or military prison, and that the
experience of all of his associates whose opinions on this question he
was able to obtain, either personally or by letter, was the same. It
is therefore most probable that the cases entered upon the sick
reports of both armies as typhus fever were in almost every case, if
not in all, cases of typhoid fever occurring in scorbutic subjects.
[Footnote 7: _A Treatise on the Practice of Medicine_, by George B.
Wood, M.D., etc., Philada., 1855.]
[Footnote 8: _The American Journal of the Medical Sciences_, February
and August, 1837.]
[Footnote 9: _Ibid._, January, 1866.]
[Footnote 10: _The Science and Practice of Medicine_, by William
Aitken, M.D., Edin.; 3d Amer. ed., p. 462, Philadelphia, 1872.]
[Footnote 11: _Camp Diseases of the United States Armies_, by Joseph
Janvier Woodward, M.D., Philadelphia, 1863.]
[Footnote 12: _United States Sanitary Commission's Memoirs--Medical_,
p. 600, New York, 1867.]
From the foregoing sketch of its history it is evident that typhus
fever has prevailed from time to time in almost all the countries of
Europe. Indeed, it is probable that no one of them has wholly escaped
its ravages, while in others--as, for example, Ireland--it has been
more or less constantly present until within the last few years, when
its visitations have been less frequent as well as less severe. Even
in countries which are popularly supposed to enjoy an immunity from it
there is evidence of an incontrovertible character that it has
occasionally occurred. Such an immunity has been claimed for France,
but in the works of Riverius,[13] {341} Ambrose Pare,[14] and others
will be found descriptions of the disease which leave no doubt upon
the mind of their entire familiarity with it; and Hirsch, in his work
on _Historico-Geographical Pathology_, is able to give references to
several writers who describe outbreaks that have recently occurred
there. The disease has also been observed in Iceland. Typhus fever is
of much less frequent occurrence in the other divisions of the eastern
hemisphere than in Europe. According to Murchison, there are no
authentic records of its having been met in Africa, or, with the
exception of India, in Asia, such as it is seen in England and
Ireland. There are, however, reports of its occurrence in Asia Minor,
Syria, Persia, Egypt, Nubia, Tunis, and Algeria, which Hirsch,[15] on
the other hand, believes place the occasional presence of this disease
in these countries beyond doubt. The same difference of opinion exists
between these two distinguished observers in regard to the accounts
which have been published of typhus fever occurring in Mexico, Central
America, and South America, the latter holding that they are entirely
reliable, the former that the cases described in them were really
cases of malarial or typhoid fever. The disease has never been met
with on the continent of Australia, in New Zealand, or in the valley
of the Mississippi and the States bordering on the Pacific Ocean in
our own country.
[Footnote 13: _The Practice of Physick_, being chiefly a Translation
of the Works of Lazarus Riverius, London, 1678.]
[Footnote 14: _Traite de la Peste, de la Petite Verolle et Rougeolle_,
par Ambrose Pare, Paris, 1568.]
[Footnote 15: _Loc. cit._]
While Hirsch's researches go to show that the tropical zone has not
been so wholly exempt from the visitation of typhus fever as some
authors have asserted, they establish the fact that it is of much less
frequent occurrence there than in the colder portions of the temperate
zone, where the modes of life are certainly much more favorable to its
extension. Natives of warm climates are as liable to be attacked by it
as others upon coming to places where it is prevailing, and in the
Philadelphia epidemic of 1836, which Gerhard[16] has described,
negroes and mulattoes suffered from it more severely than the whites.
[Footnote 16: _Loc. cit._]
ETIOLOGY.--The etiology of typhus fever will be best studied under the
heads Predisposing and Exciting Causes.
PREDISPOSING CAUSES.--It may be stated, generally, that whatever
impairs the health or reduces the strength of an individual, even
temporarily, or acts depressingly on his nervous system, predisposes
him to typhus fever. But there are among the predisposing causes some
which exert a more special influence on its production than others.
Among the more powerful of these is the overcrowding of human beings,
with deficient ventilation. Indeed, there are some authors who
consider that this has been in many cases alone sufficient to occasion
the disease; and although this opinion, as it involves the admission
that it may be generated de novo, is contested by others, there is
great unanimity among authors in attaching great importance to it. Of
the patients admitted into the London Fever Hospital with typhus
fever, a large proportion came from the more crowded districts of the
city. The disease has always been most prevalent in the poorer
quarters of Glasgow, Dublin, and Edinburgh, and when epidemic in
Philadelphia in 1836 it was confined to a portion of the town which
has always been noted for the squalor and misery of its inhabitants.
Among those admitted during that year to the Philadelphia Hospital
were seven negroes, said by Gerhard to {342} be "the entire population
of a cellar." It is probably largely due to the fact that the better
social condition of the poor in this country prevents the degree of
crowding which often exists in European cities that the disease is
comparatively rare here. The effect of overcrowding is of course much
increased by want of cleanliness, either of the person or of the
clothes.
Poverty, not merely from its own depressing influences, but also from
the fact that it leads to overcrowding, is a powerful predisposing
cause of typhus fever. Insufficiency of food, which is one of its many
consequences, by impairing his nutrition and thus diminishing his
vital resistance, renders the individual more susceptible to the
action of the specific cause. Gerhard says that of the patients seen
by him in 1836 a very small proportion came from the better class of
mechanics, and Tweedie[17] and Sir William Jenner[18] state that it is
rare to meet with instances of the disease, except in the case of
medical practitioners and students, among those in comfortable
circumstances. Bateman[19] goes so far as to assert that "deficiency
of nutriment is the principal source of epidemic fever;" and there is
certainly a remarkable coincidence in time between outbreaks of this
fever and seasons of want and distress. But, as Murchison has shown,
destitution is not essential to the production of typhus, for the
Dundee epidemic of 1865 was due to overcrowding of the town, brought
about by the inhabitants of the surrounding country flocking into it
in consequence of labor being unusually abundant and wages good.
[Footnote 17: _Lectures on the Distinctive Character, Pathology, and
Treatment of Continued Fevers_, by Alexander Tweedie, M.D., F.R.S.,
London, 1842; and _Clinical Reports on Fever_, by same author, London,
1830.]
[Footnote 18: _On the Identity or Non-Identity of Typhoid and Typhus
Fevers_, by William Jenner, M.D., London, 1880; also _Lancet_,
November 15, 1879.]
[Footnote 19: _A Succinct Account of Typhus or Contagious Fever of
this Country_, by Thomas Bateman, M.D., F.R.S., London, 1820.]
Similar in its action to the above cause is intemperance. Not only is
the habitual drunkard more likely to suffer from typhus fever than the
temperate man, but a single debauch has been followed by an attack in
individuals who had previously resisted the contagion. On the other
hand, the most rigid temperance will not afford in all cases a
complete immunity from its effects. The debility left by an illness is
also a condition favoring the occurrence of an attack of the disease
in those who are exposed to its exciting cause. Fatigue of all kinds
renders the body less able to resist the causes of disease, and typhus
fever is not an exception to the general rule. Overworked nurses are
specially liable to contract it. The depressing emotions also favor
its occurrence. It has been observed during epidemics that those who
exhibit an excessive fear of the contagion are much more likely to
suffer from it than the cheerful and courageous.
No age enjoys an immunity from the disease. In fact, it is probable
that all ages are equally liable to it. Buchanan[20] has seen it at
the London Fever Hospital in an infant a fortnight old and in a man of
eighty, and attributes the prevailing opinion that children rarely
suffer from it to the fact that they are not often taken to hospitals,
but are retained in their own homes for treatment. Gerhard[21] says
that no children in the asylum attached to the Philadelphia Hospital
were {343} attacked with the disease during the prevalence of the
epidemic there, but the distance of the asylum from the wards in which
the cases were treated was probably the reason of their escaping. In
the few cases which have come under my own observation the patients
were young men, varying in age from twenty-five to thirty-five. The
sexes also suffer from it equally. In some epidemics there may be a
preponderance of one sex over the other, but in others the reverse has
been the case.
[Footnote 20: _A System of Medicine_, edited by J. Russell Reynolds,
M.D., F.R.C.P., etc., vol. i., article "Typhus Fever," London, 1866.]
[Footnote 21: _Loc. cit._]
Occupation, except so far as it brings the individual into immediate
contact with the sick, as in the case of physicians, nurses, and
clergymen, does not predispose to the disease. There would seem also
to be no difference in the susceptibility of the different races to
the contagion. Acclimatization affords no protection from the disease,
as it does in the case of typhoid fever, and change of the habits of
life does not appear to exercise any influence upon the liability to
it. On the other hand, the susceptibility of different individuals,
and of the same individual at different times, varies considerably.
Thus, while in many persons a single exposure to the contagion is
followed by an attack, in the case of an engineer mentioned by
Murchison it did not occur until after fifteen years of continuous
service at the London Fever Hospital. A person who has once suffered
from typhus fever is not likely to contract it again, but this
protection is not complete, as there are a few well-attested instances
of a second attack on record.
The disease prevails most frequently during the winter and early
spring, principally because the cold weather of these seasons leads to
the closing of windows and all other avenues of ventilation, thus
intensifying its exciting cause. Still, some epidemics of great
severity have occurred in the warmer months of the year, as, for
instance, the one described by Gerhard. It is also doubtful if there
is any relation between variations in temperature and the amount of
moisture in the air and the prevalence of epidemics of typhus fever,
although Hirsch regards a low and damp situation as powerfully
predisposing to the endemic and epidemic prevalence of the disease. It
is usually met with in towns on the sea-coast or on navigable rivers,
but it has also been observed frequently in country districts, and
even in regions at a considerable elevation above the level of the
sea.
EXCITING CAUSE.--The principal if not the only exciting cause of
typhus fever is a specific contagion developed in the bodies of the
infected and transmitted from them to the healthy by actual contact,
by fomites, or through the atmosphere. The nature of this contagion is
unknown. A careful study of its peculiarities seems to justify the
opinion that it depends upon the presence of a minute organism in the
emanations given off by the sick, which is capable of indefinitely
multiplying itself in the human body. But this is only an hypothesis,
which rests principally upon the analogy between typhus and some other
diseases, as, for instance, relapsing fever and diphtheria, in which
such a growth is thought to have been discovered, and upon the fact
that the contagious principle whatever it may be, is destroyed by a
temperature over 204 degrees F.
The evidence in favor of the contagiousness of typhus fever is
conclusive, and may be briefly stated as follows: When it breaks out
in a community the disease not only attacks those persons who have
been subjected to the same influence as the sick--as, for instance,
members of {344} their own families, occupants of the same house,
etc.--but also those who have come from healthy localities to visit
them. In fever hospitals it is rare for any member of the household
who has not already had the fever to escape an attack, and the
probability of his suffering is in direct proportion to the intimacy
of his relations with the patients. Thus, the nurses are far more
likely to be attacked than servants whose duties do not take them into
the wards, except those employed in the laundry, who are so often
affected by it that Murchison says it is difficult to find women who
are willing to take the position. The spread of the disease may often
be promptly arrested by the complete isolation of the first few cases,
while free intercourse between the sick and the well is invariably
followed by its extension, not only in the locality in which it first
appeared, but to other localities. But the strongest argument in favor
of its contagiousness is found in the fact that patients taken into a
previously healthy place have frequently become the starting-point of
an epidemic. In this way the disease has often been introduced by
Irish immigrants into the cities on our seaboard, and even into some
of our interior towns.
Actual contact is not necessary for the communication of typhus fever
from the sick to the well. The contagion may be transmitted through
the atmosphere. How far it will be transmitted in this way will depend
upon many circumstances. In a spacious and well-ventilated ward it is
probable that the presence of one or two patients with this disease
does not seriously endanger the safety of the other patients, and that
the only persons who run much risk of contracting it are the
physicians and nurses, who are often compelled in the performance of
their duties to inhale the emanations from the bodies of the sick. At
the Pennsylvania Hospital, where cases of this disease are
occasionally admitted, it has been usual to isolate them by placing
them in a room a few feet distant only from the dining-room of the
men's medical ward and separated from the ward by a short corridor.
The steward of the hospital informs me that during his connection with
it, which extends over a period of more than sixty years, he has never
known the disease to extend to other persons, except on two occasions.
One of these was during the epidemic described by Da Costa, when an
unusual number of cases was received, and when one resident physician
and two nurses contracted the disease. On the other occasion, which
happened during my own term of service in the spring of 1881, a young
Danish sailor appeared to have taken the disease from two British
seamen. As it was ascertained positively that he had not entered the
room in which these two seamen were isolated, and as his bed in the
ward was one of the farthest removed from the room, and he had not
therefore been more or as much exposed to the contagion as the other
patients, it was difficult to understand why he alone of all of them
should have suffered from it. The explanation was, however, found in
the fact that he had been taken over to the women's ward to act as
interpreter for a countrywoman who was not known at the time to be
suffering from typhus fever, and that he had remained there some time
in conversation with her. Murchison and Buchanan both assert also that
typhus fever has never extended from the London Fever Hospital to the
inmates of adjacent houses, even when it was itself one of a row of
houses. If, on the other hand, several patients with typhus fever are
placed in a crowded and ill-ventilated ward, the contagion will then
be found to have {345} acquired so much more virulence that few of the
other patients will escape its effects.
There is also no question that typhus fever may be communicated by
fomites. Numerous instances are on record in which the disease has
been communicated by the wearing apparel and bed-clothes of patients,
and we have already called attention to the frequency with which
laundry-women in fever hospitals are attacked by it. The clothes of
persons who are themselves free from the disease, but who have been in
close attendance upon the sick for some time, are often also the
medium of communication. Indeed, Murchison goes so far as to say that
men who have not changed their clothes and "who have been living in
close, ill-ventilated apartments and on short allowance, may at length
have their garments so impregnated with the poison of typhus as to
communicate it to others without being themselves the subjects of it,"
even if they have not been brought in contact with fever patients. The
disease was communicated in this way, he thinks, in the famous Black
Assize in 1750 by several prisoners to the court that tried them,
although they were themselves free from it. On the other hand, with
proper precautions there is little danger of the disease being
conveyed by physicians to their own families or to other patients.
Some difference of opinion exists as to the stage at which typhus is
most contagious. Many authors believe that it is more infectious
during convalescence than at any other time, and base this opinion
upon the fact that the removal of fever patients to the convalescent
ward is very often followed by the occurrence of the disease among its
other occupants; but this is probably due, as Murchison suggests, to
the patients being allowed at this time to wear their own clothing,
which has not been thoroughly disinfected. It is much more likely that
the disease is more contagious during the stage when the febrile
symptoms are most marked than during either the stage of convalescence
or that of invasion. It would appear also, from the observations of
Dr. Gerhard and others, that dead bodies do not readily communicate
the contagion or that the contagious principle is easily counteracted
after death. Still, there are several well-authenticated cases on
record in which individuals have unquestionably contracted the disease
from dissecting the bodies of patients dead from this cause.
A question of great interest naturally arises here, as to whether or
not typhus fever ever occurs except as the consequence of exposure to
a previous case of the disease. Is it, in other words, ever generated
de novo? Authorities are divided upon this point, many contending that
an independent origin is impossible, and others that it may
occasionally arise in this way. Among the latter is Murchison, who
adduces in support of the position he takes several instances in which
poverty, with overcrowding and deficient ventilation, appears to have
been the only cause of extensive outbreaks of the disease, as in the
case of the Black Assize already alluded to. These cases the opposite
party explain by assuming that the germs of the disease are capable of
lying dormant for a long time until roused into activity by favoring
circumstances. If the disease is caused, as we have shown there is
good reason to believe it is, by the presence of a minute organism,
this view does not seem to be untenable. Pasteur has demonstrated that
the germs of the splenic fever of some of the lower {346} animals may
be deprived of their virulence by cultivation in appropriate liquids.
If their virulence is diminished under certain circumstances, the
assumption does not seem unwarrantable that under others it may be
increased, and if we may draw this conclusion in regard to one form of
microscopic growth, we may do the same for others; and the hypothesis
is therefore not an unreasonable one that the typhus germ needs the
atmosphere engendered by overcrowding for it to acquire the power to
produce the disease.
PERIOD OF INCUBATION.--The period of incubation of typhus fever
appears to vary considerably in length, but is usually about twelve
days. In some cases the interval between exposure to the contagion and
the occurrence of the first symptoms of the disease is asserted to
have been considerably longer, and in one instance as long as
thirty-one days; but it is probable that there has been in most, if
not in all, of these cases a second exposure which has been
overlooked. On the other hand, it is said to have followed at once
upon exposure, as in cases reported by Gerhard, in one of which a
nurse inhaled the breath of a patient whom he was shaving, and in an
hour afterward was taken with cephalalgia and ringing in the ears,
which were immediately succeeded by the other symptoms of typhus. In
this and other similar cases which are on record it is difficult to
exclude the possibility of a previous infection. In a case, however,
reported by Murchison there would seem to be no reason to suspect that
any such previous infection could have taken place, as the patient,
the matron of an orphan asylum where there was no typhus, was taken
ill immediately after opening a bundle of clothes which a child had
brought with her from a fever hospital, and which had not been
thoroughly disinfected.
SYMPTOMATOLOGY.--It will facilitate the study of typhus fever to give,
in the first place, as most of the systematic writers on fever have
done, a brief clinical sketch of the disease as it ordinarily occurs,
and then afterward to consider its leading symptoms in greater detail.
GENERAL DESCRIPTION.--An attack of typhus fever is sometimes preceded
for a few days by prodromata, such as a feeling of malaise,
indisposition to exertion, pain in the head and limbs, anorexia, and
vertigo; but it oftener begins abruptly with a slight chill, or more
rarely with a decided rigor. This is followed in a short time by
headache, by a marked rise of temperature, and by an increased
frequency of pulse and respiration. Nausea is also occasionally
present, and less frequently vomiting. The tongue is at first moist
and covered with a thin whitish fur, but soon becomes dryish, and its
coating is apt to assume a brownish appearance in a day or two. With
these symptoms there are loss of appetite, great thirst, constipation,
a dull, heavy expression of countenance, a dark, dusky hue of the
face, and injection of the conjunctivae. Mental confusion is early
observed, so that, although the patient may be able to answer
questions correctly when thoroughly roused, it is readily seen that
his mind is working with difficulty. The sleep is very often disturbed
by dreams, so that he awakes from it unrefreshed. Prostration and loss
of muscular power are so decided from the very beginning of the
disease that the patient is obliged usually to take to his bed at
once, and it is much rarer to meet with walking cases of the disease
than in typhoid fever. The urine is dense, scanty, and high-colored.
{347} Usually, about the fourth day of the disease the characteristic
eruption of typhus fever makes its appearance. It consists of numerous
spots of irregular form with ill-defined margins and of a dark red or
purplish color, occurring singly or in groups, and varying in size
from that of a pin's point to two or three lines in diameter. They
disappear at first under pressure, but in twenty-four hours become
persistent, and in severe cases may be converted later into petechiae.
Besides this eruption there is another which consists of a faint,
irregular dusky red, subcuticular mottling. The two eruptions together
constitute the mulberry rash of Jenner, and have been variously
described by different authors under the name of measly or
morbilliform rash.
As the disease advances the prostration becomes greater and the pulse
grows weaker. The tongue becomes dry and brown and trembles when
protruded. Later, it is so dry and contracted that it can scarcely be
put out of the mouth. Sordes collect about the teeth and lips, and the
surface exhales a peculiar odor. The headache grows more severe or
gives place to delirium, which may at first be active and violent, and
then pass into the low and muttering form, or the delirium may be of
the latter variety from the start. The sleeplessness of the early
stages may continue, and the condition known as coma vigil not
infrequently supervenes. The delirium is usually followed by stupor,
which is more or less profound in accordance with the severity of the
case, and which is accompanied by all the symptoms which characterize
the so-called typhoid state, such as subsultus tendinum, picking at
the bed-clothes, slipping down in bed, retention or incontinence of
urine, and sloughing of the parts exposed to pressure. In this
condition the temperature, although usually still considerably above
normal, is lower than during the first week of the disease.
Meanwhile, the issue remains in doubt, and may continue uncertain for
several days before any improvement in the symptoms can be observed,
or, the stupor passing into coma, the case may speedily terminate in
death. When death is the result, it usually takes place about the
close of the second week or a little later, but it may occur earlier
in consequence of the violence of the fever, or, when due to a
complication, may be postponed until after the end of the third week.
Fortunately, however, recovery is the rule in this disease. The
beginning of convalescence is often as abrupt as that of the attack
itself. The temperature will often be found to have fallen to the
normal or below the normal, the pulse and respiration to have returned
to a healthy condition, and all confusion of the intellect to have
disappeared in the course of a few hours. Occasionally, however, its
approach is more gradual, and a slight fall in temperature and a
corresponding improvement in the other symptoms may be observed before
it actually occurs. Diarrhoea, an excessive secretion of urine, with a
tendency to the deposition of urates, and moderate sweating, often
take place simultaneously with the cessation of the fever, and were
formerly regarded as critical discharges. The return to health is
usually rapid, and very rarely retarded by the occurrence of
complications or relapses, as in typhoid fever. The disease itself
leaves no tendency to any other disease.
DESCRIPTION OF SPECIAL SYMPTOMS.--The appearance of a patient with
typhus fever is pathognomonic, and is often alone sufficient to enable
{348} a physician or nurse familiar with it to recognize the disease
when brought in contact with it. The surface generally is congested;
the face is flushed, and in bad cases dusky red or even livid in hue;
the expression is dull and vacant, except during delirium, when it may
be wild or even fierce; the conjunctivae are injected, the eyes
watery, and the teeth encrusted with sordes. The skin is generally hot
and dry, except toward the close of bad cases, when it may be cool and
bathed in a profuse sweat.
The symptoms connected with the nervous system are among the most
characteristic of the disease, and of them none is more marked than
prostration. It shows itself early, the patient usually taking to his
bed immediately after his seizure or within a few days of it. It is
much rarer than in typhoid fever to meet with walking cases of typhus,
but Buchanan[22] mentions that patients with the rash already out upon
them do occasionally present themselves at the out-door department of
the London Fever Hospital. It generally increases as the disease
progresses, and is often accompanied by a tendency to syncope. It may
attain such a degree that the patient is unable to turn himself in bed
or to help himself in any way. Among the most distressing sensations
which attend this condition of excessive feebleness is a feeling as if
he were sinking into the earth with nothing to support him. Headache
is also an early symptom. It is often observed among the prodromata of
the disease, and when these are absent supervenes directly after the
chill. It is usually frontal, but may be diffused. It is generally
dull and heavy, but is sometimes acute, and may be accompanied by a
tendency to vertigo, increased by sitting up, and by pains in the back
and limbs. It becomes more severe with the progress of the disease
until the occurrence of delirium, when it is, as a rule, less
complained of. With the headache there is generally some dulness of
intellect, except in mild cases. This may be slight at first, and may
continue so throughout the whole course of the attack, exhibiting
itself principally in some confusion as to dates. In more severe cases
it is much more marked, and may finally pass into actual stupor. On
the other hand, it may be entirely absent, even in severe attacks, as
in a case reported by Da Costa and in some cases recently observed by
myself. It is usually soon replaced by delirium, which may be low and
muttering or wild and noisy, the former being the more common.
Delirium is said to occur most frequently among the educated classes
and those oppressed with care and anxiety, but is not rare among those
who occupy a lower position in the social scale, especially the
intemperate. It is, as a rule, most marked at night, and in mild cases
may occur only at that time or upon waking in the morning. When the
delirium is active the patient may shout and scream, or leave his bed
and attempt to throw himself from the window, being endowed apparently
for the moment with strength sufficient to enable him to commit these
acts of violence. After the paroxysm is over he sinks back in bed
exhausted. The confusion of intellect or delirium continues in bad
cases until death supervenes or until the establishment of
convalescence. Indeed, the mental disturbance does not always end with
the latter, and it is not rare for feebleness of intellect to persist
for some time after the patient has in other respects regained his
usual health, and in a few cases insanity has followed an attack of
typhus fever. Among the most {349} formidable of the symptoms of
typhus are convulsions, which are fortunately of infrequent
occurrence.
[Footnote 22: _Loc. cit._]
The patient generally suffers from wakefulness, except during the
first few days. When sleep is obtained it may be unrefreshing or
broken and disturbed by dreams. In other cases the opposite condition
of somnolence may be present. Occasionally, after having apparently
slept for hours, he may deny having been asleep at all. This
condition, which constitutes the coma vigil of Chomel, is entirely
distinct from that described by Jenner under the same name, in which
the patient lies with his eyes wide open, gazing into vacuity, his
mouth only partly closed, his face pale and devoid of expression, and
which is invariably fatal. Muscular tremor is more or less present in
all cases of the disease, and in bad cases may be a prominent symptom.
The disease, when this symptom is marked, especially if there is at
the same time low, muttering delirium and a moist skin, presents a
considerable degree of resemblance to delirium tremens. There is very
often intolerance of light, tinnitus aurium, and loss or perversion of
the senses of taste and smell. Deafness is also not uncommon, and is
regarded by many authors as a favorable symptom. In bad cases, in
addition to subsultus tendinum, there are carphologia, incontinence or
retention of the urine, and paralysis of the sphincter ani.
Some discrepancy is found to exist in the statements of different
authors in regard to the temperature curves of typhus fever. They all
agree, however, in assigning them certain characters, the knowledge of
which is often of great assistance in diagnosis. One of these is a
rapid rise of temperature immediately after the invasion of the
disease. Wunderlich[23] asserts that he has observed a temperature of
104.9 degrees F. on the evening of the first day, and Lebert has found
it as high as 106.4 degrees F. on that of the second. Such
temperatures, occurring so early in the disease, must be infrequent,
as Murchison has never met with them. Usually, the temperature attains
its maximum on the third or fourth day. The maximum is about 104
degrees or 105 degrees F. Murchison says it scarcely ever reaches 106
degrees, except in children, in whom it rarely is as high as 107
degrees, but Lebert states that he has known it to be as high as 107.8
degrees. On the other hand, it may never exceed 103 degrees, even in
fatal cases. When the maximum is attained early in the disease there
may be for several days, or until defervescence takes place, very
little variation in the evening temperatures, but, as a general rule,
they are slightly less elevated in the second than in the first week.
This usually occurs from the tenth to the fourteenth day, but it may
be postponed until the eighteenth, or even until much later. In some
cases on the day before the crisis a slight fall, and in others a
considerable fall with a subsequent rise of temperature, are observed.
Defervescence is often very rapid, the temperature falling five or six
degrees in the course of twelve hours. A true lysis is rarely
observed. The occurrence of a complication in the course of a disease
will not only cause a decided rise of temperature and a modification
of the temperature curve, but may also postpone defervescence beyond
the usual time. Not infrequently the thermometer indicates subnormal
morning temperatures with slight evening rises for several days after
the crisis, unless complications arise, {350} when fever of the hectic
type may occur. A very slight cause will also often produce a
considerable, although temporary, elevation of temperature in this
condition. The morning remissions are less decided than in typhoid
fever, especially in the first week. As a rule, they do not exceed 1
degree, but Lebert lays stress upon the fact that in the same curve
variations from 0.3 degrees to 1.8 degrees and from 0.6 degrees to 2.1
degrees often occur. Cases which terminate fatally are generally
characterized by high fever, with absence of the morning remissions,
which may continue uninterruptedly through the second and even the
third week. During the death-agony there is frequently a rise of
temperature of two or more degrees. A very high temperature in the
first week is often the forerunner of severe cerebral symptoms in the
second, and a fall of temperature unaccompanied by an improvement in
the other symptoms is not always indicative of the approach of
convalescence.
[Footnote 23: _On the Temperature in Disease_, New Sydenham Society's
translation, London, 1871.]
Anorexia is generally present in typhus fever from the beginning of
the attack, and may persist until its close. It is not, however,
usually attended by the same repugnance for food as in other fevers.
Patients can generally be persuaded at first to take nourishment.
Indeed, Dr. Gerhard asserts that the negroes who fell under his care
in 1832 frequently asked for solid food. Nausea and vomiting are rare
symptoms; the latter may occur late in the disease, and then, not
infrequently, is caused by irritation of the brain. Thirst is present
in all cases. In the later stages of the disease, when the senses are
blunted, water may not be asked for, although urgently called for by
the condition of the system. The bowels are, as a rule, constipated in
this disease. The exceptions to this rule are, however, more numerous
than is usually thought. Wood[24] says that he has frequently seen
diarrhoea in typhus fever when it occurs in recently-arrived
immigrants. Da Costa[25] mentions that it has occurred in several of
the cases which have come under his care, and Buchanan[26] says that
he has observed it in at least one-third of the patients admitted into
the London Fever Hospital in recent years. When there is no diarrhoea
the stools are of normal color and consistence. When it exists they
are watery and usually dark greenish in color, and never present the
peculiar ochrey-yellow appearance seen in typhoid fever. They are said
to be alkaline in reaction. Tympanites is rare in typhus fever. It may
be present in cases in which there is diarrhoea, and may then be
associated with gurgling in the bowels, but rarely attains the degree
common in typhoid fever. Gurgling when present is, moreover, not
confined to the right ileo-caecal region, but may be produced in
different parts of the abdomen by pressure. There may also be
tenderness in the epigastric and hepatic regions, but the enlargement
of the spleen so constantly observed in typhoid is generally wholly
wanting in this fever.
[Footnote 24: _Loc. cit._]
[Footnote 25: _Loc. cit._]
[Footnote 26: _Loc. cit._]
The tongue in the beginning of the disease is covered with a thin
whitish fur and is moist, and may continue so throughout in mild
attacks. Generally, however, it soon becomes dryish, and in bad cases
absolutely dry, and is tremulous when put out of the mouth, while its
coating becomes thicker and brownish, and finally brown, or even black
and cracked. It is rare to see the tongue itself fissured as in
typhoid fever. Less frequently it remains red, smooth, and glazed
throughout the attack. Occasionally the tongue is contracted in bulk,
and it may {351} then, in consequence of its dryness and that of the
mouth, be impossible to protrude it. Sordes frequently collect about
the gums and lips in severe cases.
The pulse is usually increased in frequency in typhus fever, and
varies from 100 to 120, but in many cases it never rises above 90, and
in very severe cases it may be as high as 150. This increase is
observed from the beginning, and generally bears some proportion to
the severity of the fever; but toward the close, when the prostration
is great, the pulse may continue frequent even after a fall in
temperature has taken place, and is always more frequent when the
patient is sitting up than when he is lying down. Occasionally,
however, a very slow pulse is associated with symptoms of great
severity. When this association occurs the prognosis is grave. In the
young and robust the pulse may be full and bounding, but it is more
often compressible or small and weak. It is not so often dicrotic as
in typhoid fever. There is sometimes, according to Lyons, a singular
want of uniformity in the force and volume of the arterial pulse in
different parts of the system, and there may be but one pulsation at
the wrist for two of the heart. A very sudden fall in the frequency of
the pulse without an improvement in the other symptoms is not a
favorable indication, as it may be due to impaired innervation or to
degenerative changes in the muscular tissue of the heart. Usually the
beginning of convalescence is marked by a gradual fall of the pulse.
Later it may fall to 50 or below it, and continue slow for some time,
just as it does in typhoid fever.
The heart shares in the general enfeeblement of the system. In severe
attacks the impulse soon becomes weak and diffused, and may be
entirely absent for some time even in cases which eventually terminate
in recovery. Stokes long ago called attention to an alteration in the
systolic sound of the heart which he taught indicated the urgent
necessity for the administration of stimulants. This sound is observed
in the progress of the disease to become shorter and less distinct,
and finally inaudible, while the second sound is unaffected. This
modification of the heart-sounds is always an accompaniment of great
prostration. Occasionally the first sound is replaced by a functional
murmur.
The characteristic eruption of the disease is generally preceded by
the fainter subcuticular mottling already alluded to, and usually
appears between the fourth and seventh days, but it has been observed
as early as the third day, and, on the other hand, its appearance is
said by Wood to have been delayed until the thirteenth. It consists of
minute spots with ill-defined margins, varying in size from that of
the point of a pin to two or three lines in diameter, irregular in
shape, slightly elevated above the skin at first only, and occurring
singly or in groups. They are pinkish in color, and disappear readily
under pressure when first observed. They may then, as Gerhard and
others have pointed out, present a considerable resemblance to the
rose-colored spots of typhoid fever. In the course of twenty-four
hours they become brownish, and later, when the attack is a severe
one, livid in color. In malignant or even severe cases they are
frequently converted into true petechiae. They do not appear in
successive crops, but usually require a couple of days for their full
development. Their duration is variable. In mild attacks they may
disappear in the course of a few days, but in bad cases often {352}
persist until after convalescence, and are recognizable after death.
They are confined to no part of the body, but appear usually earliest
and most abundantly upon the folds of the axilla and upon the abdomen.
Occasionally, however, they are first observed upon the wrists, and in
some cases are more numerous upon the arms and legs than upon the
body. They are rarely found upon the neck and face, but in children
the latter may be so much covered by them that the disease may be
readily mistaken for measles. They present some resemblance to
flea-bites, but the latter may be easily distinguished from them by
the minute discoloration in the centre left by the puncture of the
insect. The eruption is oftenest wanting in young subjects. It is
usually, but not invariably, most copious in severe attacks, but cases
have ended fatally in which it was wholly wanting from beginning to
end. Its color is also to a certain extent an index of the severity of
the attack; the darker and more livid it is, the graver the prognosis.
In malignant cases or those complicated by scurvy, in addition to the
petechiae above referred to, purpura spots and vibices are not
infrequently observed. Some authors assert that the eruption is
followed by a slight desquamation of the cuticle, but this is denied
by others. Sudamina occasionally occur, but they are much rarer than
in typhoid fever. The blue spots described by the French under the
name of taches bleuatres are also sometimes met with.
A very disagreeable odor is exhaled from the bodies of typhus-fever
patients after the first week. Although readily recognizable by those
who have once perceived it, it is difficult to describe. Gerhard spoke
of it as pungent, ammoniacal, and offensive, especially in fat,
plethoric individuals, and believed that those patients who presented
this symptom in the highest degree were most likely to communicate the
disease to others. Murchison has also expressed the opinion that the
typhus poison is associated with this odoriferous substance. Others
have compared the odor to the smell given off by rotten straw, the
urine of mice, and various other substances. Wood says that he has
often perceived the same odor in badly-ventilated rooms in which a
number of people have been shut up together for some time.
The sensibility of the skin in cases in which the stupor is not so
great as to render the patients insensible to all external impressions
is said by some writers to be much increased. There is also
occasionally so much tenderness in the epigastric region as to give
the impression at first to the attendant that there is inflammation of
the stomach or liver.
Pulmonary complications are quite frequent in typhus fever, and, as
they often come on insidiously and give no evidence of their presence
by cough, expectoration, or even more hurried breathing, that is often
seen in uncomplicated cases, it is well to make it a rule to examine
the chest of every patient with this disease. To do this thoroughly it
is not necessary to make him sit up, which, where great prostration
exists, is often attended with danger. If he be turned gently upon his
side the auscultator will usually have no difficulty in ascertaining
the precise condition of his lungs.
The respiration is usually much more frequent in this disease than in
health. Even in cases in which there is no disease of the lungs it is
often as high as 30, and in cases in which there is such a
complication it may be 60. Its frequency is generally proportional to
the severity of {353} the fever. On the other hand, in grave cases in
which cerebral symptoms are predominant it may be reduced in frequency
much below the normal. When coma or profound stupor exists, it may
become jerking and spasmodic, or even simulate the stertorous
respiration of apoplexy. Bronchitis, if not of such constant
occurrence as in typhoid fever, is certainly not rare. It usually
occurs early in the attack, and makes itself known by the presence of
sonorous and sibilant rales, which give place later to mucous rales.
Expectoration is often absent in these cases; where it exists the
sputa are either mucous or muco-purulent. In mild cases no further
lesion of the lungs occurs. When the attack is more severe hypostatic
congestion is very likely to supervene. This is a condition which is
often attended with danger, and which frequently, as has been said
already, escapes recognition unless the chest be thoroughly examined,
when dullness on percussion, feeble respiration, and subcrepitant
rales may readily be detected. Occasionally the physical signs
indicate the existence of pneumonia. This, when it occurs in the
course of this disease, is always of low grade, and is attended by the
expectoration of mucus streaked with blood.
The breath of the typhus-fever patient has a very disagreeable odor,
not unlike that given off from the body, and is said by Murchison to
contain an increased amount of ammonia.
According to Parkes,[27] the changes in the urine are those usual in
ordinary pyrexia. During the fever it is generally diminished in
quantity, dark in color, and of high specific gravity. It contains an
increased amount of urea and of uric acid, the latter of which is not
infrequently spontaneously precipitated. Sulphuric acid is also in
excess. On the other hand, the chlorides are diminished in amount or
entirely absent. This diminution cannot be ascribed to a decrease in
the quantity ingested, for when they are administered with the food
they are not found to be eliminated by the kidney. The amount of
phosphoric acid does not appear to be affected by the disease. The
urine is acid in reaction at first, but its acidity soon diminishes,
and it may become alkaline toward the close of bad cases. It may also
contain albumen, or even blood, the former being present oftenest in
cases characterized by high temperature. According to Da Costa,
tube-casts are more often present than absent in severe cases. Those
seen by this observer were either coated with rather opaque epithelial
cells, many of which were finely granular or covered with granules,
which, when tested with reagents, were sparingly soluble in acetic
acid, and which with very high magnifying powers did not present the
round shape of oil, and were probably the urinary salts collected in
the tube-casts. The crisis is sometimes marked by a copious deposit of
urates. During convalescence the urine is usually increased in
quantity, is pale and limpid, and of low specific gravity, and is
found to contain the chlorides in gradually increasing quantity.
[Footnote 27: _The Composition of the Urine, etc._, by Edmund A.
Parkes, M.D., London, 1860.]
VARIETIES.--Many of the varieties of typhus fever recognized by
authors--as, for example, jail fever, ship fever, camp fever, and
hospital fever--really differ in nothing but name and the
circumstances under which the disease has arisen. Others are mere
modifications of it, due to the predominance of one symptom or of a
certain set of symptoms or to the intercurrence of a particular
complication, and likewise do not {354} need a full description here.
To this latter class belong the inflammatory typhus, the nervous or
ataxic typhus, the adynamic typhus, and the ataxo-adynamic typhus of
Murchison. The first variety occurs in young and robust subjects, and,
it is also said, in persons of the upper class. It is characterized by
high fever, intense headache, and active delirium. In the second
variety the nervous symptoms, such as delirium, somnolence, stupor,
and muscular tremblings, are the most prominent. The most marked
feature of the third variety is the excessive prostration, which is
shown in the feebleness of the heart's action and the loss of muscular
strength and of control over the sphincters. In this form the eruption
is dark colored. Purpura spots and vibices also are very apt to
appear, and even hemorrhages from the gums, nose, or other parts to
occur. In the ataxo-adynamic form the symptoms of the ataxic and those
of the adynamic form are found united. In addition to these there are
certain other varieties, arising from differences in degree. These
differences are sometimes owing to diversities in the constitution and
habits of the patient, sometimes to variations in the character of the
epidemic, and are sometimes not readily explainable. One of these is
the mild form, in which the symptoms are those of moderate fever, and
in which the disease may run its course in seven days. In this form
the temperature may never rise above 102 degrees F., the eruption be
absent or very scanty, and the characteristic stupor or dulness be
wholly wanting. Unless complications arise recovery invariably takes
place. A walking form of typhus fever, as has already been said, is
much rarer than of typhoid, but it does sometimes occur, Dr. Buchanan
having often seen the eruption out upon patients who have walked to
the London Fever Hospital to seek admission. In this form the disease,
however, does not always run a mild course, as alarming prostration is
very apt to come on later in its course. Another variety, the abortive
form, has been described by authors. In this an individual, in due
time after exposure to the contagion, may present all the
characteristic symptoms of typhus fever, but the disease, instead of
running its usual course, may terminate abruptly with a critical
discharge of some kind. This form occurs during epidemics, and is
analogous to the abortive attack of scarlet fever or some other
diseases which are occasionally met with. On the other hand, a very
severe form, the typhus siderans of authors, also sometimes occurs. In
this variety the temperature rises rapidly, and soon attains its
maximum; there are frequent pulse and respiration, severe headache,
and early delirium and stupor. The mortality in this form is very
great. Very frequently death takes place so rapidly as often to leave
the physician in some doubt as to the nature of the disease in those
cases in which exposure to the contagion cannot be positively traced.
COMPLICATIONS AND SEQUELAE.--The complications of typhus fever often
exercise a decided influence upon the course of the disease, for they
not only retard convalescence, but are often the immediate cause of
death. Their early detection, therefore, becomes a matter of the
greatest importance. They will be found to vary in different years,
one epidemic being characterized by complications which are entirely
wanting in the next. Among the commonest of them are several different
conditions of the respiratory organs. Bronchitis, if not quite so
frequent as in typhoid fever, occurs in a large number of cases. It
may come on at any stage {355} of the disease, either immediately
after the beginning of the attack or in its course, or not until
convalescence. In cases accompanied by prostration mucus may
accumulate in the bronchial tubes, and be the cause of the patient's
death by preventing the due aeration of the blood. It would seem to be
an especially frequent complication in Ireland, and it is rather
surprising that so acute an observer as Graves appears not to have
been aware of its real relation to typhus, and speaks of it as if it
were a predisposing cause. "Nothing can be more remarkable," he says,
"than the facility with which a simple cold, which in England would be
perfectly devoid of danger, runs into maculated typhus in Ireland, and
that, too, under circumstances quite free from even the suspicion of
contagion; in truth, except when fever is epidemic, taking cold is its
most usual cause." A much more serious complication than bronchitis is
the form of pneumonia already alluded to as liable to occur in the
course of typhus. This may often occur so insidiously that it may be
considerably advanced before its presence is even suspected; hence the
necessity for examining carefully the lungs of every patient with this
disease who comes under our care. Generally, however, it makes itself
known by giving rise to rapid breathing and great lividity of the
surface, but, as has already been said, both of these symptoms may
exist in cases in which there is no chest complication. This
pneumonia, if it does not immediately prove fatal, may, by becoming
chronic, retard the convalescence. It occasionally is followed by
gangrene, and sometimes by phthisis, which may then run a very rapid
course. Phthisis is, however, a much less frequent sequela of typhus
than of typhoid fever. Pleurisy may also complicate typhus fever, but
it is much more rarely met with than pneumonia.
Perhaps next in frequency to pneumonia and bronchitis are diseases of
the kidneys. These are very serious complications, whether they
antedate the fever or have occurred in its course. Careful examination
of the urine will generally lead to the discovery of a small amount of
albuminuria in bad cases, but this is fortunately, in the majority of
them, only temporary. The urine should, however, always be re-examined
before the discharge of the patient, as there is good reason to
believe that many otherwise inexplicable cases of chronic albuminuria
have originated in an attack of typhus. The presence of albumen and of
casts in the urine of a patient apparently convalescent from this
disease should therefore make us careful in our prognosis as to his
future health. The occurrence of diarrhoea may also very seriously
affect the patient's chances of recovery. Dysentery has also been
observed in certain epidemics in Ireland, and is not infrequent when
the disease breaks out in besieged towns or when it occurs in summer.
In grave cases or those complicated with scurvy the blood may be so
broken down as to escape readily from the vessels. Under these
circumstances, in addition to the purpura spots beneath the skin, we
may have epistaxis, haemoptysis, haematemesis, intestinal hemorrhage,
or hemorrhage from any other part. Erysipelas, too, may be a
troublesome complication, for not only does it exhaust the strength,
but, when it invades the mucous membrane of the larynx, as it
sometimes does, it may prove rapidly fatal by producing oedema of the
glottis. Degeneration of the muscular structure of the heart may also
take place. This gives rise to a slow and feeble pulse and to a
disposition to syncope. Bed-sores are not so frequent as in typhoid
fever. They {356} do, however, sometimes occur, as does also gangrene
of the toes and of other parts not subjected to pressure.
Less common complications are jaundice, peri- and endo-carditis,
meningitis, local and general paralyses, cancrum oris, a diffuse
cellular inflammation ending in purulent infiltration, and
inflammatory swellings of the glands, or buboes. The salivary
glands--and especially the parotid gland--are very apt to be affected
by this inflammatory swelling. This occurs rapidly, is very tender,
and in most cases soon runs on to suppuration, although it
occasionally in children spontaneously subsides. It may occur at any
time during the course of the fever, or not until convalescence, and
sometimes affects the glands of both sides of the face. These buboes
form a connecting link between typhus fever and the Oriental plague,
and Murchison says that the distinguished Egyptian physician Clot Bey,
on seeing some cases of the former disease complicated with parotid
swellings, declared that in Egypt they would be regarded as examples
of the latter.
Many of the above-named complications may occur also as sequelae, and
in addition to these we may have pyaemia, giving rise to purulent
collections in the joints and phlegmasia alba dolens. The last named
is not in itself serious. Its chief danger is from the breaking down
of the clot and the subsequent occurrence of embolism.
Menstruation is said not to be uncommon in the early stages of typhus
fever, and may be so profuse as to greatly increase the prostration or
even to cause death. According to Murchison, miscarriage does not
inevitably occur when pregnant women are attacked with the disease,
and if it does occur it is not necessarily fatal to either mother or
child.
POST-MORTEM APPEARANCES.--Emaciation when death has occurred early in
the course of the disease, and is due solely to the violence of the
fever, is usually not well marked, but in those cases which have been
protracted through the intercurrence of complications it may sometimes
reach an extreme degree. Bed-sores, except under the circumstances
just mentioned, are also rare. Rigor mortis is generally not well
developed, and is of short duration. In a few cases it would seem,
however, to have been well marked. The typhus maculae are persistent
after death, and so are any purpura spots and vibices which may have
been present during life, but the subcuticular mottling usually
disappears. The skin of the dependent portions of the body is
discolored by the settling of blood in it, and putrefactive changes
are apt to set in rapidly.
The only constant lesion observed is a profound alteration of the
blood, which is darker in color and abnormally fluid. If clots are
found at all, they are large, soft, and friable. The fibrin is
diminished in amount. In the early part of the disease the red
blood-corpuscles are said to be slightly increased in number, but
later they are diminished, and under the microscope are observed to be
crenated and not to form themselves readily into rouleaux. The white
corpuscles are increased in number. No accurate chemical examination
of the blood appears to have been made. Many of the post-mortem
appearances which have been described as characteristics of typhus
fever are really the consequence of this abnormal condition of the
blood.
The respiratory organs generally present evidences of disease; the
lesions of laryngitis, bronchitis, pneumonia, hypostatic congestion of
the {357} lungs, and pleurisy have all been observed after death from
typhus fever. Usually, the traces of previous inflammation of the
larynx are but slight; in a few cases, however, ulceration has been
found, but the ulcers are stated to be always minute and superficial.
Ulcers are also occasionally found in the bronchi, and frequently
indicate by their appearance the pre-existence of a much higher grade
of inflammation. The bronchial mucous membrane is, however, oftener
merely reddened and softened and covered with a tenacious frothy
secretion. True pneumonia is of infrequent occurrence as compared with
that of hypostatic congestion of the lungs, but it nevertheless does
occur, and may be of either the catarrhal or croupous variety. When
pleurisy exists, it is usually accompanied, according to Murchison, by
purulent effusion into the pleural cavity. On the other hand, Lebert
says the variety of inflammation of the pleura oftenest met with is
the plastic. The intestines present no constant lesion. Gerhard says
that in fifty examinations there was but in one case, and that
doubtful in diagnosis, the slightest deviation from the natural
appearance of the glands of Peyer. In a few cases the Peyer's patches
have been found more prominent than usual, but not more so than they
are in measles and in some other diseases. Lebert alone of recent
authors makes a contrary statement. In an epidemic at Breslau, he
says, the solitary glands, as well as the patches of Peyer, were the
seat of small, isolated, and superficial ulcers, which were usually
situated in the vicinity of the ileo-caecal valve. The mesenteric
glands are generally unaffected, but in the Breslau epidemic just
referred to they were not infrequently found moderately swollen. In
cases in which dysentery has occurred as a complication the
characteristic appearances of the disease will of course be observed,
as well as those of typhus fever. The spleen is generally softened and
slightly enlarged. The enlargement is not, however, always present, as
Gerhard found it in one only out of every five or six of the cases
which he examined. Extravasations of blood into its structure are
occasionally met with. The liver is usually congested, somewhat
enlarged, and frequently under the microscope presents the appearances
of commencing fatty degeneration. The kidneys often present
unmistakable signs of renal disease in the swollen granular and more
or less fatty condition of their gland-cells according to the duration
of the disease. The muscles are darker in color than in health. Under
the microscope they are found to have undergone the peculiar granular
or waxy degeneration described by Zenker, and which have been fully
referred to in the article on typhoid fever. Extravasations of blood
are occasionally found in them, which may soften and form
pseudo-abscesses.
Other post-mortem appearances which are met with less frequently than
those above detailed are inflammation, and even ulceration, of the
mucous membrane, of the bladder, inflammation of the salivary gland,
peritonitis, and congestion of the pancreas and of the stomach.
The muscular tissue of the heart is generally softened and easily
torn. It is not, however, as stated by some authors, invariably so,
for in several cases in which it was examined by Da Costa it had
undergone this change in one case only, in which there was no reason
to suspect previous disease of the heart. The alteration is similar in
kind to that which takes place in the voluntary muscles. An effusion
of serum, which may be of a deep-red color from the transudation of
the coloring matter of the blood, is {358} sometimes found in the
pericardial sac, as are ecchymotic patches upon the surface of the
heart. The endocardium may be stained from the imbibition of blood. On
the other hand, endo- and peri-carditis are excessively rare.
Notwithstanding the severity of the cerebral symptoms in typhus fever,
there are few or no important changes found in the brain or its
membranes after death. The sinuses are occasionally filled with dark
fluid blood, and the appearances of congestion of the brain are
sometimes present. In other cases there may be an increased amount of
serum beneath the arachnoid and into the lateral ventricles, but not
more than is often seen after death from other causes. Very rarely a
slight film of hemorrhage has been found in the cavity of the
arachnoid, and sometimes also the evidences of non-inflammatory
softening of the brain. Actual inflammation of the meninges has only
been detected in a very few cases. There may also be congestion of the
spinal membranes, increase of the spinal fluid, and softening of the
cord itself. The ganglia of the sympathetic system appear to undergo a
form of granular degeneration.
DIAGNOSIS.--The diseases which most closely resemble typhus fever are
typhoid fever, measles, meningitis, and typhoid pneumonia.
The circumstances under which typhoid and typhus fever occur are
different. Typhoid is never generated by overcrowding, and if
contagious at all is much less so than typhus. Prostration occurs much
earlier and is usually much more marked in the latter. The eruption in
the former does not appear until the eighth day, and comes out in
successive crops, and usually disappears under pressure as long as it
lasts, and therefore may be easily distinguished from that of the
latter. The duration of typhus is from ten to twenty days; that of
typhoid is rarely less than twenty-one. Nevertheless, cases are
occasionally met with in which it is impossible to arrive at a correct
conclusion as to their nature unless some light is thrown upon it by
the existence of other and more characteristic cases in the same house
or neighborhood. I have recently had under my care a case which
eventually proved to be typhoid fever, but which I and many others who
saw it at first believed to be typhus in consequence of the presence
of an abundant eruption, which did not disappear under pressure, and
was finally converted into petechiae.
The eruption of typhus is sometimes found upon the face, especially in
children, and then presents a considerable similarity to that of
measles, which, however, usually appears a little earlier. There is,
moreover, rarely the same amount of prostration or stupor in the
latter disease, which is also attended by coryza and more bronchial
catarrh than is often present in the former. The eruptions in the two
diseases differ. In measles it is crescentic in shape, and is more
elevated than in typhus. It is also brighter in color, disappears
under pressure, except in malignant cases, as long as it lasts, and is
followed by free desquamation of the cuticle, which is not often
observed in typhus. The temperature may be high in the former, but it
usually falls upon the sixth day.
In meningitis the headache is much more severe, and does not disappear
upon the occurrence of delirium. It may be so severe as to cause the
patient to cry out. The senses are painfully acute. There are
intolerance of light and sound, and some hypersensitiveness of the
surface, {359} strabismus, inequality of the pupils or some other
local paralysis, and retraction of the head. Nausea and vomiting are
more common than in typhus, while the utter prostration of the latter
disease is wholly wanting, and so is of course the characteristic
eruption. The tache meningitique is wanting in the latter, but too
much reliance should not be placed upon either the presence or absence
of this sign. The diagnosis is only likely to be difficult in those
cases of typhus in which the delirium is active. In that form of
typhus in which the symptoms simulate those of delirium tremens some
difficulty may also be experienced in making a diagnosis, especially
if the patient be a drunkard. In delirium tremens it will be
remembered, however, that there is little or no elevation of
temperature, that the skin is bathed in perspiration, the tongue
moist, and the characteristic eruption absent. Typhoid pneumonia can
be distinguished from pneumonia complicating typhus fever by the
presence of the eruption in the latter.
Other diseases which have occasionally been mistaken for typhus fever
are remittent fever, Bright's disease, giving rise to uraemia and
purpura. It does not seem likely that even the severest forms of
malarial fever should ever present such a resemblance to typhus fever
as to make the differential diagnosis a matter of difficulty; but it
would appear from the history of the latter disease given by Murchison
that such a mistake has occurred in some of the Spanish American
countries. The enlargement of the spleen and liver is much less marked
than in remittent fever, and the remissions of temperature are much
less decided. Uraemia may at times present a good deal of resemblance
to the condition often seen in typhus fever after the supervention of
coma or stupor, but the history of the case, the absence of fever and
of eruption in the former, will generally enable us to distinguish
between the two conditions. It should be remembered, however, that
Bright's disease may occur in the course of typhus fever. Purpura may
generally be recognized by the absence of fever and by the occurrence
of hemorrhages from the nose, gums, and bowels.
PROGNOSIS.--The age, habits of life, and previous condition of health,
as well as the character of the prevailing epidemic, must all be fully
considered before making a prognosis in any special case. The disease
usually runs a much milder course in children and young people than in
adults past thirty years of age. After this age the mortality
progressively increases, and in advanced life it becomes very high,
being often as much as 50 per cent. or over. Sex does not of itself
exercise much influence upon the course of typhus fever, for, although
a few more men than women die of it, this appears to be attributable
to the greater prevalence of drinking among the former. Previous
intemperance acts unfavorably by producing a degeneration of the
tissues of the body, thus rendering the patient less able to withstand
the effects of the disease. Drunkards have therefore always furnished
a large proportion of the fatal cases. The mortality among patients
who are unfortunate enough to take typhus fever as they are
convalescing from other diseases is usually also very great. This has
often been observed in general hospitals in which cases of fever as
well as those of other forms of disease are admitted. Fat, lymphatic,
or muscular people more frequently die of it than those of a different
conformation. Gerhard found it especially {360} fatal among negroes in
the epidemic of 1836, and Buchanan seems to have had a similar
experience at the London Fever Hospital. It is a fact noticed by
English writers that people of the better class, although seldom
attacked by typhus, often suffer severely from it. The mortality is
always high among those patients who previously to contracting the
disease have been for some time deprived of sufficient food, or have
been overworked, or who have been the subjects of mental anxiety,
worry, or any other depressing emotion. It is high also among those
who in the beginning of the disease have exhausted their strength in
the vain effort to resist the disposition to go to bed. The chances of
recovery are, on the other hand, very much improved by the removal of
patients from crowded, ill-ventilated houses to the wards of a
spacious, airy hospital.
Unfavorable symptoms are a profuse dark-colored eruption associated
with purpura spots and vibices, general lividity of the surface, great
injection of the pupils, and a dusky hue of the countenance; extreme
prostration; an excessively frequent and feeble pulse, especially if
it is at the same time irregular or intermittent; absence of the
cardiac impulse and of the systolic sound; hurried and spasmodic or
abnormally slow respiration; great dryness and retraction of the
tongue; excessive prominence of the nervous symptoms, such as
headache, delirium, whether active or muttering; unequal or pin-hole
contraction of the pupils; strabismus or other local paralysis;
sleeplessness; muscular tremblings; subsultus tendinum; carphology;
protracted hiccough; retention of the urine; relaxation of the
sphincters of the bladder and rectum; coma and especially coma vigil,
and convulsions; continued high temperature, rising instead of falling
after the tenth day, especially if it is associated with coldness of
the extremities and of the breath; a profuse perspiration without a
general improvement in the symptoms; diminution in the quantity of the
urine, or the presence in it of albumen, blood, or casts; vomiting;
and diarrhoea. Hope, however, should never be abandoned even in the
most unfavorable cases, as recovery has sometimes occurred when the
patient seemed almost in articulo mortis. Convulsions are said to be
invariably followed by death, and Graves regarded the presence of the
pin-hole contraction of the pupils as of very grave import.
Favorable symptoms are--reduction of the frequency of the pulse, a
fall of temperature, a diminution of the stupor or a resumption of
consciousness, and a return of appetite and of moisture to the tongue.
When the patient begins to improve he will often without assistance
turn upon his side after having lain for a long time upon his back,
and this change of position is sometimes the first indication of the
approach of convalescence.
The mortality varies of course in different epidemics. The cases which
have come under my own care being too few in number to draw deductions
from on this point, I must rely upon the experience of those whose
field of observation has been more extended than my own. According to
Murchison, out of 18,268 cases of typhus fever admitted into the
London Fever Hospital during twenty-three years, 3457 proved fatal,
making a mortality of 18.92 per cent., or 1 in 5.28. Deducting 686
cases fatal within forty-eight hours, the mortality falls to 15.76 per
cent., or 1 in 6.34. Included among the fatal cases is a large number
in which {361} the disease had run its course to a favorable
termination, and in which death was really due to sequelae, such as
pneumonia, erysipelas, etc. Moreover, the death-rate in the hospital
is greater than in the community, because children, who rarely die of
typhus fever, are seldom brought to it; while, on the other hand, it
receives a large number of the infirm and aged inmates of the
metropolitan workhouses. Making allowance for these sources of
fallacy, Murchison believes that the actual mortality of typhus is not
more than 10 per cent. In Gerhard's cases the proportion of deaths
amongst the black was much greater than amongst the white men; thus,
of the whites 1 died in 4-2/3, of the blacks 1 in 2-19/28. Amongst the
women the reverse was true; thus, 1 white woman died in 4-3/5, but
only 1 colored woman in 6-1/2, nearly. Da Costa lost 6 out of 39
cases. In one of the fatal cases the diagnosis was doubtful; in
another there was a great deal of previous disease; in two others
death was due to complications--so that there were but two in which
the fatal result could fairly be attributed to the disease itself.
TREATMENT.--Typhus fever is an eminently preventible disease. It is
therefore proper that the description of its curative treatment should
be preceded by a few words in regard to its prophylaxis.
It is still an unsettled question whether or not typhus fever ever
occurs de novo, and although the recent discovery by Klebs and others
of bacillus peculiar to typhoid fever (the bacillus typhosus), and of
special bacilli in other analogous diseases, renders it highly
probable that typhus fever has also its own bacillus, and that
therefore it is not likely to arise except as the result of infection,
it must be admitted that it has often prevailed in localities into
which it has not been possible to trace its importation. Under these
circumstances it will be well to refer to those conditions which are
asserted by some authors to favor its spontaneous generation,
especially as these same conditions are certainly known to favor its
propagation. It will not be necessary to do this at any great length,
as they have all been fully described in discussing the etiology of
the disease. The most important of them is the overcrowding of human
beings, especially when combined with deficient ventilation,
destitution, and want of personal cleanliness. The knowledge of the
laws of hygiene is now so universally diffused that this combination
of conditions never occurs at the present time to anything like the
degree it often existed in the eighteenth century, and consequently
epidemics of this disease are not only less frequent, but are also
much milder in character, than formerly. Much work, however, still
remains for sanitarians in the improvement of the homes of the poor,
which even in this country are too often overcrowded and
ill-ventilated.
The extension of the disease in a community will almost always be
prevented by the prompt isolation of the first few cases. This can
often be thoroughly done, if the patient is in easy circumstances, by
placing him in an upper room, which should be stripped of its carpets,
curtains, and other unnecessary furniture; by cutting off all
communication between him and his attendants and the rest of the
household; and by the free use of disinfectants. The room should be
airy, and to ensure good ventilation a window should be left partly
open. This may be done during the febrile stage, even in winter,
without the risk of any injury to the patient. Among the poorer
classes, however, {362} isolation can rarely be effectually carried
out, and it is therefore much better to remove the patient to a
hospital. Upon the admission of such a patient to an institution of
this character his clothes should be at once disinfected. This may be
done by washing the underclothing in a disinfecting fluid, and then
exposing them to a free current of air, and by subjecting the outer
clothing to a very high temperature in an oven or to the fumes of
burning sulphur. Murchison believes that a neglect of this precaution
has often been the cause of the extension of the disease to other
inmates of the hospital, especially when the patient resumes during
his convalescence the same clothing he wore upon admission. If the
hospital is a general one, he should be placed, whenever practicable,
in a well-ventilated ward by himself or with other patients suffering
from the same disease. As this is not always possible, the number of
the other occupants of the ward should be reduced and their beds
placed as far away as possible from his. As the infectiousness of
typhus fever is very much lessened by free ventilation, this
precaution is often alone sufficient to prevent its extension to them.
It is also well, however, to supplement it by the use of
disinfectants. The diffusion of a solution of carbolic acid in the
atmosphere of the ward by means of the steam atomizer has not only
rendered the odor emanating from the patient less perceptible, but has
also appeared to diminish decidedly the risk of infection. As a still
further precaution the patient may be sponged with a weak solution of
carbolic acid or some other disinfectant. His nurses should be
selected, whenever practicable, from among those who have had the
disease themselves. They should never sleep in the sick room, lounge
about the patient's bed, or inhale his breath. They should be allowed
a certain amount of time every day for rest and recreation in the
fresh air, and should have a full supply of nourishing food. On the
other hand, they should be warned against the danger of
over-stimulation, which is often resorted to in the hope of warding
off the disease, and should be relieved as far as possible from
attendance upon other patients. It may be well here to say that the
nursing of a case of typhus fever should never be undertaken by the
relatives or friends of the patient, except as a matter of necessity.
Not only do the anxiety and distress they naturally feel unnerve them
and render them unfit to carry out the directions of the physician,
but they can rarely execute the many offices required in the sick room
with half the skill of a trained nurse or with so little annoyance to
the patient.
Before the patient is allowed to leave his ward he should have a warm
bath. If the disease has occurred in a private house, the room which
he has occupied should be thoroughly disinfected. This is best done by
replastering, repapering, and repainting it. In many cases, however,
it will be sufficient to fumigate it with burning sulphur, and then to
air it for several days. The bed and bedding should also be
disinfected, and, where this cannot be thoroughly done, the latter had
better be destroyed.
Of primary importance in the treatment of typhus fever is the
regulation of the diet. Although there are no ulcers in the bowels in
this as in typhoid fever, and although, consequently, there is not the
same imperative necessity in this as in the latter disease to restrict
the patient to liquid articles of food, experience has shown that such
articles are much more readily digested and assimilated than solids.
The diet {363} should consist, therefore, of milk, beef-tea, and
chicken or mutton broth. Of all of these, milk is incomparably the
best, and it should form, unless the patient manifest an unconquerable
repugnance to its use, a large part of the nourishment in every case.
Farinaceous articles of food are generally not well borne in this
fever, because the diminution in the secretion of the salivary glands
which almost always exists prevents their proper digestion. After the
third or fourth day nourishment should be given in small quantities at
short intervals, as every two hours, every hour, or even every half
hour when the prostration is extreme. It should be the aim of the
physician to give an adult at least two quarts of milk or their
equivalent daily.
It is sometimes necessary to put a delirious patient under some
restraint to prevent him from leaving his bed or doing some other act
of violence. Frequently a judicious nurse will be able to accomplish
this without the use of an undue amount of force, but at other times
it will be necessary to have recourse to mechanical means of
restraint. Usually, all that is necessary is to pass a folded sheet
across the patient's chest, the ends of which are fastened to the
sides of his bed.
It is now a universally accepted axiom among physicians that typhus
fever is a self-limited disease, and that any attempts to cut it short
is worse than useless. Not only do remedies which are employed for
this purpose often produce alarming prostration, but there can be no
doubt that they have in some cases been the cause of a fatal
termination, which under another plan of treatment would have been
averted. During the last century it was not uncommon to bleed, and to
bleed largely, in the beginning of an attack of typhus fever, but even
then there were physicians--as, for instance, O'Connell, Rogers,[28]
Pringle,[29] and Rutty[30]--who raised a warning voice against the
practice. Sir John Pringle goes so far as to say that "many have
recovered without bleeding, but few who have lost much blood." A very
similar opinion was also expressed by Baron Larrey in the early part
of this century. Indeed, it is very evident that the same difference
of opinion existed as to the employment of venesection in the
treatment of acute affections when these authors wrote as prevailed in
England and this country until within the last thirty years, and that
the disastrous results which occasionally follow the abstraction of
large amounts of blood from patients affected with fevers and
inflammations were as fully recognized then as now by many physicians.
This would seem effectually to dispose of the
change-of-type-in-disease theory which was generally accepted in the
first half of this century as sufficient to explain the fact which
could no longer be overlooked that this class of patients did much
better under a supporting than a depleting plan of treatment.
Purgatives were also at one time freely given for the purpose of
arresting the disease, but the results obtained from their use were
scarcely less unfavorable, and they are now never employed with this
view. The use of quinia in large doses has also been advocated for the
same purpose, but experience, while it has shown that it is a valuable
remedy, has demonstrated also that it does not possess {364} this
power. Exactly the same thing may be said of the cold-water treatment
of typhus fever. There is no evidence that it has ever shortened the
duration of the disease.
[Footnote 28: _An Essay on Epidemic Diseases_, p. 60, by Joseph
Rogers, M.D., Dublin, 1734.]
[Footnote 29: _Loc. cit._]
[Footnote 30: _A Chronological History of the Weather and Seasons, and
the Prevailing Diseases, in Dublin during the Space of Forty Years_,
by John Rutty, M.D., London, 1770.]
If the physician is called to a case of typhus fever during the chill,
before reaction has taken place, he will of course have recourse to
diffusible stimulants and external warmth to aid in the establishment
of this process. More frequently he is not sent for until after the
chill has been succeeded by fever. His treatment will then, of course,
vary with the condition of the patient. If his stomach is loaded with
food, an emetic should be administered to him. If the bowels are
constipated, a mild cathartic will often be of service, but after the
bowels have been once well moved it is generally unnecessary to
disturb them further. During the first day or two, while the fever is
still moderate in degree, and during the uncertainty which then
usually exists as to the diagnosis, it will be sufficient to prescribe
the neutral mixture or the spirit of Mindererus in tablespoonful doses
every two or three hours. Upon the third day more active remedies will
generally be required to reduce the temperature. This is best done by
the cold-water treatment in some form or other, or by the internal
administration of antipyretic doses of quinia. The manner in which the
cold water is to be used and the cases to which it is applicable must
be left in a great measure to the judgment of the physician. In the
form of the cold affusion it is now rarely resorted to, although
Currie[31] obtained most excellent results with it. It is calculated,
however, to alarm a timid patient, and it is probably owing largely to
this fact that it has fallen into disuse. The cold bath, packing in a
cold wet sheet, and sponging with cold water are the more usual means
of employing cold in the treatment of typhus fever at the present day.
The cold bath is much used in Germany in the treatment of different
forms of fever, and even of inflammation. It is also resorted to in
this country, but it has never attained the same popularity here as
abroad. The best way of using it is as follows: The patient as soon as
his temperature rises above 103 degrees F. should be placed in a bath
having a temperature between 80 degrees and 90 degrees, and which,
whenever practicable, should be brought to his bedside, as when he has
to be carried to the bathroom he is sometimes not only alarmed and
rendered very nervous by the operation, but may exhaust himself in his
struggles to free himself from his attendants. After his immersion
cold water should be gradually added until the temperature of the bath
is between 60 degrees and 70 degrees F. The length of time he should
be allowed to remain in the bath will of course depend upon
circumstances. If shivering is produced by it, he should be at once
removed from it and thoroughly dried and put back to bed. If no such
symptoms are observed, he may be allowed to remain in it longer. As a
general rule, a half hour is as long as will be necessary or safe for
him to continue immersed at any one time. His temperature will usually
continue to fall for some time after his removal from the bath, but in
the course of a few hours it will be found to have risen again to 103
degrees or over, when he should have another bath. In this way it may
be necessary to repeat the baths from eight to twelve times a day.
Some authors recommend that the patient should be placed at once in a
bath having a temperature of 50 degrees F., {365} but this method of
applying cold possesses no advantage over that above described, and
is, like the cold affusion, very apt to excite alarm in the patient.
The cold bath is not, however, well borne by all persons, and alarming
symptoms, and even fatal collapse, have followed its use in the old
and feeble. It is also contraindicated when the skin is covered with a
profuse sweat or when the disease is complicated by an internal
inflammation. When the means of giving a cold bath are not at hand,
the cold pack will often be found a very efficient substitute for it.
Sponging with cold water, although not so efficacious in reducing the
temperature, has advantages over either of these methods of applying
cold. In the first place, it is more agreeable to most patients and
less calculated to excite alarm in those who are timid. Again, it may
be more frequently repeated, and may be used in cases in which the
cold bath is contraindicated. Occasionally alcohol or vinegar may be
added with advantage to the water, with the view of increasing its
refrigerant effects.
[Footnote 31: _Medical Reports on the Effects of Water, Cold and Warm,
as a Remedy in Fever and Febrile Diseases_, by James Currie, M.D.,
F.R.S., London, 1805.]
When quinia is given for the purpose of reducing the temperature in
the treatment of typhus fever, it must be used in large doses, as much
as ten or fifteen grains repeated once or twice in the course of
twenty-four hours being required for this purpose. When given in these
quantities it has the disadvantage of producing deafness and
occasionally of increasing the headache. I have therefore contented
myself in the cases which have fallen under my own care with giving it
in more moderate quantities, in combination with one of the mineral
acids, as, for instance, a couple of grains of quinia in solution with
from eight to ten drops of dilute muriatic acid, repeated from four to
six times a day. The mineral acids were originally recommended in the
treatment of typhus fever in the belief that they neutralized the
poison which caused the fever, and which was supposed to be ammonia or
some of its compounds. Although this theory is now no longer
entertained, there can be no doubt that the tendency in this disease
to the accumulation of ammonia in the blood is prevented by their
administration. Digitalis, aconite, or veratrum viride may also be
given in appropriate doses if with a high temperature there coexists
great frequency of the pulse. The first-named remedy is especially
indicated if there is at the same time diminution of the secretion of
urine.
As the disease progresses other symptoms present themselves for
treatment. One of the most urgent of these is the prostration. This
not only appears early, but is often extreme, and if not met by
appropriate remedies will often of itself be sufficient to cause the
death of the patient. As soon as it makes itself manifest stimulants
must be prescribed. These are, however, not to be resorted to simply
because the patient has typhus fever. Many cases do perfectly well
without them. In the young and robust it is often unnecessary to have
recourse to them. On the other hand, in the old, the feeble, and the
intemperate they should be employed early. The rule laid down by
Stokes, that they should be administered as soon as the first sound of
the heart becomes indistinct and inaudible, may be adopted for our
guidance in this respect. At first they should be given tentatively.
If the delirium, headache, and other nervous symptoms are increased
after their administration, it is best to withhold them. They should
be continued, on the other hand, when under their use the delirium
ceases or grows milder, the other nervous {366} symptoms subside, and
the patient falls into a refreshing sleep. The amount required to
prevent fatal prostration will of course vary in each case. I have
rarely myself found it necessary to prescribe more than half an ounce
of whiskey or brandy every two hours, and frequently a very much
smaller quantity has been found sufficient. Cases are, however,
reported in which from twenty to twenty-four ounces daily have been
given with asserted advantage.
Another symptom which often demands prompt relief is the headache.
When not severe, it may be relieved by the application of cold to the
head, either in the form of the ice-cap or by means of cloths
frequently wrung out of cold water, and by the administration of
moderate doses of potassium bromide; but when intense it requires more
active treatment for its removal, such as the application of cups to
the back of the neck or of leeches to the temples. General bleeding
will accomplish the same result, but the good which is done by it is
often more than counterbalanced by the prostration it induces.
Sleeplessness is also sometimes the cause of a good deal of distress
to the patient. When it occurs early in the disease and is caused by
the headache, it will generally subside under the use of the remedies
which are employed for the relief of the latter symptom; but when it
comes on at a later period, it will often require special treatment.
There is some doubt as to the propriety of giving opium under these
circumstances, but Murchison, Gerhard, and others assert that it may
be given not only without injury, but with positive advantage to the
patient. Graves was in the habit of combining it with a small quantity
of tartar emetic in the condition in which the sleeplessness is
associated with active delirium. If, on the other hand, the delirium
is of a low muttering character, it should be given with a diffusible
stimulant.
In this condition I have often found a pill containing a small
quantity each of opium and camphor, frequently repeated, to answer an
admirable purpose, not only in procuring for the patient the needed
repose, but also in diminishing the restlessness, jactitation, and
subsultus tendinum. Opium should, however, not be used at all or used
very carefully in cases in which there is congestion of the lungs or
disease of the kidneys. The existence of the pin-hole pupil is also a
contraindication to its employment. In young and robust patients, if
the insomnia is attended by active delirium, chloral in twenty-grain
doses, repeated if necessary, may often be given with advantage, but
it should never be prescribed in cases in which the action of the
heart is feeble. Other remedies which have been recommended in the
treatment of this condition are belladonna, hyoscyamus, musk,
chloroform, and cannabis indica. Potassium bromide appears to have no
power to relieve it. No special modification of the above treatment is
needed when delirium occurs independently of sleeplessness and
headache. When the stupor is profound, efforts should be made to rouse
the patient by the use of counter-irritants to the shaven scalp or to
the nape of the neck. Murchison speaks well of the administration of
strong coffee under these circumstances. If there is at the same time
suppression or diminution of urine, diuretics should be administered
in the hope of stimulating the kidneys to increased secretion.
Retention of the urine is not an infrequent occurrence in this
condition, and the physician ought never, therefore, to accept the
assertions of the {367} nurse or friends of the patient that the
latter has passed water, but should satisfy himself by an examination
in regard to the condition of the bladder at every visit. He will
often find that the apparent passage of urine is nothing more than the
dribbling due to an over-distension of this organ. Neglect of this
precaution has occasionally been the cause of much subsequent distress
to the patient, as cystitis is sometimes set up as a consequence of
it. In one case which came under my observation, and in which this
precaution had been neglected, the patient suffered from incontinence
of urine for some time after his recovery from the fever. Thirst is a
symptom which is always present and complained of at the beginning of
the fever, and usually bears some proportion to the severity of this
process. Weak tea, an infusion of cascarilla-bark, and camphor-water
have all been recommended by different authors for its relief, but it
is probable that no one of them possesses any superiority over water.
If the stomach is irritable and water is not retained, small pieces of
ice should be allowed to dissolve in the patient's mouth. Later, when
the stage of stupor supervenes, it is very important to see that the
patient obtains a full supply of water. In this condition he will not
call for it, although it is even more urgently required than before.
Vomiting may occur at any time in the course of typhus fever. If it is
observed at the very beginning of an attack, an emetic will often
arrest it, but when it supervenes at a later period, it is generally
of cerebral origin, and will usually subside under the use of the
remedies already referred to which are prescribed for the relief of
the nervous symptoms. In addition to these, sinapisms may be applied
to the epigastrium, and champagne, when the circumstances of the
patient will permit it, should be given in the place of whiskey or
brandy. When everything is rejected by the stomach, recourse must be
had to nutritious enemata. Constipation is to be overcome by gentle
purgatives, as the use of powerful cathartics is very apt to be
followed by troublesome diarrhoea. If this should come on, it is best
treated by small doses of opium in combination with a mineral or
vegetable astringent. When these fail, it may sometimes be relieved by
a prescription containing sulphuric acid and morphia, and at others by
enemata of from twenty to thirty drops of laudanum in warm water. When
glandular swelling occurs in the parotid region or in other parts of
the body, an effort should be made to promote resolution by painting
them with tincture of iodine. Blisters have also been recommended for
the same purpose, but they should be used carefully, as in low
conditions of the system they are sometimes followed by sloughing of
the integuments. If these remedies fail, poultices should be applied.
As soon as pus has formed it should be evacuated by one or more free
incisions.
Very few attacks of typhus fever run their course without the
occurrence of some pulmonary complication. When this is slight it
demands no special modification of the previous treatment, and it is
sufficient to apply mustard poultices or stimulating liniments to the
chest. But in cases of greater gravity, it matters not whether the
complication is bronchitis, congestion of the lungs, or pneumonia, a
more active treatment is required. Under these circumstances the
ammonium carbonate in five-grain doses, given in mucilage of acacia,
frequently repeated, or from thirty minims to a teaspoonful of the
aromatic spirit of ammonia every {368} two hours, sufficiently
diluted, may be prescribed with great advantage. When gangrene
supervenes the prognosis is almost hopeless, but an effort should be
made to save the patient's life by the administration of potassium
chlorate and of an increased amount of stimulus. Murchison also speaks
well of the inhalation of tar vapor and of carbolic acid.
As the other complications of typhus are at least of as common
occurrence in typhoid fever, it will avoid a good deal of useless
repetition to refer the reader to the article on the latter disease
for a description of the treatment which they render necessary.
The patient should be kept in bed for some time after the subsidence
of fever. Although relapses are rare in this disease, recrudescences
of fever not infrequently occur as a consequence of undue exertion in
the early part of convalescence. Syncope is also not infrequently
produced by the patient's sitting up too soon. The diet should be
carefully regulated until the recovery is complete. It should at first
consist wholly of liquid or semi-liquid articles of food, but later
meat in some digestible form may be allowed. Stimulants are often as
urgently demanded at this time as during the fever itself. They should
be given as the strength returns in gradually diminishing quantities.
The length of time during which it is necessary to continue them will
depend in great measure upon the previous habits of the patient. As a
general rule, their use should not be abandoned until he is able to
leave his bed, and they may often be continued after this with benefit
to him. As convalescence progresses it will be well to substitute ale
or porter for the brandy or whiskey the patient had previously taken.
A return to health will also be promoted by the judicious use of
tonics, such as iron, quinia, Huxham's tincture, tincture of nux
vomica, the mineral acids, and even cod-liver oil in some cases.
{369}
RELAPSING FEVER.
BY WILLIAM PEPPER, M.D., LL.D.
SYNONYMS.--Febris recidiva, vel recurrens; Fievre a rechutes; Fievre
recurrente; Typhus icterodes, vel recurrens; Bilious Typhoid Fever;
Ruckfall's Typhus; Tifo recidivo; Famine Fever, Hunger-pest,
Armentyphus, Hunger-typhus, Spirillum Fever.
DEFINITION.--Relapsing fever is an epidemic contagious disease, the
specific cause of which is not certainly known, although a peculiar
spirillum appears to be constantly present in the blood. It occurs
chiefly among the over-crowded and destitute, but may spread widely
when introduced among more favorably situated populations. Its
invasion is abrupt, and is marked by a distinct chill or rigor,
followed quickly by high fever (104 degrees to 106 degrees), with
severe headache and pains in the back and limbs. Delirium is
comparatively rare. The tongue is heavily coated, and there are
epigastric tenderness, vomiting, constipation, and enlargement of the
liver and spleen, with frequent jaundice. There is no characteristic
eruption. These symptoms cease abruptly from the fifth to the seventh
day, with copious sweating; but after an apyretic interval of about a
week's duration a relapse occurs similar to the first attack, but of
less duration (three to five days). Second, third, or even more
numerous relapses may subsequently occur at less regular intervals.
One attack does not protect against a second one to the same extent as
with other contagious diseases. The mortality is usually small.
HISTORY AND GEOGRAPHICAL DISTRIBUTION.--It is not important to
consider here at any length the history of this disease. Allusions to
it were made by Strother, 1729, and by Huxham, 1752, but the first
reliable account on record is the description of an epidemic in the
year 1739 by John Rutty.[1] Relapsing fever undoubtedly occurred at
different times and at various places during the next hundred years,
although the records of it are scanty, and for the most part
imperfect, owing chiefly to the want of a clear recognition of its
essential difference from typhus and typhoid fevers.
[Footnote 1: _A Chronological History of the Weather and Seasons_,
etc., London, 1770, pp. 75-90.]
During the decade from 1842 to 1852 relapsing fever prevailed in a
very active and widespread form. Epidemics occurred in England,
Scotland, and Ireland, in various parts of Germany, and it was during
this time that it was first observed and described in America. In
June, 1844, an emigrant ship from Liverpool came to America with
eighteen cases on board, which were taken to the Philadelphia and
Pennsylvania {370} Hospitals. In 1848 a few cases were imported by
emigrants to New York, and in 1850 to Buffalo in the same way.[2]
[Footnote 2: See _Fevers, their Diagnosis, Pathology, and Treatment_,
Meredith Clymer, Phila., 1846, p. 99; _Clinical Reports on Continued
Fever_, A. Flint, Phila., 1855, p. 364; Dubois 1848.]
The next great outbreak of relapsing fever began in Odessa in 1863 and
lasted until 1872. It prevailed in various parts of Russia, in
Germany, France, and Great Britain, and for the first time occurred
extensively in the United States, especially in Philadelphia and New
York. The present article is based largely on a study of this epidemic
as it presented itself in Philadelphia during the years 1869-70, when
the writer, in conjunction with the late Edward Rhoads, had the
opportunity of observing about two hundred cases, in the wards of the
Philadelphia Hospital. An admirable article on the same epidemic
appeared from the pen of the late John S. Parry, in the _Amer. Jour.
Med. Sciences_, N.S., vol. lx., Oct., 1870, p. 336.
Between the years 1877 and 1880 relapsing fever occurred quite
extensively at Bombay, and was there studied by Carter[3] and Lewis;
and during 1879-80 it prevailed in Konigsberg, an account of which
epidemic has been published by Meschede.[4]
[Footnote 3: _Spirillum Fever_, by H. Vandyke Carter, M.D., London,
1882.]
[Footnote 4: _Virchow's Archiv_, Bd. lxxxvii. p. 393.]
The geographical distribution of relapsing fever is seen, therefore,
to have been very extensive; and not only has it occurred in the
above-mentioned localities, but there have also been less extensive
outbreaks in France, India, Egypt, Algeria, South America, and
elsewhere.
CAUSES.--In all probability the essential cause of relapsing fever is
a specific poison, but we know nothing of its real nature nor of the
precise conditions under which it originates. Recent investigations
have shown that the spirillum discovered by Obermeier is constantly
present during the febrile stages of relapsing fever, but it cannot
yet be decided whether this minute organism is the actual cause or
only an invariable accompaniment of the disease.
It appears that conditions of destitution, filth, and intemperance
amongst an overcrowded population favor the development of the virus,
and hence the epidemics have, as a rule, begun in towns, such as
Dublin, Glasgow, Odessa, St. Petersburg, Breslau, etc., where such
conditions prevail. Great importance has been attached, in particular,
to the scarcity of food and to destitution as powerful factors in
favoring the production of the disease. Some of its names
(hunger-pest, hunger-typhus, famine fever) have been given with
reference to this, and in the case of several outbreaks a careful
comparison has been made of the decrease of the food-supply and the
consequent advance in price of the staple commodities with the
development and progress of the disease. Although this is in all
probability true of those centres where relapsing fever originates, it
has but a partial application to the secondary centres where the
disease is imported and develops.
The presence of destitution and filth, enfeebling the vitality of a
section of the community, would favor the spread of this as of any
other specific fever, but there is considerable evidence to favor the
view that the importance of starvation as a cause of the fever has
been exaggerated. This was strongly urged by Parry[5] as the result of
his study of the {371} Philadelphia epidemic of 1870, and our own more
extended observation showed that the vast majority of the patients
appeared to be well fed. On the other hand, the influence of
overcrowding as favoring the development and spread of relapsing fever
has been clearly established by the study of many epidemics, as in the
Breslau attack of 1868, reported by Wyss and Bock, where single
tenement-houses furnished as many as seventy-one cases; in the
Edinburgh epidemic of 1869 and 1870, where Muirhead found the
breathing-space allotted to each individual in the affected houses to
vary from 250 to 400 cubic feet; and in the Philadelphia epidemic,
where the observations of Parry and ourselves showed the presence of
an extreme degree of overcrowding in most of the houses where the
disease broke out.
[Footnote 5: _Loc. cit._, p. 339.]
No age is exempt, but neither can it be said that age exerts any
influence upon the occurrence or frequency of relapsing fever. Of 1164
cases in the Philadelphia epidemic of 1869-70 in which the age was
noted, the result was as follows:
Males. Females.
Under 20 149 76
From 20 to 30 220 140
From 30 to 40 143 101
From 40 to 50 135 67
From 50 to 60 60 34
From 60 to 70 20 6
From 70 to 90 6 7
--- ---
Total 733 431 = 1164
The youngest cases were in children two or three years old; the oldest
patients were women over eighty-five years old.
Sex exerts no influence, though, on account of the larger proportion
of males likely to be exposed to the specific cause, the results of
nearly all epidemics show a preponderance of male patients in the
proportion of 33 per cent., 66 per cent., or even 85 per cent.
(Meschede).
Nationality does not act as a predisposing cause,[6] except in so far
as certain countries may present more frequently than others the
conditions favorable for the development of this disease. Of 1170
cases in Philadelphia in which the nativity was noted, 219 were Irish,
61 English, 161 German, 729 American. Of the latter 729, about
one-half, or nearly 28 per cent. of the whole number, were negroes,
while the negro population of Philadelphia was only about 3.3 per
cent. of the total. This excessive proportion of cases among the
negroes was undoubtedly due in large part to the fact that in
Philadelphia overcrowding is notoriously more common and extreme among
them than in any other portion of the population, although it is also
likely that they present an excessive susceptibility to the virus of
this as of many other specific diseases.
[Footnote 6: Hirsch's _Geog. and Hist. Pathology_, New Syd. Soc. ed.,
1883, vol. i. p. 615.]
Attempts have been made to show some connection between the period of
the year or the atmospheric conditions and the rise and spread of
epidemics of relapsing fever; but, as Murchison clearly showed, these
epidemics are wholly independent of such influences. In Philadelphia,
of 1176 cases in which the date of occurrence is known, there occurred
in September, 1869, 4 cases; December, 1869, 6 cases; January, 1870, 5
cases; February, 1870, 13 cases; March, {372} 1870, 124 cases; April,
1870, 209 cases; May, 325 cases; June, 293 cases; July, 115 cases;
August, 19 cases; September, 28 cases; October, 15 cases; November, 1
case; December, 2 cases; January, 1881, 2 cases; February, 1 case;
March, 2 cases; May, 7 cases; June, 2 cases; September, 2 cases;
October, 2 cases.
Occupation exerts no predisposing influence, but in all epidemics the
great majority of cases occur among the vagrant classes, who lead a
precarious life and commonly sleep in foul, overcrowded lodgings.
Murchison noted that in the London epidemics a considerable proportion
of cases occurred among recent residents, but he attributed this,
correctly, not to any special local cause, but merely to the fact that
this floating population is largely of the vagrant type. In
Philadelphia a careful inquiry showed that recent residence produced
no special predisposing influence, and a study of other epidemics
confirms this view.
Contagion is, however, the essential cause of the spread of relapsing
fever when the virus has once been developed. It seems clear from the
distinct periods and from the widely-separated localities in which
different outbreaks of relapsing fever have occurred that its special
poison is capable of being called into existence or activity by
favoring conditions. Murchison held the belief that it was very
intimately connected with, if not generated by, destitution, and, as
already stated, much evidence exists to show that the disease is most
apt to break out after periods of scarcity; but no just and convincing
proof exists that destitution, any more than over-crowding and other
depressing influences, can actually engender a specific contagium
capable of being transported to great distances and of originating
widespread outbreaks of the specific disease among differently
situated populations. It appears necessary to assume the existence of
some unknown special virus which finds its suitable nidus for
development in the conditions attendant on filth and overcrowding, and
which attacks with greatest facility the systems of those who are
enfeebled by want and depressed by vitiated air. When once this
specific poison has been called into active existence, however, there
can be no doubt as to the fact that it can be carried by fomites, and
that it is given off from the bodies of relapsing-fever patients so as
to affect any who may approach. Although a few observers have doubted
this contagiousness of relapsing fever, the evidence in its favor is
overwhelming. In many epidemics, as in Philadelphia in 1869, its
contagiousness is at least as intense as that of typhus fever. A
single case may, indeed, be admitted to a healthy family among the
better classes or into the wards of a well-ventilated hospital without
propagating the disease, although striking cases of contagion are on
record where a patient has communicated the disease to all the members
of a family favorably situated and living at a distance from any other
possible source of contagion. On the other hand, if admitted to an
overcrowded and filthy lodging the disease is apt to spread rapidly.
Wyss and Bock report seventy-one cases as having occurred in a single
lodging-house during the course of the Breslau epidemic of 1868, and
in Philadelphia single houses in several instances furnished more than
a score of cases, and several short streets more than one hundred
cases each.
In the Philadelphia Hospital twenty-three persons lying sick in the
wards with other affections contracted relapsing fever from the
patients {373} admitted with that disease; two of the visiting staff,
five resident physicians, and nine nurses also suffered attacks of
varying severity. This corresponds with the general experience of
those connected with fever hospitals during the prevalence of
relapsing fever.
As in the case of typhus and other contagious diseases, the distance
at which relapsing fever can be contracted by direct contagion through
the atmosphere is a very short one, not exceeding a few feet at most.
The poison may be carried by fomites. Instances are on record where
persons having visited infected districts have conveyed the disease to
others at a distance without contracting it themselves.
When rooms which have been occupied by relapsing-fever patients are
subsequently occupied by other persons, these are very liable to
acquire the disease. Parry relates two remarkable cases in which
relapsing fever was transported to a distance by infected clothes; and
it has been more than once observed that during epidemics of this
disease laundry-women engaged in washing the clothes of fever
patients, but without any means of more direct communication with the
sick, were frequently attacked (Cormack, Wyss and Bock).
In connection with the etiology of relapsing fever it is necessary to
consider the role played by a minute organism which has been
frequently detected in the blood of patients suffering with this
disease. This spiro-bacterium was first observed in relapsing fever by
Obermeier[7] in 1873, and has since been identified as a spirillum or
spiroechete. The very numerous observations of Obermeier, Albrecht, H.
V. Carter, Motschutkoffsky, Koch, Cohen, Holsti, Enke, Meschede, and
others leave no doubt that this peculiar parasite does occur at least
very frequently in the blood of patients with this disease. The
failure to detect it, which has been reported by several good
observers, may readily have been due to the extreme delicacy of the
organism, or to the neglect of the proper method of preparing the
slides of blood for examination, or to delaying the examination of the
blood until after death, when it rapidly disappears. Thus no value can
be attached to the negative observations of Rhoads and myself, made
prior to Obermeier's discovery, since our method of examination was
not sufficiently exact.
[Footnote 7: _Centralbl. f. die med. Wissensch._, 1873, No. 10.]
The following description of the mode of examining the blood, and of
the spirillum, is condensed from H. V. Carter's account: It is
necessary to employ magnifying powers of not less than 500 diameters.
The fresh blood may be examined immediately after obtaining it by
pricking the washed finger of the patient. For preservation dried
specimens are needed: a very thin layer of fresh blood is evenly
spread with the needle over the glass cover, exposed to the weak fumes
of a solution of osmic acid, and allowed to dry under protection from
dust; the dried film of blood may then be treated with glacial acetic
acid or may be stained.
[Illustration: FIG. 19. Spirillum from the blood in a case of
relapsing fever, X 700 (Koch).]
The spirillum [See Fig. 19] is a colorless, slender, twisted filament,
which when quiescent has a length of 2.66 times the diameter of a
blood-disc (1/1500 to 1/500 inch = 0.012 to 0.043 millimetre). When
unfolded they become distinctly elongated. They are very narrow (not
more than 1/40000 inch), and present four to ten spiral turns; when
fresh they are in active movement and unfold in part, becoming wavy or
bent. They {374} resist the action of concentrated acetic acid, and
are readily stained by certain dyes. In number, five or ten may be
visible in a field or they may be too numerous to count. They have not
been detected either in the secretions or in the evacuations. Both
Koch and Carter have succeeded in cultivating this special form of
bacteria outside of the body.
To judge from the observations thus far made on this difficult
question, the parasite is found first toward the close of the period
of inoculation or soon after the beginning of the fever, or it may be
detected throughout the febrile stage; but shortly before the
cessation of the fever it quickly disappears, to reappear at the time
of the relapse. There would seem, therefore, to be some close
connection between the febrile paroxysms and this organism, and it is
not remarkable that many observers have concluded that this spirillum
is the essential and specific cause of the fever, and that it is
impossible to have this disease present without the appearance of the
parasite in the blood; nor that the name spirillum fever has been
applied to the disease by Carter.
Such conclusions appear to be premature, however, and we prefer to
regard the undoubted existence of the spirillum in the blood of
relapsing-fever patients as at present only an important aid in
diagnosis, and to await the occurrence of other epidemics and the
repetition of careful studies upon this organism, both within and
without the human system, before venturing to decide whether it is
merely one of the phenomena of the disease or whether it is its true
cause and specific contagious principle.
It must be added that both Carter and Koch have succeeded in
inoculating monkeys with relapsing fever, and Motschutkoffsky[8] of
Odessa, who had the opportunity of inoculating a human being, asserts
that he succeeded in producing the disease, and found the incubation
period to be not less than five nor more than eight days. Carter also
gives an interesting table[9] of six instances of inoculation, four of
them by cuts while making autopsies, with consequent development of
relapsing fever in each instance. Some allowance must be made for the
fact that in all the instances of this series there had been exposure
to contagion by close communication with fever patients, though this
exposure had existed for several months previously without leading to
the development of relapsing fever.
[Footnote 8: _Centralblatt f. d. med. Wissenschaften_, 1876, No. 11,
p. 194.]
[Footnote 9: _Op. cit._, p. 403.]
GENERAL CLINICAL DESCRIPTION.--After a period of not less than five or
six days from the reception of the contagion the disease begins {375}
abruptly with a chill of variable severity, accompanied by headache
and aching pains in the back and limbs. The patient feels weak and is
often giddy, but is not always obliged to go to bed the first day.
Nausea and vomiting are among the earliest symptoms, and distress at
the epigastrium, with tenderness, may attend or even precede the
chill. Fever quickly follows; the pulse runs up from 110 to 130 in a
few hours; the temperature reaches from 103.5 degrees to 106 degrees
by the end of twenty-four hours; the pains increase, and there are
insomnia and great restlessness; appetite fails; thirst is extreme;
the tongue is moist and furred, and the bowels quiet. During the
subsequent six days these symptoms persist. The temperature presents a
daily remission at some period of the twenty-four hours amounting to
one or two degrees, the maximum reached in fully-developed cases
varying from 104 degrees to 108 degrees. The pulse continues very
rapid, and not rarely exceeds 140; the respirations are hurried and
rapid, and cough attends many cases. Delirium is rare, but insomnia,
restlessness, headache, and rheumatic pains in the back and limbs may
prove constantly annoying. Appetite is variable, more frequently lost;
nausea and vomiting are common; thirst is very troublesome; and the
bowels are constipated or loose. No characteristic eruption appears,
but sudamina are frequently present, since in a large proportion of
cases there is more or less sweating, even during the continuance of
high fever. Abdominal pain, tenderness in the epigastrium and
hypochondria, and demonstrable enlargement of the liver and spleen are
almost invariable. The urine is concentrated and dark or bile-stained.
Jaundice is a common symptom, though its frequency varies greatly in
different epidemics. The same may be said of epistaxis.
While these symptoms are at their height and the patient is suffering
severely the paroxysm suddenly ceases, and in a few hours he is
entirely relieved. This remarkable crisis occurs usually at the close
of the seventh day, but may occur as early as the third or as late as
the fifteenth day. It is attended with a critical discharge, copious
sweating being by far the most common, though diarrhoea, free
epistaxis, or hemorrhage from some other surface may replace it. The
patient feels weak and languid; the temperature and pulse have fallen
below the normal, and remain so for a day or two. Soon there is a
rapid improvement in the appetite and the appearance of the tongue,
and the patient regains strength day by day, and often feels so well
that it is difficult to persuade him that he must avoid exertion and
exposure. The enlargement of the spleen subsides rapidly, that of the
liver more gradually; epigastric tenderness subsides, but in many
cases some degree of it persists for several days. This interval or
apyretic period lasts about a week, when, again without warning or
provocation, the patient relapses, and is seized abruptly with the
same set of symptoms which attended the first attack. This relapse
does not usually last more than three days (one to five are the
limits), and is terminated by a similar crisis, after which a slow
convalescence is entered upon, or else after an apyretic interval of
some days' duration a second relapse ensues, and this may, in rare
cases, be in turn followed by a third, fourth, fifth, or even sixth
similar relapse. In addition, it must be noted that many serious
complications are liable to occur. The total duration of the disease
thus varies from eighteen to ninety days. Convalescence is often
tedious, and there are many troublesome sequelae. {376} The mortality,
however, is not great, averaging 5 or 6 per cent. Death may occur
suddenly from collapse at the close of the first paroxysm or from
heart-clot; it may be produced by exhaustion in protracted cases; or
be hastened by any serious complication; or the patient may sink into
a typhoid condition, with low delirium, coma, and suppression of urine
for several days before the fatal termination.
DETAILED STUDY OF SPECIAL CONDITIONS.--It is usually difficult to
determine the period of incubation. In the unique case in which
Motschutkoffsky is said to have produced relapsing fever by
inoculation the initial symptoms occurred seven days after the
inoculation. Wyss and Bock had several good opportunities of
determining the minimum period of incubation, and found it to be six
days. We may assume that the ordinary period is six to eight days, but
that it varies, in accordance with the virulence of the virus or the
susceptibility of the system, from four to fourteen days. During this
time the patient feels as well as usual, or at most suffers for a day
or two from slight malaise, with vague rheumatoid pains, headache,
giddiness, and anorexia. In only 13 out of 181 of our cases in which
this point is noted was the invasion gradual. Examination of the blood
prior to the invasion does not discover any spirilla.
The invasion is usually abrupt and during the daytime; the patient can
often fix the very hour of its occurrence, a severe chill attacking
him while at work or at meal-time. This is the most common initial
symptom (138 out of 168 our cases of sudden invasion); less commonly,
obstinate vomiting and nausea or sudden vertigo are the first symptoms
(each 8 times out of 168), or violent headache (14 times out of 168),
or sharp epigastric pain. Parry also observed that the occurrence of
obstinate and profuse vomiting as the initial symptom was especially
frequent in children.
The physiognomy is carefully noted in one hundred and seventy of our
records. The countenance is often flushed, with watery eyes and
anxious, suffering expression. The flush is less dingy and dull than
in typhus; the eye is comparatively rarely injected; and the
expression is much less dull and stupid than in that disease. In cases
where grave nervous symptoms supervene and the typhoid condition is
developed the facies assumes all the characteristics of that state.
The livid bronzing of the face, described by Cormack in 1843 and by
Carter (Bombay epidemic of 1877), was noticed in a moderate degree in
only nine of our cases, and seems to be of infrequent occurrence. When
we observed it it seemed due to an admixture of a faint jaundice tinge
with a deep flush. Jaundice, as already stated, is of common
occurrence, though its frequency varies greatly in different
epidemics. It was present in 25 per cent. of our cases, rather more
frequently in the negro patients than in whites, and in degree varied
from a slight tinge of the conjunctiva and skin to the deepest
staining of the entire body. The presence of jaundice in combination
with the general features of high fever imparts a most peculiar and
alarming appearance to such patients.
With the occurrence of the crisis the flush rapidly subsides and the
face becomes pale, or, if the discharges have been profuse, it may
appear sunken, haggard, and almost choleraic. Parry described a
peculiar puffed, velvety look at this stage, as though the skin had
been much thickened and softened at the same time.
{377} There is no characteristic eruption in relapsing fever. In 150
out of 180 cases where the condition of the skin was carefully noted
there was no eruption of any kind; in 4 cases there were small
roseolar spots, with peculiar subcuticular mottling, which resembled
the early stages of typhus eruption, but soon faded away without
becoming petechial. A similar eruption was noticed by Murchison in 8
out of 600 cases. It appears from the third to the seventh day of the
first paroxysm; it may or may not recur in the relapse, or it may
occur then only. Eruptions apparently similar to this have been
described by others as quite common in certain epidemics. Carter
describes minutely an eruption which was noted in at least 10 per
cent. of his Bombay cases, the spots of which were at first small,
slightly raised, and pinkish or rose-colored, and which either faded
away soon or changed into purplish, more persistent stains. In a
valuable report on the Konigsberg epidemic of 1879-80, Meschede[10]
remarks that roseola was observed in cases complicated by exanthematic
typhus, which prevailed simultaneously, but in no case of
uncomplicated relapsing fever. While, however, this suggestion may
apply to some few of the cases of eruption observed by others, it is
certainly inapplicable to the vast majority of them. We also noticed
an eruption of pale-reddish, slightly elevated papules in seven cases.
It must be borne in mind that persons of such a low class as are the
great majority of relapsing-fever patients would naturally be expected
to present a variety of cutaneous eruptions from filth or vermin, and
that in consequence some of the appearances above described may have
been of such origin. It is certain that the bites of either
mosquitoes, fleas, or bedbugs may in this disease be followed by
persistent reddish papules passing into petechiae. Apart from this,
however, true petechiae have been quite common in some epidemics,
while very rare in others. Parry saw "small spots of purpura" once
only, in a delicate girl; and we did not observe petechiae once in
several hundred cases, many of which had extensive internal
ecchymoses. On the other hand, they have been found in as much as 30
per cent. of all cases (314 out of 1000 cases, Smith at Glasgow). They
do not appear on any fixed day, but are more common in the first
paroxysm than in the relapses; and although sometimes associated with
a tendency to hemorrhages from other surfaces, they have been so often
observed in cases of ordinary severity that scarce any unfavorable
prognostic value can be attached to them.
[Footnote 10: _Virchow's Arch._, Bd. lxxxvii., p. 405.]
Vibices and extensive ecchymoses of the surface are of much more grave
import, and in cases where fatal sinking is threatened they may appear
accompanying a purplish lividity of the countenance.
Herpetic eruptions about the mouth or nostrils were observed in 20 out
of 181 of our cases in which this point is noted. They appeared
usually toward the close of the febrile stage, and their development
was found to have value in determining the approach of the crisis.
Barensprung mentions especially the occurrence of herpes labialis in
cases of irregular relapsing fever which bore considerable resemblance
to typhus. Sudamina are, as might be expected in a disease attended
with so much sweating, of quite common occurrence, though much more so
in some epidemics than in others, unless searched for with greater
care by the one set of observers. Desquamation was noted in 42 out of
181 of our cases, and {378} invariably at the close of the relapse. It
was usually confined to the hands and face, and occurred in the form
of comparatively small flakes. This is more frequent than has been the
case in most epidemics. Murchison quotes a case in which a piece of
epidermis ten inches square separated from the body of a lad
convalescent from relapsing fever.
A peculiar odor exhaling from patients with relapsing fever has been
repeatedly noticed. A description of this unpleasant symptom, given by
Kelly, as quoted by Murchison,[11] accords closely with what was
frequently manifest in our own cases: "The smell was peculiar, not
fetid or heavy, but somewhat like burning straw with a musty odor."
Carter, in describing a similar odor in some of his cases, notes that
the skin was not in these instances in a particularly foul state.
[Footnote 11: _Op. cit._, p. 346.]
From what has already been said, it will be anticipated that the
variations of the temperature in relapsing fever constitute the most
peculiar and characteristic feature of that disease. A careful study
of the accompanying charts will convey a more accurate impression than
can be given by any description. The temperature begins to rise before
the chill is fully developed, and when there is no initial chill the
patient may be found within a few hours of the appearance of giddiness
and headache with a temperature of 102.5 degrees to 103.5 degrees.
Before twenty-four hours have passed it has risen to from 104 degrees
to 106 degrees. During the paroxysm the febrile movement is continued,
presenting merely a diurnal variation of one to two degrees, sometimes
attended with sweating and partial relief of distressing symptoms, the
minimum being observed at different hours in different cases, or even
in the same case, though more frequently it occurs in the morning.
In a case reported by Parry a chill recurred at the same morning hour
on three successive days. Wyss and Bock report some unusual cases in
which a brief intermission occurred, with a fall of pulse and
temperature to the normal, most frequently on the day before the real
termination of the paroxysm. The highest temperature varies from 104.5
degrees to 108.75 degrees; in our cases the highest observed was 107.5
degrees. This occurs, as a rule, on the last day or the day before the
last of the initial paroxysm, and Obermeier has observed a sudden rise
of four degrees in half an hour just before the crisis. Meschede,[12]
however, found the highest temperature on the corresponding days of
the first relapse.
[Footnote 12: _Loc. cit._]
The duration of the primary paroxysm is usually six or seven days; but
this is subject to considerable variations, as will be seen from the
following table of 160 cases in which the duration was accurately
ascertained: Initial paroxysm lasted--2 days in 1 case; 3 days in 2
cases; 4 days in 10 cases; 5 days in 19 cases; 6 days in 40 cases; 7
days in 58 cases; 8 days in 18 cases; 9 days in 2 cases; 10 days in 5
cases; 11 days in 2 cases; 14 days in 2 cases; 15 days in 1 case; and
Parry, observing the same epidemic, found the duration of the first
paroxysm to vary from 4 to 11 days. It is, however, rare for the
duration to exceed ten days unless some complication be present.
{379} [Illustration: FIG. 20. Typical case of relapsing fever, with
three relapses, terminating in recovery. (From Motschutkoffsky)]
With the beginning of the crisis there is a prodigious and sudden fall
of temperature, unequalled in any other condition of disease. Within a
few hours it may fall six or eight degrees (going down at the rate of
1.5 degrees or 2 degrees an hour); and falls of 12 degrees, 13
degrees, or even 14.4 degrees (Murchison), in the course of twelve
hours have been noted. In our own cases the greatest {380} fall was
from 107.2 degrees to 95 degrees, or 12.2 degrees; and this is as low
a point as is usually reached, though temperatures of 94 degrees, 93
degrees, or even 92 degrees, have repeatedly been observed. Murchison
refers to one case in which collapse supervened, where the rectal
temperature was 90.6 degrees. In nearly all of our cases a subnormal
temperature occurred at the crisis, and lasted for a day or two
subsequently, when it gradually rose and remained normal until the
relapse, unless some transient complication caused a temporary rise in
the interval.
[Illustration: FIG. 21. Typical case of relapsing fever (Mary Collins,
aged 32), terminating in recovery. One relapse, with slight
post-critical rise of temperature.]
Occasionally, there is no relapse whatever, but convalescence follows
{381} the initial paroxysm. This occurred in 10 out of 181 of our
cases, and Murchison found that of 2425 cases reported by various
authors no relapses occurred in about 30 per cent. Carter describes
these under the name of the abortive form, and found them to
constitute 23.8 per cent. of all his cases. It is probable, however,
that in many cases so regarded either a relapse of very transient
duration has been overlooked, or else that an attack of ephemeral
fever has been regarded as of specific nature. In ordinary cases the
duration of the intermission averages six or seven days, but here,
again, considerable variation occurs. In 139 of our cases where its
duration could be accurately determined it was as follows:
3 days in 4 cases. 7 days in 64 cases. 11 days in 1 case.
4 " " 3 " 8 " " 22 " 12 " " 1 "
5 " " 12 " 9 " " 9 " 13 " " 1 "
6 " " 12 " 10 " " 9 " 20 " " 1 "
Despite these variations in the duration of the initial paroxysm and
of the first intermission, the average date of the occurrence of the
relapse in any large series of cases is about the twelfth day from the
primary chill.
The relapse is ushered in with the same striking abruptness as the
initial attack. The temperature again rises rapidly to 104 degrees or
106 degrees, and then pursues a continuous course resembling
ordinarily that of the primary paroxysm. The difference between the
maximum of the two paroxysms is rarely more than 1.5 degrees or 2
degrees, though either may be much milder than the other; as a rule,
the highest temperature is attained on the last or penultimate day of
the first attack. The duration of the relapse averages three or four
days, though it may last but a few hours or a single day, and yet
exhibit a rise of 5 degrees, 6 degrees, or 7 degrees; or, on the other
hand, it may be prolonged to six, seven, or even more days. Lyons,
observing the disease in the Crimea, reports some relapses as having
lasted twenty-one days, though it is improbable that a greater
duration than seven days occurs without the presence of some
complication. The relapse usually terminates by crisis, with an abrupt
fall to an abnormally low temperature; though we observed at this
time, much more frequently than at the close of the first paroxysm, a
gradual subsidence of fever, or lysis. Again the patient regains
strength and appetite, but in a considerable proportion of cases
subsequent relapses ensue. As a rule, the second, third, and later
relapses are attended with a febrile movement of shorter duration and
of less severity than the first two paroxysms, and are also separated
by intermissions of increasing length. Meschede[13] found from a study
of 360 cases that the average duration was for the first paroxysm six
or seven days; second paroxysm, four or five days; third paroxysm,
three or four days; fourth paroxysm, one or two days; fifth paroxysm,
one day.
[Footnote 13: _Loc. cit._]
In a remarkable case given in full at page 394, the duration of the
paroxysms and intermissions were as follows:
First paroxysm, 8 days; first intermission, 9 days.
Second " 5 " second " 1 "
Third " 1 " third " 6 "
Fourth " 6 " fourth " 8 "
Fifth " 5 " fifth " 9 "
Sixth " 4 " sixth " 10 "
Seventh " 3 " seventh " 11 "
Eighth " 3 " followed by convalescence.
{382} The proportion of cases in which more than a single relapse
occurs appears to vary in different epidemics. Murchison found that in
1500 cases reported by various authors a second relapse occurred 109
times (1 out of 14); a third relapse, 9 times (1 out of 166); and a
fourth relapse, once. Of 182 cases noted carefully by ourselves, a
second relapse occurred 24 times (1 out of 7-1/2); a third relapse, 5
times (1 out of 36); a fourth relapse, once; and in the
above-mentioned case six or seven relapses.
It follows that the total duration of the morbid process varies from
the average of about eighteen or twenty days, in cases with a single
relapse, to forty, sixty, or even ninety days. Of course the
occurrence of complications may lead to very great modifications of
the febrile movement and of the total duration of the disease.
There are several additional points about the febrile process
requiring mention. In all the paroxysms there is a greater tendency to
local or general perspirations than is met with in other continued
fevers, and occasionally there are rigors or slight chills about the
same hour on several days after the invasion or on the day preceding
the crisis. It has been noted also that, even when the temperature is
very high, the quality of the heat, as judged by the feeling of the
skin, is different from that in typhus fever, and that the peculiar
pungent irritating sensation known as calor mordax is rarely marked.
But a more important peculiarity is the fact that the extreme
temperatures (106 degrees, 107 degrees, or 108 degrees) that are
frequently observed in relapsing fever for several days in succession
do not appear to involve any great increase of danger, and in
particular are not attended with the production of the grave nervous
symptoms so often met with in connection with hyperpyrexia in typhus
and typhoid, and often regarded as the direct result of the exalted
temperature itself. This striking fact is of much interest in its
bearing on the theory of hyperpyrexia, and may possibly be explained
by some marked difference in the conditions of heat-dispersion in
these different diseases.
The pulse in relapsing fever is very rapid, and on the whole the rate
corresponds with the movement of the temperature. It usually rises
above 110, the limits being 90 and 140, the lower rate being noticed
in the milder and uncomplicated cases and in subjects of phlegmatic
constitution. The pulse rises rapidly at the invasion, and may reach
120 in the course of a few hours. Its maximum is usually noticed when
the temperature is highest, shortly before the crisis; and when this
actually begins the pulse may fall with a rapidity as remarkable as
that of the decline of the temperature. Thus, within twenty-four hours
it may fall from 152 to 80, or in even a shorter time from 140 to 54,
or even as low as 48 (Obermeier) or 44 (Muirheid), or even 30
(Stille). While this great fall is often noted, it is by no means
constant. In our own cases it was frequently observed that the
critical fall in temperature was not accompanied by a commensurate
fall in pulse. Thus, at the close of a very severe initial paroxysm
lasting nine days the temperature was 107 degrees, and fell in the
course of twenty-four hours to 99 degrees, and in twenty-four hours
more to 96 degrees; during the first day of this fall the pulse was
from 96 to 100, and during the second it fell to 76.
This want of correspondence was more marked at the close of the {383}
relapse than of the primary attack; thus, in a well-marked case, where
the maximum temperature (105.4 degrees) occurred eighteen hours before
the crisis of relapse, the temperature fell in four hours from 104.4
degrees to 96.2 degrees, while the pulse, which was 130, fell in
twelve hours to 108, and in twelve more to 92. In another case, in a
man aged twenty, the temperature at the close of the second relapse
was 106.4 degrees, with a pulse of only 100; after the crisis, as the
temperature fell, the pulse rose to 120, and did not descend until the
end of twenty-four hours; and later, at the close of thirty-six hours,
the temperature was 98 degrees and the pulse 72, lower than which it
did not go. Carter[14] states that in the Bombay epidemic it was
invariably the case that the pulse did not decline to an extent
corresponding with the temperature.
[Footnote 14: _Op. cit._, p. 140.]
During the remainder of the intermission the pulse may be normal, or
it may continue accelerated in consequence of some irritative
condition; as the time for the relapse approaches it frequently again
becomes abnormally slow. In either event it is found that any muscular
exertion causes marked acceleration of the pulse.
During the paroxysm the character of the pulse is full and bounding,
and there is considerable arterial tension. This is well shown in some
of the sphygmographic tracings by Carter;[15] while in one of our
tracings from the right radial of a man aet. 32, taken on the fourth
day of a severe initial paroxysm, the line of ascent is steep and the
summit sharp. During the crisis, and for a day or two thereafter, the
pulse may be weak, compressible, and dicrotic, and occasionally
irregular.
[Footnote 15: _Op. cit._, p. 103.]
The sounds of the heart and its impulse are weakened, except possibly
during the first few days of the primary paroxysm. Blood-murmurs over
the base of the heart and along the great vessels in relapsing fever
were first noticed by Stokes, and have been frequently observed in
subsequent epidemics. They were found in a large proportion of our
cases, not rarely in both paroxysms, and during the early stage of
convalescence when anaemia was marked; but during the intermissions
they are rarely audible, and when the action of the heart was slow
they were replaced by prolongation of the first sound.
It must be further noted that the pulse-rate is not a reliable
indication of the danger in this disease, since, just as is the case
with the hyperpyrexia, extreme rapidity of pulse may be present when
the general symptoms denote no unusual danger, and when the patient
ultimately recovers most satisfactorily.
There is a remarkable disproportion and dissimilarity between the
cerebral and peripheral nervous phenomena in relapsing fever and those
familiar to us in typhus and typhoid fevers. We have seen that
patients almost invariably complain of headache. When prodromes are
present it is commonly among them, and it may be the initial symptom
to usher in each paroxysm. When the attack is fully developed headache
is usually very severe, and no symptom is more bitterly complained of.
It varies in seat and character. More commonly it is frontal or
general; occasionally we found it occipital, and still more rarely it
was unilateral, constituting hemicrania. It rarely continues during
the relapse. Headache of an equally acute and violent character may be
present in typhoid, but the headache of typhus is much more dull and
contusive.
{384} The mental condition is only exceptionally affected, a
circumstance which greatly increases the patient's perception of his
sufferings. Delirium is not present in ordinary cases, even though
very severe and attended with hyperpyrexia; or if present is limited
to the period immediately preceding the crisis, when there may be
violent and noisy delirium of transient character. In some of our
cases forcible restraint was necessary under these circumstances.
There are numerous instances on record showing the abruptness with
which noisy, demonstrative, or even destructive delirium may appear,
and the equal suddenness with which in the course of a few hours, or
even of fifteen minutes, the patient may become rational and composed.
Such attacks resemble hysteroidal spells, and probably occur more
readily in patients of a nervous or hysterical temperament. They were
certainly more common when the patients had been of intemperate
habits; and, further, we had opportunities of noting that the
occurrence of relapses in habitual drunkards who had previously
suffered with delirium tremens was apt to develop a form of delirium
which was to all appearance of that nature.
Delirium of a different and much more grave type may appear in
connection with the symptoms of the typhoid state. In some cases this
results from the presence of serious complications which induce a
state of great prostration, while in others it is associated with
great diminution or entire suppression of urine. The delirium under
these circumstances is apt to be low and muttering, with a tendency to
pass into stupor or profound coma.
Vertigo is present more frequently and in a more persistent form than
in any other febrile disease. It was noticed as among the occasional
prodromes, and was especially severe for the first few days of the
initial paroxysm, though it often continued throughout this stage and
recurred with the relapse. Occasionally it was complained of in the
recumbent position, but usually it was excited only by a change of
position.
Wakefulness was one of the most distressing symptoms in all cases, and
appears to have been noted in all epidemics. Although the severity of
the pain in various parts of the body and the absence of blunting of
the perceptions would naturally cause much loss of sleep, the degree
of the insomnia and the obstinate resistance it offers to the action
of anodynes are apparently far in excess of what could thus be
accounted for. Parry found that several of his patients could take as
much as three grains of opium every second hour throughout the
afternoon and night without either inducing sleep or causing
contraction of the pupils.
Convulsions are rare and of very grave import. They may occur at the
period just preceding crisis, when the nervous irritation is most
intense, and are then somewhat less indicative of a fatal result than
if occurring in the course of the paroxysm, when they are apt to be
associated with extreme prostration of the nervous centres, with a
tendency to subsequent fatal coma. No connection has been observed
between their occurrence and the presence of albumen in the urine.
General tremor is rare, and was observed only in those of our cases
where there had been habitual intemperance, with presumably a tendency
to delirium tremens. Muscular rigidity was noticed occasionally, but
may have been only apparent, being induced by the hyperaesthesia and
{385} soreness which were marked in some cases. The hyperaesthesia
which was observed was both cutaneous and muscular, and was attended
with tenderness of the body of the muscle, and also of the nerve-trunk
supplying it. Meschede speaks of opisthotonos as a rare complication
in his cases.
Motor paralysis involving single muscles or groups of muscles is
occasionally noticed, as of the deltoid or of one arm (Meschede).
Parry observed transient loss of power of the extremities in several
cases, chiefly during the intermission or the period of convalescence.
In one of our cases temporary hemiplegia occurred, with partial loss
of sensation on the affected side.
The bladder and rectum are rarely affected, except in cases where the
typhoid state with tendency to coma is present. Disorders of sensation
are, however, much more common. When motor palsy occurs the affected
part may also be the seat of impaired sensibility, while in a large
proportion of all cases numbness of the extremities, with or without a
sense of tingling, is complained of; out of 182 cases we noted this
symptom in 94, affecting the fingers alone in 62, the feet alone in 6,
and all the extremities in 25 cases. Cutaneous hyperaesthesia or
partial anaesthesia are also occasionally observed. But the most
noteworthy and constant symptom of this class are the pains in the
muscles and joints which are bitterly complained of by nearly all
patients with relapsing fever. They constitute, indeed, one of the
highly characteristic features of the disease, and possess a
diagnostic value. They may occur among the rarely present prodromes,
but usually they appear with the chill and increase in intensity
during the paroxysm; they may persist with even greater severity
during the intermission, or, if they have then subsided, recur with
the relapse, and may constitute one of the most troublesome hindrances
to convalescence. It will thus be seen that in frequency, severity,
and persistency they differ widely from the aching pains in the
extremities complained of in typhus and other specific fevers. They
are one of the most potent causes of the extreme insomnia, and are apt
to dwell in the mind of the patient so vividly that he dreads each
relapse on this account, and consequently looks back upon his attack
of relapsing fever as a terribly painful experience. These pains are
usually described as rheumatic in character, and several times
patients presenting themselves at the hospital on the second or third
day of the initial paroxysm stated that they had inflammatory
rheumatism. As a fact, we observed the utmost intensity of these pains
in a few cases where the patients were of marked rheumatic diathesis.
The nape of the neck, the muscles of the trunk or extremities, or the
large or small joints, or lower parts of the spinal region, may be the
seat. At times they extend along the course of nerve-trunks. In
character they are described as a deep intense aching, with occasional
severe or excruciating, sharp, lancinating pains. Pressure or movement
increases them. The joints are not red or swollen (though swelling may
appear as a sequel), and the pains seemed to us rather to be referred
to the joints than to be caused by any local irritation therein. As
already stated, there is often tenderness of the body of the muscles,
and this was especially marked in many of our cases on pressure along
the course of the nerve-trunk.
Murchison suggests that they are due to the circulation in the blood
of an {386} abnormal substance, such as uric, lactic, or phosphoric
acid; but it appears to us altogether probable that they are rather to
be connected with states of congestive irritation of the sheaths of
the nerve-trunks (early stage of perineuritis), or possibly in some
cases of the spinal membranes also. It is true that they are sometimes
shifting in their seat and fluctuating in their severity, but this is
not inconsistent with the above suggestion, while the widespread
irritative processes found in this remarkable disease, the resemblance
of these pains and the frequently attendant numbness and tingling to
the sensations caused by other forms of perineuritis, and the
occasional development of local palsies of a single muscle or group of
muscles, all are in its support.
The special senses are acute, sometimes painfully so. The eyes are
watery and occasionally injected, but this latter condition is rare
and slight in relapsing as compared with typhus fever. At the crisis
and for a few days subsequently wide dilatation of the pupils is not
infrequently observed. Dulness of hearing was present during the
paroxysm in 14 of our cases, and a few patients complained of
tinnitus; but these symptoms are not at all common in the disease,
although it will be seen hereafter that affections of the middle ear
are among its sequelae.
Debility is not such a prominent symptom as in typhus and typhoid
fevers. Patients manage to drag themselves about for several days
during the initial paroxysm with all the symptoms fully developed, and
after admission to the hospital will often be able to help themselves,
or even to rise from bed, unless prevented by the severe pains or the
vertigo. Still, there are many cases, not necessarily of very grave
type, in which there is a marked sense of weariness and exhaustion,
and of course in all cases of typhoid character the prostration is
great. It must constantly be borne in mind that even when the patient
feels or seems able to sit up he must on no account be permitted to do
so, since the occurrence of sudden and fatal syncope is one of the
accidents constantly to be apprehended. It is not only during the
pyrexia that this precaution must be enforced; we meet with extreme
debility during the intermission in some cases, and syncope has
followed exertions made at that period as well as at others.
During the paroxysms the respirations are much accelerated, at times
to a greater degree than would correspond with the pulse-rate, while
at others extreme rapidity of pulse may be associated with moderate
elevation of the rate of respirations.
As examples of the relation between temperature, pulse, and
respirations we quote the following from our records of adult cases:
(_a_) Temperature, 108 degrees; pulse, 124; respiration, 40. In the
relapse; no chest trouble.
(_b_) Temperature, 107.5 degrees; pulse, 120; respiration, 28; falling
to temperature, 96 degrees; pulse, 68; respiration, 18, within twelve
hours, during which crisis occurred.
(_c_) Temperature, 107 degrees; pulse, 144; respiration, 31. In the
relapse.
(_d_) Temperature, 107 degrees; pulse, 108; respiration, 44. Initial
paroxysm; no pulmonary congestion.
Temperature, 106 degrees; pulse, 116; respiration, 28. Relapse; no
pulmonary congestion.
Temperature, 97 degrees; pulse, 76; respiration, 24. Critical fall;
cough, {387} congestion of lungs posteriorly, and left one relatively
dull on percussion, but pneumonia did not develop.
In many epidemics bronchitis, hypostatic congestion, and pneumonia are
of rare occurrence, while in others, as in Philadelphia in 1870, they
are comparatively frequent and lead to serious respiratory symptoms.
While the pyrexia was high there was very frequently an irritative dry
cough, with the fine crepitant and subcrepitant rales attending
congestion and imperfect expansion of the lungs heard at the middle
and lower portions of the chest posteriorly. In numerous instances the
rales would disappear entirely after a few full inspirations in the
sitting posture, just as in the corresponding condition in typhoid
fever. But in a considerable proportion of all the cases (fully 35 per
cent.) there was more troublesome bronchial cough, associated with
sonorous, sibilant and subcrepitant rales, with mucous or
muco-purulent expectoration.
Bronchitis of this character was a source of serious annoyance to many
patients. In several cases there was impaired resonance at the lower
margins of the lungs posteriorly, with imperfect bronchial
respiration, but without the symptoms of fully-developed pneumonia.
Such conditions were regarded as due to hypostatic congestion, and
proved amenable to treatment. Pneumonia occurred in eleven cases out
of 200 recorded with reference to this complication. It will be more
fully discussed under the head of Complications. It was attended with
the usual physical signs, and gave rise to extremely rapid and labored
breathing, especially when associated with painful enlargement of the
liver and spleen. In a case of double pneumonia, with enlarged and
ruptured spleen, the respirations were from 80 to 90 for two days, the
pulse being 130 to 136. It was a very fatal complication, death
resulting in all but two instances.
Leyden[16] has shown that though the percentage of carbonic acid in
the air expired during the pyrexia is diminished, the total quantity
exhaled is increased, the proportion being as 1.5 to 1 in the
non-febrile state.
[Footnote 16: "U. d. Resp. in Fieber," _Deutsch. Arch. f. klin. Med._,
1870, 536, quoted by Murchison.]
Elaborate investigations have been made of the condition of the urine
in relapsing fever by numerous observers, and in the Philadelphia
epidemic of 1870 we had the great advantage of being assisted by the
distinguished chemist, the late Horace B. Hare, who conducted an
extensive series of analyses in our cases. In a number of cases
quantitative analyses were continued daily throughout the entire
course of the disease.
As a rule, the quantity of the urine is comparatively free during the
febrile periods, very scanty at the time of crisis, except in the
cases where critical discharges of urine occur, and excessive for some
days after the crisis.
Still, there were not rare exceptions, especially to the first of
these statements. Thus on four successive days of the relapse of a
severe case with delirium, but without albumen, and which ultimately
recovered, the analysis gave--
Temperature. Amount in ccm. Sp. gr. Urea in Grm. Na. Cl.
103 400 1024 23.8 2.64
105 300 1025 15.27 1.95
106 500 1024 24.7 4.3
106 to 97 850 1021 24.735 5.525
{388} And in another severe case, also resulting in recovery, the
analysis was, for two days preceding the crisis of the initial
paroxysm--
Amount. Sp. gr. Urea. Na. Cl.
500 1014 12.9 Traces of albumen.
650 1014 15.85 1.365
After the crisis:
2250 1004 18.9 15.75 No albumen.
And again, in another case at the height of the initial paroxysm,
within twenty-four hours of the crisis, no vomiting, purging, or
epistaxis being present; temperature 105 degrees; only 500 ccm. was
passed of dark reddish colored urine, non-albuminous, and with sp. gr.
1011.
In a fatal case there was total suppression of urine for three days,
the catheter drawing off only a few drops of almost pure liquid blood.
When crisis occurs by copious urination the discharges are frequent,
large, and of light color and low specific gravity.
The urine of the intermissions is of similar character, and for
several days after crisis it is not rare to have 2000 to 2500 ccm.
passed. The largest amounts we noted were in a man who recovered, and
who passed at the crisis of the relapse and during the following days
the amounts here given.
Amount. Sp. gr. Urea. Na. Cl.
1000 ccm. 1010 14.9 2.6
2000 " 1003 20.2 42.8
3550 " 1002 26.625 130.995
2600 " 1002 19.24 27.30
2800 " 1005 24.96 22.66
2500 " 1013 47.25 11.25
2700 " 1014 59.13 7.29
Carter reports a case where the patient continued for two weeks after
the relapse to pass 130 oz. of sp. gr. 1002.6.
The amount of urea varies considerably, and is evidently under the
influence of complicated conditions. The rule appears to be that it
increases during the paroxysms, diminishes during the crisis,
increases during the few days following crisis, and then falls off
again. These results are stated upon the authority of Murchison,
quoting from Pribram and Robitschek, Wyss and Bock, and others. Our
own observations, however, while agreeing in the main with these, show
that there are numerous and important exceptions, especially to the
occurrence of the post-febrile increase in the elimination of urea.
The largest amount of urea excreted in twenty-four hours by any of our
patients was 59.13 grammes, or 912 grains, on the sixth day after the
end of the relapse, but as much as 74 grammes (1142 grains) have been
found.
Deposits of urates were very common in the urine of the paroxysms and
of the crisis. The uric acid has been found increased, and so also
have the phosphates, crystals of which are frequently found mixed with
the urates.
The chlorides diminish during the paroxysms, until just before the
crisis their amount is very small, or they may even have disappeared.
Immediately after the crisis they reappear slowly or quickly, and even
{389} very large amounts may be discharged, as seen in the figures
given by Hare's analyses: 2.6 grm. on day of crisis, 42.8 grm. the
following day, and the enormous amount of 130.995 grm. on the next
day. A copious flow of urine corresponds with great augmentation in
the amount of the chlorides.
Bile-pigment was constantly present in jaundiced cases, the amount
being proportioned to the depth of the jaundice and the quantity of
the urine. Bile-acids have been detected (Carter and Schmidt), and
also leucin and tyrosin (Pribram and Robitschek).
Albumen, with or without tube-casts, is not uncommonly found, and
traces of sugar have been detected in a few cases. More careful
consideration will be given to these under the head of Complications.
The following appearance of the tongue has been repeatedly described,
and when present may be regarded as possessing some diagnostic value:
The body of the tongue slightly swollen, so as to show the impressions
of the teeth, and by the second day the central part of the dorsum
covered with a peculiarly white fur, while the edges and a small
triangular space at the tip are clean and red. Such a tongue was seen
in many cases at the beginning of the Philadelphia epidemic, but later
it was present in but a small proportion. We find it specially
mentioned in 97 of our recorded cases, or about 50 per cent., the
general description being given that it was moist, rather large, with
pink, clear edges, and a triangular clear space at the tip, and with
heavy white fur in the centre.
Some accurate observers, as Wyss and Bock, did not notice anything
peculiar about the tongue, but merely described it as moist and coated
with a thick white fur. The tongue often remains moist throughout the
case, the coat becoming yellowish, and later brownish. Of course if
there is nasal obstruction from epistaxis or catarrh, and the patient
breathes through the mouth, the tongue will soon become dry and brown;
but in addition, this state of the tongue with sordes on the teeth and
lips, appears in a small proportion of cases (3 per cent., Zuelzer; 12
per cent. of our own patients) in conjunction with grave typhoid
symptoms.
During the intermissions the tongue clears off quite rapidly, unless
marked gastric disturbance persists, but regains its former state as
soon as the relapse occurs.
In rare cases the tongue is red and glazed, and Parry and ourselves
observed peculiar painful cracks continuing obstinately after the
relapse. It is apparent, therefore, that the tongue presents evidences
of vitiated secretions, of local catarrh of the buccal mucous
membranes, and of the high grade of gastric irritation so constantly
attendant on this disease.
As a rule, there is complete anorexia during all of the febrile
paroxysm, while in the intermission the appetite soon returns, and is
sometimes truly ravenous. We did not, however, observe in any case a
voracious appetite during the febrile paroxysms, such as was very
often present during the London epidemic of 1843 and the Irish
epidemic of 1847, and is particularly mentioned by Murchison.[17]
[Footnote 17: _Op. cit._, p. 360.]
Thirst is constant and intense, and is excited not only by the high
temperature, but by the irritation of the stomach; it may continue
through {390} the intermission, when natural appetite and the power of
digesting solid food have returned.
Nausea and vomiting are always prominent symptoms, and most especially
so in children. In some cases nausea occurs among the prodromes; and
occasionally the attack is ushered in by profuse and uncontrollable
vomiting instead of by a chill, and the stomach continues entirely
non-retentive throughout the paroxysm. Vomiting is not usually so
obstinate and severe, however, and with extreme care in feeding and
medication it will often be allayed after two or three days. It
occasionally recurs profusely immediately before the crisis, as in the
case given in full at page 394, where after a violent attack of
vomiting the patient fell asleep, and awakened in a profuse sweat.
This symptom was present in 146 out of 182 of our cases, was usually
confined to the febrile stages, and was, as a rule, worse in the
initial paroxysm.
The matters vomited consist of the ingesta colored with bile, of
glairy mucus tinged with bile, or of green bile, sometimes in
considerable quantity. Small particles of blood may occasionally be
noticed in the matters vomited, and in rare instances true hematemesis
occurs. Judging from the frequency with which in fatal cases we find
ecchymoses of the gastric mucous membranes with blood-stained mucus in
the cavity of the stomach, we should expect black vomit to be more
often observed than is the case. Murchison (p. 361) states that it was
not noted in any British epidemic except that of 1843, and then it
occurred in only a few cases, although it seems to have varied in
frequency at different places. Arrott at that time described the
symptoms as "quite common" in the fever at Dundee; and W. Reid of
Glasgow recorded the case of a girl in the same epidemic who vomited
large quantities of clotted blood, and who also had hemorrhages from
the bowels and from the ears. It has occasionally been observed in the
continental epidemics. It was observed in four of our cases. By all
who have observed blood-vomiting in relapsing fever it is recognized
as a symptom of almost invariably fatal import. Three of the four
cases in which we observed it proved fatal, but one patient, who had
copious hematemesis, both at the close of the first relapse and during
the second relapse, recovered after a desperate and protracted
struggle.
The bowels are not so often constipated as in typhus, and it is not
rare for diarrhoea and constipation to alternate, or for the bowels to
be loose throughout the paroxysms. They are noted in 181 of our cases
as regular in 32, loose in 61, and constipated in 88 instances.
Meschede states that diarrhoea was present in nearly one-half the
cases of the Konigsberg epidemic of 1879, though usually as a late
symptom, the early stage being marked by constipation, which in a few
cases persisted throughout. The stools may be consistent and dark or
thin and bilious, or occasionally, when gastric or intestinal
hemorrhage has occurred, they contain black coffee-ground matter.
Occasionally, the diarrhoea has a critical character, and occurs at
the close either of the initial paroxysm or of the relapse, though it
may not entirely substitute sweating. This mode of crisis occurred in
two of our cases, but Douglas observed it in 6 out of 33 cases.
The abdomen may appear enlarged, but this is as much the result of the
{391} enlargement of the liver and spleen as of gaseous distension,
which is rarely present in a high degree. Abdominal pain is almost
constant, and may be very severe. It is especially mentioned as having
been present in 148 out of 182 of our cases. It commonly extends
throughout the epigastrium and both hypochondria, but may be present
on one or the other side, while, on the other hand, there may be
general abdominal soreness. It is associated with tenderness on
pressure, which may be so great as to hinder the movements of the
trunk and to render the descent of the diaphragm in breathing painful.
This may be the first symptom to usher in the attack, and it occurs at
an early stage in most cases. Many of our patients when admitted to
the hospital had already been cupped or blistered over the region of
the liver or spleen. This distress was greatest in cases attended with
jaundice and marked gastric irritation; and Parry reports that in his
cases (occurring in the early part of the epidemic which we studied)
jaundice was rare (4 out of 37), and abdominal tenderness was not
present. It is not difficult to explain its almost universal presence
in view of the severe lesions of the substance of the liver and
spleen, the distension of their capsules from the acute swelling of
the organs, and the implication of the coats of the stomach.
Enlargement of the liver and spleen probably exists to a greater or
less degree in every case of relapsing fever without exception. This
statement is based on the concurrent testimony of accurate observers
in all epidemics and upon the evidence of post-mortem examinations.
The enlargement of the liver can be demonstrated in nearly all
instances by careful percussion. It varies greatly in its degree,
however; in mild cases it may be slight, while in severe ones the
liver may be found extending at least three inches below the margin of
the ribs within three or four days from the initial symptom. In our
own fatal cases the weight of the liver averaged between four and four
and a half pounds.
The spleen enlarges even more rapidly and to a greater degree than the
liver. In fact, its enlargement in relapsing fever is greater than in
any other acute disease. It may be detected by percussion by the first
or second day, and may then continue to rapidly increase until by the
fifth or sixth day a large painful mass is readily recognized by
palpation and percussion, or even by inspection. The organ often
weighs twelve or sixteen ounces, not rarely twenty to twenty-five,
and, as an instance of the extreme limit that may be reached, Kuttner
reports sixty-eight ounces in one case. This enlargement is greatest
toward the close of the first or second paroxysm, and subsides quite
rapidly in most cases during the intermissions and as convalescence
progresses; we have, however, known a moderate degree of enlargement
of the spleen to persist for some weeks after the crisis of the last
paroxysm.
The occurrence of jaundice in a considerable proportion of cases of
relapsing fever is a clinical fact of much interest. Its frequency
varies greatly in different epidemics, and even at different stages of
the same epidemic. At times it is rarely met with (1 out of 14, 20, or
35 cases), while in other epidemics it is present in 1 out of every 6,
5, or even 4 cases. Of 182 of our own cases jaundice is recorded in
45, or exactly in 1 out of 4. According to our observation, it
occurred in a larger proportion of cases among negroes (14 out of 32)
than in whites, and {392} Stille states that it occurred in nearly
every such case that came under his observation. When present it
usually occurs during the first paroxysm, and may be limited to that
stage; or, again, it may be present in each of three or four
successive paroxysms in the same case; or, finally, it may first
appear in the relapse. As a rule, it subsides speedily after the
crisis, though Carter states that in two or three cases the symptom
made its first appearance just after the crisis. It varied from the
slightest yellow tinge of the conjunctiva to the deepest staining of
the whole surface. The urine is discolored in proportion to the
intensity of the jaundice, and the serum of a blister will be deeply
tinged. It must be carefully noted, however, that the feces are not
decolorized, but, as already described, contain fully a normal amount
of biliary coloring matter. This fact has been relied on by Murchison
and others to prove that the jaundice in relapsing fever is purely
dependent on the morbid state of the blood, and is not due to
obstruction of the biliary passages; and we are prepared to admit that
the element of blood-dyscrasia may play a part in the production of
the jaundice. The anatomical evidence, however, given on page 414,
renders it probable that in many cases at least the essential cause is
to be sought in an obstructed state of the minute gall-ducts of
certain areas of the liver. If the main hepatic duct or the common
duct were obstructed, there would of course be paleness of the feces,
as the bile would be prevented from entering the duodenum. But when a
large amount of highly-colored bile is being secreted, as in relapsing
fever, it seems clear that the obstruction of a certain number of
minute ducts would cause sufficient resorption of the bile to induce
jaundice of varying degrees of intensity, while at the same time
allowing a flow of bile through the patulous ducts.
Jaundice must be regarded as an unfavorable or even a grave symptom in
relapsing fever, but not to the extent that would be the case were it
directly connected with the intensity of the blood-dyscrasia. Many of
the most violent cases in all epidemics have been unattended with
jaundice, while, on the other hand, many cases in which jaundice has
been marked "have had not a single symptom that made them differ from
ordinary cases excepting the yellowness" (Henderson). It follows,
therefore, that the gravity of a certain proportion of the jaundiced
cases does not follow directly from the presence of bile in the blood
and tissues, but from the lesions of the liver of which the jaundice
is a symptom, or from the existence of widespread irritation of many
parts of the body. Thus jaundice is present in an unusually large
proportion of the cases attended with marked enlargement and
tenderness of the liver and spleen, whether vomiting is also present
in extreme degree or not. It was noteworthy that it was
disproportionately frequent in negroes, and that in these patients the
lesions of the liver and spleen were also unusually pronounced. Again,
jaundice is present in an unusually large proportion of the cases
attended with low delirium, extreme prostration, defective secretion
of urine, and the other features of the typhoid state--so much so that
such cases have been described by various writers under the name of
bilious typhoid fever.
But, as already stated, it is not legitimate to consider the gravity
of these cases as the result of the jaundice, but rather that the
jaundice is merely a symptom of the widespread irritative lesions,
which in such {393} cases not only involve the liver and spleen, but
the kidneys, the lungs, the marrow of the bones, the muscle of the
heart, and occasionally the membranes or substance of the brain and
cord.
The true prognostic value of jaundice in relapsing fever would then
seem to be, that of itself it indicates merely an obstructed state of
a certain number of minute bile-ducts, but that its presence justifies
the apprehension that the local lesions of the liver may become
excessively developed, or that there is a tendency to widespread
tissue-changes which at a later stage of the disease may lead to the
appearance of grave constitutional disturbance of a typhoid type.
Hemorrhage in relapsing fever is not uncommon, and may occur from
various surfaces. Epistaxis is, however, the only form which is
frequent enough to justify being regarded as a symptom. It usually
occurs in from 5 to 15 per cent. of cases of relapsing fever, but in
the Philadelphia epidemic it was much more frequent than this,
occurring in not less than 83 out of 182 of our cases. It was not more
frequent or profuse in grave cases than in those of ordinary severity,
and consequently could not be regarded as a reliable indication of the
intensity of the blood-dyscrasia. Although ordinarily moderate in
amount, it was occasionally so copious and persistent as to require
prolonged plugging of the nostrils, and in at least one case
contributed chiefly to cause an intense anaemia, which long delayed
convalescence. It occurs at all periods of the paroxysms, but more
commonly toward the close. In fifteen of our cases extraordinarily
profuse epistaxis attended the crisis, and evidently replaced in part
the copious sweating by which the paroxysm more commonly terminates.
SYMPTOMS ATTENDING THE CRISIS.--We have already described the
aggravation of all the symptoms which immediately precedes the crisis
in typical cases of relapsing fever, and the abrupt fall of
temperature, and usually of the pulse, that follows. But this
extraordinary change is nearly always attended with some profuse
critical discharge, of which sweating is by far the most common,
though copious epistaxis, metrorrhagia, diarrhoea, or vomiting may
also occur, and to a greater or less degree, but seldom entirely,
replace the sweating. In 182 cases in which we carefully noted the
mode of termination of the paroxysm there was no definite crisis
(termination by lysis or gradual and irregular defervescence) in 76;
profuse sweating, 89; profuse epistaxis, 15; profuse diarrhoea, 2.
In most epidemics the proportion of true crises is greater than in the
above table--a fact dependent upon the unusually severe and
complicated form of the disease which we were studying. The beginning
of the sweat may be preceded by chilliness or rigors, by extreme and
dangerous prostration, or by violent nervous disturbances; or there
may be an attack of profuse vomiting, followed by sleep, during which
sweating begins. The sweat may be moderate in amount, but is often
extraordinarily copious; the patient is literally bathed in it, the
bed- and body-clothing is saturated, and we have seen the mattress
saturated. It has an acid reaction, but we do not know of any accurate
analyses of it. Some writers have attributed to it a characteristic
disagreeable odor, but we did not notice any in our cases that could
be considered peculiar to this disease.
CONVALESCENCE.--We have already stated the average duration of {394}
relapsing fever to be eighteen or twenty days, while the extreme
limits are from eighteen to ninety days. Despite the fact, however,
that the mortality is in most epidemics only about 5 or 7 per
cent.--greatly less, therefore, than in typhus fever--the
convalescence from relapsing fever is frequently slow and protracted.
The obvious cause is, just as in the case of typhoid fever, the
existence of numerous and serious lesions of the solids and the
tendency to many troublesome complications and sequelae. We have,
however, seen many instances of rapid recovery of strength and health,
even after prolonged attacks with several successive relapses.
The following case is quoted partly on account of the numerous
relapses, and the long duration of the sickness:
B. B. Y., medical student, was much exposed to the contagion of
relapsing fever in the wards of the Philadelphia Hospital during the
spring of 1870, and in May had an attack apparently of this disease,
which, however, subsided in four or five days and was followed by no
immediate relapse. He continued his attendance at the hospital during
the remainder of May and the whole of June; in July took a trip to the
South, where there was no relapsing fever prevailing, and after
exerting himself for several days during intensely hot weather, he
became sleepless and much prostrated. He returned home, and after
recovering from the fatigue felt quite well for about a week, until 3
A.M., August 1st, when he was attacked with a severe chill, followed
by great insomnia, obstinate vomiting, intense headache, especially in
the back of the neck, occasional sweating, violent fever, recurrence
of very severe chill the following day at 11 A.M., epigastric and
hypochondriac tenderness, decided jaundice, costive bowels, and
scanty, high-colored urine. This paroxysm lasted till the morning of
August 9th, when severe vomiting took place, followed by sleep, during
which crisis occurred by drenching sweat lasting several hours.
Appetite and strength soon began to return, though some jaundice
persisted, and by August 17th he felt able to drive out a short
distance, and retired feeling somewhat fatigued. He awoke with pain in
the back of the neck, which continued increasing till 11 A.M., August
18th (second paroxysm), when a severe chill occurred, lasting three
hours and followed by the same train of symptoms, including jaundice,
which persisted five days, till Aug. 23d, when crisis again occurred
by sweating. On the 24th he felt well enough to use slight exercise,
which was followed by prostration and by a return of chill (third
paroxysm) the next day at 11 A.M., with subsequent headache, fever,
irregular sweats, etc., lasting but one day. Again felt well until
Aug. 30th, when he was attacked (fourth paroxysm) at 11 A.M. with
severe chill, lasting three hours, followed by severe paroxysm,
lasting six days, till Sept. 5th, when crisis again occurred by
sweating. Again felt well for eight days, until Sept. 13th, when the
fifth paroxysm occurred, lasting five days, ending Sept. 18th by
critical sweating. This was followed by an intermission of nine days,
until Sept. 27th, at 11 A.M., when the sixth paroxysm occurred,
lasting four days, and less severe than the preceding ones. This was
followed by an intermission of ten days, till Oct. 11th, when the
seventh paroxysm occurred at the same hour of the day, and lasted
three days. He then went sixty miles from home to a fine, pine-bearing
district, and enjoyed an intermission of eleven days, when the eighth
and {395} last paroxysm occurred at the same hour, and lasted three
days, until Oct. 25th. His convalescence was very satisfactory, and he
was enabled to resume his studies by the middle of November. No
sequelae occurred. In 1878 Dr. Y., who had been working very steadily
with a rapidly-growing practice, was attacked with severe typhoid
fever, with grave nervous symptoms and with albumen and tube-casts in
the urine, and died on the twelfth day.
It will thus be seen that in this unusually protracted case there were
seven distinct relapses, one of which was brief and interrupted one of
the regular intermissions, while the rest were all severe.
Duration of
1st paroxysm, violent, 8 days. 1st intermission, 9 days.
2d " violent, 5 " 2d " 1 day.
3d " less violent, 1 day. 3d " 6 days.
4th " severe, 6 days. 4th " 8 "
5th " severe, 5 " 5th " 9 "
6th " less severe, 4 " 6th " 10 "
7th " less severe, 3 " 7th " 11 days,
8th " mild, 3 " followed by convalescence.
The total duration of the case, which was entirely free from
complications, was therefore ninety days.
VARIETIES.--The foregoing clinical description prepares us to
appreciate the varieties of relapsing fever that may be said to exist.
They consist of--
The abortive form, in which a single paroxysm of variable length and
severity occurs, terminating in a critical fall of temperature and
usually with some critical discharge, but not followed by any relapse.
There can be no doubt of the existence of such cases, although they
are not common; and at times the paroxysm is so slight that were it
not for the known exposure of the individual to the prevalent epidemic
influence, in the absence of any other adequate cause, the case might
readily be regarded as one of non-specific febricula. The caution
must, however, be borne in mind as to the occurrence of relapses of
such extreme shortness of duration (less even than twenty-four hours)
as to readily escape notice unless a careful watch be kept for their
detection.
The ordinary or typical form, including the cases with one or two
relapses, presenting the usual variations in the severity of the
symptoms and in the duration of the paroxysms and of the
intermissions.
The multiple or protracted form, if it be thought desirable to thus
particularize cases presenting an excessive and unusual number of
relapses, as three, four, five, six, or even seven.
The grave or subintrant form, which is designed to include the highly
congestive form of Cormack and the bilious typhoid of Griesinger and
Lebert.
Under another heading (see relations to other diseases, p. 420) we
shall give reasons for regarding the bilious typhoid fever of
Griesinger and Lebert as merely a form of relapsing fever, with which
a certain proportion of cases of true typhoid fever complicated with
hepatic catarrh may have been included.
The characteristics of this grave subintrant form are as follows:
Jaundice, occasionally absent, but usually present in an intense
degree; marked enlargement of the liver and spleen; a tendency to
hemorrhage from various mucous surfaces; extreme prostration;
defective or suppressed {396} secretion of urine; hypostatic
congestion or inflammation of the lungs in a large proportion of
cases; dry brownish tongue; low muttering delirium, often passing into
stupor or coma; hiccough; imperfect crisis; and a continuance of some
morbid phenomena, so that merely a remission occurs to separate the
paroxysms; and a high percentage of mortality. The great modification
of the intermission which is so highly characteristic of typhoid
relapsing fever is doubtless due in chief part to the serious local
lesions developed, and seems to justify the name of subintrant as
above suggested. The course of such fever is well illustrated by the
following case, in which the characters of typhoid relapsing fever
were present in the highest degree, death occurring on the fifteenth
day:
Charles Hood, colored, aet. 28, of temperate habits, was taken ill on
April 5, 1870, after malaise lasting thirty-six hours, with fever,
nausea and vomiting, headache, and general aching throughout body; and
was admitted to the hospital April 6th. There was already marked
jaundice, and epistaxis had occurred; there were also insomnia;
wandering delirium; extreme tenderness over the liver and spleen, both
of which were enlarged; dryness of tongue, vomiting, and distension of
the abdomen. These symptoms continued, his condition becoming daily
more aggravated. Restless delirium alternated with heavy sopor. The
jaundice grew deeper. Marked digital formication existed, but the
arthritic pains were not so severe as in ordinary cases. The tongue
was dry and of a red orange color. Profuse epistaxis occurred on the
seventh day of the disease, requiring plugging of both anterior and
posterior nares, and followed by great prostration. A gradual fall in
the temperature occurred during the sixth, seventh, and eighth days,
reaching 99 degrees on the latter day. During this decline the
delirium ceased and the mind remained merely dull; the jaundice
decreased, as did also the tenderness of the hypochondriac zone. The
pulse and respirations improved, and diarrhoea ceased. The improvement
was but brief; for about eighteen hours he lay apyretic, with cool
hands and feet, and with eyes closed and mind dull but free from
delirium. Fever then reappeared and with the ascent of the temperature
the unfavorable symptoms recurred. The relapse lasted but two days,
and was followed by irregular decline of fever till death occurred on
the fifteenth day of the disease. Obstinate hiccough appeared on the
eleventh day, and continued, accompanied with occasional vomiting on
the fourteenth day. Delirium alternating with sopor reappeared.
Jaundice again became marked, and again there was extreme tenderness
over the liver and spleen. The pulse grew small and feeble, the
respirations shallow and labored, with an expiratory moan. Cough began
on the twelfth day, and was soon followed by the physical signs of
pneumonia of the lower lobe of both lungs. The urine continued free
from albumen. The patient sank into deeper coma, and died on the
fifteenth day. Post-mortem examination showed highly-developed
characteristic lesions of the spleen and liver, with red hepatization
of lower lobe of both lungs. There was no affection of the glands of
Peyer. The course of the fever is shown in the following tracing (see
Fig. 22).
[Illustration: FIG. 22. From a case of the bilious typhoid or grave
subintrant form of relapsing fever.]
COMPLICATIONS AND SEQUELAE.--As would be anticipated from what has
been said of the wide range of the symptoms and of the remarkable
course of the temperature in relapsing fever, there are many
complications and sequelae liable to occur, and which require special
consideration. {397} They may be classified according as they affect
the febrile movement, the state of the blood, or one or other of the
groups of organs.
We have already described the various irregularities presented by the
febrile paroxysms and the intermissions, and no further allusion need
be made to mere variations in length, severity, or number of the
former. In rare cases, however, a peculiarity is presented, usually in
the first intermission, which is difficult of explanation. About
twenty-four hours after an apparently complete crisis, with a fall of
temperature to a subnormal point, there may be a sudden and rapid rise
or rebound of temperature to 104 degrees or 105 degrees, attended with
distressing symptoms of high fever, but lasting only twenty-four or
forty-eight hours. A good example of this is given in the case
described on page 394; and Carter[18] cites several examples of it
terminating either in recovery or in rapid death. He asserts that
examinations of the blood during such post-critical febrile rebounds
invariably showed an absence of spirilla, so that in his opinion such
fever must be considered non-specific. Their explanation seems
difficult, since the pyrexia is too brief to be associated with any
local inflammatory complication.
[Footnote 18: _Op. cit._, p. 172.]
More frequent and serious is the protracted post-critical pyrexia
which we have already described as modifying the interval, so as to
produce a subintrant type by maintaining continuous though irregular
fever until the accession of the relapse, unless cut short by death.
This post-critical fever is non-specific, is unattended with spirilla
in the blood, and is to be associated with the extensive irritative
processes in the liver, spleen, kidneys, lungs, and other parts that
are present in these grave and {398} complicated cases. It is to be
noted that the course of those paroxysms which terminate in lysis
indicates that they may represent a milder type of the above process.
The peculiarities of the delirium, amounting sometimes to maniacal
excitement, which attends some cases of relapsing fever, has been
fully described.
Less common are the following: mental hebetude, lasting some days or
even weeks after the close of the last paroxysm, or, as in a case of
Carter's, gradually increasing mental feebleness, terminating in
imbecility. In such cases suspicion must arise of the occurrence of
some local lesion of the membranes or substance of the brain.
Partial palsy is mentioned by numerous authors as occurring during or
shortly after attacks of relapsing fever. Paralysis of one or both
deltoids has been noted, the latter by Cormack, who saw it continue
ten days after the patient was well in all other respects. Temporary
paralysis of the forearm (Douglas) or of the whole arm (Parry,
Meschede) has been observed; and Parry also describes loss of power in
the legs lasting for one week. In one of our cases temporary loss of
power of the left arm and leg occurred, attended with such impairment
of sensibility that the woman had to feel for the fingers of the left
hand to assure herself of their existence. This loss of power occurred
during the initial paroxysm, and gradually passed away, but she was
unable to stand alone on the thirty-first day of the disease. In a
case reported by Tennent[19] facial palsy was developed six days after
the second crisis.
[Footnote 19: _Glasgow Med. Jour._, May, 1871, p. 379.]
Various explanations have been offered for these local palsies, but,
as already stated (see page 386), it seems probable that they are
referable to morbid conditions of the nerve-trunks, or, less commonly,
of the spinal cord. It must be noted, however, that in a certain
number of autopsies serious intracranial lesions are found, which are
evidently the results of the attack of relapsing fever. These consist
of abscess of the brain, meningitis, and specially cerebral
hemorrhage. This was present in one of our cases, but Carter found
copious hemorrhage in no less than 8 out of 54 autopsies, and in 5
others there were minute capillary cerebral hemorrhages. Still, in
nearly all the cases of large hemorrhage we have found recorded the
effusion was upon the surface of the brain, and this, combined with
the absence of true hemiplegia from the forms of paralysis noted in
relapsing fever, and the transient character of these palsies, makes
it clear that they are not to be explained by any considerable
cerebral hemorrhage. On the other hand, however, it must be admitted
that an additional possible cause of them is to be found in minute
hemorrhage into small areas known to govern the movements of certain
groups of muscles. Again, we have had occasion to note the occurrence
of both thrombosis and embolism among the lesions of relapsing fever,
and it is evident that either of these accidents, if involving a
comparatively small branch of a cerebral vessel in certain motor
areas, might cause transient paralysis, such as has been described.
Nor can we fail to see that, while such symptoms as the delirium,
mania, coma, or subsequent mental impairment may receive other
explanations, it is possible that they may arise from similar
processes of minute hemorrhage, thrombosis, or embolism involving
other parts of the brain.
{399} The frequent occurrence of severe rheumatic pains in the muscles
and joints during the course of the disease has been dwelt upon (p.
385); but in some cases they persisted during the intermissions and
for a considerable time after all other symptoms of disease had passed
away. Occasionally they greatly retarded convalescence by interfering
with exercise and sleep. These pains were mostly in the legs, and were
increased by exercise, and also seemed to be influenced by changes of
weather. Patients who suffered thus were also liable, after exposure
or in consequence of severe atmospheric changes, to sharp attacks of
similar pains elsewhere, and especially in the course of the
intercostal nerves. Occasionally violent and persistent headache
follows the disease, not improbably associated with changes in the
membranes of the brain, although in other cases severe neuralgia
occurs in consequence of the anaemia which may remain in an intense
degree after the fever. Troublesome numbness and soreness of the soles
of the feet and of the palms of the hands, increased by pressure, has
been noted as a sequel persisting for several days or weeks.
Affections of the special senses are not rare. The most remarkable
among these is the affection of the eyes, which is apt to occur far
more frequently in connection with relapsing fever than with typhus or
typhoid. The proportion of cases in which this sequel appears varies
greatly in different epidemics. In the British epidemics of 1826 and
1843, when this form of post-febrile ophthalmia was first accurately
described by Mackenzie of Glasgow, it was very frequent; and it was
equally so in Finland in 1867-68, when Estlander[20] again carefully
studied it.
[Footnote 20: "U. Choroiditis nach Febris Recurrens," _Arch. f.
Ophth._, 1869, Bd. xv., Abth. ii., 108.]
On the other hand, so far as can be stated in regard to a sequel which
may appear after convalescence is far advanced and the patient
discharged from medical care, it was very uncommon in the Philadelphia
epidemic of 1869-70. This ophthalmia may occur during the course of
the fever, but more frequently it begins during convalescence, and
even some months after convalescence has been established. It occurs
in patients of both sexes and at all ages. Usually it affects but one
eye, but both may be attacked simultaneously or consecutively.
Patients who were very ill-nourished and debilitated were most apt to
present this sequel, and Murchison regards previous starvation as one
of its main causes. The exciting cause and true pathology appear
obscure as yet, however, and the existence of a neural origin is not
improbable. In some cases the ophthalmia has seemed to result directly
from exposure to cold. Among our own patients, as already stated, eye
symptoms were less common and severe. A careful record of 184 cases
was kept in reference to this question. Several patients complained of
diplopia during the febrile stage, and one asserted that every object
appeared fourfold to him. Conjunctivitis of moderate severity, usually
associated with otorrhoea, occurred in about 5 per cent. of our cases;
it generally affected only one eye, and occurred in a few instances as
late as the third week after the relapse. In a few cases (four) also
there was dulness of vision in one eye, noted during the course of the
disease and persisting for some time after convalescence began. In
only one instance, however, did permanent impairment of vision ensue,
and this man had passed through a violent attack of the fever with
unusually grave nervous symptoms. {400} It left him with optic
neuritis on the right side, which induced partial atrophy of the nerve
and great limitation of the field of vision. Meschede reports
intraocular affections in 6 cases out of 180 specially examined,
though it is not certain that such affections were directly connected
with the febrile process. Ocular ecchymosis occurs in a small
proportion of cases, especially of the graver types.
Dulness of hearing is not so common in relapsing fever as it is in
typhoid. It was present in 14 out of 184 of our cases during the
course of the disease, and in a few instances partial or almost
complete deafness in one ear persisted after convalescence, owing
doubtless to a slight affection of the middle ear. In one case marked
deafness appeared suddenly on the day after the termination of the
relapse by crisis. Meschede[21] found disease of the middle ear in no
less than 8 per cent. of his cases.
[Footnote 21: _Loc. cit._]
Purulent otorrhoea from one or both ears is of more frequent
occurrence, and without any special exciting cause may present itself
at any time during the course of the disease or more commonly after
the relapse. In the same manner purulent coryza may occur.
The eruptions occasionally present during the fever have been
described. Bed-sores from pressure are much less common than in
typhus, but are met with in a small proportion of cases. As a rule,
they are of moderate size and heal quickly. Superficial gangrene of
the lips, nose, and ears has also been noted in rare cases (Zuelzer)
in connection with gangrene of the extremities, probably from
embolism. The occasional occurrence of painful boils, of abscesses in
the cellular tissues (Wyss and Bock), and the more rare occurrence of
erysipelas may be mentioned among the sequelae.
As already stated, the severe pains in the joints and members which so
frequently occur during relapsing fever are, as a rule, unattended by
any redness or swelling of the joints. In rare cases, however, there
is effusion into the joints during the fever, or more commonly there
are attacks during convalescence which simulate subacute rheumatic
arthritis. Such attacks may last but a few days, but in several of our
cases there was painful swelling of the knees, wrists, and fingers
which persisted for several weeks after the fever, being attended with
slight crepitation on motion, and altogether behaving like subacute
rheumatism.
As would be expected from the severity of the fever, the marked
disorder of digestion, and the lesions of the spleen and liver in
relapsing fever, anaemia is a common sequel. In cases where there has
also been free hemorrhage, usually in the form of epistaxis, the
anaemia may indeed reach an intense degree.
The cardiac murmurs which have been described as present in a certain
proportion of cases are dependent upon the blood-changes, and when the
anaemia is extreme these murmurs are also audible over the large veins
and the pulmonary artery, and persist after convalescence is fully
established.
Oedema of the lower extremities occurs in a considerable number of
cases. It is clearly due in part to the anaemia, but the cardiac
debility which follows the fever is also largely concerned in its
production. It was, indeed, marked in some of our cases where no
anaemic murmurs existed, but where there was great nervous and
muscular debility. {401} Usually limited to the feet and ankles, it
occasionally extended above the knees, and in one case, where great
anaemia and debility from fever and over-exertion coexisted, there was
oedema of the hands and wrists, with great distension of the legs up
to the hips. It is not associated with albuminuria as a rule, and
yields readily to treatment and rest, in the course of a few weeks.
Hemorrhages from various surfaces have already been mentioned, and a
full account given of epistaxis, which is by far the most common form.
Bloody vomiting has been noticed in a small proportion of cases in
various epidemics. It varies in amount, but is always attended with
great gravity of the attack, and usually is followed by fatal results.
It occurred in four of our cases, two of which presented also black
stools containing altered blood, and suppression of urine; while in
another it occurred at the close of the first relapse, and during the
second relapse was copious and repeated. In this case it was attended
with alarming symptoms of collapse, from which the patient rallied,
and after a desperate struggle recovered.
Blood may also be discharged from the bowels in such large amount as
to constitute actual hemorrhage--a symptom of great gravity; or in
small quantity and completely altered, so as to impart an inky black
color to the stools--a condition not necessarily attended with urgent
danger; or, finally, there may be frequent bloody dysenteric stools.
Hemorrhage has also been observed from the uterus, from the kidneys,
from the ears, and from the old cicatrix of a syphilitic chancre.
Hemorrhage occurred in 87 out of 183 of our cases, or in nearly 50 per
cent. It was from the nostrils in 82 cases, from the uterus in 1 case,
from the stomach in 4 cases, and from the cicatrix of a chancre in 1
case.
Sudden collapse occurs with such comparative frequency in relapsing
fever as to require special attention as one of its complications. It
may occur at any period of the disease, but it is most common at the
crisis of the first paroxysm or of the relapse. The symptoms are
usually those of cardiac failure, with rapid, small, and feeble pulse;
shallow and hurried, or slow, labored, and imperfect respiration;
coldness of the extremities, while the central temperature may remain
elevated; muttering delirium, rapidly passing into unconsciousness.
Occasionally almost instantaneous death occurs from syncope induced by
some muscular exertion, as standing up or even rising in bed. In other
cases the symptoms indicate the development of cardiac thrombosis, and
subsequent examination has verified this opinion. In still other cases
the symptoms resemble those which occur in extreme hyperpyrexia
dependent upon overwhelming and paralysis of the nervous centres.
Copious hemorrhage from the stomach and nose may also induce syncope
of alarming and even fatal severity. When from the latter cause,
reaction may be induced and the patient may ultimately recover, as we
saw in a case where after repeated hematemesis the patient sank into
profound collapse. In all of its forms, however, this complication is
of extreme and imminent danger, and death follows, as a rule, in a few
hours. The cases in which it occurs are usually of severe type,
occurring in persons who have previously been in poor health or
intemperate, or who have been subjected to privation and improper
exposure previous to and during the early stages of their attack.
Still, collapse may occur in mild cases {402} also, and whatever the
type of the disease there may be no special indication of approaching
trouble, when the patient rapidly passes into collapse, to be followed
by death in a few hours. It occurred in nine of about two hundred
cases under our observation. In one it was the result of hemorrhage
from the stomach, and ended in recovery; in one, at the close of the
initial paroxysm the patient, who was stupid, with muttering delirium,
sank into collapse as the temperature rapidly fell from 105 degrees to
97 degrees, and died in a few hours; in one, on the fourth day of the
relapse the temperature suddenly fell from 102 degrees to 96 degrees,
with free sweating, but suddenly rebounded to 102 degrees, with very
rapid, feeble pulse, distinct basic cardiac murmur, constriction of
chest, restlessness and delirium, slight convulsions, and death in
eight hours; in one, a man at the end of the initial paroxysm,
immediately after his admission to the hospital in apparently fair
condition, became violently delirious, with bounding pulse, soon grew
comatose, and died in one hour; in one, a man who was in feeble
condition, on the nineteenth day, with irregular persistent fever (he
had splenic abscess), sat up on the edge of the bed, sank back in
syncope, and died in less than an hour; in one, a man who did well
until the second day of the relapse, when pleuro-pneumonia and
pericarditis were developed, died suddenly four days later: there was
considerable pericardial effusion; in one, sudden death from syncope
or cardiac thrombosis occurred on the twelfth day in a man who had
suppurative parotitis and metastatic abscesses of the lungs; in one,
sudden collapse and death occurred in one and a half hours at the end
of the initial paroxysm; in one, a drunkard with large fatty liver had
pyrexia continuing after the initial paroxysm, and on the ninth day,
while in a state of hebetude, with mild delirium and a pulse of 112,
coma suddenly occurred, and death followed in two hours.
Pericarditis is a rare complication, and is apt to coexist with
pleuro-pneumonia. This combination occurred in one of our cases where
pleuro-pneumonia and pericarditis were developed on the second day of
relapse, and proved fatal by sudden collapse on the fifth day, with
the pericardial sac distended with serum and its layers coated with
plastic lymph.
Thrombosis of veins, as in phlegmasia alba dolens, occurs much more
rarely than after typhoid fever. Arterial embolism, on the other hand,
is not uncommon. Murchison[22] reports a case in which gangrene of the
left foot from obstruction of the left femoral artery, together with
cerebral softening from obstruction of the left middle cerebral
artery, occurred in connection with cardiac thrombosis. Zuelzer
alludes to similar cases in the St. Petersburg epidemic of 1865-66,
where, in addition to the extremities, the nose, ears, and lips became
gangrenous. Other examples of embolism are found in lesions of the
spleen and kidneys, where infarctions are of frequent occurrence.
[Footnote 22: _Op. cit._, p 384.]
Heart-clot, or cardiac thrombosis, appears to occur more frequently
than in any other acute zymotic disease, with the exception of
diphtheria. Even when the occurrence of passive hemorrhages and of
ecchymoses of various tissues indicates marked dyscrasia of the blood,
there will not rarely be found firm white clots in one or other of the
cavities of the heart. These frequently present unmistakable evidences
{403} of ante-mortem formation, and, as already stated, there is a
certain proportion of the cases of rapid and unexpected death where
the fatal result is directly due to cardiac thrombosis, attended with
the usual symptoms.
The constant affection of the spleen has been fully described; it is
not therefore surprising that both complications and sequelae arise in
connection with it. At times, in cases which ultimately recover, the
pain in the splenic region is so violent and continuous, and is
attended with so much tenderness over the enlarged organ, that
localized peritonitis is undoubtedly present. Occasionally this
perisplenitis persists, and in conjunction with the inflammatory
changes in the substance of the spleen maintains an irregular fever
after the specific pyrexia has run its course. This was noticed in
several of our cases, but especially so in a case where, after the
initial paroxysm, an irregular fever was kept up, obscuring the
relapse, until the nineteenth day, when death occurred suddenly from
syncope on rising on the edge of the bed, and where examination showed
splenic peritonitis, with a splenic abscess as large as a pigeon's
egg.
The enlargement of the spleen usually subsides during the
intermission, and disappears speedily or in the course of a few weeks
after convalescence is established. Occasionally, however, it
persists, and is attended with marked anaemia. In one case, where
death occurred from pneumonia, the sequel of relapsing fever, at about
the thirtieth day, the spleen weighed twenty-nine ounces; and in
another case, where death occurred from gangrenous pleuro-pneumonia,
at the fortieth day, the spleen was still enlarged and presented
characteristic changes in its pulp. On the other hand, in a case where
death occurred on the twelfth day of typhus, occurring forty-four days
after recovery from a very bad case of relapsing fever, making it
altogether the one hundredth day, none of the lesions of the first
disease were discoverable.
Rupture of the spleen occurs occasionally, and is usually attended
with sudden pain, collapse, and speedy death. Murchison refers to two
examples recorded by Zuelzer and one by Hudson; Petersen reports
fifteen cases, in seven of which sudden rupture occurred with speedy
death, while in the other eight the rupture followed local softening
from infarction, and resulted in death in a few days from purulent
peritonitis.
In one of our cases, where death occurred on the sixteenth day,
apparently from double pneumonia and heart-clot, it was found that
there was a rupture in the enlarged spleen near its upper end, recent
plastic peritonitis in the region of the spleen, and a moderate amount
of bloody pulpy fluid throughout the peritoneal cavity.
As we have seen, disturbances within the respiratory tract occur with
very different frequency in different epidemics. In many they are
rare, while in 1870 we noticed cough and other evidences of
respiratory trouble in no less than 90 out of 200 cases.
Severe catarrhal laryngitis is a rare and dangerous complication. It
did not occur in our cases, but both Begbie and Paterson report cases
of it which required tracheotomy, and Wyss and Bock met with
ulcerative laryngitis with perichondritis.
Bronchitis of moderate severity, although rare in many epidemics,
{404} occurs so frequently in others, as in Philadelphia in 1870, as
to rank as a symptom of the disease.
Pneumonia is one of the most fatal complications. The results of our
own observations agree with the statements of Jenner and of Carter,
that it is the next most common lesion after enlargement of the liver
and spleen. On the other hand, Murchison noted it only in 4 or 5 out
of 600 cases. It occurred in at least 11 of our cases, 8 of which were
fatal; and unquestionably less extensive inflammation was present in
other cases which recovered, in view of the marked respiratory
disturbances frequently present. Both lungs were involved in 4 cases;
of the remainder, the right and left were about equally divided. Out
of 23 autopsies, the lesions of pneumonia were found 8 times. The
lower lobes were affected in every case. The form of this disease was
croupous in 9 cases; in 1 it was that of metastatic suppuration, and
in 1 it was more properly described as splenification. The amount of
plastic pleurisy associated with it was usually great, and in one case
there was also severe pericarditis. In another case the disease
advanced to the stage of gangrene of a circumscribed area of the
pleura and of the superficial layer of the lung. In only one instance
was albuminuria present. In two cases the pneumonia occurred so late
in the course of the disease that it might be regarded as a sequel.
Death occurred in one of these on the thirtieth day, and in the other
(that in which gangrene ensued) it ran a subacute course, and death
did not take place until the fortieth day. In the other cases the
disease began at the close of the initial paroxysm, during the
intermission, or early in the relapse. As would be expected, the
sympathetic fever due to this complication modified and obscured the
characteristic course of the specific pyrexia.
This rare termination in gangrene has been noted by other observers;
in all five or six times. Parry met with a truly remarkable case of
double pneumonia, followed by gangrene, and yet resulting in recovery.
Jaundice is apt to attend cases of relapsing fever which are
complicated with pneumonia.
Pleurisy is an almost constant accompaniment of pneumonia, and
frequently occurs in marked degree. It may also be present in cases of
severe splenic inflammation. In all probability, localized plastic
pleurisy is not infrequent, and may cause some of the severe thoracic
pains so frequently present.
Metastatic abscesses of the lung occur occasionally as a result of the
profound toxaemia, and are apparently preceded by patches of
infarction, which soften in the centre, as in the usual development of
pyaemic abscesses. This condition was found in one of our cases in
conjunction with suppurative parotitis. It has been included among the
instances of pneumonia.
Acute miliary tuberculosis, involving chiefly the lungs and intestinal
canal, occurred as a sequel in one case under our observation, and
phthisis has been found to follow by other observers (Carter). It is
to be expected that if the patient did not so quickly pass from under
observation it would be found that an affection so gravely
complicating nutrition as does relapsing fever is frequently followed
by serious organic disease.
Parotitis is mentioned by so few authors as to show that it is a {405}
rare complication in most epidemics, varying from 1 in 600 to 1 in 50
cases. One gland only is affected at a time as a rule, though both may
be involved successively. The inflammation begins either during the
intermission or the relapse, and may terminate by resolution or by
suppuration. Although a painful and severe complication, it is
followed by recovery in a considerable proportion of cases. Carter[23]
states "that in some degree it was noted in 2 or 3 per cent. of all
cases, and nearly as often amongst survivors as in the casualties." It
occurred in three of our cases (185); once it underwent resolution;
once suppuration occurred in the parotid and in the masseter muscle,
with metastatic abscesses in the lungs, and death; and once the
patient, who had previously existing amyloid degeneration of liver and
spleen without albuminuria, had severe relapsing fever with two
relapses, in the first of which parotitis occurred in both glands,
successively terminating in suppuration, after which he did well
through an apyretic period of six weeks, when sudden high fever
appeared, followed by speedy death.
[Footnote 23: _Op. cit._, p. 210.]
Pharyngitis and tonsillitis of mild grade occur in from 3 to 25 per
cent. of the cases in different epidemics.
Hiccough deserves to be ranked among the complications, because it is
of frequent occurrence, obstinate and annoying. It occurred in a
considerable proportion of our cases, and much more frequently in
those who had jaundice. It was often present both in the initial
paroxysm and in the relapse, but disappeared soon after the end of the
pyrexia. It bore no constant relation to the severity of the vomiting.
Not rarely it lasted several days and nights, causing exhaustion and
interference with sleep and proving rebellious to treatment.
Hypodermic injections of morphia and atropia, chloroform internally,
and extremely careful alimentation proved most serviceable.
Hemorrhage from the stomach has already been spoken of (see p. 390).
Diarrhoea, as already stated (see p. 390), occurs much more frequently
than in typhus fever, varying from 1 per cent. (Murchison) to 15 per
cent. (Scotch epidemics) or 33 per cent. (Philadelphia), or even 50
per cent. (Konigsberg). It is usually of moderate severity, but
occasionally is so profuse and intractable as to constitute the main
cause of death. In some epidemics the attacks of looseness occur
almost exclusively after the relapse, but in others the bowels are
frequently loose during the febrile stages. In our cases there were
not infrequently from three to eight thin, dark, bilious or light
yellowish stools daily after the second or third day of the initial
paroxysm, and then the looseness would stop during the intermission,
probably to recur in the relapse. Occasionally diarrhoea with very
frequent liquid stools occurs at the close of one or both of the
febrile stages, assuming a critical character, and substituting more
or less of the sweating which is the common mode of crisis, although
in several such cases quoted by Murchison from Douglas the sweating,
despite the critical diarrhoea, was usually profuse. It can scarcely
be said that there is any relationship between diarrhoea and vomiting;
both are frequently present, and may even be severe and persistent in
the same case, though either may be marked while the other is moderate
or slight. Abdominal pain and tenderness in the epigastrium and
hypochondria are constant symptoms, but when diarrhoea is marked there
are apt also to be griping {406} pains and tenderness in the lower
segment of the abdomen. When diarrhoea occurs as a sequel, either
beginning after the close of the relapse or continuing in cases where
the bowels have been loose during pyrexia, it is apt to prove
obstinate and intractable, or even to lead to a fatal result.
The character of the stools varies much; usually thin and dark, they
may be light yellowish or even whitish. Thus, in a severe case with
deep jaundice we observed seven liquid and decidedly whitish stools in
twenty-four hours. In such instances there is undoubtedly more or less
complete closure of the biliary ducts by plugs of mucus or by swelling
of the mucous membrane. On the other hand, the stools may be inky
black from admixture with altered blood, or, lastly, they may consist
of mucus and blood, in which event the complication assumes the form
of actual dysentery and is attended with increased abdominal pain and
with tenesmus. Dysentery was, as would be expected, quite frequent in
the Indian epidemics studied by Carter.[24] It is usually of moderate
severity, but occasionally it runs into gangrenous inflammation, is
attended with perforation of the bowel, or is followed by hepatic
abscess. In one instance we noticed a peculiarly fetid puriform
discharge from the anus, which occurred during the relapse and
persisted for several weeks, gradually subsiding, as though from some
unhealthy ulceration which slowly healed.
[Footnote 24: _Op. cit._, p. 218.]
Jaundice is of frequent occurrence, but has been sufficiently
discussed at page 391.
Peritonitis is not rare in its circumscribed form. This statement is
based on the comparative frequency with which localized splenic
peritonitis, of varying degrees of severity, is found after death in
relapsing fever from various causes, and from the great frequency of
severe pain and tenderness in the region of the enlarged spleen in
favorable cases. In its lesser degrees it may not add materially to
the danger of the patient, but in more severe forms, associated with
serious splenic lesions, it may run a protracted subacute course and
maintain irregular fever.
General peritonitis is, on the other hand, a rare complication,
occurring not more than once in several hundred cases. It results from
dysenteric perforation of the bowel, from rupture of a splenic
abscess, or from rupture of the spleen itself. An example of this
latter accident which occurred under our observation has already been
given. Speedy death invariably follows, though in the case just
referred to the symptoms of peritonitis were totally masked by those
of the coexisting double pneumonia, which seemed to be the immediate
cause of death.
Suppuration of the mesenteric glands is a rare complication, mentioned
especially by Wyss and Bock. As these glands are not usually found
enlarged, there being no irritative lesion of the intestines of common
occurrence in relapsing fever, it is probable that the collections of
pus which have been found were metastatic in origin.
Dyspepsia is not an infrequent sequel, as would necessarily be the
case after a disease characterized by so much gastric irritation and
by such serious lesions of the liver and spleen. As a consequence,
care in diet is often required for a considerable period after the
course of the disease has ended; dyspeptic symptoms are frequently
complained of, and marked emaciation and anaemia often protract
convalescence.
{407} It may be observed that a striking appearance of emaciation is
often developed shortly after the crisis of the first paroxysm, or,
more particularly, of the relapse. It is partly due to the actual loss
of weight during the high pyrexia, but even more to the abrupt
transition from a state of extreme febrile turgescence to one of
equally extreme relaxation and maceration of the surface.
The amount of urine has been seen (p. 387) to vary greatly in cases
distinguished by no special disorder of the kidneys; the extremes in
ordinary cases being from twelve or fifteen ounces just before the
crisis to from eighty to one hundred and twenty within forty-eight
hours after the crisis. Suppression is, however, sometimes noted, and
is always a grave symptom, though Parry[25] reports more than one case
in which on several successive days there was not more in twenty-four
hours than one fluidounce of non-albuminous urine, and in which no
symptoms of uraemia occurred, and the sweat had no urinous odor. In
one of our fatal cases, with intense jaundice, hematemesis, inky black
stools, and oedema of the feet and of the lungs, there was not a drop
of urine secreted during the last four days of the initial paroxysm;
death occurred on the eighth day, and the kidneys were found intensely
engorged, of a deep blackish-blue color, with numerous ecchymoses in
the cortex, due to impaction of the convoluted tubules with blood,
while the renal epithelium was granular and swollen, and many tubules
were filled with epithelial cells and granular matter. At the autopsy
the urinary bladder was firmly contracted and contained a very small
amount of bloody liquid.
[Footnote 25: _Op. cit._]
More frequently, incontinence of urine, with or without retention,
occurs during the febrile stages--according to our observation, most
commonly in cases attended with mental disturbance and tending to a
typhoid condition. The symptom was not of very grave significance,
however, and after the use of the catheter for a few days the bladder
regained its tone.
Albumen is quite frequently present in small amounts during the
pyrexia of relapsing fever. Thus, in 18 cases of ordinary severity,
which all recovered, and in which the urine was carefully examined
daily, a trace of albumen was found in 5; in 2 cases it appeared both
in the initial paroxysm and in the relapse, but in all instances its
presence was of brief duration. In one of these five cases the albumen
appeared at both critical periods, when the amounts of urine in
twenty-four hours were respectively 150 ccm. and 250 ccm.; but in the
other cases the transient albuminuria coincided with free secretion of
urine (1250 ccm., 1850 ccm.). It is probable that were the same
careful search to be made in all cases the presence of albumen would
be detected in fully 20 to 25 per cent. On the other hand, in fatal
cases the occurrence of albuminuria is by no means constant, although
undoubtedly it is present in a larger proportion of such cases than of
those of ordinary severity.
Our experience does not confirm that of Murchison, who states that he
never met with typhoid symptoms in relapsing fever without albuminuria
or some other evidence of retarded elimination by the kidneys. In
several of our cases where the typhoid state was developed in the
highest degree repeated examination of the urine failed to discover
albumen.
{408} Most observers have been struck with the comparative immunity of
the kidneys from serious disturbance in a disease presenting such
complicated morbid processes and widespread lesions as relapsing
fever. To show, however, that these organs suffer specially in certain
epidemics, it may be mentioned that Obermeier[26] reports having found
albumen with tube-casts of various kinds in 32 out of 40 cases of
relapsing fever, thus showing that, in the particular epidemic he was
studying, catarrhal nephritis was of almost uniform occurrence. It is
true that serious interference with the elimination of urea and other
nitrogenous matters may occur without the coexistence of albuminuria,
so that it is impossible to deny that severe nervous symptoms may
result from impaired renal activity even when the urine contains no
albumen.
[Footnote 26: "U. d. wiederkehrende Fieber," _Arch. f. path. Anat. u.
klin. Med._, Bd. xlvii. p. 170.]
Attention has already been called to the variations presented in the
amounts of urea, but more extended observations are required to show
the precise relations of these variations to the graver nervous
phenomena. It will be found, we venture to opine, that, while in one
group of relapsing-fever cases of grave type, cerebral symptoms are
dependent upon the retention and accumulation in the system of urea
and other effete nitrogenous products, owing to interference with
renal activity from pre-existing organic disease of the kidneys or
from an exceptional degree of congestion of those organs, there are
other groups where similar typhoid cerebral symptoms are more directly
dependent upon the specific toxaemia, upon the hyperpyrexia, upon
exhaustion of the nerve-centres by intense peripheral irritation, or
upon congestion or other morbid conditions of the nerve-centres
themselves.
In all cases where cerebral symptoms manifest themselves in relapsing
fever the daily examination of the urine--which here, as in other
zymotic diseases, is a duty in all cases--becomes of extreme
importance. Three conditions should be borne in mind in such
examinations. In the first place, the attack of fever may have
occurred in one already the subject of organic kidney disease, and,
considering the classes from which the majority of the cases of
relapsing fever are drawn, this possibility cannot be of rare
occurrence. Out of eighteen post-mortem examinations in which the
kidneys were studied with especial care we found positive evidence of
pre-existing organic disease four times. In these cases the
albuminuria was marked and persistent, though tube-casts were rarely
found, and severe cerebral symptoms of typhoid type were prominently
present. In another highly interesting case the patient, who had
amyloid disease of the liver, spleen, and kidneys, contracted severe
relapsing fever; he had increased albuminuria during both febrile
stages, suppurative parotitis, but no grave cerebral symptoms, and
apparently recovered. After an apyretic period of six weeks, during
which the symptoms of the amyloid visceral disease persisted, a sudden
and rapidly fatal pyrexia occurred. Unfortunately, the existence of
spirillar infection of the blood was not known at the time.
In the second place, the attack of fever may become complicated with
acute nephritis from special localization of the poison, as in
Obermeier's cases, or from vulnerability of the kidneys. In such cases
careful study of the urine should indicate the event, and the
prognosis, though grave, is not so hopeless as in the first instance.
An interesting example of {409} this occurred under our observation,
where the patient, who had apparently an ordinary attack, was seized
with acute catarrhal nephritis, with temporary uraemia, during the
relapse, but after a dangerous illness recovered without any organic
renal disease as a sequel.
In the third place, may be found the more usual and more
readily-determined condition of slight and transient albuminuria (with
variations in urea excretion) which has already been discussed, and
which has no serious prognostic significance.
The following very interesting case deserves special mention: The
patient, a man aged thirty-six, was admitted on the fifteenth day of
an attack of acute catarrhal nephritis, with slight ascites, marked
oedema of the feet and legs, and highly albuminous urine. In the
course of ten days the oedema and albuminuria were much diminished,
when on the thirteenth day after admission he was attacked with
relapsing fever, the ward in which he lay containing a number of
persons ill with that disease. The initial paroxysm was severe, but
without any grave cerebral symptoms; the urine grew scanty, dark, and
bloody, and the oedema increased and invaded the pelvis. Crisis
occurred on the fifth day, temperature falling 9 degrees, sweating
copious, urine 473 ccm. in twenty-four hours, color of porter, highly
albuminous, and depositing blood, renal epithelium, hyaline, granular
and epithelial casts, all stained reddish. Two days later, urine 1600
ccm., light colored, with only a small amount of albumen.
A slight and brief relapse (101 degrees for two days) occurred after
an interval of four days; a second imperfect relapse (100.5 degrees
for three days) after a further interval of six days; and finally,
after a further interval of only two days, a violent relapse
(temperature rising rapidly to 106 degrees) with crisis (fall of 8
degrees in twelve hours) at close of fifth day. The oedema gradually
diminished from the time of the first crisis, did not increase in the
relapses, and disappeared completely and finally about ten days after
the last relapse. The urine was very free after the first paroxysm,
averaging from 2000 to 2300 ccm. During the subsequent febrile periods
it did not decrease, and indeed on the second day of the last relapse,
with the temperature at 105 degrees, the amount in twenty-four hours
was 3200 ccm. Four days subsequently, during crisis, the amount was
only 350 ccm.
The albumen disappeared entirely from the urine in two weeks from the
close of the last relapse; there had then been no tube-casts for some
days, and the patient was discharged entirely well a short time
afterward. The treatment consisted of hot vapor-baths, repeated dry
cupping over the kidneys, infusion of digitalis with acetate of potash
during pyrexia, and Basham's iron mixture in the intermissions. It
seemed that the occurrence of the relapsing fever interfered
wonderfully little with the recovery from nephritis.
Hematuria is a comparatively rare and very grave complication. It may
occur as an additional evidence of the dyscrasia of the blood in
connection with hemorrhages from other surfaces, or as in the case we
have before referred to or in that reported by Murchison,[27] it
results from intense engorgement of the kidneys. In Murchison's case
hematuria, with much albumen and tube-casts, occurred in both
paroxysms {410} without any uraemic or typhoid symptoms, and was
followed by satisfactory recovery.
[Footnote 27: _Op. cit._, p. 370.]
Sugar is sometimes present in small quantity as a transient symptom;
and diabetes has been observed as a sequel.[28]
[Footnote 28: Tyson, _Phila. Med. Times_, 1871, i. 418.]
Metastatic inflammation of the kidneys, with centres of suppuration,
was observed by Wyss and Bock.
When menstruation occurs during relapsing fever, as it may do at any
time, it is apt to be excessive, and may amount to severe hemorrhage.
Crisis has been known to occur in this manner.
The numerous cases reported by various observers of relapsing fever
occurring in pregnant women establish the rule that abortion almost
invariably occurs, whatever may be the stage of the pregnancy. In a
large majority of cases the mother recovers, but the child, if viable,
is stillborn or dies in a few hours. Only two of our patients were
pregnant women, and the result in each was unusual. In one, the
patient, already the mother of several children, was in the fifth
month of gestation; the initial paroxysm was severe, with delirium,
but no symptoms of abortion occurred; the intermission lasted six
days, during which she felt very well; the relapse was also severe,
and crisis occurred on the fifth day, the temperature falling below
normal, and the case promising to do well; but on the following day
there was a sudden rebound of temperature, pulse 140, severe
praecordial pain, and death occurred in twenty-four hours, the
contents of the uterus being partially expelled during the act of
dying. In the other case, a girl of eighteen years, who had aborted at
the third month of gestation eight months previously, and who was
again three months advanced in pregnancy when attacked with relapsing
fever, went safely through a bad attack and carried her baby
successfully to full term.
MORBID ANATOMY.--The surface of the body often presents patches of
livid discoloration, and jaundice persists in cases where it has been
present during life. There is but little appearance of emaciation,
except in cases where it has been present before the attack.
When death occurs while the temperature is high the body remains warm
an unusual length of time. Thus, in one case where death occurred at
11.30 P.M., the temperature at 12 was 103 degrees, and at 1 A.M. it
was 101-3/5 degrees, that of the room being 73 degrees; at 6 A.M. it
remained at 93 degrees, the room being at 73 degrees; between 9 A.M.
and 2 P.M. the room was kept at 55 degrees, but the body was still at
82 degrees at the latter hour.
The voluntary muscles are often jaundiced, and in prolonged cases they
may be found flabby and having undergone marked granular degeneration.
In many cases, however, they remain quite dark and firm. Ecchymoses of
the muscular substance are met with occasionally.
In one case, where during life there had been painful swelling of the
left parotid region, with fistulous openings on the cheek, and where
death occurred on the twelfth day of the disease, the masseter muscle
was swollen, with patches of dark, almost black, discoloration from
ecchymosis, and was studded throughout with small collections in its
substance. The fluid from these contained very numerous cells
indistinguishable from leucocytes. The muscular fibrils were friable
and granular, and there was multiplication of the nuclei of the
sarcolemma. {411} These unusual lesions seemed to have originated in
interstitial disintegrating thrombi, with consequent inflammation of
the muscle.
The muscle of the heart is more frequently affected, and in the fatal
cases our attention was particularly drawn to those lesions.
Ponfick[29] has also described them minutely. The degree of change
varies from a partial loss of transverse striation, with slight
granular appearance, up to a very high degree of granulo-fatty
degeneration. The organ is then flabby, its substance pale gray or
brownish, either wholly or in streaks, and microscopic examination
shows an extreme degree of fatty granular change. It must not be
forgotten, however, that many of the subjects of relapsing fever have
been leading irregular and dissipated lives, and that in some
instances the lesions of fatty degeneration detected in their organs
may have been the result of their previous habits.
[Footnote 29: _Virchow's Archiv. f. path. Anat._, Bd. lx. Hft. 2, p.
162.]
Lesions of the cardiac muscle were most marked in those of our
patients who had been intemperate, and in whom fatty degeneration of
the viscera (chiefly liver and kidneys) was also found. They were most
fully developed in cases where death occurred at a comparatively late
period, while in some very severe cases, in which death occurred as
early as the fifth day, the cardiac fibre presented merely faintness
of striation without actual granular degeneration.
Ponfick in particular notes that the great majority of the bodies he
examined were of persons who had been habitual drunkards.
Pericarditis is occasionally present, and is marked by the usual
lesions. In a very severe case in which it contributed largely to the
production of the fatal result it was associated with pneumonia. In
addition to this, effusions of blood beneath the endocardium and
pericardium are not rare; and we have seen them quite large and
numerous in cases where the muscular fibre was firmly contracted and
the cavities contained quite firm decolorized clots.
Thus in our case No. 62, Series C., "the heart was normal in size,
with no appearances of previous disease. There were numerous
ecchymoses of both layers of the pericardium. The right cavities
contained large, firm, yellowish, fibrous clots, forming a cast of the
upper part of the ventricle and of the auricle, and extending both
into the pulmonary artery and back into the veins, and so firm that by
gentle traction a complete cast of these vessels was drawn out. The
clot in the pulmonary artery was throughout firm, fibrous, and
yellowish. There were numerous ecchymoses of the pleura and of the
mucous membranes of the stomach and urinary bladder, hemorrhagic
infarctions in the kidneys and lungs, and granulo-fatty degeneration
of the cardiac muscle." Death had occurred in this case about the
close of the third week, and was preceded by hematemesis and
suppression of urine. We must note in this connection the tendency to
embolism that exists in this disease.
Especial interest attaches to the condition of the blood in relapsing
fever. Usually it presents no abnormal appearance if drawn during
life, though in grave cases it may coagulate imperfectly. We have no
knowledge of its minute chemical characters, save that in several
cases where there was great diminution in the amount of urine, with
uraemic symptoms, urea has been found in considerable amount in the
blood (Murchison, p. 368). The red globules present no definite or
{412} characteristic changes. In some of our examinations they
appeared of light color and became crenated very quickly on exposure.
On the other hand, the white corpuscles have repeatedly been observed
to be increased in number, at times considerably so (Cormack,
Thompson, Zuelzer, Carter, Boeckmann, and ourselves), though this
change is not regarded as constant or essential. It has, however, a
very great interest in connection with the characteristic lesions of
the spleen which will be described hereafter. In several cases we
observed that many white corpuscles were small and apparently
imperfectly developed. Boeckmann[30] concludes that they increase in
number during the febrile paroxysm, reaching their highest number at
the crisis, and then diminishing gradually to the normal. The red
globules are much decreased during the fever, and return to the normal
slowly during convalescence.
[Footnote 30: _Deutsch. Arch. f. klin. Med._, Sept. 1881, p. 513.]
In addition to these changes, various abnormal elements have been
observed more or less constantly. By far the most important of these
is the spirillum or spirochete of Obermeier, which has been already
carefully described. In proportion as this organism has been carefully
looked for it has been found constantly, so that the evidence has
become very strong in favor of its uniform presence in the blood of
relapsing-fever patients during the febrile stage of the disease.
Ponfick in 1874[31] called attention to the occurrence of large
granule-cells in the blood in this disease. They are found during life
as well as after death, when they exist in largest proportion in the
blood of the splenic, hepatic, and portal veins. Their shape is
spherical, ovoid, or elongated; the basis of the cells is a delicate,
translucent, albuminous substance; and the granules are of a fatty
nature, as shown by the action of reagents. These cells have been
found by other observers, and the view is generally received that they
are derived from the lymphoid elements of the spleen, and perhaps of
other portions of the lymphatic system; and Carter, who has studied
them carefully, is inclined to think there is some connection between
them and the development of the spirillum.
[Footnote 31: _Centralbl. f. d. med. Wissensch._, 1874, p. 25.]
Ponfick also first described[32] certain other large,
irregularly-shaped, pale, granular, nucleated cells, which occur in
smaller number in the blood in relapsing fever, and which he regarded
as altered endothelium, derived from the lining of the blood-vessels,
of the lymphatics, or of the lacunar spaces of the spleen.
Occasionally these cells are found with such highly granular contents
as to make them closely simulate the large granule-cells described
above. These results of Ponfick have been confirmed by other
observers.
[Footnote 32: _Loc. cit._]
In several of our reports of examinations of blood there is mention
made of quite abundant, free granular matter--an appearance also
observed by Carter. Finally, the latter describes the occurrence of
thread-like filaments and of short, rod-like bodies.
There are no characteristic lesions connected with the
gastro-intestinal canal. The mucous membrane of the stomach may be
normal or merely injected, though where there has been much vomiting,
and especially bloody vomiting, there is marked injection, and not
rarely ecchymosis and submucous extravasations of blood, with
softening of the membrane. {413} These extravasations are usually
small, but Cormack reports a case where one-third of the mucous
membrane of the stomach was the seat of ecchymosis and extravasation.
In one of our own cases the extravasations occupied an area of four
inches square.
The small intestines exhibit patches of congestion or ecchymosis less
frequently than the stomach, though it is usual to find injection of
the mucous membrane, especially of the lower portion, in cases where
there has been diarrhoea. Carter, observing the disease in India,
found in one-half of all autopsies some amount of congestion,
hemorrhage, or inflammation of the ileum. In two instances he found a
layer of diphtheritic deposit over the mucous membrane of the lower
part of the ileum.
There are no special alterations of the solitary or agminated glands,
and ulceration never occurs. Even in cases where the constitutional
infection is severe, whether diarrhoea has been present or not, it is
noteworthy that there is rarely any swelling of the solitary glands or
Peyer's patches, such as is met with in many other acute specific
diseases. It was not present in any of our autopsies.
The large intestine in like manner exhibits no characteristic lesions.
Patches of congestion and occasionally submucous ecchymoses may be
observed, and croupous exudation occurs here somewhat more frequently
than in the small intestine.
Wyss and Bock[33] speak of enlargement of the mesenteric and
retroperitoneal glands as of frequent occurrence, but we did not
observe it, and Murchison states that these glands present no abnormal
appearance.
[Footnote 33: _Op. cit._, p. 223.]
Alterations of vascularity of the brain or its membranes are met with,
but they are variable and bear no definite relation to the precedent
symptoms. Ecchymoses of the membranes are occasionally observed, and
in one of our cases extensive meningeal hemorrhage was found.
Murchison reported a case in which embolism of the left femoral artery
occurred, and subsequently of the left middle cerebral artery,
inducing death. The suggestion may be hazarded that in some of the
cases where there is severe delirium ending in stupor and death there
has been multiple capillary embolism of the cerebral vessels.
There is occasionally the evidence of catarrhal inflammation of the
upper air-passages, and in some epidemics diphtheritic exudation in
the pharynx and larynx has been noted (Wyss and Bock); and Ponfick
found acute oedema of the glottis in a considerable proportion of the
fatal cases at Berlin. The lesions of pleurisy are met with in a small
proportion of cases; in our own autopsies this complication was more
frequent than in most epidemics.
The lungs may be normal, and Murchison concludes that they are more
frequently so than in typhus. Still, they often present congestion or
oedema, and subpleural ecchymoses, hemorrhagic infarctions, and
pneumonic consolidation are not rare. Lobar pneumonia was present in
33 per cent. of our own autopsies, in 28 per cent. of Carter's, and in
20 per cent. of those conducted by Ponfick. The inflammation usually
presents the regular stages, and is associated with a moderate degree
of plastic pleurisy; but occasionally, as in one of our cases, it
terminates in gangrene. In the instance referred to there was an area
of gangrene about three inches square and one inch in depth, involving
the pleura and a {414} superficial layer of lung on the antero-lateral
aspect of the left lower lobe. In another remarkable instance, already
referred to on account of the suppurative inflammation of one masseter
muscle, the lungs, which were stained yellow throughout, presented
numerous deep purplish patches, which on section altogether resembled
the secondary metastatic deposits of pyaemia, with yellowish softening
or even puriform centres surrounded by a rim of purplish livid
discoloration. Very numerous similar patches, varying from the size of
a pea to that of a hazel-nut, and presenting every stage of
development, were found throughout both lungs. In a few instances we
found the lesions of chronic phthisis, which had, of course, existed
before the attack of relapsing fever. The bronchial glands were found
swollen and infiltrated in cases where inflammatory processes in the
lungs have existed.
Much interest attaches to the state of the genito-urinary organs in
relapsing fever, but caution is required to distinguish lesions that
have existed prior to the attack from those properly referable to it.
Owing to the intemperate and exposed lives of many of the patients,
renal lesions might reasonably be expected in no small proportion. The
comparative rarity of albuminuria (see p. 407), even in severe cases,
is suggestive of the view that when it is present it may at least
sometimes be due to pre-existing lesions aggravated by the acute
infectious process, and further that the extreme gravity generally
presented by such cases may be in part due to the impaired condition
of the kidneys.
The morbid changes most frequently referable to the fever are moderate
enlargement and congestion, occasionally very intense so that we find
it described in our notes as deep blackish-purple or blue; ecchymoses
of the capsule or of the mucous membrane of the pelvis; small
hemorrhagic infarctions, usually in the cortex; and cloudy swelling of
the glandular cells. Less commonly are found hemorrhagic infarctions,
or small embolic patches advanced to various stages of disintegration,
even to the formation of small puriform collections. In quite rare
cases the lesions of acute nephritis are present, while caution must
be used in interpreting other changes occasionally met with, such as
pallor with granulo-fatty degeneration or other advanced alterations
of the glandular cells, or hyperplasia of the intertubular connective
tissue, with or without contraction of the kidneys.
The mucous membrane of the bladder, as already mentioned, may present
ecchymoses, or, more rarely, croupous exudation (Wyss and Bock). The
urine contained may be bloody, or, as in one of our cases where there
had been total suppression of urine for over seventy-two hours before
death, there may be but a small amount of almost pure blood,
containing a few phosphate crystals, but no tube-casts. In this case
there were also ecchymoses of the bladder and of the pelvis of the
kidneys, with intense congestion and numerous small hemorrhagic
infarctions of the kidneys.
The liver is constantly though variously affected. It is found
enlarged in the great majority of cases, especially if death has
occurred during the febrile stage. The ordinary degree of enlargement
in our cases was from four to four and a half pounds, but in a few
instances the liver weighed one hundred or one hundred and two ounces,
though in most of these extreme cases the patients had been drunkards,
and there was such advanced fatty alteration of the liver as to make
it probable that the {415} organ had been diseased previously. These
figures correspond with the results of other observers.
In many cases, especially when death occurs early and during the
febrile stage, the capsule and substance of the liver are congested,
at times intensely so; and when ecchymoses are found elsewhere they
are apt to be present here also, appearing as purplish patches dotted
over the capsule and extending into the superficial layer of hepatic
tissue. Not rarely, however, the liver substance is paler than normal,
and presents a yellowish tinge, apart from the decided yellowish
staining present in cases attended with jaundice. Carter describes a
partial mottled paleness of the liver as having been frequently
observed in his cases, the circumscribed pale areas presenting a
corresponding localized degeneration of the cells, as though from some
local interruption of circulation.
Cloudy swelling and fatty degeneration of the liver-cells are indeed
very often present, and in some epidemics with preponderance of
bilious symptoms are constantly found (Ponfick). The degree of the
cell-alteration varies from a slight granulo-fatty change to an
advanced fatty degeneration, even with a marked tendency, in rare
cases, to disintegration of the cells, so as to produce lesions
analogous to those of acute yellow atrophy (St. Petersburg epidemic).
The whitish deposits described by Kuttner as due to albuminous or
fibrinous infiltration are probably referable to transformed
hemorrhagic infarctions, and the minute puriform collections that have
been observed at the centre of the acini (Wyss and Bock) may have been
metastatic in origin, or attributable to the disintegration of minute
thrombi associated with irritative hyperplasia of the adjacent
lymphoid elements. The consistence of the liver varies: when death
occurs early and bilious symptoms have not been marked, it may be even
firmer than normal, but more frequently it is softer, and it may be
relaxed, flabby, and friable.
The condition of the bile-ducts is of great interest in view of the
frequency of jaundice as a symptom in relapsing fever, and most
authorities unite in saying that they present no lesions capable of
explaining it.
The gall-bladder is usually found full of dark bile, but there is no
such degree of inspissation, except in rare instances, as could
interfere with its passage through the ducts. Murchison quotes the
statement of Peacock that in some instances the bile was thick and
viscid, so as apparently to cause obstruction, but all observations
agree in showing that this is exceptional. The mucous membranes of the
larger ducts may present evidences of slight catarrhal inflammation,
but in nearly all cases where they have been carefully examined, even
when jaundice had been marked, they have been found patulous and free,
so that the jaundice cannot be regarded as due to obstruction of the
larger ducts save in rare instances (Pastau). In further confirmation
of this may be stated the fact that there is no want of bile in the
duodenum and feces.
On the other hand, a careful consideration of the lesions of the
substance of the liver will show that it would be most improbable that
the minute biliary ducts in the areas most affected should escape
implication. Munch, who investigated this subject carefully, found
that there was a catarrhal state of the fine bile-ducts in every case
of relapsing fever with jaundice; and Litten found the smallest ducts
plugged with bile-stained pellets of mucus. It would appear,
therefore, that in many cases at least {416} the jaundice is really
obstructive in its origin, the seat of the obstruction being in the
too-rarely examined minute bile-ducts, though further investigation of
this interesting question is required.
The clinical bearing of these conditions has been fully discussed in
the appropriate section.
The changes in the spleen are constant, and even more remarkable than
those in the liver. It is enlarged with rare exceptions, and
especially so if death has occurred during the febrile stage. Upon the
subsidence of the fever the spleen probably returns to its normal size
more rapidly than the liver. The more common extent of the enlargement
in our own cases was from ten to eighteen ounces, though we found the
spleen in one case weighing twenty-nine and a half ounces and in
another forty-four and a half ounces. In neither of the latter
instances was there any reason to suspect malarial complication. The
most extensive enlargement we have found recorded is sixty-eight
ounces in a case reported by Kuttner.[34]
[Footnote 34: _Schmidt's Jahrb._, 1865, vol. cxxvi.]
There is usually a correspondence between the stage and extent of the
splenic and hepatic lesions, but this is not invariable, and one or
the other organ may present a far higher degree of enlargement or much
more intense interstitial changes. It may be mentioned, moreover, that
in some unusual cases the lesions of the lungs, such as ecchymoses and
hemorrhagic infarctions, may be disproportionately marked as compared
with those of either the liver or spleen.
The capsule of the spleen often presents a mottled look, with at times
large purplish ecchymoses; it is apt to be more or less opaque, and
local peritonitis, with thin layers of plastic exudation often forming
friable adhesions with the abdominal wall, may exist.
In one of our cases the capsule presented a small perforation or
rupture, with an exudation of plastic lymph over an area of four by
six inches, and diffuse peritonitis, with effusion of bloody liquid
with shreds of lymph throughout the abdominal cavity. This fatal
termination is fortunately rare, but there are several other instances
on record. The splenic pulp may retain its consistency and firmness,
even in cases that have run a long course; but more frequently it is
softened, and may be almost diffluent. The pulp is often swollen, so
that when cut it projects above the section. The color is darker than
normal, and often is of a deep maroon color. This swelling is due to
enlargement of the blood-vessels, associated with great increase of
the cellular elements of the pulp and with enlargement of the
Malpighian corpuscles.
When death occurred early in the disease we found these bodies grayish
or grayish-yellow in color and of the size of hempseed, so that the
section very thickly studded with them closely resembled shad-roe, and
this stage of the lesion is frequently described in our notes as the
shad-roe spleen. Subsequently, the Malpighian bodies enlarge still
more, and stand out above the section a line or more in diameter, and
of a lighter color; not rarely, several of them come in contact, and
thus form a considerable mass of irregular shape, resembling the
infarctions described below.[35] It is probable that central softening
may occur later in the {417} Malpighian bodies, though we are inclined
to regard the puriform collections frequently found as chiefly due to
the disintegration of hemorrhagic infarctions or of embolic patches.
Of these, hemorrhagic infarctions are by far the most common and
present the familiar appearances. They may be quite numerous,
superficial, or deep-seated, and of variable shape and size. At first
dark reddish, firm, and sharply separated from the surrounding pulp,
they grew reddish-yellow or yellowish later, softened in the centre,
and eventually were transformed into puriform collections. Doubtless,
in a large proportion of cases that recover such infarctions exist and
are slowly absorbed. Ponfick has shown that these are venous
infarctions, the arterioles leading to them being patulous. True
arterial embolism does, however, occur, though much more rarely
(Ponfick, Murchison), giving rise to firm, wedge-shaped infarctions at
the periphery of the spleen, which may undergo degenerative changes
similar to those above described. The resulting abscesses may burst
into the peritoneum, pleura, lung, or bowel. The microscopic
appearances have been most fully described by Ponfick, our own
comparatively meagre observations having accorded entirely with his
subsequent accurate description. The cells of the swollen pulp contain
red blood-discs and pigment, and some present collections of bright
granules. The lymphoid cells of the Malpighian corpuscles are at first
in a state of cloudy swelling with multiplication of their nuclei, and
later show marked granular fatty degeneration.
[Footnote 35: Thus, Wyss and Bock describe "multitudes of minute
abscesses as large as poppy or hempseed, and containing a single drop
of pus."]
The lymphatic glands present no lesions, and the pancreas is normal.
The peritoneum is not affected as frequently as other serous membranes
in this disease. Superficial ecchymoses are, however, quite common,
especially so over the solid viscera; and more rarely effusions of
blood have been found in the subperitoneal connective tissue,
involving the muscular or glandular tissues beneath. We have already
mentioned (p. 406) the occasional occurrence of local peritonitis,
most frequently of the splenic capsule, and also the rare accident of
diffuse inflammation from rupture of the spleen.
The marrow of the bones was carefully examined by Ponfick, who first
called attention to the presence of important changes in relapsing
fever, which have since been confirmed by other observers. These
changes consist in proliferation and subsequent degeneration of the
lymphoid cells of the marrow, with multiplication of the nuclei in the
walls of the minute vessels and fatty degeneration of their coats. As
a result of these changes, spots of puriform softening may form,
chiefly in the cancellous tissue of the extremities of the long bones,
with the production of localized necrosis, and possibly with extension
of inflammation to the neighboring articular cavity.
Considerable space has been devoted to the detailed consideration of
the pathological changes in relapsing fever, partly because we believe
the fact has not been sufficiently recognized that the disease is
constantly attended with important and characteristic lesions. These
consist, in brief, of remarkable changes in the blood; of widespread
ecchymoses and infarctions, which not rarely undergo puriform
disintegration; of hyperplasia and subsequent degeneration of the
Malpighian corpuscles of the spleen, with changes in the cellular
elements of the splenic pulp; of cloudy swelling of the gland-cells of
the liver and kidneys, with a {418} marked tendency to fatty
degeneration; of changes in the marrow of the long bones; and,
finally, of granulo-fatty degeneration of the muscles, and especially
of the heart.
DIAGNOSIS AND RELATION TO OTHER DISEASES.--The entire question of the
diagnosis of relapsing fever is dominated by that of spirillar
infection. Before Obermeier's discovery the differential diagnosis of
the initial paroxysm, and to a less extent that of the subsequent
events of a case of relapsing fever, was attended with considerable
difficulty. But if, as now seems established, immediately before and
throughout the initial paroxysm and subsequent relapses a
characteristic spirillum is to be detected in the blood upon proper
examination, while it rapidly disappears after the crisis, it is
evident that as soon as a suspicion is aroused as to the possible
presence of relapsing fever the question may be settled conclusively
by the microscope.
None the less is it important to consider carefully, but briefly, the
symptoms by which relapsing fever is to be distinguished from various
affections which may simulate it, because even the most experienced
observers admit that the spirillum cannot be invariably detected;
because it is not yet known that a similar organism may not be found
in some other affections; and, finally, because on the outbreak of an
epidemic of relapsing fever, especially in America, where its
occurrence has hitherto been so rare, there is strong probability that
the nature of the early cases will not be even suspected until the
relapse occurs.
Typhus fever often prevails in an epidemic form simultaneously with
relapsing fever, so that it was inevitable they should have been for a
time confused. Their essential non-identity is, however, now too well
recognized to require any lengthy demonstration. The following
statement of the heads of the argument may therefore suffice.
In typhus there is no characteristic spirillum, and the lesions which
are truly characteristic of relapsing fever are totally wanting. There
are convincing differences in the symptoms, course, and results of the
two diseases. There is no evidence to show that when fever has been
imported into a locality by a single case, typhus fever has ever
produced other than typhus, or relapsing other than relapsing fever.
The two diseases often prevail together, and may coexist in the same
house, each preserving its own distinct characteristics; and persons
exposed to the double contagion may contract one or the other, or
first one and then the other at a shorter or longer interval, so that
an attack of either exerts no protective power against the other. It
must be noted, however, that in a large majority of such cases of
successive contagion it is relapsing fever which has been followed by
typhus, while the reverse has been observed much more rarely.
In 1869-70 the two diseases were prevalent in Philadelphia, and the
wards of the municipal hospitals constantly contained a considerable
number of cases of both. Three instances came under our care in which
after recovery from relapsing fever the patient contracted typhus. All
of these patients were employed as assistant nurses, and were
continuously under observation from the early part of their attack of
relapsing fever to the end of the attack of typhus. In one case the
interval of health between the close of the relapse and the onset of
typhus was forty-four days; in the second it was thirteen days. In
both cases the original disease was {419} thoroughly characteristic
and the subsequent attack of typhus was typical. In both death
followed, and the post-mortem examination verified the above
statement. The third patient had severe relapsing fever, from which he
recovered and returned to work, though with pains in the legs,
shoulders, and forehead. After an interval of apparent health of
eleven days he developed a well-marked attack of typhus, which
terminated on the twelfth day in recovery. It may be added that
although typhus is not of frequent occurrence in any portion of North
America, there have been a number of epidemics unattended with a
single case presenting the features of relapsing fever.
Between well-marked cases of the two diseases there should be no
difficulty in making a prompt diagnosis. Relapsing fever is
distinguished from typhus clinically by the severity of the initial
chill; the rapid elevation of the pulse and temperature; the
comparative infrequency and mildness of cerebral symptoms, despite the
intense fever; the severity of the gastric symptoms, nausea and
vomiting; the enlargement of the liver and spleen, with marked
abdominal pain and soreness; the frequency of jaundice, of epistaxis,
and of other hemorrhages, and of anaemic murmurs over the heart and
large vessels; obstinate insomnia; vertigo; peculiar rheumatoid pains
and perversions of sensation; the frequency of sweating during the
high pyrexia; by the occurrence of crisis, subnormal temperature,
apyretic interval, and relapse; the rarity of measly eruption and of
bed-sores; the frequency of pneumonia, diarrhoea, ophthalmia, oedema,
and desquamation as complications and sequelae; the usual occurrence
of abortion in pregnant females; the protracted course of the disease,
and its remarkably low mortality despite the severity of the symptoms,
except in cases of complicated or typhoid type; and, finally, by the
modes in which death occurs. Of course to this must be added the
specific result of examination of the blood in relapsing fever.
Doubt will arise only in very rare cases where a measly eruption
appears on or before the fifth day of relapsing fever, with headache
and mild delirium, but without severe gastric symptoms, epistaxis, or
jaundice. If no relapsing fever were prevalent at the time, such a
case might well be regarded as one of mild typhus until the crisis and
the relapse disclosed its real nature. But if the two diseases were
known to be prevalent in the community, examination of the blood would
properly be made at once and the diagnosis be established.
The diagnosis between ordinary cases of relapsing fever and typhoid is
readily made by the gradual onset and peculiar course of the pyrexia
in the latter disease, as well as by the frequency of delirium, of
abdominal distension, and of diarrhoea, and by the characteristic
eruption. The occurrence of epistaxis, bronchial irritation, and
splenic enlargement is common to both, and an eruption of small
rose-pink spots has been noted by some observers (Carter, pp. 194,
317). But jaundice, enlargement of the liver, hypochondriac pain and
soreness, excessive nausea and vomiting, severe rheumatoid pains, and
numbness and tingling of the extremities, are very significant
symptoms of relapsing fever. Attention has already been called to the
grave type of relapsing fever in which the typhoid state is fully
developed, and to the fact that in such cases the pyrexia is often
modified, the onset less abrupt, the crisis imperfect, and the
interval occupied by an irregular post-critical {420} symptomatic
fever. It is altogether probable that such cases have not rarely been
regarded as of true typhoid character; and indeed the attempt has been
made by Griesinger to establish as a separate and independent
affection, under the name of bilious typhoid fever, a group of cases
which close examination seems to show to be chiefly composed of grave
complicated relapsing fever with a certain proportion of true typhoid
fever, complicated with jaundice.
The recognition of the bilious typhoid type of relapsing fever is
based upon the history of the case; the mode of onset; the greater
severity of the pains, arthritic and abdominal; the early appearance
and intensity of the jaundice; the more marked enlargement of the
liver and spleen; the marked tendency to hemorrhages from various
surfaces; the peculiarities which careful study of the temperature
curve will show, especially about the time of crisis; the rarity of
eruption; the characteristic spirillum;[36] and the totally different
anatomical lesions, which are, unfortunately, often demonstrable, as
this form of relapsing fever is fatal in from 33 to 50 per cent. of
cases.
[Footnote 36: As first demonstrated by Motschutkoffsky.]
Since the discovery of the spirillar test for relapsing fever it may
be said that Griesinger's bilious typhoid must be stricken from
medical nosology as an independent affection.
The case of Charles Hood, on page 396, is a good example of the
bilious typhoid form which occurred not rarely in the Philadelphia
epidemic.
Murchison points out that, owing to the frequent occurrence of
jaundice in relapsing fever, this disease has been mistaken for yellow
fever by such good observers as Graves, Stokes, and Cormack.
Difficulty in diagnosis would be likely to arise only in regard to the
bilious typhoid type of relapsing fever, and since its clinical
history has become so well known, a mistake is not likely to occur.
The geographical distribution of the diseases is widely different.
Yellow fever is influenced powerfully by season and temperature, while
relapsing fever is independent of both. Negroes are but slightly
liable to yellow fever, while relapsing fever attacks them with
special violence. Yellow fever is not contagious, but infectious, and
second attacks are extremely rare; relapsing fever is one of the most
contagious of the zymotic diseases, but one attack does not protect
against a subsequent one. The mortality, the anatomical lesions, the
course of the pyrexia, the leading clinical symptoms, are all widely
distinct in the two affections; and, finally, no spirillum has been
found in the blood in yellow fever. Yellow fever is an extremely fatal
disease; the ordinary form of relapsing fever has a mortality of 2 to
10 per cent.; the bilious typhoid form, one of 33 to 50 per cent. In
yellow fever the spleen is but slightly enlarged, and the liver is
pale and softened; in relapsing fever the liver and spleen are greatly
enlarged, and there is great tenderness over the hypochondriac region.
In yellow fever albuminuria is much more common, and the urine more
frequently suppressed, than in relapsing fever.
The sudden onset, the severe headache and pains in the limbs, the
vomiting, jaundice, epigastric tenderness, enlargement of the liver
and spleen, occasional epistaxis, hematemesis, or hematuria, absence
of characteristic eruption, liability to herpes facialis, pneumonia,
and diarrhoea; the occasional occurrence of remissions in the pyrexia,
and even of more or less fully-developed chills for several successive
days during the initial paroxysm or {421} the relapse, suffice to
explain the difficulty which may arise in distinguishing the bilious
form of relapsing fever from bilious remittent fever. But the latter
disease arises exclusively from malaria, and is therefore powerfully
influenced by season and locality; is not contagious; does not present
anything approaching to the crisis, the apyretic interval, or the
abrupt relapse of relapsing fever; presents pigmentary changes in the
blood, instead of the spirillum; and lesions of the spleen and liver
totally unlike those characteristic of relapsing fever; can be
promptly controlled by antiperiodic doses of quinine, and therefore
should have a mortality far less than that of the grave form of
relapsing fever. It is not necessary to pursue this subject further,
but a reference to the temperature charts of Carter[37] or of
Litten[38] will show that in some epidemics single paroxysms
resembling those of quotidian ague might occur during the interval
between the initial paroxysm and the relapse, or a series of two,
three, or more such paroxysms of quotidian or tertian type might
represent an entire relapse. Such phenomena are wholly uncontrollable
by quinia, and are presumably dependent upon irregularities in the
specific infection, instead of upon a blending of malaria with the
poison of relapsing fever. There is some ground for believing,
however, that those who have recently passed through an attack of the
latter are highly, perhaps unusually, susceptible to malarial
infection, as we have already seen they are liable to contract typhus.
[Footnote 37: _Op. cit._]
[Footnote 38: _Deut. Arch. f. klin. Med._, xlii. 1874.]
The chill, the sudden and high fever, the acid sweat, the high-colored
urine, the intense pains and soreness, and the occasional murmur over
the heart, will in some cases of relapsing fever suggest the idea of
severe rheumatic fever, with illy-developed articular inflammation and
with a tendency to hyperpyrexia. The urgent danger presented by the
latter condition and the necessity for immediate recourse to cold
baths and large doses of quinine or of the salicylates, render it
highly important that no such error of diagnosis should be made. It
will usually be avoided readily by observing that in relapsing fever
there are great nausea, repeated vomiting, insomnia, peculiar
formication of the extremities, jaundice, early enlargement of the
liver and spleen, with abdominal pain and soreness, and a tendency to
epistaxis; and, further, that despite the high temperature, cerebral
symptoms such as result from rheumatic hyperpyrexia are not
threatened, except in grave typhoid cases or just preceding the
crisis.
The onset of relapsing fever may suggest forcibly the invasion period
of small-pox, with its marked rigors, high fever, lumbar pain, aching
in the head and limbs, nausea and vomiting, and if the patient is
known to have been exposed to the contagion of both diseases a
diagnosis would be impossible until the third day. But such a dilemma
can rarely occur, and under ordinary circumstances the patient's
antecedents will enable a correct opinion to be formed.
Severe cases of simple febricula with marked gastric disturbance may,
as remarked by Jenner, closely simulate relapsing fever; and the same
is true of attacks of acute gastro-hepatic catarrh, with severe
headache, sharp fever, cholaemic eye, epigastric tenderness, and
frequent vomiting. Of course there is no danger under ordinary
circumstances of these simple conditions being regarded as relapsing
fever, but when the latter is prevalent in epidemic form it is
probable that the mistake is frequently made. {422} Although an
immediate diagnosis might be possible only by microscopic examination
of the blood, the peculiar clinical symptoms of relapsing fever would
soon be found wanting, and suitable treatment would bring the simpler
affection under control.
Acute yellow atrophy of the liver occurs chiefly in pregnant women,
though it is also met with in men and children; but it is so rare that
should a case of it come under observation during the prevalence of
relapsing fever there is considerable danger that its nature would be
overlooked. It resembles relapsing fever in the occurrence of jaundice
and other signs of hepatic disorder, of delirium, and of a tendency to
hemorrhage from various surfaces. The temperature, however, is more
moderate, and does not exhibit the sudden remission of relapsing
fever; the liver is usually demonstrably diminished in size; severe
nervous disturbances, such as convulsions followed by stupor and then
by coma, are more constant; while the occurrence of spirilla in the
blood of relapsing fever and of leucin and tyrosin in the urine of
acute yellow atrophy serves to distinguish completely the two
diseases. Acute yellow atrophy is, moreover, invariably fatal.
With ordinary care there is but little danger that any of the local
complications of relapsing fever will so absorb attention as to lead
to a neglect of the specific general disease, so that the cerebral
symptoms should be readily distinguished from the onset of any acute
intracranial affection; the parotitis which occasionally appears early
in the disease should not be confounded with idiopathic mumps; and so
for other complications. There is far more danger, indeed, lest some
of the complications may be overlooked; and this is especially true of
pneumonia, one of the most frequent and most important of them all.
Its occurrence is the cause of the supervention of grave typhoid
symptoms or of the modification of the normal course of the pyrexia in
so many cases that nothing but a systematic daily examination of the
lungs will avert serious oversights.
MORTALITY AND PROGNOSIS.--The rate of mortality has varied in
different epidemics from 2 or 3 to 24 per cent. Murchison shows that
out of 2115 cases admitted to the London Fever Hospital during a
period of twenty-two years, and embracing two distinct outbreaks, only
39 proved fatal, making 1.84 per cent. mortality. Adding to these the
results of Scotch and Irish epidemics, a total of 18,859 cases, with
761 deaths, is reached, giving the rate of mortality for Great Britain
as 4.03 per cent. The great Indian epidemics studied by Carter gave
111 deaths out of 616 cases, equal to 18.02 per cent. Recent German
epidemics have given from 5 to 10 per cent. The above rates are
obtained where all the cases observed during an epidemic are included.
If, however, the mortality of the ordinary form of relapsing fever is
computed separately from that of the bilious typhoid form, it does not
exceed 2 to 5 per cent., whilst the mortality of the latter form rises
to from 33 to 50 per cent., or even higher.
In the Philadelphia epidemic, out of a total of 1174 cases there were,
as nearly as can be ascertained, 169 deaths, giving a rate of
mortality of 14.4 per cent. Taking all the cases admitted to the
hospital under our observation, many of which entered at a late period
of the disease and not a few when moribund, the mortality was not less
than 13 per cent. {423} The mortality among the negroes who were
attacked with the disease was considerably greater than among the
whites. Finally, if the mortality of the bilious typhus form be
considered separately--although from the frequency of jaundice in this
epidemic and the numerous gradations of severity presented it is
difficult to form a sharply defined group of this character--it was
certainly not less than 50 per cent.
The date of death varies with the epidemic, the form of the disease,
and the previous condition of vitality of those attacked. Ordinarily,
by far the larger proportion of deaths occur during the first relapse
or the second interval, but in bilious typhoid cases, presenting grave
complications, especially pneumonia or severe hemorrhages at an early
date, or in cases occurring in intemperate subjects, or in those
previously in impaired health, the mortality is much heavier in the
initial paroxysm or the first interval than at later periods.
Youth exerts the same favorable influences upon the result of
relapsing fever as it does in the case of typhus and typhoid.
Murchison states that of 717 male patients under twenty-five years of
age admitted into the London Fever Hospital, not one died, and in most
epidemics similar, though not equally marked, results have been noted.
In some epidemics the mortality among young children has been
considerable. As a rule, the percentage of deaths increases with each
decade after thirty years.
Sex does not exert any definite or constant influence upon the
mortality. The number of males affected is far greater; they are
liable to be exposed to the contagion in its most concentrated form; a
larger proportion of them are probably the subjects of intemperance
than in the case of females; and thus most statistics agree in making
the mortality somewhat greater in the male sex; but, all things being
equal, there is no good reason for holding that sex itself has any
value in determining the result.
As in other zymotic diseases, the mortality from relapsing fever is
highest during the early period of an epidemic, and the type of the
disease grows milder as the epidemic declines. Cases of the bilious
typhoid form have become notably less frequent during the later stages
of some epidemics than at an earlier period.
Marked difference has been observed also as to the action of remedies
at different stages of epidemics, the early cases exhibiting an
extraordinary resistance to remedies, and especially to anodynes,
which passes away later. When typhus and relapsing fevers have
prevailed together, and a clear discrimination between the two sets of
cases has not been made, it has appeared that the mortality increased
as the epidemic advanced, but this apparent exception has been due to
the fact that at first the cases of relapsing fever were in the
majority, while later those of typhus, the much more fatal disease,
preponderated.
Epidemics of relapsing fever prevail at all seasons, but more commonly
they are at their height during the colder months of the year. The
total mortality will of course correspond, but the actual percentage
is not constantly greater during any one season, although it is
probable that the greater liability to chest complications during the
colder months will render the disease more fatal then.
The gravity of relapsing fever has varied so greatly in different
epidemics that it is very difficult to determine what influence upon
the mortality {424} has been exerted by mere difference of race. A
further source of difficulty is found in estimating the differences in
the physical conditions of the poorer classes in the various
communities affected. The mortality has been exceptionally high in the
Russian and Indian epidemics and in some of the German ones, while in
the British epidemics it has uniformly been light. It is interesting
to note that in the Philadelphia epidemic, where the great majority of
patients were Irish or negroes, the mortality was high, over 14 per
cent. The previous condition of the Irish patients must certainly have
contrasted favorably with that of the individuals attacked in the
Dublin and Belfast epidemics, so that the difference in result seems
attributable only to a greater virulence of the disease. As an ample
opportunity was here afforded to judge of the relative severity of
relapsing fever in the negro and white races when the cases occurred
at the same season, at the same stage of the epidemic, and in
individuals living under nearly similar conditions, it may be stated
that the conclusion of all who studied the question closely was that
the disease was much more severe among negroes, and in particular that
they displayed a greater tendency to serious complications and to the
bilious typhoid form.
Although the degree and virulence of the infection undoubtedly
constitute the most important elements in determining the mortality,
the previous health and habits of those attacked with relapsing fever
exert an influence upon the result. This is especially true of
habitual intemperance, which, by disposing to disease of the liver and
kidneys, greatly increases the liability to a fatal result. It has
been seen (page 409), however, that even when acute catarrhal
nephritis existed at the time of the attack severe relapsing fever
might terminate favorably. Another observation which we made
frequently, and which coincides with what is well known in regard to
typhoid and typhus, is that improper exertion and exposure during the
stage of incubation and immediately after the invasion produced a
highly unfavorable effect on the subsequent course of the disease, and
seemed in particular to dispose to dangerous or fatal collapse at the
critical periods.
Apart from these general considerations, there are many special points
to be considered in regard to the prognosis of relapsing fever:
If after the crisis of the invasion there is not rapid and decided
improvement, complications should be suspected.
A sharp rebound of temperature quickly following crisis may be
followed by speedy death.
Mere elevation of temperature during the invasion and the relapse,
even though to an extreme height, is not attended with the danger
which even a somewhat lower degree would indicate in other zymotic
diseases.
Increased elevation toward the expected time of crisis should arouse
anxiety, as sudden and dangerous cerebral symptoms may occur.
Prolonged duration of the pyrexia, or the substitution of irregular
gradual defervescence (lysis) for the characteristic crisis often
associated with typhoid symptoms as are these conditions, is
significant of complications and of danger.
Wild delirium during the pyrexia, or transient active delirium about
the time of crisis, is not necessarily unfavorable, but continuous low
delirium, with disposition to stupor, is associated with a typhoid
tendency and is frequently followed by death. Excessive muscular {425}
tremor or convulsions are highly unfavorable, but not necessarily
fatal, symptoms.
Cardiac murmurs are not of serious import. The pulse is not usually as
rapid in proportion to the temperature as in typhus or typhoid, and an
excessively rapid pulse toward the expected time of crisis, especially
if associated with feebleness of the heart's action, points to the
danger of sudden collapse at or soon after that time. Previous cardiac
disease, especially fatty degeneration in habitually intemperate
persons, increases this danger. Continued frequency of pulse after the
crisis indicates some complication or the danger of some accident.
Cough of a bronchial origin is not a specially unfavorable symptom,
but if associated with the physical signs of pneumonia and with marked
disturbance of respiration it indicates extreme danger.
Epistaxis, even when copious, often occurs in favorable cases, but
hemorrhage from the stomach or the kidneys is usually, though not
invariably, followed by death.
An eruption, measly or of pink spots, with or without minute
petechiae, is rare, and usually occurs in severe cases, but is not of
specially unfavorable significance unless associated with the typhoid
state or with patches of purpura.
Hiccough is a much less unfavorable symptom in relapsing fever than in
typhoid or typhus, and vomiting, even frequent and persistent, may
occur in cases of ordinary severity.
Enlargement of the liver and spleen indicates special risk only when
persistent for some time after the relapse, in connection with
persistent irregular fever. Jaundice has no necessarily unfavorable
signification, is frequent in ordinary cases in some epidemics, but
when it is associated with the other features of the bilious typhoid
form the danger is extreme, at least 33 per cent. of such cases
proving fatal.
Slight transient albuminuria may exist without special danger, but if
associated with evidences of catarrhal nephritis, or if extreme
diminution of urine, with or without albuminuria, exists, cerebral
symptoms are apt to ensue, with a high degree of danger.
All serious complications--parotitis, erysipelas, dysentery, abortion,
pneumonia, and, above all, peritonitis--greatly increase the risk.
It is not possible to determine in what cases the relapse will fail to
occur. Motschutkoffsky's statement, that when a slight post-critical
rise occurs a relapse will follow, must be applicable only to a
limited number of cases.
In all cases at least one relapse must be expected; the patient in the
interval must be regarded as still sick, and after the close of the
relapse he must still be treated with rigid care until convalescence
is permanently established. It must be remembered in hospital practice
that many patients enter toward or after the crisis of the first
paroxysm, so that caution is needed in estimating the effect of
remedies and the period of the disease.
The undue prominence of certain conditions during the course of the
disease is apt to be followed by corresponding sequelae, and
emaciation, anaemia, dyspepsia, diarrhoea, dysentery, enlargement of
the spleen and rheumatoid pains may then be anticipated. The liability
to ophthalmia and affections of the middle ear is not to be forgotten.
{426} CAUSES OF DEATH.--In fatal cases death occurs from exhaustion
dependent on the protracted and severe sufferings of the patient; from
cerebral symptoms; from hyperpyrexia; from the virulence of the
toxaemia; from uraemic poisoning; from sudden collapse; or from some
complication, such as hemorrhagic meningitis, hemorrhages, pneumonia,
dysentery, rupture of the spleen, peritonitis, or abortion.
TREATMENT.--The indications for treatment presented by regular cases
of relapsing fever seem to be--to moderate the pyrexia; to relieve
distressing symptoms, especially pain, insomnia, and gastric
irritability; to sustain the strength of the system; to prevent or
modify the relapses; and to avoid complications and sequelae.
It is needless to observe that until the nature of the specific cause
of relapsing fever is fully determined, whether the spirillum occupy
that relation or not, it is impossible to direct our efforts
rationally toward its neutralization or elimination. The various
remedies which have been employed for these special purposes have no
clinical support to recommend them. And while experiment has shown
that the activity of the spirillum is readily destroyed by the direct
action of various weak solutions, as of quinine, carbolic acid,
iodine, and mineral acids, no special curative effect follows the
internal administration of these remedies, even in the largest doses
consistent with safety. In fact, there can scarcely be any disease in
which treatment is less satisfactory or its results more difficult to
estimate. The marked difference between various epidemics, and the
wide variation presented by the development of individual symptoms in
different cases of the same epidemic, fully account for this.
Quinine, as might be expected, has been largely used, in the hope that
it might control the pyrexia or prevent the relapse. Murchison[39]
quotes a considerable amount of evidence from various sources to show
that it does not possess either of these powers. It was administered
to a considerable number of our cases, either in small and frequently
repeated doses during the pyrexia or the intermission, or else in
large doses repeated several times in immediate anticipation of the
expected time of the relapse. Thus in some cases three grains of
sulphate of quinia were given every two or three hours until tinnitus
was produced, and then this was maintained during the remainder of the
pyrexia and of the intermission. The amount given daily was from
thirty to forty-two grains. It seemed to rather increase the
discomfort in the head, and in some cases it aggravated the
irritability of the stomach. The pyrexia was certainly not controlled
by it. Given in the same manner during the intermission, it was
usually well borne, but was not effectual in preventing the relapse.
It is true that in some cases the subsequent relapse seemed to be
somewhat modified.
[Footnote 39: _Op. cit._, p. 408.]
Thus in one case 30 grains were given on the 6th of April; 39 grains
on the 7th; 39 grains on the 8th; 42 grains on the 9th; and 60 grains
on the 10th; the critical fall had occurred during the night of the
7th, and the relapse began on the evening of the 9th, but the rise in
temperature was less abrupt than usual, and the relapse lasted less
than five days. It was quite severe, however, so that it is doubtful
whether the apparent modification was anything more than is frequently
observed in cases where no quinine has been administered.
In another case the fall in temperature at the end of the first
paroxysm {427} was from 105.5 degrees to 97 degrees on March 26th: 35
to 40 grains of sulphate of quinine were given daily on April 4th,
5th, 6th, 7th, and 8th; the temperature began to rise on the 3d, but
the severe pyrexia and the usual symptoms of the relapse were limited
to a period of less than thirty-six hours. This is a less common
irregularity, and yet does not afford sufficient evidence of the
efficiency of quinine. In other cases, however, as already stated, no
appreciable effect followed its administration in this manner.
To illustrate the other method of giving quinia, a case may be quoted
in which 20-grain doses every three or four hours were given from
April 25th to April 29th, so that in four days 575 grains were taken.
The initial paroxysm was of average severity, and terminated at the
end of the seventh day, April 20th. The quinine did not postpone the
relapse, which occurred on April 28th, but was of much less than the
usual duration.
In no other case in which these large doses were given was there even
as much reason as in the above instance to attribute to quinine any
positive influence upon the course of the disease.
In order to demonstrate that the failure of quinine was not dependent
upon a want of absorption, Muirhead injected large amounts
subcutaneously with no better results.
In conclusion, it may be said that the evidence shows positively that
quinine possesses no specific influence whatever upon relapsing fever;
that in only occasional cases, if at all, will even enormous doses
given during the intermission postpone or modify the subsequent
relapse; and that it is not effective in reducing the temperature. In
view, therefore, of the usual gastric irritability and tendency to
vertigo and headache, which seem to be increased by large doses of
quinine, and, further, in view of the small mortality, and of the fact
that when death occurs it usually comes from causes over which large
doses of quinine could exert no influence, it seems clear that this
drug should be prescribed only in tonic doses and only in cases where
it is well tolerated by the stomach.
Arsenic was used in a considerable number of our cases with the view
of determining if it possessed any power of relieving the severe pains
or of influencing the relapse. It was administered in the form of
Fowler's solution (Liq. potassii arsenitis), and was given exclusively
by the mouth. If given during the intermission, it was well borne in
doses of five to ten drops every four or even every three hours, given
freely diluted with water and immediately after food. In several cases
it quickly induced puffiness about the eyes, but no effect whatever
was produced on the pains or on the succeeding relapse. In more than
one such case there was an unusually profuse crop of sudamina during
the relapse, many of the vesicles breaking and being followed by
brownish stains. When given during the pyrexia it aggravated the
nausea and vomiting, so that it had to be suspended. In one
unfortunate case, indeed, although promptly suspended, the arsenical
solution seemed to have assisted in the establishment of vomiting and
purging, which proved uncontrollable and contributed greatly to the
fatal result. Hypodermic injections of arsenic have been used
considerably with no better results. There seems, therefore, to be no
reason whatever for any further use of this drug in relapsing fever.
{428} The high pyrexia and the severe rheumatoid pains have naturally
suggested the use of salicylic acid and the salicylate of soda. We
were not sufficiently aware of their antipyretic properties in 1869-70
to have recourse to them, but in more recent epidemics Unterburger[40]
and Riess[41] have found that large doses of the latter substance (one
hundred grains or more daily) will reduce the temperature either in
the initial paroxysm or in the relapse, but that the disease is not
cut short nor are the lesions of the blood or solids prevented.
[Footnote 40: _Jahrb. f. Kinderheilk._, v. x., 1876.]
[Footnote 41: _Deutsch. Med. Wochnsch._, Dec., 1879.]
It must be borne in mind here, as in connection with the action of
quinine, that apparent modifications of the relapse are to be viewed
with great distrust, since such great irregularities therein naturally
present themselves. Care must further be taken lest such attempts to
reduce the temperature aggravate the irritation of the stomach, and by
lessening the power of taking food induce more serious exhaustion than
would have resulted from the unchecked pyrexia. The evidence in our
possession is not sufficient to justify a positive decision as to the
therapeutic value of the salicylates in relapsing fever, but,
apparently, they are applicable to only a portion of the cases, and in
these are of but limited utility.
The same failure which has followed the use of quinine, of arsenic,
and of salicin and the salicylates has attended the effort to prevent
the relapse by berberine, benzoate of soda, tincture of eucalyptus,
and other reputed antiperiodics.
Digitalis, veratrum viride, and aconite were used by us quite freely
as antipyretics. The first two of these were often suspended on
account of the irritability of the stomach, and no valuable results
followed their use when well tolerated. Aconite in small doses,
frequently repeated, as one drop every two hours, seemed to aid in
allaying nausea and to exert some slight influence upon the fever. In
cases where there was a distinct tendency to heart-failure, digitalis
was given freely with advantage.
Cold baths were not used to reduce the temperature in any of the cases
under our observation. They have been employed in other epidemics,
but, as far as we know, with no other effect than to cause merely
temporary lowering of temperature, without any decided relief to the
other symptoms and without any apparent influence upon the course of
the disease. Frequent spongings with cool water and the application of
ice to the head gave only slight and temporary relief.
Simple febrifuge remedies, such as effervescing draught or spirit of
nitrous ether with solution of acetate of ammonium, were well received
by the stomach, and appeared to promote perspiration and the more free
secretion of urine.
Finding all our efforts to control the pyrexia so unsuccessful,
recourse was had in a large proportion of our cases to the
hyposulphite of soda, given, dissolved in two ounces of water, in
doses of twenty grains every two or three hours. In two cases it
seemed to increase nausea, and at times it caused some purging, but
otherwise it was well borne by the stomach, and, indeed, frequently
appeared to aid in controlling vomiting. The records show that this
drug was given in only two or three of the fatal cases, so that
although the patients who took it regularly presented every grade of
severity of the disease, they did well uniformly. It is certain,
however, that the hyposulphite of soda exerted no specific effect
{429} upon the disease; it did not reduce temperature, it did not
prevent or modify the relapses nor relieve the severe pains; it may
have promoted more free and healthy secretions, and, by tending to
prevent vomiting, may have aided in maintaining nutrition; but, on the
whole, it may fairly be doubted whether this remedy merits any more
extended trial.
One chief reason of the failure of antipyretics in relapsing fever is
to be found in the existence of widespread irritative lesions of the
glandular and mucous tissues, which combine with the specific
blood-changes in causing and maintaining the high temperature. It is
not surprising, therefore, that the remedies which afford the greatest
relief in this disease are opiates and sedatives to the
gastro-intestinal mucous membrane. Opium, or morphia, must indeed be
regarded as the basis of the rational treatment of relapsing fever. It
is called for by the insomnia, the severe headache and the pains in
various parts of the body, the nausea and vomiting, and the pyrexia.
It does not appear to have been as prominent a feature in the
treatment of other epidemics as we found it necessary to make it in
Philadelphia. Parry[42] used it very freely, chiefly in the form of
opium, by the mouth, and found a singular tolerance exhibited by his
patients, several of whom took as large a dose as three grains every
two hours during the afternoon and night without producing any sleep
or even any contraction of the pupils. This resistance to the action
of opium was observed chiefly in the early part of the epidemic, and
we may add that it was exhibited chiefly when opium was given by the
mouth. When morphia was used hypodermically we found that one-fourth
of a grain, given at intervals of six to twelve hours, afforded very
great relief to the pains, aided and relieved vomiting, and often
induced quiet, refreshing sleep. Its use was not contraindicated by
jaundice, by cough or pulmonary congestion, or by moderate contraction
of the pupils. It was frequently given so as to maintain decided
drowsiness throughout the pyrexia. When the pains persisted during the
intermission the morphia was continued in smaller doses or at longer
intervals. It occasionally happened that when patients were thus kept
continuously under opium influence no relapse occurred; but here, as
in regard to the action of quinine, it may safely be asserted either
that what was regarded as the initial paroxysm was in reality the
relapse, or else that the absence of a relapse was a mere
irregularity, and in no way to be attributed to the action of the
opium. On the other hand, in cases presenting a tendency to the
typhoid state, with a disposition to stupor, or where the urine was
scanty and albuminous, no opiate was administered.
[Footnote 42: _Loc. cit._]
We have already stated that in our cases quinine in acid solution was
frequently ordered, and it answered very well to add to each dose of
this a suitable amount of morphia.
Atropia, in the dose of gr. 1/60 to gr. 1/40, was usually associated
with the hypodermic injections of morphia. This was done particularly
in cases where the pains were very severe, when the pupils were
disposed to be contracted, or when there was continued profuse
sweating. In addition to this, atropia was continued without morphia
during the intermission in a few cases. The patients proved
susceptible to its influence, and dryness of the mouth with dilatation
of the pupils was readily {430} produced by gr. 1/60 every six hours.
In one case gr. 1/40 every four hours for two days caused delirium,
with the usual symptoms of belladonna action, all of which passed away
quickly after withdrawal of the drug. But in none of these cases was
the relapse influenced in the least.
Other remedies may be used for the relief of the insomnia, which is
always one of the most distressing symptoms. Chloral and bromide of
potassium have been found serviceable in various epidemics, and some
observers have preferred them to opium for the relief of headache and
insomnia. They did not prove reliable in the Philadelphia epidemic of
1869-70. Bromide of potassium, even in large doses, produced scarcely
any effect, and, while in a few cases chloral in doses of gr. xx. gave
positive relief, in the majority of instances 40 grains failed to
cause sleep or relieve suffering. It must not be forgotten also that,
as there is a special tendency to cardiac failure in this affection,
the action of chloral must be closely watched.
In a small series of our cases where muscular pains, hyperaesthesia,
and twitching were marked succus conii was given quite freely, but
without any apparent benefit.
The condition of the stomach required attention in almost every case.
Nausea, vomiting, and epigastric and hypochondriac soreness were the
prominent symptoms. Anorexia was usually complete during pyrexia, and
not rarely patients were admitted to the hospital who asserted that
for one or more days they had not taken any nourishment whatever.
Under such circumstances, and in a disease where the tendency to
prostration and cardiac failure calls for stimulants and food, it is
evident that strict care must be given to the diet. In many cases
skimmed milk with lime-water, meat broths, arrowroot, or gruel, could
be taken in small amounts at short intervals, and retained. But
whenever these are rejected, no attempt should be made to persist in
their use, but koumiss, whey, or chicken-water should be substituted,
and continued until the stomach grows retentive. Equal care must be
paid to the selection of a suitable form of stimulus. It may be proper
to employ a mild and relaxing emetic if the patient be seen at the
onset of the disease and if there is reason to suspect the presence of
indigested food in the stomach, but under any other circumstances
there seems no reason for its use in a disease where vomiting is so
common and gastric irritability one of the most troublesome symptoms.
Nor should purgatives be given save when very positive indications
exist for their use.
Constipation is rarely obstinate; the amount of nourishment taken is
very small; in a considerable proportion of cases there is diarrhoea,
or at least a sensitive state of the bowels; and as a consequence it
is preferable in nearly every case to dispense with laxatives
entirely, and, if the bowels must be opened by assistance, to
administer a simple enema.
When irritability of the stomach is marked, benefit may be derived
from very small doses of calomel frequently repeated, as, for example,
gr. 1/8 or 1/4 every one or two hours. Subnitrate of bismuth may be
used in combination with this or as a substitute for it. In several
instances more prompt relief was obtained from nitrate of silver given
in the dose of gr. 1/12 every three or four hours, dissolved in thin
mucilage of acacia.
Stimulants were remarkably well borne, and their administration in
such form as was acceptable to the stomach was clearly of service,
{431} even from an early period of the disease. As a rule, whiskey was
employed, given in the form of milk punch. By carefully graduating the
amount of alcohol, and when necessary diluting the milk freely with
lime-water, the stomach usually received it well. If circumstances
favored, dry champagne, or brandy or sherry in carbonated water would
often prove preferable. The exhausting nature of the disease, the
marked tendency to cardiac failure, and the inability to digest an
adequate amount of nourishment, all indicate the early use of
stimulants. In cases where a tendency to the development of the
typhoid state existed alcohol was freely given, even to the extent of
sixteen ounces of whiskey in twenty-four hours. Other stimulants were
usually given in these cases, such as carbonate of ammonium,
especially if pulmonary congestion existed; turpentine, especially if
tympany was marked; or Hoffmann's anodyne or spirit of chloroform, if
muscular twitchings, hiccough, or insomnia with wandering delirium
were prominent symptoms. In all cases of severity the use of tonics
and stimulants should be maintained in reduced doses during the
intermission and for some days after the final fall of temperature.
It remains to allude briefly to certain special remedies and to
certain symptoms requiring special treatment. Formerly, much diversity
of opinion existed as to the propriety of venesection or local
depletion in relapsing fever, but Murchison concluded, after a careful
examination of the evidence, that it had not been shown to be of
service; and certainly the disease as it occurred in Philadelphia in
1869-70 presented no indication whatever for even the mildest
depletory measures. This corresponds with the recognized plan of
treatment in all the specific fevers.
Blisters are not so objectionable in relapsing fever as in either
typhus or typhoid, and there are several conditions in which they have
been found decidedly useful. In cases where the headache has
obstinately resisted cold applications, bromide of potassium, and
opiates, a blister to the back of the neck has afforded marked relief,
with no unfavorable result. Again, in cases where the vomiting and
epigastric distress were severe and obstinate the application of a
blister three inches square to the epigastrium is to be recommended.
Chloroform has proved of value for the relief of various symptoms in
relapsing fever. As already stated, it was found the most useful
remedy for the hiccough which was so troublesome in a number of our
cases, and especially in those where jaundice was pronounced. It also
seemed serviceable in controlling the peculiar chills which in varying
degrees of severity were present in a few cases, recurring at about
the same hour on successive days. These rigors or chills were
uninfluenced by very large doses of quinine or other antiperiodics,
but were apparently controlled by full doses of chloroform given in
advance of the expected hour of recurrence.
Jaundice, which, as has been stated, is partly of haemic origin, but
is probably also due in part to obstruction from catarrhal swelling of
the mucous membrane of the bile-ducts, is not influenced by mineral
acids, and still less should mercurials or purgatives be administered
for its relief. It would seem proper, in cases where this symptom is
marked, to observe special care in diet and the use of stimulants, and
to employ local sedative {432} astringents, such as small doses of
nitrate of silver combined with opium and belladonna.
Muscular soreness, pains, and tremor may call for special treatment on
account of their severity. The only remedy which has proved useful in
relieving the first two of these symptoms is opium, conjoined with the
external use of anodynes. Iodide of potassium fails even in doses as
large as can be borne, and the same is true of muriate of ammonium and
cimicifuga, which we used thoroughly without any effect. In the
muscular pains, however, which torment the patient during
convalescence, the ammoniated tincture of guaiacum was found of
service. Atropia hypodermically and chloroform internally have been
found useful for the relief of severe muscular twitchings.
Upon the whole, therefore, it will be seen that in ordinary cases a
supporting and expectant plan of treatment is all that is required.
Abandoning the idea of forcibly controlling the fever or of preventing
the relapse, care should be given in the first place to the diet and
to judicious stimulation.
Opium or morphia should be used to control pain, excitement, and
insomnia, aided, as far as the latter is concerned, by bromide of
potassium or the cautious use of chloral. Cooling drinks should be
allowed, cool applications made to the head, and the body should be
repeatedly sponged with cooling and disinfecting lotions. If the
stomach is retentive, quinine in moderate doses may be given in acid
solution, alternating with a simple fever mixture; but if nausea and
vomiting are present, the first purpose will be to allay them by the
appropriate measures already discussed.
Epistaxis is a frequent symptom, but usually requires no special
attention. Occasionally it is profuse, and then should be promptly
checked, since serious exhaustion may follow its continuance. If,
therefore, mild astringent applications do not arrest it, recourse
must be had to the tampon saturated with diluted Monsell's solution.
The urine must be closely watched and frequently analyzed in relapsing
fever. In some epidemics serious alterations in this secretion are
rare; in others it is not uncommon for the urine to be scanty, and to
contain albumen or blood. When this latter condition is presented,
especially if at the same time uraemic symptoms exist, dry cups should
be applied over the kidneys, to be followed by the use of dry heat,
and free perspiration should be promoted by hot-air baths or by the
hot wet pack. It is probable that jaborandi given in repeated small
doses, so as to avoid any depressing effect on the heart, will be
found valuable in such cases. Infusion of digitalis, with spirit of
nitrous ether or with acetate of potassium, may also be used with
advantage.
Absolute rest must be insisted on throughout the entire period of
paroxysm and relapse. The records of every epidemic present instances
of sudden death from cardiac syncope following trifling exertions. The
patients should therefore be kept strictly quiet in bed from the
initial rigor until their strength is fully restored after the
relapse. As the danger of collapse is especially great at the time of
the critical fall in temperature, the patient should be closely
watched as the end of the initial paroxysm and of the relapse
approaches. If there is any sudden rise of temperature, with head
symptoms due to hyperpyrexia, large doses {433} of quinine, ice to the
head, cold spraying, or the cold bath must be promptly used. As
sweating begins the body must be covered with a warm blanket and warm
stimulating drinks be administered. If any marked tendency to collapse
is observed, the subcutaneous injection of strychnia or of ether and
digitalis, conjoined with diffusible stimulants internally and hot
applications externally, are to be employed immediately. The special
remedies required for the various complications and sequelae have
already been sufficiently indicated.
I desire in conclusion to acknowledge the important assistance
received from Drs. Geo. S. Gerhard, Louis Starr, Charles Shaffner, and
R. G. Curtin, who, under the supervision of my colleague, the late Dr.
Edward Rhoads, and myself, recorded the histories of most of the cases
which serve as the basis of this article, and also tabulated them for
statistical purposes.[43]
[Footnote 43: Reference must also be made to the interesting
observations on spirilla published by Mulhauser in _Virchow's Archiv_
for July 9, 1884, after this article had been printed. His results go
to confirm the view that the spirillum of Obermeier is the essential
cause of relapsing fever.]
{434}
VARIOLA.
BY JAMES NEVINS HYDE, M.D.
Variola is an acute, febrile, contagious, and systemic affection,
preceded by an incubative period, characterized by the evolution of
symptoms in a relatively determinate order, with a cutaneous
efflorescence successively papular, vesicular, and pustular in type,
followed by crusting, and terminating either fatally or by complete
convalescence, with or without sequelae in the form of multiple,
circumscribed, and superficial cicatrices.
SYNONYMS.--_Lat._, Variola; _Eng._, Small-pox; _Fr._, Petite Verole;
_Ger._, Pocken; _Ital._, Vajuolo.
HISTORY.--Small-pox is a disease which, there is reason to believe,
was first developed in the earliest ages of which the human family has
record. Originating probably in China, India, and the adjacent
countries of the Asiatic continent, its extension over Europe and
America was, without question, in the line of progress pursued by the
advancing centres of traffic and population. The earliest traces of
its ravages can be dimly recognized in the descriptions of writers in
the middle and latter parts of the sixth century. In the early years
of the tenth century, however, a remarkably accurate picture of the
disease was drawn by Rhazes, a physician of Bagdad. His treatise,
translated by Greenhill for the London Pathological Society,[1] sets
forth the views of an Egyptian physician named Ahron, who wrote in the
sixth century. After these dates the remarkable political and social
changes in Europe, which are to be attributed either directly or
remotely to the Crusades, contributed largely to the opportunities for
the spread of the disease and to the occurrence later of those
decimating epidemics which became veritable scourges. In the last
century the resulting mortality in some of the countries of Europe was
often equal to the entire population of one of their largest cities.
If a modern traveller could find himself transported to the streets of
the city of London as they appeared in the early part of the present
century, it is probable that no peculiarities of architecture, dress,
or behavior would be to him so strikingly conspicuous as the enormous
number of pock-marked visages he would encounter among the people at
every turn. In the face of all cavil and sophistry, medical science
will always count among its greatest triumphs the modifications which
variola has undergone since its preventive treatment was established
upon a satisfactory basis by the discovery of the immortal Jenner.
[Footnote 1: _A Treatise on the Small-pox and Measles_, by Abu Becr
Mohammed Ibn Zacariya Arrazi, London, 1848.]
{435} The bibliography of the disease is extensive, and the list of
authors contributing to the subject is enriched by the names of such
men as Boerhaave, Van Swieten, Sauvages, Willan, E. Wagner, Johanny
Rendu, Hebra, and, more lately, Kaposi.
ETIOLOGY.--Respecting the etiology of variola, it can scarcely be
affirmed that our knowledge has been greatly extended since the date
of the experiments of Jenner. There is no historical knowledge of its
generation de novo; and the earliest cases of the malady must
therefore be classed with the exceedingly rare instances of
spontaneous cow-pox which have proved such a boon to the
vaccini-culturists. To-day every case of small-pox is justly regarded
as having been directly or indirectly transmitted from one or more
individuals affected with a similar disorder. It is thus recognized as
specifically infectious, contagious, and inoculable, its transmission
occurring, first, without contact, by atmospheric conduction of a
volatile contagious principle of unknown nature; second, with contact
either by (_a_) actual transference of dry or moist infectious
secretions deposited upon a susceptible surface, immediately or
through the medium of garments, bed-clothing, paper money, and similar
material substances; or (_b_) by inoculation of unprotected persons
with the pathological product of an infected organism. There is no
doubt but that the contagious principle displays its greatest
activities in connection with the contents of the lesions undergoing a
change from the vesicular to the pustular phases, though from the
beginning to the end of the disease it is probable that all the
tissues and fluids of the infected body are in various degrees capable
of producing the malady in those who are unprotected. Furthermore,
whether associated or not with an organic substance, the contagium of
the disease is known to preserve the power of reproducing itself for a
period lasting for weeks, months, and even a longer time. A field for
its activities once secured, there is a period of time during which
few if any evidences of its progress are declared, this period being
abruptly terminated by distinct and characteristic symptoms. This is
known as the period of incubation.
The nature of the contagium in small-pox has been the subject of much
speculation, careful investigation, and experiment, the results having
established but few facts of any practical value. There is at present
no proof that any bacteria, vegetable germs, or other minute organisms
foreign to the human body are the essential causes of the disease. It
is certain that in health the human body is completely enveloped in a
volatile medium emanating from the secretions of the glands of the
skin, which can be recognized by some of the keen-scented lower
animals when it is wafted through the air at a distance of several
hundred feet from a single individual. It is reasonable to conclude
that not only in small-pox, but in other contagious and infectious
diseases, these emanations possess a pathological character, and
become capable of transmitting such maladies from diseased to healthy
organisms. Certain also it is that when the subjects of these diseases
are crowded together, as in prisons, hospitals and camps, this
contagious element gathers an unwonted intensity. By far the larger
number of all transmissions of variola occur after inhalation of the
infective medium--in other words, by the avenue of the lungs. It is
probably for the same reason that the disease spreads more widely and
with greater virulence during the cold seasons of the {436} year, in
this latitude especially from December to February--a time when the
ventilation of inhabited dwelling-houses is usually much less perfect
than in warmer weather.
The disease affects individuals of all ages and both sexes, not
sparing the foetus in utero, and, in the case of the latter, occurring
both with and without previous infection of the mother of the unborn
child. Nowhere are its ravages so extensive and followed by such fatal
results as among those who have long been unprotected by previous
vaccination. Among the debilitated, as also among the very young and
the very old, small-pox is liable to be followed by severe
complications and a fatal result. Negroes, possibly in consequence of
tendencies inherited through generations of unvaccinated ancestors,
are particularly prone to the disease. Lastly, there is occasionally
noted an individual idiosyncrasy, in consequence of which either a
remarkable susceptibility to the disease exists or a no less singular
immunity against its encroachment is conferred.
Thus, physicians, much exposed to its influences in the discharge of
their professional duties, are known to be relatively exempt, while
other individuals, few in number it must be admitted, have either had
repeated attacks of the malady itself, or, after each exposure to its
contagious principle, a recurrent illness of variable type. In the
immense majority of all cases, however, one attack confers immunity
upon the sufferer against subsequent invasion of the disease for the
remainder of life. Upon a few occasions I have known variola to occur
in individuals previously affected with cutaneous diseases, especially
the eczematous--a fact which merely suggests that such pre-existing
disorder of the integument conferred no immunity against infection.
SYMPTOMATOLOGY.--The earliest symptoms of small-pox may be
occasionally recognized during the stage of incubation, which, as
described above, embraces a period of from ten to fifteen days, though
these limits are not absolutely fixed, since both shorter and longer
incubative periods have been at times established. During the interval
the patient may appear to enjoy perfect health, or, on the other hand,
suffer from an ill-defined malaise, with anorexia, languor, insomnia,
and allied symptoms. Close observation of the patient thus affected
will often reveal the existence of a peculiar pallor of the face,
accompanied by a skin-color which suggests a slight degree of
sallowness of the complexion. These rather indeterminate symptoms are
naturally most marked toward the completion of the period of
incubation.
The latter terminated, the period of invasion follows, and extends
from the conclusion of the incubative stage to the moment when the
first cutaneous lesions of variola appear upon the surface. The
symptoms which characterize the onset of this period of invasion are
conspicuous and characteristic. There is often a sharp vespertine
rigor or a more or less continuous chilliness, accompanied by
sensations of "creeping" over the surface, lasting even for several
hours. Meantime, the temperature rises to 103 degrees or 105 degrees
F., the pulse running up to 120 or 130 beats per minute. In this
febrile condition there is commonly complaint of a characteristic
aching in the head and back, intense, scarcely intermittent, and so
peculiar as to have frequently furnished a clue to the diagnosis of
the approaching malady. These sensations are quite analogous to the
substernal and other pains which frequently precede the first
explosions {437} of syphilis, and are all, without question, due to
the circulation of a poisoned blood, the influence of which is in this
manner confessed by the nervous system. In the case of infants and
young children the invasion of small-pox is frequently ushered in by
delirium and convulsions--symptoms which are to be explained by the
facts just named.
This complexus of febrile and nervous symptoms, varying somewhat in
intensity and possibly interrupted by sensations of chilliness, may be
recognized as continuing on the second and third days of the period of
invasion. Meantime, there may be noted a dusky hyperaemia of the
pharynx and tonsils, the surface of which may even display elevated
points which develop later into papules. In exceptional instances the
intensity of the poison is such that the system fails to rally before
the violence of the onset, and a fatal result ensues before the
characteristic exanthem appears upon the skin.
On the second and third days of the invasion stage of the disease, if
they are displayed at all, the variolous rashes appear. Too much
attention can scarcely be paid to the importance of their recognition
on the part of the diagnostician. Often indeed have practitioners been
deceived by their occurrence, having been either completely blinded to
the serious nature of the malady in progress, or, as Bartholow[2] has
well shown, having supposed that they were dealing with a concurrence
of variola and scarlatina or rubeola.
[Footnote 2: "The Variolous Diseases," _Med. News_, Mar. 4, 1882, p.
232.]
Hebra was the first to point out the significance of the rash known as
roseola variolosa or erythema variolosa. Occurring at about the dates
named above, it is in a few patients pronounced and vivid, even in
solitary instances rivalling in severity the exanthem which succeeds
it. In others, the majority of all patients in some epidemics, it may
be entirely wanting. The writer has certainly observed its most
typical development in women who were either menstruating or in the
puerperal state. It is said also to be relatively frequent in subjects
of a tender age. Kaposi[3] has recognized it in all its manifestations
at every age.
[Footnote 3: Consult the admirable chapter on variola in his treatise,
_Path. u. Therap. der Hautkrankt_, Wien, 1882.]
It appears in the form of puncta, striae, or diffuse and uniform
blushes covering extensive areas of the integument, livid red,
purplish, or brownish-red in hue, paling under pressure, but never
leaving upon the skin over which the finger-nail is quickly drawn the
characteristic whitish streak by which many practitioners test the
scarlatinal rash. The surfaces involved may be either not raised or
slightly elevated above the general level of the skin, and are usually
circumscribed. The regions chiefly involved have been carefully
described by Th. Simon, and are hence sometimes called Simon's
triangles. Thus the groin, the internal face of the thighs, and the
hypogastric region may be involved at once (femoral triangle of
Simon); the surface of the axilla, the pectoral region, and the inner
face of the arm (brachial triangle of Simon), as also the extensor
faces of the knees and the elbows, the dorsum of the feet, and indeed
every portion of the surface of the body.
In the midst of these rash-covered areas may also appear petechial or
hemorrhagic, dark-red, pin-head to bean-sized maculae, which undergo
color-changes both in lighter and deeper shades as the invasion period
{438} lapses. In lieu of these, however, transient wheals may come and
go over the surface, and even the erythema described above may assume
an erratic phase and appear in one part only to disappear and recur at
another. None of these flash-light warnings of the oncoming exanthem
are proportioned to the latter in the matter of extent and intensity
of development. They may be followed by grave or mild manifestations
of the disease. The subsequent eruption may also be much more
abundantly developed in regions where the invasion rashes have not
appeared, and the latter completely fade before the former have
advanced to occupy the field thus deserted.
The invasion stage of variola commonly occupies three days. Rarely it
extends into the fourth, fifth, and even the sixth, day after the
premonitory chill and fever.
Upon its subsidence the exanthem of the disease as a rule promptly
appears. Simultaneously, the temperature abates, the rapidity of the
pulse diminishes, and there is marked amelioration of the general
symptoms. The patient, frequently deceived by the completeness of this
defervescence, is apt to conclude that he is convalescent from his
disorder, and is thus often astonished at the discovery of the
exanthem upon the person, usually the face. In other cases, more
commonly those of a grave character, there is failure of this
defervescence, the febrile symptoms continuing or even increasing in
severity.
The eruption first appears in the form of pin-head sized and larger,
firm, conical, discrete, coherent or confluent, reddish papules,
sometimes accompanied by mild sensations of a pricking or painful
character, often exciting no subjective symptoms by which their
presence could be declared. To the touch they are characteristically
indurated, and suggest the hardness of small shot imbedded in the
skin. They appear first and in greatest abundance upon the face and
scalp, involving later and progressively the trunk, the extremities,
and the palmar and plantar surfaces. It is at this moment that the
eruption most resembles that to be recognized in measles (the
distinction between the eruptive symptoms of the two diseases will be
considered later). At times a reddish areola surrounds each lesion,
especially those appearing upon the trunk. All are situated about the
orifices of the follicles and glands of the skin.
On the first and second days of the eruption the papular lesions
multiply in number, involve an increasingly large area, and
individually augment in size; so they appear first upon the head, and
are successively presented to the eye upon the lower portions of the
body. The older lesions are usually recognized upon the scalp, face,
neck, and shoulders; the more recent upon the extremities. By the
third day of the eruptive stage there is usually evident at the apex
of the older lesions a minute vesicle containing a drop of pellucid
serum, which rapidly changes in character and size till a distinct
vesicle is formed with cloudy or lactescent contents. Early in their
career an apicial depression can be seen, which later deepens into a
characteristic umbilication. This umbilication in the vesicular stage
is somewhat peculiar. It is more than a mere depression of the summit,
such as might be made by thrusting a blunt-pointed pin centrally and
downward so as to carry the roof-wall before it. It is made clinically
most distinct by the fluting or puckering of the peripheral part of
the roof-wall, giving the lesion a crenated appearance which is not
{439} assumed by any other cutaneous efflorescence of multiple
development. It may be regarded as pathognomonic of variola.
The pock is usually mature by the sixth day of the eruption. It is
pea-sized and globular in shape; its umbilication has been usually
quite removed by the complete filling of its chamber with distinctly
purulent contents; it is often surrounded by a halo due to hyperaemia
or exudation; and, the total number of individual lesions being then
fairly determined, it is often closely set against its fellows, islets
of unaffected integument having meantime become fewer and more
contracted. The face, covered with this eruption, then exhibits a
typical aspect. The entire integument becomes swollen and brawny or
oedematous. The eyes are thus closed by the tumid lids, which are
separable with difficulty, and this, too, even though they be the seat
of comparatively few lesions. The nose, lips, cheeks, and ears are by
similar processes deformed and given a most repulsive unsightliness.
Mucus and puriform secretions gather and dry about the mucous outlets.
The skin of other parts of the body (hands, feet, genitalia, and the
entire extremities) is in a similar condition, merely most noticeable
in the exposed and disfigured visage.
The fever of maturation or suppuration, or, as it is often called, the
secondary fever, is lighted to activity with the onset of the
suppurative process. The temperature rises to a point ranging between
101 degrees and 105 degrees F., the pulse-rate simultaneously rising
to 100 and even 150 in the minute, varying of course with the age of
the patient and the severity of the attack. During its continuance,
from the eighth or ninth to the eleventh or twelfth day of the
disease, the victim of the malady is in a deplorable and critical
condition. The intense grade of cutaneous inflammation, with its
resulting subjective sensations of burning pain and tension, the
soreness of the mouth (tongue, pharynx, inside of lips, and palate),
due to the existence of pus-filled pocks upon the buccal membrane,
and, for similar reasons, the dysphagia and irritation of the larynx
and tracheal membrane, are all sufficient to account for the general
condition. In cases of mild grade the patient lies conscious, but in a
stolid apathy, listlessly accepting the services of his attendants. In
others there is delirium of low or high grade, often sufficient to
demand constant surveillance, lest in consequence the patient do
serious injury to himself.
The behavior of the pustules which appear upon the mucous surfaces
accessible to the eye is modified somewhat by the heat, moisture, and
friction to which these surfaces are exposed. Typical, fully-distended
pustules occasionally persist upon the soft palate and the inside of
the lips. Soon, however, the macerated roof-wall yields, leaving a
reddish floor where the mucous membrane is exposed, denuded of its
epithelial layer or covered with a new tender and hyperaemic pellicle.
In grave and severe cases these pustular lesions may extend deeply
into the mucous tracts, involving the trachea, bronchi, or alimentary
canal. In an autopsy made by the writer on the body of a male subject
dead of unmodified variola, there was no portion of the alimentary
canal from the mouth to the anus which was not studded by thickly-set
pustules. The urethra, vagina, vulva, external auditory canal, and
conjunctivae are, in severe cases, similarly involved. According to
Kaposi, the tympanum is usually exempt.
The period of desiccation begins usually on the thirteenth or
fourteenth {440} day of the disease, and, according to the severity of
the previous pathological processes, requires for its completion from
one week to a fortnight. Its onset is characterized by a second marked
but gradually developed defervescence. With a diurnal temperature
successively less elevated above the normal standard there is a
corresponding fall of the pulse-rate. As the disease has by this date
taxed the vital resources of the system to the utmost limit, the
exhaustion resulting may be declared by a pulse which is flagging,
weak, and even in the matter of frequency much below the standard of
health.
The cutaneous lesions now again undergo a change. Some of the pustules
rupture, and their viscid contents, oozing forth, concrete into a
yellowish crust which gradually assumes a brownish hue. Others
desiccate en masse, the roof-wall first collapsing upon the contents,
thus producing an appearance which again suggests umbilication of the
lesions. This is sometimes termed a secondary umbilication. The
desiccation en masse is doubtless due to the evaporation of a portion
of the fluid exuded into the superficial strata of the integument, and
the consequent inspissation of the pus. Often the face at this moment
is totally concealed by a dense, dry, brownish or even blackish mask,
composed of the crusts furnished by numerous individual lesions. At
the same time the tumefaction of the skin subsides, and the subjective
sensations to which it gave rise gradually disappear. Beneath the
crusts cicatrization advances till the former are lessened, and
finally, becoming detached, fall in quantity from the surfaces
subjected to friction. Beneath them are seen brownish and violaceous
blotches, the integument thus stained slowly losing its abnormal
color. It is thus seen to be the seat of multiple, slightly depressed,
shining scars of a dead white color, which in the course of time lose
somewhat of their disfiguring prominence, but which when typically
distinct persist for a lifetime. This exfoliation of crusts continues
till the skin is completely rid of its pathological products, the
process being completed with entire restoration to health about the
conclusion of the fourth or fifth week of the disease. Meantime, in
favorable cases, convalescence progresses pari passu. The patient has
a returning appetite, decadence of symptoms originating in impairment
of function of the mucous membranes, and gains in weight till the
restoration to sound health is complete.
Such is the history in outline of what may be regarded as a typical
form of uncomplicated variola. It should not be forgotten, however,
that in different epidemics there are marked differences in the career
and manifestations of the malady, and that even among the cases
observed in a single locality visited by the disease the same
divergence of symptoms is no less conspicuous. This diversity is due
to several causes, irrespective of the remarkable modifications
displayed in the variolous who have been previously vaccinated.
Individual susceptibility is doubtless to be considered in this
connection, as also the temperament, bodily vigor, and hygienic
surroundings of those who are infected. It is possible also that the
intensity of the poison may be subjected to occasional modifications
in its transmission from individual to individual. In this way the
following types of variola present themselves in clinical forms with
divergent features:
CONFLUENT VARIOLA (variola confluens).--This virulent form of {441}
small-pox is ushered in by a relatively short incubative period,
followed by a severe invasion of the disease. The premonitory chill is
violent; the cephalic and lumbar pains are excruciating; the fever,
rising to a high grade, 106 degrees to 110 degrees F., with few and
slight remissions, scarcely subsides, if at all, with the appearance
of the eruption, the latter developing early, and, to borrow an
expression from syphilographers, exploding with violence over large
areas of the surface of the body. The initial lesions of the exanthem
are dense and deeply-set papules, so closely coherent even at this
moment that they scarcely leave between them interspaces of sound
skin. During the vesiculo-pustular transformation which they promptly
undergo on the second day there is a more or less complete coalescence
of the elements of the eruption, which circumstance has given this
form of the disease its name, confluent variola. This confluence is
most conspicuous upon the face and hands, where large flat vesicles
run together, form pus-filled bullae, and finally convert the surface
on which they rest into a single, large, many-chambered pustule. All
this occurs upon an enormously swollen and inflamed skin, disfiguring
every feature of the face and wellnigh obliterating every external
distinction between the scalp, nose, eyes, and mouth. Here and there
the mass is elevated by the quantity of exuded pus to a more notable
projection from the surface. Pustules filled with blood may appear at
several points. At others, the suppurative inflammation may be seen to
have eroded the derma, which is covered with a diphtheritic membranous
exudation similar to that covering the mucous membranes lining the
mouth, nose, and ears. Naturally, the skin in its totality often
yields to these destructive processes and in large patches falls into
gangrene.
The confluence of the lesions is less marked in other parts of the
body than the face and hands, yet the entire surface may be covered
with a coherent exanthem which becomes elsewhere, in large areas,
confluent. The writer has seen patients in whom the head of a pin
could not be placed upon an unaffected patch of skin in any portion of
the body. The parts subjected to pressure in the reclining posture,
such as the back, shoulders, and buttocks, are especially liable to
this coalescence of the pustular lesions.
In confluent variola too, as already intimated, the mucous surfaces
suffer proportionately. Pasty accumulations of muco-pus and
diphtheritic exudation, like macerated chamois leather, cover the
tongue, which is often so enormously swollen as to bulge between the
teeth and project from the mouth. These exudations line the mouth,
pharynx, larynx, and even the bronchi. Beneath these masses the eroded
mucous surface is dry, livid red in color, and has a varnished aspect.
Gangrene here may lead to necrosis of the cartilages of the larynx.
Aphonia is often complete, deglutition impossible, respiration
difficult. The stench arising from the patient is intolerably fetid
and pervading, and a single exhalation will poison the best-ventilated
apartment. The submaxillary and sublingual glands are enlarged and the
neighboring lymphatics swollen.
The patient who is plunged into this grave condition is the victim of
a fever which is unquestionably septicaemic in character; he has a
small, frequent, and often fluttering pulse; his mental condition is
betrayed by a delirium of varying grade or he lies comatose. In this
state a fatal {442} result is often induced by either exhaustion of
the vital forces or an intercurrent malady, such as pleurisy,
pneumonia, cardiac inflammation, oedema of the glottis, or an
uncontrollable diarrhoea. In yet other cases the patient falls into a
typhoid state, and, after surviving for a fortnight or more with a low
fever, a broncho-pneumonia, or a diarrhoea, succumbs to an inevitable
exhaustion, the surface of his body being yet covered with a dry,
blackish, and fetid crust.
The expression of an intense variolous poison is known as hemorrhagic
variola; also as purpura variolosa and black pox. A large number of
such cases have been designated and treated as black measles, the real
nature of the malady having been mistaken.
The law readily observed by the diagnostician of diseases in general
must here be recognized. There are no hard and fast lines in nature.
Hemorrhagic variola occurs, without question, in different types. At
the one extreme are classed the inevitably fatal cases, where the
patient sinks smitten by the malady even before the exanthem is
developed; at the other are found the cases of confluent variola, not
necessarily fatal, in the course of which hemorrhagic lesions appear
in variable number, blood either filling the pustules after the latter
have arrived at maturity, or forming ab initio purpuric pocks
intermingled with the typical lesions of the variolous exanthem.
However ill-defined the limits between these classes may be, the
symptoms of hemorrhagic variola are sufficiently characteristic to
require separate description. According to Kaposi, it occurs in the
two following types:
The first form is termed variolic purpura. Its incubative period is
brief and distinguished by unusual conditions of malaise and lumbar
pain. On the fourth day there is an intense fever with rapid pulse,
and this is speedily followed by a deep purplish-red staining of the
face, neck, trunk, and extremities, the skin thus affected being
slightly tumid and quite dry. Minute maculo-papules can be
distinguished here and there over the surface, often closely set
together, and presenting the characteristic color described above. At
this stage of the disease the eruption greatly suggests an intense
rubeolous exanthem, and has been, as a result, repeatedly mistaken for
the so-called black measles. But the excruciating pains persist, there
is often coincident delirium, and the pin-head sized maculo-papules
noted above become lenticular in shape, cease to lose their color
under the pressure of the finger, extend peripherally even in a few
hours, flatten and become purpuric patches of a bluish-black shade,
palm-sized and even larger, covering extensive areas of the
integument, new lesions forming in unaffected islets of the skin;
conjunctival ecchymoses appear at the angles formed by the lids, and
finally encircle the cornea with an annular purplish-black cushion.
The mucous surfaces become dry, crack, and bleed where the epithelium
is torn, and become covered with offensive crusts. The odor exhaled by
the patient is intolerably fetid. He lies stupid as the march to a
fatal issue is hourly hastened. Hemorrhages occur from the larynx,
bronchial membrane, intestinal surfaces, and even into the parenchyma
of the viscera, the muscles, serous membranes, periosteum, and
neurilemma. The urine is retained in the bladder; the respirations
rapidly increase in frequency; the pulse flutters; and death closes
the scene between one and two days after the onset of the malady. In
several cases observed by the writer, {443} occurring in infants and
children, the entire course of the malady was completed in twelve
hours.
In the second and much rarer form of hemorrhagic variola there are the
usual unfavorable portents of intense prodromic symptoms. On the
fourth day the skin is swollen and indurated in consequence of the
development within its structure of numerous firm, roundish, slightly
acuminate papules, so thickly set together that it is wellnigh
impossible to distinguish between them. These are early in betraying
the bluish-black hue significant of hemorrhage into their mass. They
multiply in number and increase in size, while their hemorrhagic
stains widen and sweep from each as a centre, like the waves that
spread from a pebble thrown into smooth water. In these cases, more
often than in those first described, pus-filled pocks may develop over
some portions of the surface, while in others a species of gangrene
occurs in consequence of the separation of the derma from the
subcutaneous tissues by effused blood. At times pustules of somewhat
typical aspect are formed and subsequently filled with blood by a
hemorrhage from below. The accompanying symptoms are grave, but less
rapidly fatal than in the other types of the disease. Delirium,
stupor, an intense fever, and a rapid, feeble pulse are commonly
noted. A fatal result is usually reached in from four to five days.
Hemorrhagic lesions, isolated or confluent, are seen also in severe
forms of variola, not of the two types described above. Thus, in
confluent small-pox, especially when occurring among the unvaccinated,
some of the pustules on the face, the back, or possibly the legs,
where varicosities of the veins permit a passive engorgement of the
tissues with blood, may become the seat of a hemorrhage. For these
local causes are often etiologically effective. In other cases the
appearance of the hemorrhagic lesions seems to be due to a dyscrasia,
such as that recognized in phthisis, chronic alcoholism, and
haemophilia.
Aside from the trivial accidents to which the exanthem may be subject,
the hemorrhagic types of variola may be regarded as necessarily grave
and in a large proportion of cases inevitably fatal. That they are all
truly the results of variolous poisoning is shown, first, by the
occurrence of intermediate forms; second, by the occasional
transmission of the disease in its typical aspects to the partially
protected.
VARIOLOID is that form of variola in which the disease is modified,
either in its course, duration, or intensity of symptoms, such
modification usually resulting, directly or indirectly, from the
protective influence of vaccination or from a previous attack of
variola.
The symptoms of the class of patients commonly regarded as suffering
from varioloid are all those of variola, modified, however, in the
direction of a mitigation of their intensity and dangerous character.
It is thus evident that there is no strict line of demarcation between
the very mildest physical expression of the variolous poison and that
variola vera which presents atypically benign symptoms in any stage of
its career. Within this wide range of possibilities cases of varioloid
occur which certainly differ from each other by very marked degrees.
The invasion stage of varioloid may be shorter or longer than that
occurring in variola vera, and may be insignificant or intensely
marked as regards the severity of its symptoms. According to
Bartholow[4] the {444} invasion rashes are here of common occurrence;
and the more extensive the latter, the less copious the subsequent
eruption. It must be admitted that a personal experience has not
confirmed us in this view.
[Footnote 4: _Loc. cit._]
After the high fever and severe cephalic and lumbar pains of this
stage there may follow, in the case of varioloid, a complete
defervescence and the appearance of a very copious exanthem. With
this, however, the apogee of the disease may be reached, and the
subsequent symptoms be altogether insufficient in comparison with
those which have preceded. Thus, the maculo-papules may never reach a
vesicular stage, or, having attained this, the vesicles may not be
umbilicated, or may shrivel after their contents have assumed a
lactescent color, and be succeeded by light superficial crusts which
in a few days fall. Or, again, the pustular stage of the lesions may
be fully developed, even with the production of a halo about the
pocks, while yet there is no swelling of the skin and but trifling
subjective sensations experienced by the patient. The pustules in the
course of from four days to a week desiccate and are shed, leaving
behind them violaceous pigmentations of the surface without persistent
cicatricial sequelae.
Other cases, again, instead of producing the impression upon an
observer of being illustrations of a malady aborted or cut short at
some period of its career, seem to exhibit merely a modification in
the intensity or distribution of symptoms betrayed in a wellnigh
typical career. Thus, there may be a total absence or insignificant
reminder of the septic fever usually known as the secondary fever of
variola, and the elements of the eruption may be few or appear in
scanty number upon the face and more copiously elsewhere. The latter
may, however, pursue a perfectly typical career and be followed by
characteristic scars.
There is yet another type of varioloid with which many practitioners
become familiar who have experience in epidemics of small-pox. The
patient exhibits distinct symptoms of malaise in the period of
incubation. The fever of invasion, with its characteristic pains and
nausea, is equally well marked. Defervescence occurs with a trifling
eruption of maculo-papules, which in two days have wellnigh completely
disappeared. There is no secondary fever, but the patient is far from
well. There is a period of anaemia, mental depression, marked languor,
and unmistakable evidences of physical prostration out of all
proportion to the precedent symptoms. In these cases it may well be
believed that the poison has at last produced a strong impression upon
the nervous centres. The most characteristic feature of these cases is
the tedious convalescence from an apparently trifling form of the
malady.
The identity of varioloid with variola is abundantly shown--first, by
the occurrence of intermediate forms of every grade, from the mildest
evidence of variolous poisoning to typically developed cases of
variola vera; second, by the fact that patients affected with
varioloid are capable of transmitting variola to the unprotected;
third, by the anatomico-pathological fact that the structure of the
pock, when it appears, is the same in all.
A variation as to the form and contents of the lesion of modified
variola occasionally occurs as a consequence of individual
peculiarities or of the special surroundings of the patient. A number
of useless terms have been employed to designate these peculiarities,
the most of which {445} are relics of the superstitions of the past.
In variola siliquosa the pocks are said to contain air only; in v.
pemphicosa, bullous lesions predominate; in v. verrucosa, the papules,
after partial evolution and involution, leave minute wart-like
papillary masses upon the face; in v. crystallina, there are
superficial vesicles only filled with clear serum, which somewhat
resemble those recognized as sudamina. The older English writers with
as little reason described cases of horn-pox, swine-pox, etc.,
differing only from those of variola by the anomalous behavior of the
exanthem in the course of its evolution.[5]
[Footnote 5: Besides the terms given above, Hebra gives the following
list of Latin adjectives which have been employed to describe special
varieties of small-pox, none of which requires special explanation:
variola papulosa, conica, acuminata, globosa, globulosa, tuberculosa,
cornea, fimbriata, miliaris, lymphatica, vesiculosa, pustularis,
rosea, morbillosa, carbunculosa, etc.]
COMPLICATIONS AND SEQUELAE.--The complications and sequelae of variola
are fewer in number and more restricted in range than those of many
other maladies. This results from the remarkable unity of the disease
as it occurs in its several manifestations among the unprotected, its
relatively rapid progress, and its absolute disappearance on the
completion of its curriculum. There is no chronic form of variola
lingering for weeks and months after the violence of the fever has
abated.
Furuncles and abscesses occasionally result during or after the
pustular stage of the disease has been reached, sometimes of such
extent as to give exit to large quantities of an ill-conditioned pus.
The tissues, weakened by the suppurative process which the skin has
undergone, may then necrose, and thus lay bare periosteum, cartilage,
or bone. Erysipelas, especially about the face, may close the eyes,
encroach upon the scalp, or spread extensively over other regions.
Muscular paralyses, hemiplegic and paraplegic attacks, albuminuria,
diarrhoea, and the inflammations of chronic type affecting the
thoracic organs may each supervene, and either greatly prolong
convalescence or precipitate a fatal issue. None of them is perhaps
more common than a low typhoid and febrile state, in which the patient
lies after his variola is practically ended, his skin struggling to
regain its normal tone, a fever of remittent type taxing his energies,
his bowels in frequent movements discharging a thin and fetid feculent
matter, while a low delirium renders him insensible to the gravity of
the situation.
Reference has been made above to the implication of the eyes of the
variolous, and the possibility of the disorder terminating, after an
otherwise favorable convalescence, in total blindness, should not be
forgotten. The cornea may be the seat of pustules or a diffuse
puriform infiltration resulting in ulceration, and eventually
perforation with hernia of the iris. At times it is merely macerated
by the pus continually covering it, and in that condition yields to
even moderate pressure. At others the deeper portions of the globe
fall into inflammation, and there is a resulting cyclitis,
irido-cyclitis, or parophthalmia.
In the nose severe destructive effects may follow the pustular
involvement of the Schneiderian membrane, including necrosis of the
nasal bones and profuse epistaxis.
In a similar way, the external ear may be involved, the tympanum
disappear, a severe otitis media supervene, and the mastoid cells
become filled with pus and detritus of necrosed tissue.
{446} In the larynx, which may be well lined with pustules, as
indicated above, complications may arise in the shape of oedema of the
ary-epiglottic folds,[6] laryngo-oesophageal abscess and various
diphtheritic deposits lining every portion of the mucous membrane.
[Footnote 6: J. William White, "Surgical Aspects of Small-Pox,"
_Medical News_, March 4, 1882, p. 241.]
Other disorders noted as complicating variola are hydrocele and
orchitis in the male, ovaritis in the female, gangrene of scrotum or
labia, haematuria, peritonitis, adenopathy and lymphangitis and
arthritis, as well as peri-arthritic suppurative inflammation.
PATHOLOGY AND MORBID ANATOMY.--Ours is a day in which bacteria,
special to each of a number of infectious diseases (lepra, pemphigus,
tuberculosis, etc.), are constantly reported as coming to light under
the persuasive influence of modern staining solutions. With respect to
variola, it may be said that while Cohn, Klebs, Weigert, and others
have, without question, recognized microsphaera, micrococci, and
similar organisms in variolous pus, their causative relation to the
pathological process has certainly not yet been demonstrated.
The pathological anatomy of the cutaneous lesions of variola has been
very carefully studied by Auspitz and Basch,[7] and Heitzmann.[8] The
following is a condensed account of the results reached by these
observers:
[Footnote 7: _Virch. Archiv_, Bd. 28.]
[Footnote 8: _Trans. of Amer. Derm. Ass._, Aug., 1879.]
First appear circumscribed patches of hyperaemia, in which the
papillary layer of the corium is concerned, and which is followed by
some thickening of the rete, the epithelia involved becoming coarsely
granular. This granular condition is due to an increase of living
matter within the protoplasmic bodies, evident at the points of
intersection of the reticulum of which they are composed, the nuclei
becoming solid and shining, and the threads traversing this
cement-substance between them becoming also increased in thickness.
The papillae beneath increase in size in consequence of their vascular
engorgement, and in consequence of the change experienced by the
connective-tissue bundles, which are partly transformed into
protoplasm, while the protoplasm between them increases also. There
is, in brief, a liquefaction of the glue-giving basis-substance, which
makes visible the reticulum of living matter formerly hidden within
it. In this way the epidermis is raised into the flat solid papules
which are the early lesions of the disease.
Then follows an exudation of a serous fluid at one or more points in
the papule, the meshes of the reticulum being so stretched and torn
that small chambers are formed filled with the liquid exudate
containing granules. Between these chambers the separating strata of
epithelia are compressed so as to form septa or partition walls. The
neighboring epithelia become granular, divested of their cement
envelope, and transformed into protoplasmic clusters still connected
with the living reticulum by slender threads. An irregular cavity is
thus formed in the thickened rete traversed by septa, the contained
exudation being filled with granules, coagulated fibrin, and lymph. A
few protoplasmic bodies are here also distinguishable, which Heitzmann
regards as either debris of destroyed epithelia or colorless
blood-corpuscles.
In these changes the connective-tissue beneath participates. The
papillae eventually disappear, the superior portion of the corium
being replaced by {447} clusters of medullary or inflammatory elements
uninterruptedly connected by threads of living matter.
The pus-corpuscles which eventually appear originate mainly from
transformed epithelia. In the process of transformation the increased
protoplasm of the epithelia first exhibits shining homogeneous lumps,
which, after an intermediate stage of vacuolation, undergo an
endogenous metamorphosis into nucleated bodies with a reticulum in
each. To the number of these there is possibly an addition by the
immigration from below (diapedesis) of leucocytes.
The question of repair with or without the production of cicatrices
rests upon the behavior of the connective-tissue elements. If these
are not torn asunder, but remain in connection with each other, the
re-formation of a glue-giving basis-substance is possible, and new
bundles of fibrous connective-tissue take the place of the old. If, on
the contrary, the latter are completely destroyed, their place is
filled with the cicatricial new growth. The pigmentation, which is
such a common transitory sequela of the skin lesions, is due both to
the imbibition of the coloring matter of the blood by the epithelia
and by direct hemorrhagic exudation into both the rete and derma.
The umbilication of the mature pock is doubtless due to the situation
of such lesions at the orifices of the excretory ducts of the
skin-glands. The epidermis, in one or more of its strata, dips
downward to form a living investment for such glands, and in this
situation ties down the centre of the roof-wall of the pustules.
Eventually, it too, as a result of the maceration and tension
incidental to the complete filling of the pock with pus-elements, is
ruptured or stretched, and the umbilication of the pustule disappears.
The anatomy of the exanthematous lesions in hemorrhagic variola is not
different from that described above. The pocks in such cases are
merely filled with blood instead of with pus or sero-pus. In some
forms of hemorrhagic variola, as indeed would be suggested by their
clinical observation, there is hemorrhage directly into the tissues of
the integument, or, more probably in severe cases, a mere passive
leaking of the sanguineous fluid with its coloring matter through the
relaxed and weakened vascular walls.
The morbid changes occurring in the viscera are described by
Curschmann as follows: The mucous surfaces may be the seat of
pustules, diffuse purulent infiltration, and catarrhal, croupous, or
diphtheritic inflammation. As regards the extent of diffusion of the
pustular lesions, they occur, according to Wagner, in bronchi of the
second and even of the third order, rarely in the stomach and
intestines, and in the rectum only in its lowest portion. The bladder,
urethra, and serous surfaces are always exempt. The lungs, breast,
liver, spleen, brain, and spinal medulla are variously involved. Often
the tissues of these organs are quite unchanged as regards their
macroscopical appearance. At other times the tissues appear swollen,
granular, and undergo a fatty degeneration. In purpura variolosa the
spleen and walls of the heart, however, are seen to be firm, dark-red,
and more or less indurated.
DIAGNOSIS.--The establishment of a correct diagnosis where there is
question of variola is one of the most critical and important of the
duties of a physician. Upon such decisions have turned, again and
again, {448} professional success or disaster. To pronounce that case
to be variolous which is not of such a nature is to subject one to the
indignation of the few and the ridicule of the many. On the other
hand, to be guilty of treating a patient with small-pox, and of
remaining ignorant of the nature of the malady, is to subject many
ignorant people to the danger of exposure to the disease and to render
one's self liable for the redress sought by recourse to the civil
authorities and the law. It is difficult to decide which predicament
is the graver.
Typical variola vera is readily recognized by its characteristic
features. As usual, it is the atypical and modified forms where the
difficulty most often arises and where the danger to the physician is
proportionately increased.
In the invasion stage of the disease it is often impossible to
recognize any symptoms characteristic of variola. High fever with
severe lumbar pain, considerable gastric distress, and the appearance
of one of the invasion rashes (roseola variolosa) would, however, put
the observant practitioner on his guard. I have often noticed in these
cases a symptom which, apparently insignificant, has on more than one
occasion preceded the eruptive period. It is the occurrence upon the
centre of the two cheeks of a vivid damask-red blush, occasionally
having a purplish-red hue, and with a very remarkable circumscribed
area. This may be recognized in children and adults of both sexes when
it occurs in typical aspect, and is undoubtedly a hyperaemia of the
character of that producing the rashes in Simon's triangles.
When the variolous exanthem first appears the practitioner should
secure as soon as practicable a history of the invasion stage if this
has not been subject to his personal observation. He should then make
careful inquiry as to the possibility of a neighboring source of
contagion, and ascertain by inspection whether the person of the
patient exhibits the evidences of successful vaccination. In this
connection it is always well to estimate the value of the elements
represented by (_a_) the period ascertained as having elapsed since
the last successful vaccination; (_b_) the typical or atypical
character of the existing cicatrices of vaccinia; (_c_) the unicity or
multiplicity of the cicatrices simultaneously resulting from
vaccinations performed at one and the same date.
Without question, the first papular lesions of variola resemble those
of rubeola or measles to an extent which has often deceived the most
expert diagnosticians. The distinguishing points are--(1) In measles,
catarrhal symptoms (conjunctival, nasal, laryngeal, bronchial), which
are usually absent in the early stages of variola, and later are
obviously associated with the irritation set up of the pustules of the
maturing period. (2) The difference in the temperature record, that
noted in the invasion stage of variola varying from 104 degrees to 105
degrees F., while in rubeola it is rarely registered above 103 degrees
F. Moreover, in typical variola the defervescence is marked and
characteristic on the appearance of the exanthem, while in rubeola,
when the rash appears, the temperature is usually sustained at a
maximum, and may even rise. (3) The differences in the rashes of the
two disorders. The papules of variola, even in its confluent forms,
are, when first observed, remarkably discrete and exhibit not the
slightest tendency to grouping, while the maculo-papules of rubeola
are (_a_) developed simultaneously on the face and trunk, while those
of variola {449} commonly appear first on the face and afterward on
the trunk, the older, and larger therefore, in the site of earliest
appearance; (_b_) are set in clusters or groups having a distinct
tendency to crescentic arrangement, a symptom decidedly best
appreciated by the eye when the eruption is viewed in totality or in
large areas with the eye of the observer somewhat removed from the
surface; (_c_) are often made to disappear or pale beneath the
pressure of the finger, while there is greater persistence of color in
the variolous papules; (_d_) are surrounded by little or no halo, each
elementary lesion of the eruption being abruptly defined upon the
sound skin, while the variolous papule is apt to rest upon a circlet
of hyperaemic integument.
Even with careful observation of all the specific differences between
the two diseases, they may, for a brief time, so resemble each other
as to defy the skill of the expert. In all doubtful cases the
physician should invariably admit the doubt and defer an exact
diagnosis for twenty-four hours. During the delay the variolous
exanthem should betray its individuality by the formation of a minute
vesicular apex at the summit of several papules.
In scarlatina the uniform diffusion of the exanthematous blush, the
absence of papules and vesico-papules, the continuance of the fever
after the rash has appeared, the characteristic scarlet or
boiled-lobster color of the skin, and the anginose condition of the
throat, are all significant symptoms. In hemorrhagic small-pox the
color of the integument is a much more purplish and lurid-reddish hue,
rapidly reaching that stage where it refuses to pale under the
pressure of the finger, and never leaving in the track of the
finger-nail quickly drawn over its surface the peculiar transitory
yellowish-white line which can be usually obtained in the skin of the
patient with scarlatina.
The pustular stage of variola might be confounded with the pustular
syphiloderm. But in the latter there should be a history of a chronic
rather than of an acute affection, and, as a result, the simultaneous
appearance of lesions in very different stages of their career, some
distended with pus, others ruptured and crusted, yet others which have
recently formed in the immediate vicinity of the oldest lesions, while
the latter have been in full involution or have been replaced by
superficial losses of tissue.
The resemblance of pustular variola to certain suppurative and other
disorders of the sebaceous glands is well attested by the name given
by certain French authors to molluscum epitheliale (M. contagiosum, M.
sebaceum)--viz. acne varioliformis. But in the case of acneiform
disorders the concurrence of comedones, the chronic course of the
disease, the absence of fever and systemic disturbance, and the
particularly irregular distribution of the lesions upon the face, with
failure to appear elsewhere,--all these facts forbid the confusion of
the affection with variola. In medicamentous acne, accompanied by the
sudden appearance of numerous pustular lesions symmetrically displayed
upon the surface, there will indeed be a source of error. In such
cases, of course, a history of the ingestion of a medicament capable
of producing a rash will afford valuable aid in the diagnosis. In
pustular forms of dermatitis medicamentosa there will usually be found
a more abundant development of the pus-containing lesions upon the
head and both arms and forearms, with {450} no tendency to extension
over very large areas of the trunk and lower extremities--a
circumstance which a delay of but a few hours will often substantiate.
The absence of marked defervescence is the most characteristic
difference between variola in its eruptive stage and typhus, typhoid,
and relapsing fevers. Pneumonia, cerebro-spinal meningitis, acute
miliary tuberculosis, and gastric fever are all to be differentiated
from variola by the occurrence of symptoms characteristic of the
involvement of the several organs which in these diseases respectively
are more particularly impaired.
PROGNOSIS.--The prognosis of variola is wellnigh inseparably
associated with the question of protection by vaccination. Variola
vera in the unprotected is an exceedingly fatal malady, the death-rate
varying in different epidemics according to the severity of each and
the ages and hygienic surroundings of the victims of the disease.
Certainly, from 15 to 50 per cent. of unprotected individuals affected
with the disease occurring in epidemic form in any given community
will perish. This number may, however, be enormously increased, as,
for example, among a large number of unprotected negroes crowded
together in a filthy prison, or when the malady makes a periodical
visitation to an insular community where long isolation has begotten a
carelessness with respect to vaccination.
With respect to individual cases it may be asserted, first, that an
intense series of prodromic symptoms, followed by the appearance of an
unusually large number of cutaneous lesions, is often unfavorable.
Confluence of the latter adds to the gravity; hemorrhagic and purpuric
symptoms are in the highest degree portentous, and commonly indicate a
fatal result. Women pregnant or in the puerperal state, infants at the
breast, and persons of both sexes at advanced ages, are little able to
resist the ravages of the disease. According to Kaposi, women recently
delivered prematurely or who have lately suffered from an abortion
succumb more often than others of their sex. Chronic alcoholism among
male subjects and the cachexia induced by all chronic visceral and
systemic disorders are sources of weakness which largely increase the
death-list by adding to the heavy strain upon the vital energies. The
prognosis is rendered uncertain or unpromising by extensive
involvement of the mucous as well as of the cutaneous surfaces, by
marked visceral complications, by evidences of shock or exhaustion
before the apogee of the exanthem is reached, by grave sequelae, and
even by simple complications of the malady when, instead of entering
promptly upon convalescence, the patient lingers for weeks in a
typhoid condition. An unfavorable symptom in any case is the sudden
cessation of the processes actively pursued upon the surface of the
body. The swelling of the integument then suddenly diminishes and the
crusts by which it was covered shrivel. The eruption, in brief, seems
to undergo what may be described as a collapse. The pulse at such
moments usually flutters feebly, and there are other portents of
dissolution which the eye of the physician will hardly fail to
interpret correctly. The fluids in such instances mechanically drain
away from the surface of the body to seek the deeper parts. This is
not peculiar to small-pox. Similar phenomena occur even in the case of
other than exudative affections of the skin. In pityriasis rubra the
{451} patient dies leaving an integument apparently unaffected, and I
have seen a patient dead of even multiple sarcoma of the skin when the
tumors were reduced fully one-half in bulk as the result of a similar
cause.
On the other hand, the practitioner should never forget that even
apparently desperate cases of variola rally and are won back to life.
That the exudative process should be in full evolution at the surface
of the body is, caeteris paribus, certainly so far a good omen. The
most hideous, extensive, and stench-emitting crusts have hidden for a
time the forms that have for many subsequent years not only known the
enjoyment of life, but have made that life of inestimable value to
others. The physician in the presence of this most loathsome and
formidable disease should never despair.
PROPHYLAXIS AND TREATMENT.--The loftiest end to be reached by the
physician of our day with respect to variola is its complete removal
from all civilized countries, and indeed from the face of the earth,
by the practice of universal vaccination and revaccination. The
evident modifications which the disease has undergone in late years as
a consequence of the extraordinary attention given to this subject is
an earnest of the future. The day is probably not far distant when the
man, woman, and child unprotected by vaccination will properly be
regarded as an enemy of the human race, and treated accordingly.
Evidences of the most satisfactory character as to successful
vaccination should be imperatively required of all applicants for
admission to schools, academies, colleges, charitable institutions,
public libraries, art-galleries, and places of labor controlled by
incorporated institutions; of all members of conventions,
legislatures, political, religious, and deliberative bodies; of every
purchaser of a ticket for purposes of travel; and of every voter. In
addition, there should be in every district a systematic and
periodical inspection of all persons registered in the census by
persons qualified and competent to perform compulsory vaccination.
This is the scientific treatment of variola.
Respecting the therapeutic management of variola, it must be admitted
that there are no remedies known to exert the slightest influence in
either cutting short the curriculum of the disorder or in checking its
progress in any stage. When vaccination is practised after the disease
is fully developed, the two disorders, vaccinia and variola,
apparently concur, and proceed pari passu to the evolution peculiar to
each. Quinia, the sarracenia purpurea, the salicylate of sodium,
emetics, diaphoretics, purgatives, and other remedies and methods
vaunted as efficacious, have again and again failed to establish the
claims which have been put forth respecting the value of each.
The most important of the considerations to be regarded at the outset
of the management of the small-pox patient relate to his hygienic
surroundings and nursing--considerations which scarcely differ from
those recognized as of general importance in the case of all septic,
contagious, and filth-producing diseases.
The timid, the fearful, and the unprotected are to be at once
dismissed from the bedside, and trustworthy attendants secured who
have received protection by either recent vaccination or a prior
attack of the malady. The sick chamber should be sufficiently large
and capable of the most thorough ventilation by free access of air.
Solar light should be excluded {452} as rigidly and completely as
possible, since it is reasonably certain that its access to the face
has an etiological relation to the pitting of that part, often the
most serious sequel of the affection. It is an interesting fact that
pitting is much less frequently noted on those parts of the body from
which light is excluded by the covering of the clothing. The
temperature of the sick room during the febrile stages of the disorder
should not rise above 70 degrees F. nor be permitted to fall below 60
degrees F. Between these extremes a variation may be made in
accordance with the sensations of the patient.
During the invasion stage of the disease the patient can rarely
assimilate food, but if this be possible it should be given throughout
the entire course of the disease in the form of animal broths, eggs,
nutritious soups, and milk. Iced and acidulated beverages are often
grateful to the palate, and small lumps of ice should be permitted to
dissolve slowly in the mouth. Lime-water may be required by unusual
gastric irritability. As the disease progresses and the palate and
buccal membrane become painful and sore by reason of the localization
there of pustular and other lesions, various mouth-washes and gargles
may be ordered, such as those containing the chlorate of potassium,
the tincture of myrrh, the tincture of cinchona, or even the milder
demulcent fluids made by the addition of flaxseed, gum acacia, or
powdered elm-bark to water. In almost all such cases the skilled nurse
will accomplish a grateful result by frequently cleansing the mouth of
the sufferer (especially before the deglutition of aliments) by
covering the finger with a soft handkerchief, dipping it in pure hot
water, and then thoroughly and gently cleansing the entire buccal
cavity. The spray of a saturated solution of boracic acid in
rose-water may then be directed over the parts.
Applications of cool and iced water to the skin are commonly grateful,
and, as a rule, are accompanied by no danger to the patient, though in
the early periods of the disease they unquestionably retard the full
evolution of the cutaneous symptoms. For the pain in the back,
therefore, which is often the most urgent symptom of the invasion
stage of the disease, it is usually preferable to make hot
applications. The large rubber bags now in common use, filled with hot
water and from time to time applied to the lumbar region, may be
employed with good effect simultaneously with iced, spirituous, or
camphorated applications to the head.
Numerous indeed have been the topical applications made to the surface
of the skin in the pustular stage of the malady, both with a view to
assuage the soreness and pain and to obviate the tendency to pitting.
The opening of the pustules and the evacuation of their contents
(practicable only in other than confluent forms of the disease) has
been practised from an early date, but is ineffectual from the
standpoint of any practical results thus obtainable. The same may be
said of the subsequent cauterization of the floor of the pustular
chamber, which only adds to the distress experienced by the sufferer
in his skin. Medicated unguents, applied to the skin, containing
mercury, iodine, and other substances, are not known to be followed by
any better results. It may indeed be laid down as a general rule that
fatty applications to pus-producing surfaces where the pathological
product is virulent are apt to undergo decomposition and otherwise act
unfavorably upon the tissues--a fact first pointed out by Ricord in
connection with the treatment of the {453} chancroid. Vaseline, as not
liable to undergo chemical decomposition, is not open to this
objection.
Curschmann, Kaposi, and other authors are in agreement respecting the
value of water-compresses over the surfaces invaded by the eruption--a
method of topical treatment which I desire to fully endorse after
personal observation of its value. Curschmann recommends compresses
dipped in iced, Kaposi those moistened with tepid water. The sensation
experienced by the patient will prove the best guide to the
temperature of this fluid. I prefer a solution containing one drachm
of boracic acid to the pint of water as hot as can be discovered to be
productive of comfort, a drachm or two of glycerine being added to the
solution. The compresses dipped in this (or a carbolated solution, if
the latter is preferred by either physician or patient) should be
assiduously moistened and changed regularly by the attendants just as
long as they can accomplish good. They operate, first, by protecting
the part; second, by keeping it moist; third, by maintaining the
surface temperature at the point most pleasant to the patient; fourth,
by exercising the gentlest degree of equable compression over the
surface. When desired, this may be covered with the Lister protective
material or a piece of oiled silk to prevent evaporation at the
surface.
In Vienna warm baths, administered either by the process of continuous
immersion so generally practised there or by immersion for from two to
three hours of each day, have been found to furnish the greatest
amount of comfort to the patient. The skin is thus speedily relieved
of its tension, the exfoliation of the crusts is hastened, and the
time required for the evolution of the cutaneous lesions, if not
shortened, is at least not retarded by the accidents of exposure to
the desiccating influences of the air--ends which for the patient are
practically one. In this country, and especially in private practice
outside the larger charities with their ampler provision for these
emergencies, nearly the same result may be reached by wrapping the
patient completely in sheets wrung out of water of the temperature
desired.
From first to last in the treatment of variola, all indications should
be made subordinate to that most prominently set forth by the general
character of the symptoms--viz. the conservation by every possible
means of the vigor of the patient. The tax upon all reserves of vital
energy is here so enormous and constant that he will gravely err who
for a moment loses sight of this fact. Hence it is that anodynes,
chloral, opium and its alkaloids, the bromide of potassium, and
similar medicaments, introduced either by the stomach or by hypodermic
injection, are to be jealously reserved for emergencies when it would
seem cruel to withhold the temporary comfort they may impart.
Stimulants are of course to be freely employed whenever they are
indicated by exhaustion as this may be shown by a weak pulse and other
failing functions of the body, but are certainly best reserved for
such emergencies. In general, it may be remarked that the fewer the
medicaments ingested by the stomach, and the larger the restriction of
the labor of this organ to the task of sustaining the nutrition of the
body, the better are the chances of a favorable issue.
It is unnecessary to add that all other indications presented in any
given case are to be met, subject to the conditions indicated above.
Abscesses {454} are to be opened and antiseptically treated; delirious
patients are to be sedulously prevented from doing themselves injury;
daily movements of the bowels are to be secured; while the diarrhoea
of the typhoid state, occasionally resulting from the exhausted
condition of the system when the force of the disease is spent,
demands proper control.
Cleanliness is to be enforced by every judicious measure. The skin of
the patient is to be washed in tepid water and soap as often as
practicable in the course of the disease, and under no circumstances
are applications of ointments, washes, or lotions to be allowed to
collect in strata upon the surface commingled with the pus and crusts
of the disease. At the time of such ablution, and occasionally
oftener, the linen and other garments of the patient are to be
changed. When the crusts are regularly exfoliating from the surface of
the body general warm baths may be ordered, after each of which the
surface of the body may be anointed with vaseline or covered with a
finely-sifted dusting-powder, such as the corn-starch farina sold by
grocers.
Inasmuch as hemorrhagic variola is usually hopeless in character, and
remedilessly fatal, Kaposi's liberal use of opiates may be recommended
when euthanasia is all that can be expected. So long as there is the
narrowest chance of recovery resort may be had to ergot, turpentine
and the mineral acids internally, combined with the external use of
styptics and ice. But little confidence can, however, be placed in
these measures, which will prove entirely ineffective in the great
majority of all cases.
In all fatal cases of variola the duties of the physician are not
ended by the death of the patient. It is for the benefit of the living
that he should require destruction or disinfection and long disuse of
all domestic articles that were employed upon or about the patient.
The lifeless body should be disposed of by cremation, and medical men
should exert their influence in favor of legal enforcement of such a
wholesome practice.
{455}
VACCINIA.
BY FRANK P. FOSTER, M.D.
SYNONYMS.--Vaccina, Variolae vaccinae (Jenner), Cow-pox, Cow-pock,
Kine-pox, Kine-pock; _Fr._ Vaccine; _Ger._ Kuhpocken, Schutzpocken,
Impfpocken, Schutzblattern; _It._ Vaccina; _Sp._ Vacuna.
DEFINITION.--An eruptive disease characterized by a cutaneous lesion
closely resembling that of small-pox, going through the stages of
papulation, vesiculation, pustulation, incrustation, and
cicatrization; differing from small-pox in the mildness or almost
total absence of the constitutional symptoms, by being communicable
only by inoculation, and by the fact that the lesions, as a rule, are
developed only at the points of inoculation and in their immediate
neighborhood.
This definition holds good for the great majority of cases, but in
each of its parts we must take account of exceptions. For example, the
lesion does not always follow the regular sequence of changes
described. It may stop short at the stage of papulation, constituting
the so-called raspberry excrescence, which will be further referred to
hereafter; it may pass directly from the stage of vesiculation into
that of incrustation, without any such change in its liquid contents
as can properly be said to form a pustule; desquamation may take the
place of incrustation; and, after an evolution otherwise normal, there
may be no formation of a scar, simply because the destructive effect
of the lesion has not extended deeper than the epidermis. The
constitutional symptoms are sometimes severe, but they are always of
very short duration. The disease is said to have been communicated
otherwise than by inoculation in the case of some of the lower
animals. Thus, Chauveau succeeded in producing some of its phenomena
in the horse by causing the virus to be inhaled in the form of spray.
It is doubtful, however, if it is possible to eliminate all sources of
fallacy in such experiments. Finally, a generalized eruption is
occasionally observed, although with great rarity. In stating these
exceptions no reference is intended to cases in which complications
occur.
NATURE OF THE DISEASE.--Many considerations warrant us in classing
cow-pox among the varioliform diseases--chiefly its general
resemblance to variola, and the fact that individuals who have been
affected by it are thereby more or less fully protected against
small-pox. It has been thought, indeed, that cow-pox was in reality
but a modified form of small-pox; and this idea has been the basis of
one of the theories that have been held as to the origin of vaccinia.
Before enumerating and discussing those theories it will be well to
mention that cow-pox is spoken of as spontaneous, casual, or
inoculated, according to its mode of origin, known or assumed, in
individual instances.
{456} Spontaneous or original cow-pox is the name commonly applied to
the disease as it is met with in the cow in instances in which its
mode of origin is unknown. Strictly interpreted, this expression
implies a belief that the affection is capable of being developed in a
cow independently of contagion or infection--a notion that seems to be
held by many physicians, but not, so far as the writer is aware, by
those whose study of the subject has been such as to lend any
considerable weight to their opinions. Ordinarily, however, the term
spontaneous cow-pox is employed simply as a convenient expression to
denote the disease as it occurs naturally in cows, without implying
any belief or theory as to its mode of origin.
Casual cow-pox is the term applied in cases that have been contracted
by accidental inoculation, whether in the cow or in man. It is
manifest that the so-called spontaneous cases are really casual,
unless we accept the doctrine that infection is not necessary to the
development of the disease.
The term inoculated cow-pox implies that the affection has been
produced by intentional inoculation. Here, again, we are confronted
with an illogical expression, for a disease that is inoculated
accidentally is still inoculated, as much as if it had been conveyed
purposely. It may be said, indeed, that the casual disease is due to
some other form of infection than inoculation, but for such an
assertion there is not a particle of proof.
Passing from this unsatisfactory nomenclature to a consideration of
the theories that have been held as to the nature of cow-pox, we are
first met with that of its being a disease sui generis, like
small-pox, measles, scarlet fever, and the like, and, like them,
originating only by its own specific contagion, not being capable of
development by a modification of any other contagion, however closely
it may thus be counterfeited. This seems the most rational theory of
the nature of cow-pox, but it cannot be demonstrated except by
disproving all opposing theories; and that has not yet been
accomplished.
Another theory is, that cow-pox is really small-pox modified, as the
phrase runs, "by passing through the system of the cow." It has been
thought possible, indeed, to specify in what way the cow's system
could impress such decided changes upon the virulent disease small-pox
as to convert it into the mild affection that we know as vaccinia; in
other words, it has been imagined that the function of lactation
accomplished this remarkable result. This notion may have been due to
the observation that so-called spontaneous cow-pox is met with only in
cows that are in milk. The significance of this fact, however, is
really nothing more than that cows in milk are more exposed to
accidental inoculation than other bovine animals--namely, at the hands
of the milkers. The fact that in such cases the lesions are almost
always confined to the teats and the udder, far from affording any
ground for the notion that there is some mysterious connection between
cow-pox and the function of lactation, is but another proof that the
disease is the result of inoculation. The lesions appear at the points
of inoculation, the teats and the udder being the parts handled by the
milkers. Moreover, there is no difficulty in inoculating young calves
or adult bulls, and the lesions so produced do not vary in a single
particular from those observed in so-called spontaneous cases.
{457} Men have been so carried away with this milk theory, however, as
even to believe that the virus of small-pox might be shorn of its
dangerous properties, so that it would produce only the vaccinal
lesion when inoculated simply by mechanical mixture with milk. During
the late Civil War one of the Confederate Army surgeons actually put
this notion to the test of practice on quite a large scale,
inoculating large numbers of persons with a mixture of small-pox virus
and milk, terming the practice mitigated inoculation. We can scarcely
suppose that he did anything else than variolate these persons, just
as he would have done had he used variolous lymph without the addition
of milk. His experiments show nothing new; they merely furnish a
recent confirmation of the well-known fact, familiar to the old
inoculators, that inoculated small-pox is sometimes exceedingly mild
in a series of cases.
This theory of the variolous origin of cow-pox, and of the
practicability of converting small-pox into cow-pox at will by
"passing it through the system of the cow," has taken deep root in the
minds of men, especially in Great Britain, where the late Mr. Ceely's
experiments and Mr. Badcock's experience seemed to give it some color.
Some years ago, however, the question was investigated most
practically and thoroughly by a commission appointed for the purpose
by one of the medical societies of Lyons, Chauveau being the recorder.
Their conclusion was--and their reasoning seems to the present writer
incontrovertible--that small-pox and cow-pox were wholly distinct from
each other under all circumstances, and that it was impossible to
convert the one into the other. But the doctrines of the English
investigators, reinforced as they were by the ingenious arguments of
the late Dr. Seaton, were not easily to be overturned in their own
country or in America; consequently, the practice of variolating cows
has been resorted to from time to time for the purpose of obtaining a
stock of vaccinal virus of unquestionable authenticity--the so-called
variola vaccine. This practice is utterly fallacious, and it is also
dangerous, since the disease so produced, however mild it may seem to
be, is nothing more nor less than small-pox, with its infectiousness
by effluvium and its liability to prove serious even when carefully
inoculated.
Quite recently the experimental investigation of the question has been
undertaken de novo by a well-known English veterinarian, Mr. Fleming;
and, since his conclusions coincide with those of the Lyonnese
commission, it is to be hoped that we have seen the last of this
rough-and-ready method of improvising a case of genuine cow-pox--a
method that, in the light of our present knowledge, can only be
characterized as downright malpractice.
The third and last theory we have to consider is that which ascribes
the origin of cow-pox to infection from the horse. So far back as
Jenner's time it was conjectured that cow-pox was due to the
accidental conveyance of the virus of the grease (the eaux-aux-jambes
of the French) by reason of the cows being milked by persons who were
also employed in the care of horses affected with that disease. Grease
is an eruptive disease of horses' heels. Doubtless it has often been
confounded with a mere eczematous affection by those who have
repeatedly failed in their persistent attempts to inoculate cows with
it, and, on the other hand, a localized eruption of horse-pox may have
been mistaken for it by those who have {458} supposed themselves to
have succeeded in producing cow-pox by inoculating cows with the virus
of grease, and have consequently given in their adhesion to the grease
theory of the origin of cow-pox. At all events, so far as the writer
is aware, that theory is not now held by any well-informed writer.
Still regarding the horse as the originator of cow-pox, we must turn
our attention to horse-pox (equinia). Several years ago Depaul of
Paris took great pains to establish the fact that horse-pox (an
affection totally distinct from grease) was an eruptive febrile
disease of horses, an exanthem; that the eruption was generalized,
and, being for the most part concealed by the hair, generally
overlooked; and that it was capable of being conveyed by inoculation,
the lesion being indistinguishable from that of cow-pox. He believed
himself to have demonstrated also that it was the contagion of
horse-pox that gave rise to cow-pox in the cow.
Depaul's investigations were very keen and his conclusions were
exceedingly plausible, but they cannot be called convincing,
notwithstanding the fact that Constantin Paul succeeded for a time in
popularizing a stock of horse-pox virus as material for vaccination.
At about the same time the Beaugency case of cow-pox was discovered,
and the perfectly satisfactory use that has been made of that stock
may have thrown Depaul's theories and Paul's practice undeservedly
into the background.
We can only say, in summing up, that the small-pox theory is utterly
untenable, that the horse-pox theory has not been disproved, and that
the theory that regards cow-pox as derived neither from small-pox nor
from horse-pox, but as a disease sui generis, although not proved, is
the most rational of all, and the most in keeping with known facts.
ETIOLOGY.--Nearly everything that could be said under this head has
already been considered. It may be added that meteorological
conditions have been supposed to favor the prevalence of the disease
among cows. More precise observations are needed to enable us to
determine whether or not there is any truth in this supposition. It
has been said that the affection is most apt to prevail during warm
and moist seasons. This is contrary to what we might have imagined, as
warmth and moisture are quite destructive of the vaccinal virus. Under
ordinary circumstances, however, the contagium often proves
wonderfully tenacious of life, and the disease, once introduced among
a herd of cows, is prone to linger for months, or even years,
attacking animals recently added to the stock and young cows during
their first lactation. As has already been stated, age, sex, and
parturition can be regarded as etiological factors only in so far as
they favor the occurrence of accidental inoculation. In the human
subject vaccinia occurs generally as the result of intentional
inoculation, as will be more fully referred to when we come to the
consideration of vaccination. Insusceptibility is occasionally met
with, both in the cow and in man, but it is very rare. Perhaps it may
be explained in some instances by the subject having really had the
disease, or indeed small-pox, either before or after birth, in so mild
a form as not to have left the characteristic marks. Certain it is
that the lesion does not always leave a permanent scar, especially in
the cow.
GENERAL COURSE OF THE DISEASE.--This is best studied in cases that
have followed intentional inoculation, for here we know the {459}
chronological sequence of events. Depending somewhat upon the method
of inoculation, and perhaps also to some extent upon the state of the
skin at the site of the inoculation, or even upon a systemic condition
(since some vaccinators hail it as a harbinger of success), at the
time of the operation a ring-like erythema may be seen surrounding the
inoculation. This is exceedingly evanescent, being doubtless due to
vaso-motor action, and is not often witnessed.
Ordinarily, no effect whatever is observed until after the lapse of
two or three days, when a red papule is formed. This papule increases
in superficial area, but not in height, and gradually loses its
redness. It assumes a circular form, or, in the case of a compound
pock (for that is the proper name for the lesion), a configuration
representing segments of several circles, and as it increases in area
it becomes more and more raised at the border (the bourrelet of French
writers), while the central portion, which also increases in size pari
passu with the peripheral annular vesicle, does not become more
elevated, but remains depressed, giving the pock as a whole the
peculiar shape termed umbilication. Up to the eighth or tenth day,
inclusive, the marginal elevation contains a limpid fluid termed
lymph, and consequently presents a pearl-like lustre. At this period a
rather sudden increase takes place in the corpuscular elements
contained in the lymph, causing that liquid to become thick and
opaque, so that the elevated margin of the pock, which before had
shown the pearl-like lustre alluded to, now comes to look as if made
of tallow.
At the same time what is known as the areola forms around the pock,
and constitutional symptoms show themselves. The areola is a
circumscribed redness of the skin, perfectly circular in form and of
five or six times the diameter of the pock itself. It is sharply
defined and of a vivid red hue. Usually it is a mere hyperaemia of the
skin, but in some instances, especially where the process of
pock-formation is decidedly pronounced, a few papillary elevations are
to be seen in the immediate neighborhood of the pock, and at that
situation there may also be some lividity. After a few hours'
persistence in the form of a disc the areola begins to disappear, the
redness fading first at the central portion, so that in its declining
stage it assumes the shape of a ring which constantly grows narrower
and narrower at the expense of its inner portion, and finally
disappears altogether. In the cow the areola is only a faint line
immediately around the pock.
Constitutional symptoms are invariably present in cases that follow
the regular course. The temperature rises one or two degrees
Fahrenheit, the appetite becomes impaired, and sleep is somewhat
disturbed. In many cases, mostly those of secondary inoculation, the
symptoms are more severe; the fever runs higher, and may be
accompanied with transient delirium; nausea is experienced, perhaps
with actual vomiting; and severe pain is felt in the head and along
the spine, the latter being most marked in the cervical region. These
symptoms usually last but a few hours, and they are apt to be
accompanied by a modification of the areola whereby it loses its
disc-like outline and becomes diffused irregularly, especially, if, as
is usual, the inoculation has been done on the arm, in a downward
direction toward the elbow.
Along with these phenomena intense itching is often felt at the
situation of the pock, being an aggravation of the pruritus that in a
mild {460} form accompanies the greater part of the whole course of
the lesion. Supposing the arm to have been inoculated, the lymphatic
glands of the axilla now become swollen and tender, but their
suppuration is unusual, and is to be regarded as a complication.
To go back to the pock: some time before the contents of the marginal
elevation become opaque the central portion is converted into a crust
of a brownish color, and finally, from the tenth to the fifteenth day,
the bourrelet itself, having ceased to increase in size, takes part in
the process of incrustation, the completed crust representing the form
of the pock, having a circular ridge at the border, at which part its
color is not so deep as at the centre. The crust usually falls off
between the fifteenth and the thirty-fifth day. It is hard,
translucent, and of a prune-juice color; thick at the centre and thin
at the periphery; smooth on its attached surface and somewhat wrinkled
on its outer aspect; surmounted at the centre by the epidermal debris
produced by the operation of inoculation, mingled perhaps with more or
less dried blood.
After the crust falls off a reddened surface is left of a cicatricial
nature, usually somewhat depressed below the level of the surrounding
skin, and frequently showing lesser pits, which latter appearance is
termed foveolation. Instead of these pits, radiated striae are
frequently left. Gradually the scar loses its red color, and, like
other scars, finally becomes paler than the surrounding skin. It is
usually permanent.
IRREGULARITIES IN THE COURSE OF THE DISEASE.--Ever since cow-pox first
became the subject of medical study deviations from its typical course
have been noticed, and have been the theme of a good deal of
speculation. The older writers, indeed, bestowed no little attention
upon what they considered to be not irregular forms of vaccinia, but
distinct affections with which it was liable to be confounded. Their
descriptions of these diseases, which they termed spurious cow-pox,
are, however, so vague as to possess but little more than an
historical interest. In regard to affections met with casually in the
cow, we can often determine their nature only by test-inoculations,
and even that criterion is not always thoroughly convincing; for, on
one account or another, we may fail in the attempt to propagate true
cow-pox, and on the other hand, if we admit that there is a radical
difference between cow-pox and small-pox, it is manifest, bearing in
mind the errors into which experienced investigators have fallen, that
we may propagate small-pox through a long series of experiments
without once suspecting it to be anything but cow-pox. We may,
nevertheless, always determine, provided we succeed at all, whether we
are dealing with a disease that protects against vaccinal and
variolous inoculation.
In the human subject we seldom meet with affections that counterfeit
vaccinia, although, if we take only the lesion into consideration,
there are certain contagious forms of herpes that may give rise to
doubt, and possibly the same may be true of impetigo contagiosa.
Turning, then, to the irregularities properly so called, we have first
to consider the absence of constitutional infection. This must not be
confounded with the mere lack of obvious constitutional symptoms; what
is meant by the expression is, that in certain instances the local
lesion may appear typical, and yet no such impression be made upon the
system as to render it proof against subsequent inoculation. Early in
the {461} century the possibility of this lack of systemic infection
was insisted upon by Mr. Bryce of Edinburgh, who invoked it as an
explanation of the occasional failure of vaccinia to protect against
small-pox. The practical question was, how to decide, in a given
instance, whether general infection had or had not taken place. In the
opinion of many observers--and that notion has cropped out every now
and then up to the present day--absence of the areola furnished at
least presumptive evidence that the constitution had eluded infection.
But, whatever may be held theoretically, it must be conceded either
that the general system very rarely fails to feel the impress of the
disease, or else that the criterion is fallacious. For in an
experience of seventeen years the present writer has not known of a
single instance in which a vaccinal lesion that pursued a regular
course in other respects has failed to be accompanied by the areola.
And certainly Mr. Bryce himself must have attached little if any
importance to it, for he took great pains to establish a means of
determining the presence or absence of constitutional infection--the
so-called Bryce's test. This consists in repeating the inoculation at
a certain period in the evolution of the disease, the theory being
that systemic infection does not take place at once, but only after
the lapse of a number of days from the time of the inoculation. Up to
that time a repetition of the inoculation is possible, and, if
systemic infection results from the first one, both lesions will
mature at the same time, the second one following an accelerated
course, reaching its acme rapidly, although dwarfed in size. If, on
the other hand, the first inoculation failed to infect the
constitution, the second one will pursue its course in the usual
manner. Moreover, at a certain time, generally about the fifth day, a
repetition of the inoculation will fail altogether if the original
insertion has really infected the system. The present writer can
testify that Mr. Bryce's statements are correct; he has applied the
test in many cases, but in no instance has he been led to the
conclusion that constitutional infection had failed to take place. He
is inclined to think, therefore, that such failure is exceedingly
rare.
Passing over the multiplicity of irregularities in the lesion that
were described by the older observers, it seems that there are a few
that are of practical importance. In the first place, there is a
variety of pock to which it is not easy to give a definite name, but
which is characterized by a lack of decided elevation above the
surrounding skin (a deficiency for which it makes up in superficial
area), by the early formation of a thin, flimsy, straw-colored crust,
and by the utter failure of the characteristic firm brown crust of the
typical variety to become developed. This form of irregular pock has
not been seen by the writer of late years, but before animal
vaccination came into general use he met with it frequently, mostly in
cachectic children. Notwithstanding its sprawly, unsatisfactory
appearance, it is undoubtedly genuine, for the typical lesion may be
produced by inoculation with its contents.
Another irregularity of the pock is what is familiarly termed the
raspberry excrescence. A red elevation forms at the seat of
inoculation, and at first promises to follow the typical course,
although it may be tardy in making it appearance; but it never
advances to full development. It becomes indolent, and may last for
several weeks, or even months, in the form of a hard, flat nodule of a
bright-red color, not unlike a small {462} naevus. In many instances
it has a succulent look, but no lymph can be obtained on puncturing
it. No areola appears at any time, and finally the lesion slowly
disappears, leaving no trace of its existence. It is probably an
abortive form of pock, in which only the papillary layer of the skin
takes part, without any exudation into the epidermis. It is seldom, if
ever, protective against small-pox, for it constitutes no bar to a
subsequent vaccination. This irregular pock has been observed from
time to time ever since the early days of vaccination, but for the
past six years it has been seen more frequently in New York than for
many years before. Now, however, it seems to be growing less common.
The writer is not aware of any satisfactory explanation of its
occurrence. It is seen in all sorts of subjects, and seems to follow
the use of one variety of virus as much as the employment of any
other.
What has been termed generalized vaccinia is another form of
irregularity. The expression is a vague one, covering as it does not
only the very rare cases of true eruptive vaccinia, in which a general
eruption of pocks takes place as a consequence of constitutional
infection, playing the part of an exanthem, but in addition those
instances, not very uncommon, in which pocks are formed here and there
on the body, probably as the result of the accidental transfer of the
virus from the pock by scratching. Under such favorable
conditions--the immediate transfer of lymph from a pock in which the
specific evolution is going on vigorously--the slightest penetration
of the epidermis with the nails is enough to secure self-inoculation.
In view of this facility with which it may be effected, we should be
very careful not to jump hastily to the conclusion that in any given
case of generalized vaccinia the supplementary pocks are truly
eruptive; as a matter of fact, the present writer has never seen an
instance in which he was convinced that such was the case. Where the
pocks are very numerous, especially in subjects with an irritable
skin, much distress may be caused by the itching and by the
consequences of scratching, and marked febrile reaction may accompany
the process; so that, in view of the great similarity of the lesions
to those of the variolous eruption, much doubt is sometimes
entertained as to whether the disease is not really small-pox. This
question cannot always be definitely settled at first, but the failure
of the secondary fever of small-pox, together with the fact that the
disease does not spread by infection, will generally suffice to decide
it.
Concerning those cases of generalized vaccinia that are manifestly not
eruptive, it sometimes happens that the cutaneous receptivity is not
exhausted for several weeks, or even months. Such cases set Bryce's
test at defiance, in consequence, probably, of an idiosyncrasy. In
some of these instances the pocks appear in clusters of successive
formation, looking not unlike patches of zoster. Small supplementary
pocks in the immediate neighborhood of the original lesion are not at
all uncommon.
PATHOLOGICAL ANATOMY.--Avoiding the minute histological details for
which the prescribed length of this article gives no scope, but little
is to be added to what has already been said in the section on the
clinical features of the disease. The lesions of vaccinia are wholly
cutaneous. Confining ourselves to cases that follow a regular course,
there is, indeed, but one, the pock--a term that seems preferable to
vesicle and {463} pustule, since the latter apply only during certain
phases in the development of the lesion.
A pock may be regarded as essentially a lesion of the epidermis, for
it is in that structure that its most striking features are developed,
and in some cases, although doubtless the papillary layer of the derma
is congested, there is no permanent alteration of tissue below the
Malpighian layer of the epidermis. These are the catarrhal pocks of
Rindfleisch, and it is in such cases, if in any, that no scar (even of
temporary duration) results. The term catarrhal pock, however, is not
vitiated by an extension of the morbid process deep enough to produce
a permanent cicatrix, and it is probable that in most cases the
catarrhal type predominates. By the term diphtheritic pock the same
author refers to cases in which the congestion of the papillary layer
is so intense as to block the supply of blood to the apices of the
papillae, as a result of which they become exsanguinated and necrosed,
forming a white pultaceous layer on the floor of the pock, which is
undoubtedly what Ceely referred to when he spoke of a false membrane.
In some cases even the subcutaneous tissue undergoes necrosis, a sort
of core being included in the substance of the crust that ultimately
forms.
Whichever of these forms of pock we take into consideration, always
excluding irregularities and complications, we find certain definite
changes in the epidermis. The dome of the pock is formed by the
unbroken transparent horny layer of the epidermis, unaffected by the
morbid process. The cavity of the pock is formed by the squamous cells
of the epidermis being forced out of their normal relations by an
exudation of lymph between them, some of them being tilted up edgewise
while still retaining their connection with the surrounding cells,
thus accounting for the multilocular structure of the pock; for it is
a fact that the circular bourrelet consists not of one ring-like
cavity, but of many separate chambers. The result of this structure
is, that the liquid contained within the pock--the lymph--escapes only
partly through a puncture made in the wall of the vesicle. In order to
evacuate the pock thoroughly it is necessary to make a great number of
punctures or a circular incision following the ring-like ridge of the
bourrelet.
The lymph contained within the cells of the pock is a liquid which in
its gross physical properties differs but little from the lymph which
exudes from any traumatic surface shortly after the injury has been
inflicted, as in the glazing process that takes place in wounds.
Examined microscopically, however, it is found to contain not only the
fibrin, the salts, the corpuscular elements, and the debris that
ordinary tissue-juice presents, but also certain minute spherical
bodies--termed microspheres, microzymes, vaccinads, etc.--that give it
its characteristic infective quality and justify the title of virus
commonly applied to it. That these minute bodies really constitute the
virulent element of the lymph, or at least that they are the vehicle
of the contagium, is not a mere matter of conjecture, but has been
demonstrated abundantly, notably by Chauveau and Sanderson's diffusion
experiments. Inoculation with the supernatant liquid, containing none
of these bodies, always fails to convey the disease, but it is not
absolutely essential that they should be present in large proportion
in the lymph to render the latter virulent, for Chauveau found that
lymph diluted with thirty times its bulk of water was not without
infective {464} power. It scarcely need be said, however, that the
greater the proportion in which they are present, the greater is the
probability that the lymph will prove infective on inoculation. These
bodies have been supposed to be of a vegetable nature, and Hallier,
Kohn, and others have bestowed no little study upon their botanical
characteristics. Under favorable circumstances they retain their
virulent properties for a long time, especially if kept perfectly dry
and not subjected to a high temperature. The present writer has met
with success in the use of vaccinal virus seven years old.
The lymph differs somewhat in its gross appearances according as it is
produced in man or in the bovine animal. In the former it is clear and
limpid, and exudes freely in great drops when the pock is punctured in
its peripheral portion; in the latter it is more straw-colored and
more viscid, exuding sluggishly, or even refusing to flow without the
aid of pressure. Moreover, the vaccinads seem endowed with different
properties in the two cases: in man they have a tendency to remain
equably diffused through the liquid, while in the cow they tend to
separate from it and to be deposited upon any solid surface at hand.
The phenomenon termed umbilication, common to the vaccinal pock and to
that of variola, has given rise to some differences of opinion as to
the mechanism of its production. The term implies a depression at the
centre of the pock. This appearance is not invariable, but it is
constant enough to have met with general acceptance as a
characteristic feature, notwithstanding the undoubted fact that it is
found in lesions that have nothing whatever to do with any of the
varioliform diseases. Not to waste space in discussing the various
theories that have found supporters, it may be said that they have all
been proved to be defective, save only the simple explanation that as
the process of evolution advances the centre of the pock undergoes
desiccation, whereby that portion of the tissue involved is so glued
and drawn together as to become incapable of the swelling that is
still going on in the growing peripheral portion of the lesion.
The crust into which the pock ultimately becomes converted is not, as
is commonly supposed, mere dried lymph and nothing else; it is dried
tissue enclosing concrete lymph. It generally includes also various
sorts of debris--broken-down epithelium, blood-corpuscles,
pus-corpuscles, and even, in rare cases, a core of sphacelated tissue
like that of a furuncle.
As has already been said, the cicatrix is to a certain extent peculiar
in that it is usually depressed and foveolated. Too much stress has
been laid upon these features, however, and the truth is that some
traumatic scars cannot be distinguished readily from that of vaccinia,
while, on the other hand, many a genuine pock leaves no permanent
trace behind it. Indeed, in the cow it is the exception for a
noteworthy scar to form.
SEQUELAE AND COMPLICATIONS.--The most important sequela of vaccinia is
the fact that it protects the subject against small-pox, and on that
circumstance hinges the chief practical interest of the disease. This
leads us at once to the subject of vaccination, and therefore under
that head we shall pursue our consideration of this curious affection.
{465} Vaccination.
SYNONYMS.--"The new inoculation;" _Fr._ Vaccination; _Ger._
Kuhpockenimpfung, Schutzpockenimpfung; _It._ Vaccinazione; _Sp._
Vacunacion.
HISTORY.--Before giving the history of vaccination itself (meaning by
that term the intentional inoculation of vaccinia for the purpose of
protecting the subject against small-pox), it may be well to devote a
few words to a practice that preceded it--that of the intentional
inoculation of small-pox (or simply inoculation, latterly called
variolation). In very early times various Oriental peoples became
aware of the fact that small-pox might be very decidedly mitigated by
inoculation. This was practised in various ways, all of which may be
reduced to the process of inserting small-pox virus into a solution of
continuity. Lady Montagu, the wife of an English ambassador to Turkey,
brought the practice back to England with her, where it soon made its
way into popular favor, and whence it spread rapidly over Europe and
America. Thus contracted, small-pox was shorn of a great part of its
terrors; the eruption was usually trifling in amount, and in every way
the disease was mild as a rule. Still, the mortality was something
worth considering, and, worse than that, the inoculated disease was
communicable by effluvium, so that an inoculated person had to be
secluded carefully for fear of spreading the disease in the ordinary
way. In all cases, too, careful medical treatment was thought
necessary. On the whole, then, while inoculation was undoubtedly a
boon, it was fraught with many grave perils. So great, indeed, were
these perils, and so thoroughly were they appreciated, that the
practice was interdicted by law in most civilized countries so soon as
vaccination had become established in popular favor.
In several European countries the common people--at least those of
them who had much to do with dairies--gradually became aware of the
existence of the disease termed cow-pox, and of the fact that those
individuals who had accidentally contracted it were rendered proof
against the infection of small-pox. There is even fair testimony to
show that some of these people, particularly the English farmer,
Benjamin Jesty, relying on their observation to this effect, employed
intentional cow-pox inoculation as a protective measure. These facts,
however, do not detract in the least from the credit that all
Christendom has awarded to a man who subjected the popular impression
in question to the test of scientific investigation, proved its truth,
and demonstrated its value to the world. That man was Edward Jenner,
an English country physician. It was in the last quarter of the
eighteenth century that he entered upon his course of inquiry, and on
the eve of the present century he published his demonstration to the
world. It was not a discovery; it was not an invention: it was more
than either, "a matchless piece of induction," to quote the words of
Mr. John Simon. Filled as he must have been with the consciousness of
his great achievement, Jenner set this good example to all
investigators: that he did not make haste to convert the world; he
first convinced himself. It may almost be said, indeed, that, like
Minerva from the head of Jove, the rational and perfected practice of
vaccination sprang complete from Jenner's hands. Doubt and ridicule he
had to encounter at first, and afterward envy and detraction; but the
force of {466} his facts and the symmetry of his deductions were such
that the new inoculation soon spread through the broad world, and has
ever since maintained its sway, save with a few fanatical scoffers.
That vaccination really does protect against small-pox observation has
taught the whole civilized world, if we leave out of account the few
conscientious and intelligent doubters (made such, doubtless, quite as
much by the extravagant statements often put forth by those who from
time to time think it incumbent on them to defend vaccination, as by
their own misinterpretation of facts) who are to be found associated
with the noisy little body of actual opponents of the practice. One of
the most injurious statements ever made in the advocacy of vaccination
is, that it always protects if properly done. When one of these
illogical defenders of that proposition is confronted with an instance
that disproves his assertion, he falls back on the allegation that in
that instance the vaccination was not properly done. The manifest
absurdity of such an argument strikes the doubter most forcibly, and
inclines him to say to himself, Falsus in uno, falsus in omne.
Unbelief founded on this ground would never have arisen if the plain
truth had always been adhered to: that the protection afforded by
vaccination is not invariable, and that very often it is not
permanent. In the infancy of the practice these facts were not known,
but it is now many years since they became obvious to every
fair-minded observer. The misapprehension of facts lies chiefly in the
false deduction from the circumstance that the great majority of cases
of small-pox occur in persons who have been vaccinated. But the
explanation of this is very simple. Suppose that, of one hundred
persons vaccinated, twenty fail to be protected permanently; that all
persons not vaccinated are unprotected; and that throughout the
civilized world the proportion of vaccinated to unvaccinated persons
is as ninety to ten. Making no pretence of arithmetical accuracy, it
may certainly be said that all these suppositions are well within the
truth. It follows from them that in a community of ten thousand
persons there will be nine thousand who have been vaccinated, and one
thousand who have not. Of the former, eighteen hundred will have
failed to secure lasting protection. Therefore in case of an epidemic
there will probably be a proportion of eighteen cases of small-pox in
the vaccinated to ten in the unvaccinated; and yet this should not
obscure the fact that of the nine thousand vaccinated more than seven
thousand were absolutely protected, whereas of the one thousand not
vaccinated not one could escape the disease if exposed to it. When we
add the further observation that of the eighteen hundred cases of
small-pox among the vaccinated not more than thirty or forty would
probably prove fatal, while of the one thousand cases in the
unvaccinated about two hundred would end in death, we have a striking
demonstration of the efficiency of vaccination. As a matter of fact,
statistics show that the figures here given err rather in allowing too
little than in asserting too much in favor of vaccinal protection.
The question naturally arises, Why it is that vaccination protects
some persons and does not protect others?--reference being had, of
course, to permanent protection, for it is exceedingly rare for
temporary immunity to be attained if we exclude those instances in
which the variolous infection has taken place before the operation is
resorted to. This {467} question cannot be answered with any
certainty, but various theories have been brought forward, some of
which call for notice.
In the first place, it has been thought that the revolution of the
system termed puberty was fraught with such a radical change as to do
away with the mild modification due to vaccination. While this theory
has an air of plausibility, it seems to lack proof and not to be
upheld by analogy, for we do not find that children who have had
scarlet fever, measles, and the like often undergo those diseases a
second time on arriving at the age of puberty.
The only remaining theory that our limits will allow a consideration
of is that put forward by Marson of London, that the degree and
duration of vaccinal protection are proportionate to the perfection of
the vaccinal lesion and to the number of insertions made. In a large
experience with small-pox Marson found that the disease was more fatal
among those whose vaccinal scars were imperfect or few in number than
among those who bore evidence that several pocks had been produced and
had run a typical course. As to the influence of a perfect evolution
of the lesion, but little doubt can be entertained, for we have
already seen that in some instances its course is so different from
what it should be that no protection whatever seems to result. When we
come to consider the number of the pocks as affecting the degree or
the duration of protection, however, an obvious source of fallacy
arises in the fact that we cannot always be sure that some of the
scars on a person having a number of them were not the products of a
repetition of the operation several years after the first--that is to
say, a revaccination, the efficiency of which in restoring lost
immunity is now well established. Nevertheless, as long as the doubt
remains the best course to pursue seems to be to act as if Marson's
theory were in all respects correct, and vaccinate by multiple
insertions.
We have, then, no positive means of ascertaining who those persons are
that are likely to fail of lasting protection, or how long a time will
elapse before the cessation of their immunity will take place. The
only safety lies in revaccination. But after how many years should
revaccination be resorted to? It has been thought that this question
might be settled by noting at what age, or at what period after
primary vaccination, large numbers of people became susceptible of
revaccination. This test, however, is not altogether trustworthy, for
a renewed susceptibility to vaccinia by inoculation does not
necessarily imply that the liability to take small-pox by effluvium
has been regained. If it did, modified small-pox (varioloid) would be
far more common than it is, for it is certain that revaccination can
be made to succeed in a very large proportion of children long before
they have reached the age of puberty. The fact is, contrary to the
notions of the last generation, that success in revaccination is the
rule, not the exception. Formerly it was not expected to succeed, and
therefore no special pains were taken to ensure success.
Definite rules cannot be laid down as to the time that should be
suffered to elapse before vaccination is repeated, but in the great
majority of instances safety may be attained by revaccination every
five or six years, and always in the presence of an epidemic,
regardless of the lapse of time; also whenever one's mode of life is
to undergo a noteworthy change, {468} as in emigrating to a foreign
country, on entering the military service, and the like.
To sum up, then, vaccination almost invariably protects against
small-pox for the time being; generally for a long term of years;
sometimes for a lifetime. Often the protection is absolute; as a rule,
it is very nearly so; in rare instances it is trifling. In general
terms, it may be said that it is scarcely less protective than
variolous infection itself, for death from a second attack of
small-pox is by no means rare. Here the question comes up: Is
vaccination less protective, either in degree or in duration of
effect, than it was at the time of its adoption? Given a typical
vaccinia, we may unhesitatingly answer, No; but do we now so
invariably produce the disease in all its essential features as was
done in Jenner's time? Yes, provided we use proper virus and employ as
much care as was taken by the older physicians, who, trained to the
practice of variolation (the inoculation par excellence of bygone
days), did their work with a gusto now seldom witnessed. But there was
a time, now happily at an end, when it was not easy to obtain
thoroughly good virus, and when, therefore, the result was apt to vary
materially from the standard. This may be conceded without entering
upon the vexed question of the general deterioration of the Jennerian
stock of vaccine.
Besides immunity from small-pox, there are one or two sequelae of
vaccinia that deserve mention before we proceed to consider what it is
better to class as complications. In the first place, vaccination has
been supposed to confer temporary protection against whooping cough.
The writer is not aware, however, of any precise data going to prove
either the truth or the falsity of this supposition.
Secondly, by virtue probably of the inflammation that attends the
evolution of the vaccinal pock, vaccination practised in the immediate
neighborhood of a small naevus often cures that blemish, and it has
been done for that purpose in many cases. It has no advantage over
many other measures, however, and there is the disadvantage that the
naevus may so mask the pock as to give rise to some doubt as to the
satisfactory character of the latter. The practice, therefore, is not
to be urged.
COMPLICATIONS.--These are local and systemic. Those of them that are
at all serious are rare, and can generally be traced to fortuitous
circumstances.
Inflammatory complications are usually due to undue traumatism at the
time of the inoculation, to injury of the pock, or to the previous
existence of a cutaneous disease or of some dyscrasia. Dermatitis is
the most common. It is usually a mere erythema, but in some instances
lymphangitis, lymphadenitis, phlegmonous inflammation, with diffuse
suppuration, may result. From injury of the pock ulceration and
gangrene may take place, and septic absorption may follow in their
train. These complications are to be treated as if they had occurred
from any other cause. Generally, the mere vaccination is not
responsible for them, but in some instances putrescent vaccine may be
adduced as their source. In such cases the complications, if they can
still be called so, are apt to make their appearance long before the
pock matures, even within forty-eight hours of the vaccination.
Inflammatory complications supervening on the full development of the
pock may invariably be set down as due to some cause not connected
with the quality of the virus employed.
{469} An undue amount of dermatitis is best treated with some mildly
astringent and anodyne application. The following liniment is
excellent for the purpose: Rx. Unguenti Stramonii oz. j; Liquoris
Plumbi Subacetatis fl. drachm ss; Olei Lini fl. oz. iv.--M. fiat
linimentum. As a rule, it is best to avoid poultices applied over the
pock itself, for they soften the tender structures that make up its
dome and render it prone to rupture, with all the consequences that
may follow its conversion into an open sore. When the latter accident
has occurred, dusting powders will ordinarily suffice to absorb the
discharge, and thus prevent putrefaction--either the ordinary toilet
powder or salicylized or carbolized powders, the basis of which may be
starch with a small proportion of the oxide of zinc. Besides the
antiseptics mentioned, iodoform, boric acid, etc. may be used to
advantage. Liquid applications are not usually so appropriate, but the
writer has known the proprietary preparation termed Listerine to
answer admirably.
Circumscribed collections of pus are to be treated as under other
circumstances, and burrowing is to be guarded against. It is only in
the worst cases that constitutional treatment of any sort is demanded,
and in these it should be of a supporting nature.
Passing from the simple inflammatory complications to those of a
specific character, we will first mention erysipelas. Genuine
erysipelas following vaccination is quite rare, but when it does occur
it is prone to prove serious. The writer believes that it always
depends on secondary infection--_i.e._ that the vaccinal wound becomes
the nidus of an erysipelatous contagium already existing in the
patient's surroundings, just as any other traumatic surface might, and
that the vaccinal virus has nothing whatever to do with it. Admitting
that improper virus is apt to give rise to dangerous inflammatory
complications, the latter are not really erysipelatous, whatever guise
they may put on. Erysipelas following vaccination calls for no other
treatment than what is proper for traumatic erysipelas under ordinary
circumstances.
We now come to the subject of vaccinal syphilis. The question of the
possibility of conveying constitutional taints along with vaccinia was
raised long ago, but, partly relying on certain theoretical tenets,
and partly because of the rarity of well-ascertained facts to shake
the blind confidence felt in the utter harmlessness of vaccination,
the profession fought the suggestion without properly investigating
it. In regard to syphilis, the broad assertion was maintained that two
infectious diseases could not affect an individual at one and the same
time: either syphilis would be communicated alone or vaccinia alone;
moreover, it was affirmed that the juices of a syphilitic person were
not capable of giving rise to the disease by inoculation unless they
happened to proceed from a syphilitic lesion. There was never
sufficient basis for the former of these two doctrines, and the latter
received a rude shock when it was shown by Pallizzari and the
anonymous physician of the Palatinate that the blood of a syphilitic
subject was capable of conveying the taint. Meantime, certain horrible
outbreaks of syphilis were reported, chiefly in Italy, that could not
reasonably be imputed to the ordinary occasions of syphilitic
infection. Even these occurrences, however, failed to shake the
general incredulity, especially in Great Britain, where until quite
recently men's orthodoxy in medical matters was gauged by their
obstinacy in refusing to {470} investigate, far less believe, the
slightest proposition unfavorable to vaccination, and where, also,
observations from beyond the limits of the empire were looked upon as
in all probability fallacious.
To a Frenchman, M. Viennois, we are indebted for the first systematic
and fair-minded study of the subject of vaccinal syphilis. This writer
demonstrated that the Rivalta cases and those of other like outbreaks
were certainly due to vaccination, but he concluded that they owed
their occurrence not necessarily to the use of lymph from syphilitic
subjects, but to the fact that that lymph contained blood. By this
time it had come to be recognized that syphilis was inoculable by the
blood. But even Viennois's masterly essay, and the facilis descensus
it offered to those English authors who found themselves confronted
with proof positive of their error, failed to make any noteworthy
impression beyond the concession that syphilis might possibly be
communicable in vaccination, but that, if it were, the catastrophe
might easily be escaped by avoiding the use of lymph contaminated with
blood, and that, therefore, the danger was practically no danger at
all, for no one in England would think of using bloody lymph! In all
this the English were slavishly followed by our own countrymen. It is
proper to add, however, that Ballard of London did his best to present
the matter in a proper light to the British profession, and that it is
largely due to his labors and to those of Jonathan Hutchinson (the
latter of whom supplemented Ricord's discovery that vaccine lymph is
never free from blood with abundant clinical evidence of the existence
of vaccinal syphilis unavoidable by the mere observance of Viennois's
safeguard) that we are now freed from the clog of error in this
matter. Nor was it the English alone that so long baffled the
recognition of the truth; in the French Academie de Medicine, Jules
Guerin and his adherents fought desperately against it.
At the present day we know that syphilis is liable to be communicated
in vaccination, and that, too, without regard to visible blood in the
lymph employed. There are two ways of avoiding it. One is, to use
non-humanized lymph, since the lower animals are insusceptible to
syphilis.[1] This is simple. The other is, to select a human
vaccinifer that is free from syphilis. This is difficult. Too great
reliance, however, should not be placed upon the vaccinifer; it is
possible to convey syphilis even in the use of bovine virus. Suppose
two persons, A and B, are to be vaccinated at one sitting, A being
syphilitic. If A is vaccinated first, and the same lancet, imperfectly
cleansed, is used on B, it is plain that B will be inoculated not only
with vaccine lymph, but also with A's blood. It is of the first
importance, therefore, that this form of vaccinal inoculation of
syphilis should be carefully guarded against; and that can be
accomplished most certainly by using a fresh instrument for each
patient.
[Footnote 1: Practically, this is certain, although there is some
reason to believe that the disease may be conveyed to monkeys.]
From a medico-legal point of view it is important to note that
constitutional syphilis may follow vaccination, and yet have nothing
to do with it. Suppose an infant to be born syphilitic, but with no
visible manifestations of the taint. Let that child be vaccinated, and
let the syphilitic dyscrasia afterward break forth. The ordinary
inference would be that the syphilis was due to the vaccination; and
in most instances this view would certainly be urged by the syphilitic
parent, since it would {471} free him from suspicion. It is always
easy to disprove such an allegation, however, for syphilis
communicated in vaccination always shows itself first in the form of a
chancre at the site of the vaccination. Therefore in any given case,
unless this mode of onset can be proved, the syphilis is manifestly
not of vaccinal origin. Some observers, it is true, are of the opinion
that vaccination may evoke a pre-existing syphilis, to use Lanoix's
term--_i.e._ that it may hasten the appearance of the characteristic
manifestations, and even determine their localization at the site of
the vaccinal inoculation. But, even allowing the truth of that
proposition, in such a case the lesion would be constitutional, not
chancrous.
It is well, nevertheless, to take precautions against being placed on
the defensive in this way; and it may commonly be avoided by declining
to vaccinate infants under three or four months old, since inherited
syphilis generally manifests itself by that time. This prudence on our
own behalf should not be carried so far, however, as to lead us to
deny the benefit of vaccination to very young infants whenever the
prevalence of small-pox is such that they are in obvious danger of
exposure.
As regards its management, vaccinal syphilis does not differ from the
ordinary form of the affection, and hence demands no other treatment
than what is proper for the disease contracted in the usual way. It
simply originates in an extragenital chancre.
Concerning the conveyance of other constitutional taints in
vaccination our knowledge is very limited. The present tendency of
pathological investigation is, however, to accord inoculability to
many diseases that formerly were not imagined to possess that quality,
so that in regard to other affections than syphilis it is prudent to
use the utmost care in the choice of lymph. There is one supposed
safeguard that does not seem to have the slightest title to be so
regarded--namely, the notion that a typical pock cannot be developed
on a person affected with a specific cachexia. There is no truth in
the doctrine. Over and over again the writer has seen perfect vaccine
pocks on persons whom he knew to be syphilitic.
Cutaneous affections of a non-specific character are sometimes
observed to result from vaccination; that is to say, they follow close
upon its performance, without any other known exciting cause. It may
fairly be supposed that in many instances they would have shown
themselves even if the vaccination had not been performed, for it is
often the case that we are unable to speak positively in regard to the
exciting cause of an eruption. Several years ago a striking case in
point was related to the writer by a well-known physician of this
city, S. S. Purple, in whose practice it occurred. Purple had engaged
to vaccinate a child on a certain day, but for some reason the
vaccination was not done. In about a week from the appointed day,
however, erysipelas made its appearance, beginning on the left arm at
the usual site of vaccination, and pursued its course to a fatal
termination. To be sure, we are now speaking of non-specific
affections, but erysipelas illustrates the proposition perfectly,
notwithstanding its specific character.
Children with a tendency to eczema are prone to suffer an outbreak of
that disease as the result of vaccination. In Jenner's time, indeed,
it was considered not only that there was great risk of causing an
aggravation of any slight eczematous eruption by vaccination, but that
the mere {472} existence of the eczema, even in the most trivial form,
was likely to interfere with the success of the vaccinal inoculation.
This has been the general feeling of the profession. Quite recently,
however, many observations have been recorded tending to show that the
old dread of vaccinating an eczematous child was not altogether
warranted. The question needs further study, and, while it is probably
best to postpone the operation under ordinary circumstances, nothing
should induce us to withhold its protective influence where there is
any manifest danger of actual exposure to small-pox.
Although eczema is the most common of the cutaneous affections called
forth or aggravated by vaccination, there are various forms of skin
disease, some of them difficult to classify, that occasionally result.
They are usually vesicular, pustular, or furuncular--that is to say,
irritative. In the majority of instances it will be found either that
the pock itself has followed an irregular course, being whitish,
diffuse, and ending in an exaggerated although superficial
incrustation, or that it has been subjected to injury. Still, in some
cases neither of these conditions is the precursor of the skin
affection. In many instances the latter can only be called
nondescript. There seems to be some occult connection between
vaccination and the curious skin disease described by the late Tilbury
Fox of London under the name of impetigo contagiosa; and, indeed,
Piffard of this city has found certain microphytes to be common to the
crusting period of vaccinia and that of contagious impetigo. What the
relation of the two affections is to each other, however, it is
difficult to say.
Apart from impetigo contagiosa, the cutaneous complications that
follow in the wake of vaccination possess no distinctive features, and
their management differs in no wise from that of the same
manifestations due to other causes.
THE TECHNICS OF VACCINATION.--This aspect of our theme involves a
number of separate considerations. It will be convenient to give our
attention first to the matter of the choice of virus. The question
arises at once as to the selection between animal vaccine and the
humanized variety. In a broad sense the term animal vaccine
includes--1. Virus derived directly from a case of so-called
spontaneous cow-pox. 2. Variola vaccine--_i.e._ the virus of an
affection of the cow resulting from variolation. 3. The virus of
horse-pox (not strictly vaccinal). 4. Retro-vaccine--_i.e._ the virus
of an affection produced in the cow by the inoculation of vaccinia
from the human subject. 5. The virus of a disease (true vaccinia)
propagated through a series of bovine animals from the so-called
spontaneous cow-pox, being the virus now commonly understood by the
term, and the variety here referred to when it is not stated to the
contrary.
By humanized vaccine we understand that which is obtained from the
human subject, no matter how short or how long its descent from the
cow. As regards animal vaccine, we may practically exclude from
consideration all but the last variety mentioned, that being the one
to which, in the great majority of instances, the term is now
restricted. This narrows the question down to the choice between virus
that has been propagated through a number of bovine animals
(practically, calves) from the spontaneous disease in the cow, and
that which, whatever its original source, has already passed through
the human system.
{473} The variety first mentioned, sometimes called primary vaccine,
is generally spoken of by authors as not very trustworthy as regards
its infective power (that is, not to be counted on to take), and as
prone to give rise to undue inflammatory complications when its use
does prove successful. These unpleasant qualities might be explained
by the supposition that primary vaccine is not apt to be at its best
when it is now and then obtained. Practically, however, it may be
dismissed without further consideration, for it is seldom to be had.
The second form--variola-vaccine--is manifestly improper to be used
whenever genuine vaccine is to be obtained, unless, indeed, we shut
our eyes to the accumulating evidence that variola-vaccine, so called,
is not vaccine at all. Furthermore, it is a question whether its use,
as well as all attempts to produce it, should not be forbidden by law.
The third variety, if such it may be called, it does not seem
legitimate to use in the present state of our knowledge, since it is
not yet proved satisfactorily that horse-pox possesses the full
protective power of cow-pox, or is free from objections that do not
arise in connection with the latter.
As to retro-vaccine, while the writer is unable to see any positive
reason against its use, neither can he see any reason why it should be
superior to humanized vaccine, as such, save that during the period of
its bovine propagation it is not liable to become contaminated with
the poison of syphilis. The idea that an enfeebled stock of humanized
vaccine can have new life infused into it by passing through the
system of the cow is not reasonable prima facie, and there are no
particular facts to support it. By ensuring freedom from the danger of
communicating syphilis retro-vaccination doubtless served a good
purpose at one time, but now, since the remarkable and enduring
excellence of the Beaugency stock is so well established, there seems
to be no excuse for a further resort to the practice.
The last of our five forms of animal vaccine, that produced by the
continued propagation of spontaneous cow-pox through calves, is what
is now known as animal vaccine par excellence. Its advantages over the
other forms are so obvious that it alone should figure in any
comparison between animal and humanized vaccine. That being
understood, what are the relative merits of animal and humanized
vaccine? It should be stated, in the first place, that bovine virus
should be compared with virus that has long been humanized, for lymph
of but a few removes from the bovine animal does not show any
noteworthy differences from animal vaccine itself.
In behalf of humanized virus it is maintained--1, that it is a more
trustworthy preventive of small-pox; 2, that it is superior in its
infective property, so that it is surer to take; 3, that it is more
prompt in its action, thereby affording more speedy protection to
persons who have actually been exposed to small-pox; 4, that its
virulent property is easier of preservation, wherefore it is more to
be depended on when it is necessary to keep it on hand for a long time
or to transmit it to great distances; 5, that its use requires less
skill, or, rather, less special knowledge of the peculiarities of the
animal virus; 6, that it is less violent in its effects; 7, that it is
less apt to give rise to irregular, and therefore more or less
abortive and non-protective, forms of pock.
{474} The first of these propositions, which asserts that humanized
vaccine confers greater protection against small-pox than the animal
virus, was warmly maintained by those who opposed animal vaccination
on its first introduction into this country; but now the record of the
past thirteen years, during which period bovine virus has more and
more borne the brunt of the fight against small-pox, has disproved it
in the judgment of all competent and fair-minded observers. So far,
indeed, as the facts have been analyzed, they go to show that the
reverse is the case--that bovine virus confers a more complete and a
more lasting protection. Direct observation on this point is
strengthened by the collateral fact that revaccination became at once
astonishingly successful when the use of animal vaccine first gained
currency, whereas now it is again declining in success; the
explanation of which latter circumstance is, that it is now found
difficult to revaccinate those whose primary vaccination was done with
bovine virus--a striking indication of the permanence of the
protection accomplished with the latter.
The second assertion--that humanized virus succeeds more readily than
the bovine variety--is still maintained by many, but, it may
confidently be said, by few if any whose experience with good animal
vaccine has been large. The truth is, that every large public
vaccination service in the country is now carried on almost solely
with bovine virus, and that results are thus achieved that were not
dreamed of in former times. Individual experience cannot weigh against
this fact, but may be explained, rather, by what modicum of truth
there may be in the fifth proposition, or by the assumption (surely a
legitimate one, in view of the number of irresponsible and ignorant
purveyors of animal vaccine that have thrust themselves before the
profession since the advantages of the practice were established by
the labors of others) that those whose observation leads them to a
conclusion at variance with that reached by the great majority of
trained observers have really been unfortunate in the quality of the
virus with which they have been supplied. Whatever the explanation may
be, however, there is nothing more certain than that the use of animal
vaccine, properly carried out, is daily furnishing results that have
never been excelled, if they have been equalled, in the employment of
humanized virus on a like scale.
The third suggestion--that the humanized virus acts the more promptly
of the two, and is therefore to be preferred for immediate
protection--is plausible, since the areola (the alleged sign of
systemic infection) forms somewhat later around a pock produced by
animal virus than around one that is the result of vaccination with
the humanized variety. The difference is one of a few hours only at
the most, and it is not by any means a general occurrence; still, we
may concede that in this respect the use of humanized virus is to be
preferred under certain circumstances.
As to the fourth statement--that humanized virus is more tenacious of
its infective property--strictly speaking, there is not a particle of
truth in it. In the case of liquid lymph preserved in capillary tubes
it has the semblance of truth, but, for reasons that will be more
fully set forth hereafter, that is because it is difficult to get the
virulent portion of bovine lymph out of the tube. In the form of dried
lymph (the only form that ought to be used) animal vaccine may be sent
to all parts of the world, and may be kept any reasonable length of
time and without {475} special care, without undergoing sensible
deterioration, if tested by one who is familiar with its peculiarities
and aware of the care that should be taken in using it. Under ordinary
circumstances there is no difficulty about preserving animal vaccine
with its energy practically unimpaired.
The statement that the use of humanized virus demands less special
knowledge than that of bovine virus is conceded at once. That special
knowledge is easily mastered, however, and no man fitted to practise
medicine will look upon its acquirement as a bugbear or a hardship.
The impression, almost universal thirteen years ago, that humanized
vaccine is less severe in its local and constitutional effects than
the animal virus has been eradicated from the minds of all but those
who still follow the teachings of the older writers rather than yield
to what daily experience has been teaching during these thirteen
years, or those who reason from exceptional cases rather than from a
general drift. The truth seems to be this: with revaccinated adults
animal vaccine acts somewhat more severely than the humanized virus;
in infants, on the other hand, its action is not so violent as that of
the humanized variety.
Concerning the seventh and last claim put forward in behalf of
humanized vaccine--that it is less apt to give rise to irregular or
spurious pocks--we may say that no form of irregularity has been
observed by those who have lately used the bovine virus that was not
well known to the older writers, who founded their observations
wholly, or almost wholly, on the use of the humanized virus; nor is
there any proof that such irregularities are more common now than
formerly. The truth seems to be, that these irregular forms of pock
seem to prevail at certain times, and not at other times, regardless
of the particular stock of virus used, other things being equal. Why
this should be so we do not know, but the fact is beyond dispute.
To sum up, then, we can only say that in barely one particular--that
of promptness of action--can humanized virus justly be credited with
any superiority, while in every other essential respect it is
inferior, so far as any difference is to be observed.
What, on the other hand, are the points of superior excellence
attaching to bovine virus? Setting aside certain extravagant
assertions that have sometimes been made in its behalf, such as that
it far exceeds the humanized virus in its protective virtue (which may
be true, but is not yet proved), they may be put in general terms in
the form of a denial of all the particular claims that we have
enumerated as having been put forth for its rival. Such a denial, it
has been seen, seems to the writer to be justified, save in the one
particular that perhaps we should accord to humanized virus the merit
of speedier action, and consequently greater certainty of protection,
in cases of actual exposure to small-pox.
Besides these negative points in its favor, the foremost advantage of
animal vaccine is the guarantee it gives that, properly used, no
syphilitic contamination will result. On this point no argument is
needed, for the cow is insusceptible to syphilis.
A second consideration in its favor is, that it can always be had in
large quantities at short notice. The young practitioner of the
present day can scarcely appreciate the importance of this fact, but
whoever remembers the comparative helplessness in which, in past
years, he has found himself in the face of a sudden outbreak of
small-pox, not knowing which {476} way to turn for an adequate supply
of vaccine, will at once concede its force.
On the whole, then, it must be said that bovine virus is entitled to
the preference as a rule, but that possibly it is well to resort to
humanized lymph of early removes under the special circumstances above
referred to. On no account should long-humanized vaccine be used so
long as our present stocks of animal virus maintain the excellence
they have thus far preserved, nor should humanized virus of any sort
be preferred in the general run of cases.
Passing now to a consideration of the various forms of vaccine,
disregarding its source, there are practically these three: the crust,
liquid lymph preserved in capillary tubes, and dried lymph.
Until recently the crust, or scab, was much used in this country. Its
capability of being preserved unimpaired for a long time was a valid
excuse for this, especially in regions remote from the great channels
of communication, and it was in such districts that the use of the
crust was chiefly practised. That excuse scarcely exists now, for
there are few physicians who cannot obtain a better form of vaccine
within a very short time. The objections to the crust are two: 1. Most
crusts are inert. Especially is this true of bovine crusts, which are
wellnigh worthless. It must be confessed, however, that when once a
crust has proved itself active it may be trusted to retain its
infective property for a very long time. The writer has made
successful use of crusts seven years old that had made the voyage to
Japan and back; and they were bovine crusts too. Still, the rule is,
that crusts are untrustworthy. 2. Their use is apt to be followed by
undue inflammation, probably of septic origin, for they almost
invariably contain putrescent or readily putrescible elements. It has
even happened to the writer to cut open a crust that to all appearance
was typical and innocent, and to find in its interior a cavity
occupied by a pulpy, stinking slough. Manifestly, such material is
unfit to be introduced into the system of any human being.
In regard to liquid lymph in tubes, it is not much used in this
country, and its employment elsewhere is on the decline. At first
thought, it would seem to be the best form of all, but experience does
not bear out this view. In this form humanized lymph is vastly
superior to animal lymph, but with every possible care in charging and
sealing the tubes it is not uncommon to find their contents putrid.
There are low vegetable organisms that are supposed to prey on the
vaccinad. If there is any truth in this supposition, those organisms
are certainly favored in their destructive luxuriance by keeping the
lymph liquid, thus furnishing them with the best possible
culture-fluid. Be this as it may, the fact is well ascertained that
tube-lymph does not keep well. It has been mentioned already that
bovine lymph stored in tubes is decidedly inferior to the same form of
humanized lymph. This was long ago recognized by propagators of animal
vaccine, but the cause remained a mystery until Warlomont of Brussels
suggested that it was due to one of the physical peculiarities of
animal lymph--that, namely, as already hinted at, by virtue of which
its formed elements tend to attach themselves to any surface presented
to them, leaving the supernatant liquid a mere inert compound of
water, albumen, and salts; so that in the case of tube-lymph the
virulent elements remain attached to the glass, and only the inert
constituents {477} are really used. This theory is exceedingly
ingenious and plausible, but the writer is not aware that it has been
proved. He does know, however, that in some South American countries,
where calf lymph in tubes is used with success, the custom is to grind
the tubes to powder, and inoculate with the resulting magma, glass and
all. This practice is certainly not to be commended.
Dried lymph is the most efficient of all forms of vaccine, and, kept
as it ought to be, it retains its infective power long enough to
answer all ordinary requirements. The writer has used it three years
old with success. It may commonly be counted on for six weeks. One
fact should be borne in mind, however: the longer dried lymph has been
kept the more care is necessary in its use, for by long keeping it
becomes very hard, so that it is a work of patience to dissolve it off
from the surface on which it was deposited. Failure to accomplish its
solution is the most common cause of a lack of success in its
employment.
The various forms of stored vaccine are esteemed by the writer in the
following order: 1, dried bovine lymph; 2, dried humanized lymph; 3,
humanized tube-lymph; 4, humanized crusts; 5, bovine tube-lymph; 6,
bovine crusts.
The age and other circumstances under which it is best to vaccinate
children constitute a point for practical consideration. It may first
be mentioned that pre-natal vaccination has been advocated by some
authors; that is to say, the vaccinal infection of the foetus in utero
by vaccinating the mother during gestation. There seems to be
respectable testimony going to show that the end may thus be
accomplished, but a weighty objection arises in the fact that this
mediate vaccination of the foetus produces no physical sign of its
success, so that doubt must always be felt as to whether or not the
procedure has been efficacious. Moreover, it is seldom indeed that a
child needs protection before its birth, provided we protect the
mother, for it is well known that vaccinia will overtake and destroy
the variolous infection, even when the latter has had two or three
days' start. The practice has been chiefly urged by Bollinger. It is
not likely to come into general use.
There is no special objection to vaccinating an infant at any time
after birth, but usually it is well to defer the operation until the
child is about three months old, unless there is actual danger of
exposure to small-pox. Yet it is not well to postpone vaccination
until the period of dentition, for the combined irritation of the two
disturbing elements may prove decidedly uncomfortable if not serious.
Something is to be said as to the time of the year to be chosen. In
New York the bad custom prevails, especially among the poorer classes,
of having children vaccinated only in April, May, or June--just the
part of the year in which erysipelas is most rife. The hot months
should not generally be chosen, for any source of irritation is apt to
be felt more severely by infants during the summer heat. However, no
circumstances should be looked upon as a positive bar to vaccination
in case of actual danger of exposure to small-pox, and in large towns
children should never be taken into public conveyances or carried into
any promiscuous assemblage until they have been protected by
vaccination.
The next question is as to the part of the body that should be
selected for the inoculation. The region of the insertion of the left
deltoid muscle {478} is usually chosen--the left rather than the
right, because most nurses habitually carry an infant on their own
left arm, so that the child's left arm is uppermost, and hence less
exposed to injury. The region of the deltoid insertion is
comparatively free from the irritation of muscular contraction, and it
is easily accessible. If two insertions are made, it is well to make
one of them over the deltoid insertion and the other at a point about
an inch distant on the line of the posterior border of the same
muscle, for there the lymphatic connection with the axillary glands is
less free, so that adenitis is not so much to be feared. To avoid a
scar in a locality that may be exposed to view on certain occasions
some mothers prefer that their daughters should be vaccinated on the
lower limb. To this there is no special objection, further than that
the lower limb is rather more exposed to rough handling than the arm.
If the leg is chosen, the point of junction of the two heads of the
gastrocnemius is an eligible situation.
The actual operation is performed in various ways. The old inoculators
generally made an incision through the whole thickness of the skin, so
that a pellet of subcutaneous fat rolled up into the little wound.
This is wholly unnecessary; furthermore, it is objectionable, for it
decidedly increases the risk of inflammatory complications. Still more
to be avoided are the methods by inserting a seton imbued with the
virus and by hypodermic injection or other like procedures. The best
way is, simply to remove the horny layer of the cuticle, so as to
expose the succulent portion of the epidermis. This surface is
somewhat red, and from it a slight exudation of lymph will be
observed, but there need not be the least flow of blood. By this
procedure it is not uncommon to vaccinate a sleeping child without
waking it. It is not only admissible, but preferable, not to wound the
derma at all. Such an abrasion is easily made with an ordinary lancet,
which, contrary to the advice sometimes given, should be very sharp;
but no cutting or scratching should be done with it, only scraping
with the convex part of its edge, precisely as in using an ink-eraser.
Scratching instruments (such as the rake-like vaccinator often used or
a row of needles set in a handle) are not easy to adapt to varying
degrees of plumpness of the arm, and are apt to make too deep
scratches, one at either side, while the skin between the two is
scarcely touched. Whatever instrument is chosen, it should not be used
again until it has been thoroughly cleansed--made chemically
clean--which can be accomplished only by heating it or by wiping it
off and then dipping it into a strong disinfectant solution.
Some individuals are refractory to vaccination, but complete
insusceptibility is exceedingly rare. Various expedients have been
resorted to in rebellious cases, such as vesication with
ammonia-water, maceration of the skin for some hours with glycerine,
and the like. The writer has known these devices to succeed, but he
has not seen the slightest advantage in the plan recommended by Ceely,
that of using a wound some hours old rather than one just made,
although he has tried the experiment many times. It is not necessary
to make a large abrasion; one as large as the little finger-nail is
ample.
The next step is to apply the virus, and it should be so applied as to
bring it into contact with every part of the denuded surface. In what
is known as arm-to-arm vaccination, or its equivalent, calf-to-arm
{479} vaccination (by all means the most successful method, although
not often practicable in this country), the liquid lymph, fresh from
the vaccinifer's pock, is simply applied, when it will at once become
diffused over the abraded surface without any special pains being
taken to accomplish that end.
If dried lymph is used, particular care should be taken to see that it
is actually dissolved and transferred from the substance on which it
was dried to the abraded surface. Failure to accomplish this is the
cause of almost all the lack of success that inexperienced vaccinators
meet with. The lymph should be moistened with water, or, if it is
quite old, with glycerine, before the abrasion is made, so that it may
have time to dissolve. It should then be rubbed upon the abraded spot
vigorously, and at least for the space of a full minute.
In the use of tube-lymph no other precautions are necessary than in
arm-to-arm vaccination, but, simple as this method is, its results are
unsatisfactory.
Crusts should be reduced to a powder, and then made into a thin paste
with water or glycerine. A convenient way of powdering a crust is to
rub it on a file or between two files. The paste is to be well rubbed
upon the abrasion. The insertion of a solid piece of crust into a
valvular incision is not to be recommended.
When the operation is finished it is well to keep the arm bare for
about five minutes, but not necessarily until the spot has become dry.
It is not well to apply any sort of plaster, but means should be taken
to prevent the underclothing from sticking to the abrasion. For this
purpose there is no objection to the shields that are furnished by the
surgical instrument-makers. Usually, however, nothing of the sort is
necessary.
THE STORAGE AND PRESERVATION OF VACCINE VIRUS.--Lymph should usually
be taken on the eighth day, inclusive--never after the areola has
formed. On the other hand, the writer's experience does not lead him
to coincide with those who state that the earliest lymph that can be
obtained is the most energetic. If it is to be dry-stored, the
substance to be coated with it (slips of quill, ivory, wood,
whalebone, glass, and the like) should be laid gently in the pool of
lymph that exudes on puncturing the pock, and allowed to dry,
preferably without the aid of artificial warmth. The layer of lymph
should be plainly visible after it has dried. A second coating is
advisable, as it serves to preserve the first.
Capillary glass tubes are either cylindrical or furnished with a
bulbous expansion at the middle, the latter form being most commonly
used. To charge a tube make sure that both ends are open, and then
submerge one end in the pool of lymph. Capillary attraction will cause
the tube to fill, and the process may be facilitated materially by
inclining the tube toward a horizontal direction, so that the
capillary attraction is not opposed by that of gravitation. Care
should be taken to keep the applied end of the tube constantly
submerged, or bubbles of air will enter it. The sealing may be done
with a blowpipe, by simply holding the ends in a flame, or by means of
sealing-wax or some similar substance. The satisfactory charging of
tubes demands some practice, but a little patience will enable any
intelligent person to succeed.
In regard to crusts, they should never be removed until the surface
beneath has become cicatrized and they have been partially detached by
the natural process. A crust torn off prematurely should never be
used, {480} and the same may be said of secondary crusts--_i.e._ those
that form by the desiccation of the discharge from the raw surface
left when the primary crust has been removed forcibly.
For the preservation of vaccine in these various forms tubes need only
be kept in a cool place. Dried lymph and crusts should be guarded
against dampness even more than against warmth. Their preservation may
be decidedly favored by over-drying, either in an exhausted receiver
or by keeping them in a closed vessel in the presence of sulphuric
acid, chloride of calcium, or some other substance having a strong
affinity for water. It is needless to say, however, that they should
not come into actual contact with any such agent. While this
artificial desiccation tends powerfully to preserve dried lymph, it
makes it more difficult to use. When dried lymph or a crust is to be
sent by mail or other conveyance, it should be wrapped in some
impermeably envelope, for which purpose gutta-percha tissue is very
convenient. Both these forms of virus should be kept in a cool place.
There is no objection to keeping them on ice, provided they are well
protected against moisture.
* * * * *
In conclusion, the writer wishes to say that the limited space at his
command has compelled the assumption of a dogmatic rather than an
inductive form in the construction of this article. To the reader who
may wish to pursue the subject further--and it will well repay
thorough study--he would recommend the following bibliography:
Ballard: _On Vaccination: its Value and Alleged Dangers_, London,
1868.
Bousquet: _Nouveau traite de la vaccine et des eruptions varioleuses_,
Paris, 1848.
Bryce: _Practical Observations on the Inoculation of Cow-pox_,
Edinburgh, 1809.
Ceely: _Observations on the Variolae Vaccinae_, Worcester, 1840.
Chauveau et al.: _Vaccine et Variole_, Paris, 1865.
Depaul: _Nouvelles recherches sur la veritable origine du virus
vaccin_, Paris, 1863; _De l'origine reelle du virus vaccin_, Paris,
1864; et al.: _De la syphilis vaccinale_, Paris, 1865.
Hardaway: _Essentials of Vaccination_, Chicago, 1882.
Hering: _Ueber Kuhpocken an Kuhen_, Stuttgart, 1839.
Jenner: _An Inquiry, etc._, 2d ed., London, 1800.
Sacco: _Trattato di Vaccinazione_, Milano, 1809.
Seaton: _A Handbook of Vaccination_, London, 1868.
Steinbrenner: _Traite sur la vaccine_, Paris, 1846.
{481}
VARICELLA.
BY JAMES NEVINS HYDE, M.D.
Varicella is an acute disorder of infancy and childhood, in the course
of which appears a cutaneous exanthem of vesicular type, accompanied
at times by systemic symptoms of moderate severity, terminating in the
course of from three days to a fortnight, after the formation of
relatively few crusts upon the skin, with occasionally persistent
cicatrices.
SYNONYMS.--_Eng._, Chicken-pox; _Ger._, Windblattern, Schafpocken;
_Fr._, Varicelle; _Lat._, Variola notha, seu spuria; _Ital._,
Morviglione.
HISTORY.--The literature of the disease which is now best recognized
under the title of varicella has been, in the history of medicine,
wellnigh inextricably confused with that of variola. In the latter
part of the seventeenth and the early part of the eighteenth century
the distinction between typical forms of the two disorders became
apparent, and was described by Willan and Harvey in England, and other
writers in Germany, France, Holland, and Belgium. Among those who have
contributed to its literature may be named Hebra, Kaposi, Trousseau,
Simon, Thomas, Guntz, Henoch, Kassowitz, and Boeck.
ETIOLOGY.--Varicella is essentially a disease of early life, occurring
almost exclusively in infants and young children. It is a contagious
disorder, and at times, especially in hospitals and asylums for
children, occurs in apparently epidemic forms. The question relating
to the inoculability of the contents of its vesicular lesions is still
open, positive and negative results being recorded by different
experiments.[1]
[Footnote 1: The writer has purposely avoided, in the brief space here
devoted to the disease under consideration, entering into a discussion
of the question respecting the relation sustained by varicella to
variola. On one side are the views entertained by the Vienna school of
dermatologists, according to which there is but a single virus in
these several forms of disease--the variolous poison. On the other are
the opinions and the practice, largely based upon the latter, of most
English and American physicians, who deny the existence of any
relation between the pathological states recognized by them as
occurring in two entirely distinct affections.
My personal view may be briefly formulated as follows: Practically and
clinically, it is useful to regard these disorders as of a distinct
nature. The arguments, however, in favor of such absolute distinction
are not irrefutable. There is probably in both forms of disease but a
single virus, that of variola; but this, modified by evolution among
generations of vaccinated children, has, in this process of natural
cultivation or attenuation, produced a malady of tender years whose
attacks do not protect from variola and occur irrespective of
vaccination.]
SYMPTOMATOLOGY.--The period of incubation of the disease cannot be
said to be definitely established. At times, without question, an
entire fortnight elapses between the dates of exposure and the
evolution of the disease, but both longer and shorter intervals have
been recorded.
{482} If there be a prodromal stage of the disease, certainly in the
vast majority of the little patients it cannot be recognized. During
the last month the writer has observed the evolution of the disease in
twenty children gathered together in the Chicago Home for the
Friendless, no one of whom was recognized as ailing before the
eruption appeared. Occasionally the disease is preceded by mild or
even severe febrile symptoms, accidents sufficiently common in this
class of patients.
The exanthem, commonly the first symptom of the disorder, occurs in
the form of reddish puncta, from which rapidly develop rosy-colored
maculations, and these become tensely distended, transparent or
slightly yellowish vesicles, of the average size of a split pea,
though they are occasionally smaller or may enlarge to the dimensions
of a bean or small nut. The eruption appears first upon the upper
segment of the body, implicating the chest in front and behind, the
neck, the scalp, particularly the extremities, and quite sparingly the
face also, which may, however, entirely escape. In cases where the
eruption is profuse it may be completely generalized, involving
largely the trunk and extremities, the lesions, upon the back
particularly, being as closely set together as in discrete variola. In
many, even the majority, of cases the exanthem is much less profusely
developed, not more than a dozen or twenty vesicles springing from the
surface.
The vesicles are superficial in situation, the firm papule which
precedes the variolous rash being altogether wanting. They are at
first transparent, their contents plainly showing through their
translucent roof-wall, composed only of the stratum corneum of the
epidermis. They are both acuminate and globular, and occasionally rest
upon a slightly hyperaemic integument. Umbilication rapidly occurs at
the apex, and simultaneously their contents become lactescent and
gradually sero-purulent. Occasionally vesicles are transformed into
genuine, coffee-bean-sized, pustules. Intermingled with these are
often seen illy-developed and abortive vesicles.
By the end of a period lasting from twelve hours to the second or
third day involution has usually begun, and the lesions, with and
without rupture--more often the latter--desiccate, and are thus
transformed into yellowish or yellowish and brown, circular,
circumscribed crusts resting upon an apparently unaltered integument.
These crusts are often so firmly attached that they do not fall
spontaneously before the lapse of from five to eight days. When this
exfoliation is ended there are left slightly hyperaemic pigmented
patches of corresponding size where the crusts had rested. A
destructive process occasionally results upon the surface of the face
at the base of such vesiculo-pustular lesions as have formed there, in
consequence of which a small depressed and superficial cicatrix is
left, which does not differ from that resulting from discrete variola.
These scars may be superficially seated and transitory in character,
or much deeper and persistent through life.
Throughout the course of the disease systemic symptoms may be
altogether wanting, or may occur in a mild, and much more rarely in a
severe, type. In some cases the temperature is increased by one or two
degrees upon the appearance of the exanthem, and often a febrile
movement of moderate grade may persist for forty-eight hours or
somewhat longer. Defervescence, however, is always rapid and perfect.
In very {483} rare cases there is a subsequent successive new
development of scanty vesicles, whose appearance is heralded by mild
exacerbations of fever.
Occasionally the vesicles may be recognized upon the mucous surfaces
of the lips, inside of the cheeks, tongue, palate, conjunctivae, and
progenital regions of both sexes. Still more rarely the glands of the
throat become slightly tumid and painful.
The complexus of symptoms, in the large majority of all these little
patients, is that which pertains to a disorder of distinctly mild
type. The eruptive lesions are scanty and productive of but trifling
subjective sensations. Occasionally they are picked or scratched, and
thus become the seat of either pain or pruritus. In the febrile stage
the child is noticeably fretful for a period of perhaps twenty-four
hours. At the end of that time older children are frequently observed
engaged in their customary amusements in the nursery.
Severe types and complications of varicella are in general limited to
the little patients who are recognized as suffering from hospitalism.
Among these we see erysipelas, severe vaccinal eruptions, lesions of
inherited syphilis, and the sequelae of morebilli and scarlatina,
which the disease both precedes and follows.
PATHOLOGY.--The anatomical structure of the lesions in varicella is
largely a matter of inference, since there has been but small
opportunity of studying the disorder as displayed in sections of the
morbid integument. Manifestly, the exanthem is exudative in type, the
serum in circumscribed areas lifting the superficial layer of the
epidermis from the deeper parts of the derm. Unquestionably, septa
occur in typically developed varicella chambers, similar to those seen
in variola--a pathological fact which is the corner-stone of the
doctrine relating to the unity of the two disorders. The serum
contained in these septa possesses an alkaline reaction. The formation
of a cicatrix is evidently due to the intensity of the process in
certain exceptional lesions, as a result of which the papillae of the
corium are superficially destroyed. These sequelae are often due to
the picking and scratching of the lesions.
DIAGNOSIS.--Varicella is to be distinguished from eczema pustulosum by
its mild febrile symptoms, the discreteness of its pustular lesions,
the absence of itching, and of infiltration of the skin in patches,
and its tendency to symmetrical development.
From impetigo and the impetigo contagiosa of Fox of London it will
often be scarcely differentiated. Inasmuch as these disorders are
frequently recognized among children suffering from varicella or
varicella convalescence, it can scarcely be doubted that these
diseases have been in the past often confounded, and that in many
cases it is practically impossible to distinguish between them.
Decided elevation of bodily temperature, umbilication of
symmetrically-disposed lesions, and a rapid involution of the disease
point to varicella. The two forms of impetigo occur without fever, are
usually scantily developed, and are much more apt to be pustular in
type, lacking, moreover, the halo of the varicella lesions. The latter
are also, on an average, smaller and more numerous. The two forms of
impetigo, finally, never display the generalized eruption of severe
varicella. The non-contagious variety of impetigo is much more
decidedly pustular in its lesions, and the latter spring from a deeper
plane of the epidermis.
{484} As to the eruptions due to vaccinia and vaccination, there can
be but little doubt that these also have been frequently confounded
with varicella. Efflorescences having origin in this way are very
largely impetiginous in type, and the conditions named above are then
to be regarded as distinctive differences, so far as any distinction
can, under these circumstances, be recognized. Impetigo, impetigo
contagiosa, and varicella are all sufficiently common accidents after
vaccination. No reliance can be placed upon characteristics described
as connected with a certain stuck-on appearance of the crust regarded
by Fox as characteristic of the crusts in impetigo contagiosa. In all
these vesiculo-pustular disorders of childhood desiccating serum and
sero-pus upon the surface result in the formation of crusts which have
a similar (so-called) stuck-on appearance.
Variola and varioloid of infants and children are to be distinguished
from varicella by the evidence of origin from such contagious
maladies; by the occurrence of prodromal symptoms; by the greater rise
in temperature during the febrile stage; by the typically papular
stage of the exanthem at its outset, and no less typically pustular
stage before the occurrence of desiccation; by the confluence of
lesions in confluent cases; and by the much longer and evidently
graver stadium of the disease. Distinctions between mild varioloid and
severe varicella in infancy and childhood will always tax to the
utmost the skill of the diagnostician. The sooner it is generally
understood that intermediate forms occur which cannot be positively
assigned to the one or to the other category, the better it will be
for both the profession and the laity. The fact that in the one case
there is generation of a variolous poison capable of producing a
contagious disease in adults, and in the other a malady which is known
to affect children only, renders the decision important. Scattered
papulo-vesicular and vesiculo-pustular lesions appearing after a high
fever, and pursuing a period of evolution longer than forty-eight
hours, should always awaken suspicion. Superficial lesions, on the
contrary, distinctly vesicular on the third day, or commingled with
minute, very superficial pustules, should be regarded as
characteristic of varicella.
The so-called varicella prurigo of Hutchison of London[2] includes
several of the disorders considered above under the titles impetigo,
impetigo contagiosa, and the vaccine rashes. The irritable condition
of the skin resulting from several of the exanthemata leaves it prone
to the development of a long list of cutaneous lesions, some of them
accompanied by pruritus in various grades, to each of which might be
given, according to the caprice of authors, a separate name.
[Footnote 2: _Lect. on Clin. Surg._, Lond., 1878, p. 15 _et seq._]
PROGNOSIS.--The prognosis of varicella, per se, is always favorable.
Only in the hospital cases, complicated by erysipelas and scarlatina
convalescence, may grave results be anticipated. The milder attacks
may leave persistent relics of their career in the form of one or more
depressed and persistent cicatrices, which become less conspicuous as
the patient approaches adult years.
TREATMENT.--Varicella is, in a large proportion of cases, successfully
treated by domestic management and the simpler remedies familiar to
those in charge of the nursery. Confinement for a brief time to the
{485} cradle or bed, and a proper regulation of the temperature of the
room and of the diet, are usually all that is required. Special
remedies may be indicated in isolated cases, but certainly none such
are demanded by the varicella. Efforts should be made to protect the
face lesions from the traumatism of picking and scratching, with a
view to prevent pitting.
Isolation of patients is not requisite, nor any process of
disinfection other than that which is incidental to a fresh supply of
pure air. Vaccination should be practised alike in the case of
children who have and who have not suffered from the disease.
{486}
SCARLET FEVER.
BY J. LEWIS SMITH, M.D.
HISTORY.--The terms scarlet fever and scarlatina are used synonymously
to designate one of the most common and fatal of the eruptive fevers.
Whether this malady occurred prior to the Christian era is uncertain.
It is believed by some that the plague of Athens, 430 years before
Christ, vividly described by Lucretius, and by Thucydides, who was
attacked by it, was scarlet fever of a peculiarly malignant type
(Richardson); but, as will be seen from the following extracts from
Thucydides, the plague differed in important particulars from
scarlatina of the present time: "Internally, the throat and the tongue
were quickly suffused with blood, and the breath became unnatural and
fetid. There followed sneezing and hoarseness; in a short time the
disorder, accompanied by a violent cough, reached the chest.... The
body externally was not so very hot to the touch, nor yet pale: it was
of a livid color, inclining to red, and breaking out in pustules and
ulcers." Loss of sight and gangrene of the extremities were common
results in those who recovered, and adults appear to have been
affected as frequently as children. "The dead lay as they had died,
one upon another, while others, hardly alive, wallowed in the streets
and crawled about every fountain craving for water. The temples in
which they lodged were full of the corpses of those who died in them."
Lucretius says of this plague, "If any one for a time escaped death
(as was possible, either by reason of the foul ulcers breaking or by
means of a black discharge from the intestines), yet consumption and
destruction awaited him at last; or, as was often the case, an
excessive flux of corrupt blood, attended with violent pains in the
head, issued from the obstructed nostrils, and by this outlet the
whole strength and substance of the man passed away. He, moreover, who
had escaped this violent flux of foul blood was not certain wholly to
recover, for still the disease was ready to pass into his nerves and
joints, and into the very genital organs of the body. And of those who
suffered thus, some, fearing the gates of death, continued to live,
though deprived by the steel of the virile part, and some, though
without hands and feet, and though they lost their eyes, yet persisted
to remain in life, so strong a dread of death had taken possession of
them. Upon some, too, came forgetfulness of all things, so that they
knew not even themselves."
Gangrene of the extremities, loss of sight, a violent cough, loss of
memory, etc. are not symptoms of scarlet fever, so that in my opinion
{487} the plague of Athens, if correctly described by the historian,
was a different malady.
Caspar Morris, in his essay on scarlet fever, states his belief that
Seneca, who lived in the first century of the Christian era, described
an epidemic of the malignant form of scarlatina in his portrayal of
the pestilence that visited Thebes during the half-mythical age of
Oedipus, six centuries before Christ. Seneca's description of the
symptoms of this plague is as follows:
Piger ignavos
Alligat artus languor, et aegro
Rubor in vultu, maculaeque caput
Sparsere leves; tum vapor ipsam
Corporis arcem flammeus urit
Multoque genus sanguine tendit
Oculique regent, et sacer ignis
Pascitur artus. Resonant aures,
Stillatque niger naris aducae
Cruor; at venas rumpit hiantes.
Languor, redness of the face, light spots upon the head, distension of
the cheeks with blood, distortion of the eyes, a flushed appearance of
the limbs, tinnitus aurium, and a discharge of black blood from the
nostrils, certainly indicated a very malignant form of disease, but to
believe that it was identical with the scarlet fever of the present
time requires considerable credulity. From the fact that it devastated
Thebes we infer that it occurred largely among adults, differing,
therefore, from the modern scarlet fever, whose victims are chiefly
children. The same uncertainty hangs over epidemics during the first
centuries of the Christian era.
The first clear and undoubted portrayal of scarlet fever is found in
the medical literature of the sixteenth century. Sydenham and his
contemporaries in the seventeenth century witnessed epidemics of it,
studied its nature more thoroughly, and consequently acquired a more
accurate knowledge of it than that possessed by their predecessors. It
was in this century that measles and scarlet fever were
differentiated. During the last two hundred years scarlatina has been
the subject of monographs too numerous to mention. It has long been
regarded as one of the most important maladies of childhood, on
account of its frequency and the great mortality that attends it, so
that numerous cases and many epidemics are every year related in the
medical journals. By this vast accumulation of observations and the
patient and thorough use of the microscope our knowledge of scarlet
fever has become full and accurate.
As with most of the infectious maladies, scarlet fever extended to the
Western World through European shipping. It was brought to North
America about the year 1735. Tardily it spread to South America, where
it appeared in 1829, and more recently it has been established in
Australia. It entered Iceland in 1827, and Greenland in 1847.
ETIOLOGY.--The evidence is strong that scarlet fever does not
originate de novo--that it does not spring from certain atmospheric or
telluric conditions, but is produced by a definite specific principle,
since countries have been free from it for centuries till it was
imported by commerce. That it appears in certain localities without
any known exposure is attributed to the fact that the poison is so
subtle and transmissible that it is {488} conveyed long distances in
articles of merchandise, even in small packages, so that those who
chance to open them or come in contact with them are infected. It is
believed that reading matter transmitted through the mails has in many
instances been the medium of infection.
The theory that the acute infectious maladies are caused by
micro-organisms, or, as they are now designated, microbes, commonly
discarded at first and believed to be chimerical, is rapidly gaining
ground in the profession, and appears to be fully established as
regards certain of them. These parasites, barely visible under high
powers of the microscope, and ascertained to be vegetable by their
behavior under certain chemical agents, exist in immense numbers in
the blood, tissues, and secretions of patients suffering from the
infectious maladies, especially in the graver cases of them; and the
microscope shows that these organisms vary in shape and appearance so
as to admit of classification.
The germ theory has now become so important that it cannot be ignored
in a monograph relating to so important an infectious malady as
scarlet fever. The relation of microbes to the infectious diseases has
been made the subject of investigation by Pasteur, Toussaint, and
others in France, and by many in Germany, with most interesting
results. The belief held by many, and which seemed very plausible, was
that the microbes, instead of sustaining a causative relation to the
maladies in which they occur, were the result of these maladies--that
they sprang into existence in consequence of the vitiated state of the
blood and tissues, just as fungi appear on decaying substances or as
the Oidium albicans appears in certain morbid conditions of the buccal
surface and secretions. Obviously, in order to elucidate this matter
and determine the relation of these parasites to the diseases in which
they occur, it was necessary to experiment on animals, but,
unfortunately, as a bar to successful experimentation many of the most
important infectious maladies which afflict the human race, as typhus
and typhoid fevers, the marsh fevers, and syphilis, do not occur in
animals, or they occur in a changed and mitigated form. Others,
however, can be produced in their typical character in animals, as
diphtheria, and others still originate in animals and are transmitted
from them to man, as anthrax or splenic fever of the herbivora and
hydrophobia. Very interesting and important results have been produced
by experimental researches with the microbes of certain of these
diseases, which, if applicable to the common and fatal infectious
maladies of an analogous nature in man, may yet result in immense
benefit in mitigating the virulence of those affections which are the
scourge of childhood and which sensibly diminish the increase of
population. It has been found possible to cultivate the microbes
contained in the blood, tissues, and secretions in certain of the
infectious diseases, and after a series of cultivations, so that these
organisms are far removed from the animal substance which contained
them, and with which they were so intimately associated in the
individual, they have been employed for inoculation--with this
important result, that the primary disease was reproduced. This seems
to indicate beyond question the causative relation of these parasites
to the diseases in which they occur. Experiments with the result which
I have stated have been made with the microbes of splenic fever,
chicken cholera, murrain, and certain other maladies.
Pasteur employs as the media for cultivation--(1st) urine neutralized
{489} by a few drops of potash solution; (2d) a liquid prepared by
boiling for twenty or thirty minutes the yeast of beer in water,
neutralizing, and filtering; and (3d) chicken tea, prepared by boiling
equal parts of water and the lean of muscles a quarter of an hour,
filtering, and neutralizing. A small drop of infected blood is placed
in the liquid of cultivation, and the microbes which it contains
multiply so abundantly that the liquid becomes turbid in a short time,
and they are found in all parts of it. A drop of this liquid is added
to another portion of the medium, and this also soon becomes turbid
from the immense development of organisms which have the same
microscopic appearance and character as those in the drop of blood.
The process is repeated many times, until the microbes are far removed
from their original source in the blood and tissues, and a drop of the
last cultivation, whether it be the fiftieth or the hundredth, is
inserted under the skin of a healthy animal selected for the
experiment. If it be true, as stated by the experimenters, that the
original disease is thus reproduced with the microbes of at least
three or four distinct maladies, this age is distinguished by one of
the most important discoveries ever made in pathological studies. It
remains to determine whether this great discovery is of general
applicability to the infectious diseases with which man is afflicted.
If so, it is not improbable that we are on the eve of finding a method
by which some at least of these maladies may be prevented or
mitigated, as small-pox has been since the time of Jenner. The result
of experiments made by Pasteur with the microbes of that fatal malady
of the herbivora, known under the various names of splenic fever,
anthrax, wool-sorter's disease, and charbon, encourages this belief.
Originating among the herbivorous animals, it has in many instances
been contracted by individuals who have rapidly perished. Many engaged
in assorting alpaca and mohair have lost their lives by it, some with
all the symptoms of profound blood-poisoning, without external
lesions, and others with redness and swelling at some point of
infection where a sore or abrasion existed, but with speedy
blood-contamination.
The microbe of this malady, the Bacillus anthracis, occurs in the form
of straight filaments with little movement or only with oscillation,
and producing bright-shining spores. Now comes a very interesting and
important result of experimentation: Pasteur states if several days
elapse between the cultivations the virulence of the parasite
diminishes, so that he has been able to produce by inoculation with it
a mild and never fatal form of charbon, which affords immunity in the
animal from any subsequent attack. This opinion was sustained by a
trial experiment on sixty sheep. Toussaint and Chauveau claim that
they produce a similar attenuation of the virus by defibrinating
infected blood, heating it to 55 degrees C. (131 degrees F.) and
filtering it. These experiments awaken the hope that the time will
come when the acute infectious maladies in man, scarlet fever among
others, will be rendered less virulent. That one of them--to wit,
small-pox--has for nearly a century been under our control certainly
encourages the belief that there is some way to mitigate others of the
same class which are equally fatal if not so loathsome.
As yet, observers do not agree in regard to the parasite which is
supposed to sustain a causative relation to scarlet fever. Klebs
states that it is highly probable that both measles and scarlet fever
are produced by {490} micrococci, and he has sketched the design and
described the development of a microbe which he designates the Monas
scarlatinosum.
The _London Medical Times and Gazette_ for Jan. 28, 1882, contains an
account of the supposed discovery of the scarlatinous microbe by
Eklund of Stockholm, an authority in the microscopic examination of
parasites. He says that scarlet fever is rarely absent from the
Swedish capital and from the barracks and dwellings on the isle of
Skeppsholm. In the urine of scarlatinous patients he has constantly
found a prodigious number of discoid corpuscles, oval or round, their
diameter being less than 1/1000 millimetre and from 1/30 to 1/10 that
of a red blood-cell. They are colorless or yellowish white, surrounded
by a distinct cell-wall, each containing a well-defined nucleus of a
deeper hue. Sometimes one or more microbi may be seen. They exhibit
rotatory or oscillatory movements, especially observed when a drop of
water is added to the fluid. They multiply, as he has frequently seen,
by fission--first in the microbes, next in the nucleus, and lastly in
the cell-wall. He cannot say whether they develop into a mycelium. At
any rate, the development of fine filaments seems to be exceptional.
He has never seen them adhere in moniliform chains nor massed as
zooglaea. He considers them to be veritable schizomycetes, and
proposes the name Plox scindens.
Eklund asserts that he has found these same organisms in vast numbers
in the soil- and ground-water of the isle of Skeppsholm, in the mud of
the trenches dug for the water-mains, and in the greenish mould upon
the walls of the old barracks, where scarlet fever was most rife. He
states that scarlet fever has occurred in children after drinking milk
mixed with the ground-water of the island, and he observed a case
which followed immersion in one of the trenches of the island and the
drying of the clothes in a small room. In another instance scarlet
fever broke out in a block immediately after exposure of the
ground-water by excavations.
It is evident that the discovery of this microbe under such
circumstances does not prove that it is the cause of the disease. This
can only be determined by inoculation, or by experiments which furnish
the conditions of scientific exactness. Although great progress has
been made in parasitology during the last decade, it is evident that
several years of observation and experimentation must elapse before it
is clearly and definitely ascertained whether or to what extent
microbes cause scarlet fever and the other exanthematic fevers with
which it is classified.
Whether the specific principle of scarlet fever be a micro-organism or
a chemical substance, its mode of action and effects have been
ascertained by clinical observations. Without doubt it commonly enters
the system by the breath, but it may enter in the ingesta, and it
infects the blood. That it resides in the blood has been ascertained
by inoculation with this liquid, by which scarlet fever has been
reproduced in its typical form. From the blood it enters the tissues
and secretions. Hence handkerchiefs or linen containing the saliva or
mucus of a patient, the epidermic scales shed abundantly in the
desquamative period, and probably also the urinary and fecal
evacuations, contain the poison, so as to be highly infectious. Even
the discharge of a scarlatinous otorrhoea is thought by some to be
contagious for a considerable time.
Scarlatina is communicable not only by direct exposure to a patient,
{491} but also by exposure to objects which happen to be in his room
during his illness, and to which the poison becomes attached, such as
clothing, books, and toys; small packages, even letters, it is
believed, from cases which have occurred, sometimes convey and
disseminate the contagious principle.
In England observations have been made which show that scarlatina has
been communicated by infected milk. The disease occurred in the family
of a milkman, and the milk, before it was distributed, remained for a
time in a kitchen which had been occupied by the patients. This milk
was taken by twelve families, and in six of these the disease occurred
almost simultaneously at a time when few cases were occurring in the
locality. There had been no direct exposure to the carrier of the milk
nor to members of the affected family (Taylor). In another instance a
woman and her son had scarlet fever while they were serving milk to
several families, and the disease appeared in all these families
except one, which consisted of old people (Bell). It is known that
milk absorbs volatile substances so as to be flavored by them, as is
shown in the experiment of placing it in an open vessel in a box with
a pineapple; and it may in a similar manner become infected by the
specific principle of scarlet fever, or it may be infected by detached
particles of epidermis; which is not improbable when one convalescing
from scarlet fever is allowed to milk the cows or prepare the milk for
distribution.
The scarlatinous virus surpasses that of any other eruptive fever
except small-pox in its tenacious attachment to objects and its
portability to distant localities. Hence in the literature of the
disease are the records of many cases in which the poison was conveyed
long distances, retaining its virulence to the full extent and causing
an outbreak of the malady in the localities to which it was carried.
In New York, so frequently has scarlet fever as well as measles and
diphtheria been contracted from the persons or clothing of well
children who come from infected houses, that the Health Board now
excludes from the public schools all children who come from such
houses, even though they live on separate floors from those occupied
by the sick. In one instance that came under my notice a washerwoman
whose child had scarlet fever communicated the disease to an infant in
the household where she was employed, by placing her shawl over the
cradle in which it was lying. A physician of my acquaintance went from
a scarlet-fever patient to a family several streets distant, and took
one of their children upon his lap. After the usual incubative period
this child sickened with a fatal form of the malady, and the remaining
children of the household were in time affected. In New York scarlet
fever has seemed to me to be not infrequently communicated through
school-books, which, profusely illustrated by pictures and rendered
attractive to the young, are often allowed to lie upon the bed of a
scarlatinous patient and be handled by him during convalescence, or
even during the course of the fever if it be mild. The young librarian
of the circulating library of a Sunday-school, whose pupils came
largely from the tenement-houses, was occupied a considerable part of
a day in covering and arranging the books. After about the usual
incubative period of scarlet fever he sickened with the disease. His
two sisters were immediately removed to a rural township three hundred
miles away, and to an isolated house where scarlatina had never
occurred. About one {492} month after his recovery, and after his room
had been disinfected by burning sulphur and his bed-clothes and linen
had been thoroughly washed, and all articles suspected to hold the
poison had been either disinfected or destroyed, the brother visited
his sisters in the country. Three weeks subsequently to his arrival
one of these sisters sickened with scarlet fever, and a week later the
other also. It seems that the exposure must have occurred several days
after his arrival in the country from some book or other infected
article in his possession. About two months elapsed after the last
case; the family had returned to the city, the infected room in the
country-house had been thoroughly fumigated by burning sulphur from
morning till evening, when a little girl from an inland city remained
a few days in this house, and probably often entered the room where
the young ladies had been sick. In a few days she also sickened with a
fatal form of scarlatina. Such histories and experiences are not
infrequent. They are common during epidemics of scarlet fever. They
indicate an extraordinary attachment of the scarlatinous poison to
objects, and show that it is not gaseous nor readily volatilized.
A striking example of this fixity of the poison occurred in the
practice of the late Kearney Rogers, formerly a prominent and much
esteemed surgeon of New York City. Six children in a family had
scarlet fever. Three and a half months subsequently another child,
living at a distance, was allowed to return home and occupy the
apartment in which the sickness had occurred. One week subsequently to
the date of the return this child sickened with the same malady.
Elliotson states that a patient with scarlet fever was admitted into
one of the wards of St. Thomas's Hospital, and for two years
subsequently young persons who were admitted into the ward were apt to
take the disease. Richardson of London relates the following
experiences of a family whom he attended in a rural district: "At a
short distance from one of our villages there was situated on a slight
eminence a small clump of laborers' cottages, with the thatch peering
down on the beds of the sleepers. A man and his wife lived in one of
these cottages with four lovely children. The poison of scarlet fever
entered the poor man's door, and at once struck down one of the
flock." The remaining children were now removed some miles away, and
after several weeks one of them was allowed to return. Within
twenty-four hours it also took the disease, and quickly died. The
walls of the cottage were now thoroughly cleaned and whitewashed, the
floors scoured, and all the wearing apparel either destroyed or
washed. Four months elapsed after the last sickness when one of the
remaining children returned. "He reached his father's cottage early in
the morning; he seemed dull the next day, and at midnight I was sent
for, to find him also the subject of scarlet fever. The disease again
assumed the malignant type, and this child died." Richardson believes
that the contagium was attached to the thatch, which could not be
thoroughly disinfected. The fact of this remarkable long-continued
attachment of the poison to objects, indicating by this fixity that it
is a solid, is consonant with the theory that it is an organism.
INCUBATIVE PERIOD.--The duration of the incubative period varies in
different cases. It is sometimes less than twenty-four hours, as in
{493} the above case reported by Richardson; in the following
well-known case, observed by Trousseau, it was one day. A girl arrived
in Paris from Pau, where there was no scarlet fever, and occupied the
same apartment with her sister, who was sick with this disease.
Twenty-four hours after her arrival she also was attacked with the
same malady.
Russeberger attended a child who was exposed at noon to scarlet fever,
and took the disease on the following night. B. W. Richardson
(_Clinical Essays_, 1861, vol. i. p. 94) gives his own experience: He
had applied his ear to the chest of a patient suffering from scarlet
fever, and was conscious of a peculiar odor emitted from the patient.
He was immediately nauseated and chilly, and from that moment he dated
the beginning of an attack of scarlet fever. In the _Transactions_ of
the Clinical Society of London, vol. xi. 1878, the late Charles
Murchison gives the statistics of 75 cases, showing the incubative
period, as follows:
In 4 cases it was not more than 24 hours.
" 2 " " " " 30 "
" 3 " " " " 36 "
" 4 " " " " 40 "
" 1 " " " " 41 "
" 4 " " " " 58 "
" 1 " " " " 54 "
" 1 " " " " 2-1/2 days.
" 31 " " within (time not accurately ascertained) 4 days.
" 2 " the incubation did not exceed 4-1/2 days.
" 17 " " " " " 5 "
" 2 " " " " " 6 "
In three cases Murchison believes that the incubation was precisely
fixed at thirty-six hours, three days, and four and a half days.
Watson says that a man reached Devonshire on mid-day to see his
daughter, who had scarlet fever. Two days later he was also attacked.
Rehn saw a child who was attacked two days after its grandmother
returned from a case of scarlet fever; and Zengerle, a girl of ten
years, residing at Wangen, where there was no scarlet fever, who took
the disease two days after her mother had returned from visiting a
family affected with it. Loochner states that a boy aged four and a
half years was attacked one and a half days after admission into the
infected wards of a hospital. Armistead, in his annual report on the
health of the Newmarket rural district, states that three children,
coming from a different part of the district, visited Westley, and
stayed next door to a child who had scarlet fever six weeks
previously, and who was allowed to play with these children on the
evening of Aug. 13th and morning of the 14th. The family then returned
home, and on the 18th, four days after the exposure, all three
children sickened with scarlet fever (_Brit Med. Jour._, Sept. 30,
1882).
Ordinarily, therefore, the incubative period, though varying in
different cases, is within six days. Many cases, however, occur in
which it seems to be longer. Thus in my practice scarlet fever
appeared in a family on April 26, 1882. The patient was immediately
removed to the third floor and the other children to the basement. All
communication between the infected room and the basement was
forbidden, but on May 8th, twelve days after the separation, one of
these children sickened with the disease. {494} Many observers--among
whom may be mentioned Niemeyer and Copland--believe that the
incubative period may be longer than one week, but, on account of the
subtlety of the poison and the many modes of transmission, it is
possible that in the instances of an apparently long incubative period
there were other and unsuspected exposures. When scarlet fever has
been communicated by inoculation, as in the experiments of Rostan and
others, the incubative period has been about seven days, but Gerhardt
states that a man was attacked four days after an abscess was opened
by a knife used upon a scarlatinous patient. This variation in the
incubative period, which also occurs in some other infectious
diseases, as diphtheria, is probably due mostly to individual
differences, some being more susceptible than others; but it may be
due partly to those obscure meteorological conditions which we
designate the epidemic influence. Probably, as a rule, when the
disease is quickly developed after exposure, the attack is more severe
than when several days elapse.
CONTAGIOUSNESS.--The area of the contagiousness of scarlet fever is
small. It apparently embraces only a few feet. Therefore, close
proximity is the necessary condition of its propagation. Hence many
who are exposed, particularly of those who are remotely exposed, do
not contract the disease. There is also an idiosyncrasy in some
children, so that they resist infection even when repeatedly and
closely exposed. In the _New York Medical Record_ for March 23, 1878,
C. E. Billington states that of 90 children in 26 families who were
exposed to scarlet fever, 43 contracted the disease and 47 escaped;
whereas, as is well known, comparatively few unprotected children
escape pertussis, variola, varicella, or measles if exposed to either
of these diseases. By strict isolation, therefore, the spread of
scarlet fever is more easily prevented than that of most other acute
infectious maladies. In the New York Foundling Asylum for a number of
years children with scarlet fever were isolated in a small room
attached to one of the wards. The door between the two rooms was
closed, and not opened during the continuance of the sickness.
Entrance into the small room was through another door, and a nurse was
assigned to the scarlet-fever cases, with strict directions that she
should not mingle with the other children. These simple precautions
were found sufficient in the various epidemics of scarlet fever which
occurred in the city to prevent the spread of the malady through this
institution; whereas, similar measures were much less effectual in
arresting the spread of measles and pertussis. Consequently, an
outbreak of scarlet fever in this institution was usually limited to a
few cases, while the extension of measles and pertussis was arrested
with difficulty till a more efficient quarantine was established.
VARIATIONS IN TYPE.--The type of scarlet fever varies greatly in
different epidemics, and frequently also in cases which occur in the
same epidemic, even in the same family. One child may have scarlatina
so mildly that little treatment is required and convalescence soon
begins, while another has the malignant form, and soon succumbs,
notwithstanding the prompt employment of the most efficient and
appropriate measures. Ordinarily, however, if the first case in a
family be very severe, subsequent cases will present a similar type;
but there are notable exceptions. This variation in type in different
years and different epidemics is probably not equalled in any other
infectious malady. Consecutive {495} epidemics may present this
variation, or the same type may continue for a series of years, and
then, from some unknown cause, change to one milder or more severe. In
England, during Sydenham's life, scarlet fever was so mild that he
regarded it as a trivial affection, requiring little attention, like
rotheln of the present time, but after the death of Sydenham, Morton
and his contemporaries in London found, to their sorrow, that the type
of scarlet fever was very different from that described by Sydenham's
pen. The late Graves of Dublin and his contemporaries treated a mild
type of scarlet fever with a very small percentage of deaths--much
less than that during the preceding generation--and they attributed
their success to their greater knowledge and more appropriate use of
remedies than their ancestors possessed and employed. By and by the
type changed, the mortality of former years was restored, and they
discovered that their previous success in saving life had been due not
to their skill, but to the mild form of the malady. A distinguished
physician of New York treated more than fifty cases of scarlet fever
in one of the institutions without a single death. A few months
afterward the type of the malady changed, and his own son perished
from it.
SURGICAL AND OBSTETRICAL SCARLATINA.--After surgical operations, and
sometimes in surgical cases not requiring operative measures, a
scarlatinous efflorescence occasionally appears upon the whole or
nearly the whole body, and remains for several days. The following
were cases of the kind alluded to. They occurred in Guy's Hospital,
and were published by H. G. Howse in _Guy's Hospital Reports_ for
1879: On March 15, 1878, Jacobson performed osteotomy upon a child
suffering from extreme rachitis. The operation was followed by a
moderate febrile movement (100 degrees to 101 degrees), and after
three days by the appearance of an efflorescence, with sore throat and
the strawberry tongue. The osteotomy had been performed under carbolic
acid spray and with all the details of antiseptic surgery. The rash
soon faded, the temperature fell, and the child, temporarily separated
from the other patients from the suspicion that the disease was
scarlet fever, was brought back to the ward. The subsequent history
confirmed the diagnosis of scarlet fever, for the skin desquamated,
and on April 1st abundant albumen was found in the urine. The case
terminated favorably. Three months previously the same operation had
been performed on the other leg, with no unfavorable symptoms. On
April 5th, three weeks after the osteotomy, a lipoma was removed from
another patient aged twenty-one years. The following day the
temperature rose to 101 degrees, and remained at that till April 8th,
when it suddenly increased to 103 degrees, and a rose-rash occurred
over the body, with sore throat. On April 9th, Howse excised the
elbow-joint of a girl of sixteen years having pulpy disease. On the
10th her temperature began to increase, and on the 11th reached 105.8
degrees. Toward evening a roseoloid eruption appeared over her body,
and she was isolated. On April 12th, Dr. H. excised a fibroid bursa
patellae from a woman of twenty-nine years. On the following day her
temperature was 99 degrees, but on the 14th it rose to 100 degrees,
and on the evening of the 15th she had rigors and headache. On the
morning of the 16th the temperature was 102.5 degrees, and a roseoloid
eruption occurred over the face and chest. The surgeons now perceived
that an epidemic of the so-called surgical scarlatina was occurring,
so as to justify the postponement of other operations.
{496} In the same volume of _Guy's Hospital Reports_, James F.
Goodhart gives the histories of nearly thirty cases of this disease
occurring during a series of years in the same hospital. The patients
were chiefly children, having the most diverse surgical ailments,
among which may be mentioned hip disease and abscess, genu valgum
without operation, necrosis of femur, hydrocele with explorative
operation, a scald, a sinus over the great trochanter, spinal disease
with abscess, tenotomy for club-foot, and vesical calculus with
operation. The most common disease was caries or necrosis with
abscess. In cases operated on the intervals between the operations and
the occurrence of the efflorescence varied from two days to more than
two weeks. Goodhart, after a careful examination of these cases, came
to the conclusion that they were for the most part examples of true
scarlet fever, especially as a considerable proportion of them
occurred in groups, and there was a known exposure of some of the
patients to children admitted into the hospital with the sequelae of
scarlet fever.
In the _British Med. Jour._ for Jan., 1879, George May, Jr., reported
a case of efflorescence in surgical practice which appears to have
been scarlatinous. A child was operated on for the radical cure of
hernia on Dec. 4th. Toward the close of the same day he became
restless, vomited, and his pulse on the following day rose to 136.
Forty-eight hours after the operation a rash appeared on the chest and
arms, the abdomen became tense and painful, and on the following day
he died. The poison, however, in this case may have been septic.
Hillier remarks (_Diseases of Children_): "In the hospital for sick
children, of the children who contract scarlatina a very large
proportion have been the subjects of a surgical operation within a
week before the rash appears." Gee says (Reynolds's _System of
Medicine_): "It has been doubted by some whether the scarlatiniform
rash which sometimes follows operations is really scarlatinal. The
eruption appears from the second to the sixth day after the operation,
and in the cases which have caused the doubt is very fugitive and the
first and only symptom. Yet that the disease really is scarlet fever
would seem to be proved by the following observations: first, that the
disease occurs in epidemics; secondly, that in a given epidemic a
severe case occasionally relieves the monotonous recurrence of the
very mild form; thirdly, that a precisely similar scarlatinilla
attacks in the same epidemic patients who have not been subjected to
operation and who have no open sore; and lastly, by way of a veritable
experimentum crucis, that, however freely these patients are exposed
to ordinary scarlet fever contagion afterward, they do not contract
that disease." Paget and other distinguished London surgeons who have
observed this complication of surgical cases, believe that the
patients have been previously exposed to the scarlatinous poison, and
that the surgical diseases or operations furnish favorable conditions
for the occurrence of scarlet fever, so that the exposure, which
probably would have been without result in ordinary health, causes an
outbreak of the malady.
Those who have reported cases of this form of efflorescence have for
the most part neglected to state whether the patients had had scarlet
fever previously, knowledge of which would have aided in the
diagnosis; but from an examination of the histories of cases,
especially those {497} published in the London journals in the last
four or five years, there can, I think, be little doubt that surgical
maladies of a certain kind, especially traumatism, do produce a state
of system which predisposes to scarlet fever, so that this class of
patients are especially liable to contract it. Therefore, in my
opinion, a considerable proportion of reported cases of surgical
scarlatina are genuine, but in a considerable number, perhaps an equal
number of such cases, the histories and symptoms indicated a septic
rather than scarlatinous efflorescence, and in not a few instances,
when consultations have been held, opinions differed, some
diagnosticating scarlet fever, others septicaemia. In some of the
cases I find it stated that the fauces presented the normal
appearance. Now, faucial redness is so generally present in scarlet
fever, antedating that of the skin and coexisting with it, that its
absence is strong evidence that the disease is not scarlatinous.
Moreover, when, as was true of certain of the reported cases, the rash
appeared irregularly upon the surface, and faded away in two or three
days with the abatement of the fever, and the conditions for septic
absorption were present, the efflorescence was probably septicaemic.
The following were apparently cases of septicaemia efflorescence: A
child aged five years (_Brit. Med. Jour._, Feb. 15, 1879) had
inflammation of the lymphatic glands in the groin, which suppurated.
At the time when the abscess was fully formed a rash appeared over the
entire body. It consisted of numerous red points, but was paler than
that of ordinary scarlet fever; temperature never above 99 degrees; no
sore throat nor desquamation of cuticle. No child exposed to her took
scarlet fever, and her sickness could not be traced to infection. In
the _British Med. Jour._, Jan. 4, 1879, L. Braxton Hicks states that
his son, attending school at Reading, was seized with a severe attack
of pyrexia, accompanied on the second day by delirium and the
occurrence of a rash like scarlet fever over the entire surface. He
had no decided redness of the fauces, though it was perhaps slightly
flushed. The right buttock was swollen from inflammation, and a large,
deep-seated abscess formed near the tuberosity of the ischium. When
the delirium abated the boy said that he was standing the day before
the fever began with his legs far apart, when a schoolfellow stretched
them farther by suddenly pulling on one of them. The rash, which was
nearly universal, lasted three days, and was not followed by
desquamation. No case of scarlet fever occurred in the school before
or afterward. In the same volume of the _British Medical Journal_,
Surgeon Frolliott of the East India Service relates the case of a
private, aged twenty-three years, and three years in India, who, when
on duty in the Punjab, was injured by the explosion of an Afghan
powder-magazine. The accident occurred Dec. 21, 1878. On Dec. 25th a
bright scarlet rash appeared upon the abdomen and spread over the
entire body. The following day the eruption was very vivid, like a
boiled lobster, and it lasted five days. The temperature, which in the
beginning had been 101 degrees, abated to the normal after the rash
appeared. No soreness of throat nor redness of the buccal surface
occurred, but the epidermis desquamated even from the palms of the
hands and soles of the feet. Now, the febrile movement of scarlet
fever does not cease while the efflorescence is distinct. It does not
even diminish when the eruption appears, while in the above case it
fell to the normal--a common {498} occurrence in septicaemia, even
when the blood-poisoning is profound. Moreover, scarlet fever is so
rare in India that Frolliott, after twelve years' service, had only
heard of one case among Europeans and natives. The surgeons who
consulted over the case of this private disagreed in opinion, some
regarding the disease as septicaemic, others as scarlatinous. But a
better knowledge of the clinical history of scarlet fever on the part
of these army surgeons would, I think, have removed all doubt as to
the diagnosis.
It is the opinion of some reputable surgeons that the exposure of
traumatic patients to the scarlatinous poison sometimes aggravates the
inflammation of wounds, causing them to assume an unhealthy appearance
even though no scarlatina be produced. The late Solly made the remark,
"Whenever a case of surgery in private practice takes on a highly
phlegmonous appearance I am always sure to find break out, in the
inmates of the house, either erysipelas or scarlet fever" (_British
Med. Jour._, Feb. 15, 1879). We will see that the scarlatinous poison
sometimes causes pharyngitis or nephritis without producing the
general disease. In a similar manner it seems that it may aggravate
open wounds, intensifying the inflammation in them, while there is no
efflorescence or other symptom to show that scarlatina itself is
present. The poison appears to act entirely locally in such cases.
Paget, in his _Clinical Lectures_, says: "I think it not improbable
that in some cases results occurring with obscure symptoms within two
or three days after operations have been due to the scarlet-fever
poison, hindered in some way from its usual progress." Playfair, in
his remarks on the puerperal state, adds: "Mr. Spencer Wells informs
me that he has seen cases of surgical pyaemia which he had reason to
believe originated in the scarlatinal poison; and his well-known
success as an ovariotomist is no doubt, in a great measure, to be
attributed to his extreme care in seeing that no one likely to come in
contact with his patients has been exposed to any such source of
infection." Opinions like these, held by such prominent members of the
profession and sustained by many observations, should certainly induce
physicians to prevent, so far as possible, any exposure of their
surgical patients, especially if they have any sores or wounds,
whether by traumatism or the scalpel, to the scarlatinal poison.
OBSTETRICAL SCARLATINA.--Women during convalescence after childbirth
are very liable to contract scarlet fever. In the New York Infant
Asylum, which has maternity wards, a woman was admitted from a house
in which scarlet fever was prevailing, and assigned to a cot next that
occupied by one of the waiting women, who was confined soon afterward.
Her labor was favorable, but three days afterward she took scarlet
fever, and another lying-in-patient contracted it from her. The sore
throat and desquamation were characteristic. It has come to my
knowledge that a physician of New York, in whose family scarlet fever
was occurring, attended three women in succession in their
confinement, and all contracted scarlet fever, which presented the
characteristic symptoms, and two of them died. Experienced and
cautious physicians of New York, aware of the danger, do not go
directly from a scarlatinous patient to an obstetrical case, but avoid
the risk by intermediate visits to other patients or by remaining for
a time in the open air.
{499} Playfair, remarking on this subject, says: "There is good reason
to believe that the contagium of zymotic diseases may produce a form
of disease indistinguishable from ordinary puerperal septicaemia, and
presenting none of the characteristic features of the specific
complaint from which the contagium was derived. This is admitted to be
a fact by the majority of our most eminent British obstetricians,
although it does not seem to be allowed by continental authorities,
and it is strongly controverted by some writers in this country. It is
certainly difficult to reconcile this with the theory of septicaemia,
and we are not in a position to give a satisfactory explanation of it.
I believe, however, that the evidence in favor of the possibility of
puerperal septicaemia originating in this way is too strong to be
assailable. The scarlatinal poison is that regarding which the
greatest number of observations has been made. Numerous cases of this
kind are to be found scattered through our obstetric literature, but
the largest number are to be met with in a paper by Braxton Hicks. Out
of 68 cases of puerperal disease seen in consultation, no less than 37
were distinctly traceable to the scarlatinal poison. Of these, 20 had
the characteristic rash of the disease, but the remaining 17, although
the history clearly proved exposure to the contagium of scarlet fever,
showed none of its usual symptoms, and were not to be distinguished
from ordinary typical cases of the so-called puerperal fever. On the
theory that it is impossible for the specific contagious diseases to
be modified by the puerperal state, we have to admit that one
physician met with 17 cases of puerperal septicaemia in which, by a
mere coincidence, the contagion of scarlet fever had been traced, and
that the disease nevertheless originated from some other source--a
hypothesis so improbable that its mere mention carries its own
refutation."
Parturition, like traumatism, furnishes in an eminent degree the
conditions in which septic poisoning occurs, and the efflorescence
which often accompanies septicaemia bears, as we have seen, a very
close resemblance to that of scarlet fever. Hence in many instances
the same difficulty is present in making a differential diagnosis
between septic and scarlatinous blood-poisoning in obstetrical cases
which occurs in surgical practice. But, according to my observations,
an efflorescence occurring during the week following parturition is in
most instances septic. It is only in exceptional cases that it is
scarlatinous, and there is little danger that the accoucheur, engaged
in general practice and visiting scarlatinous patients, will
communicate scarlet fever through his person or clothing if he
exercise proper precautions. His short stay in the sick room and his
out-door exercise in visiting cases prevent infection of his person or
dress. But if, as Playfair believes, the scarlatinal poison sometimes
produces in parturient women a puerperal fever in which the
characteristic scarlatinal symptoms are lacking, and which, in the
present state of our knowledge, is not distinguishable from ordinary
septic fever, certainly the scarlatinous virus sustains a much more
frequent causative relation to childbed fever than has been heretofore
supposed.
Infants under the age of six months do not ordinarily contract scarlet
fever, although fully exposed, and those under four months nearly
possess immunity. Still, this disease has been observed in new-born
infants, contracted, apparently, through the placental circulation.
{500} Tourtual states that a woman waited upon her own husband and
child, both of whom had scarlet fever, during the eighth and ninth
months of her pregnancy, till near her confinement. Though she had no
symptoms of scarlet fever, her infant had unusual redness of the skin
and buccal surface and difficulty of swallowing up to the fifth day.
On the ninth day desquamation began, and at a later stage the nails of
the fingers and toes separated. A case having a history in some
respects similar is related by Megnert, but the symptoms were
anomalous for scarlet fever, and the disease may have been ordinary
septic fever. On the other hand, in one instance in my practice a
mother had scarlet fever, beginning about the third day after her
confinement, and although she suckled her infant and it was constantly
in bed with her, it had no symptoms of scarlet fever, although it
became affected immediately afterward by a severe form of eczema,
probably from the altered quality of the milk; and in two instances
observed by Murchison new-born infants remained healthy, although
their mothers suffered from scarlet fever.
After the age of six months the liability to scarlet fever increases
till the close of infancy, children between the ages of six months and
one year being less liable to contract the malady than during the
second year, and those in the second year being less liable to it than
those in the third year. Murchison collected the statistics of deaths
from scarlet fever in England and Wales during a series of years
ending with 1861. The number of deaths aggregated 148,829, and the
percentage of deaths at different ages was as follows:
Deaths under 1 year, 6.7 per cent.
" between 1 and 2 years, 14.09 " "
" " 2 " 3 " 16.00 " "
" " 3 " 4 " 15.13 " "
" " 4 " 5 " 11.9 " "
" " 5 " 10 " 25.9 " "
" " 10 " 15 " 5.8 " "
" " 15 " 25 " 2.6 " "
" " 25 " 35 " 0.8 " "
" over age of 35 years, 0.8 " "
Among the deaths were ten cases above the age of eighty-five years, so
that scarlet fever, though especially a disease of childhood, may
occur in any decade of life; but old age, like early infancy, almost
possesses immunity from it.
I have preserved the records of the ages of 145 consecutive cases
occurring in private practice. If we add to these 58 cases observed by
Prof. Octerlony (_Amer. Jour. of Med. Sci._, July, 1882) we have the
statistics of the ages of 203 cases, which are embraced in the
following table:
Under 1 year, 3
From 1 to 2 years, 25
" 2 " 3 " 43
" 3 " 5 " 57
" 5 " 10 " 53
" 10 " 15 " 13
" 15 " 20 " 3
" 20 " 30 " 4
" 30 " 40 " 2
---
Total, 203
{501} CLINICAL FACTS REGARDING SCARLET FEVER.--As a rule, scarlet
fever occurs but once, one attack conferring immunity from the disease
for life; but there are exceptions. In 1869, I attended a child with
fatal scarlet fever who three years previously, it was stated, had
passed through a first attack with all the characteristic symptoms.
The following case occurred in a family attended by the late Dr.
Herzog: R----, a boy of six years, had scarlet fever in a mild form in
January and February, 1875, followed by moderate desquamation. In July
of the same year he was kicked by a horse in the street, receiving a
deep scalp-wound which required three stitches. Three days afterward
he had, to appearance, a second attack of scarlet fever, attended by
high febrile movement, and followed also by desquamation. It was
believed by Dr. H. to be a genuine case, and was so treated. I am not
able to state as regards the presence of soreness of the throat, and
doubt arises whether this second attack may not have been septicaemic.
In April, 1876, a third attack occurred, which I saw from the
beginning. It was accompanied by all the characteristic
symptoms--injection of the fauces, an efflorescence continuing the
usual time, followed by desquamation and albuminuria, the latter
continuing several weeks. Richardson states that three distinct
attacks occurred in his own person, and a student attending the
lecture at which this was mentioned informed the doctor that he also
had had scarlet fever three times.
Sometimes a second attack occurs so soon after the first that it has
been described as a relapse. The following was a case in point in the
practice of Godneff (_Meditz. Vestnik._, No. iv., _N.Y. Med. Rec._,
April 30, 1881): A youth of seventeen years contracted scarlet fever
while taking care of a child. It began with a chill, and he had the
usual efflorescence, sore throat, and tumefaction of the cervical
glands. An exudation appeared upon his tonsils and uvula, and his
temperature reached 104 degrees. The urine contained a trace of
albumen, the rash in due time faded, and the epidermis exfoliated. On
the fifteenth day, when he was about ready to leave the hospital, he
again had a chill, followed by fever. The temperature reached 105.2
degrees, the rash reappeared over the entire surface except the face,
diphtheritic exudations occurred upon the fauces, and the urine, the
quantity of which was diminished, again became albuminous. This second
efflorescence faded on the twenty-fourth day, and on the
twenty-seventh exfoliation began. Hillier says: "I have seen a young
woman in the fever hospital suffering from a second attack of
scarlatina, the first attack having occurred five weeks previously.
She had quite recovered from her first illness, and was acting as
nurse. In both seizures the rash, the sore throat, and other symptoms
were characteristic. The relapse or recurrence was less severe than
the primary disease." Cases of a fourth, or even of a greater number
of attacks, have been reported. The first seizure is sometimes milder,
but in other instances is more severe, than those which follow.
Exposure to the scarlatinous poison not infrequently produces
pharyngitis without the occurrence of scarlatina, and the inflammation
is apt to be severe, accompanied by pain in swallowing and marked
febrile movement. This phlegmasia is distinguished from scarlet fever
by its shorter duration and the absence of the efflorescence. It
occurs in adults as well as in children, and in those who have had, as
well as in those who have not {502} had scarlatina. So far as I have
observed, it is very seldom accompanied or followed by any of the
complications or sequelae so common in and after scarlet fever. It
cannot be distinguished from ordinary pharyngitis except in the manner
in which it occurs, and one attack does not preclude another. The late
George B. Wood made the remark that he never attended a case of
scarlet fever without suffering from sore throat. The following were
examples of this form of pharyngitis: On Jan. 17th, 1882, I was called
to a boy of three years with severe scarlet fever, ushered in by
convulsions. On the following day his sister, aged seven and
three-fourths years, whom I had attended a year previously during a
severe attack of scarlatina, and who had been almost constantly with
the brother, became very ill, with a temperature of 103.5 degrees.
Examination revealed severe inflammation of the fauces, without
pseudo-membrane or any other exudation except muco-pus. On Jan. 19th
an older brother, nine years, whom I had attended in scarlet fever
three years previously, was affected in the same way, his temperature
being 104 degrees and his respiration guttural and noisy, especially
during sleep, in consequence of the great amount of faucial swelling.
At times he was delirious. The inflammation in both cases began to
abate about the third day, and had disappeared by the close of the
week. That the contagium of scarlet fever may be received into the
system and cause pharyngitis, while the patient has immunity from
scarlet fever through a previous attack, and that this inflammation
may occur any number of times, as in the case of Dr. Wood, are
remarkable facts.
Now and then cases occur which appear to show that the scarlatinous
poison may affect the kidneys, producing nephritis, while there is no
other manifestation of its influence. Thus in my practice a lady of
about forty-five years constantly attended her son, sleeping by his
side, during an attack of scarlet fever. Her health had previously
been good. When the boy was convalescent, as her appetite failed and
she was indisposed, a careful examination revealed the fact that she
had albuminuria, although she had had no sore throat or other symptom
of scarlet fever. After several weeks of treatment her disease was
removed, and she has remained well since. In the _British Med. Jour._
for Nov. 29, 1879, it is stated that in a family four girls were found
to be suffering from desquamative nephritis. One of them had recently
had scarlet fever, but the other three had presented no symptoms
whatever of this disease. Such cases, although probably rare, appear
to show that, as the scarlatinous poison may produce inflammation of
the fauces without the occurrence of scarlet fever, so it may cause
nephritis without producing the general disease, or apparently
disturbing the functions, or changing the state of other parts, except
the kidneys.
SYMPTOMS.--ORDINARY FORM. Scarlet fever usually begins abruptly, so
that the exact time of its commencement can be fixed. If any
premonitory symptoms occur, they are slight, so as scarcely to attract
attention, as languor or the appearance of fatigue. A dusky aspect of
the surface may occasionally be observed during the few hours
preceding the attack. In some children the first symptom is
chilliness, and occasionally a distinct chill occurs. In the adult a
chill is ordinarily the first symptom. With or without the initial
chilliness, febrile movement occurs, of variable intensity according
to the severity of the type, and {503} accompanied by such symptoms as
usually arise in a febrile state of system, as cephalalgia, anorexia,
and thirst. The pulse rises to 110, 120, or more per minute, the
temperature to 102 degrees, 103 degrees, or 104 degrees; the skin is
hot, face flushed, and the eyes bright. Even in cases that are not
malignant or grave, and that give indications of a favorable result,
there is often more or less stupor, with transient delirium and sudden
starting or twitching of the extremities, showing that the
cerebro-spinal axis is involved.
Vomiting is a common symptom in the beginning of scarlet fever,
occurring before the appearance of the efflorescence. It therefore has
diagnostic value when the nature of the case is still doubtful. In
some patients it is an initial symptom, but in others some hours have
elapsed when it occurs. I recorded its presence or absence in 214
patients, with the following result: present in 162 patients, absent
in 52. In severe forms of the disease it is rarely absent, and if it
do not occur it is probable that the case will be mild, requiring
little treatment and having a favorable termination. In epidemics of
unusual mildness the number of cases without vomiting may be in excess
of those in which this symptom occurs. It appears to be due to
functional disturbance of the cerebro-spinal system, and it may
therefore be properly regarded as a nervous symptom. In severe cases
the vomiting is apt to be repeated, not only on the first but on
subsequent days, and we shall see that in cases of great gravity, in
which a fatal termination is not improbable, persistent vomiting, by
which the food and stimulants so urgently required are rejected,
interferes seriously with successful treatment. In a few cases
embraced in my statistics nausea without vomiting was recorded. The
bowels in ordinary scarlatina act regularly or are slightly
constipated. Diarrhoea, which so commonly accompanies the persistent
vomiting in malignant cases, if it occur in this form of the malady is
slight and transient and due to accidental causes. The food, if it be
given in the liquid form and cool, is usually taken readily, on
account of the thirst, except when deglutition is rendered painful by
the pharyngitis.
The symptoms pertaining to the nervous system vary according to the
severity of the disease and the temperament of the patient. Many
children during the progress of the common form of scarlet fever
present a dull or apathetic appearance. They lie much of the time with
their eyes closed; others are more restless, and not a few, if the
fever be considerable, have occasional twitching of the limbs and more
or less headache. Eclampsia sometimes occurs on the first day,
especially in those predisposed to it, even when the subsequent course
of the disease is mild and favorable. This complication, very grave
and usually fatal when it occurs at a later stage, is in most
instances, when it takes place on the first day, readily controlled by
proper remedies and with little detriment to the patient. But if it be
attended by high elevation of temperature and marked drowsiness,
approaching the comatose state, it is very serious upon the first as
well as upon subsequent days. Nervous symptoms occurring in the
beginning of scarlet fever, when it has the ordinary favorable type,
begin to abate in three or four days, but if they supervene at a later
date, and especially in the declining stage, they possess more
gravity, since they then not infrequently result from and indicate
renal complication.
{504} Early in the disease, nearly as soon as the commencement of the
fever, the faucial and buccal surfaces become inflamed, as shown by
redness, swelling, and tenderness. The physician summoned in the
beginning of an attack will already, at his first visit, observe
hyperaemia of the fauces, with points of deeper injection than over
the general faucial surface, and soon the buccal surface also
participates. The inflammation at first produces preternatural
dryness, and this is followed by a viscid secretion. The papillae of
the tongue enlarge and become prominent, giving rise to the appearance
known as strawberry tongue which is so common in scarlet fever. This
state of the buccal and faucial membrane continues throughout the
disease. A thin fur appears upon the tongue on the first day, and it
increases on the second and third days, after which it is apt to be
detached, exposing the surface of the organ, which has a deep red hue,
but in not a few patients the fur remains or is reproduced as soon as
shed. Except in the mildest cases the Schneiderian membrane also
participates in the inflammation as the disease advances, so that a
thin, irritating discharge, containing leucocytes or pus-cells, flows
from the nostrils. The skin is hot and dry, and cutaneous
transpiration nearly checked. The respiratory system is rarely
involved in any notable manner unless there be a complication. Many
have no cough whatever, while others have a slight cough, due to the
fact that the inflammation, of a catarrhal form, has extended from the
fauces to the surface of the glottis. Slight acceleration of
respiration, corresponding with the degree of fever, may also be
observed. The kidneys commonly act regularly and normally during the
first days, any serious impairment of their functions being rare
before the close of the first week.
When the symptoms described above have continued from six to eighteen
hours the efflorescence appears. It is first observed about the ears,
neck, and shoulders, in reddish patches fading into the normal hue.
These patches extend and unite, and in the course of a few hours the
trunk and upper extremities, and finally the legs, are covered. The
scarlatinous rash usually, when fully developed, resembles that
produced by external heat or the application of a sinapism. It has
been likened to the appearance of a boiled lobster, but there are
numerous minute points of a deeper or duskier hue than the surface
generally. In many patients the rash appears, especially over the
abdomen and lower extremities, as minute, thickly-set points, with the
skin of normal appearance between them. Henoch of Berlin says of
scarlet fever: "In general, the moderate grades of eruption prevail,
the skin, when seen from a distance, presenting a diffuse, more or
less scarlet redness, while on closer inspection it is found that this
redness is composed of innumerable red points closely situated
together, and separated from one another by very small paler portions
of skin. The dark-red points appear to correspond to the
hair-follicles." On passing the finger over the efflorescence no
distinct prominences are observed, but a sensation of roughness is
sometimes imparted from engorgement of the cutaneous papillae. The
rash disappears on pressure, but it immediately reappears when the
pressure is removed. Its slow return is evidence of sluggish
circulation, and it indicates a grave and dangerous form of the
malady. The color is then usually a dusky instead of a bright red. The
efflorescence is most marked in dependent parts, as along the back,
over the chest and {505} abdomen, and in the flexures of the joints.
Parts pressed upon by the bed-clothes, which confine and intensify the
heat, present a deeper coloration than other portions of the surface.
Often, especially in mild cases, the rash is absent from portions of
the surface where it commonly appears, while it presents a typical
character elsewhere. Tardy and incomplete establishment of the rash
when the symptoms indicate an attack of ordinary or more than ordinary
severity is commonly due to some perturbating cause, especially
diarrhoea. In the _London Lancet_ for Aug. 16, 1879, cases are related
of supposed scarlet fever without the rash, cases in which pharyngitis
and stomatitis with the strawberry tongue occurred, without
efflorescence upon the skin; but it is to be remembered, as stated
above, that the inflammations which commonly attend or follow scarlet
fever, particularly the pharyngitis and nephritis, not infrequently
occur in those who have already had scarlatina, and occur more than
once from fresh exposure to scarlatina patients. These inflammations,
occurring under such circumstances, appear to be purely local
maladies, produced by the scarlatinous virus; and it seems to me a
question whether, in the so-called scarlatina without efflorescence,
the inflammations which are present, and which undoubtedly have a
scarlatinous origin, are not local in their nature, instead of being
local manifestations of the constitutional disease. The burning and
itching sensation produced by the rash increases the restlessness of
the patient, and is sometimes the most annoying of the symptoms.
The temperature in the common favorable forms of scarlet fever usually
varies from 101 degrees in the mildest cases to 103 degrees or 104
degrees in those more severe. If it attain 105 degrees or over, the
case is properly designated grave or severe. The febrile movement
commonly fluctuates but little from day to day till the fourth or
fifth day, when, if the case be favorable and no complication occur,
it begins to decline. The temperature is as high in the beginning of
the attack as subsequently.
The symptoms pertaining to the digestive system during the initial
period of scarlet fever have been sufficiently described. The
subsequent symptoms referable to this system do not differ materially
from those present in the beginning, except the absence of vomiting.
The lips are dry and often cracked. The inflammation of the mouth and
throat continues, with anorexia and thirst. With the decline of the
disease the appetite gradually returns, but it is not till the close
of the second week that it is fully restored. Great and continued
disturbance of the digestive apparatus, seriously interfering with the
nutrition, pertains to the malignant forms of scarlet fever.
The urine is high-colored, and in robust children during the first
days of scarlet fever it frequently deposits urates on cooling. Gee,
who has carefully investigated the state of the urine in scarlet
fever, says that the quantity of water is diminished and the urea is
not necessarily increased during the pyrexia; that the chloride of
sodium is diminished till the fourth, fifth, or sixth day, and that
the phosphoric acid is diminished during the climax of the pyrexia,
though not during the first three or four days. In one case he made a
daily estimation of the amount of uric acid, and found it greatly
diminished on the second and third days, normal on the fourth, and
much increased on the fifth. He believes that similar variations are
common in the quantity of the products excreted {506} in the urine.
Bile may also appear in the urine, coincident with a yellow tinge of
the conjunctiva.[1]
[Footnote 1: Article on scarlatina in Reynolds's _System of
Medicine_.]
The duration of scarlet fever varies in different cases. If the attack
be very mild, with little efflorescence, the febrile movement may
decline by the fourth or fifth day; but if the disease be severe,
little or no amelioration of symptoms may occur before the twelfth or
fourteenth day, even when no complication has occurred to increase the
temperature or cause aggravation of symptoms. Octerlony, who estimated
the duration of scarlet fever from the commencement of febrile
symptoms to "the disappearance of fever, with marked improvement in
leading symptoms," ... "found that the average duration of the disease
in forty cases was six and one-sixth days. The minimum duration in a
very slightly-marked case was three days: the maximum duration was
fourteen days." In general, prolongation of fever beyond the usual
time is due to some complication--more frequently to unusually severe
pharyngitis, with accompanying cellulitis, than to any other cause.
The malady whose commencement was so abrupt declines gradually. In
ordinary cases, by the close of the first week or in the beginning of
the second the rash becomes less and less distinct, and finally
disappears, as do also the redness and swelling of the buccal and
faucial surfaces. The engorgement of the tonsils and of the papillae
of the tongue subsides, the appetite returns, the countenance
brightens and becomes natural, and the child, who during the height of
the fever scarcely noticed objects or noticed them with indifference
or even repugnance, can be amused as before his sickness.
Desquamation succeeds. This begins at about the sixth day, and is not
completed till the tenth or twelfth day; often not till the close of
the third or in the fourth week. The amount of desquamation
corresponds with the intensity and duration of the efflorescence, or
rather of the dermatitis which produces the efflorescence. If the
efflorescence have been slight and partial, it will be slight, perhaps
scarcely appreciable, but if the rash have been general, full, and
protracted, exfoliation occurs upon every part. It begins about the
face and neck, and within a day or two appears upon other parts. Where
the skin is thin the epidermis as it is detached presents a
furfuracous appearance; where it is thick, as upon the palms of the
hands or soles of the feet, it separates in layers of considerable
thickness.
Such is a brief description of scarlet fever when it pursues its
normal course without any disturbing element, but there is no other
disease in which complications and sequelae so frequently occur. The
liability to them renders the prognosis in every case doubtful. They
largely increase the percentage of deaths. They occur both in mild and
severe forms of scarlatina.
The difference in type in different cases and epidemics has already
been alluded to. Scarlet fever is sometimes so mild, and its symptoms
so slight, that the diagnosis is necessarily uncertain. In the spring
of 1866 I was called to an infant thirteen months old who had slight
pharyngitis and an indistinct rash over a part of the surface. In two
days the eruption had disappeared, and the health within a day or two
later was apparently fully restored. Diagnosis would have been
doubtful except for sequelae {507} which clearly indicated the
scarlatinous nature of the attack. In another instance two children
passed through the entire course of scarlet fever playing every day in
the street. Although the intelligent grandmother saw the rash upon
them, its nature was not suspected, as it was midsummer and cases of
prickly heat common, till nearly two weeks afterward, when one of the
children had nephritis and anasarca ending fatally. In cases so mild
as these the heat of surface is but slightly increased, the pulse but
little accelerated, and the rash usually does not occupy so much of
the surface as in ordinary cases; the appetite is not lost, though
diminished, and the thirst is moderate.
Between scarlet fever so mild that it terminates in four or five days,
and that of the grave or malignant type presently to be described, all
grades of severity exist. Scarlet fever occurs in all forms from mild
to severe, but certain symptoms characterize grave or malignant
cases--symptoms which are absent or much less prominent in ordinary
scarlet fever. Therefore the grouping of cases according to the type
is proper, and facilitates the studying of the disease.
GRAVE FORM (malignant scarlet fever).--This form of the disease is in
some epidemics common, while in others it is rare. The symptoms which
characterize it are severe from the beginning, those of the nervous
system predominating at first, such as intense cephalalgia,
restlessness or stupor, sudden twitching of the muscles, and perhaps
delirium, or even convulsions. Many pass rapidly into coma and die
within two or three days, succumbing to the intensity of the
scarlatinous poison while the malady is still in its commencement. The
rash is dusky. It disappears by pressure, and returns slowly when the
pressure is removed, showing extreme sluggishness of the capillary
circulation. Some patients are very drowsy, lying in a semi-comatose
state except when aroused, and if aroused are very restless. Others
are constantly restless. If placed in one position on the bed, they
throw themselves in another in a half-conscious or unconscious state.
They do not speak, or they mutter like those affected by the graver
forms of typhus, calling the names of playmates or talking
incoherently about things which interested them when well. The
thermometer placed in the axilla is found to rise above 103 degrees,
which is a safe average, to 105 degrees or even 107 degrees, and the
heat of the surface is pungent except when the case approaches a fatal
termination, when the extremities, ears, and nose may be cool while
the trunk and head are extremely hot. The pulse from the first is
rapid, ranging from 130 as the minimum in a malignant case to a
frequency which can scarcely be counted. A very frequent pulse is
nearly always feeble and compressible. Irritability of the stomach is
one of the most common symptoms in grave cases, so that many patients
immediately reject the nutriment and stimulants which are so urgently
required to sustain the vital powers. The vomiting, therefore, if
frequent and severe, greatly increases the danger, and in not a few
instances this symptom is associated with diarrhoea, which also tends
to increase the prostration.
Severe and dangerous nervous symptoms, due to the intensity or
activity of the scarlatinous poison, occur chiefly within the first
three or four days. Grinding the teeth, sudden muscular twitching,
delirium, convulsions, and profound stupor occur for the most part
within this time. Afterward the danger is mainly from exhaustion,
unless in the {508} second week or subsequently, when nervous symptoms
may arise from uraemia.
Those who survive the onset of malignant scarlet fever often have in
the course of a few days severe pharyngitis, with extension of the
inflammation to the lymphatic glands and connective tissue around the
angle of the jaw. These inflammations cause more or less external
swelling. The faucial turgescence around the entrance of the larynx,
with the accompanying secretion of viscid mucus or muco-pus, often
causes noisy respiration, and many at this stage of the attack breathe
with the mouth constantly open to facilitate the ingress of air.
Ordinarily, no discharge occurs at first from the nasal surface, but
as the disease continues, if the type remain severe, defluxion of thin
muco-pus takes place from the Schneiderian surface, which frequently
excoriates the cheek. The lips also are apt to be sore and swollen.
In malignant cases the disease is more protracted than when the type
is mild. Thus in a recent case in my practice the rash was still
distinct at the close of the second week, though the temperature had
fallen from 105 degrees to 102 degrees and some desquamation had
appeared. Long continuance of the febrile movement is, however,
oftener attributable to some inflammatory complication than to the
primary disease.
In all epidemics of a severe type cases now and then occur in which
the poison is so intense, or it acts with such frightful energy, that
death occurs even within the first day. The patient is overpowered at
the outset of the disease by the virulence of the specific principle,
perishing in coma, preceded perhaps by convulsions. The autopsy in
such cases reveals hyperaemia of the brain and cranial sinuses, blood
of a dark-red color, capillary hemorrhages in various parts, a flabby
heart, and perhaps some engorgement of the spleen and kidneys.
Usually, malignant scarlet fever exhibits its severe type from the
first, but cases sometimes occur which seem mild and favorable for a
few days, when severe symptoms suddenly supervene. This change from a
mild to a dangerous disease is, however, most frequently, I think, due
to some complication.
IRREGULAR FORMS.--Deviation from the normal type in scarlet fever is
usually due to some perturbating cause, which is often a pre-existing
or co-existing disease, or a disordered state of system through causes
distinct from the scarlatinous disease. Thus, a little girl in my
practice had the symptoms of scarlet fever, such as febrile movement
and inflammation of the buccal and faucial surfaces, nearly a week
before the scarlatinous eruption appeared. During this time the
patient had an intestinal catarrh, with diarrhoea, which declined when
the rash occurred. This intestinal disease was the apparent cause of
the irregularity in the malady. If scarlatina occur during a severe
attack of entero-colitis attended by purging, the defluxion from the
external surface may be such that no efflorescence appears. Severe
scarlet fever itself sometimes appears to cause gastro-intestinal
catarrh so as to produce an afflux of blood toward the intestinal
tract and away from the skin. Practitioners occasionally meet cases
like the following, which I recall to mind: In a family where
scarlatina was prevailing a little child early after the commencement
of symptoms which seemed to be plainly referable to this exanthem was
seized with vomiting and purging, which continued till death {509}
occurred on the third day. No efflorescence appeared upon the skin,
but the symptoms indicated the presence of severe intestinal catarrh,
complicating and masking scarlatina. We are aided in the diagnosis of
such cases by observing the faucial redness, and we may discover a
faint efflorescence upon parts of the surface, as about the groin or
in the flexures of the joints. In another instance an infant in the
warm months having protracted entero-colitis, the usual summer
epidemic of the cities, had the characteristic symptoms of scarlet
fever, which was present in the family, but the diarrhoea continued
and no rash appeared.
In one who is much reduced by an antecedent disease, as phthisis, or
who has a disease, chronic or acute, which produces a decided afflux
of blood away from the surface and toward the interior of the body,
the eruption is commonly tardy in its appearance, indistinct, or
wholly absent. Thus, severe inflammations of internal organs not
infrequently render scarlet fever irregular. On the other hand, some
maladies occurring in connection with this exanthem do not change its
symptoms, but themselves undergo modification. Pertussis may be cited
as an example, the cough of which is sometimes modified by an
intercurrent attack of scarlet fever, the symptoms of the latter
disease undergoing little change.
Scarlet fever may also be irregular without any apparent perturbating
cause. In 1867 I attended a young lady whose previous health had been
good, and whose brother was sick at the time with scarlet fever. She
had considerable febrile movement, with severe pharyngitis, and,
though her surface was repeatedly examined, no efflorescence was seen.
Two weeks subsequently she was affected with severe nephritis,
anasarca, effusion into at least one of the pleural cavities, oedema
of the lungs, and probably hydro-pericardium, the case ending fatally.
Rilliet and Barthez state that a second attack of scarlet fever is
more apt to be irregular than the first. Probably this opinion is
correct, especially if only a short time have elapsed between the two
seizures. Still, as we have already stated, both seizures may be
typical, and the second more severe than the first.
It would be impossible to make a clear and positive diagnosis of
certain cases of irregular scarlet fever, in which cerebral,
pulmonary, or gastro-intestinal symptoms predominate, were it not for
the fact that they occur in connection with other cases of scarlet
fever or are followed by sequelae which evidently have a scarlatinous
origin.
Occasionally, the eruption, if it be intense or if a certain condition
of system be present in the patient, is accompanied by more or less
extravasation of blood-corpuscles from the capillaries, so that the
redness does not entirely disappear on pressure, usually in points. In
rare instances certain of the exanthematic fevers present an extreme
hemorrhagic character, so as to be beyond the reach of remedies, and
of necessity speedily fatal. Hemorrhagic cases of this severe form are
probably more common in variola than in the other fevers, but I have
met a notable case in what was diagnosticated scarlatina. In June,
1881, a man in his thirty-second year, whose previous health had not
been good, though he had no defined ailment and had been able to
follow his occupation of harness-maker, suddenly became very ill, with
high febrile movement and faucial inflammation, attended by marked
prostration. After some hours an intense eruption of a scarlatinous
appearance covered nearly the entire surface, and on the following day
hemorrhages began to occur. The urine {510} contained a large
proportion of blood; each conjunctiva was raised by hemorrhages
underneath (ecchymosis), so that its natural color was lost and the
eyelids closed with difficulty; and blood flowed from the nostrils,
gums, and under the skin, forming hemorrhagic points and blotches. One
of the consulting physicians, perceiving the resemblance to
hemorrhagic variola as described by Hebra, suspected that we had a
case of this formidable malady to deal with, but the time for the
appearance of the variolous eruption passed by without its occurrence.
Death took place on the fifth day. The temperature during the sickness
was high, though the record of it has been mislaid. Fortunately, such
severe hemorrhagic cases, which are necessarily fatal, are rare.
COMPLICATIONS AND SEQUELAE.--Scarlet fever, if its type be severe, is
in itself dangerous to life. Many, as we have seen, perish from its
direct effects when it produces profound blood-poisoning. But, while
the ordinary epidemics of this malady are necessarily attended by a
large mortality from the virulence and depressing effect of the
specific principle, unfortunately, of all the diseases of modern
times, scarlatina ranks first as regards the number and gravity of its
complications and sequelae, so that nearly or quite as many perish
from these as from the direct effect of the poison.
Nervous accidents occur chiefly at two periods--to wit, in the first
days, when they are due to the severity and malignancy of the malady
and to the impressible nervous temperament of the child, and in the
declining stage, or after the termination of the fever, when they
occur from uraemia. If the type be malignant, delirium, jactitation,
profound stupor, and convulsions frequently occur on the first and
second days; and they are symptoms which properly excite the utmost
alarm and demand all the resources of our art, since they indicate a
form of the disease which is apt to end in speedy death. The eyes have
a dull or wild expression, the conjunctiva is suffused, the heat of
surface pungent, the pulse rapid and compressible or feeble, rising
above 150, even to 200, per minute, and the temperature is always
elevated to a degree that involves danger, the thermometer not
infrequently indicating 105 degrees or 106 degrees. But this severe
form of scarlet fever, attended by so great elevation of temperature,
is much less dangerous than in former times, even though it be
complicated by delirium and convulsions, since we no longer hesitate
to reduce bodily heat, when excessive, by the free use of cold baths,
and have discovered potent agents in the bromides and chloral for
controlling convulsions. Nevertheless, not a few perish in the
commencement of scarlet fever with predominating cerebral symptoms, as
delirium or eclampsia, followed by coma, under the best possible
treatment. Sometimes the symptoms have closely simulated those of
acute meningitis, and if the rash have been delayed and the sore
throat is as yet slight, the physician may suspect that he is dealing
with this disease; but autopsies in such cases show no inflammatory
lesions, but only congestion of the cerebral and meningeal vessels.
As is stated in a preceding page, in every case of normal scarlet
fever inflammation of the faucial surface is present, as indicated by
redness, tenderness, and increased secretion of mucus or muco-pus. It
precedes the efflorescence on the skin, and is announced by pain in
swallowing and on pressure with the fingers behind and below the
angles of the jaw. In that form of scarlet fever which has been
designated anginose the {511} pharyngitis is severe, and is a
prominent element in the malady, the uvula, the pillars of the fauces,
and the faucial surface in general being infiltrated and swollen.
Nevertheless, this inflammation, with the accompanying tumefaction, is
properly a part of the disease, rather than a complication, if it
abates with the subsidence of the scarlet fever or begin to abate soon
after, and if it produce but slight destructive change in the tissues
of the neck. The secretions from the fauces may be foul and offensive;
even superficial ulcerations or gangrene may occur upon the faucial
surface, causing it to present a dark brown or jagged appearance, and
the tissues of the neck may be infiltrated to a certain extent, and we
designate the disease a form of scarlet fever under the title
anginose. But when this condition is greatly aggravated, so that there
is extensive infiltration and swelling of the tissues of the neck,
with an amount of ulceration or gangrene which in itself involves
danger, continuing after the primary disease abates, prolonging the
fever and reducing the strength, it is proper to regard the state of
the throat as a complication. In addition to the pharyngitis, which is
severe as described above, the sides of the neck around the angles of
the jaw become swollen, hard, and tender. The inflammation has been
propagated to the deeper structures of the neck. Poisonous substances,
the result of decomposition or vitiated secretions, traverse the
lymphatic vessels from the faucial surface, and, being intercepted in
the lymphatic glands, cause adenitis, and the inflammation extends
from the glands to the adjacent connective tissue, which becomes hard,
tender, swollen, and infiltrated with inflammatory products. This
tumefaction sometimes begins by the second or third day, but it is
usually about the close of the first week or in the beginning of the
second week that it becomes so considerable as to constitute a source
of danger and anxiety. It is in most cases bilateral, though one side
may begin to swell before the other and remain larger throughout.
In severe cases of this complication the tumefaction extends from ear
to ear, filling up the space below and around the angles of the jaw
and under the chin. Not only is deglutition difficult, but it is
difficult to open the mouth sufficiently to inspect the fauces, and
attempts to do so cause much pain. The lymphatic glands, which lie in
the inflamed area and participate in the inflammation, are greatly
enlarged by hyperplasia, the round granular lymph-cells multiplying so
abundantly that the glands increase to many times their normal size.
Most of the tumefaction is, however, due to extension of the
inflammation to the connective tissue of the neck. The cellulitis,
which resembles that occurring in other conditions, is attended by
distension of the capillaries, the abundant formation of young round
cells, and transudation of serum (Billroth). A moderate amount of
tumefaction may disappear by resolution, but if it be considerable it
seldom abates in this way, but by the tedious and exhausting process
of suppuration or gangrene. If the swelling at its most prominent
point present a reddish hue, all hope of producing resolution must be
abandoned; it cannot be effected by any medicine or appliance within
the resources of our art. The abscess which forms is apt to be
diffuse, so as to involve danger of pyaemia, unless it be soon opened
and properly washed out. With the discharge of the pus the swelling
gradually softens and declines. In other cases gangrene results. The
vessels in the inflamed part are compressed by the inflammatory
products, so that {512} they no longer convey the blood which is
required for the purpose of nutrition. It is a law of the economy that
whenever the circulation ceases, the tissues which receive their
nutritive supply through the obstructed vessels lose their vitality.
Hence gangrene occurs in all that portion of the swelling in which the
circulation is arrested. The skin over it peels off, the dead tissue
underneath is brown or dark, and soon, if life be prolonged, the
slough begins to separate. The prognosis as regards this complication
depends largely on the size of the slough. If it be large, death will
probably result, since the strength of the system is already reduced
by the primary disease, and the reparative process will necessarily be
slow, while abundant suppuration tends to increase the exhaustion. In
some of the worst cases of cervical gangrene which I have seen the
slough has laid bare the muscles and vessels of the neck, producing in
one case a cavity or excavation sufficiently large to admit a hen's
egg. Often the slough extends under the skin, so that the deepest
recesses of the cavity are not visible, and occasionally in cases
which have ended fatally in my practice severe hemorrhage occurred
from the concealed vessels. If the ulcerative or gangrenous process
extends so deeply into the tissues of the neck that hemorrhages occur,
death is the common result; but if the destructive action be of
moderate extent and other conditions favorable, we may expect recovery
through cicatrization, with perhaps some deformity by contraction of
the cicatrix.
When the inflammation of the connective tissue of the neck is
extensive, involving both the lateral and anterior regions of the
neck, the patient is in a perilous state. The cellulitis, when
extensive and accompanied by much swelling, may produce oedema of the
glottis, may obstruct respiration by compressing the air-passages or
the laryngeal nerves, may cause compression of the jugular veins, and
thus give rise to dangerous cerebral symptoms, or may lay bare and
injure important muscles and nerves, as we have seen. If the
ulceration or gangrene be extensive, and death do not occur by
hemorrhage from arterial or venous twigs, septic poisoning may occur,
increasing still more the fatal nature of the malady.
Some cases of this complication are melancholy in the extreme, as one
related by Cremen, in which ulceration of the pharynx occurred,
allowing the escape of food and preventing deglutition. In severe
scarlatinous pharyngitis the inflammation is apt to extend along the
Eustachian tube, causing its occlusion. This accident will be
considered when we treat of otitis media, another grave complication.
It often also extends into the nares, causing catarrh of the
Schneiderian mucous membrane, with discharge of muco-pus from this
surface. Not infrequently ulceration or gangrene occurs in the faucial
surface, producing more or less destruction of tissue and forming
excavations which connect with the throat, while the cutaneous surface
retains its integrity and is not even reddened. The following case
shows how grave the complication which we are now considering
sometimes is when the external surface of the neck is not involved,
and how the inflammation by extension outward from the fauces may
involve the middle ear.
_Case 1._--Annie K----, aged two and a half years, an inmate of the
New York Foundling Asylum, was well, except an eczema of the scalp,
until the night of April 3, 1882, when she was attacked with vomiting
and {513} diarrhoea. She was feverish and drowsy, and at 2 P.M. on the
4th the scarlatinous efflorescence appeared upon her neck, body, and
lower extremities; tongue coated; pharynx red; temperature (axillary)
103 degrees; pulse 160. The symptoms and aspect indicated a grave form
of the malady, and the usual sustaining treatment was ordered. On
April 5th the temperature was 102 degrees, pulse 144, tongue less
coated, eruption fading, less stupor, no albumen in urine. April 6th,
morning temperature 102 degrees, pulse 160; passed a restless night;
stools thin and too frequent; has grayish patches in the throat: P.M.
temperature 103-1/5 degrees, pulse 150. April 7th, the diarrhoea
continues, and she has a copious muco-purulent discharge from the
nostrils; P.M. temperature 103-3/5 degrees, pulse 160. April 10th, the
temperature has continued at about 103 degrees; the patient is very
sick, with a constant foul-smelling discharge from the nostrils;
breath very offensive; temperature 103.5 degrees, pulse about 180.
April 12th, general appearance a little better, but the posterior
surface of the fauces is completely covered by a thick
pseudo-membrane; had four loose stools last night; temperature and
pulse the same as at last record; a dark, offensive, and jagged
coating over the fauces, and a dark, foul discharge from the nostrils,
as before; examination of the chest negative. April 14th, is much
prostrated; temperature 104.5 degrees, pulse rapid and weak;
respiration noisy, diminished resonance over lower two-thirds of left
side of chest; ulcers upon the mouth and tongue; fauces red and
ulcerated. April 17th, pulse 150, temperature 100.5 degrees; general
appearance somewhat better, but the diarrhoea continues, and patches
of a diphtheritic character have appeared upon the lips; moist rales
in left side of chest. The symptoms continued nearly the same until
April 23d, when she died. A dull percussion sound and distinct
bronchial respiration were observed in the left scapular region during
the last days of her life.
Autopsy nine hours after death by the curator, Dr. W. P. Northrup:
Body well nourished; the tissues have a jaundiced hue; lips sore; on
turning the head to one side pus runs from the left ear and dirty
muco-pus from the mouth. Brain normal; on opening the petrous portion
of the left temporal bone the middle ear is found full of pus, which
communicated freely with the external ear through a perforated
membrana tympani; the Eustachian tube cannot be traced in the sloughy
tissue, and a passage filled with pus extends from the ear to the
fauces; opposite the greater cornua of the hyoid bone are two deep
ulcers, each having about the diameter of a ten-cent piece, with
sloughy and offensive base and sides; the left ulcer communicates by a
ragged and wide sinus with a dark and sloughy cavity of about four
drachms capacity; this cavity is located in the neck under the angle
of the jaw, apparently occupying the site of a disintegrated gland,
and it opens upon the surface of the fauces. The surface of the larynx
has a dusky, dirty appearance, sprinkled with little cheesy-looking
spots, and covered by a dirty, foul-appearing liquid, as if some of
the ichorous pus had escaped into it from the neck; about one and a
half inches below the vocal chords there is an unmistakable
pseudo-membrane; below this, near the bifurcation, the trachea has a
bright-red color, as if a pseudo-membrane had been peeled from it,
leaving the surface raw. The detachment of a pseudo-membrane from this
part, if it did occur, must have been ante-mortem, for the organ had
been carefully handled {514} in making the autopsy. Between the apex
of the left lung and the median line the tissues of the neck,
dissected upward, are found indurated, yellow, and giving an offensive
odor, showing that the cervical cellulitis had extended downward
farther than usual. The bronchial glands have undergone hyperplasia,
being enlarged and hard. The right lung is normal; about one-half of
the left lower lobe is consolidated, and when cut is found to be
gangrenous and offensive. The liver is apparently somewhat enlarged;
spleen normal in size; gastric mucous membrane has a congested
appearance and is covered with mucus; mesenteric glands enlarged,
pale, and firm; Peyer's patches swollen and pale; at lower end of
ileum some pigmentation of these glands; in large intestine the
solitary glands are enlarged, and a few of them pigmented; kidneys
pale, cortex thickened, and markings indistinct. Microscopical
Examination.--In the pia mater perhaps a little increase of cells;
meninges of brain otherwise normal. The trachea shows well-marked
diphtheritic inflammation; it contains a film of pseudo-membrane;
evidences of inflammation occur also upon the laryngeal surface,
though less marked than in the trachea. The solidified portion of the
lung exhibits the ordinary lesions of broncho-pneumonia, with some
interstitial change. In the kidneys we find parenchymatous nephritis,
with some cell-growth in the Malpighian bodies.
The above case has been related at length, not only because it shows
how severe and destructive the inflammation of the throat, extending
into the tissues of the neck, sometimes is, but because four other
complications or sequelae were also present--to wit, otitis media,
diphtheria, nephritis, and pneumonia. We see from the above case how
formidable a disease scarlet fever sometimes is when attended by the
inflammations to which it so frequently gives rise, for a child older
and stronger than this, if thus affected, would necessarily have
perished with the best possible treatment.
In localities where diphtheria is endemic, as in New York City and
Paris, scarlet fever is often complicated by a pseudo-membranous
inflammation of the fauces and air-passages. In severe cases of
scarlet fever the Schneiderian as well as the faucial surface is
covered with it, so that it can be readily seen on inspecting the
anterior nares. Occasionally, the pseudo-membrane appears upon the
laryngeal and tracheal surfaces, as in the case which I have related
above and in others presently to be related, causing dangerous
embarrassment of respiration. This complication sometimes begins
almost at the commencement of scarlet fever, but in most instances it
does not occur before the third or fourth day, and it sometimes does
not appear till in the declining stage of the fever. When it begins,
it intensifies the febrile movement and produces general aggravation
of symptoms.
The common opinion is, that whenever a pseudo-membrane occurs upon the
inflamed mucous surface in scarlatina true diphtheria has supervened;
but there are those who hold that scarlet fever itself, when the
inflammations which attend it are severe, may give rise to
pseudo-membranes, so that what seems to be diphtheritic is but an
element in the primary disease. My convictions are strong that when
pseudo-membranes occur on any of the inflamed mucous surfaces in
scarlet fever, true diphtheria has, with few exceptions, supervened if
the patient live in a {515} locality where diphtheria is prevalent.
That scarlet fever may occur in an individual along with another acute
infectious malady is shown by abundant cases. It often occurs with
varicella, and J. Herzog relates the following case, in which measles
and scarlet fever coexisted:[2] A boy aged eight years had measles,
with the usual catarrhal symptoms, and on the fourth day, as the
temperature was returning to the normal, it rose again suddenly, and
the scarlatinal rash and sore throat appeared. In due time these
subsided, and desquamation occurred. I have seen a similar case in
consultation during the current year, so that there is nothing
improbable in the theory that scarlet fever may coexist with other
infectious maladies; and it is admitted that diphtheria, like
erysipelas, may complicate the most diverse constitutional diseases.
Moreover, when a child with pertussis, measles, typhoid fever, or
tuberculosis suddenly develops a high fever with the occurrence of a
pseudo-membranous inflammation upon the fauces or air-passages, all
admit that diphtheria has supervened, since such inflammation is not
an element in any form or type of either of these diseases; and I see
no reason in the nature of the disease why scarlet fever should not be
equally liable to this complication.
[Footnote 2: _Berl klin. Woch._, 1882, No. 7.]
The elaborate treatise by Sanne of Paris on diphtheria contains a
chapter entitled "Secondary Diphtheria." In it the author says, what
all who are familiar with diphtheria will agree to, that secondary
diphtheria does not differ in nature from the primary form, and that
it exhibits a tendency "to occupy the organs which are themselves the
seat of the more pronounced local determinations of the primitive
malady.... Diphtheria is seen in the course or sequel of numerous
diseases. Some appear to have a special proclivity for engendering
diphtheria; these are specific maladies: measles, scarlet fever,
pertussis." I have tabulated as follows Sanne's statistics of
secondary diphtheria:
Cases Deaths Cures Doubtful
----- ------ ----- --------
Diphtheria complicating measles, 100 83 15 2
" " scarlet fever, 43 22 17 4
" " pertussis, 20 12 6 2
" " typhoid fever, 8 8
" " tuberculosis, 19 19
Sanne's statistics relating to the seat of scarlatinous diphtheria are
as follows:
Fauces alone attacked, 15 cases.
" with larynx " 4 "
" " nasal fossa " 8 "
" " larynx and nasal fossa " 4 "
" " larynx and bronchi " 1 "
" " nasal fossa and lips " 1 "
" " lips and skin " 1 "
" unaffected, 3 "
Diphtheria generalized, 2 "
Larynx only affected, 2 "
Nasal fossa " 1 "
The opinion of so good an observer as Sanne, that when in scarlet
fever, pseudo-membranous exudation appears upon the mucous surfaces
which are the seat of scarlatinous inflammation, diphtheria has
supervened, and not a croupous form of scarlatinous phlegmasia,
carries with it great {516} weight. That it was diphtheria in four
instances in my practice I had sufficient proof, for this disease
became dissociated from scarlet fever, and extended to other members
of these families as idiopathic diphtheria.
Nevertheless, one of the most difficult problems which we have to deal
with in certain cases is to distinguish diphtheritic from
non-diphtheritic inflammation; and I see no reason why the
scarlatinous inflammation when intense may not be sometimes
membranous; and those no doubt err who ignore this, and consider every
inflammation attended by a pellicular exudation diphtheritic. We know
that in some cases of dysentery a fibrinous exudation occurs upon the
surface of the colon; that in croupous pneumonia fibrin exudes into
the bronchioles and alveoli of the lungs; and that physicians in
localities where there is no diphtheria meet, though at long
intervals, cases which they designate croupous pharyngitis and
laryngitis; and it seems to me that the intense inflammation of
anginose scarlatina probably sometimes produces the same exudation.
Moreover, it is very difficult to distinguish in the swollen fauces
between a membranous exudation and ulceration or superficial gangrene
so common in malignant scarlet fever. The grayish-white surface,
jagged and foul, may be the one or the other, an exudation or a
sphacelus, and in certain instances it is impossible to discriminate
between the two conditions at the bedside.
Diphtheria complicating scarlet fever sometimes begins nearly
simultaneously with the latter. Henoch states that exceptionally he
has observed suspicious patches upon the fauces before the appearance
of the scarlatinous eruption upon the skin; and he adds: "I have had
repeated opportunities of observing this unusual beginning. In such
cases we must ask ourselves whether the first affection was really
connected with the second, or whether the former was a true primary
diphtheria, rapidly followed by scarlatina. This opinion is favored by
the fact that I have only observed such cases in the hospital, in
which infection with various forms of contagion can scarcely be
avoided."
But usually it is not till the third or fourth day of scarlet fever
that this complication begins. The patient has been progressing
favorably with the scarlet fever, till on a certain day a marked
aggravation of symptoms occurs. A higher temperature, more pungent
heat, and the physiognomy of a more serious malady are present. On
inspecting the fauces to discover the cause we observe a pellicle
forming over the tonsils and perhaps other portions of the faucial
surface. Often the entire aspect of the case changes by the occurrence
of this complication, a mild case of scarlet fever becoming grave and
fatal in consequence. Thus in a case which I saw with Dr. Hardy of New
York the membranous inflammation of diphtheria, commencing upon the
fauces on the third day of scarlet fever, extended to the Schneiderian
membrane, and thence along the left lachrymal sac to the eyelids,
producing redness and swelling along the side of the nose and upon the
cheek like that of erysipelas. A thick diphtheritic pellicle occurred
upon the under surface of each eyelid on the left side, with great
tumefaction of both lids, gangrene of the cornea, and destruction of
the eye. The case soon ended fatally.
The diphtheritic inflammation sometimes extends to the larynx and
trachea, producing hoarseness and more or less obstruction to {517}
respiration. A thin film or flakes of fibrinous exudation, rendering
the respiration noisy, developed on the laryngeal or tracheal surface,
is, I think, not infrequent in diphtheria complicating scarlet fever,
but the rapid development of a thick and firm pseudo-membrane, so as
to imperil the life of the patient from the stenosis in the
air-passages, has been much less frequent in my practice than it is in
primary diphtheria and in diphtheria complicating measles or
pertussis. The following were cases of this severe complication
occurring in a recent epidemic in the New York Foundling Asylum. In
these cases the respiration was noisy, but the obstruction to
breathing seemed to be due to infiltration and swelling around the
aperture of the glottis, rather than to diphtheritic croup, which the
autopsies showed to be present.
_Case 2._--A child aged three and a half years, who previously had
symptoms of mild catarrhal croup, with moderate redness of the fauces,
sickened with scarlet fever on Oct. 1, 1882, the rash being profuse
and soon covering nearly the entire body. The axillary temperature was
103 degrees, pulse 140; slight stridor in breathing and some cough;
fauces very red, but free from membrane. Oct. 2d, restless, sleeping
but little; has vomited four times. Oct. 3d, temp. 103.5 degrees,
pulse 120; fauces much swollen; still vomiting; rash abundant. 4 P.M.,
temp. 104.3 degrees, pulse 128; tongue clean; some discharge from
nares; urine not albuminous, but its quantity diminished. Oct. 4th,
aspect that of very severe sickness; profuse discharge from nostrils;
fauces of a deep red color, and a diphtheritic pellicle over tonsils
and uvula; tumefaction along the sides of the neck; temp. 104 degrees,
pulse 140; breathing moderately stridulous; urine is passed more
freely than yesterday; evening temp. 105 degrees. Oct. 6th, croupy
symptoms more marked; tonsils and uvula greatly swollen, so that the
fauces are almost occluded; temp. 103.5 degrees; breathing difficult,
but apparently sufficient oxygen is received; profuse nasal discharge,
and other symptoms as before. About 1.30 P.M. he was raised to take
some milk, and suddenly became asphyxiated. His face was dusky, his
eyes protruded, and he voided urine and feces. Dr. Swift, who attended
the child, and to whom I am indebted for this history, immediately
performed tracheotomy, which gave temporary relief by the expulsion of
a considerable quantity of pseudo-membrane through the opening. On the
following day the respiration again became obstructed at some point
below the canula, so that it could not be removed; the features grew
livid, and death occurred in convulsions twenty-six hours after the
tracheotomy.
The autopsy was made by Dr. W. P. Northrup, curator of the asylum, who
found the pharynx covered by a membrane which was traced to the
posterior nares; larynx, trachea, and bronchial tubes as far as the
third divisions also covered with membrane; portions of the tracheal
surface denuded, and the mucous membrane underneath of a bright red
color and smooth; tonsils sloughy and fetid; mucous membrane of
smaller bronchial tubes very red and covered with viscid mucus and
pus; a portion of the left lung, extending from the root posteriorly
to the surface, gangrenous, discolored, and honeycombed; two or three
intensely hyperaemic spots, as large as a bean, in left lung; right
lung congested, but not consolidated; slight catarrh of stomach;
circumscribed areas of congestion in intestines; solitary glands of
intestines swollen, and some {518} of them ulcerated; spleen of normal
size, rather pale; liver congested and somewhat enlarged.
_Case 3._--Katie, aged six and a third years, was returned to the
asylum on Nov. 18th. Three days later (Nov. 21st) she had sore throat,
reddened fauces, coated tongue, and a faint rash upon the neck, chest,
and arms; eyes injected; temperature 102 degrees. In the afternoon
temperature 103 degrees; eruption still faint. Nov. 22d, temperature
103.5 degrees; an eruption on chest, abdomen, arms, and legs in
patches. Evening, temperature 104 degrees; voice clear. Nov. 23d,
temperature 103.5 degrees; tongue red; fauces deeply reddened, but
without any visible pseudo-membrane; eruption of a scarlatinous
appearance over the back and abdomen; on the extremities dusky, livid
patches. P.M., temperature 104 degrees; is slightly delirious;
eruption abundant. Nov. 24th, temperature 103.5 degrees; eruption well
out on abdomen; it is the same as yesterday upon the extremities,
except perhaps a little more dusky; still no pseudo-membrane to be
seen upon the fauces; is restless and delirious. P.M., during the day
has been very restless, suffering from dyspnoea; no croupy voice nor
croupy cough, though the dyspnoea continues, and a pseudo-membrane is
now visible over the tonsils and adjacent faucial surface; eruption
dusky; skin cool; pulse very frequent and feeble. From this time she
sank steadily, and died at 11.30 P.M. During her sickness her urine
seemed to be diminished, but it was not properly examined.
Autopsy Nov. 25th by Dr. W. P. Northrup, curator: Points of redness,
apparently a hemorrhagic eruption, over the face, shoulders, and parts
of the trunk; a few of the same on the extremities; no pseudo-membrane
visible in nostrils or in buccal cavity; brain not examined.
Naso-pharynx covered by a thick fibro-purulent membrane. Larynx
contains a well-marked pseudo-membrane, but not continuous. Trachea
covered by a pseudo-membrane, continuous over most of its surface, but
in places broken and flaky. Where it is detached the mucous membrane
is seen underneath, dusky and deeply injected. At the root of the
lungs the pseudo-membrane can be traced along the tubes about an inch
in all directions. Lungs oedematous, with deep congestion in places,
but apparently no pneumonia; about two drachms of clear, straw-colored
fluid in pericardium; a few stringy decolorized clots in the cavities
of the heart; left ventricle contracted. The heart-fibres, carefully
examined, microscopically, in the laboratory, are found to be normal,
not having undergone granular or fatty degeneration. Liver normal in
size; pale-yellow areas upon the superior surface, either from anaemia
or fatty deposition. Kidneys of usual size, capsule not adherent;
pyramids congested; cortex pale; markings distinct. Spleen enlarged
about one-third; consistence normal. Stomach and intestines not
examined.
_Case 4._--Scarlet fever complicated by diphtheria, nephritis, and
broncho-pneumonia. (History by house physician, Dr. Swift.) Phoebe,
aged three and a quarter years, was delicate, but in her usual health
till Oct. 29, 1882, when she became languid and vomited several times,
and her tongue was coated. Oct. 30th, occasional vomiting; fauces
reddened; tongue coated. Oct. 31st, remains languid; fauces deeply
reddened; a faint scarlatinous eruption over back, wrists, and feet;
temperature 100.5 degrees. P.M., eruption of scarlet fever well out
over the surface; tongue cleaner. Nov. 1st, {519} rash over entire
body; temperature 100.2 degrees. Nov. 2d, fauces deep-red; tonsils and
uvula swollen; diarrhoea and vomiting. Nov. 3d, temperature 102.5
degrees; the eruption, which has been bright red, is now more dusky.
Nov. 5th, temperature 104.5 degrees; dusky-red color of the eruption;
skin beginning to desquamate in places; urine normal; a discharge from
nostrils. Nov. 6th, temperature 103.5 degrees; eruption still present,
but skin of abdomen and back desquamating; has otorrhoea on both
sides; fauces deeply hyperaemic, but no pseudo-membrane visible upon
them. Nov. 7th, temperature 103 degrees; respiration and cough have a
slight croupy character; other symptoms as yesterday. Nov. 8th,
temperature 101 degrees. A careful inspection of the fauces shows that
it contains no pseudo-membrane; nostrils discharging a dark-brownish
liquid; examination of urine negative. Nov. 11th, eruption, which
appears to have been hemorrhagic in points, is fading and the
desquamation is less. Nov. 14th, nostrils still discharging; glands of
neck swollen. Nov. 16th, temperature 103 degrees; sp. gr. of urine
1010, no casts, nor albumen; the chest seems clear; less discharge
from nostrils; fauces clean and but slightly inflamed. Nov. 17th,
18th, temperature 103.5 degrees; vomits; lungs healthy, but breathes
with considerable effort, though without stridor; urine diminished;
its sp. gr. 1020, albuminous, contains blood-corpuscles and granular
casts. Nov. 19th, is very pallid; temperature 104 degrees; very
restless; vomits; urine diminished; bowels freely open. Nov. 20th,
respiration still embarrassed; subcrepitant rales over the entire
chest and percussion resonance not clear; temperature 102.5 degrees.
Nov. 21st, physical signs the same; temperature 103.5 degrees;
respiration 80. Nov. 22d, urgent dyspnoea; dulness on percussion over
top of right lung and over lower part of left lung; is delirious; no
perspiration; urine scanty; bowels freely open. From this date the
dyspnoea became more urgent, and death occurred at 4 P.M. on the 23d.
Autopsy by Dr. W. P. Northrup, curator: Body well nourished; slight
oedema of both legs; swelling at angles of jaws, most marked on left
side. Vessels of brain moderately injected; otherwise appearance
normal. Cicatrizing ulcers on both sides of fauces; a diphtheritic
pseudo-membrane on septum of nose, larynx normal. Trachea, upper half
apparently normal; a thin film of pseudo-membrane extends from just
above the bifurcation upward to nearly the middle of trachea. About an
ounce of fluid in each pleural cavity; on the right side a few loose
flakes of fibrin floating in the serum, and consolidation of lung at
apex; collapse in one or two places. Left side, recent adhesions over
whole of posterior surface and base; surface of lower lobe dark, and
when it is detached strings of fibrin adhere to it, and it is
consolidated. The cut surface shows marked oedema, injection, increase
of mucus in bronchi, and disseminated miliary tubercles in every part;
no tubercles in the pleura, and none elsewhere in the body except in
the left lung; tubercles in the lower lobe larger and more thickly
grouped than in the upper lobe. Decolorized clots in heart, extending
from ventricles into auricles of both sides. The capacity of the
ventricles seems normal. Liver and spleen, normal. Kidneys rather
large; capsules not adherent; superficial veins injected. The cut
surface shows congested pyramids and pale cortex; markings indistinct
and irregular; about four ounces of clear straw-colored fluid in
abdominal cavity, and the solitary follicles of {520} large intestines
show pigmentation; two simple intussusceptions, each three-fourths
inch in length, in small intestines.
Coryza frequently commences at or about the time of the pharyngitis.
The inflammation of the Schneiderian membrane is continuous
posteriorly with that of the fauces, and is announced by redness and
swelling, inability to breathe freely through the nostrils, and an
irritating ichorous discharge. Simple coryza in itself involves little
danger, though it is an unpleasant complication, and in the nursing
infant it may interfere with sucking. Diphtheritic coryza, on the
other hand, which is frequently present when diphtheria complicates
scarlet fever, involves danger, since it is apt to cause ulcerations,
hemorrhages, and septic poisoning. When the local symptoms are
unusually severe and the discharge abundant, it is probable that
inflammation has in some cases extended to the antrum of Highmore.
Inflammation of the middle ear is another unpleasant and not
infrequent complication. It is attributed to extension of the catarrh
from the pharynx along the Eustachian tube to the tympanum. In a
considerable proportion of cases of otitis media this tube is occluded
by the infiltration and swelling of its mucous membrane, so that the
muco-pus escapes with difficulty or is retained. Hence severe earache,
an increase of the febrile movement, and outward bulging of the
membrana tympani occur. Sometimes headache or other cerebral symptoms
arise, probably from the fact that the meningeal artery, which
supplies the meninges, is connected by anastomosing branches with the
tympanum. In one of the cases related above it will be recollected
that the ulceration and abscess extended from the fauces to the middle
ear, the entire Eustachian tube having disappeared in the ulcerative
process.
Frequently, the otitis escapes detection, its symptoms being masked or
obscured by the general disease, until the membrana tympani is
perforated and otorrhoea begins; but by careful examination the nature
of the complication can usually be ascertained before the ear is
injured to this extent, for a patient too young to speak will often
press with the fingers against the painful ear or lie with the ear
pressed upon the pillow, evidently having an increase of suffering if
placed in any other position. One old enough to speak and in proper
mental condition makes known the earache as soon as it occurs.
The mucous membrane of the tympanum, red and swollen from
inflammation, secretes muco-pus abundantly; and this, pent up in the
cavity, must obtain an exit before relief occurs. It is well if this
secretion escape, though with difficulty, down the Eustachian tube.
The destructive action of the pus upon the delicate structure of the
ear is often such that, within a few days, irreparable harm is done
and more or less deafness results. Relief can occur, if the Eustachian
tube remain closed, only by perforation of the membrane and the
discharge of the secretions into the external meatus. When this occurs
the inflammation in the most favorable cases gradually abates, the
aperture in the drum closes, and the integrity of the auditory
apparatus is preserved. In severe cases the mastoid cells
participating in the inflammation become filled with muco-pus and
tender to the touch, and often the collateral oedema causes
tumefaction and narrowing of the external ear, which subside with the
discharge of pus from the tympanum.
{521} Unfortunately, there is for many a more melancholy history--a
more destructive inflammation, involving permanent impairment or total
loss of hearing. This is especially apt to occur in strumous and
feeble children. All grades of inflammation and destructive action
occur in different cases. The perforation in the drum-membrane may be
large or the membrane may be completely destroyed, and the detached
ossicles escape one by one into the external meatus, and in a few
instances, fortunately rare, this occurs in both ears, producing
complete and permanent deafness. In my own practice this has never
occurred, but I have met one or two adults who were totally deaf from
this cause.
The mucous membrane which lines the bony wall of the middle ear has
the function of the periosteum, and therefore, when inflamed and
subjected to pressure, is liable to ulcerate. As in other parts of the
skeleton under similar conditions, superficial caries or necrosis of
the underlying bone is apt to occur. The carious or necrotic process
may extend to the mastoid cells. An offensive otorrhoea, continuing
for months or years, indicates the persistence of this pathological
state of the tympanum, which is rendered so obstinate by the presence
of dead bone. A moment's survey of the anatomical relations of the
middle ear shows the danger to which these patients are liable. A thin
bony septum, perforated with blood-vessels and sometimes containing
congenital apertures, separates the tympanum from the cranial cavity
above. Posteriorly lie the mastoid cells, connected with the tympanum
by one large and several small apertures. Anteriorly is the
commencement of the Eustachian tube and in close proximity to the
tympanum lies the carotid canal, and at one point also the superior
petrosal sinus. Virchow has shown how inflammation extending from the
ear in otitis media sometimes produces such compression of the veins
or sinuses by the swelling from the infiltration and exudation that
the circulation is arrested, and the fibrin contained in the blood of
these vessels is precipitated, forming thrombi, with the most
disastrous effect upon the individual. Pus may also burrow in the
interstices of the bone, causing great pain, or the pent-up
secretions, having no outlet for escape, may in time undergo caseous
degeneration, producing the conditions in which tuberculosis so often
originates.
Death not infrequently occurs in chronic otitis media in another way.
The otorrhoea, after months or years, suddenly ceases, the child
complains of constant severe headache and is feverish, and the case
ends in coma, preceded perhaps by convulsions. Meningitis has
occurred, produced by extension of the inflammation through the thin
bony septum which divides the tympanum from the cranial cavity, and at
the autopsy hyperaemia of the meninges, fibrin, pus, perhaps softening
of the brain and an abscess, are formed in the portion of the
encephalon adjacent to the tympanum. Therefore, otitis media, though
it often ends favorably, is in many patients an obstinate, dangerous,
and even fatal sequel of scarlet fever.
The complication known as scarlatinous rheumatism is regarded by some
as a synovitis, but its symptoms, especially its shifting from joint
to joint, seem to ally it to the rheumatic affections. In some
epidemics it is common. It usually begins toward the close of the
first week or in the second week, and its common seat is in the ankle,
phalangeal, and wrist joints. It is attended by very little swelling
in {522} most patients, though the joints are tender and painful on
pressure. It does not seem to retard convalescence materially, though
it produces suffering and involves danger as regards the heart. It
subsides in a few days with the ordinary treatment of acute
rheumatism, and even without special treatment, the chief danger being
that, as in idiopathic rheumatism, endocarditis may arise, with
permanent crippling of the valves. The following was a case of
valvular disease having this origin. It occurred in my practice.
_Case 5._--Freddy M., aged four years, sickened with scarlet fever
March 6, 1879. The usual vomiting occurred on the first day, and the
temperature was 104 degrees. The case progressed favorably till March
14th, when he complained of pain in both wrists, both ankles, and both
knees. On March 17th the general condition was good, the urine
contained no albumen, and apparently few urates, but he still had pain
in the joints of the upper and lower extremities and in the back;
pulse 140, temp. 103 degrees; breathes with a slight moan; urates in
the urine, but no albumen. A distinct mitral regurgitant murmur is now
heard for the first time. Under the use of salicylate of sodium the
pain in the joints soon ceased, but the mitral murmur is permanent.
The following prescription is for a child of five years:
Rx. Ol. Gaultheriae fl. drachm iss;
Sodii Salicylat. drachm iii;
Syrupi fl. oz. ii;
Aquae fl. oz. iv. M.
S. Give one teaspoonful every four hours.
Of the serous inflammations occurring in scarlet fever, pericarditis
has been, according to Rilliet and Barthez, most frequently observed.
In this country it is probably more frequent than is usually supposed,
but it is less frequently detected than pleuritis, the symptoms of
which are more conspicuous. It is apt to occur in connection with
endocarditis.
The following case, showing the liability to pericarditis and other
serous inflammation which exists in scarlet fever, occurred in my
practice:
_Case 6._--C----, girl aged five years and ten months, sickened with
severe scarlet fever on April 4th. Was delirious; pulse 158; had
vomiting and constipation. April 10th, pulse varies from 124 to 153,
no delirium; a considerable quantity of urates in the urine. April
11th, has to-day, for the first time, severe pain in the epigastrium,
with tenderness and moderate distension. Otherwise symptoms favorable,
but severe; pulse 140; respiration moderately accelerated, and
vesicular in every part of the chest. From this date the symptoms
continued about the same till April 14th, when the dyspnoea became
more marked and the action of the heart rapid and tumultuous. The
epigastric pain, distension, and tenderness continued; the percussion
sound was dull over the lower part of the chest; the dyspnoea became
rapidly worse, although the pulse had considerable volume; and at 5
P.M. death occurred. At the autopsy about one ounce of turbid serum,
with a soft deposit of fibrin, was found in the pericardium. Each
pleural cavity contained from six to eight ounces of transparent
serum, and both lungs were readily inflated, except a little of the
posterior portion of each lower lobe, which could not be; no fibrinous
exudation over the lungs. The liver extended four inches below the
margin of the ribs, and upon its convex {523} surface in the
epigastrium, corresponding with the seat of the pain, was a rough
patch of fibrin about one and a half inches in diameter. The bronchial
mucous membrane was moderately injected, as was also that of the
colon, and the kidneys appeared hyperaemic.
Among the serous inflammations which complicate or follow scarlet
fever, pleuritis is one of the most important. It usually begins in
the desquamative stage, and is apt to be suppurative on account of the
feeble state of the patient when it commences. It has always, in my
practice, been tedious, as all empyemas are, and it does not differ in
its clinical history from the idiopathic disease. I have met cases of
scarlatinous empyema in which, from opposition of the family or for
other reasons, thoracentesis was not performed, and death occurred;
others in which this operation effected a cure, and one at least in
which the patient recovered by escape of pus through a bronchial tube.
The pleuritis is seldom latent, or so masked by the symptoms of the
general disease that it is apt to be overlooked. On the other hand,
the cough, embarrassment of respiration, and pain referred to the
affected side render diagnosis easy.
Dilatation of the heart is common in grave cases of scarlet fever,
such cases as are properly termed malignant. It is indicated by a
feeble and quick pulse. Acute infectious maladies, especially those of
a malignant type and accompanied by high febrile movement, are very
apt to cause parenchymatous degenerations in organs, prominent among
which is granulo-fatty degeneration of the muscular fibres of the
heart. This weakens very much the contractile power of these fibres.
But early in malignant cases, probably before the muscular fibres are
damaged, the contractile power of the heart is feeble from impaired
innervation, the result of the general weakness. Hence this organ,
when weakened by structural change and insufficiently stimulated
through diminished innervation, may not fully empty itself during the
systole, and consequently it becomes dilated. Dilatation of the heart
and imperfect contraction of the auricular and ventricular walls are
apt to result in the formation of clots in the cavities of the heart;
and this appears to be the immediate cause of death in not a few
instances. An ante-mortem clot occurring in any of the cavities of the
heart necessarily seriously obstructs the circulation, unless it be of
small size. Hence the dyspnoea, which may occur perhaps suddenly, and
the change of pulse to one of marked feebleness and frequency. Large,
firm white clots are most frequently found in the right cavities. They
interlace with the chordae tendineae, lie even within the
auriculo-ventricular opening, and send prolongations into the
pulmonary artery and the cavae. Associated with the white clots are
dark, soft clots and fluid blood. The left cavities may be contracted
and empty, or they may contain dark, soft clots or white ante-mortem
clots. Clots in the left ventricle are sometimes prolonged into the
aorta as far as the brachio-cephalic branches, while those in the left
auricle may extend to the pulmonary veins. If dilatation of the heart
be so great that clots form in its cavities, speedy death is probable.
Sometimes a patient passes through scarlet fever and appears in a fair
way to recover, when he succumbs to some exhausting sequel distinct
from the heart, and at the autopsy the heart is found dilated and
containing whitish clots, which are probably ante-mortem, and which
hastened {524} death by obstructing the circulation. Under such
circumstances this state of the heart is attributable in great measure
to the complication which has weakened its contractile power.
The following was a case in point. It occurred in the New York
Foundling Asylum:
_Case 7._--R. A., aged three years, had scarlet fever, beginning March
23, 1882. The symptoms were favorable at first, but serious
complications and sequelae occurred, which were fatal. The record of
April 18th reads: "Appears well nourished, but is anaemic; has
otorrhoea; no oedema; skin desquamating; dulness on percussion over
upper third of right side of chest, anteriorly and posteriorly; mucous
rales and rude breathing over same area; fine rales posteriorly over
lower part of left side of chest; pulse 160, respiration 68,
temperature 101-2/5 degrees." April 20th, is feeble and takes
nutriment with difficulty; tongue thickly coated; pulse 160,
respiration 68, temperature 101-2/5 degrees. April 26th, condition
about the same as at last record, but he is evidently weaker; the lips
are ulcerated and fauces still swollen. May 2d, cannot speak
distinctly; a brownish, foul-smelling secretion lodges on the spoon
used in depressing the tongue; left side of face swollen. On the
following night eight convulsions occurred, attended by orthopnoea,
and mucous rales in the chest from pulmonary oedema. Diarrhoea
supervened and the patient died about midnight. Autopsy: Body
moderately wasted and very white, several dark-blue spots on scalp and
face from hemorrhages underneath; lips covered with dry crusts; brain
of normal appearance; aperture of the larynx narrowed at the chink by
infiltration and swelling of the tissues; surface of the vocal cords
covered by a thin white film, apparently a fibrinous exudation;
tracheal surface hyperaemic; about a drachm of straw-colored fluid in
each pleural cavity; right lung wholly adherent by recent exudation of
fibrin; left lung also largely adherent. A careful examination showed
the presence of broncho-pneumonia in each lung, with considerable
infiltration of the walls of the bronchi, and cylindrical dilatation
of many of them; cavities of the heart dilated, so that this organ
appears much enlarged, and its shape approaches the globular; its apex
is rounded or obtuse; transverse diameter of the right ventricle, when
its walls were open and drawn apart, was three and one-quarter inches;
that of the left ventricle three and a half inches. Similar
measurements of the heart of another child of about the same age,
believed to be normal, were about one inch less in each direction. All
the cavities contain white firm clots along with soft dark clots.
Liver of normal size, pale; the outer surface and all cut surfaces are
studded with nodules of the size of a pin's head, of a dull, opaque
white color. These white spots, examined microscopically by Professor
Delafield, are found to be neither tubercles nor gummy tumors, but to
consist of polygonal cells, lying in the meshes of the capillary
plexus of veins, which are perfectly preserved. He has not observed a
similar case. The walls of the gall-bladder are one line or more in
thickness, and the gall-duct is pervious. The microscope shows general
hypertrophy of the gall-bladder and hypertrophy of its papillae. The
urine removed from the bladder was found to contain albumen and
hyaline casts, and a microscopic examination showed a small amount of
parenchymatous inflammation. The spleen was somewhat enlarged.
Punctate congestion of small areas of {525} gastric surface, no
increase of mucus; mesenteric glands uniformly enlarged; jejunum,
ileum, and colon exhibited a slightly increased vascularity. The
immediate cause of death appeared to be imperfect contraction of the
heart and the formation of clots in its cavities, due, apparently to
the pleuro-pneumonia as much as, or more than, to the primary disease,
scarlatina.[3]
[Footnote 3: Dr. Goodhart (_Guy's Hospital Reports_, 1879) reports
several interesting cases to confirm his opinion that acute dilatation
of the heart is a not infrequent sequel of scarlatinous nephritis, and
is the cause of death in some apparently inexplicable cases.]
There can be little doubt that nephritis in its milder form is much
more common than was formerly supposed. A few years since little
attention was given by a large proportion of physicians to the state
of the kidneys, and the urine was not examined till dropsy made its
appearance, which only occurs in the more severe forms of nephritis
and is a late symptom. It is now known that catarrh of the renal tubes
frequently occurs in a mild form early in scarlet fever, without
causing albuminuria, dropsy, or any notable symptom. It may produce a
smoky color of the urine, and the appearance in it of granular
epithelial cells, with an increase of mucus, but no albumen. With
careful treatment and no exposure to cold, the renal catarrh abates
with the decline of the scarlet fever. It is scarcely severe enough to
merit the name desquamative, tubal, or parenchymatous nephritis,
though it is a mild form of the same pathological state. Steiner
states, as the result of many careful examinations of cases, that
hyperaemia of the kidneys was always present in those who died early
in scarlet fever, and that in a certain proportion of these cases
catarrh of the renal tubules was present in addition to the
congestion. Even in some who died on the second or third day he found
cloudiness of the epithelium in the renal tubes, although the urine
had not indicated such a change. The opinion has even been expressed
that catarrh of the renal tubes is as common in scarlet fever as that
of the bronchial tubes in measles; that is, that it is a uniform
element in the disease; but this appears to be an exaggerated
statement, for others have failed to find any evidence of renal
catarrh in certain cases.
The nephritis which gives rise to symptoms, and therefore interests
the practitioner, commonly begins in the declining period of scarlet
fever or during the desquamative stage, and is in many instances
plainly attributable to exposure to cold or to currents of air. It
originates either during this period, or, if it have previously
existed as a mild renal catarrh, it now becomes aggravated. Dropsy,
which always attracts attention, does not occur till the nephritis has
continued for some time.
Why nephritis, with the subsequent dropsy, so frequently occurs after
scarlet fever is not fully understood. Rilliet and Barthez attribute
it to disturbance of the function of the skin. The fact has long been
observed that the kidneys become affected nearly if not quite as
frequently after mild as after severe cases. Indeed, the chief danger
in mild cases, when the patients are but a short time in bed and are
soon allowed to go about, is from the nephritis. Chilling the surface
and checking cutaneous transpiration appear to be the immediate cause
of this inflammation in a considerable proportion of cases. Therefore,
severe attacks of scarlet fever with abundant rash and desquamation,
which require the patient to be kept in bed the proper time and in a
warm room two or three {526} weeks, appear to be less frequently
followed by this renal disease than are milder cases which are more
carelessly treated.
The most thorough and minute microscopic examination of the state of
the kidneys in scarlet fever which have come to my notice were those
by E. Klein, published in the _Lond. Path. Soc. Trans._, and
illustrated by microscopic drawings. It appears from these
examinations that the changes in the kidneys are complex, among which
we recognize both those of parenchymatous or desquamative nephritis
and interstitial nephritis; but we would infer that the interstitial
nephritis is mild in degree and quite subordinate, or else confined to
portions of the organ, from the fact that so many permanently and
fully recover. The following is a resume of Klein's examinations in
twenty-three cases: We conclude from these microscopic researches that
the anatomical changes of both parenchymatous and interstitial
nephritis are commonly present in greater or less degree in cases of
scarlet fever. If they are mild or confined to portions of the
kidneys, no symptoms occur; but if they are sufficient in extent or
degree to impair the function of these organs, then symptoms, as
albuminuria, diminution of urine, etc., appear.
1. Parenchymatous Nephritis, Proliferation of Nuclei, Hyaline
Degeneration of Arterioles, the Glomerulo-Nephritis of Klebs.--Klein
found increase of nuclei (probably epithelial) upon the glomeruli and
hyaline degeneration of the intima of minute arteries, especially
marked in the afferent arterioles of the Malpighian bodies. The intima
of these vessels was in places so swollen as to resemble cylindrical
or spindle-shaped hyaline masses, and cause narrowing of the lumina of
the vessels in which this degeneration occurred. Klein observed in
some specimens so great hyaline degeneration of the capillaries of the
Malpighian bodies that circulation through them was obstructed. In the
more advanced or protracted cases this hyaline substance in the
glomeruli began to assume a fibrous appearance. Bowman's capsule was
considerably thickened. This hyaline degeneration of the Malpighian
bodies Klein discovered in the earliest cases which fell under his
observation.
Also in the earliest cases the multiplication or germination of the
nuclei of the muscular coat of the arterioles was observed, with a
corresponding increase in the thickness of the walls of these vessels.
This change in the muscular element was observed in the arterioles in
different parts of the kidney, but it was most conspicuous in
arterioles at their point of entrance into the Malpighian bodies; and
it was distinctly observed in other arterioles, both in the cortex and
in the base of the pyramids.
In the glandular portion of the kidneys other anatomical alterations
were observed, indicating parenchymatous nephritis. There were
swelling of the epithelial lining of the convoluted tubes;
multiplication of nuclei of epithelial cells, especially in ascending
tubules, which lay close to the afferent arterioles of Malpighian
corpuscles; granular matter, and even blood, in the cavity of Bowman's
capsule and in the convoluted tubes; cloudy swelling and granular
disintegration of epithelium in some parts of the convoluted tubes;
detachment of epithelium from the membrane of larger ducts of the
pyramids in some cases. These parenchymatous changes are already known
to the profession through the observations and writings of Dickinson,
Fenwick, Johnson, John Simon, and others.
{527} Klein, in commenting on the hyaline degeneration which he
observed, states that Neelsen found the walls of the capillaries of
the pia mater thickened, highly refractive, and of a lardaceous
appearance in certain acute infectious maladies, as variola, typhoid
fever, measles, and in one case of scarlet fever.[4] Usually, only a
small portion of the capillaries were thus affected, most frequently
at the point of division into branchlets. In a few instances Neelsen
observed degeneration of arterioles extending a considerable distance,
with fusion of the intima, media and adventitia, and chemical
examination showed that the substance produced by this degeneration
had similar properties to elastic tissue. Although the examinations by
Neelsen relate to the pia mater, two of his observations are
especially interesting--first, that the hyaline change affects chiefly
vessels near their point of branching; and, secondly, that the hyaline
substance is of the nature of elastic tissue, for in the kidney in
scarlatinous nephritis the arterioles undergo the change in question
chiefly near their point of branching into the capillaries of the
glomerulus; and the intima being the part which undergoes the hyaline
change, it is probable, in the opinion of Klein, that the same
substance is produced by the degeneration in walls of the vessels of
the kidney which Neelsen observed in the pia mater, and therefore that
it is of the nature of elastic tissue.
[Footnote 4: _Archiv der Heilkunde_, 1876.]
This hyaline degeneration of the arterioles is also very marked in the
spleen in scarlet fever; and in studying the minute anatomy of the
intestines and spleen in typhoid fever Klein has found the same
degeneration of the intima of the minute vessels. He believes that
this hyaline change and the proliferation of muscle-nuclei which thus
occur at an early period in scarlet fever in the renal vessels when
the kidneys become affected are due to an irritating cause acting
similarly to that in typhoid fever.
Klein calls attention to the interesting examinations of the
scarlatinous kidney made by Klebs, who attributed the diminished
urination and the uraemic poisoning in certain cases in which the
kidneys do not exhibit any marked change to the naked eye, to what he
designates glomerulo-nephritis. Klebs says: "In the post-mortem
examination the kidneys are found slightly or not at all enlarged,
firm, ... the parenchyma very hyperaemic. Only the glomeruli appear,
on close inspection, pale like small white dots. The urinary tubes are
often not changed at all. Occasionally the convoluted tubes are
slightly cloudy. The microscopic examination shows that there are
neither interstitial changes nor proliferation of epithelium, the
so-called renal catarrh generally supposed to be present in these
conditions on account of the absence of other perceptible
derangements; and there seems, therefore, leaving out the glomeruli,
the congestion of the kidneys alone to remain to account for the
symptoms during life." But that mere congestion is insufficient to
produce the symptoms appears from the fact that it does not produce
them under other circumstances. Klebs finds, "on microscopic
examination of the glomerulus, the whole space of the capsule filled
with small somewhat angular nuclei, imbedded in a finely granular
mass. The vessels of the glomerulus are almost completely covered by
nuclear masses."
Klein, commenting on these examinations by Klebs, states that in all
{528} early cases which he examined he observed great abundance of
nuclei of the glomeruli, but a condition like that described and
figured by Klebs[5] he has seen in only a few glomeruli; for a general
state of these bodies, as described by this observer, and such an
excessive proliferation of the nuclei that the blood-vessels are
completely compressed, was not seen in one of the twenty-three cases.
Klein therefore questions whether the diminished urination and
retention of urea in scarlet fever, when the kidneys do not exhibit
any conspicuous catarrhal or other change, is due, unless in
exceptional instances, to compression of the vessels of the glomeruli
by nuclear germination, but believes, rather, that the obstructed
circulation, and consequent diminished urinary excretion, is largely
due to the changed state of the arterioles. Klein adds that perhaps
undue contraction of the arterioles, through stimulation by the
blood-irritant, may also be a factor in causing arrest of circulation
in the Malpighian corpuscles. As regards cases that perished early, he
found the parenchymatous change slight, so that a careful examination
was required in order to detect cloudy swelling and granular
degeneration.
[Footnote 5: _Handbuch der Pathol._, p. 646, fig. 72.]
2. Interstitial Nephritis.--A second set of changes Klein observed in
cases that died on about the ninth or tenth day. In such cases he
found changes due to interstitial, in addition to those produced by
parenchymatous, nephritis. Round cells, lymphoid cells, or whatever
else they should be called, were seen in the connective tissue of the
kidneys. In the kidneys of those that died at the end of the first
week after the commencement of nephritis, infiltration with round
cells was observed in the connective tissue around the large vascular
trunks. At a later stage this infiltration had extended into the bases
of the pyramids and into the cortex. The gradual increase in extent
and intensity of this infiltration was so decided in the cases which
Klein observed that he has no hesitation in concluding that when
interstitial nephritis occurs it begins about the end of the first
week, in the manner already stated--to wit, as a slight infiltration
of the tissue around the large vascular trunks, and gradually extends,
so that portions of the cortex, and rarely portions of the base of the
pyramids, are changed into firm, pale, round-cell tissue, in which the
original tubes of the cortex become lost.
The infiltration of the cortex with round cells, beginning at the
roots of the interlobular vessels, spreads rapidly toward the capsule
of the kidney, and laterally among the convoluted tubes around the
Malpighian bodies.... In the course of this process considerable parts
of the peripheral cortex, occasionally of a more or less distinctly
cuneiform shape, with the base nearest the capsule of the kidney,
become changed into whitish, firm, bloodless, cellular masses, in
which Malpighian corpuscles and urinary tubes are only imperfectly
recognized, being more or less degenerated. In some cases attended by
this infiltration of the cortex Klein observed a more or less dense
reticulation of fibres, especially around the interlobular arteries,
containing in its meshes lymph-cells, chiefly uninuclear.
In a child of five years that died after a sickness of thirteen days
Klein found evidence of intense interstitial inflammation, and also
emboli, consisting of fibrin with a few cells, in the arteries, both
in those of large size and in the arterioles, chiefly where they enter
the Malpighian corpuscles. {529} He states that in the specimens which
he examined the more intense the degree of interstitial change, the
greater was the enlargement of the kidneys, and the more distinct also
were the evidences of parenchymatous nephritis in the urinary tubes,
which either contained casts or were in the process of destruction. By
being crowded with inflammatory products, especially cells, the
Malpighian corpuscles were obliterated, undergoing fibrous
degeneration. A very curious fact observed was the deposit of lime in
the urinary tubes, first of the cortex, and then also of the pyramids,
at an early stage of scarlet fever, when the kidneys otherwise showed
only slight change. Several observers, as Biermer, Coats, and Wagner,
have each described a case of scarlet fever with interstitial
nephritis, which they consider unusual; but Klein has apparently
demonstrated, as we have seen, by a large number of microscopic
examinations, that this form of nephritis is common after the ninth or
tenth day.
Nephritis, in proportion to its extent and gravity, is accompanied by
languor, febrile movement, thirst, loss of appetite and strength. At
first the patient experiences but slight pain in the head or
elsewhere, and the quantity of urine is not notably diminished; but as
the disease continues urination becomes less frequent and the urine
more scanty. Albuminuria occurs, while the urea is only partially
excreted, and therefore accumulates in the blood. If the nephritis be
so severe or protracted that this principle accumulates to a certain
extent, grave symptoms occur, as headache, vomiting, apathy or
restlessness, and, more dangerous than all, eclampsia, which is not
unusual in these cases. Microscopic examination of the urine shows the
presence in this liquid of blood-corpuscles, granular epithelial
cells, and hyaline or granular casts, or both. The specific gravity of
the urine is diminished. But a large quantity of albumen in the urine
may render the specific gravity as high or higher than in health.
The altered state of the blood soon gives rise to transudation of
serum, first observed in most cases as an anasarca occurring in the
feet and ankles. The oedema, if not checked by treatment or through
mildness of the disease, extends over the limbs, scrotum, and
sometimes upon the trunk. It is well if the dropsy remain limited to
the subcutaneous connective tissue, but, unfortunately, it is apt to
occur, if the nephritis continue, in and around the internal organs,
producing, mentioned in the order of frequency, pulmonary oedema,
effusion into the pleural and peritoneal cavities, the pericardium,
the encephalon, and lastly into the connective tissue of the larynx,
causing that very fatal complication, oedema of the glottis. Although
this is the common order in which dropsies occur, exceptions are not
infrequent. Even the anasarca may not be the first to appear, although
in the vast majority of cases it has the precedence. Thus, Rilliet
relates the case of a boy of five years who twenty days after the
occurrence of scarlet fever, and six hours after the appearance of
bloody and albuminous urine, had double hydrothorax, rapidly
developed. As long as the hydrothorax continued no anasarca was
observed, but as it declined anasarca appeared. Legendre cites a case
in which oedema of the lungs occurred without anasarca or other
dropsy. Occasionally, the anasarca and internal dropsies take place
nearly simultaneously. The nephritis and consequent serous effusions
usually appear within three weeks after scarlet fever ends, but cases
occur in which the effusions are first observed as late as the fourth
and fifth weeks. The patient may be {530} considered to possess
immunity from this sequel if he have reached the close of the fifth
week after the abatement of scarlet fever without its occurrence.
The dropsy is usually acute, but it may assume the chronic form, since
the nephritis which causes it, happily curable in most instances, may,
if neglected, become chronic. Whether the dropsy in itself involve
danger depends in great part on its location. Anasarca and ascites may
exist a long time with little suffering or danger, but a small amount
of serum in certain other localities causes alarming symptoms and
speedy death. Oedema of the lungs, hydro-pericardium, oedema of the
glottis, and intracranial effusions are always dangerous, and the last
two are sometimes fatal within twenty-four to forty-eight hours.
Oedema of the lungs has been fatal within twelve hours from the
occurrence of the first symptoms of obstructed respiration.
Cerebral symptoms occurring during scarlatinous nephritis are probably
sometimes due to the irritating effect of the retained urea on the
nervous centre. In other cases the cause appears to be cerebral oedema
or compression of the brain by effusion of serum within the ventricles
and upon the surface of the brain. Headache, dull or severe,
dilatation of the pupils or their oscillation in the same degree of
light, vomiting with little apparent nausea, are common symptoms of
scarlatinous nephritis when it has continued a few days, and the
excretion of urea is so diminished that this substance begins to exert
its poisonous effect on the system. Such symptoms are apt to be
followed by somnolence, threatening coma, or by eclampsia, unless the
patients are promptly and properly treated. In some patients that die
of scarlatinous nephritis, death occurring in convulsions or coma, no
appreciable lesions are observed within the cranium, unless more or
less congestion, the fatal ending being attributable to the uraemia.
In other instances we find an effusion of serum within the ventricles
or upon the surface of the brain. Although the symptoms in
scarlatinous nephritis and uraemia may appear very unfavorable, the
prognosis is usually good under prompt and appropriate treatment. Thus
severe convulsions and a degree of somnolence that bordered on coma
may abate, and convalescence be fully established within a few days,
and Rilliet and Barthez announce ten recoveries in thirteen patients
affected with convulsions due to this renal affection.
ANATOMICAL CHARACTERS.--Scarlet fever being, as we have seen, a
constitutional febrile disease of an ataxic nature, and accompanied by
certain inflammations, necessarily affects the composition of the
blood; but since this disease varies so greatly in type or severity,
the state and appearance of this liquid also vary. At the autopsies of
the more malignant cases we find the blood dark and fluid, with small,
soft, and dark clots in the heart and large vessels. In other cases
the clots are large, firm, and solid, as described in a preceding
page. In malignant cases that end fatally Rilliet and Barthez state
that both the large and small vessels of the cerebral meninges and the
brain are found hyperaemic, but in a variable degree. In those who die
in coma, preceded by delirium or convulsions, during the eruptive
stage, the intracranial congestion is usually marked, with perhaps
some transudation of serum, but without inflammatory lesions. The
fibrin in scarlet fever remains in about normal proportion, except as
it is increased by inflammatory {531} complications. Andral found an
increase in the proportion of blood-corpuscles from 127 to 136 parts
in 1000.
The respiratory apparatus, except the Schneiderian membrane, is
usually normal when no complications exist. Samuel Fenwick[6] made
post-mortem examinations in sixteen cases of scarlet fever, and
concludes from them that inflammation of the mucous membrane of the
stomach and intestines occurs like that of the skin, followed by
desquamation of the epithelial cells, like that of the epidermis. I
have had the opportunity of examining the stomach and intestines of
those who died of scarlet fever in the eruptive stage, and have not
found any unusual hyperaemia of the gastro-intestinal surface, except
when gastro-intestinal inflammation, usually indicated by diarrhoea,
had occurred as a complication.
[Footnote 6: _London Lancet_, July 23, 1864.]
In some cases the abdominal organs exhibit changes which suggest a
resemblance to typhoid fever. The spleen is enlarged and somewhat
softened, and Peyer's patches and the solitary glands are thickened
and prominent, but less in degree than in typhoid fever. The
mesenteric glands also are in a state of hyperplasia. In other
patients these parts appear normal.
Klein made microscopic examination of the liver in eight cases, and
states that he found granular opaque swelling of liver-cells, and
changes in the internal and middle coats of certain arteries similar
to those observed in the kidneys, which have been described above. He
also found evidences of interstitial inflammation, as an increase of
round cells and connective tissue in the liver. He remarks also that
he observed hyaline degeneration of the intima of arteries in the
spleen. Rilliet and Barthez state that swelling and softening of the
spleen are exceptional in scarlet fever, but are sufficiently common
to merit attention. In post-mortem examinations which I have witnessed
nothing noteworthy has appeared to the naked eye in the state of the
liver, nor ordinarily in that of the spleen.
The efflorescence, though one of the anatomical characters, has
perhaps been sufficiently described in the foregoing pages. It begins
over the neck, chest, and groins as numerous reddish points not larger
than a pin's head, closely crowded together, but with skin of normal
color between. It is estimated that the aggregate efflorescence and
aggregate normal skin over a given area are about equal. If the
cutaneous circulation be active and the febrile movement be
considerable these spots extend and coalesce, producing an
efflorescence like erythema or like the hue of a boiled lobster, to
which it has been likened. The efflorescence, less upon the face than
upon the trunk, contrasts in this respect with that of measles, in
which the rash is full in the face, often causing some swelling of the
features. It is also less upon the palmar and plantar surfaces than
elsewhere. It scarcely causes any perceptible elevation of the skin,
but in certain localities, as upon the backs of the hands and upon the
fore-arms, it communicates the sensation of slight roughness. The seat
of the efflorescence is mainly in the superficial layers of the skin,
but it is said that it sometimes has occurred upon a cicatrix, as that
from a burn. In the robust and in favorable cases in which the
circulation is active the rash has a scarlet hue, and when the
cutaneous capillaries are emptied and the skin rendered pale by
pressure with the {532} fingers, the circulation immediately returns
when the pressure is removed. In malignant cases the color is not
scarlet, but dusky red, and so sluggish is the capillary circulation
that the skin when pressed upon recovers the blood very slowly. In
grave cases also extravasation of blood in minute points or
transudation of its coloring matter is apt to occur in portions of the
surface, when of course decolorization is not fully produced by
pressure. In cases ending fatally, during the eruptive stage the
efflorescence may entirely disappear in the cadaver, or it remains
upon parts of the surface, especially depending portions. Desquamation
is attributable to the exaggerated proliferation of the epidermis and
the loosening of its attachment by the inflammation.
DIAGNOSIS.--In the commencement of scarlet fever, prior to the
eruption, no symptoms or appearances exist which enable us to make a
positive diagnosis. Positive statement in reference to the nature of
the attack should be deferred, for the credit of the physician. Still,
if a child with no appreciable local disease sufficient to cause the
symptoms a few days after exposure to scarlet fever, or during an
epidemic of this malady, be suddenly seized with fever, the pulse
rising to 110, 120, or more, and the temperature to 102 degrees, 103
degrees, or 105 degrees, scarlatina should be suspected. The diagnosis
is rendered more certain at this early stage if vomiting occur, and
especially if the fauces be red, for hyperaemia of the fauces, due to
commencing pharyngitis, is one of the earliest and most constant of
the local manifestations of scarlatina.
When the eruption has appeared the nature of the malady is in most
instances apparent. The punctate character of the eruption before it
becomes confluent, its occurrence within twenty-four hours after the
fever begins over almost the entire surface, but its absence or
scantiness upon the face, and especially around the mouth, serve to
distinguish it from other diseases.
Scarlet fever and measles were long considered identical by the
profession, and, though the ordinary forms of these maladies can be
readily distinguished from each other, cases occur in which the
differential diagnosis is attended by some difficulty. But there are
differences in the symptoms and course of the two diseases which aid
in discriminating one from the other. Measles begins with marked
catarrhal symptoms, as if from a severe cold. Mild conjunctivitis,
causing weak and watery eyes, coryza, and mild laryngo-bronchitis,
with accompanying cough, precede the eruption three or four days and
continue during the eruptive stage. The febrile movement in the
prodromic stage of measles is remittent, the evening temperature being
two or three degrees higher than that in the morning. Contrast this
with the invasion of scarlet fever, in which the only catarrh is that
of the buccal and faucial surfaces, and there is consequently little
or no cough, and the febrile movement, ordinarily high in the
beginning, is nearly uniform in the different hours of the day. The
scarlatinous eruption appears, as we have seen, within twelve to
twenty-four hours about the neck and upper part of the chest, and
spreads over the body in a shorter time than that of measles, which
appears on the third day. The rash of measles begins to fade at the
close of the third or in the fourth day after its appearance, that of
scarlet fever not till from the sixth to the eighth day. In nearly all
cases of measles, even when the rash is confluent upon the face and a
{533} considerable part of the trunk, in consequence of the high
febrile movement and vigorous cutaneous circulation, we observe the
characteristic rubeolar eruption upon certain parts of the surface, as
the extremities, which, in connection with the history, renders
diagnosis certain.
Erythema resembles the scarlatinous eruption, but its duration is
commonly shorter. It is limited to a part of the surface, and it is
accompanied by much less febrile movement. The temperature in erythema
does not usually rise above 100 degrees, unless for a few hours,
whereas in scarlet fever it continues considerably above 100 degrees
for several days. The scarlatinous efflorescence has also a brighter
red or more scarlet hue than that of erythema, except in the more
malignant cases, in which the severity of the symptoms renders the
diagnosis clear. But an important aid in differentiating the one from
the other of these diseases is the fact that in erythema there is,
with few exceptions, no faucial inflammation, and in the few instances
in which it is present it is slight and transient, fading within a day
or two.
Scarlet fever is readily diagnosticated from diphtheria, although the
affinity is close between these two maladies. The early appearance of
the pseudo-membrane upon the fauces in diphtheria, its absence in
scarlet fever, and the absence of any appearance resembling it until
the fever has continued some days, and the characteristic
efflorescence upon the skin in scarlet fever, render diagnosis easy.
If scarlet fever have continued some days when first seen by the
physician, the diphtheritic pseudo-membrane may be present as a
complication, or the fauces may present an appearance like diphtheria
from ulceration or sloughing and the presence of foul and offensive
secretions, which produce a dark-grayish and fetid mass over the
faucial surface. Under such circumstances the character of the disease
is ascertained by the history of the case, and especially by the
occurrence of the scarlatinous eruption. An erythema transient and
limited to a part of the surface sometimes appears in the commencement
of diphtheria, and at a later period, as a result of the toxaemia,
points of a roseoloid appearance and irregular patches, often located
upon the extremities. Both kinds of rash can be readily diagnosticated
from that of scarlet fever, for the erythema, as has been stated, is
transient and partial, and does not exhibit minute points of deeper
injection, while the toxaemic rash differs in form and aspect from
that of scarlet fever, and appears at a stage of the case when the
scarlatinous efflorescence would have faded or begun to fade.
The efflorescence of rotheln sometimes closely resembles that of
scarlet fever, though it is usually more like that of measles; but it
is ordinarily accompanied by symptoms which are much milder than those
of scarlet fever, and it begins to abate as early as the third, and
disappears on the fourth, day. The eyes have a suffused appearance,
the temperature may reach 102 degrees or 103 degrees, and the
efflorescence may be as general over the body as that of scarlet
fever, but there is not the aspect of serious indisposition, and the
speedy abatement of the symptoms shows that the disease is not scarlet
fever.
PROGNOSIS.--The prognosis depends on the form of scarlet fever,
whether mild or severe, the strength of the patient, and the presence
or absence of complications or sequelae. The type of this disease is
sometimes so mild throughout an epidemic or during a series of years
that {534} death seldom occurs, whatever the mode of treatment; but
afterward the type changes, and the percentage of deaths increases and
remains high till another mitigation in the type occurs.
Sydenham in the middle of the seventeenth century stated that scarlet
fever, as he saw it in London, was so mild that it scarcely deserved
the name of disease: "Vix nomen morbi merebatur." Morton some years
later, and Huxham in the following century, had abundant reason to
regret the change of type, and now throughout Great Britain scarlet
fever is one of the most fatal and most dreaded of the diseases of
childhood. In Dublin during the present century, prior to 1834,
scarlet fever was uniformly mild, so that on one occasion of eighty
patients in an institution all recovered. In 1834 the type of the
disease totally changed and epidemics of unusual virulence occurred.
The type frequently changes from mild to severe or severe to mild, not
only in consecutive years, but in consecutive months. A few years
since a distinguished physician of New York treated about fifty cases
of scarlet fever in one of the institutions without a single death,
but a few months later the type of the malady changed, and his own son
was among those who perished from it. The prevailing type of the
disease should therefore be considered in giving the prognosis when in
the commencement of a case we are asked the probability as regards the
termination.
Extensive statistics, including those collected by Murchison from
various sources, show that in different epidemics the mortality may
vary as much as from 3 per cent. (Eulenberg of Coblentz) to 19.3 per
cent. (cases seen by myself in New York City in 1881-82, many of which
were complicated by diphtheria), or even to 34 per cent. (epidemic in
the Palatinate in 1868-69). The hospital statistics of Rilliet and
Barthez gave 46 deaths in 87 cases, or about 53 per cent.
Observations have thus far failed to establish any connection in the
atmospheric conditions of temperature or moisture and the type of
scarlet fever. Grave as well as mild epidemics have occurred in all
climates and seasons.
The mortality is nearly equal in the two sexes, but age bears a marked
influence on the percentage of deaths. Comparatively few contract
scarlet fever under the age of one year, and the period of its
greatest mortality, since it is of its greatest frequency, is between
the ages of one and six years. The following are statistics bearing on
the relation of the age to the percentage of deaths:
From the
close of From the
1st till 5th to
Under close of the 12th
1 year. 5th year. year.
------- --------- --------
Fleishman, Cases 8 204 260
Deaths 6 88 51
1st to From the
close of 6th to 12th to
6th year. 12th year. 20th year.
--------- ---------- ----------
Kraus, Cases 13 113 106 40
Deaths 4 29 10 2
7th to
16th year.
----------
Voit, Cases 5 166 109
Deaths 1 24 10
1st to
close of Over
5th year. 5 years.
--------- --------
Roset, Cases 43 156 88
Deaths 26 31 3
{535} Under 5th to 10th to Over
5 years. 10th year. 15th year. 15 years.
-------- ---------- ---------- ---------
Rusigger, Cases 101 126 47 27
Deaths 21 20 3 0
These statistics, which I believe correspond with the observations of
others, show that although few cases occur in the first year, the
percentage of deaths is large, and that a majority of the deaths occur
under the age of six years. After the sixth year the greater the age
the less the proportionate number of deaths.
Scarlet fever is liable to so many complications and sequelae that a
physician should not predict a certain favorable termination in the
beginning, however mild and regular the symptoms may be. But a
favorable result may be expected if the attack be mild, the
efflorescence appear at the proper time and extend over the entire
surface, the angina be moderate and accompanied by little or no
cellulitis or adenitis, with pulse under 140, temperature not above
103 degrees, and no marked nervous symptoms.
Whether the complications or sequelae be dangerous depends upon their
character. Rheumatism has never in my practice been dangerous, nor has
it materially retarded convalescence, except when it affected the
heart, causing pericarditis or endocarditis, when it involves great
danger. Nephritis, if it be moderate, attended by little albuminuria
and serous effusion, and by the occurrence of few renal casts in the
urine, commonly ends favorably under judicious treatment, as we have
already stated; but severe nephritis, with abundant albuminuria and
casts and serous effusions, soon gives rise to alarming symptoms, and
is the cause of death in a considerable number of instances. A similar
remark is applicable to the angina, which occurs in all grades of
severity. If it be attended by much cellulitis, with considerable
ulceration or necrosis, the state is one of danger, in consequence of
the difficulty in administering sufficient nutriment, of the
diminished assimilation and of the loss of strength from the prolonged
inflammatory fever, the septic poisoning, and the occasional
hemorrhages. Complication by pharyngeal or nasal diphtheria, now so
common where diphtheria is endemic, also greatly increases the danger.
Many cases, even when their course is normal and without
complications, involve danger, and some are necessarily fatal, from
the direct effect of the scarlatinous blood-poisoning. Such are grave
or malignant forms of the disease which the experienced eye recognizes
at a glance. Death often occurs rapidly from the toxaemia. Such cases
are characterized by high temperature (105 degrees or 106 degrees),
rapid pulse, a dusky-red hue of the surface from languid capillary
circulation, pungent heat, frequent vomiting, diarrhoeal stools, a
dry-brown tongue, and marked nervous symptoms, such as delirium, great
restlessness, or stupor. Not a few in this form of scarlet fever take
eclampsia, which is apt to be severe and repeated, and to end in fatal
coma.
Other inflammatory complications and sequelae, which have been
described in the preceding pages, retard convalescence and jeopardize
the life of the patient, such as empyema, endocarditis, pericarditis,
and pneumonia. Otitis media is seldom immediately dangerous, although
it may be painful and involve serious consequences, even a fatal
meningitis, as has been stated above, after months or years of
otorrhoea. Anomalous cases are believed to be, as a rule, more
dangerous than such as are {536} attended by an early and full
efflorescence and have the usual symptoms.
TREATMENT.--PROPHYLAXIS. Since the discovery by Jenner of the
prophylactic power of vaccination as regards small-pox, the attention
of the profession has been frequently directed to the prevention of
scarlet fever. Belladonna has been employed for this purpose by a
class of practitioners who believe in the theory that an agent which
produces symptoms similar to those of a disease is antagonistic to
that disease, and therefore tends to prevent it, or, if it be present,
to render it milder; and since this herb causes an efflorescence upon
the skin and redness of the fauces, it was selected as the proper
preventive and remedial agent for scarlet fever. Its use, however, for
this purpose has been fruitless, and it is now nearly or quite
discarded.
It is probable, from a considerable number of observations, that
scarlet fever occasionally occurs in the domestic animals during
epidemics of the disease in children. It is stated that Spinola
observed it in the horse; that Heim saw a dog that occupied the same
bed with a scarlatinous patient sicken with fever, which was followed
by desquamation; that Letheby saw scarlatina in swine, and Kraus in
young cattle. Prominent veterinary surgeons, as Williams of Great
Britain, admit the occurrence of scarlatina in animals, and the hope
has arisen that since small-pox is modified in cattle so as to afford
us the vaccine virus, perhaps scarlet fever may also be modified by
passing through one of the lower animals, so that a milder and less
fatal form of the disease might be produced in man by inoculation from
the animal. This theory, though it deserves investigation, is far from
being established. It has not yet, so far as I am aware, been shown
that scarlet fever is milder in any animal than in man, nor, if we
admit that it is modified in the animal, is it certain that the
disease could be returned to man in the modified form. In the _N.Y.
Medical Record_ for March 24, 1883, some experiments are detailed by
S. W. Strickler of Orange, New Jersey. He cites the experiments of
Caze and Feltz, who injected scarlatinal blood under the skin of
sixty-six rabbits, and of these sixty-two died within eighteen hours
to fourteen days, which indicated a highly poisonous state of the
blood employed, either septic or scarlatinous, and certainly no
mitigation of the virulence of the scarlet fever. Strickler obtained
from Williams of Edinburgh nasal mucus from a horse supposed to have
scarlatina, and with it inoculated twelve children, all of whom had
sores at the point of inoculation, with redness of the skin around the
sores, and in some instances swelling of the adjacent lymphatic
glands. It is stated that the children thus inoculated did not
contract scarlet fever subsequently when they were exposed to
scarlatina. Obviously, there is a serious objection to such
experiments upon children, so that they may not be repeated, but a
movement has been made in one of the New York medical societies
looking to the appointment of a competent committee to investigate
them. Some of the prominent veterinary surgeons of this city do not
attach much importance to the experiments thus far made, as they are
in doubt whether the virus employed was that of the genuine disease.
It is a matter of great interest and importance, and one not yet
elucidated, whether or to what extent disinfectant and antiseptic
remedies administered internally prevent the occurrence of the
infectious maladies {537} in those who have been exposed, and aid in
curing those who are sick with them. Sodium sulpho-carbolate, from
which, by decomposition in the system, carbolic acid is supposed to be
set free, has been used for this purpose. It is administered to adults
in doses of ten to thirty grains, and to children in doses
proportionate to their age. Declat has prepared a syrup of phenic
(carbolic) acid as a preventive and curative agent in the infectious
diseases. It is now employed by several of the New York physicians,
but thus far the statistics of its use are not sufficient to determine
its efficacy. It is a question whether the so-called antiseptics can,
on account of their toxic properties, be used with safety in doses
sufficiently large to be antidotal to the specific principle of any of
the infectious maladies.
It is not my intention to recommend in this treatise any remedial
agent that has not been fully tried and its efficacy determined; but
from observations made by myself in nearly twenty families in which
scarlet fever was prevailing, I am convinced that boracic acid (acidum
boricum), an antiseptic recently introduced into our Pharmacopoeia,
deserves trial as a preventive and antidote of scarlet fever as well
as diphtheria. The good result in my practice from the use of this
agent, which only extends over about six months, may be due to the
present type of scarlet fever, but I have been surprised at the
favorable progress of the cases which appeared very grave in the
beginning, at the small mortality, and at the large proportion of well
children exposed to scarlatinous cases that escaped infection, to whom
this medicine was regularly administered. Boric (boracic) acid has
been recently used by aurists with remarkable success in suppurating
and granulating otitis media, and by oculists as an eye-wash. E. R.
Squibbs says of it (_Ephemeris_, May, 1883): "A solution saturated at
ordinary temperatures contains between 4 and 5 per cent.... It is a
very bland and soothing application, whether applied in powder or
solution, relieving irritation and reducing suppuration.... It has
been administered internally in large doses without any disturbing
effects." The preparation which I have employed is one found in the
shops, with the name listerine, prepared by a Western pharmaceutical
firm. It contains, according to the manufacturers, the "essential
antiseptic constituents of thyme, eucalyptus, baptisia, gaultheria,
and mentha arvensis," and also two grains of benzo-boracic acid in
each drachm. The dose of listerine which I have employed for an adult
is one teaspoonful, considerably diluted with cold water. A child of
five years can take ten to fifteen drops every two to four hours. I
call the attention of the profession to the use of boracic acid as an
antidote to the scarlatinous poison, without sufficient experience to
enable me to speak positively of its efficacy, but with the hope and
expectation, from observing its apparent effects in seventeen families
afflicted with scarlet fever, that it will be found a useful addition
to our means of controlling this much-dreaded and fatal malady.
In the present state of our knowledge the most reliable and certain
prophylaxis is the isolation of patient and nurses, and the thorough
and judicious employment of disinfectants upon their persons and in
the apartments. All furniture and articles not absolutely required
should be removed from the sick room, and no one should be allowed to
enter it except the medical attendant and nurses. Constant ventilation
should be {538} insisted on by lowering the upper and raising the
lower sash of the window two or three inches in mild weather. Even in
stormy weather sufficient ventilation can be obtained in this way
without exposing the patient to currents of air, which should be
avoided.
Since the exhalations from the body, the various excretions, and the
epidermic cells shed so abundantly in the desquamative period contain
the scarlatinous poison, measures should be employed to disinfect
them, in so far as the comfort and well-being of the patient will
allow. Vessels which receive the excretions should contain carbolic
acid, chloride of lime or other disinfectant, and they should be
immediately emptied and cleaned after use. By the frequent application
of disinfecting washes to the nostrils and fauces the secretions from
these surfaces are to a great extent deprived of their contagiousness.
If otorrhoea occur, boracic acid, so serviceable in its treatment,
acts as a disinfectant, but in addition the ear should be syringed
with warm carbolized water, one drachm of carbolic acid to the pint of
water, and this should be continued during convalescence, for cases
occur which show that the discharge from the ear is probably the
vehicle by which the virus is communicated. Even as late as the fourth
week after the disappearance of the rash children in scarlet fever
experience relief from inunction of the surface, and if carbolic acid
be added to the substance which is employed for this purpose, and the
inunction be made twice daily over the entire surface, contamination
of the air through the exfoliations and exhalations from the skin is
in great part prevented. The late William Budd of Bristol, England,
was in the habit of recommending inunction of the surface twice daily
with sweet oil, which answered the purpose of preventing dissemination
of epidermic particles through the air; and we will presently see how
successful were his precautionary measures.
A convalescent child should not be allowed to mingle with other
children till three or four weeks have elapsed and desquamation has
ceased; and all who are liable to take the malady should be excluded
from the room in which a case has occurred for a longer period, and
until it has been thoroughly disinfected by burning sulphur or other
methods.
The New York Board of Health enforces the following excellent
regulations to prevent the spread of scarlet fever as well as other
acute infectious maladies:
"Care of Patients.--The patient should be placed in a separate room,
and no person except the physician, nurse, or mother allowed to enter
the room or to touch the bedding or clothing used in the sick-room
until they have been thoroughly disinfected.
"Infected Articles.--All clothing, bedding, or other articles not
absolutely necessary for the use of the patient should be removed from
the sick room. Articles used about the patients, such as sheets,
pillow-cases, blankets, or clothes, must not be removed from the sick
room until they have been disinfected by placing them in a tub with
the following disinfecting fluid; eight ounces of sulphate of zinc,
one ounce of carbolic acid, three gallons of water. They should be
soaked in this fluid for at least an hour, and then placed in boiling
water for washing.
"A piece of muslin one foot square should be dipped in the same
solution and suspended in the sick room constantly, and the same
should be done in the hallway adjoining the sick room.
{539} "All vessels used for receiving the discharges of patients
should have some of the same disinfecting fluid constantly therein,
and immediately after being used by the patient should be emptied and
cleansed with boiling water. Water-closets and privies should also be
disinfected daily with the same fluid or a solution of chloride of
iron, one pound to a gallon of water, adding one or two ounces of
carbolic acid.
"All straw beds should be burned.
"It is advised not to use handkerchiefs about the patients, but rather
soft rags, for cleansing the nostrils and mouth, which should be
immediately thereafter burned.
"The ceilings and side-walls of a sick-room after removal of the
patient should be thoroughly cleaned and lime-washed, and the woodwork
and floor thoroughly scrubbed with soap and water."
By such measures of prevention there can be no doubt that the number
of cases of scarlet fever would be greatly reduced.
Budd for years recommended similar precautions in the families which
he attended, and the following is his testimony in regard to the
result: "The success of this method in my own hands has been very
remarkable. For a period of nearly twenty years, during which I have
employed it in a very wide field, I have never known the disease to
spread beyond the sick-room in a single instance, and in very few
instances within it. Time after time I have treated this fever in
houses crowded from attic to basement with children and others, who
have nevertheless escaped infection. The two elements in the method
are separation on the one hand, and disinfection on the other."[7]
[Footnote 7: _British Medical Journal_, Jan. 9, 1869.]
HYGIENIC TREATMENT.--The room occupied by a scarlatinous patient
should be commodious and sufficiently ventilated. Its temperature
should be uniform at about 70 degrees during the course of the fever.
When the fever begins to abate and desquamation commences, a
temperature of 72 degrees to 75 degrees is preferable, so that there
is less danger that the surface may be chilled during unguarded
moments, as at night, when the body may be accidentally uncovered,
since sudden cooling of the surface at this time may cause nephritis
or some other dangerous inflammation. Henoch does not believe in the
theory that the nephritis is commonly produced by catching cold, but
many observations show that those who are carefully protected from
vicissitudes of temperature, who remain during convalescence in a warm
room, and are protected by abundant clothing, more frequently escape
this complication than such as are under no restraint of this kind and
are carelessly exposed in times of changeable weather. Nevertheless,
it is true that a certain proportion suffer from nephritis however
judicious the after-treatment may be. The best hygienic management
does not always prevent its occurrence. The patient should not,
therefore, leave the house until four weeks after the beginning of the
fever, and in inclement weather not till a longer time has elapsed. So
long as desquamation is going on and the skin has not regained its
normal function the patient should remain indoor, and when finally he
is allowed to leave the house he should be warmly clothed.
THERAPEUTIC TREATMENT.--In order to treat scarlet fever successfully
it is necessary to bear in mind that it is a self-limited disease,
running for a certain time and through certain stages, and that it is
not {540} abbreviated by any known treatment. Therapeutic measures can
only moderate its symptoms and render it milder. The severity of the
disease is indicated by its symptoms, and the symptoms are to a
certain extent under our control.
MILD CASES.--A patient with a temperature under 103 degrees, and with
only a moderate angina, does not require active treatment, but,
however light the disease, he should always be in bed and in a room of
uniform temperature, as stated above. Instances have come to my notice
in the poor families of New York in which scarlet fever was not
diagnosticated, and the patients were allowed to go about the house,
and even in the open air, in the eruptive stage, till some severe
complication or an aggravation of the type created alarm and medical
advice was sought, when it appeared that a grave and dangerous
condition had, through carelessness and ignorance, resulted from a
mild and favorable form of the malady. The physician, when summoned to
a case however mild, should never fail to take the temperature, note
the pulse, inspect the fauces, and inquire in reference to the fecal
and urinary evacuations, that he may detect early any unfavorable
changes which may occur.
Since in all cases angina and more or less blood-deterioration are
present, the following prescription will be found useful in mild as
well as severe scarlet fever:
Rx. Potass. Chlorat. drachm ii;
Tr. Ferri Chloridi fl. drachm ii;
Syrupi fl. oz. iv. M.
S. Half a teaspoonful every hour to two hours to a child of three
years; a teaspoonful to a child of six years.
Small doses of this medicine frequently administered act beneficially
on the surface of the throat and tend to prevent the anaemia which is
so common after scarlet fever. If the medicine be given gradually
diluted with only a moderate amount of water, the effect is better on
the inflamed fauces. Potassium chlorate is known to be an irritant to
the kidneys in large doses, causing intense hyperaemia of these
organs, with bloody urine or suppression of urine. The melancholy fate
of Fountaine, who died from the effects of one ounce of this medicine,
is known to the profession. I have seen a similar instance in a child.
But doses of one to four grains, according to the age, can be
administered with safety to children, so that half a drachm to a
drachm and a half are taken in twenty-four hours. A quantity much
exceeding this amount involves risk. In mild cases it is not necessary
to treat the throat by topical measures, the above prescription
producing sufficient local effect, but camphorated oil may be used
externally. I ordinarily prescribe quinine in small doses for this
form of scarlatina, as in the following formula:
Rx. Quiniae Sulphat. gr. xvi;
Ext. Glycyrrhizae scruple ss;
Syr. Pruni Virginianae fl. oz. ii. M.
S. One teaspoonful every fourth hour to a child of three to five
years, the potassium chlorate and iron mixture being administered
twice between.
The treatment of scarlatina by antiseptic remedies will be considered
hereafter.
{541} The itching and dryness of the surface, which increase the
discomfort of the patient in mild as well as severe scarlatina, are
relieved by frequently anointing the whole body with vaseline, cold
cream, or butter of cocoa. Carbolic acid is an efficient remedy for
pruritus, while it is also a disinfectant. It may be used in the
following formula:
Rx. Acidi Carbolici drachm i;
Vaseline oz. iv. M.
S. To be applied over the entire surface.
In New York leaf lard has long been employed as an unguent over the
entire surface in scarlet fever, and patients experience benefit from
it. Alcohol and water or vinegar and water are sometimes employed for
the same purpose. The linen should be changed every day and the bed
thoroughly aired.
ORDINARY CASES AND CASES OF SEVERE TYPE.--A safe temperature in
scarlet fever may be considered at or below 103 degrees. If it rise
above this, measures designed to abstract heat are very
important--more important even in many cases than the medicinal agents
which are commonly used to combat this disease. Since a high
temperature retards assimilation, promotes deleterious tissue-change,
and causes rapid emaciation and loss of strength, measures designed to
reduce it are urgently needed. "The production of heat depends chiefly
on oxidation of the constituents of the body" (Billroth). Therefore
fever indicates an increase of the oxidation and a molecular
disintegration above the healthy standard. Hence the augmentation of
urea in the urine and the progressive emaciation and loss of weight
which characterize the febrile state. Fever also diminishes the
secretions by which food is digested and destroys the appetite, so
that repair of the waste is insufficient. Moreover, a high temperature
continuing for a time tends to produce degenerative changes,
albuminous and fatty, in the tissues, the more rapidly the higher the
temperature, so that the functions of organs are seriously impaired.
Among the most dangerous of the tissue-changes is granulo-fatty
degeneration of the muscular fibres of the heart. In dogs and rabbits
that have perished from a high temperature artificially produced by
experimenters granular clouding of the elementary tissues has been
found after death.[8] A high temperature, therefore, in itself
involves danger, and if it occur in an ataxic disease like scarlet
fever, and be protracted, it greatly diminishes the chances of a
favorable issue.
[Footnote 8: See experiments by Mr. J. W. Legg, _Lond. Path. Soc.
Trans._, vol. xxiv., and others.]
The temperature can be reduced without shock or injury to the child by
the judicious use of cold water externally. The cold-water treatment
is not necessary if the temperature be under 103 degrees, though
useful if judiciously employed by sponging when the temperature is at
102 degrees or 103 degrees; but if it rise above 103 degrees it is
required, and the more urgently the higher the temperature. The
external use of cold water as an antipyretic in the febrile diseases
is now almost universally recommended by physicians, but it still
meets with opposition on the part of families, especially in the
treatment of the exanthematic fevers, and the directions for its
employment are therefore not apt to be fully carried out during the
absence of the medical attendant. The old theory that the fevers
require warmth and sweating has such a firm hold on the popular mind
that some years longer will be required for its removal.
{542} The modes of applying cold water recommended by cautious and
experienced physicians are various. Von Ziemssen recommended that the
patient be immersed in water at a temperature of 90 degrees, and cool
water be gradually added till the temperature fall to 77 degrees. In a
few minutes the patient is returned to his bed, his surface dried, and
he is covered by the proper bed-clothes, when his temperature will
probably be found reduced two or two and a half degrees. If the
patient complain of chillness or his pulse be feeble, he should be
immediately removed from the bath and stimulants administered, either
whiskey or brandy, for if the extremities remain cool and the
capillary circulation sluggish, the effect may be injurious, since
some internal inflammation may arise to complicate the fever. Under
such circumstances increased alcoholic stimulation is required.
The cold pack is also effectual for reducing the temperature. The
patient is placed upon a mattrass protected by oil-cloth, and is
covered by a sheet wrung out of water at a temperature of 70 degrees.
This is covered by one or two blankets. In half an hour he is returned
to bed, and will be found to have a temperature two or three degrees
less than that before the bath. Another method is to apply the sheet
wrung out of water at 90 degrees, and then reduce the temperature by
adding water at a lower degree from a sprinkler. In most cases,
however, I prefer to reduce the temperature by the constant
application to the head of an india-rubber bag containing ice. The bag
should be about one-third filled, so that it should fit over the head
like a cap. At the same time, as a potent means of abstracting heat,
at least when the temperature is at or above 104 degrees, a similar
application should be made by an elongated rubber bag lying over the
neck and extending from ear to ear. Cold applied over the great
vessels of the neck promptly abstracts heat from the blood, while it
diminishes the pharyngitis, adenitis, and cellulitis; which is an
important gain. At the same time, it is proper to sponge frequently
the hands and arms with cool water. If the temperature with this
treatment be not sufficiently reduced, one or two thicknesses of
muslin frequently wrung out of ice-water should be placed along the
arms and upon either side of the face. By such local measures, which
are agreeable to the patient and without any shock or perturbing
effect on the system, we can reduce the temperature two or three
degrees. By adding alcohol or one of the alcoholic compounds to the
water the popular objection to the use of cold is overcome.
Trousseau, in the treatment of sthenic cases attended by a high
temperature, was in the habit of placing the patient naked in a
bath-tub and directing three or four pailsful of water to be thrown
over him in a space of time varying from one quarter of a minute to
one minute, after which he was returned to bed and covered by the
bed-clothes without being dried. Reaction immediately occurred, often
with more or less perspiration. This treatment was repeated once or
twice daily, according to the gravity of the symptoms. Trousseau,
alluding to this treatment, says: "I have never administered it
without deriving some benefit." But the application of cold water in a
manner that does not excite or frighten the patient seems preferable.
Henoch, having a large experience, gives the following advice in
reference to the water treatment: "If the fever continue high and the
apparently malignant {543} symptoms described above develop, the head
should be covered with an ice-bag, ... and the child placed in a
lukewarm bath, not under 25 degrees R. (88.25 degrees F.). I decidedly
oppose cooler baths, because in scarlatina, which presents a tendency
to heart-failure, cold may produce an unexpected rapid collapse more
than in any other affection. But I strongly recommend washing the
entire body every three hours with a sponge dipped in cool water and
vinegar."[9] In grave cases with a high temperature the application of
cold should be sufficient to produce a decided reduction of heat,
otherwise the full benefit from its use is not obtained. With proper
stimulation and proper precautions prostration does not occur from the
ice-bags to the head and neck and cool sponging of other parts, so
long as the temperature does not fall below 102 degrees or 103
degrees. The danger alluded to by Henoch can only occur from the use
of the pack or general bath, and the water treatment can be
efficiently carried out and the temperature sufficiently reduced
without resorting to these. Even Currie of Edinburgh, who first drew
attention to the benefit from the cold-water treatment of scarlet
fever in an age when the sweating treatment, and even the exclusion of
cool and fresh air from the apartment, were deemed necessary,
recommended cold affusion only in sthenic cases with full and strong
pulse, and he mentions as a warning two cases with quick and feeble
pulse and cool extremities in which death occurred immediately after
the use of the water.
[Footnote 9: _Diseases of Children._]
Sodium salicylate is in some instances a useful remedy for the
reduction of heat in the infectious diseases. It seems to be more
decidedly antipyretic than quinine in the febrile and inflammatory
diseases, though somewhat depressing to the heart's action. James
Couldrey writes to the _London Lancet_ (Dec., 1882, p. 1064) that he
has derived great benefit from its use in seven cases of scarlet
fever. He administered it every two hours till ringing in the ears was
produced, and afterward every four hours, prescribing one grain for
each year in the age of the patient. It is, in my opinion, a proper
remedy when the pulse is full and strong and the temperature is not
sufficiently reduced by the cold-water treatment.
Aconite and veratrum viride reduce fever, but they are too depressing
to be safely employed in grave scarlet fever, and their antipyretic
effect is less than that of water. The use of digitalis might be
suggested by the quick and feeble pulse in certain cases that are
attended by high temperature, but the judgment of the profession is
for the most part against its use in such cases. What Stille and
Maisch state of its employment in typhoid fever appears equally
applicable to scarlet fever: "Even its advocates have not shown that
it abridges the disease or lessens its mortality, while it is
abundantly demonstrated to impair the digestion, reduce the strength,
and even to occasion sudden death. The use of digitalis in other forms
of fever is equally unsatisfactory, and justifies the judgment of
Traube, that the true field of action for digitalis is not fever."
Quinine is the medicine which above all others has been heretofore
most used, by almost common consent of the profession, to reduce the
temperature in malignant scarlet fever, but its use for this purpose
is, according to my observations, far from satisfactory. To obtain its
{544} antipyretic action it must be administered in large doses, and
if any of the quinine salts in ordinary use be administered by the
mouth in sufficient quantity, they are apt to be vomited. To a child
of five years five grains should be administered twice daily by the
mouth, or ten grains of a soluble salt, as the bisulphate, may be
given per rectum, dissolved in a little warm water. Administered per
rectum, it is frequently not retained unless held for a time by a
napkin. A considerable proportion of the malignant cases are attended
by not only irritability of the stomach, already alluded to, but by
diarrhoea, so that quinine, if administered at all, should be employed
hypodermically. The double salt of quinia and urea answers for this
purpose, as it is very soluble in water and does not produce
inflammation of the connective tissue. When the antipyretic doses of
quinine are discontinued, this agent may be prescribed as a tonic in
the doses recommended for the treatment of mild scarlet fever.
In severe cases with frequent and rapid pulse, in which ante-mortem
heart-clots are apt to occur, the ammonium carbonate is often useful.
It should be dissolved in water and given in milk, in as large doses
as five grains every hour or second hour to a child of five years. It
aids in producing stronger contraction of the cardiac muscular fibres,
and thus diminishes the danger of the formation of thrombi. Ten-drop
doses of the aromatic spirits of ammonia may be employed instead of
the carbonate, given in sweetened water. It is especially useful if
the stomach be irritable.
In severe cases attended by considerable angina and foul and offensive
secretions upon the faucial surface an antiseptic, as boracic acid in
small quantity, should be added to the potash and iron mixture
recommended above. If no drink be allowed for a few minutes after the
dose, so as not to wash it too soon from the fauces, the antiseptic
effect is more certainly produced. Those old enough should be directed
to hold the medicine for a moment like a gargle in the throat before
swallowing it. I employ boracic acid by preference, as in the
following formula:
Rx. Acid. Boracic. drachm ss;
Potass. Chlorat. drachm ii;
Tr. Ferri Chloridi fl. drachm ii;
Glycerinae,
Syrupi _aa._ fl. oz. i;
Aquae fl. oz. ii. M.
S. Give one tablespoonful every two hours to a child of five years.
More minute directions will presently be given for the treatment of
the pharyngitis when we speak of the complications.
Alcohol, whether administered in one of the stronger wines, as sherry,
or in whisky or brandy, is a most useful remedy in scarlet fever, and
is indeed indispensable in all grave cases which are attended by
feeble capillary circulation and evidences of prostration. Milk is
also the best vehicle for this agent. The wine-whey or milk-punch
should be given every hour or second hour. In scarlet fever, as well
as diphtheria, comparatively large doses are required, as a
teaspoonful of the stimulant every hour or second hour for a child of
five years.
During convalescence the hygienic treatment already described is
important. Nutritious diet and a moderate amount of alcoholic {545}
stimulants are required, while the patient is kept indoors and
protected from currents of air as long as desquamation is occurring.
More or less anaemia is present in most convalescent patients, so that
a mild tonic containing iron will aid in restoring the health. Elixir
of calisaya-bark and iron; preparations of beef, iron, and wine, or
the following prescription, will be found useful under such
circumstances:
Rx. Ferri et Ammon. Citrat.,
Ammon. Carbonat. _aa._ gr. xxiv;
Syrupi fl. oz. i;
Aquae fl. oz. ii. M.
S. Dose, one or two teaspoonfuls, according to the age, every third
hour.
ANTISEPTIC TREATMENT.--It is still to be determined whether or to what
extent antiseptics, administered internally, antagonize and control
the scarlatinous poison, and are therefore curative of scarlet fever.
The most important agent of this class, carbolic acid, can only be
employed in small doses, for a dose much exceeding a drop for a child,
or even exceeding a fractional part of a drop for a young child, might
produce poisonous symptoms. Carbolic acid is a cardiac and arterial
sedative, and it appears to reduce temperature. Intra-uterine
injections of carbolized water in the treatment of puerperal fever are
known to reduce temperature, even when there is no septic matter in
the uterus to be disinfected and washed away, as in a case related to
me in which the fever proved to be due to measles. It is not
improbable that the antipyretic action in patients of this class who
have no septic substance within the uterus is due largely, if not
mainly, to the absorption of carbolic acid from the uterine surface
and its sedative action on the vascular system. Whether this agent, so
highly extolled by Declat, and to which I have alluded in a preceding
page, can be safely employed in doses large enough to be efficient and
curative will be determined by future observations. The same remark is
applicable to the sulphocarbolate of sodium, whose antiseptic action
is supposed to be due, as already stated, to the liberation of
carbolic acid in the system. Since boracic acid does not seem to have
any deleterious action, this agent has been administered to most of my
scarlatinous patients during the last year, in addition to the older
and better known remedies, and with a very small percentage of deaths.
What may be the result in a more severe type of the disease remains to
be seen.
TREATMENT OF COMPLICATIONS AND SEQUELAE.--Local measures designed to
diminish or cure the pharyngitis are important in all but the mildest
cases. They are more especially required in the anginose variety and
in those not infrequent cases in which diphtheria complicates
scarlatina. Formerly it was necessary, in making applications to the
fauces, to employ the brush or probang for those too young to use the
gargle, but hand-atomizers, as Richardson's or Delano's, which are now
in common use, afford a quick and easy method for making such
applications. Six or eight compressions of the bulb of a good atomizer
are sufficient to cover the fauces with the spray. Those
hand-atomizers in the shops which have slender metallic points are apt
to prick the buccal surface and cause bleeding if the child resist and
toss the head. To prevent this, I am in the habit of directing
india-rubber tubing to be drawn over the point in such a way as not to
obstruct its action. The following will be found useful mixtures for
the atomizer: For ordinary cases, {546}
Rx. Acidi Carbolici drachm ss, vel. Acid. Boracic. drachm ii;
Potass. Chlorat. drachm ii;
Glycerinae fl. oz. ii;
Aquae fl. oz. vi. M.
If the surface of the throat be covered by foul secretions,
Rx. Acidi Carbolici drachm ss;
Potass. Chlorat. drachm ii;
Glycerinae fl. oz. j;
Aquae Calcis fl. oz. vii. M.
Or else,
Rx. Tinc. Ferri Chloridi fl. oz. ss;
Acidi Sulphurosi fl. drachm ii;
Potass. Chlorat. drachm ii;
Glycerinae fl. oz. i;
Aquae q. s. ad. fl. oz. vi. M.
If diphtheritic exudation complicate the scarlatinous angina, or the
surface of the throat in consequence of ulceration or necrosis present
an appearance like that in diphtheria when the exudation begins to
soften, being foul, jagged, of a dirty brown appearance from dead
matter and fetid secretions, the following should be prescribed for
use in the atomizer:
Rx. Acidi Carbolici drachm i, vel. Acidi Boraci drachm iii;
Liq. Potassae fl. drachm i;
Potass. Chlorat. drachm ii;
Glycerinae fl. oz. ii;
Aquae Calcis fl. oz. viii. M.
Liquor potassae, although a very efficient solvent of
pseudo-membranes, is too irritating for use in the atomizer unless
largely diluted. One part to eighty, as in the above mixture, will not
be found too concentrated. The following powder, used every third hour
through the insufflator, is also useful in cases of diphtheritic
exudation:
Rx. Acidi Salicylici drachm ii;
Bismuth. Subnitrat. oz. ii. M.
To be used every third hour. It is the favorite remedy of some of the
prominent New York physicians in the local treatment of diphtheria.
The following mixture is also beneficial for local treatment when the
faucial surface is foul and offensive from the exudations and
secretions. It should be applied by a large camel's-hair pencil every
three to six hours:
Rx. Acidi Carbolici gtt. x;
Liq. Ferri Subsulphatis fl. drachm ii;
Glycerinae fl. oz. i. M.
In all cases of scarlatinous pharyngitis sufficiently severe to
require special treatment, cool applications should be made over the
neck from ear to ear, as by two thicknesses of muslin frequently
squeezed out of cold water, or by the elongated india-rubber bag
already recommended in our remarks relating to methods to reduce
temperature.
In the first days of scarlet fever the coryza is slight, and no
discharge from the nostrils occurs, so that no local treatment is
required; but before the termination of the malady, in cases of
ordinary gravity, a nasal discharge usually supervenes, producing more
or less redness and {547} excoriating the upper lip. Moreover, in
localities where diphtheria occurs, if this malady complicate scarlet
fever, it is apt to affect the nostrils at the same time that the
fauces are invaded. These conditions require local treatment of the
nares. It should be remembered that the Schneiderian membrane is
midway in sensitiveness, as it is in location, between the
conjunctival and buccal surfaces, and is readily irritated by strong
applications. Medicinal applications made to it must be much milder
than those which the fauces tolerate. They should always be applied
warm, and a teaspoonful of any mixture properly employed is sufficient
for each nostril at one sitting. The applications should usually be
made every two or four hours, according to the gravity of the case and
the amount of discharge. The best instrument for this purpose is a
small syringe of glass or brass with curved neck and bulbous tip. The
child's head should be thrown back and the piston depressed rapidly,
so as to thoroughly wash out the nasal cavity. The application can
also be made through an atomizer with a rounded tip or a tip covered
by rubber tubing. The following is a useful prescription:
Rx. Acidi Carbolici drachm ss;
Sodii Chloridi drachm ii;
Aquae Oj.
The substitution of 2 or 3 drachms of boracic acid in place of the
carbolic acid makes a nicer preparation. If the diphtheritic
pseudo-membrane appear in the nares, the officinal lime-water,
injected every hour or second hour, is beneficial in consequence of
its solvent action on pseudo-membranes.
It is evident, from what has been stated above, that the condition of
the ear should be closely observed in and after scarlet fever. If the
patient have earache, considerable relief may be obtained in the
commencement by dropping a few drops of laudanum and sweet oil into
the ear and covering it by some hot application, either dry or moist,
which will retain the heat. A light bag containing common table-salt,
heated, or dry and hot chamomile flowers will also answer the purpose.
Water as hot as can be well tolerated dropped into the ear or allowed
to trickle from a fountain syringe, so as to fill the ear, is also
very beneficial in allaying the pain. If a few drops of laudanum be
added it is more useful. If the pain be not quickly relieved, a leech
should be applied at the base of the tragus. O. D. Pomeroy, an
experienced aurist of New York, says: "Leeching employed at the right
time rarely fails to subdue the pain and inflammation. The posterior
face of the tragus is ordinarily the best place for applying the
leech, but it may be applied in front of the ear or behind, wherever
the tenderness on pressure is greatest. In my opinion, paracentesis
may frequently be rendered unnecessary by the timely use of one or two
leeches applied to the meatus."
If the otitis continue, as shown by pain in the ear, of which children
old enough to speak bitterly complain, and which causes those too
young to speak to press their fingers into or against their ears, this
inflammation should not be neglected, as it may involve serious
consequences. Multitudes of children have had permanent impairment or
even loss of hearing, with caries or necrosis of the walls of the
middle ear and of the mastoid cells, which might have been prevented
by prompt and skilful {548} management of the ear in the early stage
of the inflammation. If, therefore, the otitis continue without
mitigation of pain after the above measures have been employed,
paracentesis of the drumhead is probably required. The following
directions for performing this operation, which will be useful to
country practitioners who may not be able to obtain the assistance of
a specialist, are from the pen of Pomeroy: "The forehead mirror should
be worn, in order to leave the hands free to operate by either
artificial or day light. A good-sized speculum is introduced into the
meatus. Then an ordinary broad needle, about one line in diameter,
with a shank of about two inches, such as oculists use for puncturing
the cornea, should be held between the thumb and fingers, lightly
pressed, so as not to dull delicate tactile sensibility. The part
being well under light, the most bulging portion of the membrane
should be lightly and quickly punctured with a very slight amount of
force. The posterior and superior portion of the membrane is most
likely to bulge. The chordae tympani nerve ordinarily lies too high up
to be wounded. The ossicles are avoided by selecting a posterior
portion of the membrane. After puncture the ear should be inflated by
an ear-bag whose nozzle is inserted into a nostril, both nostrils
being closed, so as to force the fluid from the tympanum. The puncture
may need to be repeated at intervals of a day or two, provided that
the pain and bulging return."
Albert H. Buck of New York, in a highly instructive paper read before
the International Medical Congress in 1876, writes as follows of
paracentesis of the membrana tympani in scarlatinous otitis: "In this
one slight operation, which in itself is neither dangerous nor very
painful, lies the power to prevent the whole train of disagreeable and
dangerous symptoms." Buck relates an instructive example: The age of
the patient was three years, and the earache had been complained of
only about twenty-four hours. "Toward morning," says he, "I was sent
for, as the pain had become constant.... An examination with the
speculum and reflected light showed an oedematous and bulging membrana
tympani (posterior half), the neighboring parts being very red, though
as yet but little swollen. In the most prominent portion of the
membrane I made an incision scarcely three millimetres (one-tenth
inch) in length, and involving simply the different layers of the
membrana tympani. This was almost immediately followed by a watery
discharge (without the aid of inflation), which ran down over the
child's cheek. At the end of three or four minutes the child had
ceased crying, and in less than a quarter of an hour she was fast
asleep. At first, the discharge was very abundant and mainly watery in
character, but it steadily diminished in quantity and became thicker,
till finally, on the fourth day, it ceased altogether. On the tenth
day the most careful examination of the ear could not detect any trace
of either the inflammation or the artificial opening." The ear had
probably been saved from ulceration of the drum membrane,
long-continued suppurative otitis, and perhaps from permanent
impairment of hearing.
When an opening has been made in the membrana tympani either by
incision or ulceration, it is advisable in some instances to inflate
the tympanum by Politzer's method, which has been alluded to above.
The nozzle of an india-rubber bag, with a flexible tube attached, is
introduced into the nostril on the affected side, and both nostrils
are compressed {549} against it. The patient fills his mouth with
water, which he swallows at a given signal, as after the words one,
two, three, spoken by the operator. During the act of swallowing,
which opens the Eustachian tube, the rubber bag is forcibly
compressed, which forces the air along the tube into the middle ear
and facilitates the escape of the pent-up secretions in the tympanic
cavity.
If the otitis have continued unchecked by treatment until the
secretions within it, after days and nights of suffering, have escaped
by ulceration through the drumhead, the opportunity for prompt and
certain cure is passed. Still, the patient under these circumstances
may quickly recover, or there may be the other alternative described
above, in which the ear is badly damaged and chronic inflammation
established in the walls of the tympanum, giving rise to an offensive
otorrhoea. In this state of the ear internal remedies are indicated,
such as surgeons employ in suppurative inflammations of bone occurring
in other parts of the system. Cod-liver oil and iodide of iron are
required, especially by patients of strumous diathesis, the object
being to promote a more healthy state of system, so as to prevent
extension of the inflammation and facilitate the healing process.
Carbolized solutions, as the following, syringed warm into the ear in
which otorrhoea is occurring, are useful in promoting cleanliness and
increasing the comfort of the patient:
Rx. Acidi Carbolici drachm ss;
Glycerinae fl. oz. ii;
Aquae fl. oz. iv. M.
But recently a much more effectual curative agent for local treatment
has been discovered in boracic acid, by the use of which the discharge
more quickly diminishes and the condition of the ear more certainly
and rapidly improves than by the use of the carbolized mixtures. When
the inflammation is recent and the ear sensitive and painful, the
following prescription should be used:
Rx. Acidi Boracici drachm iiss;
Morphiae Sulphat. gr. i;
Glycerinae,
Aquae _aa._ fl. oz. i. M.
S. Drop one to three drops into the ear three times daily.
If the acute stage of the otitis have passed, with fever and pain, and
no tenderness be present on pressure, the following prescription,
which causes too much pain in the acute stage, will be found useful to
check the inflammation and otorrhoea and restore a healthy state to
the granulating surface:
Rx. Acidi Boracici drachm iiss;
Alcohol.
Aquae _aa._ fl. oz. i.
S. Drop one to three drops into the ear three times daily.
The beneficial effects observed from the use of boracic acid in aural
surgery have given it nearly the same position as a curative agent to
diseases of the ear which atropine holds to diseases of the eye.
Recently, aurists are employing finely-triturated powder of boracic
acid dusted into the ear. The patient lies upon the side with the
affected ear uppermost. The ear is thoroughly cleaned by syringing
with tepid water, and by means of a little scoop made of stiff paper
or pasteboard or the segment {550} of quill as much of the powder is
introduced into the ear as would cover a five-cent silver piece. By
working the ear it descends to the drumhead. I can bear witness to its
efficacy in the otorrhoea of children when it is used in this manner
three times daily.
The following astringent has also been employed with good results for
the otorrhoea resulting from scarlet fever as well as from other
causes:
Rx. Zinci Sulphatis,
Aluminis _aa._ gr. v;
Aquae fl. oz. i. M.
A few drops of this should be dropped into the ear, or, if the ear be
sensitive and painful, five drops should be added to a teaspoonful of
warm water and dropped or syringed into the ear.
But in recent times aurists have discovered a remedy superior to the
above in iodoform, the action of which is safe and efficient for
protracted otorrhoea with granulations, and it is superseding to a
great extent the agents heretofore used in the treatment of this
disease. The ear should first be thoroughly cleaned by syringing with
warm water and dried, and iodoform, to which a little balsam of Peru
is added to cover the disagreeable odor, should be pressed down to the
bottom of the auditory canal by any convenient instrument. It is
anodyne, astringent, and disinfectant, and should be employed in a dry
state in considerable quantity.
The sequelae of otitis media, such as granulations sprouting out from
the drumhead, some of which may be of large size and are known as
polypi, may require treatment by the aurist. A polypus may sometimes
be removal by the forceps or better by the snare. Polypi not large and
favorably located can sometimes be cured by an astringent powder, as
iodoform, sulphate of zinc, or alum, or by applying the liquid
subsulphate of iron. The otitis externa produced by the irritating
discharge which flows from the middle ear soon disappears when the
flow ceases.
The renal affection, which, as we have seen, so often commences in the
declining period of scarlet fever or during convalescence in mild as
well as severe cases, is frequently more dangerous than the primary
disease. It largely increases the percentage of deaths. A clear
appreciation of its therapeutic requirements is important, since by
judicious treatment many recover who would inevitably be sacrificed by
improper measures. The family should be informed that the danger from
scarlet fever does not cease with the decline of the eruption, and
that the kidneys may become seriously affected by too early exposure
of the patient to currents of air or sudden changes of temperature, by
which cutaneous transpiration is checked. He should therefore be kept
indoors in a comfortable and uniform temperature three or four weeks
after the termination of the fever, until desquamation has entirely
ceased and the new epiderm is sufficiently thick and firm to protect
the surface. During the changeable temperature of the autumnal,
winter, and spring months even longer confinement at home may be
advisable.
The nephritis and consequent albuminuria antedate by some days the
occurrence of dropsy, and a physician should never discharge a
scarlatinous patient without one or more examinations of his urine.
When his visits cease the nurse should be instructed to make the
examinations by heat and nitric acid during the ensuing month, and if
any evidence, however slight, appear that the kidneys are involved, he
should be notified, {551} in order that appropriate treatment may be
immediately commenced. Early and correct treatment of the nephritis is
attended by much better results than delayed treatment, and many more
patients are doubtless now saved than in former times, when little
attention was given to the state of the kidneys until dropsy or other
prominent symptoms appeared. I have found no mother or nurse so
ignorant that she could not properly employ the test of nitric acid
and heat, and, if she be solicitous for the welfare of the child, she
will not hesitate to carry out the directions and immediately notify
the physician if the tests employed produce the least cloudiness or
turbidity of the urine.
The patient as soon as nephritis commences, as shown by the state of
the urine, should be put to bed in a room of warm and equable
temperature (72 degrees to 75 degrees F.). His diet should be liquid,
consisting of milk, farinaceous food, and a moderate quantity of
animal broths. He may drink liquids freely, especially water not too
cool, to which spiritus aetheris nitrosi is added. If he be prostrated
by the primary disease, alcoholic stimulants should be allowed.
The indications are to relieve the hyperaemic kidneys by diaphoresis
and purgation. To produce the former the patient should be immersed in
a warm bath at about the temperature of the body (98 degrees to 100
degrees), in which, if he be quiet and comfortable, he should remain
from fifteen to twenty minutes, but if restless and frightened by the
water a less time, after which he should be placed in a warm bed and
well covered by blankets. If perspiration result, the bath has been
useful, and it may be employed in grave cases two or three times
daily. If perspiration do not result, it may be produced by
surrounding the body either by hot dry or moist air. Hot dry air may
be produced by burning alcohol in a thin layer upon a plate under a
chair upon which the patient sits while he is surrounded by a blanket,
or he may be covered in bed and the hot air introduced under the
bed-clothes. In New York a convenient apparatus is used for this
purpose, consisting of a small sheet-iron pipe enclosed in a small box
of the same material. The box is in the form of a trunk, with a handle
for convenience in carrying, and the lower end of the pipe, which
extends nearly to the floor, contains an alcohol lamp. Hot moist air
may be produced by placing against the patient bottles of hot water
surrounded by towels wrung out of water. The steam arising from them
and enveloping the body and limbs produces a prompt sudorific effect.
There is in use in this city, in the treatment of these and similar
cases requiring diaphoresis, a convenient apparatus for generating
steam. It consists of a cylinder pierced with holes for the admission
of air and containing a spirit lamp, over which is a pan or pail
holding a little water. The patient, nearly naked, is placed in a
chair with the apparatus underneath, and is covered by a blanket, so
that the steam surrounds the body. This gives rise to free
perspiration, which continues after the patient is placed in bed. This
treatment should be repeated one or more times daily, according to the
gravity of the case.
The sudorific effect of the treatment by external warmth described
above should be aided by employing diaphoretics. Those which have been
most used are the acetates of ammonium and potassium, the bitartrate
and citrate of potassium, and spiritus aetheris nitrosi. If employed
when the surface is cool, they act rather as diuretics than
diaphoretics. {552} These agents, being simple in their action and
without deleterious effects, may be given frequently and in large
proportionate doses for the age.
But lately a diaphoretic which far surpasses these in efficiency has
been discovered in pilocarpine, the active principle of jaborandi.
Being soluble in water and tasteless, it is easily administered, and
is retained when, on account of the uraemic poisoning present in
scarlatinous nephritis, the stomach is irritable and other medicines,
as digitalis, are rejected. Ether may be employed with it, or the
amount of alcoholic stimulant may be increased at the time of its
exhibition in order to guard against any depressing effect. To a child
of two years one-fortieth to one-twentieth of a grain may be given
every six hours by the mouth. It may also be employed hypodermically,
as one-twentieth of a grain to a child of five years. It has both a
diaphoretic and diuretic action, while it stimulates both the salivary
and mucous secretions. According to one observer, an adult when fully
under the influence of pilocarpine secretes from one pint to one quart
of saliva within two hours, and Leyden reports a case of diphtheritic
nephritis in which the quantity of urine rose from half a pint to five
pints daily. But its most prompt and certain action is upon the
sweat-glands. Hirschfelder speaks of its beneficial action in
relieving various forms of dropsy, and adds: "In one morbid condition
of the kidney, however, jaborandi is the remedy par excellence, and
that is the acute parenchymatous nephritis which frequently follows
scarlatina.... This disease heals spontaneously if the danger that
threatens life from reduction of the urine and from the effusions of
fluid into the cavities of the body be averted. In this disease
jaborandi works wonders." I have also found it an invaluable agent
when the older remedies failed and death seemed imminent. The
following cases, in which the beneficial action of this agent was
apparent, occurred in my practice:
_Case 8._--G----, male, aged five years and six months, sickened with
scarlet fever on June 2, 1882. It began with vomiting, and was
attended by a degree of febrile movement which indicated an attack of
rather more than the average gravity. The fauces at one time exhibited
a slight exudation like that of diphtheria. In the declining stage of
the malady rheumatic pain and tenderness occurred in the wrist and
finger-joints, but not in those of the lower extremities. The case,
however, progressed favorably, and during the convalescence my
attendance ceased. On June 24th my attention was again called to the
child, when the urine was found to be scanty and very albuminous.
External measures, such as are described in the foregoing pages, were
employed, and the infusion of digitalis with potassium acetate ordered
to be given every three hours, but this medicine was for the most part
vomited. The bowels were kept open by jalap and the potassium
bitartrate. The urine, however, continued scanty, and on June 28th
severe convulsions occurred. At this time the quantity of urine was
only fl. oz. ij in twenty-four hours. The pulse in the convulsions was
quick and feeble, the skin very hot, and the axillary temperature 103
degrees. The eclampsia continued one hour, and were controlled by
large and repeated doses of bromide of potassium, aided by clysters of
five grains of hydrate of chloral in water. Muriate of pilocarpine was
now directed to be given in doses of one-thirty-second of a grain
every three hours, dissolved in cold water. This agent was not
vomited, and it must have been given by the parents in their fright
and {553} anxiety in larger or more frequent doses than were directed,
for on July 1st the bottle containing one grain was empty. Free
diaphoresis resulted from the pilocarpine, and the quantity of urine
was increased. The mother stated that the child had taken only two
doses, or one-sixteenth of a grain, of pilocarpine when the diuretic
effect was apparent and free diaphoresis also occurred. She also
stated subsequently that the quantity of urine was larger when the
pilocarpine was administered every third hour than when given at a
longer interval. A flaxseed poultice on which mustard was dusted was
also applied over the kidneys. On June 29th the pulse was 96,
temperature 100.5 degrees; occasional convulsive attacks occurred,
which were readily controlled by enemata of hydrate of chloral. On
June 30th the symptoms were all better; no more attacks of eclampsia
had occurred, and the urine was more abundant and less albuminous. The
mother remarked that the new medicine (pilocarpine) had settled the
stomach and increased the urine. The patient continued to improve, and
on July 4th the record states: "Now takes the pilocarpine, gr. 1/32,
every six hours; passes urine freely since yesterday; has not vomited
since he began to take the pilocarpine; pulse 106, axillary
temperature 99 degrees; is playful and takes milk freely, nearly three
quarts in twenty-four hours, with some farinaceous food. Digitalis
with potassium acetate is also given in occasional doses." July 6th,
pulse 92, temperature 99 degrees; perspires much, and urine nearly
normal in quantity and character.
_Case 9._--Mary S----, aged five years, on Dec. 22, 1882, presented
the symptoms of severe nephritis. Her brother had scarlet fever two
weeks previously, and she had sore throat at about the same time, but
without efflorescence; pulse 98, temperature 98.5 degrees; her urine
highly albuminous, and reduced to fl. oz. iv in twenty-four hours;
bowels constipated. Ordered a single dose of
Rx. Hydrarg. Chlor. Mitis gr. iii;
Resin. Podophylli gr. 1/6. M.
The muriate of pilocarpine was also ordered, gr. 1/20, but the patient
vomited soon after taking it. Another dose was retained, and was
followed by considerable perspiration. Dec. 23d, had one stool from
the powder of yesterday. Has taken five doses of pilocarpine, but
vomited after three of them. The last dose was administered at 10
P.M., and the mother says she "sweat fearfully" during the night. The
patient was kept warm in bed; stimulating poultices of mustard and
flaxseed, one to sixteen, were constantly in use over the kidneys, and
the pilocarpine was administered three or four times a day. The record
for Dec. 26 states: "Took the pilocarpine four times since yesterday
morning, and each dose is followed by perspiration lasting from one to
one and a half hours; quantity of urine, from fl. oz. vj to fl. oz.
viij daily; vomited twice yesterday, not to-day; pulse 104,
temperature 97.75 degrees; complains of frontal headache; bowels
regular; has considerable salivation. The patient is warm in bed, and
the flaxseed and mustard poultice over the kidneys is continued." Dec.
28th, specific gravity of urine 1019; urine still quite albuminous,
and containing blood-corpuscles and granular casts, also crystals of
oxalate of lime. Dec. 30th, takes gr. 1/20 pilocarpine twice daily,
and occasional doses of infusion of digitalis; urine more abundant;
its specific gravity 1014, slightly albuminous, and containing {554}
very few granular casts and blood-corpuscles; has lost its smoky
appearance; reaction alkaline; perspiration slight; patient
convalescent.
In another instance, a child of five years, from three to four weeks
after scarlet fever was noticed to have anasarca of the face and
extremities, with scanty and albuminous urine. One-thirty-second of a
grain of muriate of pilocarpine was administered every six hours
without the desired sudorific effect. It was then administered every
four hours, with an increase of perspiration and urination, so that
the nephritic symptoms were relieved and the patient apparently out of
danger within three or four days.
In a fourth patient, a girl of three years, having scarlatinous
nephritis, with symptoms very similar to those in the last case, the
administration of one-twentieth grain doses of pilocarpine in
conjunction with the hot-air bath, was followed by increased
perspiration and urination, and progressive and rather rapid
convalescence. This child had been taking bichloride of mercury in
one-fiftieth grain doses, prescribed by a homoeopathic physician,
without appreciable benefit. It had been for the most part vomited.
Given, as in the above cases, in moderate doses and with sufficient
interval, pilocarpine has never in my practice had any deleterious
effect, and I regard it as a very important addition to the remedies
for the relief of scarlatinous nephritis. It is apparently the most
useful and important diaphoretic for this disease which we possess.
Cathartics, especially those of a hydragogue nature, are also very
beneficial. Their action is more certain than that of most
diaphoretics and diuretics, and their employment is imperatively
required in severe or dangerous cases in which it is necessary to
remove as soon as possible the serum or urea which endangers life.
Young children or those with delicate stomach, and those much
enfeebled by the primary disease, may take magnesia, either the
citrate or the calcined. A good cathartic for ordinary cases is a
mixture of jalap and potassium bitartrate, the pulvis jalapae
compositus, consisting of one part of jalap and two of cream of
tartar. Ten grains of the mixture may be given to a child of five
years, and repeated according to circumstances. Its effect is
increased by dissolving a teaspoonful of potassium bitartrate in a
gobletful of water, and allowing the patient to drink from it. The
following is a good cathartic in some instances, especially if the
stomach be irritable, so that the more bulky and nauseating cathartics
are rejected. Care should be taken to obtain a good article, as some
of the podophyllin of the shops is not reliable:
Rx. Resinae Podophylli gr. j;
Sacchari scruple j. M.
Ft. in chart. No. v.-x.
S. Give one powder, and repeat according to circumstances.
In the treatment of one of the cases reported above it will be
recollected that the mild chloride of mercury mite was given with the
podophyllin, with a good result.
After the use of laxative agents the kidneys, being less congested on
account of the diversion that has occurred, often begin to excrete
urine more freely. But if the patient be anaemic or enfeebled and the
symptoms are not urgent, it is frequently better to avoid active
catharsis, which {555} more or less reduces the strength, and employ
remedies of a sustaining character, as in the following case, which
occurred in my practice: A little boy, pallid and scrofulous, began to
have anasarca after scarlet fever, chiefly in the scrotum, accompanied
by a moderate degree of ascites. The urine, which was passed in nearly
the normal quantity, contained albumen, but not in large amount. This
patient gradually and fully recovered, with no treatment except the
use of an oil-silk jacket over the kidneys and abdomen to promote
diaphoresis, and the use of iron. Such a patient, treated by the
powerful eliminatives which we employ for the more urgent and robust
cases, would probably have been injured rather than benefited. No
treatment can therefore be recommended in a treatise on scarlatinous
nephritis which will be strictly applicable for all cases. Variations
are demanded according to the state of the patient and the form and
gravity of the disease.
Diuretics which do not stimulate the kidneys are proper at an early as
well as late period of the renal malady, and digitalis is the one
usually prescribed. I do not hesitate to order it from the first day
in combination with the acetate of potassium. One teaspoonful of the
infusion may be given every third hour to a child of five years. The
following formula is for one of this age in good general condition:
Rx. Potass. Acetatis oz. ss;
Infus. Digitalis fl. oz. vi. M.
The following formulae are recommended by Meigs and Pepper:
Rx. Potass. Bitart. drachm i;
Spt. Junip. Comp. fl. drachm ii;
Spt. Aether. Nitros. fl. drachm i;
Tr. Digitalis, minim xv;
Syrupi fl. drachm v;
Aquae fl oz. ii. M.
Dose one teaspoonful every two hours to a child of two to four years.
Rx. Potass. Acetat. drachm i;
Tr. Digitalis fl. drachm ss;
Syr. Scillae, fl. drachm i-ii;
Syr. Zingib. fl. drachm v;
Aquae q. s. ad fl. oz. iii. M.
Dose, a teaspoonful every two or three hours to children two or three
years old.
Local treatment is important. L. Thomas, Romberg, and others recommend
the application of leeches, three or more, over the kidneys. Thomas
says: "In many cases the abstraction of blood causes immediate and
permanent relief; the fever and the pain in the region of the kidneys
cease, the secretion of urine becomes augmented, the albuminuria
lessens from day to day, and the moderate degree of dropsy that has
been developed disappears." It is only in the more robust children,
who have been but little reduced by the primary disease, that leeching
is, in my opinion, admissible. In the majority of cases instead of
depletion a poultice slightly irritating, so as to cause redness of
the skin, should be applied over the kidneys, or for older children,
not likely to be frightened by the process, the dry cups may be
applied daily. In subacute cases, not attended by any alarming
symptoms, sufficient redness may be produced by one of the irritating
plasters which the shops contain, constantly worn.
{556} Eclampsia, described in the preceding pages, is produced, as we
have seen, during the course of scarlet fever by the irritating effect
of the scarlatinous poison upon the nervous centres, but, occurring
after the decline of scarlet fever, it is ordinarily produced by the
retained urea. The same remedies are required to control the
convulsive movements as when they occur under other circumstances. The
bromide of potassium should be immediately administered in large and
frequent doses whenever eclamptic symptoms arise. During eclampsia a
child of three years should take five grains of this agent every five
to ten minutes till the attack ceases, and then at longer intervals.
The hydrate of chloral is a more powerful agent, and if the eclampsia
be not quickly controlled, I commonly employ it per rectum, dissolved
in one or two teaspoonfuls of water. For a child of three to five
years five grains should be thrown into the rectum by a small glass or
gutta-percha syringe, and retained by pressure. Properly administered
and retained, it rarely fails to control the eclampsia within ten or
fifteen minutes. Subsequently, occasional doses of the bromide should
be given to prevent the occurrence of eclampsia while the measures
described above are being employed to relieve the uraemic condition.
Rheumatism, endocarditis, and pericarditis, arising as complications
or sequelae, require the treatment which is appropriate when they
occur under other circumstances, but the remedies should not be
depressing, as the system is already enfeebled by the primary disease.
The rheumatism, if mild, usually abates in a few days without
medication, and the affected joints require only some soothing lotion
and support by a bandage. The following liniment may be applied upon
muslin and covered by cotton wadding:
Rx. Acid. Carbolici fl. drachm i;
Tinc. Belladonna fl. oz. i;
Ol. Camphorati fl. oz. ii;
If the rheumatism be severe and affect several joints, the sodium
salicylate should be prescribed, as in the idiopathic disease, with an
occasional opiate to procure rest.
Endocarditis and pericarditis require rest in the horizontal position,
avoidance of all excitement, the use of the tincture or infusion of
digitalis or of the fluid extract of convalaria to procure a slow and
steady action of the heart. Three drops of the tincture of digitalis
or five minims of the fluid extract of convalaria may be given every
four hours to a child of five years. The same external measures should
be employed as in acute pleuritis. I prefer the application of a thin
poultice of flaxseed containing one-sixteenth part of mustard and
covered with oiled silk. The cardiac inflammations, as well as
rheumatism, require opiates in sufficient doses to procure rest and
sleep.
Pleuritis, which we have stated is apt to be suppurative, demands the
same treatment as the idiopathic disease when it occurs in cachectic
patients.
{557}
RUBEOLA.[1]
BY W. A. HARDAWAY, M.D.
[Footnote 1: In the preparation of this article the writer has
consulted the following works: Thomas, in _Ziemssen's Cyclop. Pract.
Med._, vol. ii., N.Y., 1875, Am. edit.; Bohn, in _Gerhardt's Handbuch
der Kinderkrankh._, Zweiter Band, Tubingen, 1877; Squire, in Quain's
_Dict. Med._, N.Y., 1883; Ringer, in Reynolds's _System Med._, vol.
i., Phila., 1879; Meigs and Pepper, _Dis. of Children_, Phila., 1882;
J. Lewis Smith, _Dis. of Children_, Phila., 1882; Hebra, _Dis. of
Skin_, London. 1866; Vogel, _Dis. of Children_, N.Y., 1871; Niemeyer,
_Handbook of Pract. Med._, N.Y., 1869; Trousseau, _Clinical Med._,
Phila., 1871. Other references will be found in the foot-notes to the
text.]
SYNONYMS.--Rubeola, Morbilli, Measles, Masern, Flecken, Rougeole.
DEFINITION.--Measles is an acute infectious disease involving the skin
and mucous membranes, characterized by successive stages and a
maculo-papular eruption, which terminates in a fine branny
desquamation. In normal cases it runs a definite course, which from
the date of invasion to the end of desquamation occupies about
fourteen days. It is highly contagious, and occurs, as a rule, but
once in the same person.
HISTORY.--The word rubeola is probably of Spanish origin and was
formerly written rubiola or rubiolo. The designation morbilli is the
diminutive of the Italian il morbo, the plague. Although it is
doubtful, as claimed by Willan, that the Greek and Roman physicians
were acquainted with measles, there is no question that Rhazes was one
of the first to describe the affection correctly. Rubeola is said to
have been distinguished from variola by the Arabians in the twelfth
century; but, nevertheless, as late as the middle of the seventeenth
century we find Sennertus discussing the question "why the disease in
some constitutions assumed the form of small-pox, and in others that
of measles;" and in a posthumous work of Diemerbroeck, published in
1687, it is asserted that small-pox and measles are only different
degrees of the same affection.[2] According to Mayr, the merit of
having shown measles to be a distinct malady from scarlatina must be
ascribed to Forestus and Sydenham. It is not clear, however, that the
two diseases were accurately differentiated till the close of the last
century, and notably by Withering in 1792.
[Footnote 2: _Cyclop. Pract. Med._, London, 1834, p. 625.]
ETIOLOGY.--The exact nature of the measles contagium has never been
satisfactorily established, although we are in possession of numerous
researches in that direction, which, however, are to a great extent
contradictory. A brief examination of these various observations will
not prove uninteresting. Hallier found in the blood and sputa numbers
of free cocci, which fructified upon various substrata, but was
invariably the same fungus--mucor mucedo verus, Fres. In 1862,
Salisbury[3] published {558} his observations on the relation of the
straw fungus to measles. He recorded instances of inoculation with
this organism that resulted, according to him, in the production of a
modified form of rubeola, and, moreover, was protective against
further attacks of the same disease. In an exhaustive paper bearing on
this question H. C. Wood[4] quotes certain experimental inoculations
made by William Pepper, which showed conclusively that measles was not
propagated in this way, and that where any symptoms were developed
they were not those of true measles, nor did they protect the subjects
from unquestioned measles. Salisbury also claimed that measles had
occurred in camps where damp and mouldy straw had been employed for
bedding. J. J. Woodward in his work on _Camp Diseases_ points out that
camp measles prevailed almost exclusively in regiments from the rural
districts, while men enlisted in towns and cities were more or less
completely exempt. The explanation was, that those from the country
had hitherto escaped the disease, while townspeople had suffered from
it at some previous time--a condition of affairs inconsistent with the
theory of the straw fungus. Coxe and Felz found numerous bacteria in
the blood of measles patients, especially in regions where the
eruption was most pronounced. The nasal mucus also contained similar
germs. Inoculation of the blood from the subjects of measles upon
rabbits did not produce an analogous affection (Thomas). Klebs[5]
obtained micrococci from the trachea and from blood taken from the
hearts of infant cadavers. "In the latter, collected in flattened
capillary tubes, there developed balls of micrococci; in the trachea
both micrococci and bacteria were present in large quantities. Under
observation, pale, finely-granular micrococcus balls developed and
changed very quickly to bacteria, which moved about very actively.
These sought the periphery, about 1/2 mm. distant from the centre of
development, and formed a zone, comparable with a hedge or fence that
is composed of rods. From this were formed new masses of micrococci,
but further no regular process of arrangement or development could be
observed."
[Footnote 3: _Am. Jour. Med. Sci._, July and Oct., 1862.]
[Footnote 4: _Ibid._, Oct., 1868, p. 333.]
[Footnote 5: _Wurzbr. Verh._, N. F., v., 1874, quoted by Forchheimer
in Supplement to _Ziemssen's Cyclopedia_, W. T., 1881, p. 102.]
Braidwood and Vacher,[6] as the result of a number of experiments,
believed that they had sufficient evidence for concluding that the
most active mode of the transmission of measles was through the
breath, and accordingly instituted a series of experiments by
carefully examining the breath of children in the acute stage of the
disease.[7] With this object in view they coated over with glycerine
the inside of several clean glass tubes of a diameter of a half to
three-quarters of an inch. As soon as the nature of the eruption was
manifest the patient was required to breathe through one or more of
the tubes, and so on each day till the eruption had faded. Upon
examination of the glycerine with an one-eighth objective every
specimen showed numerous sparkling bodies, something like those found
in vaccine, but larger. Some were spherical; others were elongated,
with sharpened ends. They were most abundant during the first and
second days of the eruption. Healthy children and patients suffering
from typhoid and scarlet fevers were made to imitate these {559}
experiments, but no such bodies were to be seen in their specimens.
They conclude from these observations that the small spherical
elements discovered in the breath are perhaps the active agents in the
propagation of measles. Upon post-mortem of patients who had died of
rubeola these germs were found in the lungs and liver, and,
particularly, close to the walls of the capillaries. They believe that
the "lungs are the favorite breeding-ground of the contagium."
[Footnote 6: _Brit. Med. Jour._, Jan. 21, 1882.]
[Footnote 7: Several years ago Ransome of Manchester obtained
particles from the breath of two persons suffering from measles
(Squire).]
That inoculation of morbillous blood may convey the disease was first
demonstrated by Home in 1757, which experiments were verified by
Speranza in 1822 and by Katona in 1842. The inoculations of the latter
are especially noteworthy, as they numbered more than a thousand. No
person inoculated by him died, and only 7 per cent. of the
inoculations failed. On the other hand, inoculations made by Mayr gave
negative results. It is stated that Monro and Locke communicated
measles by inoculating with the tears and saliva. Attempts of the same
kind were fruitlessly made in Philadelphia in 1801, although the
blood, the tears, the nasal and bronchial mucus, and the exfoliated
lamellae of the epidermis were successively employed in the trials.[8]
[Footnote 8: Rayer, _Diseases of the Skin_, Phila., 1845.]
Mayr has shown that the nasal mucus is capable upon inoculation of
propagating the disease. He performed the experiment upon two healthy
children living at a distance from each other, at a time when the
disease had ceased to be epidemic. Some nasal mucus taken from the
patient during the stadium flavitionis, and kept fluid in a glass
tube, was the same day placed upon the mucous membrane of each of
these children. In one of them the first symptom of sneezing occurred
after eight days, in the other at the expiration of nine days. Febrile
symptoms set in two days later. In each child the rash appeared on the
thirteenth day after infection. The inoculated disease was mild and
regular in its course.
While it is perhaps true that the contagion of measles is not so
tenacious as that of small-pox and scarlatina, it is a matter of
observation that susceptible persons are liable to contract the
disease, even if not directly exposed to its influence. There is
incontestable evidence that it is conveyed by fomites--a fact well
worth bearing in mind.
It is but just to say that so excellent an observer as Mayr taught
that measles could not be conveyed by clothes, linen, etc. unless
transferred immediately from one individual to another. Panum,
however, showed that contagion could be carried many miles by an
unaffected third person without losing its activity. Aitken[9] has
also pointed out the fact that children's clothes sent home in boxes
from schools where the disease has raged communicated the disease, and
that susceptible children who had slept in the same beds, in the same
rooms, after they had been occupied by persons suffering from measles,
have taken the malady. Squire observes that the contagium of measles,
except in the catarrhal stage, is not far diffusible in the air, but
clings to surfaces, and may be thus carried from place to place; on
the other hand, children have been brought, while in full eruption,
into a house among others, and nursed in a room apart, without any
extension of the disease to the most susceptible.
[Footnote 9: _Science and Pract. of Med._, Phila., 1868.]
{560} Various circumstances render it probable that measles is most
readily propagated during the stage of efflorescence; but that it is
also highly infectious during the prodromal period is now universally
acknowledged.
According to Niemeyer, the probability of infection during the
prodromal stage is supported by the wonderful spread of measles
through schools; for, while the strictest surveillance is established
over children with any suspicious eruptions, and those known to have
had the disease are not allowed to return till long past the stage of
desquamation, no heed is paid to those exhibiting the premonitory
cough and coryza. There is no reason for believing that measles can be
propagated during the period of incubation; on the other hand, there
is no satisfactory argument for the denial of its infectiousness in
the desquamative stage. Although Panum is inclined to doubt its
contagiousness at this time--and his observations are worthy of the
greatest confidence--other good authorities differ from him
materially, and extend the stage of personal infection to a period of
from three weeks (Squire) to forty days (Hillairet).
Reasoning from analogy, we would naturally expect that the period of
incubation in measles suffered a certain amount of variation; the
result of numerous observations confirms this expectation. It is
manifestly a difficult matter in densely populated communities to
establish with accuracy the date of a given infection, but from a
study of more or less carefully noted cases it will be found that the
period of incubation may vary from three to thirty days. For the vast
majority of cases the average time between the reception of the
measles poison and the appearance of the characteristic eruption will
be about from thirteen to fourteen days. Panum, under exceptionally
favorable surroundings, found it more frequently fourteen than
thirteen days. Therefore, deducting the three or four days occupied by
the invasion stage, we shall find that the real incubation period is
from nine to ten days from the date of exposure. Mayr's two cases of
inoculation with nasal mucus showed no departure from this rule, but
in the inoculations made by Katona with blood the prodromic symptoms
made their appearance in seven days, the cutaneous lesions developing
two, and at the most three, days afterward.
Minor epidemics of measles are said to occur every three to five
years, more extensive and severe ones every seven or eight years. In
the centres of population measles may be said to be endemic; in
isolated regions the visitations of the disease may be widely
separated. Measles is a less severe disease in warm than in cold
climates, and, as a rule, we also find the affection more common and
more intense in the fall, winter, and spring than in the summer
months.[10] Epidemics of measles are usually short, and it is thought
that there is a definite relation between the severity of their onset
and their duration, this being in general short in proportion as the
given epidemic was at first severe (Mayr). Intestinal complications
are more frequent in summer, and involvements of the respiratory
organs more common in winter. The varying aspects of different {561}
epidemics--sthenic, asthenic, etc.--depend on changes in the weather,
season of the year, the presence of complications, and other agencies
not very clearly understood. Epidemics of whooping cough may precede,
accompany, or follow in the wake of measles, and it has therefore been
suggested that it stands in some peculiarly close connection with the
latter; but, aside from this often-observed coincidence, we are not
justified in our present state of knowledge in assuming any definite
relation of cause and effect between the two diseases.
[Footnote 10: Aitken (_op. cit._, p. 295) declares that the mortality
returns from England and Wales show that the influence of season is
most trifling. Occasionally it has been found that the deaths in
summer exceeded those in winter, but we believe that the statement
made above is, in the main, correct. For instance, Parson's figures
for Berlin for the years 1863-67, inclusive, are: spring, 11.9 per
cent.; summer, 13.3; autumn, 33.4; winter, 41.4. Voit's statistics in
an average of thirty years at the Children's Clinic at Wurzburg
establish the same general principles (Thomas).]
There would seem to be neither geographical nor racial bar to the
propagation of measles, for it has been observed in all countries and
among all peoples. As in the case of other zymotic diseases, a
tolerance is established for measles in countries where the disease is
more or less constantly prevalent; but where the affection becomes
epidemic for the first time, or reappears after many years, it rages
with terrific violence. This fact was particularly exemplified in the
epidemic in the Faroe Islands, and more especially in the recent
(1877) visitation of the Fiji Islands, where one-fourth of the
population succumbed in a comparatively short time.
It is quite probable, as asserted by Mayr, that children affected with
scrofulous complaints, as well as those who are the subjects of
diseases of the respiratory organs--pertussis, bronchitis, or
tuberculosis--are eminently susceptible of measles; but his statement
that sufferers from epilepsy, chorea, and paralysis exhibit an unusual
power of resistance cannot be accepted without reservation. Acute
diseases often appear to delay the outbreak of measles, so that the
latter does not appear till convalescence from the former (Thomas).
The development of vaccinia is occasionally interfered with by an
attack of rubeola; on the other hand, the two diseases may be seen
running their courses together.[11] The emphatic statement made by
Hebra, that measles is never seen to occupy a patient simultaneously
with another acute exanthem, has not been confirmed by other
observers. My own experience furnishes several examples. Measles may
also occur during the course of other acute or chronic maladies. From
a study of the literature of measles complicating pregnancy and
parturition Underhill[12] finds it to be quite uncommon, due probably
to the fact that most adults are insusceptible of further attacks; but
when it does occur in pregnancy he regards it as a very serious and
frequently fatal complication. Underhill believes measles to be most
fatal when it supervenes soon after delivery, while those who are
confined during the course of the malady stand a better chance of
recovering from it. That puerperal women are not always unfavorably
affected by measles is well shown in two remarkable cases reported by
Nelson[13] of St. Louis and Chantier[14] of Geneva, in which the
mothers were safely delivered, though suffering from measles
contracted at the end of their pregnancies.
[Footnote 11: Hardaway, _Essentials of Vaccination_, p. 60.]
[Footnote 12: _Obstet. Jour. Great Britain and Ireland_, July, 1880.]
[Footnote 13: _St. Louis Courier of Med._, Sept., 1879.]
[Footnote 14: _Annales de Gynecologie_, May, 1879.]
All ages are susceptible to the measles poison, and the apparent
exemption enjoyed by adults is due to the fact that most grown-up
people have already suffered the disease in childhood; but in Panum's
epidemic, mentioned above, it was discovered that nearly all who had
not had measles {562} elsewhere, or were not old enough to have been
exposed at the last visitation, sixty-five years before, acquired the
affection regardless of age. It is quite probable, however, that the
law of decrease of susceptibility with age holds good for measles as
well as for variola, etc., but to a less degree. It will therefore be
seen that measles is not essentially a disease of childhood. Although
there is no special limit to the susceptibility of rubeola at one
extreme of life, it would seem to be quite well established that it is
much modified at the other--namely, that infants under six months are
rarely attacked. This latter fact is conceded by individual
experience, by the records of epidemics, and by the testimony of most
observers.[15]
[Footnote 15: On the other hand, as quoted by Forchheimer (_loc.
cit._), H. C. Fox publishes some tables which show that for England
and London a much larger number of young children are attacked by
measles than other statistics would lead us to believe.]
+-------------+-------------+
| England. | London. |
+------+------+------+------+
| | Fem- | | Fem- |
|Males.| ales.|Males.| ales.|
---------------------------------------+------+------+------+------+
Under one year | 3022 | 2530 | 3571 | 2987 |
One and under two years | 6086 | 5825 | 8630 | 8050 |
Two " " three " | 3178 | 3255 | 4683 | 4757 |
Three " " four " | 1730 | 1851 | 2594 | 2620 |
Four " " five " | 980 | 1028 | 1358 | 1466 |
|------+------+------+------|
|------+------+------+------|
Five and under ten years | 255 | 278 | 301 | 316 |
Ten " " fifteen " | 29 | 38 | 24 | 32 |
Fifteen " " twenty " | 9 | 13 | 9 | 11 |
Twenty " " twenty-five " | 7 | 9 | 5 | 7 |
Twenty-five " " thirty-five " | 5 | 8 | 5 | 7 |
Thirty-five " " forty-five " | 3 | 5 | 2 | 3 |
---------------------------------------+------+------+------+------+
Even sucklings do not enjoy a complete immunity from measles.
Steiner[16] states that he has met with it in children only four or
five weeks old. Monti has recorded ten cases of rubeola in children
under two months of age. A case is reported by Kunze where a mother in
the stage of efflorescence gave birth to a child, which contracted the
disease five days afterward. Quite a number of cases of congenital
measles have been put on record from time to time; but Thomas, after a
careful investigation, says that he has been able to discover but six
authentic accounts of such occurrences.[17] That children born to
mothers suffering at the time of parturition from measles may yet
escape it themselves is proven by the cases of Nelson and Gautier
mentioned above. Whether a pregnant woman attacked by measles
transmits the disease to the foetus in utero, thereby securing
immunity from it in after life, is a question difficult of decision,
especially as we have not yet been able to decide this same inquiry,
with infinitely better opportunities, for vaccinia.[18]
[Footnote 16: _Compendium of Children's Diseases_, N.Y., 1875, p.
396.]
[Footnote 17: I believe that, under certain circumstances, the
erythema papulatum of the new-born is often mistaken for measles.]
[Footnote 18: See experiments of Burckhardt, Rickett, Gart, and
others, quoted in Hardaway's _Essentials of Vaccination_, p. 38.]
There is no good reason to believe that sex is of much importance in
establishing a predisposition to measles, although the statement has
been repeatedly made that males are more frequently attacked than
females. {563} Fox's statistics show a slight preponderance in favor
of the male sex; but a careful examination of accessible statistics
proves, as would be expected, that this degree of susceptibility
varies at different times in obedience to circumstances not readily
understood.
By the older writers (Willan, Rosenstein, Fuchs) it was very
dogmatically asserted that one attack of measles completely
extinguished all future susceptibility to the disease. Of late years
this dogma has met with much opposition, and numerous observations
have been recorded which, if entirely trustworthy, would lead us to
believe that rubeola may occur not only twice, but several times, in
the same individual. While from analogy and actual experience we are
quite sure that the recurrence of measles is not so uncommon an event
as it was once held to be, a closer examination of the question in all
its bearings clearly confirms us in the belief that subsequent attacks
are much more infrequent than is now thought to be the case by many,
and that other diseases, more or less resembling true measles, are
largely responsible for errors of diagnosis in this regard. Panum
found that all the old people who had measles during the epidemic on
the Faroe Islands in 1781 escaped it in 1846. Both Rosenstein and
Willan declared that they had never witnessed an instance of the true
recurrence of measles. Among other facts, it may be stated in this
connection that Woodward (_loc. cit._) has shown that during our late
war, while members of regiments recruited from the rural districts,
who had never before had measles, largely took it when exposed to its
influence, regiments from the cities, who had presumably acquired the
disease in childhood, remained almost entirely exempt.[19] Other
arguments of a similar sort could be readily adduced. There is no
question that mistakes in diagnosis have occurred from confounding
rotheln, roseola, etc., which closely simulate measles, with that
disease. Those particularly engaged in the treatment of cutaneous
affections could multiply instances of such errors. It is quite
significant that for certain analogous infectious diseases--_e.g._
variola and scarlatina--the same frequency of recurrence is not
claimed, although as a matter of fact they do occur. The explanation
would seem to lie in the fact that neither small-pox nor scarlet fever
is so closely counterfeited by other skin affections, notably by
rotheln, as is measles. But it would be entirely contrary to analogy
and indubitable experience to go to the extreme of the older writers
and absolutely deny the possibility of second, and even third, attacks
of rubeola. The frequency of such cases is, however, as Henoch[20]
truly states, much overestimated.
[Footnote 19: These observations of Woodward were made without any
reference to the question at issue.]
[Footnote 20: _Lectures on Diseases of Children_, N.Y., 1882, p. 282.]
Occupying quite a different position from the measles induced by
reinfection from without are the so-called relapses of rubeola. These
relapses, which may occur in from two to four weeks after the original
invasion, are analogous to the similar occurrences in scarlatina and
typhoid fever. I am cognizant of but a single case of this sort, but
Steiner and other accurate observers record a number of such
instances.
SYMPTOMS AND COURSE.--It is generally stated that the stage of
incubation exhibits no symptoms whatever; but it is undoubtedly true
that the patient will sometimes appear dull and listless, and, on
occasion, even give evidence of some slight and ephemeral elevations
of temperature. {564} As a rule, however, this period is devoid of any
marked indication of the presence of the measles poison in the
system.[21]
[Footnote 21: Some writers describe a much more marked train of
symptoms as prevailing at this time than seems warranted by general
experience, and Rehn has gone so far as to declare that the prodromal
period, as usually understood, properly commences in the stage of
incubation. Bohn is inclined to a similar view. The prodromic stage of
authors is, then, to be looked upon as the "period of the mucous
membrane exanthem."]
The prodromal stage is usually ushered in by symptoms of general
malaise, fretfulness, more or less frontal headache, shiverings,
nausea, loss of appetite, excited sleep, and sometimes delirium.
Vomiting is not so common in measles as in scarlatina, and may occur
at any time previous to the appearance of the rash. The tongue is apt
to be coated, although it may remain clean; the taste is bad, and
pressure over the stomach and bowels occasionally elicits considerable
pain; an aching pain over the sternum is also noted. As a general
thing, at this time patients are drowsy and inclined to sleep much.
Meigs and Pepper found this a very constant symptom, which they state
is in no way alarming unless associated with other more serious
symptoms of local or general disturbance. Constipation is present in
some cases, or the bowels may be relaxed or remain in their natural
state.
The prodromal fever of measles follows a peculiar course. It is
remarkably remittent in character, and is rarely of such intensity as
to threaten life, as is often the case in scarlet fever. The
temperature will rise on the first day to 102 degrees-104 degrees F.,
and the height of the fever at this time will measurably foreshadow
the character of the subsequent course. On the second day of the
prodromal stage the fever suffers a marked remission, or may even
entirely disappear, to again rise in the evening. Smith has observed
two exacerbations in the day. Again, in some instances, after the high
initiatory fever, the temperature may remain normal till just before
the rash comes out (Bohn). It is this peculiar behavior of the fever,
together with the fact that the child may regain its usual vivacity in
the fever-free intervals, which so often misleads the physician into
the diagnosis of malarial poisoning.
The most pronounced feature of this stage of the disease is, beyond
all others, the catarrhal affection of the mucous membranes. The
mucous membranes of the eyes, nose, mouth, and air-passages are all
more or less involved, and the patient suffers in varying degrees from
photophobia, coryza, hoarseness, cough, and pain in swallowing.
Sneezing is frequent and annoying, and slight epistaxis is not
uncommon. The cough usually appears on the first day, simultaneously
with the fever. It is not very troublesome at first, but by the fourth
day it becomes more frequent, assuming a hoarse, barking, paroxysmal
character. Expectoration is scanty, and auscultation reveals a harsh
vesicular murmur or else sibilant rales. Alarming but not dangerous
attacks of false croup may come on during the night. Many observers
have called attention to the red spots (papules) in the oral cavity,
which make their appearance during the period of invasion. According
to Bohn, usually on the second or third day from the beginning of the
fever there appear upon the slightly hyperaemic mucous membrane of the
soft palate, palatal arch, and uvula small or large, dark, red spots
that spread to the mucous membrane of the cheeks, and sometimes to the
hard palate, lips, and gums. Soon they become more defined, and are to
be distinguished by shape and coloring {565} from the membrane upon
which they are situated. According to the same authority, they also
afford an index to the intensity and extent of the coming cutaneous
eruption. It is also stated that if the latter partakes of a
hemorrhagic character, the spots on the mucous membrane may also
become livid. This same punctate reddening has been demonstrated in
the epiglottis, larynx, and trachea (Gerhardt), and upon the bronchi
and small intestines of children who had died during this stage of the
eruption. It is also to be noted on the conjunctivae. It has been
assumed that this period of this disease is not to be looked upon as
the stadium prodromorum, but as the period of the "exanthem of the
mucous membrane." This view of the pathology of measles seems to me
most reasonable; but in whatever way we may look upon the question,
the practical importance of this precutaneous eruptive stage is to be
insisted upon for diagnostic purposes, just as is the analogous
eruption upon the mucous membrane in small-pox.
In ordinary cases of measles we do not find such profound reaction of
the nervous system as in scarlatina. I believe that convulsions in the
prodromal stage are much more common than available statistics would
have us believe; at least, this is my own experience. Meigs and Pepper
met with convulsions but five times in 314 cases at the beginning of
the eruption, while Rilliet and Barthez observed but one convulsion in
167 cases. Thomas says that convulsions are almost always absent. On
the other hand, Trousseau and Bohn expressly declare that they are
very common, the former stating that they occur with greater frequency
than in scarlatina. I consider that convulsive seizures occurring in
connection with marked catarrhal affection of the mucous membranes are
very important aids in forecasting a probable attack of rubeola.
Fortunately, convulsions at this stage are not very serious unless
repeated or injudiciously treated.
The duration of the period of invasion in regular cases is from three
to five days, with an average of about four, but in perfectly
uncomplicated attacks this period may be extended to six or eight
days, or even longer. But that the duration of this stage may be much
shorter than the average is not sufficiently insisted upon by writers.
Ringer,[22] for instance, says that he had an opportunity of testing
the earliest appearance of the rash in an epidemic of measles in a
large public school for boys under twelve. In every case during the
epidemic the rash appeared on the first day, the cases being severe,
though of short duration, the temperature rising to 103 degrees and to
104 degrees F. In some instances the rash preceded (?) the fever.
Thus, several of the boys feeling poorly, their temperature was
carefully taken night and morning under the tongue, and in several
cases the rash appeared in the morning about the face and collar-bone,
while the temperature remained normal, and did not rise till the
evening, when it ran up to 101 degrees-103 degrees F., and even
higher. These cases certainly resemble rotheln more than measles. In
two cases, which I observed under very favorable conditions, the
eruption commenced to appear on the morning of the second day, and
more or less similar experiences are recorded by others.
[Footnote 22: _Handbook of Therapeutics_, 6th ed., London, 1868--note
to p. 26.]
The skin eruption, which appears, as a rule, on the third, fourth, or
fifth day of the attack, is ushered in with an increase in the general
and {566} local symptoms of the disease. It is particularly to be
remarked that the fever does not subside at this time, as is the case
in variola. The eruption appears first upon the face, about the cheeks
and forehead, then on the chin and neck, and thence gradually
overspreads the trunk, and finally reaches the extremities. When the
eruption is intense no part of the body is free from it, the rash
being found upon the palms and soles and upon the hairy scalp. The
cutaneous lesions proper consist at first of hyperaemic spots of about
a line in diameter, which gradually increase in size, until at their
full development they may attain a diameter of from one-twentieth to a
quarter of an inch. In the beginning they bear a very close
resemblance to the sub-papular lesions of small-pox. The
maculo-papules, when fully developed, are slightly elevated above the
level of the skin, the elevation, however, being more appreciable to
touch than sight, have a smooth velvety feel, and are so arranged as
to enclose areas of healthy skin. In the individual spots we may
frequently observe one or several minute, darker-colored papules, due
to follicular congestion, which when more intense constitutes the
morbilli papulari presently to be described. The maculae are, as a
rule, roundish, or they may be moon-shaped, or their borders may
present an indented or notched appearance. Where the capillary
circulation is active--on the cheeks, for example--or upon parts
subjected to pressure, the eruption may become confluent; that is to
say, the usually pale intervening skin becomes injected or the papules
coalesce, and in this way produce a uniform redness over large single
tracts of skin. This scarlatinoid rash, however, never occupies the
whole surface of the body, but only limited regions, and in other
situations may be detected the characteristic discrete papules of
rubeola; the color is not uniform, but is broken here and there by the
darker streaks and spots of the measly eruption. The rash, which
disappears upon pressure to return when the pressure is removed, is of
a more or less rosy red, with a tendency in some to deep red, and has
occasionally a purplish hue. According to Mayr and Hebra, it is of the
precise color which is obtained by adding a little yellow or brown to
a red pigment.
According to the researches of Thomas, Squire, and Wunderlich, as
abstracted by Seguin, the fever of the eruptive period is divided into
a moderately febrile stage and the fastigium or acme. The moderately
febrile stage averages thirty-six to thirty-eight hours, and is made
up of one or two exacerbations of 100.4 degrees to 102.2 degrees F.,
but not quite so high as the initial fever. If there are two
exacerbations, the second one is the higher; the intervening
remissions are not so low as those of the prodromal stage, yet even
now the norm may be noted on a single occasion. The fastigium
commences early in the day or in the evening; if the rise should occur
in the morning, the evening temperature rises still higher, with or
without a slight remission the following morning, and the next evening
attains the maximum. If the acme begins in the evening, the remission
on the next morning is either absent or very slight. The greatest
height of the fever in normal cases corresponds to the greatest
intensity and development of the eruption. This rule is not
invariable, however, for sometimes the fever is higher soon after the
eruption appears, and has fallen when the exanthem has reached its
highest point. The whole fastigium lasts from one and a half to two
{567} and a half days, so that the complete eruptive fever occupies
from three to four and one-half days.[23] The pulse in general
preserves a proportionate correspondence to the temperature, and never
attains the great frequency to be observed in scarlatina.
[Footnote 23: According to Ringer, the highest temperature reached in
normal cases is 103 degrees F. Thomas places it as high as 104 degrees
F., but states that it may go up to 105 degrees F. without the
intervention of any complication.]
The general symptoms, with the exception of the fever, do not greatly
differ from those common to the prodromal stage. The skin is hot and
more or less swollen, particularly about the face; there are anorexia,
photophobia, lachrymation, and sometimes epistaxis; the cough
continues, and is generally frequent and harassing, and attended with
little or no expectoration; the voice is hoarse. The tongue is coated,
principally in the middle, through which the swollen papillae
protrude, while the tip and sides are red. The blotchy redness of the
oral cavity is visible for some days, and finally becomes
indistinguishable from the surrounding congestion. The tonsils
sometimes become considerably enlarged, though suppuration must be
rare. Enlargement of the glands behind the jaw and in the neck and
groin are to be observed. At the outset of the eruption a profuse
diarrhoea supervenes in most cases--a symptom which Trousseau rightly
insists to be an essential feature of measles. This occurrence is
interpreted by some writers as an evidence of the implication of the
mucous membranes in the specific exanthem of the disease. This flux,
which is sometimes accompanied by a little blood and tenesmus, rarely
continues long, and may be succeeded by a degree of constipation. The
respiration is generally somewhat accelerated, mostly in
correspondence to the amount of fever present. Some degree of deafness
is not uncommon, owing to the extension of inflammation along the
Eustachian tubes. The urine is scanty and high colored; there is
sometimes scalding in urination and vesical tenesmus, and at the acme
of the fever traces of albumen may be detected.
The eruption, in fact, generally occupies the skin an average of four
days, and, although this period may be shortened materially, it is
less apt to be lengthened. The duration of the eruption at its maximum
of development over the whole surface is about half a day, more or
less, and, as a rule, corresponds with the greatest elevation of the
temperature. The retrocession of the rash takes place in the order of
its appearance--viz. first from the face, then from the trunk and
upper parts of the extremities, and last from about the feet and
hands, where, indeed, it may remain vivid, or even progress for a
short time longer, after the eruption has begun to subside in other
situations. Sometimes the almost faded spots will be temporarily
renewed by an abnormal rise in the temperature.
With the decline of the eruption the other symptoms begin to subside.
The cough loses its hacking, paroxysmal character, and becomes less
and less frequent, and gradually disappears. The voice regains its
normal tone, the tongue loses its fur, cleaning up in patches, and
expectoration, which was absent or scanty and viscid in the beginning,
increases and is free, the masses coughed up being coin-shaped and
floating in a clear watery mucus--a symptom much dwelt upon by the
older writers. The behavior of the temperature at this period--the
stage of decline--is quite {568} characteristic. The fall usually
begins at night, and generally the next morning it has reached the
norm or else fallen below it. On the other hand, the descent may be
less precipitate, and the fall continues less rapidly all through the
day; or there may be a slight rise again in the evening, the norm
being reached the following morning. The termination by lysis--that
is, slight elevations in the evening for several days--is much rarer,
and while it may occur in perfectly regular cases, it should put the
medical attendant on his guard against complications.
The comparatively normal course of measles portrayed in the preceding
paragraphs does not always occur, but, on the contrary, the disease
may depart from the more usual type in one or more particulars, either
in especial stages of its progress or in the greater or less intensity
of the malady as a whole.
In addition to those cases of measles where the eruptive and catarrhal
symptoms are so slight as to almost escape observation, except for the
existence of other cases in the same house or family, there are to be
recognized two other trivial varieties of the disease--namely, measles
without the catarrh, and measles without the rash.
That the eruption of measles should occur upon the skin without
implication of the mucous membranes seems to be much more doubtful
than that the catarrh should appear without the eruption. It is quite
probable, at any rate, that many so-called cases of rubeola sine
catarrho are merely instances of rotheln, which we know may occur
without any reference to an existing epidemic of measles. But that
this form of measles does exist is admitted by trustworthy observers,
although its diagnosis under any circumstances must be a matter of
great difficulty. Measles without the eruption (rubeola sine
eruptione) is more readily recognized, especially and only, however,
when a susceptible person is exposed, and as a result acquires the
characteristic catarrhal symptoms. Since in recent years more
attention has been paid to the eruption on the mucous membranes, it
may be that its discovery in these situations may lend positive
assistance to the diagnosis in such cases. It is hard to understand
how this variety of measles, which presents no inflammatory changes in
the skin, should be followed by desquamation; yet this observation has
been made. The assertion that these anomalous forms of the affection
afford no protection against subsequent attacks seems to be founded in
error, and is undoubtedly due to the confusion existing between
measles and rotheln or other exanthems.
Continental writers, especially, describe a form of measles called by
them inflammatory or synochal. It is simply an exaggeration of the
symptoms, particularly those appertaining to the mucous membranes,
found in ordinary measles (morbilli vulgaris). The prodromal stage is
much more violent, the nervous symptoms more threatening, the
implication of the mucous membranes more pronounced and persistent,
the febrile movement is of a higher inflammatory character, and the
eruption, which instantly covers the whole body (Vogel), is made up of
dark-red or purplish spots which fade slowly. It is this form of
measles, according to Niemeyer, which is chiefly attended by croupous
instead of catarrhal laryngitis, in which the inflammation of the
air-passages often extends to the alveoli of the lungs, and in which
the gastric and intestinal coats are often affected with catarrh.
{569} Let the contagion of measles be a grade more virulent, or
perhaps the resisting power of the patient more feeble, and the case
will assume the features of the septic, typhous, or hemorrhagic
variety (rubeola nigra). It is said that the hemorrhagic measles is
most apt to occur in epidemics; certain it is that the dreaded black
measles of former times is very infrequent now-a-days, due, no doubt,
to a more rational treatment and a better hygiene. Isolated cases,
however, are occasionally encountered. As a rule, from the beginning
all the symptoms evidence an overwhelming of the system by the
virulence of the poison--a condition of things much more common in
scarlatina. The pulse becomes weak, thready, and frequent; the
temperature lacks the typical remittent character of normal measles;
there is unusual prostration; and the nervous centres are profoundly
concerned, as shown by delirium, convulsions, and coma. The eruption
lags, and finally makes its appearance in an imperfect or irregular
manner. The spots are of a livid hue, interspersed with larger or
smaller ecchymoses. Hemorrhages from the mucous cavities take place,
and the patient dies in convulsions or sinks into fatal coma. It has
been said that the grave constitutional symptoms do not generally make
their appearance till the eruptive stage, but I know from experience
that the patient may be overwhelmed quite early, as in purpura
variolosa.
Too much stress should not be laid on these different types of the
disease, whether mild or grave, since they depend upon a common cause,
however much modified in one way or another; but they may be allowed
to stand for the sake of clinical convenience.
Measles may also present certain irregularities in its various stages
without necessarily departing from the otherwise benign character of
the disease.
As stated elsewhere, it is believed by some writers that a greater
part of the period of incubation is occupied by symptoms which already
indicate the activity of the measles poison in the system, and that,
therefore, this stadium in reality lasts but a few days. This opinion
does not seem to be generally accepted; at any rate, I think we are
quite safe in saying that in the majority of cases no departure from
the usual latency is observed. The deviations in the stage of invasion
have been considered above, and mostly concern its duration and the
character of the temperature. Evanescent rashes, which have nothing in
common with the specific exanthem, are sometimes observed at this
period. The eruption of measles may present certain peculiarities.
First, as to localization. Instead of coming out on the face first, it
may primarily develop on other parts of the body, provoked into
existence, as it were, by local exciting causes; thus, where ointments
or plasters have been applied or upon a part subjected to constant
pressure. It may affect only one-half of the body, or entirely spare
paralyzed extremities (Mayr). In some instances the papules are so
sparse, indistinct, and short-lived as to be scarcely appreciable.
Second, as to the physical characters of the eruption. Hebra and Mayr
recognize the following modifications:
Morbilli laevis. The efflorescence is smooth and flat, and the
individual lesions are separated from each other by normal integument.
This is the common form of measles.
{570} Morbilli papulosi. The papules are dark red and more elevated,
are about the size of hempseeds, and situated at the mouths of the
hair-follicles.
Morbilli vesiculosi. In this variety the mouths of the hair-follicles
are filled with fluid and produce delicate transparent vesicles.
Morbilli confluentes. The maculae are here so crowded together that no
healthy skin intervenes.
Morbilli haemorrhagici. The efflorescence consists of maculae or
papulae of a dark-red color, due to extravasations of blood, and do
not fade on pressure. It is well to mention in this connection the
fact, particularly noted by Meigs and Pepper in this country, that
hemorrhages into the skin may occur in cases which otherwise run a
benign course. They are best seen after the eruption has faded. In
some cases the efflorescence of measles may remain visible for a week
or ten days.
As heretofore observed, there may be a relapse of the measles eruption
after some weeks, accompanied by fever. It is said that the spots
appear on parts of the skin hitherto normal (Thomas). So far as I
know, Hebra was one of the first to point out the fact that the
so-called striking-in of the eruption was the result, and not the
cause, of some complication in the disease; for, as this author
states, before the rash fades or disappears the internal disease is
always present. It is well known, for instance, that syphilitic
eruptions will sometimes disappear upon the supervention of some acute
intercurrent affection, such as pneumonia, acute rheumatism, etc.; but
no one will suppose for a moment that the retrocession of the
syphilides was the cause of these affections.[24] The pathological
explanation seems obvious.
[Footnote 24: See Bumstead and Taylor on _Venereal Diseases_, 4th
edit., p. 513.]
COMPLICATIONS.--The complications of measles consist, as a rule, in
the exaggerated morbid action of organs or parts that are essentially
implicated in the disease; therefore we are most apt to encounter such
affections as laryngitis, bronchitis, pneumonia, etc. Inflammation of
serous membranes, on the other hand, are rare; thus, pleurisy is
infrequent unless in connection with a lobar pneumonia.
The exact causes of the complications are not always obvious, but in
many instances can be traced to the previous bad health of the
patient, to the influence of insanitation, or, finally, to certain
ill-understood features attendant upon some epidemics.
Simple bleeding from the nose, not associated with the hemorrhagic
diathesis, is not an uncommon accompaniment of the prodromal stage,
and is rarely a dangerous symptom--rather the contrary. It may also
arise after the development of the rash, and occasionally proves a
complication of serious import.
The aural complications, unlike those in scarlatina, are generally not
sufficiently prominent at first to attract attention. The symptoms,
particularly pain and deafness, are apt to be masked. Purulent
processes and consequent perforation may occur during the eruption,
but are more frequent at the stage of desquamation (Spencer).[25]
[Footnote 25: Oral communication.]
Various disorders of the skin have been observed during the course of
measles--viz. miliary vesicles, and even pustules, as already
described; herpes facialis, zoster femoralis (Thomas), and
erythematous rashes, which {571} may precede, accompany, or, it is
said, follow the eruption. Of considerably more importance is the
pemphigoid eruption mentioned by several observers. In Henoch's[26]
case, a girl of four years, the usual remission of the fever on the
evening of the second day was absent, and from the third day there
appeared over nearly the whole surface blebs filled with a limpid
fluid, which varied in size from a hazel-nut to a thaler, and even
larger. The cheeks and the backs of the hands were each covered with a
single bleb. The exanthem was of a hemorrhagic character, and the
intervening skin was red and the face swollen. The bullae appeared not
only where the eruption existed, but also on parts of the body free
from it. The fever remained at the same height till the fifth day,
when, upon the cessation of the bullous eruption, it fell to 100
degrees F. A.M., and 101 degrees F. P.M. The child died on the eighth
day of a pneumonia which developed between the sixth and seventh days.
Other cases have been reported by Steiner, Kluppel, and Loschner.
Henoch rejects the theory that the bullae are the result of the
morbillous dermatitis, but thinks that they are merely instances of
the coincidence of a contagious pemphigus.
[Footnote 26: _Berl. klin. Woch._, No. 13, 1882.]
The severe affections of the eye described by continental
writers--blennorrhoea, keratitis, iritis, etc.--are certainly very
rare in this country as complications of measles. Various so-called
strumous disorders of this organ, as will be seen hereafter, not
uncommonly, however, come under the care of the ophthalmologist as
sequelae of the disease.
The tonsils and the mucous membrane of the pharynx may become severely
inflamed. The tonsils are sometimes very much enlarged, but
suppuration, if it occur, is certainly rare. Slight ulceration of the
gums close to the teeth is occasionally noted, also aphthous
ulcerations on the lips, tongue, and gums (Ringer).
Some degree of laryngitis is an accompaniment of all cases of measles.
It has already been stated that catarrhal or false croup is frequently
observed during the stage of invasion. Inflammation of the larynx may
be present in all grades of severity. Rilliet and Barthez found
ulcerations and erosions, especially of the vocal cords, upon
post-mortem examination of a large proportion of measles subjects; and
Gerhardt, both during life and by autopsy, has verified these
observations. Loeri[27] states that inflammatory changes are more
marked in the larynx and trachea than in the pharynx. According to his
examinations, hemorrhages or ecchymoses seldom occur, but more
frequently superficial or even deep catarrhal ulcers, especially on
the anterior aspect of the posterior wall of the larynx at the apices
of the cartilages of Santorini, or on the posterior portion of the
vocal cords. The physical condition of these parts readily accounts
for the frequent and harassing cough and attacks of spasmodic
laryngitis which are such frequent complications of the invasion and
eruptive stages of measles.
[Footnote 27: _Jahrb. f. Kinderheilk._, xix. B., 1 H.]
There may be an extension of the tracheo-bronchitis to the finer
bronchial tubes, thus producing capillary bronchitis (suffocative
catarrh). It is apt to prove fatal to very young children. It occurs
more generally during or after the eruption.
Pneumonia is one of the most frequent and, directly and indirectly,
most dangerous complications of measles. Catarrhal pneumonia
(broncho-pneumonia) is, for obvious reasons, more common than the
lobar or {572} croupous variety. Pneumonia may develop at almost any
stage of measles, but experience does not confirm the statement
occasionally made that it is most frequent in the initial stage. Most
observers will agree as to its greater frequency just at the end of
the eruption or during the desquamative period. The occurrence of
epileptoid convulsions, or an untoward increase of the fever, or an
unexplained continuance of the same, should direct the attention of
the attendant to the chest, if his anxiety have not already been
aroused by a change in the character of the respiration or other
symptoms. It may be mistaken for meningitis (Squire). In estimating
the prognosis it should be remembered that croupous and catarrhal
pneumonias run quite different courses. The influence of inflammation
of the lungs upon the rash is quite decided. If an intense pneumonia
should develop in the initial stage, the eruption will be pale and
sparse, or else absent; if the eruption is already out at the time of
the attack, it may become temporarily more vivid, to rapidly fade
later.[28]
[Footnote 28: A scanty rash by no means indicates an unfavorable
course of the disease; this symptom is only serious when evidently due
to some complication.]
Chadbourne[29] has the merit of calling attention to the occurrence of
heart-clot and subsequent pulmonary oedema as a fatal complication of
measles. In a number of autopsies he found that in each case the heart
contained clear gelatinous clots of a very firm consistence, which in
most instances extended to the pulmonary arteries, and in some to the
extent of one and one-fourth inches. In the series of cases observed
by him pneumonic consolidation was mostly absent, and there was very
little evidence of collapse, but the lungs were exceedingly
oedematous. But Keating has also found heart-clot to be the cause of
death in some cases, and believes, as the result of his
investigations, that the presence of large numbers of micrococci in
the blood and in the white blood-corpuscles is responsible for this
condition.[30]
[Footnote 29: _Am. Jour. Obstet._, Oct., 1880.]
[Footnote 30: _Phila. Med. Times_, Aug. 12, 1882.]
There is a strong tendency in measles to intestinal catarrh. As
already stated, a quite sharp diarrhoea is not uncommon at the
beginning of the eruptive stage; but, unless it should prove very
profuse and long-continued, it is not to be looked upon as of very
serious import, especially if the other general symptoms of the
disease are following a normal course. In other instances the bowel
affection may be much more severe, giving rise to tenesmus, bloody
stools, and the other phenomena of colitis. In weakly children the
early diarrhoea may persist in spite of treatment for many days;
indeed, under the influence of high temperatures it may take on a true
choleraic character. Diarrhoea is a very frequent and grave
complication of the broncho-pneumonia of measles.
Acute miliary tuberculosis as an immediate concomitant of measles is
rare. According to Thomas, the disease at times immediately follows
the exanthem, and reaches a fatal issue in a few days or weeks. The
tubercles are more particularly to be found in the lungs and in the
membranes of the brain.
Among the more common disturbances of the nervous system convulsions
play an important role. The epileptoid seizures of the prodromal stage
generally terminate favorably, but in some cases of a malignant
character the onset of the disease may be ushered in with fatal {573}
convulsions. Convulsions in the later stages are apt to have a lethal
termination, as they usually occur in connection with some grave
complication, particularly of the thoracic organs.
Diphtheria is an exceedingly grave complication of measles, although
not necessarily a fatal one. It is of less frequent occurrence than in
scarlatina. It may attack any of the usual oral, nasal, or laryngeal
regions, sometimes extending into the bronchi, but suffers no
modifications in its symptoms and course from the primary disease. It
may also rarely involve other parts--_e.g._ genitals, eyelids, etc.
There is reason to believe that it is most prone to attack those cases
in which the mucous membranes have undergone the greatest inflammatory
alterations.[31]
[Footnote 31: Loeri (_loc. cit._) says that diphtheria may appear at
any stage of measles, and commences generally in the larynx, and
sometimes in the trachea simultaneously; seldom in the pharynx, as in
primary diphtheria or in that complicating other diseases than
measles.]
Many other complications of measles have been recorded in literature
(see Thomas, _op. cit._); but it is no doubt true, as observed by
Bohn, that very few of them have a real essential connection with that
affection, and might as readily be associated with any other malady,
especially in already vitiated constitutions. In the above sketch the
endeavor has been made to indicate those disorders which from the
nature of measles would seem to have a more or less close and definite
relationship to it. It is certain that the more serious complications
and sequelae of measles are comparatively infrequent in private
practice in America, although common enough in continental Europe, and
to a certain extent in the children's asylums and foundling hospitals
in this country.
SEQUELAE.--It is a difficult matter to dissociate the complications
and sequelae of measles. Properly speaking, the sequelae are to be
looked upon as the complications which have continued in existence
after the subsidence of the exanthem; but it is also customary to
include under this head certain affections that are the result of the
derangement of the system by the morbillous process.
As would be expected, among the most frequent sequelae of measles are
those diseases which have their seat in the mucous membranes. Thus, we
may observe various grades of inflammation and ulceration of the
larynx, trachea, and bronchial tubes. According to Loeri, follicular
ulcers of the larynx always give a bad prognosis, for these cases
usually succumb to tuberculosis. It is not uncommon to observe a
bronchial catarrh, apparently simple in nature, which persists with
frequent exacerbations for many months. The very frequent
broncho-pneumonia, which occurs as a complication, always remains as a
sequel, or it may develop after the morbillous process has come to an
end. In favorable cases recovery may take place in two or three weeks,
or, preceded by hectic and progressive emaciation, the disease may
prove fatal after a number of months. But even here it is not
impossible for affected persons to recover.
Chronic pulmonary tuberculosis is one of the most formidable and
frequent sequelae of measles. It is a not uncommon occurrence that,
with the exception of some trivial bronchitis, a patient may
apparently recover his health completely, and only after a lapse of
time slight daily elevations of temperature, accompanied by loss of
appetite and emaciation, {574} first give warning of the impending
danger. This form of phthisis may follow either croupous or catarrhal
pneumonia. Granular meningitis or general miliary tuberculosis also
frequently follows in the wake of measles, connected in many cases
with foci of caseous degeneration in the involved lymphatic glands or
unabsorbed pneumonic exudation.
Various gangrenous affections, particularly of the oral cavity (noma)
and genitals, but also of the skin, subcutaneous connective tissue,
cartilages of the nose, ear, etc., are often to be observed after an
attack of measles. Cancrum oris is to be especially noted.
Albuminuria is not an essential sequel of measles, although it may
occasionally occur as the result of great exposure and neglect.
A large group of chronic affections may follow in the track of
measles, either in the form of sequelae to the complications which
arise during the course of the disease or in the nature of secondary
accidents. Some few, perhaps, are more common after measles than after
any other complaint, but the majority are such as might arise in
weakly children subsequent to any specific disturbance of the health.
In addition to those already mentioned we may especially designate
chronic intestinal disease, together with ulcerations and strictures
of the bowel; chronic coryza, in varying degrees of obstinacy and
severity; chronic ophthalmia, under which title may be included
ciliary blepharitis, granulations, trachoma, phlyctenular
conjunctivitis, ulcers of the cornea, etc. (Michel[32]); aural
affections in the form of chronic suppurative inflammation, and, more
rarely, chronic catarrh of the middle ear (Spencer); certain cutaneous
diseases, more especially in my experience furunculosis and pustular
eczema; chronic bone and joint disorders (strumous), which, according
to Gibney,[33] may not only be evoked in the already hereditarily
predisposed, but also induced when the diathesis has not heretofore
existed; and, lastly, various derangements of the nervous system.
[Footnote 32: Oral communication.]
[Footnote 33: See valuable statistical article in _N.Y. Med. Record_,
June 3, 1882.]
In Thomas's valuable and freely-quoted monograph on measles (_op.
cit._) it is stated that secondary measles can exert various
influences upon the primary disturbance. In most instances when
measles attacks a person already the subject of some other disease,
particularly when the latter belongs to the common complications of
the former, it usually is aggravated. This is a matter of common
experience; but this author further declares--and supports his
assertion with numerous references--that, on the other hand, should
measles appear during the existence of a disease to which it does not
usually give rise, it may favorably influence the course of the
latter. In spite of the cases quoted in support of this view, such
results would appear to be contrary to pathological laws.[34]
[Footnote 34: Thus, while Thomas seems to be without personal
experience in the matter, he quotes without dissent a number of
observations in support of his assertion--viz.: Behrend saw a chronic
eczema of the scalp permanently disappear after measles; Rilliet found
that a chronic coxitis improved noticeably after measles; various
chronic skin symptoms, and also chorea, epilepsy, incontinence of
urine, mania, worms, dropsy, joint diseases, ophthalmia, gonorrhoea,
etc., have been known to recover under the same influence. Gibney
(_loc. cit._) in his valuable paper states that he can readily believe
that, occasionally, any acute disease, occurring in the course of a
chronic one, will prove beneficial to the other, but that he is far
from considering this to be anything more than an exception to a very
general rule to the contrary. Chronic joint disease, he continues, is
especially a disease of exacerbations, and any one not familiar with
their natural history may interpret the post hoc as a propter hoc.
Gibney has collected 24 cases of chronic bone disease in {575}
children, 21 of whom were under ten years of age and all under
thirteen. On analysis he found that 12 of these came out of the
intercurrent disease in a worse condition, 11 were unaffected, and 1
only seemed a little better. In my personal experience I have
invariably seen the eczemas of children made worse by measles. I have
no wish to dispute the trustworthiness of the statistics quoted by
Thomas; indeed, I regard them as mostly thoroughly reliable instances
of exceptions to a general pathological law; but I wish it to be
clearly understood that they are such, and that measles is not a
disease to be slightly regarded as to its effects upon the system.]
MORBID ANATOMY.--The normal rash of measles is not to be observed on
the dead body, and the only lesions of the skin to be noted are those
resulting from extravasation of blood into that tissue. Examination of
the skin removed during life from a patient with measles reveals the
following anatomical changes, according to Morris.[35] In the earliest
stages are found usually slight hyperaemia around the orifice of a
sebaceous follicle, with slight swelling from effusion of plasma.
Occasionally swelling alone is present, and more rarely hyperaemia
only. Round the small hyperaemic papule thus developed--often pierced
by a hair--a roseolar patch, due to congestion of the papillary body,
soon makes its appearance. Slight exudation of plasma, with a few
corpuscles, usually follows, and produces elevation of the papule
itself. As most of the deaths in measles are due to the presence of
some complication, the post-mortem changes will be found to correspond
to the lesions produced by these diseases, principally affections of
the respiratory organs and intestinal tract.
[Footnote 35: _Skin Diseases_, Phila., 1880, p. 57.]
DIAGNOSIS.--As a rule, the diagnosis of measles offers no great
difficulties, especially if a correct clinical picture of the disease
has been thoroughly impressed upon the mind. The salient points may be
thus summarized: A period of incubation of about fourteen days--_i.e._
from the date of infection to the commencement of the eruption; a
prodromic stage of about four days, ushered in with fever and marked
implication of the mucous tract, notably cough, coryza, epistaxis, and
photophobia; in this stage may also be noted the punctated redness of
the conjunctivae and of the palatal mucous membrane, which is to be
regarded as a diagnostic sign of great value and importance; finally,
there appears at the conclusion of the stage of invasion,
simultaneously with increase of the febrile movement, a characteristic
eruption upon the cutaneous surface, this eruption coming out first
upon the face, and composed of large maculo-papules of brownish-red
color, arranged in a crescentic form with tracts of normal integument
intervening. Of all the symptoms of measles, the catarrh of the mucous
membranes is undoubtedly the most pathognomonic. In the colored races,
where the recognition of the skin lesion is often a matter of
difficulty, this combination of symptoms should be borne in mind.[36]
[Footnote 36: Corre (_La Mere et l'Enfant dans les races humaines_,
Paris, 1882) states that measles and scarlatina exist in all climates
and among all races; however, they are less frequent in warm than in
cold climates. This relative rarity may be only apparent, and has only
been established by reason of the difficulty of recognizing exanthems
among dark-skinned peoples. In the negro the eruption (of measles)
often escapes observation, but the general symptoms, the angina,
coryza, and bronchitis, and the special coloration of the
bucco-pharyngeal membranes, permit the establishment of the diagnosis.
The skin appears more tense, and the face especially is puffed and
glossy; in passing the hand over the different regions of the body
slight elevations are felt--a difference in the level of the skin
exists in the affected and unaffected portions. On examining the
surface of the body obliquely at a well-pronounced angle of incidence,
these elevations can be perceived by the eye. Desquamation, which is
very manifest in the negro, also confirms the diagnosis; this
desquamation is formed of epidermic debris; it gives rise to a {576}
white dust, which is well defined against the black skin. The skin
itself seems to have lost its gloss; it is completely dry, and no
longer gives the abundant and odoriferous secretion characteristic of
the subjects of that race.]
In the way of conjectural diagnosis, the presence of an epidemic of
measles in the community should be taken into account. Although
measles possesses features so characteristic and pronounced, there are
a number of other diseases with which it may be confounded, especially
in its earlier stages.
There is no other disease which presents so close a resemblance to
measles as does rotheln, and it must be confessed that under certain
circumstances the question of diagnosis is a perplexing one. In
rotheln the appearance of the eruption is often the first symptom of
the affection, whereas in measles there is a prodromic period, having
a peculiar remittent type of fever, which continues for three or four
days. According to Liveing, the short duration of the febrile attack
before the eruption appears is one of the most constant and
distinctive features wherein rotheln differs from ordinary measles. In
some instances, in rotheln the premonitory fever is not at all
appreciable. The catarrhal involvement of the mucous membranes is not
nearly so marked as in measles, while the very frequent sore throat
bears more resemblance to the angina of scarlet fever. In many
instances, although by no means constantly, the eruption of rotheln
first appears on the chest, and not on the face, as is the rule in
measles. It is quite evident that the eruptive spots of rotheln have
presented different physical features in different epidemics; but, as
a general thing, it may be said that they are smaller than those in
measles, of a paler color, and, according to Thomas, not so angular,
less indented, and not so often provided with processes, therefore
less apt to assume the crescentic arrangement so often seen in
measles.[37] The incubation period is longer in rotheln than in
measles.
[Footnote 37: According to Curtman (_St. Louis Courier Med._, June,
1882), the eruption of rotheln consists, when not confluent, of single
papules, each separated by a distinct small red areola. Not
infrequently the papules are large, and sometimes a few pass into
vesicles or pustules. In measles the papules are very small, mostly
confluent, from four to six landing on a single areola, which is
larger than that of rotheln.]
In scarlet fever the incubation stage is shorter than in measles, and
the constitutional symptoms are apt to be more pronounced; the
temperature is higher, the pulse more rapid, and vomiting more
frequent. The stage of invasion in scarlatina is but twenty-four
hours; in measles, seventy-two. There is absence of the characteristic
catarrh of measles, and the presence of severe sore throat, strawberry
tongue, and swelling of the lymphatics at the angle of the jaws. In
measles the rash begins on the face; in scarlatina, on the neck and
chest. In measles the eruption consists of large papules arranged
somewhat crescentically, with intervening normal skin, followed by
bran-like desquamation; in scarlatina the rash is made up of large
patches formed of minute red spots on a bright red, hyperaemic base,
and is followed by desquamation in large lamellae. In measles the rash
is brightest on exposed parts; in scarlatina, most vivid on covered
regions. The sequelae of the two diseases are quite different.
There is no great difference in the duration of the invasion stages of
variola and rubeola; but in the former disease we have the marked
lumbar and sacral pains and vomiting, while in the latter the
catarrhal symptoms and photophobia are pathognomonic. When the
eruption of {577} small-pox appears there is subsidence of fever; in
measles, an exacerbation. A point of great importance in the diagnosis
of variola is found in an examination of the mouth and pharynx, for in
these situations on the fourth day we will often find the vesicles
fully developed, while on the skin they are still in the stage of
papulation. When measles assumes the papular form (morbilli papulosi,
rougeole bouttoneuse), it is often confounded with the papular stage
of small-pox. I have seen a number of such mistakes made. Attention to
the general symptoms of the two diseases, however, and particularly an
examination of the mucous membranes, will generally clear up any
doubt. At any rate, the question will generally settle itself in the
next twenty-four hours, for if it be variola the papules will have
undergone their specific development and the rubeolous elevations will
have become more decidedly macular.
Typhus sometimes offers a certain resemblance to measles. According to
Buchanan,[38] the eruption of typhus is occasionally, though not
commonly, a good deal like that of measles, and appears about the same
time after invasion. Coryza, when present and distinct, points to
measles. The eruption of typhus is of a smaller pattern, discrete, and
not raised; that of measles, often coalescent, crescentic, and
elevated. Subcuticular mottling is present in typhus, and absent in
measles. The palatal mucous membrane should always be examined in
suspected measles.
[Footnote 38: Art. "Typhus" in _Reynolds's System Med._, Am. ed., p.
262.]
As I have never been able to convince myself of the existence of an
independent disease called roseola, I am at a loss to give the points
of differential diagnosis; on the other hand, the various forms of
symptomatic erythema, occurring either as the result of numerous
slight derangements of the system, or in connection with grave
constitutional disease, should be carefully considered. In the first
group of cases the absence of premonitory symptoms, catarrh, etc., and
the presence of the smooth, rose-colored macules, mostly on the trunk,
and in the latter the existence of symptoms belonging to the primary
disease, should prove of assistance. The erythema papulatum of
new-born children I have seen mistaken for measles, but the fact that
rubeola is exceedingly rare in sucklings, and the absence of fever and
catarrhal disturbances, are sufficient grounds for a differential
diagnosis.
The erythematous syphilide (roseola syphilitica), particularly when
accompanied by fever, may bear some resemblance to the rash of
measles; but the history of the case, the circumscribed, indolent
character of the syphilide, in many instances sparing the face, the
absence of pathognomonic catarrhal symptoms of measles, and the
coexistence of other features of syphilis, are quite distinctive.
PROGNOSIS.--The prognosis of normal uncomplicated measles is very
favorable. Thus, of 257 cases observed by Meigs and Pepper (_op.
cit._), all terminated favorably. But in coming to any conclusion in
regard to prognosis a number of different factors must be taken into
consideration. Among the more important are--the hygienic surroundings
of the patient, the age, the nature of the complications, whether the
measles be primary or secondary, and the character of the epidemic. In
the first place, rubeola in foundling hospitals and among the poorer
classes in large cities gives a larger ratio of deaths than among the
well-to-do members of the community. For instance, Bartels has shown
that catarrhal pneumonia, one {578} of the most frequent causes of
mortality in this disease, is particularly prone to occur among those
dwelling in crowded, poorly-ventilated houses. Then, again, the
asylums and hospitals for children are peopled in many instances with
the victims of depraved constitutions, who readily succumb to
intercurrent maladies.
Leaving out of consideration sucklings under six months of age, in
whom measles is rare and said to be slight, most deaths from the
disease occur among very young children, from their greater liability
to complications. According to Beddoes,[39] the mortality from measles
is, beyond all comparison, greatest in the second year of life, and by
the tenth has become quite trifling. An examination of the statistics
bearing on this question coincides with this general statement; but
Fox's tables, already quoted, would show that more infants under one
year of age die of measles than has hitherto been supposed. The
susceptibility to measles decreases with years, perhaps on account of
the fact that most adults have already contracted the disease; but
when it does attack the unprotected adult it may prove fatal. This
statement is borne out by the large death-rate in the so-called camp
measles of our late war.[40] The ravages of measles in virgin
communities have been referred to in preceding pages. The general
temper of the epidemic must also be considered, since it is well
recognized that the essential character of epidemics differs much as
to severity.
[Footnote 39: Art. "Mortality" in _Quain's Dictionary Med._, p. 1002.]
[Footnote 40: In the general field hospital at Chattanooga the
death-rate was 22.4 in 100 cases. In General Hospital No. 1, at
Nashville, it was 19.6 in 100, or nearly 1 in 5. Many died or became
permanently disabled from the sequelae (Bartholow).]
Such complications as diphtheria, catarrhal pneumonia, diarrhoea,
convulsions, etc. necessarily affect the prognosis of measles most
seriously. More patients die of measles in the second than in the
first week of the disease. The careful studies of temperature made by
Thomas, Bohn, and others show that an unusually high and increasing
fever in the prodromal stage is of ill omen, particularly on the
second and third days, and a fever heat measuring over 105 degrees F.
at any stage should be considered as very unfavorable.[41]
Particularly to be feared is continuation of the fever after the
subsidence of the eruption, or a sudden elevation after the normal
curve has been reached. In fact, it is a safe rule to look upon all
anomalies of the curve with suspicion. Secondary measles, or measles
grafted upon some serious existing affection, is particularly fatal.
[Footnote 41: In adolescence a body heat of 107 degrees F. has been
safely passed during the decline of measles with no marked
complication (Squire).]
TREATMENT.--There is no remedy which will destroy the susceptibility
to measles. The future may develop some form of vaccination against
rubeola, for, certainly, the hopes held out by the inoculation of
measles upon the healthy subject have not been realized, as this
procedure merely reproduces the original complaint, without any
diminution in its intensity, and does not lessen the probability of
complications (Mayr). The matter of carrying out a practical and
efficient quarantine in measles is one of unusual difficulty, for the
reason that the disease is capable of active propagation at a
time--the prodromal stage--when it is not yet sufficiently
characteristic for positive diagnosis. But, as measles is by no means
as trivial a disease as would seem to be the common impression, I hold
it as a well-established principle of preventive medicine that a {579}
strict isolation should be enforced whenever, from the nature of the
case, it is at all possible; certainly, very young children and those
suffering from or showing a tendency to other diseases should be
jealously shielded from exposure.
The usual precautions as to disinfection and purification of the room,
bedding, and utensils used by patients should be observed, as in other
infectious diseases. Squire is of opinion that there is danger of
personal infection for perhaps a month, and Hillairet that isolation
for forty days should be enjoined. It is quite certain that inunction
lessens the danger of infection, and Kaposi[42] is authority for the
statement that a warm bath administered after the completion of
desquamation, or about fourteen days from the beginning of the attack,
will effectually prevent contagiousness.
[Footnote 42: _Pathologie u. Therapie der Hautkrankh._, Wien, 1880.]
The apartment occupied by a patient suffering from measles should be
kept at a uniform temperature of from 66 degrees to 70 degrees F., and
free ventilation, at the same time avoiding draughts, should be
enforced. The room should be kept moderately dark. The bed-clothing
should be light, yet sufficiently warm, and the old notion of keeping
the patient in a profuse sweat the better to bring out the eruption
should be discouraged. The diet should be bland and nutritious, and
may preferably consist of milk, gruel, tapioca, and such like
substances. As convalescence progresses there may be a gradual return
to more substantial food. The patient may be allowed cool water in
moderation, as it is cruel and useless, and even harmful, to restrict
one suffering with fever to warm or sweetened drink. The patient
should be confined to his room until convalescence has been fully
established, and should not be allowed to leave the house, both on his
own account and that of others, until the usual health has been
regained. Any of the lingering results of the disease, such as
bronchitis, otorrhoea, conjunctivitis, etc., should receive prompt
attention; iron and cod-liver oil should be prescribed for the weakly
and strumous, and regular hours of sleep, careful diet, and
appropriate bathing and exercise should be advised. It may be said,
without exaggeration, that neglect of the after-care of measles
patients is, in some instances, more to be deprecated than a similar
neglect in the actual treatment of the disease itself.
Since we are powerless to cut short an attack of measles by any
remedial agents at present known to therapeutics, the intervention of
the physician is limited to assisting the cases through to a safe
termination. Quite a number of cases, as seen in private practice,
require no special medicinal treatment, or at most one that is merely
symptomatic. The value of the so-called specific treatment, such as by
carbonate of ammonium, etc., has not been verified by experience.
In ordinary uncomplicated attacks, if the temperature should run high,
in addition to the general rules as to diet and hygiene referred to
before it will usually be found advisable to put the patient on some
diaphoretic mixture, to which may be added a mild opiate. I know of
nothing better than the formula found in the work of Meigs and Pepper
on the _Diseases of Children_:
Rx. Potass. Citrat. drachm i;
Spt. Aetheris Nit. fl. drachm ii; {580}
Tr. Opii Deodorat. minim xii vel xxiv;
Syrupi fl. drachm ii;
Aquae fl. oz. ii. M.
S. A teaspoonful every two or three hours for a child of five years of
age.
Aconite in small doses has been well spoken of in this connection, but
I have no personal experience in its use. Bromide of potassium,
together with a few drops of syrup of ipecac., dissolved in syrup of
wild cherry, acts pleasantly both on the cough and the nervous system.
The inunction of fatty substances, as originally proposed by
Schonemann, and recently urged by Milton,[43] is an excellent routine
practice, and in addition to adding very much to the patient's
comfort, has, perhaps, the merit of lessening somewhat the danger of
infection to others. For this purpose one may use leaf lard, cold
cream, or vaseline, to each ounce of which it is well to add a few
minims of carbolic acid.
[Footnote 43: _Archives of Dermatology_.]
Stimulants are rarely needed in uncomplicated measles, but Squire very
wisely calls attention to the great value of wine in the depression
following upon the crisis.
In spite of some excellent authority to the contrary, I cannot see
that any benefit is to be derived from using severe measures to bring
out an eruption that has undergone retrocession. As stated in another
part of this article, the so-called striking-in of the rash is the
result of the supervention of some complication, and not the cause of
it; therefore, a rational course of action would be to ascertain the
nature of the complicating trouble, and to endeavor to correct it,
which, at the same time, would be the very best means of restoring the
normal course of the disease.
Quinia is of great value in controlling the excessively high
temperature which is sometimes observed either in connection with, or
independent of, complications. If the quinia should prove ineffectual
or else be rejected by the patient, the physician should not hesitate
to abstract heat by cold water in the shape of the wet pack or the
general bath. I think the latter method is to be preferred. It is but
to employ the gradually cooled bath of Ziemssen, perhaps, commencing
at 90 degrees F. and going to 80 degrees or 70 degrees F. The
condition of the patient, as ascertained by the thermometer and also
the state of the pulse, must be the guide as to the duration and
repetition of the baths. In Germany excellent results are claimed for
the treatment of hyperpyrexia in measles by the cold pack, even when
the excessive temperature is due to such a complication as
broncho-pneumonia.
There is little hope from therapeutical interference in malignant
forms of measles, but the medical attendant should endeavor to reduce
temperature and support the strength by free stimulation and
nourishing food.
It will now be advisable, at the risk of some repetition, to call
attention to the treatment of some of the more prominent disturbances
and complications of measles.
Epistaxis, if severe, should be checked by cold applications and
astringents. Plugging will rarely be found necessary. Trousseau
recommends the injection of water as hot as can be borne. Ergotine by
the mouth or hypodermically will sometimes prove highly valuable.
The lids should be anointed with vaseline or cold cream to prevent
their sticking together, and it is well to occasionally evert them to
see that no {581} serious mischief has happened to the eye. If the
conjunctivitis is intense, the discharges should be removed and cold
compresses applied.
Since aural complications are due to extension of inflammation from
the oral and nasal cavities, Spencer urges the importance of early and
systematic treatment of these parts. He advises astringent
applications (Monsell's solution 1 to 4 of glycerine) to the
pharyngeal mucous membrane. Ointments of boracic acid, zinc, or
iodoform are likewise useful when introduced through the nostril.
Earache will require warm opiated poultices and inflation. Otorrhoea
is best treated after the dry method.
For sickness of the stomach a spice poultice may be applied and small
bits of ice given to suck. If constipation exist, a little oil or
syrup of rhubarb or some stewed prunes, or an enema, may be ordered.
Active purgation should be withheld.
The early diarrhoea need give little concern, as it usually soon
ceases; but if it should persist, recourse must be had to more
energetic measures, such as the use of opium by mouth or enema, given
cautiously in the case of children, vegetable and metallic
astringents, and the application of hot poultices to the abdomen. The
diet should be carefully guarded.
The cough, even in mild cases, generally requires some slight
palliative, such as syrup of ipecac., and an occasional small dose of
Dover's powder. Loeri very properly advises against the use of
irritating expectorants. I think it advisable to keep the chest well
smeared with camphorated oil, over which should be worn an oil-silk
jacket. These simple measures, perhaps, diminish the tendency to
thoracic complications. The sometimes violent paroxysms of false croup
are very satisfactorily managed, after the manner of Graves, by gently
pressing a sponge, soaked in very hot water, under the chin and over
the front of the neck. When the dyspnoea is alarming, emetics, and the
general warm bath should be brought into requisition.
Convulsions in the early stage require little treatment other than the
warm bath and appropriate doses of the bromide of potassium; occurring
later, they are very fatal under any treatment, as they generally
supervene in connection with some of the grave complications of the
disease. Chloral, preferably by enema, and chloroform may be tried.
The management of the severe bronchitis and pneumonia of measles
requires great care and circumspection on the part of the physician.
The application of a well-made flaxseed poultice, which should be
neither too heavy nor too hot, is to be regarded as invaluable. To the
flaxseed may be added a small quantity of mustard. Over the whole is
to be placed an oil-silk jacket. Alcoholic stimulants, nourishing,
easily-digested food, and expectorants containing carbonate of
ammonium are to be recommended.
For the treatment of the other complications and sequelae of measles
the reader is referred to the appropriate sections of this work.
{582}
ROTHELN.[1]
BY W. A. HARDAWAY, M.D.
[Footnote 1: In the preparation of this article the author has
consulted the following authorities: Emminghaus, in _Gerhardt's Handb.
der Kinderkrankh._, Zweiter Band, 1877; Thomas, in _Ziemssen's Cyclop.
Pract. Med._, vol. iii., Am. ed., 1875; Squire, in _Quain's Dict.
Med._, 1883. References to current literature will be found in
foot-notes to the text.]
SYNONYMS.--Rubeola, Rubella, Roseola, Epidemic Roseola, German
Measles, French Measles, Hybrid Measles, False Measles, Rubeola
Morbillosae et Scarlatinosae.
DEFINITION.--Rotheln is an acute infectious disease, presenting an
eruption of reddish macules upon the skin, accompanied by mild
catarrhal symptoms, and usually producing but slight disturbance of
the general system. It is self-protective, and occurs but once in the
same individual. It has no relationship to measles or scarlatina.
HISTORY.--A rapid glance at the interesting historical evolution of
rotheln to a specific position among the acute infectious diseases is
all that our space will allow. Some writers have attempted to show
that this affection was known to the Arabian physicians; but since it
is only in comparatively recent times that the contagious epidemic
exanthemata in general have been thoroughly differentiated, it is
quite likely that the modern conception of it was not held by them nor
by other medical men till many centuries later. Indeed, in our day,
physicians are yet to be found, though the number is rapidly
diminishing, who refuse to recognize in rotheln a distinctive specific
malady. Certain German observers in the middle of the last century (De
Bergen, 1752; Orlow, 1758) favored the idea of specificity, but these
views were soon disputed. In the years following a number of other
physicians announced their belief in the specific nature of rotheln,
while, on the other hand, various noted authorities still insisted
upon its connection with scarlet fever or measles. In 1815, Maton, an
English physician, most unequivocally declared that he had observed
cases of an eruptive disorder which resembled neither measles,
scarlatina, nor roseola, and which was worthy of a new designation.[2]
In the second and third decades of this century Hildebrand, and
afterward the celebrated Schonlein, taught that rotheln was a hybrid
of measles and scarlatina, although at this time Wagner (1834)
advocated the essential independence of rotheln. There is no doubt
that under the name of rubeola sine catarrho Willan, Bateman, and
later writers described what we now call rotheln, for they stated that
this variety of measles was not self-protective. Space will not allow
of a detailed mention of the various writers who, during the first
half of this century, {583} have contended for or against the autonomy
of rotheln. It will be well to state, however, that Hebra, from the
standpoint of the dermatologist, very properly regards the manifold
roseolae of Willan as in many instances merely symptomatic erythemata,
or else as irregular forms of measles or scarlatina; but he also fails
to recognize the distinctive features of rotheln. Even so recent a
writer as Niemeyer declares that roseola arising from infection
consists in a modification of measles or scarlet fever. It is only in
the last twenty years that our present exact ideas of rotheln have
obtained. For example, while Trousseau[3] asserts that rubeola
(rotheln) is a perfectly distinct nosological species, he speaks of
the rash as appearing and disappearing alternately for some days, of
its frequent recurrence in the same individual, etc. American
physicians were almost entirely ignorant of rotheln till within the
last ten years, when they were made acquainted with it through the
medium of a careful paper on the subject from the pen of J. Lewis
Smith of New York.[4] Before this time, however, cases had been
described by Homans, Sr., of Boston (1845), and in 1853 and 1871 by
Cotting. Very few authorities now dispute the distinctive specific
nature of rotheln; which statement is borne out by the fact that at
the last meeting of the International Medical Congress, held at London
in 1881, there were but two dissentients to this view in the section
before which it was discussed.[5]
[Footnote 2: Squire, _Trans. Internat. Med. Congress_, London, 1881.]
[Footnote 3: _Clinical Medicine_, vol. ii.]
[Footnote 4: _Archives of Dermatology_, Oct., 1874.]
[Footnote 5: See especially Kassowitz's paper, "Die Wirkliche Stellung
der sogenannten Rubeola," etc., _Trans. Internat. Med. Cong._, 1881.]
ETIOLOGY.--The contagium of rotheln is unknown, but that the disease
is contagious has been fully demonstrated by numerous observations of
epidemics and sporadic cases. From my own experience I should judge
that unprotected persons are not so susceptible of it as is known to
be the case under similar conditions in measles;[6] yet cases are
recorded which would prove that the contagion may be conveyed through
a third person and for some distance. It is probable that the vehicles
of contagion are the same as in measles. At what period of its course
the disease is most capable of transmission has not been
satisfactorily determined. Squire is of the opinion, however, that the
disease is contagious before the appearance of the rash, and may
continue so for some days or for two or three weeks. Rotheln may be
called a disease of childhood for the same reason that the other
contagious exanthemata are--namely, that the majority of adults have
already been attacked. From an examination of available statistics I
am inclined to regard the ages between five and fifteen--the years of
school attendance--as the period of life most susceptible of the
influence of rotheln, although, of course, no time of life is entirely
exempt. The non-susceptibility of sucklings, as in measles, holds true
as a rule, although I am in a position to supply exceptions to this
from my own experience, as well as from that of others. Sex seems to
be without influence in determining liability to the disease.
[Footnote 6: In this regard it resembles scarlatina more than measles,
for I have a number of times seen the disease introduced into
families, where it would attack one or two of a number equally
exposed. J. L. Smith regards it as feebly contagious, and quotes
Chadbourne's experience to the same effect. Liveing declares that
rotheln is more distinctly epidemic in Great Britain than either
measles or scarlet fever, although probably less contagious.]
The period of incubation is not very definitely settled, and, indeed,
{584} owing to the generally trivial character of the affection,
evidence on this point is difficult to obtain. Taken as a whole, it is
probably longer than is observed in measles. According to J. Lewis
Smith, in the epidemic observed by him the incubation period varied
from seven, or less than seven, to twenty-one days; Emminghaus places
it at from two to three weeks; Thomas, from two and a half to three
weeks; Squire, mostly a fortnight, the extreme being twenty-one days;
Cheadle, from eleven to twelve days.
There is nowhere recorded a trustworthy instance of a second attack of
rotheln, although from analogy such an event is to be expected. As in
measles, true recurrences of rotheln--that is, the result of a fresh
infection--are not to be confounded with relapses. I have never
witnessed a relapse, but cases of such a nature have been recorded by
other observers (Lindwurm, Emminghaus, Kortlin, Kingsley).
Rotheln is a disease sui generis, and is in no way related to either
measles or scarlatina; that is to say, it is not an irregular form of
either of these nor a hybrid of them, nor has it ever been observed to
propagate anything but itself. That it is not connected with any of
the symptomatic skin eruptions--the so-called roseolae--is proved by
its contagiousness and epidemic character. I quite agree with other
observers in declaring that rotheln has very little clinical
resemblance to scarlatina, and that, on the other hand, in the
greatest number of cases the points of likeness are with measles. In
the section on diagnosis the differential points between rotheln,
measles, and scarlatina will be considered; therefore in this place it
will only be necessary to call attention to certain general facts.
Thus, aside from the marked divergence in clinical
symptoms--incubation, invasion, fever, eruption, complications, and
sequelae--we are at once met by the positive fact that epidemics of
rotheln, while always presenting identical features, prevail without
regard to the existence of similar epidemics of measles and
scarlatina--following or preceding them--and that attacks of rotheln
offer no bar to the reception of their contagions, or vice versa.
Literature is so full of examples of this statement that it need
scarcely be dwelt upon. By way of illustration, however, the accurate
observations of J. Lewis Smith may be quoted in this connection. Of 48
cases recorded by him prior to May 1st in the New York epidemic of
1874, 19 had had measles. Rotheln in the N.Y. Foundling Hospital in
1873-74 followed an epidemic of measles. During the epidemic of
1880-81 the same fact was observed--namely, that a previous attack of
measles, as well as scarlatina, afforded no protection from rotheln. I
could multiply such examples from my own experience. A single
interesting instance may be noted here. A physician asked the writer
to examine his child, suffering, as he thought, from measles. A
careful investigation revealed a typical rotheln. A number of weeks
later an older child got measles, from which the rotheln patient
acquired a characteristic attack of the same. In the following year
both children were taken with scarlet fever.
The only escape for those who would deny the autonomy of rotheln is in
the bold assertion that both measles and scarlatina more frequently
recur in the same individual than universal experience and observation
will allow; and this leaves them in the dilemma of determining to
which group rotheln must be relegated. The hypothesis of the hybrid
nature {585} of rotheln cannot be accepted by the pathologist nor the
clinician, if for no other reason than that no one has ever seen
rotheln generate anything but rotheln, and in no case give rise to
either scarlatina or measles.
SYMPTOMS AND COURSE.--As already stated, the probable average duration
of the incubation period in rotheln is about fourteen days, varying,
however, within the limits of from six to twenty-one days. In this
respect rotheln resembles scarlatina more than measles, the period of
latency in the latter observing considerable uniformity. No deviations
from the general health are to be noted in the incubation stage.
In most cases prodromal symptoms are entirely absent, the presence of
the eruption being the first thing to show the existence of rotheln in
the system. On the other hand, in a certain proportion of cases there
will be present for a half day, or even longer, the general symptoms
of malaise, such as slight nausea, some sore throat, pain in the
limbs, stiffness of the neck, etc. Vomiting is generally absent. J. L.
Smith records one case of convulsions in the stage of invasion, and I
have notes of a single case in which the prodromal stage was initiated
by mild delirium and fever, the latter anticipating the eruption for
two days and a half, and disappearing when the rash came out. As
Thomas well observes, however, such cases are anomalous, and indicate
either abnormal sensibility on the part of the patient or are due to a
secondary rotheln.
Most observers (Emminghaus, Thomas, Smith, Squire) describe the rash
as coming out in the order usual in measles--namely, first upon the
face, scalp, and neck, then the trunk and arms, and finally the legs.
Others (Liveing, Morris) have stated that the rash first appears upon
the back and chest. In many cases in my own experience this has seemed
to be true. It is quite probable that the situation of the exanthem in
rotheln, as in measles and scarlatina, may present various
irregularities; but I am inclined to believe that a careful
investigation will in most instances show that the normal course of
the eruption is as first stated. Now, a marked characteristic of the
rash of rotheln is that, unlike that of measles, there is no period,
however short, in which its maximum is simultaneous over the whole
body; on the contrary, the eruption will have reached its full
development upon the face, and will be almost or quite faded again,
before the exanthem, for example, will have blossomed upon the trunk,
and especially upon the lower extremities. The duration of the
eruption upon individual parts of the body is probably from a few
hours to half a day at most (Thomas). A consideration of these facts
explains, according to Emminghaus, how different observers have
described the eruption as having its seat upon this or that region of
the body; in other words, it is probable that in a certain proportion
of the cases in which the rash was supposed to have begun on the chest
it had already run its course upon the face. The eruption usually
continues altogether about four days, sometimes disappearing sooner,
and sometimes being visible, especially as a fine mottling, for some
days longer. So far as the individual lesions of the eruption are
concerned, there is no question that they present, within a certain
range, varying aspects; and this clinical fact has been taken
advantage of by the opponents of the idea of specificity in order to
make it appear that the disease is not sui generis, inasmuch as it
lacks uniformity of expression. Such an argument wants force when we
consider that in making up a given diagnosis we lay stress {586} not
upon special, but upon the ensemble of, symptoms. For example, no one
would deny to measles an independent position because the eruption, as
is well known, may assume this or that form (morbilli laevis, m.
papulosi, etc.); on the contrary, we recognize a particular case or
series of cases to be measles from a due appreciation of all the
symptoms present. So it is to be expected that while the cutaneous
lesions will present a certain similarity of feature, as they do,
there will also exist minor differences in detail.
In the greatest number of cases in my own experience the exanthem is
composed of ill-defined, roundish, punctate macules, without special
grouping. These are usually discrete, but in certain situations they
may coalesce. The color is of a pale rosy red, quite difficult to
describe, but less purplish than in measles, and not so livid a red as
in scarlatina. I have occasionally observed large irregular spots not
unlike those of measles.[7]
[Footnote 7: According to Emminghaus (_op. cit._, p. 345), the
eruption generally forms roseolae of pin-head, lentil, or small bean
size. They are mostly round, sometimes oval, and bordered by
well-defined or by blurred edges. The intervening skin is not always
unchanged, for here and there we find upon it small dilated
blood-vessels, and from the spots processes extend with a certain
regularity to other spots in such a way as to give the skin a marbled
appearance.]
Thomas distinguishes three types of eruption--one with large spots,
which is rare; one with medium-sized spots; and one with small spots.
Emminghaus describes a discrete and a more confluent variety. I have
observed one case where the maculae on the back had undergone a
vesicular transformation. Others have mentioned this occurrence.
Itching of the skin is marked in some cases, and a fine desquamation
is observed after the rash, but by no means invariably.
The mucous membranes are implicated to a slight degree in rotheln, but
the amount of involvement varies considerably. In some cases that I
have observed the catarrh of the mucous membranes has been barely
appreciable. As a rule, however, the eyes are somewhat suffused, and
there is slight lachrymation and photophobia. Sneezing may be noted,
but there is little discharge from the nose. Sore throat is not
uncommon, perhaps the most constant feature, and, according to
Liveing, is apt to persist after the subsidence of the rash. The
fauces are injected, and the tonsils are red and swollen, but with no
evidence of ulceration. J. Lewis Smith and others state that the
buccal mucous membrane shows a more or less diffuse patchy and spotted
redness. The tongue may be, and usually is, covered by a white fur,
through which protrude a few enlarged red papillae. There may be
slight cough. Loeri[8] describes the mucous membranes of the pharynx,
larynx, and trachea as presenting a spotted or uniform hyperaemia.
There is no marked participation of the intestines in the catarrh.
Some few writers have noted a transient albuminuria, but it is safe to
say that such cases are entirely anomalous, if not, indeed, in some
instances, examples of mistaken diagnosis.
[Footnote 8: _Jahrb. f. Kinderk._, xix. Bd., 1 Heft.]
A very constant feature is the swelling of the lymphatic glands of the
neck, especially those back of the sterno-mastoid; the swellings may
come on before the rash appears. In all the cases that have fallen
under my notice this symptom has not been absent in a single instance.
Less constantly, and it would seem in proportion to the development of
the rash, engorgement of the glands may be noted elsewhere.
{587} There is but slight disturbance of the temperature in rotheln,
and when it does occur it is usually limited to the first few hours of
the eruption. This has been the rule in my observation, and certainly
holds good for the majority of cases. In a minority, varying degrees
of fever may be present; thus, the temperature may reach 102 degrees
F. or 103 degrees F., and then rapidly sink by the second day of the
disease, or, having fallen a degree, it may continue at this point
till the subsidence of the rash, or, it is said, may retain its
initial height till the end of the disease. During the following week
Squire states that the temperature may be readily disturbed--either
elevated by exertion or depressed by fatigue or chill. A relapse or
recrudescence of the rash may be looked for at this time.[9]
[Footnote 9: Cheadle (_Trans. Internat. Med. Congress_, London, 1881)
has reported an epidemic of rotheln of a very severe type, all the
symptoms of the disease as ordinarily recognized being very much
exaggerated.]
COMPLICATIONS AND SEQUELAE.--In the vast majority of cases neither
complications nor sequelae have been observed in connection with
rotheln. J. Lewis Smith has recorded instances of diphtheritic
inflammation as a complication, which, however, as he justly remarks,
may, when prevalent, attack any inflamed surface. Pneumonia and
bronchitis have been occasionally reported as complicating or
following rotheln. Liveing and Duckworth mention albuminuria, but, so
far as I know, they are alone in this experience. I have known
otorrhoea and ciliary blepharitis to occur as sequelae. It would not
be a matter of surprise that in weakly children various chronic
ailments should be set up by rotheln, as by any other disturbance of
the general health.
DIAGNOSIS.--There is no other disease which so much resembles rotheln
as measles. Especially is this true of atypical cases occurring
sporadically. In rotheln the whole course of the disease is much
milder than in measles, the incubation is longer as a rule, and the
fact of a previous attack of rubeola is of much importance, since we
know that recurrences are very rare. In measles there is a prodromic
period, having a characteristic temperature curve, and presenting
pathognomonic catarrhal symptoms, which precedes the eruption for
three or four days; in rotheln the appearance of the rash is often the
first sign of the affection. The sore throat of rotheln resembles that
seen in scarlatina more than the angina of measles, and the general
catarrhal implication of the mucous membranes, so marked a feature of
measles, is either absent in rotheln or exists to a very trivial
extent. Measles is essentially a febrile disease, having a peculiar
type of fever; rotheln may run its whole course without appreciable
rise of temperature. As will be seen in the preceding pages, the
development and progress of the exanthem of measles differs materially
from that witnessed in rotheln. In measles the lesions are larger,
more vivid, more angular and indented, more frequently provided with
processes, and therefore more apt to assume the crescentic
arrangement, than in rotheln. Finally, it must be urged that the tout
ensemble of the case should be taken into consideration, and not some
special feature of the skin eruption.
The incubation period of scarlet fever is much shorter than in
rotheln, and all of the constitutional symptoms are, as a rule,
infinitely graver. In scarlatina there is a febrile invasion stage of
twenty-four hours; in rotheln, if fever is present at all, it is most
generally simultaneous with {588} the rash, and rapidly disappears,
while in the former it persists for a number of days longer. Vomiting
is common in scarlet fever, rare in rotheln. In scarlet fever the
lymphatic glands are notably involved at the angles of the jaw, in
rotheln at the sides and back of the neck. Sore throat is a feature
common to both scarlet fever and rotheln, but it is very much less
marked in the latter. Thomas[10] says that in scarlatina only the
posterior parts, the uvula, the arches of the palate and their
vicinity are affected, while in rotheln the anterior parts are also
affected, and both in much the same degree. In scarlet fever the rash,
which mostly begins on the neck and chest, is made up of large patches
formed of minute red spots on a bright-red hyperaemic base; in rotheln
the eruption is composed of roundish pea-sized macules, with normal
integument intervening. In cases of doubt--for example, when the rash
of rotheln consists of very small spots which have become
confluent--the further development and persistence of the scarlatinal
efflorescence, the temperature, the pulse, the angina, and the
character of the desquamation must be taken into consideration. The
complications and sequelae are very different in the two diseases.
[Footnote 10: Article "Scarlatina," _op. cit._]
The symptomatic eruptions of the skin which pass under the name of
roseola bear no resemblance to rotheln. They usually occur as the
result of some trivial derangement of the system or in the course of
some primary affection. They are not contagious, the lymphatic glands
and the mucous membranes are not involved, and the rash is quite
different in character.
PROGNOSIS.--The prognosis of simple uncomplicated rotheln is
invariably good. Complications arising in delicate children
necessarily affect the prognosis, as would any other disturbance of
the general health.
TREATMENT.--Simple cases of rotheln require no treatment, as the
patients are rarely sick enough to be confined to bed. Graver forms of
the disease must be met by such measures as are indicated by the
symptoms present. The after-management must be conducted on general
principles having reference to the previous and present condition of
the person attacked.
{589}
MALARIAL FEVERS.
BY SAMUEL M. BEMISS, M.D.
In the medical nomenclature of this country the term malaria is
synonymous with swamp or ague poison.
Malarial affections, therefore, comprise all those diseases or morbid
manifestations which the swamp poison produces in the human organism.
This article is not designed to notice in a systematic manner any of
these disorders which are not properly classifiable under the head of
malarial fevers. It will, however, be necessary to make such
references to the pathology of chronic malarial toxaemia as may serve
to explain the influence this condition exerts in occasioning
departures from type in the febrile attacks.
When a poison generated outside the human system obtains admission to
it, and produces deleterious effects, three questions naturally arise:
What is the essential character and natural history of this noxious
agent? How does it obtain access to the human system? What is its mode
of action when received?
In reference to the first of these questions, it must be admitted that
the substantive essentiality of the malarial poison remains as yet
undemonstrated. It is true, however, that the attempts at an objective
study of this poison by means of the microscope and the cultivating
retort point to the conclusion that it is an organism.
Its subjective or analogical study affords quite incontestable
evidence in support of this conclusion. The leading features in the
natural history of malaria are closely coincident with those of
certain known organisms. It requires for its production suitable
conditions of moisture, temperature, and a properly circumstanced
breeding-place. Within certain bounds these conditions are requisite
to the life and perpetuity of all organisms.
Again, when all the above-enumerated conditions correspond apparently
in the most favorable degree, their continuous concurrence for a lapse
of time is necessary before the poison manifests its presence. It is
not improbable that this period of development may differ in different
climates, but in this country we assume it to be about thirty days. If
these facts related to some noxious organism visible to the eye, no
doubt would be entertained that the presence of its germs in the
places where it appeared was the indispensable condition. It would
then follow that the concurrence of suitable meteorologic and telluric
conditions with sufficient time for its growth and maturity were
merely accessories to its perfect development. According to this
theory, the coincidence of five circumstances is necessary before
malaria can be fully matured--viz.: Its own {590} specific germ;
suitable soil or pabulum; suitable moisture; suitable temperature;
sufficient time for its growth and development.
Certain physical qualities which pertain to the malarial poison can
also be profitably made points of subjective study. These are very
closely connected with the answer to the second question, or "How the
malarial poison obtains access to the human system." They will
therefore be briefly noticed in relation to the instrumentality of
each in conveying malaria into the system.
The first to be mentioned is ponderability, which the following facts
prove that malaria possesses:
Those different atmospheric states which affect the range of diffusion
of known air-borne yet ponderable substances exert similar influences
upon the malarial poison.
Altitude illustrates the ponderability of malaria by powerfully
retarding its diffusion.
High readings of the barometer favor its aerial dissemination.
Fogs, smoke, dust, or floating particles presumably more buoyant than
this poison may exert greater or less influence in overcoming the
obstacle which ponderability attaches to malaria as an air-borne
agent.
Currents of air passing continuously and steadily in one direction
over the breeding-places of malaria increase the limits and intensity
of toxic range.
The atmosphere is undoubtedly the medium by means of which malarial
poison is most frequently brought into the human system. Liability to
intoxication is increased in direct ratio to the proximity of points
of exposure to places of development; to similarity of level; to
situation in the line of prevailing winds which have traversed the
breeding-ground; and, lastly, to the extent and fertility of the
locality of production.
Whether malaria passes through the respiratory apparatus directly into
the circulation, or is lodged upon the fauces and absorbed through
some other surface, is not clearly ascertainable. It is certainly not
deprived of its noxious qualities by stomach digestion, and therefore,
sometimes at least, may reach the blood through the alimentary canal.
Malaria is miscible with water. It is capable of being carried by
currents of water through distances and periods of time altogether
undetermined, without losing either its toxic effects or, perhaps, the
faculty of reproduction. It is more than likely that this means of
conveyance has effected its distribution to continents and islands too
widely separated to justify a belief that it was wind-wafted. No
observations need be adduced to establish the water-borne habit of the
malarial poison, or the positive liability to its toxic effects when
received into the stomach through this medium. These facts have been
well understood from the time of Hippocrates.
The matter of communicability of malaria by means of drinking water
should not be dismissed without some allusion to the great probability
that other fluids or solids are open to a similar charge. There is a
widespread popular prejudice, especially notable in the southern part
of the United States, that drinking milk occasions attacks of the
endemic fevers. It is the usual custom to pour the evening supply of
milk into broad uncovered pans, and allow it to remain exposed in the
open air for {591} consumption at the morning meal. This viscid fluid,
so tenacious of ordinary air-borne particles, may well be suspected of
entangling sufficient quantities of swamp poison to produce sickness
if exposed where it is rife during a whole night.
A similar popular prejudice exists in regard to the muscadine grape,
which flourishes best in swampy localities. The rough skin of this
fruit, frequently covered with its own juice, offers favorable
conditions for the adhesion of air-borne particles.
The malarial poison is not reproduced within the human system. This
proposition is undeniable, since no intensification of the poison is
produced by any degree of crowding of the sick which can be practised;
neither do any conditions of contact with the sick ever impart
malarial affections.
Malarial poison is specific. This allegation is sufficiently
established by its specific effects on the human economy. There is no
other agent known which is capable of originating morbid phenomena
characterized by such marked diurnal periodicity.
It is not interchangeable with other specific poisons. This statement
may be rested upon all fairly collected clinical observations.
There are no facts which justify the belief that malaria is capable of
becoming mixed in the atmosphere, or outside the system, with any
other specific morbific germ, so as to produce a third something which
may give rise to compound forms of disease.
The answer to the second question which is best supported is, that the
malarial poison is brought into the system principally by breathing an
atmosphere impregnated with this miasm.
It is also ingested by being held in suspension in fluids used as
drink or food; perhaps also by eating certain fruits or vegetables in
their natural state whose external surfaces afford favorable
conditions for its lodgment.
MORBID EFFECTS AND PHENOMENA WHICH FOLLOW ITS INTRODUCTION INTO THE
HUMAN SYSTEM.--The discussion of the morbid process established by the
malarial poison involves some difficult problems. A period of
incubation must be admitted to follow the inception of the ague germs.
But this period has no definitely marked limits. Perhaps it is a
shifting one, according to the quantity or quality of the poison
received, or the sudden or gradual manner in which it is received, or
the state of receptivity of the system.
Certain facts seem to indicate very clearly that malarial poison is
very slowly removed from a system which has been brought under its
influence. These evidences of long systemic residence of the poison
are principally displayed in those attacks which occur after long
periods of removal from any surrounding where intoxication was
possible. Vernal attacks may be classed in the same connection. In
many instances the subjects of these long-delayed attacks have never
suffered a paroxysmal seizure, and yet when some accidental
derangement of health occurs, as from a fit of indigestion or a sudden
wetting, they fall sick with one or another form of malarial fever.
It does not appear to me that we are justified in assuming that such
attacks as I refer to are to be ascribed to secondary changes produced
in either the fluids or solids of the system by the malarial poison.
In so {592} far as the clinical phenomena are worth anything in
demonstrating the presence and agency of the specific malarial poison
in these deferred attacks, they are precisely similar to those
observed in paroxysms arising after a few hours' or a few days'
exposure to marsh miasm.
But we find further proofs of the long-continued and silent manner in
which malaria exerts its pathological influences in those enlargements
of the spleen which occur without specific attacks of sickness. The
alterations of nutrition in this organ are so characteristic of
malaria that they can scarcely be supposed to depend upon those
chances which determine the nature of secondary blood-impurities.
Intermittent Fever--Simple Forms.
The clinical phenomena of intermittent fevers afford strong support to
the opinion that this type of malarial attacks illustrates more
strongly than any other the primary influence of the poison upon the
human system. Fits of ague often occur very shortly after exposure in
infected localities, and the persons thus suddenly attacked may
present little or no evidence of cachexia before or after the
paroxysm. Indeed, they frequently resume their ordinary avocations
after the paroxysms, apparently as well as if they had not occurred.
It is therefore my opinion that the pathology of an intermittent fever
does not necessarily involve an hypothesis that the attacks are the
results of certain changes which the poison undergoes after its
inception, nor, on the other hand, that certain perversions of
systemic chemistry are required to inaugurate the paroxysms.
In accordance with these conclusions, it seems likely that the
phenomena of intermittent malarial fever result from the primary
effects of its specific poison exerted directly upon the fluids and
solids of the system, and disturbing their functions, and especially
the nerve-function.
Those malarial attacks which ensue almost immediately after exposure
are principally manifested in persons exposed at points of unusually
abundant evolution. The rule of malarial attacks in temperate
latitudes is, that they require repeated exposure to infection for
their production. The long residence of the poison in the system may
render additional doses possible, until a point of saturation is
reached which occasions paroxysmal explosions. In these cases the
period of incubation is reckoned from the first date of exposure, thus
forming the most striking contrast with the incubative periods of the
cases occurring almost immediately after exposure.
Whether the quiescent period after exposure to malaria be long or
short, attacks are seldom abrupt in their announcement. The symptoms
which usually precede pronounced attacks consist, for the most part,
in some derangement of the functions presided over by the organic
nervous system. Derangement of digestion, vitiated taste, coating of
the tongue, loaded urine, and sallow skin are ordinarily found among
the prodromic symptoms. Next in succession come feelings of malaise,
hot and cold flushes, and those neuralgias which precede and attend
malarial paroxysms.
The symptoms of an ordinary or typical malarial paroxysm are so
characteristic, as to be generally readily interpreted. Creeping,
chilly, {593} sensations over the surface, especially along the spine,
yawning, livid coloration beneath the finger-nails, retreat of blood
from superficial capillaries, and that consequent papillary elevation
which is commonly called goose-skin, comprise the earliest symptoms.
Then decided shiverings with chattering of the teeth come on, and the
patient asks for blankets to be heaped upon him and hot applications
to be made, even though the atmospheric temperature may be decidedly
elevated.
Nausea and vomiting are frequent symptoms, no doubt due to the fact
that the portal system of blood-vessels is so often the seat of
congestion during a chill. No intelligent practitioner can watch a
patient during the cold stage of a malarial paroxysm without realizing
how important the attendant congestion is as a pathological state. It
should first be considered that every chill necessarily implies a
condition of congestion in some part of the system. The blood driven
from the surface and extremities must be accounted for elsewhere; and
the amount of blood which is lost from one part of the circulatory
tree must correspond with that accumulated elsewhere. But in treating
of the pernicious forms of malarial fevers this question will again
receive notice.
In our present state of knowledge we are no more able to explain those
perversions of the normal action of the physical forces of the system
which occasion the phenomena of a chill than we are to explain how the
altered circulation in the first steps of an inflammation is brought
about. The theory which Cullen adopted is quite as explanatory and
consistent as any which has been promulgated since his time. According
to this, a state of spasm of the arterioles and capillaries causes the
chill, while the fever is merely the rebound of functions held in
abeyance during the chill.
After a variable length of time there occurs a change in these
symptoms: the patient begins to remove the blankets which covered him;
the face shows signs of returning circulation; the veins of the whole
surface gradually fill again, apparently beyond their normal state.
But the reaction goes far beyond any normal physiological state. The
face becomes flushed and the eyes injected, and the patient complains
of headache, thirst, dryness and heat of the surface; he will not
permit any covering, and constantly shifts his place in the bed in the
hope that some new position may afford him more comfort. Nausea and
vomiting are commonly present. If the fever runs high, delirium is apt
to occur. The thermometer seldom shows a temperature above 105
degrees, but I have seen 106.5 degrees recorded in the axilla in the
hot stage of a paroxysm of simple intermittent fever.
The duration of the hot stage is different in different cases.
According to Aitken, the mean duration is three to eight hours.
There is a very old and quite well-supported opinion, that the cold
stage is shorter in the quotidian than in the tertian type, and also
that the hot stage is longer in the former than in the latter. It may
certainly be affirmed that in individual cases of either type there is
no fixed relation between the duration of the chill and that of the
hot stage.
The decline of the hot stage begins by the appearance of a gentle
perspiration, limited at first to the forehead, face, and neck. This
gradually extends itself over the surface and increases in quantity
until the whole body is bathed in a profuse sweat. During this period
the {594} patient's symptoms, both subjective and objective, undergo
wonderful mitigation, and, although this stage is usually short, it
often happens that by the time it is concluded a restoration to
ordinary health seems to have occurred.
The sweating stage terminates a malarial paroxysm. The intermission
now begins, and lasts until the inauguration of another paroxysm. The
intermission is longer or shorter accordingly, first, as the paroxysm
occupies less or more time; and, second, as the interval may affect
it. The interval is that period of time which reaches from the
beginning of one paroxysm to the beginning of another. It therefore
furnishes the basis of classification of simple intermittents into the
following forms: quotidian, tertian, and quartan.
Statistics gathered from a great many sources and relating to many
countries and climates indicate that quotidian intermittents are more
common than tertian. It may then be assumed that the natural type of
intermittents is that form characterized by diurnal paroxysms. It must
be remarked, however, that if any natural law does exist establishing
the quotidian as the typical form of intermittent fevers, it is very
often set aside by unknown influences. In certain epidemics the
tertian cases preponderate, and under all circumstances convertibility
may be witnessed between the various forms.
It is probable that the statistics gathered by the medical staff of
the United States Army during the late Civil War afford the most
valuable data which we possess touching these points, in so far as
they relate to this country. During three years of the war 724,284
cases of intermittent fever were recorded, tabulated as follows:
Quotidian, 370,401 cases, 388 deaths--equivalent to 1047 + deaths per
1,000,000 cases.
Tertian, 318,704 cases, 324 deaths--equivalent to 1007 + deaths per
1,000,000 cases.
Quartan, 35,179 cases, 79 deaths--equivalent to 2245 + deaths per
1,000,000 cases.
It has been remarked by several writers that quartan attacks have a
smaller ratio in the Southern States than in other parts of the Union.
My observations on this point have not been sufficiently well recorded
to make them especially authoritative, but they support such a
conclusion.
The morbid anatomy of malarial fevers is more properly discussed in
treating of the graver forms, since the paroxysms of simple
intermittent do not often occasion death.
TREATMENT.--This must necessarily vary with the stage of the paroxysm
and condition of the patient at the time of the first visit.
Let us suppose this to be the incipiency of the paroxysm, or the early
part of the cold stage. However little the danger to life from the
paroxysm of a simple intermittent attack, the practitioner should not
forget that whatever danger does exist is to be ascribed to damages
suffered during or in consequence of the chill. There are few
exceptions to this rule, and those will be noticed presently. With
this fact in view the practitioner's duties are much simplified. He
should first endeavor to remove any complications present which tend
to aggravate the cold stage. If the chill has come on after a full
meal or after eating indigestible food, the stomach should be promptly
emptied; otherwise the cold stage will {595} be prolonged and rendered
more violent. Large draughts of warm water will frequently produce
sufficient emesis. If this should fail, ipecacuanha may be added. The
warm infusion of eupatorium perfoliatum answers well as an emetic,
producing also a laxative effect. But it is disgusting to the palate,
and sometimes prolongs its action beyond desired results. The effect
of an emetic in abridging a chill by revulsive action are uncertain,
and I avoid resorting to them for this purpose alone in simple
intermittents.
The patient's subjective complaints of suffering should receive a due
degree of attention. Additional blankets and warm applications should
be allowed when solicited. I always discourage hot or heating drinks,
except for the purpose just mentioned. I especially oppose alcoholic
stimulants, because they seldom do any good in mitigating the chill,
oftener aggravating the patient's symptoms during the hot stage,
particularly the headache and vomiting, and sometimes directly
occasioning perplexing perturbations. For example, I have seen
convulsions speedily follow a strong brandy toddy given to shorten a
chill.
While the removal of complications is imperatively indicated, it is
also important to use promptly those means which are designed to
modify and shorten the chill. It is a remarkable fact that all the
agents found to be useful for this purpose are such as directly
influence nervous function. Opium in some form enters into all
prescriptions which I have found efficient in modifying a chill. It is
quite efficacious when given alone, but I think its therapeutic energy
and certainty are increased by the addition of other agents of the
same class. I have often exhibited twenty to thirty drops of
chloroform with an equal quantity of laudanum with excellent results.
The tincture of opium may be combined with aromatic spirit of ammonia,
or with bromide of potassium, or with chloral hydrate. In combination
with either of the latter medicines it may be given by rectal
injection. If the stomach is intolerant, or by preference because of
facility of dosage and quickness of effect, the opiate may be given
hypodermically. For this purpose one-sixth to one-quarter of a grain
of morphia may be given, together with one-sixtieth to one-fortieth of
a grain of atropia. It is rarely necessary to repeat the dose
whichever form may be adopted.
After much experience in these methods of mitigating and abridging the
chills of intermittent fever, I feel entitled to say that, whether the
objects be achieved or not, no injurious consequences ensue.
The conditions of the circulatory and digestive organs are not
favorable for the introduction of quinia or of any preliminary
purgative which may be supposed to be necessary, and I therefore delay
their exhibition. It may be excepted, however, that sometimes a very
obstinately irritable stomach or exceedingly vitiated state of the
fluids can be appropriately met by gr. x to xx of calomel.
The hot stage of a simple intermittent seldom calls for medical
interference on account of excessive temperature. If the headache is
very violent or the vomiting troublesome, a subcutaneous dose of
morphia will bring speedy relief. The existence of high temperature
does not contra-indicate its use.
I am in the habit of giving opium in the following combinations:
Rx. Morphiae Acet. gr. ss;
Liq. Ammon. Acet. fl. oz. iv. M.
S. Two tablespoonfuls every second hour.
{596} Or, occasionally, the following:
Rx. Sodii Bicarb. gr. xx.
Morphiae Sulph. gr. i;
Aquae Lauro-Cerasi,
Aquae Menth. Pip. _aa._ fl. drachm iv. M.
S. Teaspoonful pro re nata.
I do not limit the use of opiates in the hot stage to old and infirm
subjects, as Dickson suggests, but give them in all cases where
vomiting, headache, or other neuralgias are excessive, or where
unusual restlessness and jactitation are present.
The propriety of giving purgatives as a preliminary measure of
treatment during the hot stage must be determined by symptoms
connected with individual cases. In the majority of cases falling
under my care purgatives are avoided. When regarded necessary, gentle
purgation is solicited by administering bitartrate of potassium in
lemonade or by combining mild mercurial doses with antiperiodics when
these latter are resorted to during the fever. In some cases a very
furred tongue, sallow skin, and costive bowels indicate more active
purgatives, which may be exhibited during the febrile stage.
The most important question which relates to medication during the hot
stage is in respect to the administration of antiperiodics. It may be
safely stated that practitioners of this country were the first to
adopt this method of procedure in malarial fevers. Here it has been
well demonstrated that a competent dose of quinia, given during any
part of the hot stage, is so often followed by the defervescence of
the fever that it would be illogical to attribute the change to any
other cause. Sometimes the remedy fails in producing this result; then
excessive physiological disturbances may follow, and perhaps some
general aggravation of the patient's symptoms.
There are four different circumstances, each of which, in my opinion,
calls for the exhibition of quinia during the hot stage, whether the
fever has reached its maximum point or not:
_First._ If the period which has elapsed since the beginning of the
paroxysm is so considerable that further delay might prevent
sufficient cinchonism to intercept the next accession.
_Second._ When the fever is so excessive that quinia should be given
as an antipyretic.
_Third._ When apprehensions exist that the fever will occasion some
complication or accident.
_Fourth._ When the tongue is clean and the state of the system is
favorable to absorption.
The hot stage is not usually favorable to absorption, and consequently
the economical use of quinia must not be attempted. It should be given
in doses varying from ten to twenty grains, preferably in solution. I
may remark that I have seldom failed in getting good results from the
powder or pills if lemonade or some fluid facile of absorption be
given at the same time. The mixtures previously formulated answer this
purpose very well, and at the same time mitigate the disagreeable
physiological effects of the quinia.
Allusion has been made to certain symptoms occasionally connected
{597} with the hot stage which involve danger. Convulsions are among
the most important of these. They occur most often among children, but
occasionally with adults. They should be met by chloroform, cold to
the head, hypodermic injection of morphia, and cupping or leeching if
the face is flushed, the eyes injected, and the carotids pulsating
forcibly.
The sweating stage may be classed with the intermission in respect to
medication. No time should be lost in securing cinchonism. From the
moment the sweating stage announces itself the fluids of the system
begin to resume their normal physiological functions. Absorption from
the intestinal surfaces is again restored, and remedies may be
administered with confidence in their effects.
The question is now no longer whether antiperiodics should be
administered, but how they shall be given. Many practitioners prefer
exhibiting them in one large dose; others think it better to give them
in repeated small doses. I have usually adopted the latter method.
Beginning with the sweating stage, I give three grains of quinia every
hour or two hours, until eighteen grains have been taken. This would
occupy periods of five to ten hours to complete the doses, ordinarily
quite a sufficient length of time to obtain cinchonism before the
advent of another paroxysm. If the physician elects to give his
antiperiodic in one or two large doses, he should not trust to so
small an amount as eighteen grains. Allowance must be made for the
loss incident to the probable over-taxation of the power to dissolve
and receive a large amount into the circulation.
Purgation should not be induced to a sufficient degree to hurry the
quinia off before absorption takes place. Some practitioners favor the
employment of adjuvants to the quinia. Very few of these have appeared
to me to be of service except opium. A very convenient formula is a
solution of quinia in peppermint-water by addition of dilute sulphuric
acid, in such proportions that fl. drachm j of the solution shall
represent five grains of quinia and seven and a half drops of
laudanum.
But, however we may boast of the efficacy of cinchona as the anceps
remedium for malarial diseases, we are forced to admit that it is not
certainly an immediate cure, and very commonly fails in producing a
permanent curative effect. If we could in all cases discern and remove
the impediments to its immediate or temporarily curative action, its
claims to be regarded as a practical specific would be undeniable. It
is probable that these impediments generally rest upon the fact that
either the remedy does not gain admission to the circulation or that
some complication exists not within the range of its therapeutic
action.
The failure of cinchona to cure a malarial attack in such a permanent
manner that it shall not be liable to return is probably owing to the
incompetent action of the drug because of its transitory stay in the
system as compared with that of the malarial poison. Some objections
apply to this theory, because when the succession of intermittent
attacks is broken by quinia and it is continuously administered
afterward, the paroxysms occasionally recur in spite of its presence
in the system. These objections may be answered by pleading that under
these circumstances secondary blood-poisons precipitate the attacks,
and cinchona should not be expected to cure these conditions.
The best methods of practice I know of to prevent a recurrence of
{598} intermittent fever after having interrupted the succession of
attacks are, first, to continue the cinchona for at least forty-eight
hours, giving at least three three-grain doses a day. After this no
medicine need be given except such as may be required to correct
chronic toxaemic states of the system or to act as blood-restoratives
until such time as prodromes of another paroxysm may exhibit
themselves. At the instant when these manifest themselves ten to
fifteen grains of quinia in solution should be taken. In order that no
loss of time should occur in applying this method, I always advise
patients to keep a solution of quinia within immediate reach. The
following prescription has sometimes appeared to effect a permanent
exemption from recurrence of paroxysms:
Rx. Ferri Redacti gr. xl;
Acid. Arseniosi gr. j;
Quiniae Sulph. gr. xl;
Ol. Pip. Nigr. gtt. x. M.
Ft. pil. No. xx.
S. One pill three times daily.
It seems sometimes to occur that intermittent attacks so impress the
nervous system that they become, like epilepsy, more liable to recur
because of an established habit. I have known chills to occur when the
ears were ringing with quinia. Strychnia fails to arrest them; arsenic
has more value, but frequently fails. Pure nitric acid, properly
diluted, in doses of six to ten drops, given every four to six hours
without regard to the stage of the paroxysm, succeeds more often than
any medication I have ever resorted to.
Before dismissing the subject of the treatment of simple intermittent
fever it may be proper to mention that I have made trials of cure by
carbolic acid, administered by mouth and subcutaneously, and also of
the sulphites, with no results worthy of recommendation.
Remittent Fever.
The difference in definition between the words remittent and
intermittent expresses the clinical distinction between these two
forms of fever in a very satisfactory manner.
Remittent fever exhibits oscillations of temperature regulated as to
hours of recurrence by laws similar to those which govern the periodic
returns of intermittent fever; but there is no complete defervescence
of the fever. While the lowest angles of the fever curve approximate
the normal body heat more or less closely, they never decline to a
standard of apyrexia.
That remittent fever is a malarial disease, produced by a cause
identical with that which produces intermittent fever, is well proven
by the following facts:
First. Cases occur in close relation with cases of intermittent fever
in populations similarly exposed to malaria, and at the same periods
of the year.
Second. The two forms of disease are readily convertible, the one with
the other.
In non-tropical countries remittent fever cannot be regarded as the
{599} natural type of malarial fevers. At least, it may be affirmed
that the proportion of cases which begin as remittent attacks is so
small that we are warranted in looking upon them as departures from
type. In the United States army during the years 1861-66, inclusive,
there occurred 286,490 cases of remittent fever. The fatal cases were
3853, being a mortality-rate of 13,450 per 1,000,000 cases. By
comparing these statistics with those of intermittent fever recorded
in a previous section it will be found that remittent fever is more
than twelve times as fatal to life as the simple intermittent forms.
If we accept this view of the pathology of remittent fever, it is of
interest to the sanitarian or practitioner to endeavor to arrive at
the causes which occasion these departures from type. Some of these
are undoubtedly extraneous to the system, and relate wholly to
circumstances affecting the malarial poison as a disease-producing
agent. Increased quantity of malaria is well understood to enlarge the
ratio of remittent cases. There is also strong presumptive evidence
supporting the hypothesis that different annual crops of malaria vary
in respect to the noxious qualities of this agent. The same
presumption relates to all crops produced in certain localities as
contrasted with others. Other causes which determine remittent rather
than intermittent attacks are personal to patients. They may be
classed as follows:
First. Unusual personal receptivity or impressibility to malaria may
exist, either because of some constitutional idiosyncrasy or of some
state the system at the time of exposure.
Second. Want of timely medical treatment or of proper medical
treatment may convert intermittents into remittents.
Third. The rapid occurrence of secondary blood infections,
extraordinary in character or amount, may cause the fever to be
continuous.
Fourth. The existence of complications, inflammatory in their nature,
may change intermittent into remittent attacks.
However various or complex the causes may be which operate to convert
intermittent attacks into remittent forms of fever, each one must be
supposed to act by disturbing the functions of those centres which
preside over the normal physiological and chemical changes of the
system.
SYMPTOMS AND DIAGNOSIS.--Attacks of remittent fever are, as a rule,
more abrupt in their advent than intermittents. When prodromic
symptoms exist, they are similar to those which precede ordinary cases
of ague.
The chill is seldom attended by such violent symptoms as the cold
stage of intermittents. The duration of the cold stage is also more
brief. In a small proportion of cases severe vomiting with large
bilious ejections complicate the cold stage. The chill is quickly
followed by the hot stage.
The mildest cases of remittent fever are not readily distinguishable
from the intermittent forms. In these cases the temperature curves are
marked by sharp angles and long tracings between the lowest and
highest records. As cases become more decided in diagnosis, and
consequently represent higher degrees of departure from the
intermittent type, the angles of temperature curves become more obtuse
and exhibit a more or less high average range. The accompanying
temperature diagram (Fig. 23) shows the thermometric record of an
unusually protracted and grave case. The patient was a near relative
of my colleague, Prof. Logan, a leading practitioner of New Orleans,
and the clinical records may be {601} accepted as altogether accurate.
It is somewhat to be regretted that the records of temperature were
not begun at an earlier period, but the gravity of the case was not
manifest until the continued type of fever was found to exist. The
latter part of the diagram illustrates the lapse of the remittent
fever into an intermittent. This is so commonly a mode of cure that
the practitioner watches with solicitude for increasing oscillations
of temperature to announce mitigations of severity in his gravest
cases.
{600} [Illustration: FIG. 23. Temperature chart showing the lapse of a
remittent fever into an intermittent. NOTE.--From the third to the
fifteenth day after attack a half drachm of quinia was given daily.
Observing no good result, it was omitted until the twenty-ninth day,
on which date two doses of eight grains each were administered. On the
morning of the thirty-fourth day eight grains were again given; on the
thirty-fifth day one scruple was given.]
The differential diagnosis of intermittent and remittent fevers may be
looked upon as practically unimportant. All cases so near the
borderline as to make differential diagnosis a question should receive
identical treatment.
There are, however, two other very grave forms of fever which are
liable to give trouble in differentiation from remittent fever. These
are typhoid and yellow fevers. The sanitary protection of communities
exposed to cases of the latter, and also the practical treatment of
the sick, call for early and correct differentiation.
But it is only in the early stages of the pathological processes of
these affections that difficulties of diagnosis are liable to obtain.
The facial expression of patients suffering with remittent is
sufficiently characteristic to afford some diagnostic inferences.
During the pyrexia the face is flushed and the eyes injected, but the
redness is more vivid and the countenance more animated than in either
typhoid or yellow fever. It would not be inaccurate to say that,
however great may be the flushing or other alterations of the
countenance in remittent fever, the natural facial expression is
better preserved than in either of the fevers under comparison with
it. Sallowness of the skin is an early and almost constant event in
remittent fever. It comes on as a secondary manifestation, and appears
in a large ratio of cases to bear some relation to the high
temperature preceding its occurrence. The icteric hue is seldom
intense, indeed very infrequently equalling the orange-yellow of
jaundice resulting from obstruction. There is an exception to this
statement in those cases in which remittent fever attacks a person
already jaundiced. I have seen many cases in which the jaundice
preceded the remittent fever, and became more strongly marked after
its incursion, particularly in those persons who had remained for some
time in a malarial region and suffered repeated attacks. In all cases
of remittent fever it seems reasonable to ascribe the more or less
jaundiced state to one or both of two factors, viz.--the accumulation
of excrementitious material and bile constituents in the blood from
primary derangement of its chemistry; and that excessive activity of
the liver which the malarial poison appears to induce. Whether the
latter mentioned factor results from some action of malaria directly
affecting the nutritive processes of the liver, as it does those of
the spleen, or whether the altered blood-currents during the paroxysms
cause this supposed hypersecretion of bile, we certainly know that to
malaria only can we ascribe those fevers which are marked by such
peculiar symptoms of biliousness or superabundance of bile as to
justify the prefix bilious fever or bilious remittent fever.
The state of the alimentary tract may properly receive notice after
these remarks. In the early stages of remittent fever the tongue may
be moist and large, and covered with a white or lead-colored or
yellowish coat. The edges may be indented with imprints of the teeth.
This is {602} Osborne's malarial tongue, and its appearance is worth
something in diagnosis.
Later in the progress of remittent fever the tongue may become dry,
brown, cracked, and difficult of protrusion, but seldom showing the
tremulousness of a typhoid-fever tongue, and differing also from the
yellow-fever tongue in the fact that in this disease the appearance of
the tongue is usually indifferent as a symptom, except that in
advanced stages it is liable to be smeared with blood.
The stomach is irritable from the very beginning of an attack, and the
acts of emesis are generally in striking contrast with those of
typhoid or yellow fever, both in respect to their violence and to the
relative amount of bile they eject.
The bowels are ordinarily costive, and when moved by purgatives the
stools contrast strongly with those of typhoid or yellow fever by
presenting evidences of the bile-coloring principles which attend all
excretions in malarial fever, and are found in the urine, the
perspiration, and occasionally the sputa.
Some unusually violent cases of malarial fever, which may become
remittent, are inaugurated with convulsions, profuse diarrhoea, and
coma.
Before closing the remarks concerning the digestive organs in
remittent fever I should mention that in the long array of cases I
have treated I cannot recall one solitary instance of black vomit. It
is, however, true that I have observed hemorrhage from the bowels in
quite a number of cases. These occurred late in protracted cases, and
were sometimes the cause of death. Whether it be merely a coincidence
I am unable to say, but it is true that the majority of these cases
have been in young females just after the establishment of the
catamenia.
Hemorrhage from the nose is frequent in remittent fever, but I have
never seen a case with general tendency to hemorrhage.
The pulse in remittent fever differs from that of the typhoid or
yellow fevers by being more synochal in character, firmer, and more
resisting to pressure. The longer the duration of the case the less is
this characteristic discernible.
The nervous system shows less ataxia. Delirium may occur in any stage
of the disease, but differs from the delirium of typhoid and yellow
fevers in showing a lessened degree of perversion of the reasoning
faculties. The neuralgias have nothing special.
The urine is acid, high-colored, and scanty. I have never found much
albumen in the urine of a case of remittent fever, unless there was
some other cause to account for its presence. A small amount may be
detected during excessive fever. Blood is a rare constituent.
Mild cases of remittent fever should terminate in recovery in from
five to seven days. Fatal attacks usually end from the fifth to the
tenth day. Many cases pursue a course which lasts from twenty to forty
days. Under proper treatment the usual termination is in recovery,
either directly or by conversion into the intermittent type.
POST-MORTEM APPEARANCES.--When death occurs in remittent fever the
post-mortem changes generally consist of those which are principally
due to chronic malarial toxaemia and those ascribable to the acute
attack.
Under the former division are permanent enlargements of the spleen and
liver, and pigmentary matter in the blood and deposited in various
{603} organs. Under the latter are to be classed hyperaemic or even
inflammatory states of the stomach and intestines, and those
degenerative changes which are the consequence of continuous
hyperpyrexia. The post-mortem changes which are so uniformly found as
to be most often appealed to in the establishment of diagnoses are
enlargements of the liver and spleen. These may be due in part to
hyperplasia and in part to blood-engorgement. The brown or slate color
of an enlarged liver is strongly diagnostic of malarial affections. It
contrasts strongly with the yellow and natural-sized liver of yellow
fever and with the negative liver of typhoid fever.
The skin is generally yellow, sometimes quite intensely icteric, but
seldom showing the ecchymotic extravasations of yellow fever. In
remittent fever we never find the cadaver oozing blood from the nose
and the mouth, nor are the stomach or intestines ever found to contain
black vomit.
TREATMENT.--The indications of treatment in remittent fevers differ
from those of intermittents in two leading essentials.
First. It is a far graver form of fever, and calls for more
promptitude and energy in treatment for its successful management.
Second. The important pathological condition to be combated is the
hyperpyrexia, and not the cold stage, as in intermittents.
But even with a clear realization of the practical importance of these
facts in governing the treatment of remittents, the practitioner must
still exercise care and self-control, lest he shall unconsciously
adopt the doctrine that inflammatory lesions must be present to
occasion such violent pyrexia as often exists. The physician who comes
directly from a case of pneumonia or rheumatic fever and finds a
patient suffering from remittent fever, with temperature higher and
pulse more bounding than those of the patient he has just left, is
pardonable for finding it difficult to realize that these furious
symptoms are not also associated with inflammation.
Attempts to cure remittent fevers by an exclusively antiphlogistic
treatment either result fatally or induce long periods of confinement
and suffering before recovery is reached. The great indication is to
secure cinchonism as promptly and completely as possible. Nothing
should divert our attention from this object. The condition of the
patient as it respects fever, delirium, or state of the tongue, should
form no bar to the administration of quinia. There are no
practitioners who have had much experience in treating these grave
forms of malarial fever after this method who are not able to recall
the numerous instances of most astonishing and gratifying amelioration
of symptoms as soon as saturation with quinia was brought about. The
dry tongue becomes moist, the skin is bathed in gentle perspiration,
the delirium ceases, and the patient sinks into a quiet sleep.
The amount of quinia necessary to produce cinchonism must be estimated
for each particular case according to the measure of its severity or
to states of the system more or less favorable to its absorption. It
must be borne in mind, however, that questions concerning the
patient's safety are paramount to those of economy. In the mildest
cases I never trust to a smaller amount than from twenty to thirty
grains. In violent attacks I have administered scruple doses every
fourth hour until a {604} sufficient test had been made of its
capability to arrest or modify the febrile paroxysm. I have never met
with any of those exaggerated physiological effects which some
observers teach us to fear from the exhibition of cinchona
preparations during fever. Certainly, I can declare that no permanent
deafness or other lasting lesion of nerve-function has ever occurred
under my observation. I must also add that I know of no reasons why
remissions afford more favorable conditions for the administration of
quinia, beyond the fact that the system is in a better state for its
absorption and assimilation. The quinia is preferably given in
solution, but may be exhibited in the form of pills, or in powder
suspended in black coffee, or in the thick mucilage of the slippery
elm.
The considerations of treatment which are naturally connected with
those just advocated relate to measures which it may be proper to
associate with the quinia. The answers to the two following questions
comprise all that is necessary to be said on this point--viz.:
Are conditions of the system present which may interfere with the
specific treatment by quinia, and which are not, in themselves,
curable by it?
Are any medicines to be given as succedanea to the specific remedy for
the purpose of rendering its action more sure or prompt?
In regard to the first inquiry, it must be admitted that in quite a
large proportion of cases of remittent fever specific treatment fails
to cure. I suppose that may be a reasonable proposition which holds
that in the majority of these cases the presence of secondary
blood-impurities annuls the ordinary specific effects of cinchona.
These must be gotten rid of by depurative medicines. The intestinal
canal, the skin, and the kidneys are the emunctories through which
elimination must be effected. It is therefore proper for the physician
to endeavor to recognize cases where such impurities exist, and to so
modify his treatment as to remove them. The indications for depurative
treatment are jaundiced skin and eyes, furred tongue, costive bowels,
and scanty, loaded urine. These are more or less positively expressed
symptoms in a large majority of cases. It is therefore proper that in
this large majority of cases of remittent fever depurative treatment
should be conjoined with the specific treatment. In my opinion, no
drugs meet this indication so well as mercurials and saline purges and
diuretics. Calomel or blue mass may be given either simultaneously
with the quinia or in alternate doses.
There are three very important rules to be observed in regard to
cathartics: They should never be carried to such an extent that
absorption of the quinine is interrupted. They should not be given in
such large or repeated doses as to produce prolonged irritation, or it
may be even inflammation, of the alimentary canal. Purgatives should
be used for their depurative effects, and never as antiphologistics.
Opium exercises excellent effects in preventing local irritation or
hypercatharsis, and in relieving derangements of nerve-function and
insomnia. It is preferably given in small doses, combined either with
purgatives or with the quinia.
I have found bitartrate of potassium the most grateful and efficient
saline for depurative action. I have generally given it in lemonade in
such amounts as to secure a gentle aperient and diuretic effect. I
hold strongly to a conviction that all drugs as soluble as this
facilitate the absorption of those less soluble--as, for example, of
quinia.
{605} If the first efforts to break the febrile paroxysms fail, it is
better to discontinue the quinia and place the patient under
symptomatic treatment, and await conditions of the system more
favorable for its repetition. Of course the high temperature is
generally the symptom requiring most care and attention.
Vomiting is one of the troublesome symptoms of remittent fever. As
internal medication minute doses of morphia, dry upon the tongue or in
solution in cherry-laurel water, or in combination with eight or ten
drops of chloroform, are generally efficacious. Swallowing pellets of
ice or frequently taking iced effervescing mixtures are good measures
of treatment. Occasionally, a mild emetic, such as warm chamomile
infusion, or warm water alone, will arrest the vomiting temporarily.
It is doubtful, however, whether this relief is secured by the
ejection of any offending matter from the stomach. It is more than
probable that the forced dilatation of the stomach has arrested the
spasms, for filling this viscus with cold drinks to repletion will
often effect the same result.
Of all applications to the epigastrium, a cold wet towel occasionally
sprinkled with chloroform is the best.
A tympanitic or tender abdomen requires stupes wrung from warm water.
They may be dashed with turpentine at first, and afterward consist of
warm water with whiskey. I have occasionally given two or three doses
of turpentine emulsion with benefit, but from much observation I am
forced to protest against the turpentine treatment, as it is called,
which is to give twenty drops of turpentine every two to four hours as
a curative agent.
Hemorrhage from the bowels must be met by haemostatic
treatment--preferably, in my experience, by the use of five grains of
gallic acid in half an ounce of camphor-water every two hours, of
morphia subcutaneously, and of cold cloths over the bowels. As in all
diseases liable to cause death from exhaustion, careful attention must
be paid to the nutriment, and stimulants must be administered as
required.
Pernicious Malarial Fever.
Certain departures from the ordinary types of malarial fever are
termed pernicious, because of their great tendency to inflict more
than usual systemic damage and danger to life upon those who suffer
such attacks. The word pernicious is used in its common English sense
of being hurtful or injurious.
It is entirely unnecessary to enter upon a discussion respecting the
propriety of employing this adjective to designate a class of cases of
disease which are primarily due to the same poison which produces
simple intermittent attacks. The extreme hurtfulness and danger of the
attacks to be described in this section, and the awful suddenness with
which they often occasion death, form striking contrasts with the more
typical forms of malarial fever, and appear fully to justify the use
of the qualifying adjective pernicious.
While all these various departures from type to be grouped under the
term pernicious possess the quality ascribed to them, they
nevertheless differ so widely in their modes of inflicting injury that
it seems desirable to arrange them under distinct sub-classifications.
{606} Some cases of pernicious malarial fever preserve the periodicity
of simple attacks sufficiently well to enable one to classify them as
intermittent or remittent in form. But more commonly it is impossible
to determine this classification, and for practical purposes it is
unimportant to attempt to make any such distinction.
The classification which appears to me most true to nature is the
following:
First. The algid or congestive form;
Second. The comatose form;
Third. The hemorrhagic form.
The algid or congestive form occurs more frequently than either of the
others. Its perniciousness is due to an aggravation or sheer
exaggeration of the cold stage of an intermittent attack.
The following brief clinical histories of two cases will serve to
illustrate the symptomatic phenomena of this form of pernicious
malarial fever:
M. S., aged fourteen, had accompanied his father to a malarious
locality in the country, and had remained with him during September
and a portion of October. Shortly after his return I was asked to
visit him because of some unusual symptoms attending a chill. I found
him in a stupor, from which he was with difficulty aroused
sufficiently to be able to swallow a dose of quinia combined with
laudanum. His face was pallid and inexpressive; the skin cool and
moist; extremities shrunken and cold; pulse small, easily obliterated
by pressure, and irregular; tongue large and moist; and pupils rather
dilated.
My second visit was at 12 M., one hour and a half later than the
first. Patient was found in a deep stupor; surface cold; extremities
and face shrunken and blue; pulse barely perceptible; large liquid and
offensive stools occasionally escaped from the bowels without the
consciousness of the patient. Death at 3 o'clock P.M.
Miss H., living in a malarious situation, complained about noon of
September 19th of great cerebral fulness and unaccountable sleepiness
and debility. She retired to her room, and after a few hours' sleep
resumed her household occupations. On the 20th similar symptoms
manifested themselves, but earlier in the day. She again slept for
some hours, but complained of great prostration after the sleep. On
the 21st, about 10 A.M., she complained of a return of the stupor, and
while retiring to her room requested that I should be called if she
did not awake in a better condition. At 1 P.M. she was found
profoundly comatose, with cold extremities and surface and bathed in
perspiration. When I reached her residence at 3 P.M. she had expired.
There is a common belief among non-professional people that the third
congestive chill is necessarily fatal. There is no foundation for this
opinion, except in the fact that when congestive chills are waxing in
their perniciousness the subject is seldom able to survive the third
recurrence if the second or first should not prove fatal.
It is difficult to account for the pathological dissimilarity between
the simple and congestive types of malarial fevers. If we say that
congestive chills are produced by an intensification of those causes
which produce and govern an ordinary chill, we make an explanation
which, however unsatisfactory, represents very nearly the full extent
of our knowledge on this point.
{607} It cannot be admitted that alterations of quantity or quality of
the malarial poison exercise the sole influence in determining the
occurrence of congestive cases. All experienced practitioners
understand that certain constitutional conditions may pervert simple
chills into congestive forms by producing prolongation or aggravation
of the states of congestion always present in ordinary chills.
Weakened cardiac function, from whatever cause, may be reckoned among
these conditions. In these cases the feeble vis a tergo yields readily
to those perturbations of vaso-motor influence which occasion passive
blood-accumulations in the small veins and capillaries. I may say
further, in speaking of the influence of the vaso-motor nerves in
governing the phenomena of a chill, that we know that in congestive
chills the cerebro-spinal system is much less the seat of symptomatic
phenomena than in simple attacks. On the other hand, the organic
system is far more profoundly affected.
However we may account for the perversions of normal circulation
underlying and producing congestive chills, the great degree of injury
they are liable to inflict is so well understood as to awaken the most
serious apprehensions whenever we are called upon to treat them.
Congestion, however occasioned, may destroy life through abolishment
of function by the sheer physical change of infarction, or, again,
through those inevitable consequences which arrested circulation
entails upon the blood. Blood-stasis is followed by separation of its
constituents, and its disqualification as a circulatory fluid in a
degree proportionate to the duration of the stoppage, and probably
also to the actual extent of the passive engorgement. Thence result
the formation of coagula in the congested vessels and deposits of
pigmentary matter. If partial reaction should occur, portions of this
blood-debris may be floated to various parts of the circulatory
system, and give rise to greater or less important alterations of
function.
Among the white soldiers of the United States army from May 1, 1861,
to June 20, 1866, 13,673 cases were diagnosed as congestive
intermittent fever. Of this number, 3370 died, being a mortality-rate
of 23.91 per cent. The aggregate number of malarial cases returned was
1,255,623. It would therefore appear that 1 case in not quite 372 was
congestive in its type, or 1.08 per cent. The late Dr. Cook of
Washington, La., estimated 2 per cent. of his malarial cases to be of
the congestive type. It can scarcely be doubted that the ratio of
congestive attacks is greater in the more southern belts of latitude
than in the middle or northern parts of the United States. Chronic
malarial toxaemia and the enervating effects of long-continued heat
upon the circulation must occasion an increased proportion of such
attacks, but my own observations show slightly more than 1 per cent.
of the cases treated in the Charity Hospital to have been of the
congestive form.
The cure of a congestive chill is one of the most difficult problems
the physician can possibly encounter. It is nothing less than the
proposition to remove a perverted state of the blood-vessels which is
dependent upon some influence exerted through a nervous apparatus
whose therapeutics and experimental physiology are imperfectly
understood. While a satisfactory solution of this problem will
probably be a remote achievement in medicine, it was long ago
empirically ascertained that certain {608} agents exercised some
degree of control over the cold stage of febrile attacks. For the most
part, these agents are addressed to those perversions of
nerve-function which constitute so important a part of the pathology
of a chill. They are identically the same remedies whose aid we invoke
to allay many other forms of perturbed nervous action. Opium,
chloroform, belladonna, chloral hydrate, and bromide of potassium have
proved more or less valuable, according to the idiosyncrasy of the
patient or the circumstances under which they have been used. I
consider opium the most valuable of these remedies. It should be given
in moderate doses, and preferably combined with chloroform or ammonia,
or, if more expedient to administer per rectum, combined with
solutions of chloral hydrate or bromide of potassium. One-sixth of a
grain of morphia, combined with one-fortieth or one-fiftieth of a
grain of atropia, is an available and useful prescription when given
hypodermically. Rubbing the extremities or the spine, or indeed the
whole surface, with ice, is a mode of practice well worthy of
attention. In the event of inability to procure ice, douches of cold
water, followed by frictions with coarse towels, may be substituted. I
have used nitrite of amyl by inhalation, but its effects are too
transitory to prove serviceable.
Some practitioners speak highly of alcoholic stimulants. My own
experience has not been favorable to their use. Perhaps their benefits
are altogether restricted to those cases in which previously weakened
heart-function existed. But it is important that alcohol be added in
all those cases of pernicious malarial fever, whatever the type may
be, where cardiac stimulation and improvement of nutrition are leading
indications.
I am sure I have often derived benefit from enemas consisting of four
ounces of well-prepared beef essence with a half ounce of whiskey or
brandy and a half ounce of strong infusion of coffee.
The value of the hypodermic syringe in treating congestive chills must
never be lost sight of. The suspension, or even reversal, of normal
systemic currents is made evident by the serous vomiting and purging
attending congestion of the abdominal cavity. Medicine placed in the
stomach under these circumstances is virtually thrown away.
The term comatose is applied to certain cases of pernicious malarial
fever because they present coma as a marked symptom. To appreciate the
propriety of this classification, it must be well understood that the
coma present is not due to cerebral congestion. Further than this one
restriction upon the application of the word there is in its
employment no declaration of any pathological views respecting the
cases it is intended to define. While, therefore, the term is
unquestionably liable to criticism, I suppose its use may still be
admitted, provided it is accompanied by a satisfactorily explicit
account of the symptoms and probable pathological conditions of the
cases included under its caption.
There is a sharp line of distinction between the symptoms and
conjectural pathology of comatose cases and of those of the congestive
form of pernicious fever. The following notes of cases will
sufficiently establish this statement:
C. L., fisherman, aged forty-four, brought into Ward 20, Charity
Hospital, in an insensible condition, November 18, 1875. Temperature
at time of admission 104.8 degrees, pulse 120, respiration 40; able to
swallow liquids placed far back in his mouth. Ordered scruple ij of
quinia in {609} solution, ten grains to be given every fourth hour.
Nov. 19th, patient has taken and retained all the quinia ordered; is
perspiring profusely; temperature 97.8 degrees, pulse 88; more
conscious; takes food and water when offered him. Ordered blue mass,
comp. extr. colocynth., _aa_ gr. v, to be taken at once. To drink
through the day bitartrate potass. oz. j, dissolved in lemonade, until
bowels are moved. Evening temperature 99.3 degrees. Nov. 20th,
temperature 98 degrees; patient placed under convalescent treatment;
discharged from hospital Nov. 29th.
Another comatose patient was admitted to Ward 19 on the 29th of
October, entirely insensible. He was treated by large doses of quinia
in solution per rectum, and by calomel gr. xx, sodii bicarb. gr. v,
placed upon base of tongue, and caused to be swallowed by a
tablespoonful of water trickled over the powder. As the patient began
to recover it was noticed that his right arm was paralyzed. A history
subsequently obtained showed that the patient was an engineer, and had
been engaged in making some land surveys in a swampy portion of the
State of Louisiana, and had been often obliged to wade or swim across
the bayous and to sleep at night in the open air, sometimes without
any protection from the weather. He had previously enjoyed good
health, and was altogether unable to account for the paralysis of his
arm. During convalescence he was treated with iron, strychnia, and
preparations of cinchona, and by cold douches and frictions to the
paralyzed arm. Convalescence was slow, but he was discharged,
completely recovered, on November 20th.
In typical cases the differential diagnosis between the congestive
form and the comatose is made without difficulty. In a congestive
chill the surface is cold, blue, or livid, the pupils dilated, and the
pulse generally slower than natural and irregular. In the comatose
form the surface is preternaturally warm, of a muddy, semi-jaundiced
hue, and the pulse and temperature both indicate the feverish rather
than the algid state.
The subjects of attacks of the comatose form of malarial fever are for
the most part persons who, having contracted attacks of fever in
malarial regions, continue to reside in the same localities and yet
use no proper medication, either for cure or for prophylaxis. We have
in these cases accumulations of secondary blood-poisons quite
sufficient to greatly impede brain-function, and the additional doses
of the primary toxic agent must exercise more or less influence in
determining the phenomena of the attacks.
Very little need be said of treatment, beyond a recommendation of the
courses pursued in the cases cited. Hypodermic medication must be
resorted to when necessary. Efforts to nourish the patient must never
be relaxed. One must see many of these cases before he can realize how
often they recover, from conditions apparently utterly hopeless, when
promptly treated and properly nourished.
The hemorrhagic form of pernicious malarial fever can scarcely be
regarded as an original type. Malaria is not a hemorrhage-inducing
poison. Indeed, it may be positively stated that malaria never
establishes the hemorrhagic diathesis as a primary effect; and it is
only by changes effected in the human economy by its prolonged
influence that it appears to become capable of doing so. The most
experienced and accurate observers of malarial affections concur in
the opinion that this rule is almost without exception.
{610} The morbid conditions whose concurrence entails upon malarial
fevers a tendency to hemorrhages may be classed together as follows:
First. The blood-changes of chronic malarial toxaemia so alter the
consistency of that fluid as to favor the occurrence of hemorrhage.
Second. The long persistent states of malnutrition in chronic malarial
cachexias produce textural weakening of the vascular walls and
increased liability to their rupture. Third. There should be added to
these one other factor, which is mainly operative during a malarial
paroxysm--namely, the increased blood-pressure put upon the vascular
walls by passive congestions.
Two of these factors, as above enumerated, are more or less general to
the system, being the consequence of general cachectic states. The
third factor acts in a purely dynamical manner in causing hemorrhages,
and must necessarily have its area of influence confined to some
certain portion or portions of the vascular tree, since the
congestions of malarial paroxysms cannot by any possibility be
general. It is an interesting fact that the influence of this
last-mentioned factor is so frequently paramount in producing malarial
hemorrhages. These hemorrhages occur in such immediate relation to
chills that we are forced to the conclusion that while altered blood
and weakened blood-vessels were previously present, yet some increase
of pressure beyond the normal was required to precipitate the
hemorrhage.
More than once in the presence of medical classes I have illustrated
the influence of these various factors, respectively, by showing the
arm of a patient suffering with chronic malarial cachexia, with no
extravasation of blood, but upon which the slightest suction with the
lips would produce exaggerated ecchymoses. This explains the fact that
hemorrhages in malarial fevers are never general, but only manifest
themselves upon those surfaces or into those structures which are the
seats of congestion during the cold stage of an intermittent.
I do most earnestly assert that during a practice of almost half a
century, nearly all of which has been passed in malarious localities,
I have never once seen a malarial-fever patient with a general
hemorrhagic tendency, if yellow fever and other hemorrhage-inducing
diseases could be authoritatively excluded. The medical profession
cannot be too watchful in guarding itself against erroneous entries
upon mortuary records to account for deaths from fevers accompanied by
hemorrhages from multiple surfaces of the body. Such aliases as
hemorrhagic malarial fever, climatic fever, rice fever, haematemesic
paludal fever, and many more of the same character, should receive the
severest examination before approval and adoption.
When hemorrhage does attend malarial fevers, it may occur from one or
another of a variety of surfaces or into shut cavities or in
parenchymatous structures. Some years ago I visited a gentleman who
was suffering from an attack of malarial fever, with haematuria. He
made a rapid and, apparently, a complete recovery. Disobeying my
injunctions, he returned to the intensely malarious locality where he
had formerly resided. After a few weeks he was seized with a chill,
followed by apoplectic symptoms, hemorrhage, and death on third day.
It is hardly to be doubted that his death was caused by cerebral
hemorrhage. But, however much in consonance with ascertained facts the
foregoing remarks may appear to be, there are certain points of
pathology connected with {611} malarial hemorrhagic fevers not easy of
explanation. Within the last score of years haematuria has been a far
more common form of hemorrhage in malarial fevers than formerly. In
many localities and during certain seasons it has been very prevalent.
In the present state of our knowledge it is not at all possible to
explain why it is that different epidemics of malarial diseases should
give rise to such a diversity of phenomena, so that one epidemic will
be characterized by a peculiar train of symptoms which shall be absent
in another, being there replaced by different symptoms equally
distinctive of the second epidemic. Whatever may be the cause of these
epidemical peculiarities, it must rest in a something which is capable
of acting as a force upon the human system. We must think of that
unknown agency which exercises this force and gives it some peculiar
direction as possessing at least a conventional essentiality. It is
not satisfactory to say that the renal blood-vessels are the first to
give way, because they are accidentally more weakened than other parts
of the vascular system, or accidentally more often the seat of
congestion. When accidents become as numerous as these cases sometimes
are, they acquire the authority of laws.
The following notes of two cases of malarial hemorrhagic fever may be
found of interest:
C. E., aged twenty-six years, was admitted to Ward 19, Charity
Hospital, Nov. 18, 1872. Had been in America more than a year, and for
several months had been working in an intensely malarial district
preparing the bed of a railroad; has had malarial diseases for several
months, and suffered a severe chill the day before admission. A few
hours after admission temp. 103 degrees, pulse 120, respiration 29;
effusion in both thoracic cavities, and very marked in abdominal
cavity; lower lobe of right lung oedematous, legs anasarcous, pitting
greatly on pressure, with several ulcers of long standing. Urine
loaded with albumen and showing under the microscope abundant
blood-corpuscles; considerable jaundice present, which the patient
states to have occurred suddenly. Ordered five grains each of calomel
and bicarbonate of sodium, to be followed after catharsis with ten
grains of quinia in solution every two hours. Nov. 22d, patient has
taken and retained one hundred and eight grains of quinia; secretion
of urine abundant; no blood present, and only a trace of albumen;
ordered twenty drops of tincture of chloride of iron three times
daily. Discharged cured December 12th. The above comprises the whole
treatment in this case, except one important measure, which consisted
in determined and persistent efforts at forced nutrition. Meat
essences, milk, eggs, and milk-punch were given as methodically as
drugs.
H. K., fifteen years of age, was admitted to Charity Hospital Sept.
15, 1872; has a history of malarial poisoning for several months; was
considerably jaundiced at time of admission, with anasarcous legs.
Under the administration of a mercurial, followed by quinia and iron,
he improved so greatly that he was discharged from my wards and placed
upon some duty in the hospital. Dec. 19th, at 11 A.M., had a chill
which lasted several hours; this was followed by violent fever, with
rapid but compressible pulse; much jactitation; incessant vomiting of
a greenish-black fluid; urine loaded with blood; and sudden
supervention of intense jaundice. Ordered quinia gr. xij by hypodermic
injection; {612} small doses of calomel and soda to be placed upon the
base of the tongue and washed down with ice-water. Secretion of urine
ceased on the morning of the 20th, followed by death at 11 P.M.
Autopsy showed both kidneys dark-colored and swollen from complete
blood-engorgement.
The treatment of hemorrhagic malarial fevers may be included under the
following indications:
First, to secure cinchonism as early as possible;
Second, to arrest the extravasation of blood;
Third, to sustain the patient's strength, and to preserve the systemic
fluids at as near a healthy standard as may be possible.
The first-mentioned indication is certainly the first in importance.
If the hemorrhage originates during a chill, or exhibits degrees of
aggravation in such close relation to the cold stage of malarial
paroxysms as to point to a relation of cause and effect, then that
course of treatment which breaks the recurrence of paroxysms will at
the same time mitigate the hemorrhage, if, in truth, it should fail to
stop it entirely. Quinia should be given in large doses by the mouth
or rectum, or both, or subcutaneously if demanded by the urgency of
the symptoms. I have generally used carefully prepared solutions of
the sulphate for hypodermic injections, but many practitioners prefer
solutions of the hydrobromate for this mode of exhibition. I have
never witnessed any symptoms following the administration of cinchona
salts which justified a belief that they increased the hemorrhage. My
rule of practice has invariably been to endeavor to prevent the
occurrence of another paroxysm, without regard to this very
questionable charge.
In regard to the second indication, it may be stated that patients are
not likely to die from actual loss of blood in any form of hemorrhagic
malarial fever. The blood which is poured out on free surfaces and
escapes by some outlet is seldom so much as to endanger life, but the
hemorrhagic process is likely to involve deeper-seated vessels. This
is especially true in malarial haematuria. Hemorrhages into the stroma
of the kidneys, the Malpighian tufts, and the uriniferous tubules
arrest urinary secretion, and thus entail death. In order to prevent
these results haemostatics should be resorted to as often as attendant
circumstances will permit. Generally these are such as to admit of the
use of haemostatics without prejudicing the effects of other remedies.
In my experience ergot in combination with gallic acid and dilute
sulphuric acid has been very efficient. The following prescription has
been usually given:
Rx. Ext. Ergot. Fluid. fl. drachm iv;
Acid. Gallic. gr. xl;
Acid. Sulphuric. dil. fl. drachm j;
Syr. Zingiber. fl. drachm iij;
Aquae q. s ad fl. oz. ij. M.
S. Dessertspoonful every four hours, diluted with water.
Some practitioners place a very high estimate upon the haemostatic
effects of turpentine. This is undoubtedly a most valuable and
accessible remedy. Dr. Schnell of Plaquemine Parish, La., has found
the tincture of chloride of iron the best haemostatic. He places fl.
drachm ij in fl. oz. iv of water, and directs a dessertspoonful every
hour as long as the hemorrhage continues. In a great majority of cases
of malarial haematuria occurring under my observation solutions of
bitartrate of potassium have {613} been given with great apparent
benefit. Its action is certainly not that of a direct haemostatic, but
by setting up currents through the kidneys, and perhaps by some
solvent power over exudations in the uriniferous tubules, it has acted
as a renal deobstructive.
In the arrest of renal secretion diuretics, cupping over the lumbar
region, and large injections of warm water into the bowels may be
resorted to. Some practitioners state that they have found buchu
beneficial.
The third indication involves a twofold duty. One relates to judicious
and vigilant attention to the patient's nutrition; the other relates
to such measures for depuration as may be called for in each
particular case.
It must be admitted that there is a degree of antagonism in the
measures of practice proper to effect these two purposes, which
renders their coincident exercise a difficult practical question. In
many cases of hemorrhagic malarial fever a competent supply of
properly prepared foods is sufficient. In other cases--and this is
especially true of malarial haematuria--depurative medication becomes
paramount. A person suffering under the effects of chronic malarial
poisoning is seized with a chill; this is followed by bloody urine,
and in the course of four or five hours intense jaundice appears.
Incessant vomiting, delirium, and jactitation also occur. The
experienced physician is at once brought to the conclusion that he has
to deal with a case of blood-poisoning bearing a close resemblance in
symptoms to uraemia. To render this conclusion still more absolute, he
has only to recall the suddenness of the occurrence of the jaundice
and to inquire what has occasioned it. Its appearance is too rapid to
permit us to ascribe it to obstruction. It is altogether improbable
that it is due to sudden hypersecretion in such pathological states of
the system as are present. If, however, we account for it by saying
that the addition of a new toxic constituent, urea and its congeners,
to an already profoundly poisoned fluid suddenly arrests those
processes which dispose of bile in physiological conditions of the
system, it seems to me that we adopt the most rational theory. It is
then jaundice from lack of consumption. The mere probability of truth
in this theory will impress the practitioner with the great importance
of eliminant practice in these conditions.
Calomel has been the medicine to which I have principally trusted. I
give it merely as a depurative, and not as an alterative. Doses of
from two to ten grains may be repeated at suitable intervals until
catharsis has been produced. Bitartrate of potassium, Seidlitz
powders, or solutions of citrate of magnesia may be also administered
if indicated. After purgation the vomiting is mitigated, if not
altogether relieved. On this account, and because of bettered states
of the system for absorption and assimilation, the way is now clear to
the physician. He can ply his antiperiodics, his properly prepared
sustenance, and his alcoholic stimulants according to the exigencies
of each particular case.
The following propositions may seem not inappropriate in closing this
section:
1st. Attacks of pernicious malarial fever are attended by more danger
to life or subsequent health than simple attacks; therefore more
prompt and energetic efforts should be made to cut them short by
cinchonism.
2d. The blood depravations of pernicious malarial fevers far exceed
those of simple cases; and therefore it becomes a leading indication
of treatment to correct faulty conditions of this fluid as early as
possible. {614} In endeavoring to secure this end assimilable foods,
stimulants, and depurants must have a shifting scale of value
according to the exigencies of each particular case.
3d. The complications of attacks of pernicious fever are far more
important than those of simple forms; and therefore symptomatic
treatment is often urgently required.
4th. Attacks of pernicious fever may be greatly diminished in number
by properly directed treatment of chronic malarial toxaemia, and
especially also by the removal of persons suffering under this
cachexia to non-malarious localities.
Typho-Malarial Fever.
The prefix typho- is properly applicable to a class of malarial fevers
which are complicated by the specific poison which produces typhoid
fever.
This term was introduced into medical nomenclature by Surgeon J. J.
Woodward of the United States Army. His classical paper on this
subject has been published in the _Transactions_ of the International
Medical Congress at Philadelphia in 1876. The following extract from
the proceedings of this congress will show the interpretation of this
term by Woodward:
"On motion of Dr. Woodward, seconded by Dr. Pepper, the following was
adopted as expressing the opinion of the section: Typho-malarial fever
is not a specific or distinct type of disease, but the term may be
conveniently applied to the compound forms of fever which result from
the combined influence of the causes of the malarious fevers and of
typhoid fever."
It follows, therefore, that the term should be so restricted as to
define a disease compounded of the two pathological factors which when
acting separately produce either typhoid or malarial fever.
When understood in this sense, and carefully employed, the term
appears to me unobjectionable. Perhaps, indeed, it may be a convenient
addition to medical nomenclature. If such a name had not been
introduced, we would be forced to speak of these cases of compound
disease as complications. As it is customary to regard the minor or
less important affection as the complicating disorder, we would often
have confusion in determining whether the case should be typhoid fever
complicated by malaria or malarial fever complicated by typhoid. This
term leaves all questions of precedence or predominance in abeyance.
There are no facts, however, which support a conclusion that the
malarial poison is capable of forming combinations with the particular
poisons of other specific fevers and give birth to a new special
poison, which may be perpetuated by successive generations, and thus
produce epidemics of a new but compound disease.
The importance of a proper use of the term typho-malarial implies
co-ordinate care in diagnosing the true nature of the malady it should
define.
It may be said, in brief, that the diagnosis of typho-malarial fever
must rest upon the blending of the symptomatic phenomena peculiar
{615} to each one of the two fevers which enter into combination. In
other words, if the differential diagnosis between the two diseases
when they are distinct is made by contrasting the symptoms peculiar to
each, the compound disease is to be recognized by more or less
positive combinations of these symptoms.
These blended symptoms should not be expected to exhibit the results
of a copartnership in which each member exerts equal influence. It is
well understood that when two diseases coincide, that one which is
more violent or excessive in its morbid process holds so much sway as
in some cases almost to extinguish the symptoms of the weaker member
of the combination. Consequently, in typho-malarial fever, the
typhoid, being the graver of the two forms of disease, ordinarily
rules the pathology.
The following notes, accompanied by a temperature chart, will
illustrate the clinical course of a case of typho-malarial fever:
J. L., aged thirty years, of French nativity, but a resident of New
Orleans for three years, was admitted to Ward 21, Bed 311, Charity
Hospital, on the night of December 10, 1881. Had been ill some days
with ague. The house-surgeon administered gr. x. of quinia in solution
and gtt. xv. of tincture of opium.
The records and temperature date from the 12th of December. During the
11th he took drachm ij sulph. cinch. in solution.
{617} [Illustration: FIG. 24. PART I., showing the temperature-curve
from December 12th to 31st, inclusive, during which time the more
characteristic typhoid symptoms predominated. PART II., showing the
temperature-curve in same case from January 1st to 20th, inclusive,
during which the influence of the associated malarial poison was
prominent.]
Dec. 13th, tenderness and gurgling in ileo-caecal region; epistaxis;
rose spots on abdomen; deafness and ataxia; no stools since 11th.
Ordered
Rx. Acid. Sulphuric. dil.,
Syr. Aurantii Cort. _aa._ fl. drachm ij;
Tinct. Cinchonae Co. fl. oz. j. M.
S. Teaspoonful in water every four hours.
Also ordered beef-essence, milk-punch, and milk.
Dec. 13th, two very offensive liquid stools; ataxia greater; skin
yellow and countenance dull and listless. Dec. 14th, fresh rose spots;
tongue brown and dry; three stools; much jactitation. Dec. 15th, more
ataxia; some delirium; pulse 100, weak. Gave gr. iiss quinia in
solution, with tincture opium gtt. iii, every two hours. Dec. 16th,
pulse 128, weak; delirious. Dec. 17, new rose spots; belly tympanitic;
tongue brown, dry; sordes on teeth and lips; eyes injected; very
delirious. Treatment continued; nutrition and stimulants given
methodically. From 17th to 22d but little change in condition or
treatment. Diet and stimulants administered regularly. Dec. 22d, coma
vigil; completely delirious. Ordered
Rx. Liq. Morphiae Sulph.,
Tinct. Digitalis _aa._ fl. drachm iij;
Spts. Aether. Nitrosi fl. drachm ij;
Liq. Potass. Citrat. fl. oz. iij. M.
S. Tablespoonful every three hours.
As the oscillations of temperature became more marked, quinia was
resorted to, apparently with good effect. The patient was discharged
from the hospital Feb. 8, 1882.
It should be observed that after the 14th of December the patient's
bowels were rather costive, and the stools occasionally moulded and
very {616} dark in color. On the forty-fifth day after admission the
patient had a severe chill, followed by a rise of temperature to 104
degrees. This yielded to competent doses of sulphate of cinchonidia.
This was a typical case of typho-malarial fever. The blended symptoms,
as well as those special to each disease, are sufficiently exhibited
in the clinical account. The presence of typhoid fever was established
by the rose spots and the marked nervous symptoms. The typhoid process
seems to have been unusually mild in so far as evidence of bowel
lesions were made manifest.
The history of the patient before admission, the color of his skin and
stools, and the temperature curves gave abundant proofs of the
malarial element in the pathology of the case.
Perhaps nothing need be added on the subject of diagnosis. I may,
however, remark that I am very cautious in asserting the diagnosis of
typho-malarial cases unless the nervous symptoms, positively-marked
bowel symptoms, or rose spots are present to vindicate such a
decision. The presence of malarial poison may be determined with less
difficulty from the previous history of the case and its special
symptoms in the early stages of an attack. But if the morbid processes
of the typhoid poison are violent, there are likely to be stages of
the disease when it is not possible to detect symptoms which indicate
the presence of malaria. On the other hand, it is unquestionably true
that the typhoid condition, as it is termed, which so often
complicates malarial fevers, can very generally be differentiated from
true typhoid fever. While certain cases, or even epidemics, of
malarial fevers are attended by remarkable adynamia, often manifesting
itself from the very incipiency of attacks, it differs widely from
that utter nervous ataxia which characterizes typhoid fever. Again,
the adynamia of malarial attacks is generally ascribable to some cause
not essential to those affections. Imperfect reaction from a chill,
long persistent hyperpyrexia, diarrhoea or vomiting, or chronic
paludal cachexia, or, it may be, some epidemic influence, may produce
it. The ataxia of typhoid fever is part of its morbid process.
Woodward's statistics show that 49,871 cases of fever diagnosed as
typho-malarial occurred among the white forces of the United States
during the late Civil War. Of this number, 4059 proved fatal, a
mortality-rate of 8.13 + per cent. Among the colored troops 7529 cases
occurred, with 1301 deaths, a mortality-rate of 17.27. Statistics
borrowed from the same excellent authority give the number of cases of
unmixed typhoid fever (or fever classed as typhoid without reference
to any complication) as 75,368 among the white troops, with 27,056
deaths, a mortality-rate of 35.89. Among the colored troops 4094 cases
occurred, and 2280 died, a mortality-rate of 55.68. These figures show
very singular comparative results. They prove that typhoid fever as an
uncomplicated malady, was four and a half times as fatal among the
whites as the same disease when in combination with malarial poison.
Among the colored troops typhoid fever was three and a half times more
fatal than typho-malarial fever.
It is highly probable that inaccuracies exist in statistics gathered
in the confusion of a great civil war, but I am not prepared to say
that the conclusions they point to are incorrect. When an acute
inflammation is complicated by malaria, its prognosis is rendered more
grave. This, no doubt, {618} is due in part to degradations of the
fluids of the system by the malarial poison, and in part to the
revulsions of circulation during paroxysms. But it does not follow
from this fact that the presence of malaria in the blood, or its
effects upon that fluid, exercise an unhappy influence upon diseases
due to other specific poisons. It may, on the contrary, be ascertained
in the future that it modifies the typhoid process, so as to deprive
it of some of its most dangerous features.
Further investigations are required to determine the facts in regard
to these questions. But it may be premised that if such a conclusion
shall ever be reached, it will influence our expectations of cure
rather than our practice. If the malarial poison is capable of
modifying the toxic effects of the typhoid poison, it must do so in
the very formative stages of that affection, if not in its incubative
period, so that, having accomplished all the good it is capable of
effecting, we may proceed at once to rid ourselves of its presence.
In entering upon the treatment of two diseases compounded in the same
patient, if one should ordinarily be amenable to specific treatment,
it must certainly be wise practice to endeavor to simplify the case by
subtracting that one from its composition. This is more especially
true if the treatment does not affect the course of the other disease
in any injurious manner. It is therefore proper to begin the treatment
of a case of typho-malarial fever by administering large doses of
quinia. A scruple may be given every fourth hour, until its effects in
eliminating symptoms ascribable to malaria, and also as an
antipyretic, have been sufficiently tested. In the early stages of
typho-malarial attacks the febrile exacerbations conform to those laws
of periodicity which govern uncomplicated malarial fevers. After the
first week, or when the typhoid process has become well established,
periodic returns of the fever are less plainly observable. It is
possible that in some cases in which the typhoid process manifests
itself with great severity the temperature curves may be very
characteristic of that disease. I am satisfied that the indications
for giving quinia to eliminate the malarial element must be based upon
the fever curves which mark the case. Perhaps a more frequent
application of the thermometer would often exhibit malarial
periodicity where it may otherwise remain unsuspected. I know this to
be very often the case in pneumonia complicated by a malarial fever.
Whether thorough cinchonism in the early progress of the attack rids
the case of symptoms due to malaria or not, only a very few days are
likely to elapse before oscillations of temperature call for its
repetition.
The typhoid processes require very much the same measures which are
applicable in uncomplicated cases of that disease. The stools of the
early stages of attacks should not be checked unless excessive, and
mercurials and laxatives should be more freely used than in simple
typhoid fever. The effects of the malarial fever and of the
hyperpyrexia of typhoid fever, when combined, must almost necessarily
entail more accumulation of excrementitious material in the blood than
would occur either disease existing separately. On this account
eliminating treatment is an important indication. When it becomes
necessary to check the diarrhoea because excessive or on account of
failing strength, diuretics subsequently prove serviceable.
Effervescing solutions of potassium or ammonium, lemonade, Apollinaris
water, iced tea, strawberry, mulberry, or raspberry juice, are {619}
grateful beverages and increase renal activity. The mineral acids may
be given during the ulcerative periods of the disease. Insomnia must
be relieved by opiates, chloral hydrate, or other hypnotics.
Tympanites should be met by warm stupes, large enemas of warm water
with fl. drachm j tincture of asafoetida or fl. oz. j of whiskey.
Small doses of turpentine in emulsion are often beneficial.
In the early progress of cases the diet should consist of farinaceous
foods, with milk and the pulps or juices of fresh fruits, given either
cooked or in their natural state as the physician may determine for
each patient. Methodical and forced nutrition becomes necessary at
more or less early periods in different cases.
The stools and all ejecta of the sick should be disinfected and
disposed of with the same care and for the same purpose as those of
unmixed typhoid fever.
{620}
PAROTITIS.
BY JOHN M. KEATING, M.D.
The term parotitis is applied to a condition of painful enlargement of
one or both parotid glands, inflammatory in nature, acute in its
course, and usually subsiding by resolution, but sometimes ending in
suppuration. The different methods of termination, together with
certain etiological distinctions, form the basis of a division of the
affection into two sub-classes--namely, 1, idiopathic parotitis; and
2, symptomatic or metastatic parotitis. These demand separate
consideration.
I. Idiopathic Parotitis.
Idiopathic parotitis, parotitis epidemica, or mumps, as it is
variously named, is an acute contagious inflammation of one or both
parotid glands, which usually appears but once in a lifetime, and
which, although by no means limited to children, is commonly met with
between the second year and the age of puberty. In certain exceptional
cases the disease affects the submaxillary glands alone.
NATURE.--The undoubted contagiousness of mumps, with the fact of its
frequently occurring in extended epidemics, entitles it to a place
among the zymotic diseases, from which it differs, however, in the
marked disproportion between the local and constitutional symptoms,
the former being well developed, the latter but slight or altogether
absent.
ETIOLOGY.--While it is more than probable that, like the other
diseases of the zymotic class, mumps is due to a contagium that finds
its way into the body in the inspired air or with the food or drink,
nothing is known of the nature of this infecting principle.
The predisposing agencies are better understood. Age is one of these,
the greater number of cases occurring, as already stated, between the
second and the fifteenth year. Infants at the breast are almost
entirely exempt, and so, too, are individuals advanced in years. In
extended epidemics it is not unusual to meet with cases in adults, but
it will generally be found on careful examination that these patients
have escaped the disease during childhood. Sex exerts some influence,
a much larger percentage of males being attacked than females.
Epidemics appear more frequently in the spring and fall than at the
other seasons of the year, so that cold and dampness of the atmosphere
must be looked upon as predisposing causes. Mumps bears a peculiar
relation to measles, scarlet fever, and diphtheria, epidemics being
apt to occur directly before, during, or immediately after the
prevalence of either of these affections, especially {621} the first.
The popular idea of mutual protection is entirely without foundation.
Certain peculiarities are presented by the disease in its mode of
occurrence and in the duration and intensity of its epidemics. Thus,
some localities are visited annually, others only at intervals of
thirty years or more; again, one epidemic may last but a few weeks and
affect a small number of individuals, while another extends over
months and attacks all the children and many of the adults in the
affected region.
ANATOMICAL APPEARANCES.--The exact pathological lesion in mumps is
obscure, since the trifling nature of the disease and the almost
invariable termination in recovery afford no opportunity for
post-mortem investigation. According to Foerster, who seems to have
made examinations in cases where mumps occurred as one of the
accidental complications of other and fatal diseases, the affected
gland at first becomes hyperaemic, and is then the seat of serous
exudation. It is reddened, swollen, and on section presents a uniform
flesh-like, moist appearance, in place of the ordinary granular
aspect. The tumor is often greatly increased in size by a simultaneous
serous infiltration of the periglandular connective tissue, and
occasionally this tissue alone is involved, the gland itself being
entirely free from lesion. The great point in favor of this view of
the pathology is the rapid and complete subsidence of the parotid
swelling by resolution--a termination to be expected only when the
inflammatory process stops short of suppuration or fibrinous
exudation.
Virchow regards all cases of parotitis as the result of an extension
of a more or less malignant catarrh originally affecting the
gland-ducts. This is undoubtedly true in some cases, but that it is
far from being the rule is proved by the infrequency of parotitis as a
secondary complication of catarrhal affections of the mucous membrane
of the mouth.
COURSE AND SYMPTOMS.--The course of the disease is susceptible of a
division into three stages--a period of incubation, of invasion, and
of actual attack.
The stage of incubation extends over a period variously estimated as
from seven to fourteen days. It is marked by no symptoms, though
sometimes a history of impaired appetite and digestion, irregular
bowels, and languor during the last two or three days may be obtained.
The period of invasion is short, lasting only twelve, or at the most
twenty-four, hours. The patient is pale and languid, has slight
rigors, pains in the breast and head, and loss of appetite; later,
local pain in the parotid region on moving the jaws or on taking acid
liquids into the mouth. The surface temperature increases from hour to
hour, and just before the glandular swelling appears it reaches 100
degrees or 101 degrees F. In some cases the invasion is characterized
by the same train of symptoms that ushers in the acute exanthemata,
such as repeated vomiting, diarrhoea, restlessness and anxiety, a
disposition to syncope, and, in very irritable children, convulsions.
Contrasted with this violent invasion other cases are met with, in
which there are no prodromes whatever except a gradual rise in
temperature, imperceptible without the use of the thermometer.
The first symptom of actual attack is a peculiar slight stitch-like
pain in one parotid region, usually the left. This radiates toward the
ear of the affected side, and is increased by movements of the jaw, as
in {622} chewing or talking, and by external pressure. The pain
rapidly grows more intense, and soon becomes associated with swelling.
The tumor first appears in the depression between the mastoid process
and the ramus of the jaw, which it fills up, and at the same time
thrusts outward the lobe of the ear. As the gland alone is swollen at
first, the tumor has the outline of a triangle, with the apex directed
downward and forward; soon, however, the connective tissue becomes
oedematous and the swelling is greatly extended, involving the cheeks
and neck, in the latter region, in severe cases, running forward as
far as the median line, downward nearly to the shoulder and backward
toward the spine. The most prominent point is directly in front of the
ear. The oedema also extends internally, involving the pharynx, the
tonsils, and sometimes even the larynx. The skin covering the tumor is
either perfectly natural in color or slightly reddened. The central
portion is firm and elastic to the touch, the periphery doughy, and
pressure here often produces pitting. There is but moderate
tenderness. The swelling reaches its height in three days, remains
stationary for two days longer, and then rapidly declines, the oedema
first disappearing and afterward the glandular swelling, the process
of resolution occupying four or five days and being attended with a
slight desquamation of the cuticle.
While mumps almost uniformly begins on one side, both glands are, as a
rule, affected during the attack. The second tumor begins to develop
twenty-four to forty-eight hours after the first, though its
appearance may be delayed much longer, even until resolution has begun
on the side primarily affected. As the course of the inflammation is
similar in both parotids, the whole duration of the attack will depend
on the time of involvement of the second gland.
Among the other symptoms an alteration of expression is prominent. At
first, the head is inclined toward the affected side; later, when both
glands are involved, it is held perfectly erect, and, as the slightest
movement increases the pain, it is maintained stiffly in this
position. The swelling of the cheeks prevents all play of the
features, and this, combined with widely-open, staring eyes and
increased thickness of the neck, gives the patient a stupid, almost
idiotic, expression. The swelling of the neck is sometimes so great
that its diameter exceeds that of the head, and the shoulders, neck,
and head, viewed together, have the outline of a truncated pyramid.
As any movement of the lower jaw greatly augments the suffering, the
mouth is kept closed, often so tightly that it is impossible to see
more than the tip of the tongue. All efforts at mastication are
suspended, and deglutition is so painful, especially when the tonsils
become enlarged, that the sufferer bears the pangs of hunger and
thirst rather than endure the agony entailed in satisfying his wants.
The act of speaking even augments the pain; the voice, when heard, has
a nasal tone. The acuteness of hearing is impaired, there are singing
noises and shooting pains in the ears, headache, and sometimes, in
extreme cases, symptoms of cerebral hyperaemia due to pressure upon
the cervical veins.
The tongue is heavily coated, the mouth is either dry or there is an
increased flow of saliva, and the fluid dribbling from the mouth adds
another element to the idiotic expression already referred to. There
is loss of appetite, increased thirst, occasionally vomiting, and
commonly {623} constipation. The temperature is elevated and the pulse
increased in frequency, both to a moderate degree. The respiration is
unaffected, except when the oedema has invaded the submucous
connective tissue of the larynx; then the movements are increased in
frequency and difficult.
Throughout the attack the pain, unless intensified by some extraneous
influence, as pressure or the act of speaking or swallowing, is only
moderately severe. In ordinary cases the patient rests quietly and
sleep is undisturbed, unless the tonsils are enlarged, when it is
liable to interruption from loud snoring. When the attack is severe
and in nervous, excitable children there is restlessness,
sleeplessness, and slight delirium at night.
The general symptoms keep pace with the local in their increase, but
they commence to subside before, beginning to disappear while the
swelling remains stationary. As soon as resolution sets in the general
and local improvement are both rapid, and by the end of the week
nothing is left but a trifling weakness and pallor, which disappear in
a few days more, leaving the patient perfectly well.
Besides the ordinary symptoms, mumps in certain instances shows a
peculiar tendency to metastasis, or secondary involvement, of the
testicle and scrotum in males, and the mammae, vulva, and ovaries in
females. This metastasis occurs much more frequently in males than in
females, and is usually met with in pubescents and adults, being very
rare either in childhood or old age. It generally begins six or eight
days after the appearance of the parotid tumor. The latter, as a rule,
subsides on the occurrence of any of these metastatic affections,
though occasionally the two run a simultaneous course. This
occurrence, together with the fact of the secondary inflammation
appearing at the date on which the parotitis naturally begins to
disappear, tends to support Niemeyer's view, that the two affections
are in reality due to the same cause, and that no true transference of
inflammation takes place from one point to the other. Occasionally,
the parotitis disappears a variable time before the onset of the
metastatic affection; then the interval is marked by grave symptoms of
depression and cerebral disturbance, but there are no proofs of actual
meningeal involvement. In these cases there is, at times, an excessive
elevation of temperature, which may account for the brain symptoms.
The most constant secondary manifestation is swelling of the testicle
proper, or true orchitis; less frequently there is epididymitis, and
with it acute hydrocele and oedema of the scrotum. The orchitis in
most cases is unilateral, the right testicle being affected, just the
opposite to the parotids, of which the left is the one first involved.
When the orchitis is double, both testicles do not become swollen at
once, the one preceding the other by an interval of several days.
The course of the orchitis is very similar to that of the mumps, the
inflammation increasing gradually for from three to six days, then
undergoing rapid resolution, the gland returning to its normal
condition by the end of two weeks.
The local symptoms are swelling, the testicle being enlarged to two or
three times its natural size, dull pain, and moderate tenderness,
while in very severe cases there is burning on micturition and a
purulent discharge from the urethra. The spermatic cord does not
sympathize in the {624} inflammation, and neither the swelling, pain,
nor tenderness is so great as in specific orchitis.
The general symptoms are confined to a moderate elevation of
temperature and increase in the frequency of the pulse, thirst, and
loss of appetite. This fever is separated from that of the parotitis
by an interval of two or three days.
The course of bilateral orchitis is longer by forty-eight hours than
that of the unilateral form, and the attending fever is more intense.
The rapid return of the testicle to its natural size and shape shows
that, as in the parotid glands, the inflammation does not extend
beyond the stage of serous exudation.
THE DIAGNOSIS of mumps is easy after the disease is sufficiently
developed to produce the characteristic alterations in the facial
expression. In the earlier stages the position of the swelling,
immediately beneath and in front of the ear, its triangular shape, and
the elevation and outward displacement of the lobe of the ear of the
affected side, distinguish it from the enlargement of the cervical
lymph-glands so liable to occur in strumous subjects. The acute onset
and course of mumps are the points of distinction between it and
morbid growths, or the very rare condition of chronic hypertrophy of
the parotid gland. The metastatic orchitis cannot be mistaken for
gonorrhoeal orchitis if the least care is taken to investigate the
history in either case.
THE PROGNOSIS is extremely favorable, there being no record of a fatal
case of uncomplicated mumps. Suppuration may occur, but it is an
exceedingly rare event. In scrofulous children the course may be
protracted for several weeks, and in them resolution is occasionally
imperfect, a degree of enlargement and induration of one or both
parotids remaining for some time.
Metastatic orchitis, as a rule, leaves the testicle in a normal
condition, but, according to Vogel, in some epidemics complete atrophy
results.
Dogmy reports an epidemic which raged in a garrison of Mount Louis in
January, 1828. Of sixty-nine bilateral and eighteen unilateral cases
of parotitis, metastasis to both testicles occurred in four cases, all
of which resulted in atrophy of the affected testicle.
THE TREATMENT is simple. The patient should be kept in a uniform
temperature, confined to one room, or, better still, to bed, until
resolution is well established. While the difficulty in swallowing and
fever continue the food should consist of milk and beef-tea; later,
other nutritious articles of diet may be added as the appetite
demands. Water, iced carbonic acid water, or lemonade may be allowed
as freely as the patient will take them, to allay the thirst. A daily
evacuation of the bowels must be secured by the use of saline
laxatives. During the early stage, if the fever be high, tincture of
aconite-root should be cautiously administered; afterward liquor
potassii citratis will sufficiently fill the indications for a
febrifuge. Tonics are required during the decline of the disease; of
this class of remedies, syrup of the iodide of iron, bitter wine of
iron, and ferrated elixir of cinchona are most useful.
Special symptoms may demand attention. For example, headache and
delirium should be relieved by hot mustard foot-baths and moist cold
to the forehead; difficult deglutition from enlargement of the
tonsils, by the frequent swallowing of bits of ice, or, if possible,
by the application of {625} astringent lotions, as tannic acid and
glycerine (one drachm to the ounce); sleeplessness, by the
administration of bromide of potassium, with or without small doses of
hydrate of chloral in children and of some preparation of opium in
adults.
In the way of local treatment the best results and greatest relief to
suffering will be obtained by gently rubbing the swollen glands with a
mixture of tincture of opium and sweet oil (one drachm to the ounce),
three times daily, and in the mean while keeping the parts enveloped
with a moderately thick layer of cotton wadding covered by oiled silk.
Water dressings or light poultices may be used with advantage. When
resolution begins a more stimulating lotion will hasten the
disappearance of the swelling.
In the exceptional instances in which the skin covering the tumor
becomes tense and red, and suppuration is threatened, two or three
leeches may be applied behind the ear of the affected side. When
suppuration has actually taken place the abscess should be immediately
opened to prevent further destruction of the gland-tissue and
perforation into the external auditory meatus.
If, particularly in strumous subjects, resolution be incomplete and
glandular enlargement and induration remain after the cessation of the
acute symptoms, cod-liver oil and iodide of iron are demanded for
internal administration and the compound ointment of iodine for
external application. It is well to dilute the latter sufficiently to
prevent its causing irritation of the skin, and to apply it twice
daily.
When metastasis occurs, the return of fever calls for the same general
treatment as in the early stage of parotitis. In addition, an emetic
should be given, as this often cuts short the fever or causes it to
disappear more rapidly. The patient must be kept at perfect rest in
bed, with the scrotum elevated by a cushion and covered with warm
anodyne lotions. Salines must be administered sufficiently often to
secure regular and free action of the bowels.
When the mammae or ovaries are secondarily attacked, the seat for
local treatment is of course different, but in all other respects the
management must be the same.
For the uncommon cases in which the transference of the inflammation
is attended with depression stimulants are required, and for those in
which meningitis is threatened cutting off the hair and the
application of cold to the head, hot mustard foot-baths, local and
general venesection, drastics, and irritants to the cutaneous surface,
are necessary.
II. Symptomatic or Metastatic Parotitis.
Symptomatic, metastatic, malignant, or suppurative parotitis, as the
condition is variously designated, is an inflammation of the parotid
gland which occurs during the course of different grave acute
diseases, is usually unilateral, and terminates in suppuration, or
much more rarely in gangrene, of the gland involved.
ETIOLOGY.--It may occur in association with typhus, typhoid,
relapsing, puerperal, and scarlet fevers, or with the plague, measles,
dysentery, cholera, and pyaemia, springing into notice at different
periods of the {626} course of these affections, which may be regarded
as predisposing causes. The exciting cause is perhaps mechanical in
nature--namely, the excessive dryness of the mucous membrane of the
mouth so common in the severe fevers. This dryness may lead to an
occlusion of the orifice of the parotid duct, with retention of the
saliva, which fluid, undergoing decomposition, may act as an irritant,
producing inflammation, and finally suppuration, of the glandular
tissue. This is a likely enough explanation of the causation in some
cases, but dryness of the mouth is such a uniform symptom in fever,
and suppurative parotitis such a comparatively rare complication, that
it cannot be a very active or common cause. Nevertheless, it is
impossible to fix upon any other direct cause, though the altered
condition of the blood in the conditions mentioned must not be lost
sight of as an important etiological factor.
ANATOMICAL APPEARANCES.--The character of the pathological lesions
have been well established, owing to the frequent opportunities that
arise of examining the diseased gland at different stages of the
inflammatory process. When the inflammation has lasted a short time, a
day or two, the tubes and acini of the gland are seen on section to be
swollen and reddened, and the connective tissue infiltrated with serum
and yellowish-red in color; a fluid, either viscid, ropy, grayish in
color, or more purulent in character, fills the duct, and may be
forced out into the mouth by stroking it in the direction of the
orifice. If of several days' longer duration, purulent softening will
be noticed in the centre of the acini; this gradually extends until
each acinus is converted into a little sac of pus. Then the
inter-acinous connective tissue breaks down, and the multiple, minute,
purulent collections become converted into a single large abscess or
into two or more smaller ones. Next, the pus seeks an outlet. The
position of pointing may be on the cheek or in the external auditory
meatus--a very common location; again, the abscess may break into the
mouth, the pharynx, the oesophagus, or into the anterior mediastinum,
the pus burrowing its way along the sheath of the
sterno-cleido-mastoid muscle.
While the parotid abscess is forming, suppurative inflammation is apt
to be set up in the masseter, pterygoid, and temporal muscles, and
from these positions the pus forces its way upward to the temporal or
zygomatic fossae. The periosteum of the neighboring bones, and even
the bones themselves, may become involved, and sometimes the cranial
bones are partially destroyed, and there is an extension of the
inflammation to the brain or its membranes. The middle ear may
participate in the general destruction, and the patient is left
permanently deaf, if indeed he escape with his life.
The lymphatics, veins, and nerves traversing the parotid are affected
by the suppuration in the gland. Irritation of the lymph-vessels
results in swelling, tenderness, and suppuration of the lymph-glands.
Thrombi form in the jugular vein and its branches, and by breaking
down lead to septicaemia and ichorization of the sinuses of the dura
mater. The nerves resist for a long time, but seem to act as paths of
conduction of the inflammation, the facial nerve leading it to the
ear, and the branches of the trifacial to the brain. When gangrene of
the gland takes place, the traversing nerves as well as the gland
elements are rapidly destroyed.
SYMPTOMS.--Symptomatic parotitis, occurring during the course of {627}
any of the diseases already named, produces no change in the general
symptoms; if, on the other hand, it occurs during convalescence, the
onset is marked by a moderate elevation of temperature and increase in
the frequency of the pulse, by thirst, loss of appetite, and sluggish
bowels. The tumor, which occupies the same position and thrusts
outward the ear-lobe as in mumps, is hard, dense, well defined, and
the seat of considerable pain until suppuration takes place, when the
latter subsides greatly. The skin over it is red, hot, and tense, and
there is much tenderness and little or no pitting on pressure. After
the abscess has formed there is well-defined fluctuation on palpation,
and at the position of pointing the skin becomes very thin and assumes
a bluish-red hue. Gangrene of the gland is manifested by the
cadaverous odor, blackening of the skin, the formation of a cavity,
and the discharge of ichor and shreds of tissue. The alteration in the
expression, the pain in the ear, the difficulty in moving the jaw and
in swallowing, are as constantly present here as in idiopathic mumps.
It must not be forgotten, though, that when the disease arises during
the course of any of the severe infectious diseases, the brain may be
so overcome that the subjective symptoms are frequently not complained
of.
The course is usually rapid, the abscess pointing on the fourth or
fifth day after the appearance of the parotid tumor; occasionally,
however, the inflammatory process is much slower, extending over a
period of several weeks. The course is also much protracted when
secondary abscesses form in other parts of the gland or in the
surrounding tissues, when the abscess is transformed into an ichorous
cavity, and when gangrene sets in. Ordinarily, where the pus is
evacuated by spontaneous rupture or by incision the abscess heals
quickly by granulation, leaving the gland enlarged and indurated for
some time.
THE PROGNOSIS depends upon the gravity of the original disease, the
period of the disease at which the complication occurs, and whether or
no mortification sets in. When the vital processes are greatly
impaired by the primary disease, the onset of the parotitis, trifling
in itself, may prove sufficient to determine a fatal result. The
danger of such a result is much increased, too, if the inflammation
begins in the earlier stages or during the height of the disease which
it complicates, while if it commences during convalescence by far the
most frequent result is recovery. Gangrene of the gland involves great
risk of life--a risk which increases in proportion to the early date
of its onset in the course of the original disease. Even when the
gangrenous process ends in recovery, the face is much distorted, the
hearing is lost in the ear, and the facial muscles are paralyzed on
the affected side. Bilateral symptomatic parotitis has naturally a
graver prognosis than the unilateral form.
DIAGNOSIS.--The disease is readily distinguished from idiopathic mumps
by the history, the less marked degree of the enlargement and
surrounding oedema, the greater degree of pain and tenderness, the
hardness of the tumor, the red discoloration of the skin covering it,
and the termination in suppuration. Further, it never displays an
epidemic tendency.
TREATMENT.--The general treatment of this form does not differ from
that of the disease it complicates, though the employment of
stimulants in increased quantities may be indicated.
{628} Before the first appearance of tumefaction of the parotid the
introduction of a probe or canula into the duct of Steno, associated
with pressure on the gland from the outside, may, by forcing from the
duct a collection of mucus or muco-pus, abort the inflammation. If
this is unsuccessful, a poultice should be applied over the gland to
encourage suppuration and pointing externally. As soon as the abscess
points the pus must be evacuated by an incision, and, as this has a
tendency to close again, a piece of lint must be kept between the lips
of the wound.
The enlargement and induration left after the healing of the abscess
require the application of tincture of iodine or of compound iodine
ointment to the surface.
When gangrene occurs it demands the same treatment, both local and
general, as when it is seated elsewhere.
{629}
ERYSIPELAS.
BY JAMES NEVINS HYDE, M.D.
DEFINITION.--Erysipelas is an acute disorder, characterized by the
systemic symptoms common to the febrile state, and by an involvement
of the integument and deeper parts, the affected surface being tumid,
hot, reddened, painful, and often the seat of well-defined bullae, the
process terminating either in complete resolution after cutaneous
desquamation or in a fatal result commonly due to complications of the
malady.
SYNONYMS.--_Eng._ St. Anthony's Fire; _Fr._ Erysipele; _Germ._
Rothlauf; _Ital._ Risipolo.
CLASSIFICATION.--Erysipelas is properly recognized as one of the acute
infectious diseases. Though by its symptoms and career it would seem
to be properly assigned to the category of the exanthemata, it is yet
by most authors set apart from the latter--first, because its career
is less specifically defined; second, because its contagiousness is
less demonstrable in every case; third, because one attack is not
known to confer upon its victims immunity against a second; fourth,
because the occasional prevalence of the disease in apparently
epidemic form is evidently due to extrinsic causes, and does not
depend exclusively upon its sudden appearance among the unprotected;
fifth, because no definite period of incubation precedes its earliest
manifestations; and, sixth, because at times it appears in local
manifestations apparently unaccompanied by systemic phenomena.
HISTORY.--The earliest writers on medicine bear witness to the fact
that the disease was recognized at the date when men first made record
of human ailments. It has occurred in all parts of the world and at
all seasons of the year, sparing neither age nor sex in its
development. Zuelzer[1] refers to epidemic occurrences of the
disorder, described by Rayer, as visiting the Paris hospitals in 1828;
by Schonlein, as existing in Zurich in 1836; by Gintrac, as spreading
in Bordeaux in 1844-45; and by Trousseau, as prevailing in the
Maternite in Paris in 1858.
[Footnote 1: _Cyclop, of the Prac. of Med., Ziemssen_, vol. iv. p.
424.]
ETIOLOGY.--Authors have in general assigned different causes to the
forms of erysipelas hitherto regarded as either idiopathic (or
medical) or traumatic (or surgical). The modern view, however, is that
which regards all cases as alike produced by the absorption of the
toxic agent capable of exciting this peculiar inflammation of the
skin. The peculiarly well-characterized symptoms of the disease--for
example, when it affects the head and face--were long regarded as
etiologically distinct from the affection which complicates surgical
injuries and wounds. But {630} a closer study of many of the cases
first named has again and again disclosed the fact that they
originated in such traumatism, for example, as the piercing of the
lobule of the ear for the insertion of an ear-ring, a carious tooth,
an alveolar abscess, or a pathological product in the antrum of
Highmore.
The disease is equally common--apart from the puerperal state--in both
sexes and at all ages, and occurs under favorable circumstances in all
seasons of the year. It is unquestionably at times spread by direct
contagion, either from the living or dead body affected with the
disease. Such contagion may occur mediately or immediately. It is,
however, not readily shown to be producible by the media of clothing
and other articles which have been in contact with a diseased surface.
The contents of the bullous lesions which appear upon the
erysipelatous surface are inoculable; and the disease has in this way
been transferred not only to men, but also, by Orth and others, to the
lower animals, and even from one of the latter to another of the same
species.
Certain it is, however, that the disease does occur, characterized by
symptoms indistinguishable from those to be recognized in the
contagious type of the malady, where the most careful investigation
wholly fails to reveal the cause, and where the disorder rapidly
spreads if the conditions for its extension are favorable. Under these
circumstances it is wisest at present to admit that the exact etiology
of erysipelas is unknown. Its relative frequency in the puerperal
state is unquestionably to be explained by the favorable local
conditions which at such times exist in the female for the development
of all septic disorders.
As regards the circumstances which might be supposed to specially
favor its development, these the capriciousness of the disease, which
is its striking characteristic, often quite disregards. Thus, on the
one hand, it may and often does prevail, year after year, in certain
hospitals, and even in certain wards of a single hospital, especially
where these are crowded with patients. But it may also repeatedly
spare masses of men affected with disease of a different type when the
latter are gathered together in prisons or camps, and indeed even may
appear among such individuals and fail to spread to others who are in
close proximity to them.
With respect to the propagation of erysipelas from infected to sound
individuals, a contrast is exhibited when the transmission of variola,
for example, is compared with it. Thus, it is well known that the
mildest cases of varioloid may be sources of malignant forms of
variola to the unprotected, while those who are partially protected
and exposed to the virus of confluent forms of the disease may exhibit
the mildest symptoms of varioloid. In erysipelas, however, it is
tolerably certain that there are different degrees of virulence to be
recognized in different cases, and that the disease at times is
transmitted in its different types. Thus, traumatic erysipelas is much
more closely related to childbed fever than the varieties of the
disease appearing upon the head and face, which cannot be attributed
to traumatism, surgical accidents, dental abscesses, or local injuries
of the antrum of Highmore. Parturient women frequently escape
infection when the erysipelatous disorder is of the so-called medical
type. Per contra, it is to be noted that women who are prone to the
relapsing and so-called chronic forms of erysipelas are {631}
particularly apt to suffer from that involvement of the genital
organs, peritoneum, spleen, and febrile movement whose sudden
occurrence after confinement is so portentous.
SYMPTOMATOLOGY.--The disease is usually announced by the occurrence of
a chill, which may precede by a day or but a few hours the appearance
of the cutaneous disorder. The rigor may be severe or mild in grade,
so that it may even be forgotten by the patient till his attention
reverts to it in connection with the resulting symptoms. There may be
simultaneously some gastric distress, rarely of severe character.
These symptoms are commonly followed by a febrile reaction. In other
cases the first recognized symptoms of the malady occur in the skin,
the patient scarcely recalling the fact of a slight preceding malaise.
The cutaneous lesions appear in the form of a circumscribed oedema and
redness of the surface, often preceded and usually accompanied by a
sensation of tension, heat, and burning pain. This macule, plaque, or
patch of diseased integument is in its typical features
characteristic. It is distinctly or irregularly circumscribed; its
oedematous condition elevates its level decidedly above that of the
adjacent integument, so that there is a somewhat sudden descent from
the former to the latter for a space of from one to two or more lines.
The redness is also of a bright crimson hue, and the reddened surface
has a sheen or glossy appearance uniformly displayed over its area. It
disappears under the pressure of the finger, leaving a yellowish-white
color in the region of impact, the erysipelatous blush rapidly
returning when the circulation at the surface is restored. This smooth
and shining condition of the reddened patch is so characteristic of
erysipelas that it arrests the attention of the diagnostician as soon
as he observes it. According to Zuelzer, it is caused simply by the
tension of the epidermis. When first observed it may occur in the form
of circular, small or large coin-sized patches, or in streaks, striae,
and radiations, or as very irregularly disposed, rosy, and shining
marblings or mottlings of an oedematous surface.
The skin thus affected is hot to the touch, tender, firm, and smooth.
It is occasionally the seat of pruritic sensations, more commonly of a
peculiar sensation of heat and burning.
In the course of two or three days the involved area spreads uniformly
or irregularly and centrifugally from the point first involved, after
which time, in mild cases, the disease persists without apparent
change for a few days more, prior to its decadence by resolution. This
final stage of the malady is characterized by a progressively
diminishing fever, moderate desquamation, gradual disappearance of the
oedema, and a color-change to the darker shades of bluish-red or to a
light brown. In this form of the disease the erysipelatous patch,
after being fully developed, does not tend to spread from the affected
to the unaffected surfaces; and, as a consequence, the affection may
complete its entire career in less than a fortnight.
In other cases, however, a remarkable tendency is developed to the
progressive spreading of the inflammation from one point or surface of
the body to another, the parts first affected paling as the disease
passes on to involve those in the vicinity, or being yet deeply
involved while the process of peripheral extension is in progress. In
yet other cases the red blush sweeps away from its first position in
tongue-like projections over a {632} tumid and painful skin, while the
region first invaded becomes paler, though still preserving its
oedematous features. In still another class of cases the advancing
ribbon or band of elevated and reddened integument passes over to a
new area, leaving the regions it has traversed tumid, painful, and
here and there streaked with rosy lines, patches, or irregular
gyrations.
In yet severer types of the malady the intensity of the inflammatory
process is such that the epidermis is raised from the tissues below by
the free exudation of the serum of the blood. In this way vesicles,
or, more commonly, bullae, develop upon the surface. Bullae thus
formed may be typically perfect, but are often exceedingly irregular
in contour, having an appearance which is suggestive of the blistering
of a surface by boiling water. The bullae may be well distended and
filled with a perfectly limpid serum. This fluid may, however, in the
course of a few days become purulent, the contents in such case drying
into crusts. In the severest types of the disease gangrene results
from the intensity of the dermatitis, and the loss of tissue which
thus occurs is repaired by the processes of granulation and
cicatrization.
The migration of erysipelas from one part to another of the surface is
sometimes so extensive as to invade from time to time the larger part
of the superficies of the body. Erysipelas of this ambulant character
may also, after invading the entire surface of the body, be relighted
at the point where it first appeared. In other cases this phenomenon
of recurrence or reawakening on patches of skin traversed by the
disease may be noticed only after moderate extension from a given
point. Reddish or rosy-colored islets then appear as new centres of a
fresh extension-process upon an integument whose swollen tissues still
exhibit the evidences of the prior invasion. In still other cases
similar islands of fresh disease are recognized in advance of the
elevated edge and tongue-like prolongations which mark the onward
progress of the erysipelatous inflammation over areas previously
unaffected.
The swelling of the involved tissues is one of the most characteristic
features of erysipelas. By this is meant not the tumefaction simply of
the superficial portions of the integument, nor the tumefaction which
may be measured by the height of the affected above the level of the
unaffected skin at the edge of the involved area, but a swelling much
more than this, involving the entire skin, and often indeed the
subcutaneous tissues, differing, of course, in the extent to which it
advances in different cases. In those of severe grade the swelling is
enormous, an affected limb assuming the elephantiasic aspect, while
the deformity thus induced in the head is fully as great as that seen
in the height of confluent variola. In such cases the neighboring
ganglia are, as a rule, enlarged and often painful.
It is indeed this swelling which gives to erysipelas of the head and
face its peculiar physiognomy. The disorder is apt to find its
starting-point in the ear, the side or point of the nose, or one
cheek. At this moment it may be possible to recognize the fact that
the adjacent mucous membrane is also involved. Thence the disease
progresses over the face, and possibly over the scalp also, the
resulting tumefaction being occasionally, as already stated, enormous.
Thus the eyes are usually closed and sealed by the swollen lids and
the orbital depressions are effaced. The lips, enormously pouting and
reddened, project from the swollen visage to as {633} great an extent
as the tumid ears, which, for similar reasons, depart from the usual
plane. The mouth, nares, and eyes alike are covered with mucous
secretions, possibly commingled with the contents of bullae which have
formed and broken. Crusts may thus collect near the mucous outlets.
The tongue is dry, parched, and cracked, and exhibits a reddish-brown
hue. In less severe cases it may be seen to be covered uniformly with
a thick yellowish or yellowish-white paste. The fauces and buccal
membrane are reddish in color, glazed, and dry.
The patient having this serious form of the malady is indeed in a
critical condition. There is usually a coincident coma or delirium.
The pulse is either greatly accelerated and full, or thready,
fluttering, and destitute of rhythm. The temperature rises to 105
degrees F., and even higher. In this condition a fatal issue may be
heralded by collapse, with decadence of the external evidences of the
disease, or by the occurrence of blood-filled blebs, or indeed by
larger or smaller areas of the surface falling into gangrene. This
latter accident may also involve the mucous surfaces, large patches of
the buccal membrane, the gums, and even the palate, losing their
vitality and showing as greenish-black, insensitive tracts, quite
firmly attached to the healthy tissue. These accidents may be of very
rapid occurrence, more particularly in the case of individuals prone
to exhibit the severest forms of the malady, such as very young
infants and those enfeebled by advanced age, by alcoholism, or by any
of the cachexiae.
Other types of erysipelas, chiefly noticeable by reason of their
location, are those spreading from the umbilicus, the genital region,
the sites of vaccination, of varices of the lower extremities, and the
surfaces near the seat of surgical accidents and operations.
The various names which have been, especially by older writers, given
to the several expressions of this disorder relate almost exclusively
to their external characteristics. Among these may be mentioned--E.
ambulans, e. erythematosum, e. bullosum, e. glabrum, e. levigatum, e.
miliare, e. oedematosum, e. pemphigoides, e. phlyctenulosum, e.
puerperale, e. vaccinale, e. variegatum, e. verrucosum, and e.
vesiculosum.
The resolution of erysipelas in favorably terminating cases is
accomplished by very gradual amelioration of symptoms. The swelling
begins to subside, usually between the third and sixth days. The blebs
that have formed then disappear by absorption, bursting, desiccation,
or crusting, and subsequent exfoliation. Desquamation of the involved
surface may be a prominent or a very insignificant feature. When the
patient with erysipelas capitis enjoys a favorable crisis in his
disease, there is occasionally noted a very rapid amelioration of the
symptoms. The tumefaction speedily subsides, the features become
recognizable, and defervescence is complete. Throughout the course of
all attacks the febrile process and the erysipelatous blush proceed
pari passu with but little deviation of the severity of the one from
the intensity of the other.
The complications and sequelae of the disease are less numerous than
they are grave. In erysipelas of the head there is usually a rapid
shedding of the hair, though in convalescence the growth of the hair
may be restored. An obstinate seborrhoea sicca may, as after variola,
linger long afterward upon the scalp; here also, as in other {634}
portions of the body, one or many abscesses may form in the
subcutaneous tissue after the resolution of the dermatitis; while in
phlegmonous erysipelas these abscesses may accompany the disease at
its height.
Lymphangitis and adenopathy are common complications of erysipelas,
the former betrayed in thickened and often knotted cords, which may be
felt radiating from involved areas to neighboring glands. A singular
modification is often undergone by the integument affected with
erysipelas which has also been the seat of other cutaneous disorders.
In this way lupus, psoriasis, chronic eczema, and some of the
syphilodermata have been relieved.
Besides the surfaces of the nasal, pharyngeal, and buccal mucous
membranes which have been indicated as at times involved by the
disease, the inflammatory redness and swelling may extend to the
epiglottis, the larynx, and the trachea. Croupous and other forms of
pneumonia, pulmonary oedema, and pleuritis have been not rarely noted.
In erysipelas of the head the membranes of the brain may inflame and
serous effusions distend the ventricles.
The joints may be inflamed either by sympathy or by direct extension
of the erysipelatous inflammation to the periarticular tissues, or yet
by the occurrence, in or about them, of metastatic abscesses in
septicaemic conditions.
The peritoneum may be also acutely or subacutely inflamed in
erysipelas, though it is doubtful whether the accident occurs in
consequence of the extension of the disease to this membrane from the
skin of the abdominal wall. The same may be said of the endocarditis
and pericarditis noted by several authors. Of all other complications,
it may be said that they can usually be assigned to the occurrence of
either septicaemia, or pyaemia, or to the development of metastatic
abscesses.
With respect to the eyes, a distinction should be drawn between those
attacks originating in deep or superficial affections of the globes
and those in which the visual organs are merely involved as by
accident in the extension of the disease. In the former case deep
orbital abscesses or inflammatory affections of the iris and retina
may be followed by erysipelas of the lids or neighboring parts, while
in the latter event the issue is more commonly a transitory
conjunctivitis, lachrymation, and photophobia, which soon disappear
when the disease has declined. The cornea, being unmacerated with pus
as in severe variola, commonly escapes perforation.
Erysipelas is a disorder which, without question, produces in a
certain proportion of patients a susceptibility to recurrent attacks.
This susceptibility, however, is less a systemic tendency to the
development of the disease than a peculiar liability to recrudescence
originated by chronic local ailments. Thus catarrhal, ulcerative, and
other affections of the nasal mucous membrane are particularly apt to
originate repeated erysipelatous attacks in the integument covering
the nose, and the same is true of the skin in the vicinity of the
orifices of fistulous sinuses and varicose veins.
The forms of disease which are often described as instances of chronic
erysipelas belong to several classes. There are, first, those in which
are observed recurrent attacks of true erysipelas. Second, those in
which a chronic eczema or dermatitis produces a circumscribed patch of
infiltration {635} in a skin having a lurid reddish hue, which is also
the seat of marked subjective sensations, chiefly itching. The
well-known forms of chronic eczema erythematosum of the face in middle
years or advanced life are commonly, and erroneously, regarded as
erysipelatous in character. Third, there is a peculiar dermatitis, of
the cheeks chiefly, with regard to whose identity as an erysipelatous
affection there is much doubt. The skin is infiltrated in a
circumscribed patch, and has a peculiarly glossy red hue. It is
essentially a chronic disorder, the affected patch remaining unchanged
for months at a time, and then exhibiting aggravation in consequence
of accidental exposure to heat or traumatism. These patches may be
relics of relapsing forms of erysipelas; and in my experience are more
commonly encountered in the subjects of chronic alcoholism.
PATHOLOGY AND MORBID ANATOMY.--The pathological changes exhibited in
the erysipelatous skin are those of an exudative process involving the
cutaneous and subcutaneous tissues. Nothing specially different from
the phenomena observed in a simple dermatitis can be recognized by the
microscope alone. Biesiadecki's careful investigations[2] certainly do
not disclose any such specificity. The epithelia are swollen with
serous fluid, and the exudate, though largely serous, contains also
the corpuscles recognized in plastic lymph. It is this serum, rapidly
invited to the surface by the acuity of the exudative process, which
raises the epidermis into the bullae described above. The nuclei of
the bodies recognized in the exudate are evidently in a state of
division and consequent multiplication. The epithelia of the rete
mucosum are swollen and stretched. The connective-tissue elements in
the derma are also swollen, and exhibit reversion to the embryonal
state. There is within each a relative increase of protoplasm, as a
consequence of which they undergo a species of liquefaction. The
blood- and lymph-vessels enlarge and are crowded with corpuscles. The
subcutaneous tissue participates in this process, its elements being
filled with finely granular cells disseminated or in aggregated
masses. The chief peculiarity of this exudation, and of these changes
in the tissue-elements where it recurs, is the rapidity with which,
when involution is in progress, the fluid is absorbed and the
inflammatory elements disappear. When abscess or gangrene complicates
the erysipelatous inflammation the changes are not different from
those recognized in dermatitis calorica.
[Footnote 2: _Sitzungsber. d. k. Acad. der Wissen._, Wien, ii., 1867.]
The changes noted in the viscera are also of a congestive and
inflammatory type. According to Ponfick,[3] there is at times a
parenchymatous degeneration of the muscular tissues of the large
vessels, and of the extremities, as well as of the kidneys, liver, and
spleen, the latter organ occasionally undergoing softening. The mucous
surfaces of the mouth, larynx, lungs, and alimentary canal have also
been found affected with oedema, congestion, and infiltration, rarely
terminating in ulcerative changes.
[Footnote 3: _Deutsch. klin._, No. 20, 1868.]
DIAGNOSIS.--The diagnosis of a typical case of erysipelas is so simple
that the nature of the malady is often recognized by those unskilled
in such matters. It is difficult to mistake for any other affection
the circumscribed, swollen, shining, and rosy-reddish patch of skin,
accompanied by fever or marked malaise, with adenopathy of near
glands, and often with a history of traumatism to which the origin of
the disorder may be readily referred.
{636} It is to be distinguished from dermatitis in its various forms
(venenata, medicamentosa, phlegmonosa, suppurativa) by its
characteristic features, and by the frequent absence in these
inflammations of a febrile reaction and of a shining, rosy-red hue of
the skin, and by the peculiarities described above of the elevated
margin of the erysipelatous area.
Eczema, especially in its chronic erythematous forms, exhibited in the
face of adults in middle and later life, is of much slower
development, is productive of itching, is ill-defined in contour, and
is not accompanied by fever.
Erythema in all its varieties is a purely hyperaemic affection and
unaccompanied by fever. In erythema multiforme there is an exudative
process by reason of which various papules, nodosities, and at times
even bullae, appear upon the surface. None of them, however, are
accompanied by a diffused area of redness spreading at the periphery.
All of its lesions are circumscribed, and rarely affect the face.
Pemphigus could only be mistaken for the form of erysipelas bullae,
but its lesions do not rise from a broadly inflamed area; they rather
have attended with each a distinct individual halo when the integument
from which they spring is at all congested. They are also rarely
accompanied by a febrile process.
Scarlatina, though a febrile affection, is readily distinguished from
erysipelas by the appearance of its exanthem, symmetrically and
generally developed over the entire surface of the body, or
progressively and symmetrically from the upper to the lower segment of
it. The exanthem has also a dull scarlet color or the boiled lobster
hue, differing thus from the rosy-red and shining patch of erysipelas.
Urticaria also is often of symmetrical development, is rarely
accompanied by fever, and is characterized by typical wheals, which,
however closely packed together, never have the smoothness of the
surface affected with erysipelas.
PROGNOSIS.--The prognosis of a simple case of uncomplicated erysipelas
occurring in an individual in fair health and possessed of a
reasonable degree of vigor may be regarded as favorable. Even in the
weakness of infancy a large area may be involved in the disease and a
high degree of fever be aroused without alarming results.
Erysipelas should, however, always be regarded as a serious disease or
a serious complication of any existing malady. It is often a grave
feature in surgical injuries. Erysipelas involving the entire surface
of the face and head is always a formidable affection. In the
puerperal state it is dreaded by every accoucheur.
All these circumstances are rendered more portentous by the existence
of the disorder as a complication of any other grave malady, or by its
occurrence among the subjects of alcoholism, struma, phthisis, or
various other cachexias, and among the aged. Occurring in epidemic
form among the inmates of prisons, camps, and hospitals, the mortality
of the disease may be increased tenfold.
TREATMENT.--The prophylaxis of erysipelas is that of all contagious
diseases. It involves isolation of the affected individual,
disinfection of body- and bed-clothing before the latter are again
employed upon the persons of others, and destruction by fire of all
dressings which have been in contact with the integument.
{637} The hygienic management of the patient is not to be neglected.
The complete ventilation of the sick chamber is to be secured, and its
temperature uniformly sustained at a point between 65 degrees and 70
degrees F.
The general treatment of the sufferer need not greatly differ from
that commonly pursued in the febrile state by modern therapeutists.
There is but little confidence to-day in the methods by venesection
and purgation, upon which at one time reliance was placed. Cool or
cold water may be freely employed when there is hyperpyrexia, either
by general bathing or by wrapping the patient in sheets dipped in and
wrung out of the same fluid. The results are favorable as regards the
bodily temperature, and are not productive of danger, though water
thus applied has no effect upon the local disorder of the skin. Iced
or cool water, by the ice-bag or compresses, is specially indicated as
a topical application for the head when there is delirium or other
indication of disturbance of the cephalic centres, irrespective of the
invasion of the scalp and face by the erysipelatous inflammation. The
sulphate of quinia in full doses is indicated especially when there is
any tendency to remittence in the febrile accessions, but is not known
to possess any power to cut short the disease. In many cases of
erysipelas the febrile condition is readily managed by the
administration of the simpler remedies found grateful to the palate of
the sufferer, such as iced, acidulated, and effervescing draughts,
with perhaps the employment of the spiritus Mindereri or the spirit of
nitrous ether. In other cases the mineral acids can be substituted
with advantage for the latter. With many American physicians it is
customary to add to these remedies the tincture of the root of
aconite, with a view to its effect upon the pulse.
Few internal remedies, however, have in this country enjoyed as much
popularity with the profession in the treatment of erysipelas as the
muriated tincture of iron in full doses. Its use, first suggested for
this purpose by Bell in 1851, has here steadily gained in favor since
its general adoption. It is well to give it in doses of not less than
20 or 30 drops, repeated every two or three hours, diluted with water.
When there is high fever, and especially if the secretion of urine is
scanty, the following formula will be found valuable:
Rx. Tr. Ferri Chloridi;
Sp. Aetheris Nitrosi;
Glycerinae _aa._ fl. drachm i. M.
S. A teaspoonful in water every three hours.
This preparation of iron certainly seems, in many cases, to shorten
the disease, but, per contra, it is to be remembered--first, that in
many other cases it has been found to exercise no control whatever
over the severest manifestations of the disease; second, that in other
countries, especially in Germany, where it is rarely employed, the
mortality from the disease is no greater than elsewhere.
The widest difference in practice has obtained relative to the local
treatment of the affection. They who have had the fortitude to content
themselves with watching the evolution of the specific dermatitis,
merely protecting the skin by dusting over it a simple powder or
leaving it covered with a cold compress, have certainly no worse
results to tabulate than those who entertain a belief in the efficacy
of the abortive treatment of the local disorder.
{638} No remedies, locally applied, can be recognized as certainly
possessing the power to cut short the inflammation. Those which enjoy
the highest reputation for topical employment are saturated solutions,
hot and cold, of the hyposulphite of sodium, of boracic acid, and of
the bicarbonate of sodium; salicylic acid; iodoform in powder; and,
quite lately, resorcin. Hot fomentations of the erysipelatous patch
are in general most grateful to the patient, and with these an opiate
and astringent effect can be obtained, as by a hot lead and opium wash
or by solutions of the sulphate of iron or of alum and tannin. Useful
methods of applying these are by the medium of borated cotton, oakum,
tow, or spongiopiline, covered with oiled silk or the Lister
protective material.
Other medicaments which have enjoyed favor in the topical treatment of
the disease are lime-water and linseed oil (carron oil), sulphur in
powder, carbolic acid, camphor, the oil of turpentine, collodium,
cataplasms and ointments containing mercury, lead, zinc, tar, and
tannin.
Respecting the measures adopted with a view to checking the extension
of the disease at the periphery of the patch, the belief in such a
possibility has been wellnigh abandoned. For this purpose the nitrate
of silver, caustic potash, tincture of iodine, and similar substances
have been boldly and broadly applied, alike over the sound and
affected integument, with the production of an artificial dermatitis
intended to supplant that which was previously in progress. Again and
again has the local inflammation transgressed these artificial limits;
and when they have been by it apparently respected there has been
little ground for believing that the result was due to the treatment
pursued. Inasmuch as the disease is often self-limited and distinctly
limited in its progression over the surface, it is manifestly
difficult to determine that its limitation in any given case is the
result of topical agencies. These agencies have, moreover, the marked
disadvantage of adding their irritative effects to those incidental to
the dermatitis.
The surgical treatment of erysipelas invading special regions of the
body or the deeper tissues is a matter of importance. Free incisions
are requisite for the liberation of pus, and all abscess cavities
should be treated antiseptically and stuffed with iodoform or
resorcin. Great tension of the lids demands free incisions in the long
diameter of either, and the same surgical procedures are often
demanded in erysipelas of the scrotum or of the labia in the female.
Gangrene and sloughing are to be treated in accordance with the
principles recognized as important in the management of these
accidents in general.
The mouth when involved may be benefited by gargles containing the
chlorate of potassium, alum, tannin, the compound tincture of
cinchona, or by the use of the spray with a saturated solution of
boracic acid in rosewater. Kaposi lays stress, in all cases of
erysipelas of the face, upon the importance of searching for and
evacuating all dental abscesses and pustules seated upon the
Schneiderian membrane. Crusts in the nasal cavity are to be soaked
with vaseline and removed by washing, their re-formation being
prevented by the insertion of small tampons smeared with a bland
ointment or oily fluid. Abscesses in other portions of the body, not
suspected as being etiologically significant, are to be carefully
searched for and emptied, whether occurring about the anus, the
genitals, or the legs.
{639} Subcutaneous injections of carbolic acid and other antiseptic
solutions have not been rewarded by such results as to establish in
any degree their special efficacy.
In all ordinary cases the expectant treatment recommended by Zuelzer
is abundantly to be commended. The inflamed tissue is to be dusted
with finely-powdered starch, and protected by a layer of soft
cotton-wool which exercises a moderate degree of pressure upon it.
Antiseptically, the highest ends are thus reached.
The diet of the patient should consist of animal broths, soups, milk,
and eggs, with a view to the reparation of the waste incidental to the
febrile process. Stimulants are to be freely used in all asthenic
conditions. In convalescence the warm water and soap bath is to be
employed, followed by dusting of the surface with starch powder or by
inunction with vaseline.
{640}
YELLOW FEVER.
BY S. M. BEMISS, M.D.
Yellow fever is a specific, infectious, and communicable disease of
one febrile paroxysm.
This definition includes some of the most prominent characteristics of
the disease. The malady, however, derives its name from a symptom not
mentioned in the definition. The yellow color of the skin and
scleroticae which appears in advanced stages of grave cases of yellow
fever, and which becomes especially marked in the cadaver, has ruled
its nomenclature. Whatever objections may be urged against the term
"yellow fever" as being founded upon a symptom of the disease not
always present, it is too strongly fixed in both medical literature
and popular usage to justify efforts to change it.
Neither is it liable to beget confusion as long as it is understood
that it is to be restricted in its application to a specific fever
induced by a specific poison, and that as an incident of its morbid
process it produces yellow coloration of the surface so frequently as
to suggest the prefix yellow to its title.
ETIOLOGY AND SYMPTOMATOLOGY.--In this day of almost general belief in
the theory which holds that each specific disease has its own specific
poison or morbific germ, it is scarcely expedient to occupy much space
in discussing the propriety of classing yellow fever among the
specific maladies.
Whether we rest the decision of this question upon the uniformity of
those circumstances and conditions which originate and develop
epidemics of yellow fever, or upon the sameness of its symptomatic
phenomena wherever observed, we find very nearly as substantial claims
to a specific individualization of the disease as any one of the
eruptive fevers possesses. Not only are its morbid phenomena so
characteristic that even non-professional observers designate it by
such epithets as Bronze John, Yellow Jack, Vomito Prieto, etc., but it
is inconvertible with other specific affections. This inconvertibility
of yellow fever with other diseases is absolute, and affords
irrefrangible evidence of the specificity of that germ or poisonous
principle which produces it.
The study of yellow-fever poison after the objective method has
hitherto been unproductive of definite results. When such experienced
and truthful observers as Sternberg, Woodward, and Schmidt, working
with the most approved microscopes, have failed to identify any
organism or object peculiar to the products from the bodies of
yellow-fever subjects or to the circumfusa of the sick, this
declaration is sufficiently supported.
{641} But when we turn to a subjective method of investigating that
toxic agent which causes yellow fever, it is found to possess
sufficiently well-marked characteristics to justify practically
valuable conclusions. Some of these characteristics or modes of
behavior merit notice.
1st. The human system is a field of reproduction and multiplication of
yellow-fever poison. This is sufficiently established by two facts:
(_a_) A person in the incubative stage of yellow-fever intoxication
may be divested of all fomites and yet originate other cases after a
developed attack.
(_b_) The infection is intensified by aggregation of the sick.
These propositions are indisputably true.
2d. The poison or infection undergoes some change after leaving the
human system. This appears to be susceptible of proof, because
communication of the disease from person to person is not a common
event. When this does apparently occur, there is often very strong
reason for a belief that the contagion was resident in some fomites
connected with the patient's bed or clothing.
3d. There are no sustained observations which prove that yellow-fever
poison is ever created de novo.
The autochthonous birthplace of the poison is unknown. The suggestion
of Niebuhr, that yellow fever may have been one of the causes of death
during the plagues of Athens, can not be authoritatively denied. It
may have been called into existence at the moment when all things else
were created which were to perpetuate each its kind.
4th. Some of those conditions and circumstances which favor or retard
the development or maturation of yellow-fever poison outside the human
body are quite well understood. Warm, damp weather is most prominent
among those climatic conditions which are favorable to the growth of
yellow-fever epidemics.
5th. A freezing temperature ordinarily destroys the contagium of
yellow fever. A high degree of artificial heat produces a similar
result. It is highly probable that certain chemical agents would also
effect its destruction if brought in contact with it.
6th. If yellow-fever fomites are hermetically enclosed in situations
protected from cold or other agents which are destructive to their
infection, its vitality may be preserved for an undetermined length of
time, and its toxic qualities again made manifest when unacclimated
persons are exposed to it.
7th. Yellow-fever poison possesses ponderability. This characteristic
is so distinctly marked that it has been frequently termed a
"low-lying poison."
8th. It is incapable of being air-borne through any great distance, at
least without being deprived of its toxic effects.
9th. It is transportable in fomites through great distances, either on
sea or land, and as often as its toxic effects are manifested after
these portations they are so uniform as to be promptly recognizable.
A great number of different materials in common use may act as
fomites, such as loose wool, cotton, or hair, or textile fabrics of
various descriptions.
The following facts, which illustrate how yellow-fever infection may
be conveyed in the most unsuspecting and innocent manner, are well
{642} authenticated. There can be no ground for accusation of error
except in the hypothesis that the infection was encountered
simultaneously in some unexplained manner. The facts are furnished by
Dr. Shannon of Ocean Springs, Mississippi: "On the 14th of October,
1883, Maj. J. B. B. died of yellow fever in Ocean Springs, Miss. I
moved the family at once to the healthy locality where you saw Miss
B., not allowing them to take any article from the room where the
husband and father had died. The children applied to me for a lock of
their father's hair, which I refused, but the oldest daughter, now
dead, prevailed upon the nurse to give it her. She placed it in an old
envelope that had been torn open at the end and carefully folded the
torn end down, thus practically sealing it, and laid it away among
other old letters. On Sunday, the 4th of November, at 12.30 P.M., she
brought this envelope out upon the open gallery, and opened it for the
first time to examine the lock of hair and show it to her aunt, Miss
S., who was visiting her, and upon inhaling the concentrated poison
confined in the envelope and emanating from the hair, exclaimed, 'Oh,
what a peculiar smell!' She then handed the envelope to her aunt, Miss
S., who, unconscious of danger, also inhaled the 'messenger of death'
with a similar exclamation, when Mrs. B., who was standing near,
reached out her hand for the envelope, but was prevented from getting
it by the entreaties of a fretful child to be taken up in her arms.
This gave time for sufficient reflection, and she admonished the young
ladies of the possible danger. The envelope was then carefully folded,
and with its fatal contents replaced in the drawer where it had been
since the 14th of October. This drawer had been almost daily opened.
On the following Saturday night, Nov. 10th, at 9 P.M., Miss S. was
taken sick with a chill, and Miss B. at about 2 A.M., some five hours
later, the period of incubation being less than seven days in both
cases. No other person handled the fatal envelope or in any way came
in contact with it, and there is, after the most careful inquiry, no
suspicion of any other source of infection in these two cases. Miss S.
died on Oct. 14th, Miss B. on Oct. 16th."
10th. These qualities of yellow-fever infection, and especially its
faculty of reproduction (which only organisms possess), furnish almost
conclusive evidence that yellow fever is a germ disease produced by a
specific contagium vivum.
Many facts are patent which sustain the generally accepted opinion
that yellow-fever poison gains admission to the system through the
medium of atmospheric air. On the other hand, I know of no
observations which prove that the disease is ever communicated by food
or drinks, or through any other vehicle than atmospheric air.
In respect to atmospheric infection by yellow fever, localizations of
aerial impregnation are often observable, not common in other
air-infecting diseases. A certain district of a large and populous
city may become the seat of a sweeping and fatal epidemic, and yet no
case occur outside of this area of prevalence. It is customary to
speak of these points of epidemic prevalence as infected localities.
If unprotected persons visit such infected places, even for a short
period of time, they are liable to attacks of yellow fever, although
they may take neither food nor drink within the limits of infection
and bring no fomites away with them. Under these circumstances
atmospheric impregnation is conclusive.
{643} But it is difficult to determine how this infection of a
locality has been produced in the first place, and how, in the second
place, it is maintained sometimes for periods of from one to three
months, with so little apparent diminution or change in the liability
to communicate yellow fever to unprotected visitors within the limits
of infection.
It seems highly probable that yellow-fever poison, after its exit from
the human body, attaches itself to various solid surfaces in proximity
to the sick, where, under suitable climatic conditions, it undergoes
more or less speedy processes of maturation in toxic qualities. The
poison thus matured is capable of being preserved with but little
change for the periods indicated above, and is communicable through
the atmosphere for short distances. It is also capable, by virtue of
some unexplained process or quality, of spontaneously extending its
area of infection. But this is at all times slow, and is readily
interrupted by streams of water, high walls, or even by much-travelled
thoroughfares.
There are no instances in which the water-supply of cities has been
shown to have distributed yellow fever.
The periods of time which may intervene between exposure to
yellow-fever poison and attacks of the disease are extremely variable.
The shortest period of incubation which has come under my observation
was about twenty hours. In three cases in which I was able to fix the
hours of first exposure with precision attacks followed in 72 hours,
83 hours, and 101 hours, respectively. Of 55 unacclimated physicians
who exposed themselves at Memphis during the epidemic of 1878, 54
suffered attacks of yellow fever. In these cases the periods of
incubation varied from one to twenty-five days, the average duration
being ten days. These physicians all remained steadfastly at their
posts of duty; consequently, the attack which occurred on the
twenty-fifth day was postponed for that length of time during constant
exposure in a locality most intensely infected.
It must be true that many cases of individual resistance to the
effects of yellow-fever infection depend upon states of the system or
idiosyncrasies which diminish liability to the action of the poison.
In other words, their personal receptivity to it is lessened by
certain constitutional states.
That this position is correctly taken is proved by the fact that many
circumstances which violently disturb the system determine attacks in
persons who may have for a long time enjoyed immunity from them.
Anxiety, grief, fright, fatigue, or exposure to sudden wettings or
cold may precipitate attacks, either by disturbing vital processes by
which the system is ridding itself of the poison--so far, at least, as
to prevent an accumulation great enough to occasion attacks--or by
lowering powers of resistance through enfeeblement of nerve-force.
But it can be affirmed in regard to yellow-fever poison that it is not
more capricious or eccentric in its behavior as an infection than that
of scarlet fever. Each of these diseases may appear in a large family
of unprotected persons with a degree of violence which results in
death in every instance, and suddenly cease, leaving a greater or less
number of the household without attacks, though equally exposed with
those who have died.
One attack of yellow fever confers immunity from the disease during
after life. A person who has suffered an attack is said to be
acclimated {644} or protected. Neither of these terms should be
applied to those who have not suffered attacks, however long they may
have withstood exposure during epidemics. It often occurs that persons
who have escaped attacks through many years of renewed exposure at
last succumb to the disease. On the other hand, I know of three
well-authenticated instances of immunity in a sweeping epidemic of
persons whose mothers had suffered attacks during the gestations which
respectively resulted in their births.
While negroes are susceptible to yellow-fever infection, attacks are
far less fatal than among whites.
SYMPTOMS IN MILD OR SIMPLE CASES.--Yellow fever is usually sudden in
its onset. Persons are liable to be seized while pursuing their
ordinary avocations, or, as often occurs, the attack may begin during
the night. The initial symptoms are chilliness or cold sensations,
seldom amounting to a decided rigor. Reaction is usually prompt and
decided, the temperature reaching within a few hours 102 degrees to
105 degrees F. Yellow fever is not a disease in which it is very
common to observe excessive body heat.
As the fever is established, the countenance becomes flushed and the
eyes injected and glistening. Frontal headache and lumbar pain are
experienced very early in the attack, and are liable to become more
intense during the progress of the fever. Muscular neuralgias,
especially in the lower extremities, are not uncommon.
During the early period of the attack the tongue is indifferent as a
symptom. It is generally moist and free from any coating. In cases
attended by much furring of the tongue careful investigation is pretty
sure to disclose the fact that it has been brought about by some
pre-existing state of disease.
The bowels are generally inactive, though naturally impressible to
cathartic drugs. The stomach is querulous from the inception of the
attack to its conclusion. Vomiting may not occur spontaneously, but it
is easily provoked by repletion of the stomach with any description of
ingesta or by harsh or disgusting medicines. The acts of emesis are
sudden and short in duration. Bile is a very uncommon constituent of
the matters ejected. Whether vomiting has occurred or not, patients
nearly always express repugnance to the weight of the physician's hand
over the epigastrium. In the very mildest cases it seems to excite
gastric distress and a tendency to emesis. The stomach and bowels are
liable to distension by flatus, sometimes to the extent of producing
colicky pains. Gaseous eructations are common.
During and shortly succeeding the cold stage the urine may be somewhat
increased in amount, but after the fever is established both the
quantity and the specific gravity are notably lessened. Albumen seldom
appears in the urine during the first twenty-four hours of an attack.
In very mild cases it is altogether absent throughout.
Delirium is not unusual during the fever. Among children attacks are
often ushered in by convulsions. In such cases delirium may be
persistent and alarming in violence.
The pulse in the early stage of yellow fever is slower in proportion
to the temperature than in most other acute diseases. This is more
especially true in respect to mild cases. Another characteristic
feature of the pulse in {645} yellow fever is that it declines in
frequency before the fever has reached its maximum. In the mildest
forms of the disease the temperature will attain its highest record
within twelve hours. It then rapidly defervesces, never to return
again. But in some cases of a moderately mild form the body heat does
not reach its acme of intensity until the second day, occasionally not
until the third or fourth day. In these cases also the pulse is apt to
decline in frequency before the fever has culminated. There are
therefore no fixed laws which govern the duration of the hot stage of
yellow fever. Those which relate to the pulse are more uniform.
The following clinical reports of two cases support this statement.
The detailed account of the symptoms establishing their diagnosis as
mild cases of yellow fever is omitted.
Susie W----, white, aged seventeen years, was admitted to Charity
Hospital on August 28, 1878. First observation, nine hours after the
beginning of the attack, pulse 100, temperature 104.6 degrees. Morning
of 29th, pulse 94, temperature 102.8 degrees; evening, pulse 80,
temperature 101.5 degrees. Sanguineous discharge from vagina began on
29th; patient supposed it to be her proper period. Aug. 30th, pulse
80, temperature 99.2 degrees; convalescent and dismissed from further
observations. In this case the urine presented a trace of albumen
early on the second day, but as the menses appeared shortly after the
urine was obtained, the presence of albumen may be in that manner
accounted for.
Bessie L----, white, age twenty-seven years, admitted to Charity
Hospital on August 28, 1878. First observation, twelve hours after
beginning of attack, pulse 100, temperature 100.6 degrees. 29th, pulse
76, temperature 102.3 degrees. 30th, pulse 64, temperature 101.5
degrees. Sanguineous discharge from vagina began on 30th and continued
until Sept. 4th; this was two weeks before the patient's regular
period. The urine showed traces of albumen at date of admission.
Discharged, cured, Aug. 31st.
It may also be stated of the pulse of yellow fever that it is easily
compressible and often gaseous in character.
Perspiration is probably an incident in the natural clinical history
of a case of yellow fever. It occurs spontaneously if the patient's
surface is protected from those influences which conflict with its
appearance. It is not critical in any sense of the word, and may
coexist with high temperature.
Yellow fever is considered to have two clinical stages. The first is
the paroxysm. This is made to include the cold stage and succeeding
fever. The cold stage is often almost or quite inappreciable, and when
this is not the fact it is in simple cases a very unimportant event.
It is therefore quite convenient to include it with the fever under
the term paroxysm. The paroxysm of a simple case is terminated by a
subsidence of the fever to nearly or quite a normal temperature.
Sometimes the temperature falls below the normal standard.
The neuralgias and subjective sufferings are greatly mitigated or
cease altogether. Thirst and restlessness are relieved, and the
patient sees before him a delicious, but too often treacherous, mirage
of restoration to perfect health. This is termed the stage of calm,
perhaps because it often precedes a tempest of fatal symptoms.
In mild cases convalescence begins at the termination of the paroxysm,
and may proceed without interruption until complete re-establishment
of {646} health has been accomplished. But in the very mildest cases
the process of recovery is easily interrupted.
In these simple forms the tendency to hemorrhage first manifests
itself in the calm stage. The gums become red, tumid, and spongy, the
tongue pointed and red at the tip. Epistaxis is liable to occur. The
eyes and skin may be slightly yellow, and the urine may show traces of
albumen. However mild the other symptoms may appear, the tendency to
hemorrhage, to albuminous urine, and to jaundice in the calm stage
bears a direct relation in frequency of occurrence and in degree to
the blood-stasis, or sluggish capillary circulation, of the first
stage.
The foregoing is a recital of the clinical phenomena of typical and
simple forms of yellow fever. The departures from type have been
divided by different writers into a variety of forms. The most
important of these will be referred to in connection with suggestions
as to treatment.
PROGNOSIS.--Prognosis is variable in different epidemics, this
observation being understood to apply to the same localities. Some of
those circumstances which affect epidemic force, so as to increase the
mortality-rate, are appreciable. If an epidemic invades a population
after an interval of exemption sufficiently long to allow a large
number of unprotected persons to have accumulated in its midst, the
crowding of the sick will increase the death-rate. We may naturally
assume that this is attributable, first, to sheer multiplication of
the infection; second, to lack of proper attention to the sick, and to
fright, grief, exhaustion, etc.
_Tabulated Abstract of Practice in Yellow-Fever Epidemic of 1878, New
Orleans Charity Hospital._
---------+---------+-----------+-----------+---------+-----------+-----
AGES. | July. | August. | September.| October.| Total. |
---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------
| N | N | N | N | N | N | N | N | N | N | P
| o | o | o | o | o | o | o | o | o | o | e
| . | . | . | . | . | . | . | . | . | . | r
| | | | | | | | | | |
| t | f | t | f | t | f | t | f | t | f | c
| r | a | r | a | r | a | r | a | r | a | e
| e | t | e | t | e | t | e | t | e | t | n
| a | a | a | a | a | a | a | a | a | a | t
| t | l | t | l | t | l | t | l | t | l | .
| e | . | e | . | e | . | e | . | e | . |
White. | d | | d | | d | | d | | d | |
| . | | . | | . | | . | | . | |
---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------
Under 5 | .. | .. | 7 | 3 | 3 | 1 | .. | .. | 10 | 4 | 40.0
5 to 10 | .. | .. | 2 | 1 | 1 | 1 | .. | .. | 3 | 2 | 66.66
10 to 20 | 8 | 3 | 26 | 7 | 25 | 6 | 7 | .. | 66 | 16 | 24.2
20 to 40 | 18 | 9 | 246 | 141 | 175 | 91 | 61 | 24 | 500 | 265 | 53.0
40 to 60 | 9 | 6 | 75 | 45 | 83 | 45 | 18 | 10 | 185 | 106 | 57.3
60 to 80 | 2 | 2 | 7 | 6 | 5 | 1 | 1 | 1 | 15 | 10 | 66.66
---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------
Total. | 37 | 20 | 363 | 203 | 292 | 145 | 87 | 35 | 779 | 403 | 51.7
---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------
Black. | | | | | | | | | | |
---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------
10 to 20 | .. | .. | 2 | ... | 5 | ... | 1 | .. | 8 | ... | ...
20 to 40 | .. | .. | 11 | 3 | 8 | 1 | 5 | 1 | 24 | 5 | 20.8
40 to 60 | .. | .. | 2 | 1 | 1 | 1 | 3 | 1 | 6 | 3 | 50.0
---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------
Total. | .. | .. | 15 | 4 | 14 | 2 | 9 | 2 | 38 | 8 | 21.0
---------+----+----+-----+-----+-----+-----+----+----+-----+-----+------
Grand total. | 817 | 411 | 50.3
-----------------------------------------------------+-----+-----+------
{647} Prognosis is especially bad in hospital practice. The foregoing
statistics of cases admitted to the Charity Hospital of New Orleans
during the greater part of the epidemic of 1878 illustrate the usual
results of hospital practice.
Many of these patients were conveyed to the hospital in extreme
conditions; occasionally they were moribund on admission. It is
hazardous to the life of a yellow-fever patient to transfer him over
the rough streets of a city, often for two or three miles, unless this
is done in the very earliest hours of the attack.
Prognosis is seriously influenced by the condition of the patient at
the moment of attack. If pregnancy exists or delivery has just
occurred, it is, under most circumstances, extremely unfavorable.
Fatigue, anxiety, despair, or grief, all render prognosis more gloomy.
The march of temperature is also important in determining fatal
results.
The following statistics show the influence of temperature in relation
to mortality from yellow fever:
Deg- |First| |Second| |Third| |Fourth| |Fifth|
rees.| day.|Died.| day. |Died.| day.|Died.| day. |Died.| day.|Died.
-----+-----+-----+------+-----+-----+-----+------+-----+-----+-----
106 | ... | ... | 3 | 2 | 1 | 1 | 2 | 2 | ... | ...
105 | 9 | 3 | 5 | 4 | 2 | 5 | 2 | 2 | 2 | 2
104 | 18 | 10 | 23 | 13 | 8 | 3 | 2 | 2 | 3 | 2
103 | 14 | 4 | 11 | 8 | 2 | 2 | 3 | 1 | 2 | ...
-----+-----+-----+------+-----+-----+-----+------+-----+-----+-----
It will be seen from this table that the danger line of temperature in
yellow fever descends as the case progresses.
It may again be stated that yellow fever, like scarlet fever, exhibits
such striking contrasts in its mortality-rate that it is hardly
possible to assert any average standard. It is true that in this
disease, as in all others, statistical accumulations tend to correct
their own errors in exact proportion to the magnitude of the
collections.
In 1878 some 36,000 cases occurred in Louisiana, of which number not
less than 6000 were fatal, a percentage of 16.66. The results of
private practice in New Orleans are exhibited in the following
statistics: Four of the principal practitioners in the city treated in
private practice 975 patients--909 white and 66 colored. Of the
former, 92, or 10.11 per cent., died; of the colored only 2 died. The
cases and deaths among the whites, classified by age, were as follows:
AGE. | Cases. | Deaths. | Per Cent.
---------------------------+---------+----------|----------
Under 5 years of age | 206 | 26 | 12.67
From 5 to 10 years of age | 233 | 20 | 8.61
" 10 to 20 " " " | 183 | 9 | 4.9
" 20 to 40 " " " | 232 | 39 | 16.7
" 40 to 60 " " " | 47 | 6 | 12.7
" 60 to 80 " " " | 4 | 2 | 50
---------------------------+---------+----------+----------
The physicians above quoted lived in different parts of the city. All
of them extended their visits and professional services to the sick to
the {648} very limits of physical endurance, and consequently included
in the above lists some patients who were not able to procure the
comforts and attention necessary to the sick. Some cases also were
included to which the physician was only brought that he might sign
the death-certificate and so avoid the coroner's inquest. After making
allowance for increase of mortality on these scores, I think it safe
to assert that the best results obtained in private practice varied
from 7 to 10 per cent. of mortality-rate.
DIAGNOSIS.--While there is no one symptom pathognomonic of yellow
fever in every stage of the disease, its differential diagnosis is
nearly always possible. The morbid action of its special poison
produces phenomena sufficiently characteristic to prove its presence.
The sudden attack, the slight cold stage, the frontal and lumbar pain,
and the capillary congestion are important diagnostic symptoms.
Even in mild attacks this capillary blood-stasis is usually sufficient
to alter the patient's countenance to such a degree as to attract
attention. A great many different adjectives are used in description
of the countenances of yellow-fever patients. While no one among them
is constantly applicable, the presence of a changed facial expression
should enlist the physician's attention and incite investigation. If
this altered countenance be associated with watery or glistening
injected eyes, the probability of yellow fever is increased.
The slow pulse which coexists with elevated temperature is a point of
much diagnostic value. But it must be remembered that this symptom is
not peculiar to yellow fever. I have noted this lack of correlation of
pulse and temperature in several cases of dengue. It is also not
infrequently found in ordinary cases of jaundice. The slow pulse of
yellow fever must be attributable to the special action of the poison
upon the nervous system. The heart's action may be slowed by
influences exerted directly or through the retrograde effects of the
delay of blood-currents in the capillary distribution.
Albuminous urine is a symptom of much diagnostic importance.
A tendency to hemorrhage may be safely stated to exist in all cases of
yellow fever. In the mildest cases hemorrhage may not actually take
place unless the patients be non-gravid females within the ovulating
limits of life. These patients seldom pass through yellow-fever
attacks without sanguineous vaginal discharges. But even in the
mildest cases yellow fever establishes the hemorrhagic diathesis to an
extent sufficient to render the occurrence of hemorrhage an imminent
event. This fact is shown first, by the congested and tumid gums, from
which blood can be readily pressed, and also by the still more
important circumstance that medical or hygienic mismanagement is so
quickly and certainly followed by black vomit or by hemorrhages from
other parts of the system. Capillary congestion is undoubtedly an
important factor in the production of hemorrhages in yellow fever,
since we cannot otherwise account for the liability to hemorrhage
which is so general in this disease.
The yellow color of the skin and eyes during life, and of the tissues
and serum of the cadaver, is probably due to the coincident influence
of two causes: first, to the coloring matter of the red corpuscles
diffused in the serum of the blood; second, to an accumulation of
secondary blood-poisons. The occurrence of the yellow color and its
intensity bear a {649} direct relation to the sluggishness of
capillary circulation during the paroxysm. It appears likely,
therefore, that the yellowness is principally ascribable to coloring
principles derived from dissolution of the blood, to which capillary
obstruction would so strongly predispose this fluid.
Schmidt has made a very careful resume of the pathological changes
found after death from yellow fever. The most important and uniform of
these affected the nervous system, liver, and kidneys. They consisted
for the most part of hyperaemic conditions, not infrequently attended
by points of extravasation and of degenerative changes. The latter are
principally found in the liver, and bear some relation to the duration
of the case, and it may be also to the degree and persistence of the
pyrexia. When the liver is the seat of fatty degeneration, it is
yellowish in color in whole or in parts. It is then sometimes spoken
of as the cafe au lait or the box-wood liver.
In cases which run a very rapid course these changes are not observed,
but only those which indicate congestion are found, and often
hemorrhagic puncta. In these instances the depending portions of the
body have dark or livid ecchymoses.
TREATMENT.--There are two propositions to which due attention should
be given before formulating rules for the treatment of yellow fever.
The first of these is, that yellow fever is strictly a self-limited
disease, and therefore is insusceptible of jugulation. Both clauses of
this proposition are indisputably true. Cases have been observed in
which mitigation of symptoms and abridgment in duration appeared to
follow spontaneous diarrhoea. Such events must be extremely uncommon,
since in my large experience I know of but one such instance supported
by good testimony.
Efforts to abort the disease by purgatives, bleedings, cold baths,
quinia, etc. have all signally failed. Among the possibilities of the
future is the discovery that some drug or combination of drugs is
capable of meeting yellow-fever poison in the field of the circulation
and antagonizing it sufficiently to rescue the victim from its fatal
toxic effects.
The second proposition is, that the formative stages of the
disease--that is, the early hours of the paroxysm--afford the most
precious moments for instituting such medication as may be considered
proper. This proposition applies no doubt to a number of other acute
affections, but in no one among them all is it so important to be
regarded as in yellow fever. The primary effects of the poison are so
boldly outlined that it appears highly probable that the damage it
exerts upon the economy is chiefly inflicted during the paroxysm. This
affords an additional reason why efforts at medication should be
principally restricted to the paroxysm and to the earliest periods of
that stage.
It is probable that during an attack of yellow fever the patient's
hold upon life is more or less secure in direct ratio to the number of
functions which retain their physiological integrity fairly well. The
suggestion of such a fact should exclude all scholastic or routine
rules of treatment.
In simple forms of yellow fever the first desideratum of the
practitioner is to become acquainted with the patient's condition at
the moment of attack. If this has occurred after eating indigestible
food or after a hearty meal of any description, the stomach should be
emptied. Ipecacuanha may be given in warm water or chamomile infusion
until this result {650} has been accomplished. After emesis, provided
this should have been considered necessary or as a first step of
treatment under other circumstances, a purgative is usually given. The
benefits of purgation are, in my opinion, limited to the act of
ridding the bowels of any fecal accumulations present. For this
purpose those purgatives which combine a due degree of efficiency with
inoffensiveness in operation have appeared to me to be the best.
Castor oil is at the head of this class. An ounce may be given to an
adult in some acceptable vehicle. This may be followed by an enema of
tepid water when required. Salines are more agreeable to the palate,
but far too unmanageable in their cathartic effects to be adopted
generally.
Some very good practitioners believe that a mercurial purge at the
onset of the attack impresses the subsequent career of the case in
some favorable manner. I do not share in this opinion, but I do select
calomel as the preliminary purgative in cases where much gastric
irritability attends the early periods of the attack. I exhibit it
also in those cases in which previous indisposition had occasioned
coating of the tongue, or in which other conditions of systemic
derangement existed for which calomel is usually prescribed.
In many cases it is desirable to avoid the disgust at taking a
purgative or the perturbation it may occasion by its action. Enemas of
tepid infusion of linseed or of milk and water may be substituted,
with the addition of castor oil when necessary.
In the early hours of the attack warm pediluvia are always grateful
and proper. They are to be given by placing a basin of warm water near
the foot of the bed, beneath the covering of a light blanket or sheet,
and allowing the patient's feet to remain immersed for ten or fifteen
minutes. If the feet are cold, mustard should be added. During the
foot-bath the patient usually falls into a perspiration which is
sometimes profuse and general.
Perspiration is a desirable event during the paroxysm, although it is
not, like the sweatings of the malarial fevers, critical, in the sense
of being accompanied by a marked decline in temperature. The idea that
sweating is beneficial is so strongly and generally prevalent as to
give countenance to the erroneous practice of resting the cure of the
disease upon its production and maintenance. I have seen valuable
lives sacrificed by obstinate persistence in measures to promote
diaphoresis, more especially in the later hours of the paroxysm or in
the succeeding or calm stage. It is quite sufficient to encourage the
perspiration by the pediluvia and by a moderate allowance of cool,
palatable drinks. Much value is attached by non-professional persons
to a warm infusion of orange-leaves or some other warm and grateful
beverage. When agreeable to patients I permit them in moderate
amounts, but do not regard them as especially valuable.
Jaborandi has been used in yellow fever. Strong hopes were quite
naturally based upon the action of this drug in exciting excretory
functions, especially diaphoresis, but the observations of my friend
Dr. Thomas Layton and of others show that it possesses no special
value, while it frequently increases the vomiting and has to be
discontinued.
After the bowels have been relieved of fecal accumulations it is good
practice to exhibit a scruple of quinia in solution with ten to thirty
{651} drops of tincture of opium, by rectal injection. Infusion of
linseed or mucilage of elm-bark or gum-arabic are the best vehicles.
The combined action of the quinia and opium mitigates the patient's
headache and lumbar pains. But the influence of these drugs is not
limited to their effect on the nerves of sensation. In quite a
proportion of cases reaction is not so prompt or complete as usual; or
reaction may be quite pronounced, and still the surface may alternate
between a dry and a perspiring state. These oscillations of function
of the organic nerves are also often corrected by this prescription.
In the great majority of simple cases no other medication than this is
requisite or proper, for no medication is proper in yellow fever
unless it is requisite.
When the neuralgias are excessively violent, opium may be again
administered, preferably by enema, and in combination with bromide of
potassium or chloral hydrate. But the effects of opium in limiting
excretory function must always be borne in mind and carefully avoided.
External applications are very efficacious in relieving the
neuralgias. In the southern part of this country the "eau sedative" of
Raspail is greatly used. This is a mixture of ammonia, camphor, and
common salt in solution, and may be prepared extemporaneously. The
applications may be made hot or cold, but if used cold they must be
continuously kept up. It is therefore better to use them warm if
sufficiently effective. Stimulating embrocations of turpentine or
mustard, or dry or wet cups, are sometimes resorted to for relief of
pain.
Excessive temperature demands attention and antagonistic treatment in
direct measure with its persistence, its degree, and its occurrence in
advanced periods of an attack.
In the epidemic of 1867, I used gelsemium as an antipyretic in fifty
cases or more, but the results were so unsatisfactory that I have
quite abandoned its exhibition. I have given quinia as an antipyretic,
but never in doses of more than a scruple. In these doses it has
failed to accomplish the desired result in the great majority of the
cases. Perhaps its antipyretic effects are limited to those cases in
which malaria is a known or an unknown complication.
I have exhibited small doses of digitalis with apparent benefit, but
aconite and veratrum viride I have long since discarded. The physician
cannot afford to sacrifice gastric quietude and competency of function
to the use of remedies whose value as antipyretics is, to say the
most, quite doubtful.
Cold has for a long period of time been brought into use as an
antipyretic in yellow fever. Its positive value and instantaneous
action should be constantly borne in mind, and in the hyperpyrexia of
yellow fever it constitutes by far the most reliable remedy, though
its mode of application must be carefully adapted to the degree of
fever present and to the susceptibilities of the patient. Cold drinks
in limited quantities, but frequently repeated; cold spongings of the
surface, or the use of the cold pack, especially in very high degrees
of body heat; large injections of cold water per rectum, which may be
passed off and repeated once in two to four hours,--form safe and
effective modes of treatment.
Hemorrhages are a constant source of anxiety in yellow fever. It is
very true that persons do not often die from actual loss of blood. I
do not know that I have ever witnessed such an event except when the
{652} blood was poured out from a recently-emptied uterus. But the
chances of recovery are lessened, because the hemorrhagic state
indicates a degree of spoliation of both the fluids and solids of the
system incompatible with maintenance of life. When this condition of
constitution is once established, the stomach rarely escapes, and in a
majority of instances it is the first, and sometimes the only,
bleeding surface. The treatment should be directed, first, to the
great indication of correcting the hemorrhagic diathesis; secondly, to
quiet gastric irritability, in order that vomiting shall not cause
rupture of capillaries. To meet the first indication I regard
nutrition and stimulants as the most important measures of treatment.
The mode of administration will be specially referred to under the
head of alimentation.
Haemostatic remedies, given as specific treatment, generally fail in
accomplishing the purpose for which they are administered. It has
always appeared to me that those therapeutic agents which are capable
of controlling hemorrhage where yellow fever is not present are
completely neutralized by the effects of its toxic agent upon the
vaso-motor nerves. Consequently, while ergot, turpentine, gallic acid,
and other like remedies may be resorted to, too much hope should not
be entertained as to their good effects.
Some excellent practitioners rely greatly on preparations of iron. The
tincture of the chloride is undoubtedly the best. This may be given in
water or upon shaved ice in doses of five or ten drops every half
hour. To allay the gastric irritability pellets of ice should be
swallowed. Effervescing drinks may be given with benefit.
I have often used with good results the following prescription:
Rx. Sodii Bicarb. gr. xx;
Morphiae Sulph. gr. ss.
Aquae Lauro-Cerasi,
Aquae Menth. Pip. _aa._ fl. drachm iv. M.
S. Teaspoonful after every act of emesis.
Occasionally I have given the following prescription:
Rx. Creasoti gtt. viij;
Tinct. Opii Deodorat. gtt. xl.
Aquae Menth. Pip.,
Muc. Acaciae _aa._ fl. drachm iv. M.
S. Teaspoonful after every act of emesis in iced Seltzer or
Apollinaris water, or in champagne.
Sometimes a few drops of chloroform in a spoonful of iced mucilage of
acacia act favorably.
In cases which appear utterly hopeless the physician, acting
desperately, is sometimes able to save life by treatment which could
scarcely be safely recommended. I once administered a fourth of a
grain of morphia to a child of seven years, who, after a sleep of ten
hours, ceased to throw up black vomit and recovered.
External applications to the epigastrium usually afford some relief to
nausea at any stage of yellow fever. Mustard or aromatic cataplasms
may at all times be used with hopes of favorable effects. Towels wrung
from cold water are very efficacious. Sometimes a drachm or two of
chloroform dashed over them increases their anti-emetic action.
Suppression of urine is generally a symptom of fatal import. {653}
Attempts may be made to establish the secretion by dry or wet cups in
the lumbar region, by warm applications around the loins, or by
mustard cataplasms or blisters. If the condition of the patient's
stomach is such as to permit this practice, copious diluent drinks and
diuretics should be given. Lemonade holding bitartrate of potassium in
solution is generally the most acceptable, and probably the most
efficient. Some physicians think they oftener obtain good results from
small and frequently repeated doses of turpentine. I can bear
testimony to the good results which sometimes follow large rectal
injections of warm or cold water, the latter being preferable when
there is high fever.
In certain cases of yellow fever reaction from the cold stage is
feeble and imperfect, or perhaps may not occur at all. This departure
from type is very fatal. The patients are stupid, sometimes
semi-comatose and incoherent, from the earliest hours of the attack.
The face is listless, drunken, or idiotic in expression. The color of
the skin is dark olive and almost livid. The print of a hand on the
chest is very slowly effaced. Sometimes the surface is covered with a
peculiarly unctuous perspiration. The pulse is feeble and
compressible; the temperature seldom more than one or two degrees
above the normal standard. Albuminous urine is found during the first
day. Death, attended by convulsive rigors, generally closes the scene
within seventy-two hours from the moment of seizure.
Hot mustard-baths should be resorted to. Blood may be drawn by cups or
leeches from the back of the neck or temples, and this may be followed
by the application of a blister. Morphia and atropia may be exhibited
subcutaneously in small doses, to be repeated as often as proper.
Quinia may be administered per rectum or by the hypodermic method.
Lastly, pilocarpine may be thrown into the tissues in sufficient doses
to procure its vigorous physiological action.
Almost in precise symptomatic contrast with these cases of failure in
reaction is another form of attack, in which violent disturbances of
nerve-function occurs; such cases often being characterized as
congestive in type. The most typical of these attacks are among
children or adolescents. If attended by noticeable chill, it is
ordinarily slight. Reaction is quick and excessively violent. The face
is flushed, the eyes injected, and convulsions with delirium are
liable to occur as early symptoms. I have watched with much interest
the alternate flushings and pallor of the countenance occurring in
these cases, such as are often observed in basilar meningitis.
The treatment in this type of attacks should include chloroform by
inhalation in sufficient amount to control convulsions. Chloral
hydrate may be administered by enema, or morphia hypodermically.
Cathartic doses of calomel often exert a beneficial effect. Leeches or
cups, to be followed by cold applications or by blisters, may be
applied about the head or neck. But cupping and leeching should only
be resorted to in the treatment of grave symptoms, since obstinate
hemorrhage is liable to occur from any and every point from which the
cuticle has been removed.
Yellow fever is often masked during the paroxysm by some pre-existing
disease. Malarial fevers, the febrile states of pulmonary consumption
or of the recently-delivered female, may all mask the early clinical
{654} phenomena to such a degree that the most experienced and
vigilant practitioners are sometimes astonished to find black vomit,
suppression of urine, and all those symptoms which mark the last
stages of the disease, suddenly developed.
Walking cases should be classed in the same category as masked forms.
In these instances the early symptoms are so slight as to be
overlooked or neglected by their subjects. They continue to prosecute
their usual pursuits until, by sheer exhaustion, they are driven to
beds from which they seldom arise.
The hygienic and dietetic management of yellow-fever patients is
extremely important, and the strictest attention must be paid to the
condition and discipline of the sick chamber. In this disease those
occurrences and circumstances which in other affections would be
reckoned as unimportant and trivial become matters of serious
magnitude.
The physician, by a composed and cheerful demeanor, often decides
which end of the balance shall go down. But an intelligent,
experienced, and faithful nurse is equally as important as the
excellent physician.
The patient should be confined in strictly recumbent positions, and
all drinks and foods must be given through tubes or from pap-cups. It
frequently occurs that patients are unable to void the bladder in such
positions. In these cases the catheter should be used, rather than
suffer any violation of the rule which demands a maintenance of
unbroken decubitus.
The sick room should be kept freely ventilated, and the patient's
bedding should be changed, when requisite, by removing him to one side
of the bed while the other is renovated. If the patient's night-shirt
becomes soiled and disagreeable, it may be cut so as to remove it, and
another, cut in the same manner, may be substituted and stitched
together. The room must be kept quiet, and useless visiting entirely
forbidden.
Cool and grateful drinks may be given in any stage or state of yellow
fever if demanded by patients. The quantity allowed at one time should
be small, since over-distension of the stomach almost certainly causes
vomiting. Effervescing drinks are nearly always grateful, and are
better tolerated than others. Seltzer-water and lemonade, or Seltzer
or Apollinaris on shaved ice, are to be recommended. Sometimes
patients call for sparkling wines or beers. I never refuse them or any
other alcoholic drink asked for in any stage of the disease. Wine
surely possesses valuable therapeutic effects in yellow fever.
Alimentation must be severely controlled by the physician, and the
tolerance and effects constantly watched. Even to the most experienced
physician the kind of food to be selected, and the time and manner of
administration, constitute difficult problems. In simple forms of the
disease food had better be strictly withheld during the continuance of
the paroxysm. Even after the stage of calm has been reached,
sufficient time should be allowed to elapse to enable the physician to
form some estimate of the degree of damage his patient has suffered
and his competency to retain foods and be nourished by them. This
question can seldom be answered in a decided manner, except through a
cautious trial of some bland and inoffensive food.
{655} On the third or fourth day of sickness a single tablespoonful of
iced milk may be given, and the immediate consequences closely
watched. If no retching or gastric uneasiness should ensue, it may be
repeated at the end of thirty minutes. Some physicians prefer to begin
with spoonful doses of equal parts of sweet milk and thin
barley-water. In my own experience chicken-water has proved to be the
most universally acceptable, as well as the most beneficial, of all
the various forms of nutriment to be chosen as a first venture. I have
frequently combined this with barley-water when first given. In this
cautious and tentative manner even the most experienced physician
prefers to proceed, rather than to attempt to prescribe rules of diet
in an abstract and arbitrary manner.
If these light articles of diet are well borne, they are to be
gradually and watchfully exchanged for beef-essences, the blood of a
rare beefsteak, and the more substantial broths. Solid articles of
food should not be allowed during the first ten days after an attack,
and for still longer periods patients should be admonished against
excesses in eating, and especially in respect to indigestible
articles. Those lesions of the blood and of the stomach, and those
grave disorders of nerve-function which occasion haematemesis in
yellow fever, are slowly repaired. Instances are reported in which
black vomit and death have followed excessive eating and drinking ten
or twenty days after dismissal from treatment.
There are, however, certain conditions which are liable to complicate
yellow fever which demand a course of dietetic procedure different
from that which I have recommended. Thus, children cannot bear
privation of food until the paroxysm is over if its duration is long.
In like manner, a more supporting course is required in most of those
cases in which yellow fever occurs as an intercurrent affection, in
all those cases which are termed typhoid or adynamic per se, and, more
emphatically still, in every case in which hemorrhages are occurring.
A failing pulse should in all instances admonish us to resort to
nourishment and stimulants.
It is a fortunate circumstance that in yellow fever the lower bowel is
generally in a state favorable for the retention of nutritious enemas.
In the most trying and critical hours of desperate cases I have seen
patients tided through by the use of skilfully prepared and skilfully
administered injections of some suitable meat-essence. When insomnia
exists, chloral hydrate or bromide of potassium may be conveniently
given in these vehicles.
It is evident that the discussion of the vastly important sanitary
questions pertaining to the prevention of yellow fever cannot be
appropriately discussed in the present article.
{656}
DIPHTHERIA.
BY A. JACOBI, M.D.
DEFINITION; SYNONYMS; HISTORY.--Diphtheria is a specific, infectious,
and contagious disease, characterized principally by epithelial
changes in, and the exudation of fibrin on and into mucous membranes,
the surface of wounds, and the rete Malpighii, thereby constituting
the so-called pseudo-membrane. Under the names ulcus syriacum, ulcus
aegyptiacum, garotillo, morbus suffocans, morbus suffocatorius,
affectus suffocatorius, pestilentis gutturis affectio, pedancho
maligna, angina maligna, angina passio, mal de gorge gangreneux,
ulcere gangreneux, angina polyposa, angine couenneuse, cynanche,
croup, diphtheritis, and diphtheria, the disease has been known and
described at different periods by the writers of different nations.
The Hippocratic writings and some remarks in the Talmud allow of some
doubt in regard to their explanation. Whether their authors observed
or recognized diphtheria cannot be proven. There is less doubt in
regard to Archigenes, quoted by Oribasius. Aretaeus of Cappadocia is
notably the first, if we except Asclepiades only, who is said to have
performed laryngotomy. The description of the pharyngeal and laryngeal
manifestations furnished by the former, however, can leave no doubt in
our minds that he knew diphtheria and recognized it. Galen, in his
remarks on the Chironian ulcer, tells us that the pseudo-membrane was
gotten rid of by coughing when the respiratory passages were affected
by the disease, and by hawking when the disease was in the pharynx.
Caelius Aurelianus recognized diphtheria of the pharynx and larynx, as
well as the diphtheritic paralysis of the soft palate; it is to him we
are indebted for the information that Asclepiades resorted to
scarification of the tonsils, and even to laryngotomy. Aetius in the
fifth century distinguished white and grayish patches and gangrenous
degeneration, observed paralysis of the soft palate, and advised
against energetic local treatment and the forcible removal of the
deposits before they were in a condition to fall off spontaneously.
The Arabs and Arabists contain no allusions to the subject, but early
chronicles tell of an epidemic raging in St. Denis in 580, subsequent
to a great inundation. There appear to have been memorable epidemics
in Rome in 856 and 1005, in Byzantium in 1004. The former are
mentioned by Baronius, the latter by Cedrenus.[1]
[Footnote 1: Haeser, _Lehrb. a. Gesch. du Med. u. d. Epidem. Krankh._,
3d ed., vol. iii., p. 434.]
According to Morejon, Gutierrez wrote his _Tradado del enfermedad del
garrotillo_ in the second half of the fifteenth century. A malignant
form of angina raged in 1517 in Switzerland, along the Rhine, and in
the Netherlands; in 1544 and 1545 in Northern Germany and on the
Rhine; {657} in 1557 in France, Germany, and Holland; to the latter
refer the reports of Tetrus Fosterus. Antonio Soglia, quoted by
Chomel, describes an epidemic in Naples and Sicily (1563), which
spread in the following year as far as Constantinople; Joannes Wierus,
epidemics in Dantzic, Cologne, and Augsburg (1565); Ballonius
(Baillon), in Paris (1576). At the same time this disease was frequent
in Denmark. From Spain there are reports on severe epidemics between
the years 1583 and 1618; the year 1613 was long known as the year of
diphtheria (anno de los garrotillos).
Mercado (1608) speaks of a child that had communicated the disease to
his father by biting his finger. Casealez advised gargles containing
alum and sulphate of copper. Herrera described diphtheria of the skin
and of wounds, and looked upon the pseudo-membrane as the essential
characteristic of the disease. Heredia, in 1690, recognized the
suffocative and asthenic forms, as well as the paralysis of the soft
palate, the pharynx, and the limbs; he also called attention to the
occurrence of relapses, which he attributed to the absorption of the
morbid products, and endeavored to prevent by cauterization.
Naples had diphtheria 1610-45, in its worse form 1618-20, together
with erysipelas, and diphtheritic affection amongst cattle. About
those times tracheotomy was often performed by Severino, the same who
found pseudo-membrane in the larynx at a post-mortem examination made
in 1642. In 1620 the disease was in Portugal, Sicily, and Malta; in
1630 in Spain, according to Fontechu, Villa Real, and Herrera. It was
remarked that in some instances no membranes were perceived in the
throat, but the cases were liable to terminate fatally with large
glandular swellings round the neck and general symptoms of adynamia.
Sicily was again invaded in 1632, Rome in 1634, Italy from 1642 to
1650, Spain in 1666. The Italian reports emphasize the marked
contagiousness of the disease and its tendency to depress the vital
powers, also the weakness of the mental faculties left behind. In
Germany the disease was described by Wedel in 1718. The epidemics
observed by him were not very instructive, yet they sufficed to teach
the importance of isolating the sick.
In the New England States diphtheria appeared in the seventeenth
century. Samuel Danforth lost the four youngest of his twelve children
by the "malady of bladders in the windpipe" within a fortnight in
December, 1659, in Roxbury, Mass. John Josselyn mentions an epidemic
in New England, mainly in Maine, which lasted at least until the year
1671. Mr. Douglass reports another, which commenced on the 20th of
March, 1735, in Kingston township, about fifty miles east of Boston,
and extended all over, and also to Boston, where it was mild at first.
But in 1738 it was very severe, and remained so for some time. Indeed,
it did not abate for a long time, to judge from a letter of Cadwalader
Colden written in 1753 to Dr. Fothergill, and the two letters of Dr.
Jacob Ogden, written in 1769 and 1774 to Mr. Hugh Gaine of New York;
as also from John Archer's "Inaugural Dissertation on Cynanche
Trachealis, commonly called Croup or Hives," published in 1798.[2] In
1809 there was a severe epidemic in Philadelphia;[3] in 1816 in Crete.
[Footnote 2: For extensive quotations from these and other writers on
diphtheria at a very interesting period of our medical literature, see
A. Jacobi, _A Treatise on Diphtheria_, New York, 1880.]
[Footnote 3: Caldwell, in ed. of Cullen's _First Lines of the Practice
of Physic_, Philadelphia, 1816, 1, p. 260.]
{658} The reports of Le Cat concerning epidemics in Rouen in 1736 and
1737 being doubtful, the first great epidemic must be set down, in
France, for 1745. It commenced in Paris, and invaded the provinces
afterward. Chomel gave an accurate description of the diphtheritic
paralysis of the soft palate, and reports a case of strabismus.
Epidemics are reported from the Netherlands in 1745, 1746, 1769, 1770,
1778-86; from Spain in 1764-71; from England in 1744-48 (by Starr),
from Plymouth, England, in 1751-53 (Thurham) and 1776. Dropsy and
glandular swellings were frequent; emetics and pure air were the
sheet-anchors of treatment. The Netherlands, France, and the West
Indies were invaded from 1770-80 by the disease, which was found often
complicated with scarlatina; Portugal in 1786 and 1787; France again
in 1787 and 1788; Northern Germany in 1790. At that time, particularly
in France, the main reliance was had on the internal administration of
cinchona and the insufflation into the throat of alum.
Epidemics have been described since from different localities in
different years: in Glasgow, 1812 and 1819; Switzerland, 1823-26;
Norway and St. Helena, 1824; New York and Kentucky, 1826 and 1828;
French provinces, 1834; Paris, 1841; several parts of Europe and North
America, 1845-56; Paris, 1853-55; England, 1854 and 1859, when 95 per
cent. of all the cases of nasal diphtheria proved fatal; Netherlands
and Sweden, 1855; all Western Europe, 1855-65, up to the present time,
and all Europe since; California, 1856 and 1857; Portugal and France,
1856; Eastern Prussia, 1850, 1852, 1856, 1857; and all the countries
with a cold or moderate climate to this very day.
During the second half of the eighteenth century but two writers are
worthy of especial notice--Home, a Scotchman, 1765, and Samuel Bard,
an American, 1771.
Home deserves credit for having distinctly drawn the line between the
pseudo-membranous and the gangrenous affections. He also endeavored to
prove that croup and angina maligna were two distinct diseases,
notwithstanding all that had been said since the time of Aretaeus in
favor of their identity. The false membrane of croup he looked upon as
an aggregation of mucus. He sought for it exclusively in the
respiratory tract, and disregarded any connection between it and the
false membrane found in the pharynx.
Bard's experience was very extensive; he saw membranous pharyngitis,
laryngitis, and pharyngo-laryngitis; he speaks of the membrane as met
upon the skin, of paralysis of the muscles of deglutition and of the
larynx, and likewise of paralysis of the lower extremities, as
sequelae. He looked upon the morbific process as the same whichever
were the mucous membranes attacked, and made a distinction only
according to the localization of the disease. The influence which he
might have exercised in shaping the professional opinion on the nature
of the disease did not make itself felt, partly because of his
classical modesty, and partly because of his remoteness from the
centres of European learning. Not before 1810 was his book translated
into French (by Ruette). While his style is classical in its
simplicity, his observation is astonishingly correct, and his
conclusions as to the actual identity of all the diphtheritic
processes in the most various clinical symptoms unimpeachable this
very day. His description of the various forms of pharyngeal
diphtheria is painfully {659} good, his observations on cutaneous
diphtheria very accurate, his few dissections well recorded,
particularly when he speaks of tracheal and tracheo-laryngeal
diphtheria, and his historical reviews very judicious indeed. "Upon
the whole, I am led to conclude that the morbus strangulatorius of the
Italians, the croup of Home, the malignant ulcerous sore throat of
Huxham and Fothergill, and the disease I have described and that first
described by Douglas of Boston, however they may differ in symptoms,
do all bear an essential affinity and relation to each other, or are
apt to run into each other, and, in fact, arise from the same leaven.
The disease I have described appeared evidently to be of an infectious
nature, and, being drawn in by the breath of a healthy child,
irritated the glands of the throat and windpipe. The infection did not
seem to depend so much on any prevailing disposition of the air as
upon effluvia received from the breath of infected persons. This will
account why the disorder sometimes went through a whole family, and
yet did not affect the next-door neighbors. Here we learn a useful
lesson--viz. to remove young children as soon as any one of them is
taken with the disease, by which many lives have been saved and may
again be preserved."
Jurine, in his prize essay of 1807, denies the gangrenous nature of
angina maligna and emphasizes the frequent complication of membranous
croup with membranous pharyngitis. It was reserved for Bretonneau to
enforce attention to the ideas of Bard by asserting (though he did not
mention either his monograph or its French translation of 1810) the
identity of angina maligna, or by whatever other title it may be
known, with membranous laryngitis, and by inaugurating his theory with
a new name for the disease to perpetuate the views expressed therein.
First and foremost, he called attention to the continuity of the
membrane (according to him, composed of coagulated mucus and fibrin)
of the nose, pharynx, and respiratory tract, its identity with certain
morbid conditions of the skin, and promulgated the theory that
"diphtherite"--the name dates from that time--is a specific disease,
an affection sui generis, and differs both from a catarrhal and a
scarlatinous inflammation.
The modern history of diphtheria may be dated from June 26, 1821, when
Bretonneau read his first essay on that subject before the French
Academy of Medicine, and gave to the disease the name it now bears.
His second and third (Nov. 25th) papers belong to the same year; his
fourth was read in March, 1826; his fifth appeared in the _Archives
gen._ of January and September, 1855. It was only in 1826 that the
material, previously gathered, was summed up in his celebrated
monograph.[4] Before this time, however, the separate essays had
received prominence from the reports and commentaries of Guersant, who
laid particular stress on the statement that diphtheria was a
non-gangrenous affection, identical, and even synchronous, with croup
in the majority of epidemics. Since that epoch the literature on the
subject has assumed enormous proportions. It is a matter of regret
that the limited space allotted to this subject should exclude much
historical detail of the etiology, pathology, and therapeutics of
diphtheria. If the history of any disease is interesting, and the
neglect of its study has ever punished itself, it is diphtheria. {660}
Particularly would the treatment have been more successful if the
knowledge of former times had been available and more heeded. As long
ago as in the seventeenth century depletion in diphtheria was
condemned, and in the seventeenth and eighteenth centuries the local
treatment with muriatic acid and the internal administration of
cinchona, camphor, and roborant diet were held to be the only
admissible ones. Bretonneau urged the same principles, and still in
our own times, for want of historical knowledge, we had to learn the
old lesson over again.[5]
[Footnote 4: P. Bretonneau, _Des Inflammations speciales du tissu
muqueux, et en particulier de la Diphtherite, etc._, Paris, 1826.]
[Footnote 5: See history and bibliography of diphtheria in Chatto;
Sanne, _Traite de la Diphtherie_, Paris, 1874; Jacobi, in _Gerhardt's
Handb. d. Kinderk._, vol. ii., 1877; Seitz, _Diphtheric und Croup
gesch. u. Klin. dargest_, Berlin, 1879; _Index-Catalogue of the
Library of the Surgeon-General's Office, U.S.A._, vol. iii.,
Washington, 1882.]
The following is a brief review of the main points of discussion upon
subjects connected with the symptomatology and pathology of diphtheria
since Bretonneau's first paper:
Bourquoise and Brunet express their belief (1823) in the contagious
character of this disease. Desruelles (1824) sees a diagnostic
difference between the sporadic and the epidemic forms in the
participation of the brain in the latter. Louis referred a number of
cases of croup in adults to pharyngeal diphtheria as their source.
Mackenzie considers that croup has its origin in the fauces, and urges
the employment of lunar caustic. Billard (1826) denies the specific
character of diphtheritic inflammation. Hamilton describes cases that
terminated in suppuration, and which he therefore distinguishes from
Bretonneau's cases. He describes two modes of termination of the
disease--one in croup, the other in a state of debility arising from
the effect of the absorbed secretion on the respiratory nerves. Pretty
looks upon those cases of croup that have their original seat in the
tonsils as contagious. Bland (1827) explains the difference between
croup and diphtheria. Deslandes declares them to be identical.
Bretonneau publishes a work in which he compares diphtheria with
scarlatina anginosa, and recommends the use of alum. Emmangard is the
first one of the physiological school who, likening diphtheria to
typhoid and claiming its origin in a malarial infection, calls it
angina gastro-enterica. Abercrombie is in favor of distinguishing
diphtheria from croup, but reports a number of cases of diphtheria of
the pharynx that terminated fatally by stenosis of the larynx. Ribes,
who encountered the disease in nine members of a single family,
asserts that croup rarely occurred without a preceding diphtheria in
his experience; he advises an examination of the throats of apparently
healthy individuals. Fuchs relates the history of epidemics of angina
maligna, and declares croup to be a genuine angina maligna trachealis,
which only does not run through all the stages. Broussais opposes the
identity of croup and diphtheria (1829), and gives a report of cures
by means of antiphlogistic regimen and laryngotomy. Diphtheria and
gangrenous angina are synonymous with him. Gendron expresses a belief
in the identity of diphtheria and gangrenous angina. Roche considers
the membrane rather of hemorrhagic than of inflammatory origin, and
consisting of discolored fibrin. About the same time Trousseau is
endeavoring to clearly establish the diagnosis between diphtheria and
scarlatinous angina. Shortly after (1830), he reports cases of
diphtheria which originated in blistering wounds, and of diphtheria of
the skin giving rise to throat affections, and {661} diphtheria of the
throat followed by skin disease. T. F. Hoffmann cites a severe case,
that ultimately recovered, with consecutive paralysis of certain
cranial nerves. Cheyne (1833) makes a stand against the "confounding
of croup and cynanche maligna under the name of diphtheritis."
Bourgeois witnessed an epidemic succeeding mumps.
Fricout and Burley (1836) declare their belief in the contagiousness
of the disease. Bouillaud attacks the theory of its specific character
on the ground that abstraction of blood produced favorable results.
Stokes makes a distinction between primary and secondary croup
according to the original seat of the affection (1837). Kessler
advocates (1841) the view of its contagious nature, and Rilliet and
Barthez adduce evidence of the occurrence of ulceration and gangrene
in the course of the disease. Taupin, like Ribes, enjoins a methodical
examination of the throat of every patient during the prevalence of an
epidemic of diphtheria, whatsoever be the disease from which the child
suffers. Boudet (1842) opposes Bretonneau's hypothesis that croup is a
descending diphtheria, and holds to the identity of diphtheria and
gangrenous angina. In this contest Durand (1843) also takes sides
against Bretonneau, and lays particular stress on the point that the
diphtheritic patient succumbs rather from the severity of the
constitutional symptoms than from suffocation. Rilliet and Barthez, on
the other hand, rally to the support of the attacked master, asserting
that the usual form of croup and that resulting from a descending
diphtheritis are one and the same, while they claim that diphtheritis
and gangrenous angina are distinct affections.
Meanwhile, the strife regarding the nature of the disease continued.
Guersant and Blache (1844) describe the stomatite couenneuse (noma,
stomacace, according to them, the rarest kind of gangrenous angina) as
a form of Bretonneau's diphtheritis, and Landsberg raises the question
whether a nerve-inflammation, present in a certain case, was to be
looked upon as an accidental or an essential feature of the disease,
and finally comes to the conclusion, with Schonlein, that it was a
neurophlogosis dependent on the disease. Bouisson (1847) reports a
case of diphtheritic conjunctivitis resulting in loss of the eye.
Robert publishes his observations on diphtheria of the skin and of
wounds, which he attributes to an atmospheric contamination in crowded
wards of hospitals, and looks upon it, with Delpech and Eisenmann, as
a form of hospital gangrene. Virchow, in the same year, distinguished
the catarrhal, croupous, and diphtheritic varieties of the disease.
Meanwhile, reports of paralysis of the soft palate after diphtheria
came from Morisseau, from Trousseau and Lasegue, and lastly (1854-59)
from Maingault. The subject of diphtheritic conjunctivitis was studied
by A. v. Graefe (1854), who encountered the disease as a complication
of diphtheria of the pharynx, nose, and skin, and hence considered it
a part of the general disease rather than an independent local
affection. Diphtheria, in its effects on the system, had at the same
time been investigated by Trousseau, who sums up with the statement
that the principal source of danger lies in the invasion of the
larynx, and that the large majority of cases of croup began as a
diphtheria of the pharynx, but that, even without the occurrence of a
laryngeal localization, many cases terminate fatally owing to
adynamia.
Outside of France, too, the subject had attracted attention. West, who
had never seen the disease occur primarily, describes diphtheria as a
{662} complication of measles. Bamberger (1855) divides the
inflammations of the mouth and pharynx into the catarrhal and croupous
forms, and considers croup and diphtheria to be subdivisions of the
latter form, differing only in degree. The paralysis of the muscles of
deglutition is discussed by Dehaenne (1857) who had contracted the
disease, and the paralysis of other muscles by Faure. A case of
diphtheria of the tonsils, nipples, and vagina in a woman recently
confined, followed by infection of the new-born and the death of both,
is reported by Mathieux; and cases of diphtheritic conjunctivitis by
Grichard, Warlomont, and Testelin. The same year Isambert published a
work in which he divided the diphtheritic affections into three
forms--viz. angine couenneuse, scarlatinous angina, and diphtheritic
angina. The last-mentioned is further subdivided into a
croupous-diphtheritic angina, in which croup of the larynx plays an
important part, and into that form in which death results from
adynamia; in the latter form there is a marked swelling of the
lymphatic glands. Apparently, at this time the epidemic in Paris
underwent a considerable change, for the croupous form does not occur
by far so frequently as Bretonneau had asserted, and croup of the
larynx without a preceding diphtheria of the pharynx was observed more
frequently than he would lead us to believe.
The various changes in the symptoms of the epidemics of diphtheria
which were observed in different places and countries, and at
different times, explain many of the differences of opinions in regard
to the nature of the disease. The literature of that subject is in the
last twenty-five years simply stupendous, and a few more notes must
suffice for the elucidation of the drift of theories and observations.
Beale was the first to look for organic beings as the cause of the
disease, without finding any. Laycock sees it in the bacilli and
spores of oidium albicans; Wilks, however, found the same parasite in
other affections. Cammack declares the diphtheritic membrane to be
herpetic. Feron also calls Bretonneau's mild form of the disease a
herpetic angina with pseudo-membrane; so does Gubler. Bouchut writes
against the identity of diphtheria, croup, and gangrene. Condie
describes the disease as occurring with scarlatina. Litchfield claims
that it is a concealed scarlatina, and Hillier that it has some
connection with it. Millard cites one case in the course of which
gangrene occurred, and another in which skin, mouth, pharynx,
respiratory passages, oesophagus, and vulva were affected at the same
time. Harley vainly endeavored to inoculate the disease in animals.
Stephens declares the disease to be infectious. Sanderson looks upon
it as identical with the angina maligna of the aged. Farr considered
the exhalations from sewers an important etiological factor.
Sellerier, Kingsford, and Harley (1859) report paralyses as sequelae.
Maugin speaks of a specific eruption; Ward, of an accompanying
purpura. Bouchut and Empis remarked the frequent presence of and
danger from albuminuria; so did Wade. Maugin calls attention to the
fact that, when present in diphtheria, it occurs early, whereas in
scarlatina it is seen during the period of desquamation, and is not of
frequent occurrence even then. Gull gives an account of cases in which
death resulted from asthenia, and speaks of a nerve-lesion which he
attributes to the severity of the local inflammation. Hildige
describes diphtheritic conjunctivitis as seen in Graefe's practice,
and looks upon it as contagious. Magne denies its contagious or {663}
infectious character. Mackenzie, while probably having seen false
membrane appear on the conjunctiva when in a state of inflammation,
yet refuses to recognize diphtheritic conjunctivitis as a distinct
disease.
In the same degree that observations of cases and epidemics increased
in number, the nature of the disease and its cause commenced to be
studied. The assumption that the latter was a chemical poison was soon
doubted, and the parasitic nature of diphtheria considered by many as
proven.
After Henle had (1840) expressed his belief in the existence of a
contagium animatum, and morbid processes had for some time been
compared with the phenomena of fermentation, Schwann demonstrated the
presence of lower organisms in fermentation and putrefaction. The
discovery of the cause of the silk-worm disease by Bassis, of the
achorion by Schonlein, of the acarus by Simon, of bacteria in
malignant pustule by Pollender, Brauell, and, above all, by Davaine,
in relapsing fever by Obermeier, the teachings of Pasteur concerning
the conditions under which putrefaction occurs,--all tended to explain
the various infectious and contagious diseases by analogy also, and to
stimulate the search for a vegetable organism in diphtheria. Buhl was
the first to discover schizomycetae in diphtheritic membrane, but
expressed no opinion as to the part they played in the process. Huter
found them in the gray diphtheritic covering of wounds, in the
surrounding apparently healthy tissues, and in the blood. Huter and
Tomasi found them in the diphtheritic membranes of the pharynx and
larynx, inoculated them on the mucous membranes of animals, and
described them as small, round or oval, dark-colored, active little
bodies. The latter observers look upon these organisms as a part of
the infectious element. Oertel found them in diphtheritic membrane and
in inflamed mucous membranes in the lymphatic vessels, lymphatic
glands, kidneys, and other organs; he considers them as the contagious
element of diphtheria. Nassiloff, too, after inoculations in the
cornea resulted in an enormous multiplication of the microscopic
organisms and their appearance with pus-cells in the lacteals and in
the lymphatics of the palate, and even in the bones and cartilages,
asserts that the development of organisms is the primary step in the
diphtheritic process. Eberth made successful inoculations in living
tissues; the micro-organisms, introduced into the cornea, proliferated
actively and caused an inflammation of irritative character in the
surrounding tissue. He asserts, with the positiveness of an
evangelist, that diphtheria cannot occur without bacteria. Klebs
inoculated the micrococci in pigeons and dogs, and found them in the
blood of the animals after death. Orth found them in the pleura,
lungs, kidneys, and urinary bladder. But what their action is, whether
they are directly pernicious, or deprive the body of certain elements
(as of oxygen in malignant pustule, according to Bollinger), or injure
mechanically by acting on the coats of the blood-vessels (either
directly or by means of altering the blood), thus depriving whole
territories of their blood-vessels, is a question upon which the
principal advocates of the parasitic theory have not yet agreed. Even
Oertel acknowledges the impossibility of explaining the manner in
which bacteria act (Ziemssen, _Handbuch_, ii., 1, p. 581, 2d ed.).
This much is positive, at any rate: that no one has yet proven that
the vegetable organisms alone, and not other, free or fixed, parts of
the {664} diphtheritic membrane, are the vehicles of the infecting
elements (Steudener); and even now the question has not been decided
whether the bacteria met with in diphtheria constitute the cause of
the disease, or are a part of the process, or co-effects of the
poisonous action--whether they are the carriers of the poison or
entirely indifferent entities.
The most important observations made by those who deny a direct
etiological connection between micro-organisms and septic diseases in
general, and diphtheria in particular, are those of Hiller and
Billroth. The latter has proven the morphological identity of the
various kinds of bacteria, although it cannot be denied that the
apparent similarity may mask a yet unknown difference. Hiller calls
attention to the fact that large numbers of micrococci have been found
in the cadaver where death has not been the result of septic disease,
and also that septic infection is not always severest where the
bacteria most abound, but where an extensive chemical decomposition or
a mass of putrefying tissue is found. This would indicate that the
septic process is rather dependent on chemical decomposition than on
the presence of bacteria.
Panum, Bergmann, and Schmiedeberg have isolated poisons that contained
no bacteria. Rawitsch and many others prove that septic infection is
not dependent on the existence of bacteria. Davaine has shown that an
infinitely small amount of a chemical poison, free from bacteria, can
kill quickly.
The presence of cocco-bacteria (Billroth) in the blood during life has
not once been proven, not even in pyaemia or septicaemia. Yet their
being swept into the lungs with the atmospheric air is indisputable.
It would therefore seem as though living blood had a greater tendency
to destroy bacteria than to allow itself to be decomposed by them. Not
only, however, would it seem so, but P. Grawitz (_Virch. Arch._, vol.
lxx., p. 546) proves that sporules do not grow in the (tissue and)
blood, but that they are in part dissolved, in part eliminated through
the kidneys, and that this result is accomplished through the
combination of the following four factors--viz. the elasticity of the
blood, its constant motion, the absence of oxygen in sufficient
quantity in the circulating blood, and the presence of living animal
cells. All of these factors appear to be of great importance. Thus it
is that, where the constant motion of the blood and the animal living
cells are not present (as in the anterior chamber of the eye or in the
humor vitreous) a rapid proliferation and accumulation of bacteria can
take place. They are also known to increase rapidly and emigrate into
the liver when deposited in the abdominal cavity.
The destruction of bacteria in the circulating blood, into which they
may have penetrated, accounts for some microscopical facts in
connection with (actually or apparently morbid) blood. Their remnants
are probably the pale and dark particles which are discovered in the
blood alongside the red and white blood-corpuscles. They could not be
identified as micrococci, while in the tissue they are more
recognizable. In autopsies they have been found in the urinary
tubules, pressing forward and piercing the walls, not occupying a
nidus of inflammation, however, and probably are even here a
post-mortem phenomenon. A direct necrosis or inflammation by the
inoculation of diphtheritic elements can only be produced in the
cornea, as was shown by Recklinghausen, and particularly Eberth.
Besides, there is nothing characteristic in the cocco-bacteria of
{665} diphtheria, with the exception, perhaps, of their browner color,
to justify their being looked upon as a distinct variety, certainly
not as another species. It is more likely that a difference of action
is not so much to be sought for in a different parasite as in the
peculiarity of the corneal tissue. When fluid containing
cocco-bacteria was injected into the eye of a rabbit, in twenty-four
hours the eye was destroyed. If injected into the eye of a dog or
guinea-pig, only a slight inflammation resulted (Billroth and
Ehrlich). If these experiments were continued on a larger scale, we
might eventually, by analogy, infer, and even prove, that the immunity
against certain diseases enjoyed by some animals is owing to
peculiarities in the very structure of their own tissues. In a similar
manner I shall prove hereafter that even peculiarities and variations
in the tissue and epithelium of the human body give rise to different
shades and variable clinical symptoms in the diphtheritic processes.
The views of Curtis, Satterthwaite, and Charlton Bastian fully agree
with those of the above observers. The latter is rather inclined to
look upon bacteria as an effect of the disease than as a cause.
Similar views were expressed by Burdon Sanderson.
Nor are the researches of Weissgerber and Terls, Lukomsky, Weigert,
Lucke, any more conclusive; and, finally, Furbringer, in his most
recent and careful studies of diphtheritic nephritis, insists upon
this, that it is not caused by immigration of fungi into the kidneys,
that the very best methods employed for the finding of parasites
result in the absence of micrococci from the inflamed organ, and that
the renal inflammation following diphtheria is the result of a
chemical process.
H. C. Wood and Henry F. Formad, in Supplement 7 of the _National Board
of Health Bulletin_ (1880), declare it altogether improbable that
bacteria have any direct function in diphtheria--_i.e._ that they
enter the system as bacteria and develop as such in the system, and
cause the symptoms. It is, however, possible that they may act upon
the exudations of the trachea as the yeast-plant acts upon sugar, and
cause the production of a septic poison which differs from that of
ordinary putrefaction, and bears such relations to the system as to,
when absorbed, cause the systemic symptoms of diphtheria. Now, these
bacteria may be always in the air, but not in sufficient quantities to
cause tracheitis, but enough when lodged in the membrane to set up the
peculiar fermentation; whilst during an epidemic they may be
sufficiently numerous to incite an inflammation in a previously
healthy throat.
The same authors publish a number of other experiments and conclusions
in Suppl. 17 (Jan., 1882): "There is no proof as yet that the
micrococci are the cause of the disease. Their presence in the exposed
dead tissue is no evidence, for the membrane represents but the
necrotic mucous lining.... Indeed, when the healthy mucous membrane of
the mouth or trachea is destroyed by caustics--for instance,
ammonia--the eschar into which it is converted--really a
pseudo-membrane--contains the same micrococci as are found in true
diphtheria, as Wood and Formad have learned. Moreover, in the
scrapings of the healthy tongue the same micrococci can be seen. Of
more significance is the detection of the same or similar micrococci
in the blood of the living patients during severe attacks. But since
these parasites were found only in the more severe cases, and not in
all instances of the disease, were seen also {666} in the blood of
other septic disorders, and since no cultures have been made with the
fresh blood, there is not yet enough evidence for any decision. In the
internal organs bacteria are not found with any regularity in
diphtheria."[6]
[Footnote 6: H. Gradle, _Bacteria and the Germ Theory of Disease_,
Chicago, 1883, p. 186.]
O. Heubner, while studying both the local affection and the general
infection of diphtheria, availed himself of the methods of Cohnheim
and Litten, who produced diphtheritic deposits by cutting off the
circulation of the blood. He ligated the neck of the bladder in
rabbits for two hours. On the first day he noticed a hemorrhagic
oedema of the mucous membrane, with loosened and tumefied epithelium;
on the second a firm and coagulated exudation took the place of the
normal tissue; on the third there were genuine diphtheritic spots in
the mucous membrane. The newly-formed pseudo-membrane exhibited all
the morphological elements of human diphtheria (genuine or
scarlatinous) and epidemic dysentery.[7] Thus Heubner's results agree
with the definition of diphtheria as the compound of severe
inflammation and necrosis. The inoculation of his diphtheritic
artefacts he found sterile. Animals, however, which were inoculated
with diphtheritic masses taken from the diseased human patient fell
sick with tumor of the spleen, hemorrhages, and general sepsis,
besides a local diphtheritic affection. Scarlatinal diphtheria used
for the same purpose had the same effect. Bacilli were developed, but
they were not found in the blood-vessels (differing in that respect
from the bacilli of anthrax), in spite of continued examination. Thus,
Heubner refuses to accept the bacilli as the diphtheritic poison; they
are, in his opinion, the result of the morbid process, and not its
cause. Thus, though he believes the diphtheria poison to be organic,
he concludes that its nature is not yet explained; contrary to the
assertions of many prolific prophets of the bacteria literature, who
now and then claim for this year's microscopic revelations the same
infallibility which was claimed for last year's opposite views.[8]
[Footnote 7: _Die Experimentelle Diphtherie_, Leipzig, 1883.]
[Footnote 8: L. Letzerich recognized in former years the specific
parasites of diphtheria, whooping cough, and typhoid fever as if they
were labelled. Then, again (_Arch. f. Experim. Pathol. u.
Pharmacol._), he admitted the great difficulty in discriminating the
specific schizomycetae of diphtheria, croupous pneumonia, epidemic
influenza, and typhoid fever.]
E. Rindfleisch[9] expresses himself as follows: "The microphytes of
diphtheria, septicaemia, and pyaemia have not been isolated and
cultivated as yet. But experimenters are convinced that there are a
great many species of microphytes underlying genuine putrefaction. In
producing septicaemic conditions in animals their efficacy differs.
Not every animal is influenced by the same microphyte. Thus it becomes
probable that the human organism is endangered by a certain number of
the putrefaction microphytes. Some one may have a particular
predilection for granulating wounds and mucous membranes, and thereby
produce a diphtheritic inflammation. Another may enter the blood from
a recent wound and give rise to a septicaemic fever with rapidly fatal
termination. The third may invade the body by means of a phlegmonous
inflammation, purulent infiltration, thrombosis, embolism, and
metastatic abscesses, accompanied with a pyaemic fever of a remittent
type."
[Footnote 9: _Die Elemente der Pathologie_, Leipzig, 1883, p. 301.]
After all, it does not appear to me that the bacteria question has
come {667} any nearer its solution in the last few years, in spite of
the most eager researches and the fact that some of the best medical
names in the world of medicine take the parasitic nature of diphtheria
for granted. For instance, in the second Congress for Internal
Medicine (Wiesbaden, 1883) C. Gerhardt rises in its favor. He makes
the statement, or rather admits, that several parasites have been
found by different men, that every one considers his the genuine one,
that several writers assume that there are several diphtheria
parasites, and suggests that, in his opinion, the disease may be
produced by different varieties of bacteria. At the same time, he
contends that the essence of the disease consists in the erosion (and
change) of the epithelium and the emigration of leucocytes. If that be
the case, I understand less than ever why diphtheria is, or is to be
called, a parasitic disease.
Panum's words seem still to be the soundest expression of all our
knowledge on the subject when he says: "It is a matter of rejoicing
that physicians have come to the conclusion that certain microscopic
organisms, be they considered vegetable or animal, and designated as
bacteria, fungi, monads, micrococci, or vibriones, do not exist merely
in the minds of theorists as causes of disease, but are in reality
enemies that must be combated with all the known efficient weapons in
our possession. But, while thus rejoicing, it must be borne in mind
that we have but a feeble insight into the relation between these
organisms and diseases, and in order to effect that much-desired
advance in scientific knowledge--a matter of considerable importance
in the practice of medicine--it is necessary not only to grasp at
isolated data, but carefully and deliberately to observe and study all
the facts before us, and even to devote some attention to those which
would tend to prove that there are bacteria and fungi which, under
certain circumstances, are perfectly harmless, and that even some of
the malignant ones among them do not commit all those outrages with
which they are charged, directly and personally."
SYMPTOMS.--In the majority of cases the disease has a prodromal stage,
which usually lasts a day or two, and may run a similar course to that
of a catarrhal pharyngitis. The patient feels somewhat indisposed, has
slight fever, is dejected, complains of painful deglutition, more
marked when swallowing fluids than solids or semi-solids, has headache
and occasionally vomiting. The occurrence of the latter, however, is
very much less frequent than in the outbreak of scarlatina. In very
severe cases convulsions have been observed, chills very rarely;
elevations of temperature of from 102.5 degrees to 104 degrees F. are
frequent; higher ones, from 105 degrees to 107 degrees, rare. At this
time it is often difficult or impossible to distinguish a catarrhal
angina from a diphtheritic by the subjective symptoms. Slight
glandular swellings under the jaw may occur in either. The
characteristic objective symptom of the latter disease is the presence
of membrane on the reddened mucous membrane of the fauces, which,
usually, is markedly injected over all or part of the surface. The
arches of the palate and the tonsils, less frequently the posterior
wall of the pharynx, are so affected. A distinctly localized redness
cannot be but either traumatic or diphtheritic. Larger or smaller
deposits are found thereon, lying loose on the surface or deeply
imbedded according to the locality. At times the first examination
reveals their presence in large numbers; at other times but a single
one can be {668} detected, which is soon followed by others, however.
Within a certain period of time, as a rule twenty to twenty-four
hours, the single deposits coalesce and form a membrane of greater or
less extent. Mostly in the same proportion to its increase in size it
increases in thickness. On the uvula, soft palate, and the posterior
wall of the pharynx the membrane is located superficially, and at
times can be easily removed; on the tonsils it has a firmer hold, and
is usually amalgamated with their uppermost tissues. On the other
hand, there are cases in which no actual membranous formation is
observed; in such cases the tissues are more or less swollen, the
surrounding portions more or less reddened, and the grayish-white
discoloration is the result of an infiltration of the tissues
themselves, and cannot be removed.
There are still other cases in which deposits of membrane and tissue
infiltration are found at the same time, and where both history and
evidence indicate that these two phenomena are the result of one and
the same process. When the uvula takes part in the process the
swelling is, as a rule, more marked than when the remaining parts of
the fauces only are implicated. Its circumference is very
considerable, and amounts sometimes to the treble or quadruple of the
normal, in consequence of the oedematous condition of the entire
tissue.
We have to deal, then, with three different manifestations of the
diphtheritic process: first, with a membrane lying on the mucous
membrane, and removable without causing much injury to the epithelium
or any to the basement membrane; such membranes were given by some the
name of croupous deposits; secondly, with a membrane implicating the
epithelium and upper layers of the mucous membrane; to this the title
of diphtheritic membrane has been given by preference; thirdly, with a
whitish or grayish infiltration of the surface and the deeper tissue,
which, if abundant, may give rise to a necrotic destruction of the
tissue.
The severity of the disease does not always depend on the predominance
of one of these three forms, for any of them may accompany a mild or a
severe attack. By a severe attack we understand one attended with
chills, temperatures as high as 105 degrees and 107 degrees F., and
marked nervous symptoms, such as vomiting and convulsions. It is
characteristic of such cases that when the membrane is accidentally or
forcibly removed it is speedily reproduced; the lymphatic system, in
addition, takes an active part in the process. The neighboring glands
become swollen; the periglandular tissue does likewise, so that the
circumference of the neck becomes enormous, and the space between the
lower jaw and the clavicle appears one immense tumefaction. These are
the cases in which, as a rule, loss of strength and general debility
speedily ensue, and death occurs from exhaustion. The membrane in
cases of this description frequently undergoes changes in appearance;
under the influence of the atmosphere and of foreign substances, and
by admixture of blood, its color becomes yellowish or brownish. The
odor of the membrane and surrounding parts becomes sweetish and musty,
and occasionally so fetid that it contaminates the atmosphere of the
room, and the air in its transit through the nose and over the pharynx
becomes by inhalation dangerous to the patient. His throat becomes
more swollen, his respiration loud; he keeps his mouth open
constantly, has an indifferent expression; the saliva dribbles
continually, the color of the skin is sallow and livid, the {669}
appetite very poor, and pulse both frequent and small. When the
symptoms are of long duration, and a deep infiltration of the affected
parts occurs, hemorrhages not infrequently make their appearance.
These may be slight although frequent; occasionally, however, larger
blood-vessels are encroached upon in the process of destruction, and
dangerous, nay even fatal, hemorrhages may be the result. The septic
forms which I have here described are more dangerous than the mild
ones previously mentioned. Still, even in the latter bad results may
ensue from a direct absorption into the blood of putrid substances and
by the penetration of fetid gases to the lungs.
Occasionally, where the infiltration has been extensive, we meet with
a condition that can only be considered as gangrene. In such cases we
see collections of a grayish pulpy mass, which on falling off leaves a
considerable loss of tissue, the further course of the disease being
either favorable, or dangerous through absorption of septic material,
or accompanied by local hemorrhages. When, after a time, health is
completely restored, marked cicatrices are left behind. Such loss of
tissue is generally seen in the tonsils only, but it may also be
encountered in the soft palate. Its cicatrices on the soft palate are
always a source of inconvenience, partly in swallowing, partly in
speaking. Actual local perforation of the soft palate I have seen but
five times in twenty-five years, sloughing without perforation very
often.
The diphtheritic membrane not infrequently spreads from the pharynx to
the neighboring organs. From the posterior aspect of the soft palate
or pharynx the disease gradually ascends to the nasal cavities; this
is particularly apt to occur when the uvula is the seat of extensive
deposits, and by forced inspiration and deglutition its posterior
surface becomes affected. In such cases the membrane which extends
thence to the nasal cavities is very dense, and capable of narrowing
the capacity of the nasal cavities anteriorly, and occasionally even
to close them entirely; as a rule, however, several days elapse before
the membrane assumes such a condition. Usually, when this form of
nasal diphtheria is in its incipient stage, it is impossible to
diagnosticate it; the most important sign thereof, besides a more
nasal articulation and sometimes greater difficulty in deglutition,
and the result of close ocular examination while the uvula is turned
sideways or drawn forward, is a swelling of the deep facial glands at
the angle of the lower jaw; when these swell rapidly it can be
asserted positively that the nasal cavities have been invaded. There
is little or no discharge from the nostrils under these circumstances.
The picture is a very different one, however, when the nose becomes
primarily affected. This usually occurs only where an acute catarrh
with but little secretion, not so often where a chronic catarrh, has
preceded infection. When the secretion is thin and serous, the
diphtheritic infection renders it no thicker, but makes it slightly
flocculent, and it may become very profuse. This form is frequently
attended with a disagreeable odor, equally unpleasant to the patient
and to those around him. During the prevalence of an epidemic one must
always be prepared to see an acute nasal catarrh or an influenza, or
even a chronic nasal catarrh, become complicated with diphtheria or
pass into it. Schuller reports the case of a five-weeks-old male child
who, having had a nasal catarrh since birth, became affected with
diphtheria of the nose. The glandular {670} swelling of which I spoke
above is a very important diagnostic, and likewise a decidedly
unpleasant symptom, which becomes very marked inside of twenty-four
hours; frequently a partial swelling remains long after the
disappearance of the diphtheritic membrane. Such glands rarely
suppurate or undergo a necrotic degeneration; sometimes they become
permanently indurated. This induration and a chronic pharyngeal and
nasal catarrh are very serious matters in many instances. Both of
these conditions are starting-points for a number of acute or subacute
attacks of diphtheria in the same person. It is they which constitute
the liability of persons once affected to be taken sick again. Not
only are they liable to be affected themselves, but they are a
constant danger to all around them. Diphtheria, in a large family of
children living in one of the best houses of the city, after having
returned half a dozen times in the course of a year, disappeared
instantaneously, not to return, when a seamstress living in an
infected neighborhood and suffering from occasional sore throats was
relieved of her daily work in the house. Oedematous swelling of the
mucous membrane and submucous tissue is often observed for a long
period to come; elongated uvulae, enlarged tonsils, often date back to
such an acute attack. Thus it is with the upper portion of the larynx
about the posterior insertion of the vocal cords (see below); its
large amount of loose submucous tissue is liable to swell considerably
in acute attacks. Frequent spells of croupy cough and a certain degree
of dyspnoea are often observed for years afterward. Though the cases
of genuine cicatrization between the arytenoid cartilages, as
described by Michael,[10] be rare, with their result of permanent
paresis of the thyroarytenoid interni muscles, when they do occur they
are either obstinate or altogether incurable.
[Footnote 10: _Deutsch. Arch. f. klin. Med._, 1879, xxiv. p. 618.]
Diphtheritic conjunctivitis occurs either primarily or as a
complication of pharyngeal or nasal diphtheria. Fortunately, it is not
of frequent occurrence; the cornea may become destroyed either by
pressure through the considerable swelling of the eyelid or by
diphtheritic keratitis. Usually the upper eyelid is the first to
suffer; it is red, rigid, swollen. In the beginning the conjunctiva
palpebrae is smooth, dry and pale, while that of the eye is chemosed;
afterward diphtheritic deposits take place either in floccules or in
solid masses. Knapp distinguishes between croup and diphtheria of the
eyelid according to the facility or impossibility of removing the
deposit. In favorable cases the membranes begin to macerate and the
eyelids to soften after a few days. In those less favorable
perforation of the cornea, prolapse of the iris, or total destruction
of the eye take place.
The ear is but rarely the primary seat of diphtheria. A girl of three
years died of laryngeal diphtheria on Sept. 6, 1882, after an illness
of four days. A girl of seven years was removed from the house on
Sept. 6th and returned on Sept. 8th. On the afternoon of the 10th an
earring taken from the corpse was attached to the left ear of the
sister, after having been washed with soap and water only. About noon
on the 11th the lobe of the left ear reddened, on the 12th it
exhibited a membrane and became swollen, and some glands enlarged in
the neighborhood. On the right mastoid process the skin was not quite
healthy, a vesicatory having been applied three weeks previously. This
surface became {671} diphtheritic on the 12th, without consecutive
glandular swelling. On the 13th the membranes grew thicker; on the
14th the pharynx was also affected, and the physician called in.
Most diphtheritic affections of the ear, however, are secondary. In
pharyngeal and nasal diphtheria the narrow orifice of the Eustachian
tube is easily obstructed by either catarrhal swelling or diphtheritic
deposit. The disease may invade the middle ear and the drum membrane
with perforation, caries, and deafness following.
The descent of the diphtheritic process into the respiratory organs
may give rise to various conditions. The membrane is not always found
to pass uninterruptedly from the mucous membrane of the fauces into
the larynx; not infrequently isolated diphtheritic spots are found in
the pouches on either side of the attached extremity of the
epiglottis, or on the epiglottis, or in the larynx. At such times the
epiglottis is moderately swollen, its margins hard and reddened.
Occasionally the redness is interrupted by small diphtheritic
deposits, which may remain isolated for a considerable time, but
generally coalesce so as to coat the edges of the epiglottis with a
continuous membrane. As a rule, the upper surface of the epiglottis is
not completely covered by membrane, while only now and then
diphtheritic deposits are found on its under surface.
The subjective symptoms accompanying the affection of the epiglottis
are not always in direct proportion to the extent of the membranes.
Dyspnoea and hoarseness occasionally occur where the only abnormal
condition is a marked oedema at the entrance of the larynx,
particularly of the posterior wall near the arytenoid cartilages and
the attachment of the vocal cords. The oedematous condition causes a
functional paralysis of the vocal cords, together with marked dyspnoea
on inspiration. The difficulty of breathing may become so excessive
that the clinical diagnosis of croup is unquestionable, and
tracheotomy resorted to, while expiration is comparatively free and
the voice not markedly affected. Furthermore, cases occur in which
there is no marked oedema, but merely a general catarrh of the
epiglottis and larynx; here, too, the subjective symptoms of
hoarseness and dyspnoea may become severe and necessitate the
performance of tracheotomy. Still, bearing this in mind, I have on
several occasions refrained from performing this operation where I
judged that, aside from the diphtheria of the pharynx, I had to deal
with a moderate oedema of the glottis or a laryngeal catarrh.
Frequently, however, membranes form in the larynx in the same way as
in the pharynx or nose; then inspiration and expiration are equally
interfered with, and hoarseness is a more constant symptom than in the
above-mentioned cases. Fever and pain are not necessarily prominent
symptoms; in fact, they are frequently unimportant, but in proportion
as the degree of narrowing of the larynx increases the respiration
becomes more difficult, long-drawn, and loud.
It may happen that the trachea and bronchi may become affected,
although diphtheria of the fauces does not exist. This does not occur
as rarely as Henoch and Oertel seem to believe. They think that
diphtheritic tracheo-bronchitis is mistaken for the primary condition,
because the throat is not examined early enough.
Oertel is of the opinion that the membrane in the fauces is {672}
overlooked in such cases. Steiner,[11] too, asserts that "the tendency
of the times is to question, nay, rather to deny, the existence of
croup extending from below upward." Now, on the contrary, repeated
experience enables me to assert with positiveness that diphtheritic
tracheo-bronchitis may occur without an affection of the pharynx at
the same time. I do not deny that it may last for days without giving
rise to dangerous symptoms. I know it does. But when the process
reaches the larynx, the symptoms of suffocation become so urgent that
tracheotomy may be absolutely required at once, and, in spite of the
operation, death soon after occurs.
[Footnote 11: _Ziemssen's Handb._, iv., 1, 126.]
Of course these cases are exceptions; as a rule, laryngeal and
tracheal diphtheria result from a descent of the disease from the
fauces. More or less uncomplicated cases of primary laryngeal
diphtheria, or so-called sporadic membranous croup, were, however,
observed before the end of the sixth decade of this century. They were
then almost the only cases of diphtheria, and linked former epidemics
and the present one together.
Inflammatory affections of the lungs may occur at various times and in
various forms during an attack of diphtheria. That which appears after
tracheotomy is usually a broncho-pneumonia, and results from
rarefaction of the air in the respiratory passages during the period
of impeded respiration, with consequent collapse of pulmonary tissue
and dilatation of the blood-vessels, and hence a disturbance of the
circulation. It may not fully develop until after tracheotomy, and is
a frequent cause of death on the second or third day after the
operation. Now and then a case of lobular pneumonia will result from
the aspiration of pieces of membranes into the smallest bronchi. It
can be easily recognized when the trachea is opened, but previous to
the operation the auscultatory signs are of little or no value, being
masked by the laryngeal rales. Percussion is equally useless, for a
dulness may just as well indicate collapse of the lung as
infiltration. The second form of pneumonia associated with diphtheria
is from the beginning fibrinous in character. Here, too, auscultation
and percussion are of little assistance in establishing a diagnosis
when there is a laryngeal diphtheria at the same time, for the above
reasons. Where, however, the dulness on percussion is accompanied by
high fever, and the long-drawn inspiration is replaced by rapid
respiratory movements, the diagnosis of pneumonic complication is
justified.
Diphtheria of the mouth, as a primary affection, is not of very
frequent occurrence; not rarely, however, is it associated with
diphtheria of the fauces and nose, mainly when they have assumed a
septic or gangrenous character; it appears on cheeks, tongue, angles
of the mouth and gums, and, after the fetid discharges have excoriated
the skin, on the lips also. In all of these localities it appears less
in the form of an extensive, thick membrane than an infiltration of
the tissues. It is most apt to occur where, from the start, the mucous
membrane of the mouth was eroded or ulcerated. The ulcerated base of a
follicular stomatitis is very frequently the starting-point of a
general diphtheria of the mouth. It is always a disagreeable symptom,
points to a long duration of the whole process, and threatens septic
absorption.
The oesophagus and the cardiac portion of the stomach are the seat
{673} sometimes of very massive and extensive, mostly fibrinous
exudations, in typhoid fever, dysentery, cholera, measles, and
scarlatina, or after injuries following contact with mineral acids,
alkalies, corrosive sublimate, or antimony. When the normal tissue was
not injured I never saw any that were not superjacent and could not
easily be peeled off (croupous). In cases of extensive pharyngeal and
laryngeal diphtheria the upper part of the oesophagus is often covered
to a distance of half an inch or an inch with membrane, the lower part
of which is thinning out into a mere film. A case of local
diphtheritic deposit near the cardiac portions of the oesophagus, upon
the seat of a stricture, I have described in my _Treatise_, p. 83.
Actual diphtheria of the stomach is rare. So is that of the intestine,
which is much more liable to be affected in animals than in man. In
the cow intestinal diphtheria is frequent (Bollinger). In the
gall-bladder, resulting from the irritation produced by calculus, it
was seen by Weisserfels. The diphtheritic form of inflammation of the
human colon and rectum--dysentery--is frequent enough, but will be the
subject of discussion in another place. But, besides this, in the
lower portion of the small intestines and in the colon long, tough,
coherent membranes are sometimes found in the male and female (not in
the hysterical female only). As a rule they are not diphtheritic, but
consist mostly of nothing but mucus hardened and flattened down by
protracted compression. The few cases of intestinal diphtheria I have
met with gave rise to the usual symptoms of enteritis, and were
diagnosticated as such.
Wounds of all kinds are easily and rapidly infected by diphtheria; for
instance, vaginal abrasions and erosions of the external ear, tongue,
and corners of the mouth. Scarification or removal of part of the
tonsils is followed in half a day or a day by a deposit of
diphtheritic membrane on the wound. The wound caused by tracheotomy
becomes liable to be infected with diphtheria within twenty-four
hours. Leech-bites, skin denuded by vesicatories, removal of the
cuticle by scratching during cutaneous eruptions, all furnish a
resting-place for diphtheria in a short time. What Billroth has
described under the name of muco-salivary diphtheritis, as it occurs
after the extirpation of a large portion of the tongue and resection
of the lower jaw, belongs to this class.
At times immediately at the beginning of an invasion of diphtheria, at
other times only on the second or third day, an erythematous eruption,
more or less general, appears on the skin. Now and then it appears on
the chest, shoulders, and back; at other times it covers the body, and
has not infrequently led to its being confounded with scarlatina. It
is not always accompanied by much fever, and cannot therefore be
mistaken for that form of erythema which frequently appears in
children with delicate skins during high fever from any source. I
cannot say that I have found this complication to give a more
malignant character to the disease, but true erysipelas does. I am not
prepared to prove that the two processes, erysipelas and diphtheria,
are identical under some circumstances, but the complication of the
two, and the ferocity with which they combine, renders a close
relationship probable. I have seen an infant dying from an erysipelas
added to a post-auricular diphtheria, this being due to a slight
abrasion of the surface. Erysipelas originating in the tracheotomy
wound, though ever so carefully disinfected and secured, is {674}
frequently observed after two or three days, and is a very ominous
symptom. Erysipelatous surfaces, denuded of their epidermis by
spontaneous vesication or injured by ever so slight a trauma, are very
liable to be covered with diphtheritic membranes.
An eruption resembling urticaria in the beginning is as innocent as
erythema, but purpura in the latter stage is a symptom of mostly
ominous nature.
On the vulva and vagina of little girls diphtheria is sometimes met
with; probably in every case it is due, under the epidemic influence,
to a local catarrh or erosion. In but few cases, comparatively, the
inguinal glands are swollen. There are not many cases of vaginal
diphtheria which are followed by the pharyngeal affection. Diphtheria
of the vagina in puerperal women is liable to become the cause of
general sepsis, and is a dangerous disease; it is seldom complicated,
but uterus, Fallopian tubes, and peritoneum may become the seat of
inflammatory and septic disturbances. In the bladder it may occur when
the urine is alkaline, in chronic cystitis, after lithotomy,
urethotomy, the operation for vesico-vaginal fistula, and in ectopia
vesicae. This form has a marked tendency toward localization, but by
extension of the phlegmon, when of putrid character, to the
retro-peritoneal cellular tissue, peritonitis may ensue and terminate
fatally. Sepsis from absorption is also frequent. Vesical diphtheria
is sometimes quite unsuspected. A man of sixty had urinary trouble a
long time; his urine was frequently very offensive, containing blood
and pus. About five days before his death he suddenly collapsed. I
found the bladder well filled, and introduced a catheter, but
succeeded in removing but a few drops of fetid liquid. Assuming the
presence of a malignant tumor at the neck of the bladder, I attempted
to draw off the urine by puncturing above the symphisis pubis; again
without success. At the post-mortem examination a thick membranous
lining of the bladder was found detached in the form of a sac
containing about a quart of urine. During life the beak of the
catheter evidently passed into the space between the bladder and the
membranous sac, which accounts for the unsuccessful attempts at
catheterization.
Diphtheria of the placenta was observed by Schuller. The membrane was
between uterus and placenta, and attached to the latter. It resulted
from puerperal sepsis. Balano-posthitis is liable to result in local
and general diphtheria; so are circumcision wounds. They are apt to
become affected either primarily, without apparent cause, or when
other members of the family are suffering from the disease.
The kidneys may become affected in various ways. Albuminuria is not
always of significance, as it occurs in severe and mild cases alike,
both before and after tracheotomy, and therefore is not connected
always either with the height of the fever or the degree of dyspnoea;
at times it disappears in a few days, in other cases it is of longer
duration. It is not invariably complicated with changes in the kidney,
neither do we always discover casts or degenerated epithelial cells in
the urine. In other respects also it does not behave like albuminuria
in scarlatina. In the latter it appears seldom before the second week
of the process, and frequently later, while in diphtheria it is often
seen early. It sometimes lasts but a few days, particularly in many
cases which set in with a high fever, which rapidly diminishes, and
terminates in speedy recovery. In {675} these occurrences the presence
of albumen appears to attend the rapid elimination of the poison.
Albuminuria seldom lasts longer than a week, and is not often
complicated with oedema, but sometimes it is but a symptom of a local
or general nephritis, and then hyaline, epithelial, and fibrin casts
and granular cells are found in the urine. Nephritis then assumes as
serious a character as it possesses in scarlatina. Cases of nephritis,
fortunately rare in a very early period of diphtheria, are liable to
run a rapid and often fatal course.
The heart and blood are affected in various ways by the diphtheritic
process. Where the disease runs a slow course, accompanied by high
fever, a granular degeneration occurs, similar to that appearing in
other acute infectious disorders--typhoid, for example. In diphtheria,
however, it would seem that this condition may arise even without
marked elevation of temperature. The pathological changes in the heart
produced by diphtheria are not always the same. Ecchymoses, cellular
hypertrophy, and granular degeneration have frequently been noticed
after death where the symptoms had been severe. The result, of course,
is considerable weakness of its muscular tissue, evidenced by the
formation of local (Beverly Robinson) thrombi, general sluggishness of
the circulation, dyspnoea, muffled heart-sounds, a cool and pale skin,
and sudden death, preceded by a very feeble and frequent, sometimes,
however, by a very slow, pulse. Aside from this, there is actual
endocarditis during the course of diphtheria or convalescence
therefrom. It affects especially the valves, and among them
particularly the mitral. It is characterized by high fever, precordial
pain, attacks of syncope, and a systolic murmur.
The rapid decrease of red blood-cells and a moderate increase of
leucocytes were demonstrated by Bouchut and Dubrisay, but the
disproportion was not such as to necessitate the diagnosis of
leucocythaemia. Wunderlich reports two cases of Hodgkin's disease, the
pseudo-leukaemia developing during diphtheria. And the slowness of
final recovery in many cases, even of but short duration and not
complicated with nervous disorders, appears to point to a serious
disintegration of the elements of the blood. The dark color and
defective coagulation of the blood in autopsies of diphtheria cases
have often been remarked.
The direct and rapid introduction into the blood of a foreign
substance has amongst its earliest symptoms fever. This reaction of a
nervous system depends both on the quantity and quality of the
substance or poison introduced, and on the susceptibility of the
patient. High temperatures are, however, not the only, nor are they
the most dangerous, nervous symptoms. To the latter belong the
different shades of paralysis met with during or subsequent to
diphtheria.
Sudden and unexpected collapse is sometimes observed, not infrequently
in the earlier part of the disease. The changes found in autopsies,
such as a dark color of the blood, deficient coagulability,
extravasations into and friability and granular degenerations of the
tissues, accumulations of degenerated cells, and granules between the
fibres, degeneration mainly of the heart-muscle, the presence of
heart-clots, thrombi in remote veins,--they all show to what extent
the disease can destroy life in the shortest time possible. In the
heart either the pneumogastric or the ganglionic {676} nerves may be
affected, and the symptoms will vary accordingly. Paralysis of the
former will accelerate the pulse, degeneration of the sympathetic will
diminish its frequency, yet death may ensue in either.
The usual form of diphtheritic paralysis makes its appearance during
the period of convalescence, at a time when all danger seems to have
passed by. As a rule, the soft palate and the muscles of deglutition
are the first to be attacked, while the condition of these organs is
apparently normal (and no longer oedematous, and thereby inactive, as
in the first period of the disease). While they are recovering, or
before, the accommodation muscles of the eyes become paralyzed.
Sometimes, however, these are the first to be affected. This paralysis
does not, as a rule, follow severe cases; on the contrary, it is not
uncommon to observe it after apparently mild attacks of the disease.
In consequence of the former paralysis, deglutition becomes difficult;
fluids are expelled through the nose or enter the larynx and bronchi,
thereby giving rise to pneumonia; in the latter there is strabismus.
The upper and lower extremities become paralyzed afterward. As a rule,
a number of muscles are affected at the same time, and improvement
will take place in about the same order in which the individual
muscles became affected. After paralysis has become affected,
circulation begins to suffer. The extremities now and then become
bluish, cool, emaciated; rarely atrophy and fatty degeneration have
been observed. The muscles of the neck also become paralyzed; the head
cannot be carried, or with difficulty only. The fingers are but seldom
affected. The same holds good of the bladder and intestines. The
respiratory muscles are not frequently attacked. Their paralysis is
very ominous, and may prove fatal in a short time from apnoea.
Not only motory but sensory paralyses may occur. Anaesthesia,
amaurosis, deafness have been observed; a number of cases of locomotor
ataxia are on record, and but lately Hadthagen[12] publishes a case
which he claims as disseminated sclerosis.
[Footnote 12: _Arch. f. Kinderheilk._, vol. v., 1883.]
Sometimes the nervous affection in diphtheria is localized in a
peculiar manner; it seems as if there is a predisposition on the part
of a certain nerve to become diseased. The case of a boy, active and
healthy, in the practice of H. Guleke, is very interesting. In the
course of three years he had three attacks of diphtheria. In the very
beginning of the disease he always became soporous with an almost
normal temperature and a slow but regular pulse. Probably the heart's
ganglia are the first to submit to the influence of the poison and
exhibit symptoms of flagging function. In most of the cases of
diphtheritic paralysis the prognosis is good; the large majority will
run a favorable course in from six to ten weeks.
INVASION.--Is diphtheria, primarily, a local or a constitutional
disease? Mercado's well-known case of diphtheria, engendered by the
biting of a finger, has been alluded to. I know of one case in which
the vagina became first affected, and later the pharynx. Bayles saw
denuded portions of skin assume a membranous character, and general
diphtheria develop afterward. Fresh wounds become diphtheritic, and
the general disease arises from this source. Even paralysis will
follow. I had a death from diphtheria when a long incision into a
phlegmon of the thigh had become diphtheritic. A little girl, who had
a considerable amount {677} of discharge from a catarrhal vagina, and
sore thighs in consequence, exhibited first, during the epidemic of
1877, membranes on the denuded cutis, and afterward general
diphtheria. Brehm reports the case of a woman on whom he performed
colotomy. The wound became thoroughly diphtheritic and gangrenous, but
the pharynx and respiratory organs remained intact. A few days after,
her daughter, who attended her in her sickness, was infected. In her
the pharynx was the seat of disorder. Besides, the tonsils are very
frequently coated with a membrane without any general symptoms in the
beginning, fever and general illness occurring only later on. Now, all
of these facts tend to show that there are cases in which the origin
of the disease is purely local.
It must, however, not be forgotten that during the prevalence of an
epidemic every one is more or less under its influence, and but little
is wanting to call forth the disease. Some years ago a well-known
physician, with whom I was intimately acquainted, died from facial
erysipelas and meningitis which had originated in a slight abrasion of
the upper lip. During an epidemic of typhoid we daily see persons with
fever, headache, and lassitude. Diarrhoeas are frequent during an
epidemic of cholera. An epidemic of diphtheria is accompanied by a
great number of cases of pharyngitis. When, in the year 1860,[13] I
reported two hundred cases of bona fide diphtheria, I at the same time
observed one hundred and eighty-five cases of non-membranous
inflammations of the throat. Such occurrences may be considered as
possible or incipient cases of pharyngeal diphtheria. Therefore,
contrary to the view of a local origin of diphtheria, it may be
claimed that the individual taking the disease was already saturated
with the poison, and the local membrane represented perhaps nothing
but a symptom, or at the utmost the causa proxima. Accordingly, then,
there are undoubtedly cases in which the pharyngeal membrane is the
first cause and symptom of the final affection, and others in which
the poisoning of the blood through inhalation is the first step in the
development of the disease, amongst the symptoms of which the
pharyngeal or nasal membrane counts as one.
[Footnote 13: _Amer. Med. Times._, Aug.]
In these cases the first complaints of the patients relate to their
general condition. Sometimes they are ignorant of any local trouble
when they consult a physician. When it is perceptible, however, it is
usually found on the visible pharyngeal and respiratory mucous
membranes. This would seem to indicate that the infectious elements
while being inhaled are there deposited. Thus there is a possibility
of simultaneous affections of both the throat and the blood in the
lungs, in either equal or variable proportions. We are easily led to
defend at least a partial admission of the poison by the respiratory
act, when we reflect that the membranes which are swallowed are
rendered innocuous by the action of the gastric fluids, and,
therefore, the alimentary canal, from the oesophagus downward, cannot
be made responsible for the admission of the poison into the system.
Thus it is that the general symptoms--as fever, lassitude,
etc.--precede the local phenomena in very many cases, while there are
exceptional cases in which the membrane appears first and the fever
later. This is especially the case when the tonsils are very large and
occupy a prominent position in the throat.
Those cases which begin with high fever and moderate or no local {678}
symptoms must be looked upon as constitutional diseases. If a person,
in the course of several hours or a day, be taken with high fever and
a moderate membrane-formation, these symptoms subsiding in one or two
days, leaving the patient weak and exhausted, but fully restored to
health at the end of a week, we would be justified in assuming
(caeteris paribus) that there was a rapid absorption of a large amount
of poison, and an equally rapid elimination thereof. They are,
moreover, the same cases in which the second or third day of the
disease furnishes albuminuria, with rapid elimination and speedy
recovery. When, however, the process is slow in developing,
accompanied by moderate fever, and the course is indolent, we have
reason to infer that moderate amounts of the poison are being
continually taken into the system and making their influence felt to a
moderate degree, but for a longer period. Such are the cases which,
without any violent symptoms, are accompanied by frequent local
relapses, or run, when the absorption is constant as well as copious,
a septic course, or terminate in paralysis.
Thus there are cases in which a local infection of the skin or of a
wound may be one of the causes, or the only cause, of the disease, and
there are cases in which the poison, in passing through and caught in
the pharynx, gives rise to local phenomena before the system at large
gives evidence of infection. But, as a general thing, diphtheria must
be looked upon as a constitutional disease, giving rise to local
phenomena, in the same way as scarlatina does on the skin, on the
mucous membrane of the alimentary canal, and in the uriniferous
tubules; measles on the skin and respiratory mucous membrane; or
typhoid in the lymph-follicles and on the mucous membrane of the
intestine; or, in other words, the diphtheritic poison may enter the
system locally through a defective, or sore, or wounded integument or
through the lungs.
Is diphtheria contagious? Undoubtedly it is. The contagious element is
liable to be directly communicated by the patient; it also clings to
solid and semi-solid bodies, and in this way is transmitted even after
a long time. There is hardly any disease which can cling so
tenaciously to dwellings and furniture; it can be transported by the
air, though probably not to a great distance, and hence in houses
artificially heated, while the windows and doors are mostly closed,
rises from the lower to the upper stories; and it is for this reason
advisable to keep the sick on the top floor. It is certainly
transmitted by spoons, glasses, handkerchiefs, and towels used by the
patient. The contagious character increases directly in proportion to
the neglect of proper ventilation. That it is spread by the feces is
not clearly established in my mind. I can give personally no examples
of its being carried by visitors or by the attending physician; this
is said to have occurred, however. The character of the disease
communicated, and the local manifestation, do not depend on that of
the original sufferer; thus mild cases may produce severe ones, and
vice versa, and convalescents can convey the disease in its full
force. Naturally, the softer character of the tissues in children
renders them more susceptible to infection, and the activity of their
lymphatic system more liable to severe forms of the disease.
Many tragic cases are recorded in literature of infection by direct
contact from pharynx to pharynx, or from the opening in the trachea to
the mouth of the surgeon; and one of the saddest cases, perhaps, is
that of {679} the much-lamented Carl Otto Weber. Myself and others
have contracted diphtheria from sucking tracheotomy wounds.
In regard to the length of the incubation periods, there can be no
better authenticated facts than those contained in a report of Elisha
Harris to the National Board of Health, an abstract of which is found
in No. 1, _National Board of Health Bulletin_, June 28, 1879. The
report says that in the fourth school district of the township of
Newark (Northern Vermont), amidst the steep hills where reside a quiet
people in comfortable dwellings, the summer term of school opened on
the 12th of May. Among the twenty-two little children who assembled in
the school-room in the glen were two who had suffered from a mild
attack of diphtheria in April, and one of them was, at the time school
opened, suffering badly from what appeared to have been a relapse in
the form of diphtheritic ophthalmia. Besides, it is proved that these
recently sick pupils had not been well cleansed, one of them having on
an unwashed garment that she had worn in all her sickness three weeks
previously. At the end of the third day of school several of the
children were complaining of sore throat, headache, and dizziness, and
on the fourth day and evening so many were sick in the same way that
the teacher and officers announced the school temporarily closed. By
the end of the sixth day from school opening, sixteen of the
twenty-two previously healthy children became seriously sick with
symptoms of malignant diphtheria, and some were already dying. The
teacher and six of the pupils were not attacked, nor have they since
suffered from the disease.
A case[14] is reported of a surgeon who, while attending a
diphtheritic child, had some secretion thrown into his face. Twelve
hours after his right eye was inflamed and painful. The affection
proved diphtheritic, and recovery was completed after several weeks
only. In a case seen by me, with Dr. L. Bopp, a child removed from a
house infected with diphtheria was attacked after fourteen days and
eight hours.
[Footnote 14: _Wurt. Med. Corresp. Bl._, 1878, No. 2.]
It would then appear that, in the direct communication of the disease
to healthy or nearly healthy mucous membranes--as healthy as the
prevailing epidemic will allow--the period of incubation is from one
or two to fourteen days. In only a small number of cases the disease
has an even shorter period of incubation than this, as when
tonsillotomy or a similar operation is undertaken during the
prevalence of an epidemic. One may rest assured that any operation on
the tonsils while an epidemic of diphtheria is at its height will be
followed within twenty-four hours by diphtheritic deposits on the
wounded part. To what extent we are justified in considering this a
bona-fide incubation of the disease in a previously healthy body is,
of course, another question. It seems to me that these cases
positively prove that the operation is only the causa proxima of a
diphtheritic affection, and that we may take it for granted that
during an epidemic every individual is more or less under its
influence and affected by it, so that it needs but a wound or an
accidental abrasion of the surface of the mucous membrane to call the
disease into action. In a similar way, fresh wounds or morbid
conditions of the mouth may call forth the disease. The ruptured
vesicles of a follicular stomatitis are liable to serve as
resting-places for diphtheritic membranes, and thus I have seen the
complication of a follicular stomatitis with oral diphtheria; and any
{680} lacerations of the vagina during labor may become diphtheritic
within twenty-four hours. If now, on the one hand, incubation depends
on the condition of the affected surface, it is probable, on the other
hand, that the intensity of the poison at the time plays an important
part in determining the period that is to elapse between infection and
the invasion of the disease.
ETIOLOGY.--Diphtheria is pre-eminently a disease of early life; in
this respect it is said to differ from the genuine fibrinous
bronchitis, which by some is held an absolutely different disease, and
stated to occur but rarely in children. But even this statement is
probably incorrect. In the spring of 1879 I met with four cases of
fibrinous bronchitis in children under three years of age. The number
of cases of diphtheria in adult life is not very large, while in old
age it is very small. Of 501 deaths in Vienna in 1868, only 1 had
reached the age of sixty-two; of more than 300 cases in which I
performed tracheotomy but 2 were over thirteen years old.
I do not know that sex exerts any predisposing influence over
diphtheria, yet of the six hundred cases or thereabouts of laryngeal
diphtheria in which I either personally performed tracheotomy or
observed the progress of the disease in the practice of others, I
found the majority in males, and the recoveries in inverse proportion
to the number thereof, the mortality being greater among boys. As far
as age is concerned, nearly all the zymotic diseases are seen most
frequently in children. They exhibit a greater disposition to submit
to diphtheria than adults, if we except those under ten months. Where,
however, the disease has occurred previous to the seventh or eighth
month, the greater number of cases has been found under three months.
Tigri reports the disease in a child of fourteen days. A child of
fifteen days was seen with diphtheritic laryngitis and oesophagitis by
Bretonneau, one of seventeen days by Bednar, one of eight by Bouchut,
one of seven days by Weikert; Parrot mentions several cases, and
Siredey[15] reports eighteen cases of diphtheria in the newly-born.
They occurred in the Hospital Lariboisiere in the spring of 1877, and
were probably infected by the nurses of a neighboring children's
asylum. Membranes were found on the soft palate, tonsils, or larynx,
and also on both pharynx and larynx. One case occurred where the
posterior nares alone were affected. I have met with four cases of
diphtheria of the pharynx and larynx in the newly-born myself. One of
these became sick on the ninth day after birth, and died on the
thirteenth day; the other died on the sixteenth day after birth; the
third was taken when seven days old, and died on the ninth day. The
predisposition to diphtheria during childhood[16] seems to be
explainable by several circumstances. The mucous membrane of the mouth
and pharynx in the child is more succulent and softer, and frequently
the seat of a congestive and inflammatory process. The nasal cavities
are small and frequently affected by catarrhs, the buccal cavity often
the seat of catarrh and of stomatitis, and insufficient cleanliness
leads here to irritation of the mucous membrane. Any abnormal state of
the mucous membrane, with {681} the exception of an atrophic condition
and cicatricial changes, affords an excellent abode for diphtheria.
The tonsils are proportionally large; in fact, we rarely see the
tonsils in children completely sheltered by the arches of the palate.
On the other hand, the pharynx is anything but spacious, and while the
protuberant condition of the tonsils affords a resting-place for the
invading disease, the remaining space is so small that it becomes a
source of uneasiness to the well in many instances, and very much more
than that to the child during diphtheritic tumefaction. Furthermore,
we must take into consideration the large number and size of the
lymphatics, which can be more easily injected in the child than in the
adult, according to Sappey, and the fact of greater intercommunication
amongst the lymphatics and between them and the system; for S. L.
Schenck has found that the network of lymphatics in the skin of the
newly-born, at least, are endowed with stomata, loopholes through
which the lymph-ducts can communicate with the neighborhood, and vice
versa.[17] These circumstances, although they may have no influence in
calling the disease into existence, yet assist in its development and
in adding to the severity of the symptoms.
[Footnote 15: These, Paris, 1877.]
[Footnote 16: W. N. Thursfield (_London Lancet_, Aug. 3d, 10th, 17th,
1878) collects 10,000 cases of diphtheria in England between the years
1855 and 1877. Of these 90 per 1000 were under a year, 450 per 1000
from 1-5 years, 260 from 6-10, 90 from 11-15, 50 from 16-25, 35 from
26-45; 25 per 1000 were 45 years and over.]
[Footnote 17: _Mittheil. aus d. Embryol. Instit._, i., 1877.]
On the other hand, while the above reasons go to prove that diphtheria
attacks children by preference, there is again an anatomical and
physiological condition--to wit, the free slightly acid secretion of
the mouth, beginning with the third month--that acts as a hindrance to
the frequent occurrence of diphtheria after the third month. A poison
or poisonous product of whatever nature can less readily find a
hiding-place so long as it can be readily--we might always say must
surely be--washed away. During these months of eruptive secretion from
the mouth diphtheria, therefore, is not very frequent; thus teething,
in the case of diphtheria, cannot be held responsible by mothers fond
of diagnosticating dental diseases. In this connection the remark of
Krieger ought not to be overlooked, who explains the relative scarcity
of the disease in the first year of life by the fact that cumulative
influences will produce a great number of cases, and cumulation
requires time. Undoubtedly, however, an important etiological
consideration is the fact of having had the disease previously. We can
cite a host of zymotic diseases the occurrence of which once serves as
a protection against future attacks. Not only can no such security be
expected after one attack of diphtheria, but, caeteris paribus, the
disease shows a preference for those who have survived a previous
attack. The statement that only the mild cases, with but slight
elevation of temperature and freedom from severe constitutional
symptoms, are likely to suffer a relapse is founded on error. True, I
have more frequently seen relapses after mild cases--which,
fortunately, are in the majority--but the disease has also recurred
where originally high fever and an extensive lymphadenitis proved it
to be a severe case. Besides, second attacks of membranous croup are
also recorded (Guersant, N. F. Gill, Quincke).
As there are individuals, so there are families, which have a
predisposition to diseases, as there are others in whom,
notwithstanding ample exposure, infection does not easily take place.
Yet in the families in which diphtheria is of frequent occurrence it
cannot always be attributed to enlarged tonsils and a tendency to
pharyngeal or nasal catarrh.
{682} Still, catarrh and the vulnerability of mucous membranes must be
considered as a frequent source of diphtheria; children will get
numerous relapses often after a nasal or pharyngeal catarrh. Sudden
changes in the temperature of the atmosphere or of the surface of the
body are therefore dangerous in predisposed persons. And thus it is
that while severe epidemics have spared no climate or land known to
us, the majority of cases have occurred in winter and spring; in other
words, at a time when catarrhal disorders are of most frequent
occurrence. In my experience at New York, the first quarter of the
year yielded more cases than any other. Still, they are frequent
enough in warm seasons. Krieger insists upon the injurious influence
of hot summers and dry hot rooms. I do not doubt the correctness of
his views, which cannot but be strengthened by the damaging results of
our furnace-heating. But the influence of season on the invasion and
course of diphtheria is but indirect and conditional, and may be,
perhaps, after all, compared with that exerted by filth--a term which
is lately used to express all sorts and forms of nastiness, from
filthy bodies of men to their clothes, their habits, their food, and
the air they breathe, whether polluted by carbonic acid, by
excrementitious gases, or by exhalations of sewers.
Cases of diphtheria which are traced to exhalations from sewers (or
even to filthy habits of life) are very frequent. Yet typhoid is
attributed to the same causes. So is dysentery. Can, then, foul
exhalations produce alike diphtheria, typhoid, and dysentery? Do these
diseases arise from a common poison? Or is the poison of a treble
character, so that a part may give origin to diphtheria, another part
to typhoid, a third to dysentery?[18] Have we to deal, in such
occurrences, with specific influences, or only with a lowering of the
standard of health, thereby affording other morbid influences an
opportunity to exercise their power? These questions are still
involved in darkness, and constitute problems the solution of which
still engages the minds of both individual writers and authorities. A
report of the Board of Health of Massachusetts, closely adhering to
the results of exact observations,[19] leaves them doubtful, and the
affirmative reports of some modern writers do not bear scrutiny.[20]
[Footnote 18: In regard to the causal connection of the two latter
diseases with sewer exhalations we can be more positive than in regard
to the former.]
[Footnote 19: Author's _Treatise on Diphth._, p. 35.]
[Footnote 20: M. A. Avery, _Med. Jour. and Obst. Rev._, Feb., 1882.]
Air polluted by bad drainage or leaky sewers has been considered
responsible for diphtheria as well as for typhoid fever and dysentery.
Not only the impairment of general health, but the direct and
unmistakable disease, has been attributed to it. Thus Bayley refers,
in the endemic of Bromley,[21] the first cases to unventilated sewers
and cesspools. School-children multiplied the disease. Thursfield
attributes the diphtheria at Ellesmere[22] to the accumulation of
excrements under the school-room, and to deficient supply of water,
which, moreover, was of bad quality. Tripe (like Railton, Bailey,
Russell, Bell) accuses sewer gas;[23] others polluted waters or bad
drainage.[24] I have not been convinced, however, that diphtheria can
be considered a sewer-gas disease, in the same way as typhoid fever.
The deterioration of the general health resulting from the inhalation
of foul air is sufficient to explain the outbreak of the individual
attack during a prevailing epidemic.
[Footnote 21: _Sanit. Record_, Aug. 10, 1877.]
[Footnote 22: _San. Rec._, 158, 1877.]
[Footnote 23: _Ibid._, June 14, 1878.]
[Footnote 24: _Ibid._, April 18, May 2, 1879.]
{683} In regard to polluted water, I do not think that pathologists
who attribute infectious diseases to bacteria only are justified in
condemning it. It may not be so guilty, after all, for the admixtures,
inorganic and organic, minerals, admixtures of wood and plants, also
lower fungi and their products--algae, infusoria--would render water
rather disagreeable, but not exactly unhealthy. The latter effect can
be accomplished--always assuming the bacteria theory correct, for the
sake of argument--by bacteria only. But when they arrive in the
stomach, their doom is sealed; they are decomposed. The only places
where, possibly, they could take root would be diseased or ulcerated
places in either the oral cavity or the upper portion of the
oesophagus.
Not only water, but the milk of animals also, has been accused of
being the direct cause of diphtheria. Powers concludes, though a
connection between diphtheria and the consumption of milk have not
been proven as yet, that it is very probable indeed. His careful
investigations into the causes of some local epidemics in North London
exclude any other source from which the people could have been
affected. Perhaps one of the forms of garget, cow mammitis, is of an
infectious character. His reasoning, however, is not accepted by A.
Dowrus,[25] who still believes that the milk which gave rise to
diphtheria at a distance may have been soiled and infected. For though
the connection between milk and scarlatina and typhoid fever had been
known for years and variously studied, no observation of the kind had
yet been made in regard to diphtheria. Besides, where the young, in
England, drink much milk--viz. in the cities--diphtheria was very much
less frequent than where little or no milk was taken--viz. in the
country. Even in the country the well-to-do classes, who drink milk,
had but little diphtheria, while the children of the poor, who
obtained none, suffered a great deal from it.
[Footnote 25: "Diphtheria and Milk-Supply," _Brit. Med. Journ._, Feb.
1, 1879.]
In regard to this transmission of diphtheria by means of milk O.
Bollinger[26] hesitates to express any opinion, except that the matter
is very doubtful indeed. Probably the possibility of contracting
diphtheria directly from animals is very much greater than the danger
from water or milk. On a Pomeranian farm, during the winter 1875-76,
every newly-born calf died of diphtheria. The superintendent of the
farm and the woman who attended to the calves were taken with
diphtheritic angina.[27] Similar occurrences have been recorded.
Bollinger reports a mycotic disease of the trachea and lungs in birds.
[Footnote 26: _D. Z. f. Thiermed. u. vergleich. Pathol._, vi., 1879,
p. 7.]
[Footnote 27: Damman, in _D. Zeitsch. f. Thiermed._, 1876, p. 1.]
Friedberger's report,[28] presented to the Veterinary Society of
Munich, on croup and diphtheria of domestic fowls, leaves no doubt as
to its frequency, particularly amongst the nobler varieties.
[Footnote 28: _D. Zeitsch. f. Thiermed._, v., 1879, p. 16.]
Nicati[29] studied an epidemic diphtheria amongst hens which had
similar symptoms and a course very much like that in man; it could be
inoculated into other animals, and was contemporaneous with the
outbreak of the epidemic amongst the human population of Marseilles.
Trasbot[30] succeeded in inoculating a healthy hen from a diphtheritic
one, but the {684} attempts at transmission to dog, pig, and man were
unsuccessful. The _Med. and Surg. Journal_[31] contains the following:
In a house at Ogdensburg, N.Y., five children were ill with
diphtheria. Three kittens who had been playing with them from time to
time took the disease and died. Post-mortem examination showed
diphtheritic membranes in their throats.[32]
[Footnote 29: _Revue d'Hygiene et de Police sanitaire_, 1879, p. 3.]
[Footnote 30: "De la transmission de la Diphth. des Animaux a
l'Homme," _Gaz. hebdom._, 1879 Avril 25.]
[Footnote 31: _Med. Rec._, Nov. 8, 1879.]
[Footnote 32: An elaborate description of the croupo-diphtheritic
inflammations of mucous membranes in hens, turkeys, pheasants, and
pigeons may be found in _Zurn. Krankh. d. Hausgeflugels_, 1882, p.
104.]
Gerhardt[33] reports the following: 2600 hens were imported from
Verona, Italy, into a village, Messelhausen, in Baden. Some of these
hens were affected with diphtheria when they arrived. Within six weeks
600 of their number died of diphtheria, and 800 more soon after. In
the following summer 1000 chickens were raised by artificial breeding,
all of which died of diphtheria within six weeks. Five cats kept in
the place also died of diphtheria; a parrot fell sick with it, but
recovered. An Italian cook, suffering from diphtheria, in the month of
November, 1881, while being subjected to local treatment with carbolic
acid, bit the head-nurse's left foot and hand. Both these wounds
became diphtheritic, the man falling sick with high fever, and
requiring three weeks for his gradual recovery. Besides, four of the
six workingmen employed in taking care of the hens of the
establishment were taken with diphtheria. Not a single case, however,
occurred in the neighboring village. Thus, it is safe to assume that
the diphtheritic disease of hens can be transmitted to man.
[Footnote 33: _Verhandlungen des_ (ii.) _Congresses fur Innere
Medicin_, Wiesbaden, 1883, p. 129.]
Diphtheria may be also produced by outside influences. In this regard
the attempts at generating pseudo-membranes by artificial means are
very interesting indeed. As early as 1826, Bretonneau, by the
introduction of tincture of cantharides and olive oil into the
trachea, succeeded in producing a "dense, elastic, reed-like
membranous concretion." Delafond called croup into existence by the
use of ammonia, oxygen, chlorine, corrosive sublimate, arsenic, and
sulphuric acid. On the other hand, H. Mayer asserts that it is
impossible, by means of ammonia, to produce a croup in the windpipes
of animals which in the slightest degree resembles that occurring in
human beings. Trendelenburg, however, after producing membranes in the
trachea by the use of a solution of corrosive sublimate (1:120),
succeeded in hardening the entire mass with bichromate of potassium,
which it was impossible to do with the most tenacious mucus.
Rey observed croup in horses that inhaled smoke in a burning
stable.[34] In the collection of the veterinary school of Zurich there
is a croup membrane from a heifer which had been exposed to a fire; at
Munich, one from the trachea of a horse, produced by forcibly
injecting medicines into the nose. Hahn made an observation on cows,
W. Ammon on horses, of long croup membranes after the animals had been
exposed to smoke and fire; and Oertel constantly insists on there
being "no actual difference between croup as it ordinarily occurs and
that excited in the windpipe of a rabbit by means of ammonia. The
color and texture, the physical, chemical, and histological
characteristics, are identical."
[Footnote 34: _Journ. de med. vet. de Lyon_, 1850, p. 249.]
{685} MORBID ANATOMY.--Either the membrane or the granular
infiltration is characteristic of diphtheria. The statement that the
former occurs only when atmospheric air can gain access thereto, as A.
d'Espine and C. Picot still hold,[35] is plainly contradicted by its
appearance on the mucous membrane of the lower intestines. The
condition of the membrane is not unalterable, any more than the
clinical symptoms of the disease, for, according to different
circumstances, epithelium, mucus, blood, and vegetable parasites are
added thereto. The membrane can either be lifted from the mucous
membrane on which it lies or is imbedded into and underneath it. In
the first instance, it consists to a great extent of fibrin, the
result either of epithelial changes or derived directly from the
exuded blood-serum. E. Wagner, who makes no anatomical distinction
between croup and diphtheria, considers epithelial changes the
principal source. The pavement epithelium becomes altered in a
peculiar manner. It becomes turbid, larger, dentated, and dissolves
into a network; it is at first uninhabited, but serves later as the
vehicle of newly-formed cells; there also occurs a considerable
infiltration of the mucous membrane pus-cells and granules; besides,
the cellular tissue is studded with granules, the granular
degeneration resulting sometimes in necrotic destruction, which is
looked upon by Virchow as the most important element in severe forms
of diphtheria. The several conditions or degrees may occur independent
of each other, associated or in succession. Classen shares Wagner's
views, but, according to Boldygrew, the pseudo-membrane consists of
successive coagulations of a fibrinous fluid which exudes from the
diseased surface. Steudener also opposes the views of Wagner. He does
not believe in the probability of an exclusively endogenous origin of
the cellular elements of croup membrane; in fact, he doubts the
occurrence of an endogenous formation of pus-globules in epithelium.
Croupous membrane, according to him, is formed by the migration of
numerous white blood-globules through the walls of the vessels in the
mucous membrane, and by a direct formation of fibrin from the
transuded plasma. In addition to this, the mucous membrane is stripped
of its epithelium (except at the mouths of the acinous glands) and
infiltrated with migrating cells. Fresh croupous membrane consists of
a delicate network of homogeneous structure and shining appearance, in
which numerous cells and the epithelium of the various layers of the
trachea are imbedded. In old membranes the cells are destroyed by
granular degeneration and general maceration. Tenacious mucus with
pus-cells and detritus are then found. C. Weigert looks upon the
deposits as analogous to those on serous membranes. Every inflammation
yields an exudation which may coagulate when the coagulating ferment
is added. This latter is probably produced by the white blood-cells
when in disintegration. But he does not say why it is that there is no
such coagulation in suppurative processes, where the leucocytes are
more numerous. He believes himself justified in establishing
pathological differences of croup, pseudo-diphtheria, and diphtheria.
A croupous inflammation means destruction of epithelium, which gives
rise to a fibrinous exudation upon the surface, while the cellular
tissue remains intact. The only difference between it and the
pseudo-diphtheritic inflammation is looked for in the larger number of
emigrated white {686} blood-cells. The superficial deposit consists,
to a great part, of them and the fibrinous exudation. When there are
but few leucocytes the deposit is a network of fibrillae (croup). When
there are many, the masses are more solid and voluminous
(pseudo-diphtheritis). When, however, the tissue is changed into a
hard substance resembling coagulated fibrin, when the exudation does
not exist on the surface, but takes place into the mucous membrane,
the process is diphtheria. Zahn also establishes three varieties--viz.
1st, such as result from a peculiar degeneration of pavement
epithelium; 2d, such as originate in the solidification of a
muco-fibrinous, and, 3d, of a fibrino-purulent, exudation. Each of
these varieties may contain colonies of micrococci, but these
organisms are neither essential nor are they constantly found.
[Footnote 35: _Man. prat. des mal. de l'enfance_, 1877, p. 81.]
The diphtheritic process does not merely consist of the membranous
changes in the pharynx and air-passages. Its fatal cases have afforded
marked evidence of the implication of most of the organs. Reimer's 17
cases give the following post-mortem results: the lungs were
hyperaemic in 8 cases, twice the seat of pneumonia, and three times of
embolic infarctions; in addition, emphysema in 12, oedema in 6,
atelectasis in 7, subpleural ecchymoses in 7, pericardial ones in 4.
The heart-muscle had undergone fatty degeneration in 6, and was the
seat of ecchymoses of the size of a pin's head in 3. In addition to
frequent hyperaemic conditions of the abdominal viscera, emboli of the
liver in 3 (with capillary hemorrhages of the peritoneal covering in
1), emboli of the spleen in 5, desquamative nephritis in 7 (in 6 of
which there were colonies of micrococci in the uriniferous tubules),
cellular hyperplasia of the cervical and mediastinal glands in 14
(complicated in 6 with capillary hemorrhages in the glandular tissue).
The blood was frequently normal, very often watery and dark, at times
leucocythaemic. Thus the disease exerts its influence everywhere.
Rindfleisch defines diphtheritic inflammation as that form of
inflammation which produces a coagulating necrosis in the tissues by
the immigration of schizomycetae. The coagulating necrosis differs
from the usual form of necrosis in this, that the change from life to
death is accompanied with the coagulation of fluid albuminoids. This
process takes place mainly in the interior of cells and other parts of
tissues, and therein differs from the coagulation of fibrin. In the
cells there is taking place a peculiar homogenization of protoplasm;
at the same time the nuclei disappear, and are changed into irregular
masses liable to cohere and form membranous conglomerates, which owe
their peculiar wax color to the invasion of a solid albuminoid endowed
with a strong tendency to refract the light. Coagulating necrosis is
found in circumscribed localities, and gives rise, in the
neighborhood, to a marked amount of inflammation and suppuration,
which leads to the expulsion of the necrotic part, with more or less
loss of substance--either mild or phagedenic ulceration.
Leyden describes a gray degeneration of the muscular tissue which he
believes to be truly inflammatory, and Unruh has lately published an
account of some cases in which myocarditis occurred. In Leyden's
cases, the muscular nuclei were increased, became atrophied, and
underwent fatty degeneration, giving rise thereby to extravasations,
softening, dilatation and debility of the heart, with general
debility, collapse, {687} and--probably by reflex action on other
branches of the pneumogastric--vomiting. Micrococci he found neither
in the heart nor in the kidneys.
In the heart, particularly on the right side, numerous thrombi are
frequently found in various stages of development; its muscular tissue
is often in a state of fatty degeneration or the seat of
parenchymatous inflammation and hemorrhages. Bridges first called
attention to the occurrence of endocarditis in diphtheria.[36] This
complication, which, however, occurs more frequently with rheumatism,
puerperal fever, diphtheria of wounds, pyaemia, and old valvular
affections than in the course of an acute diphtheria, does not, as
found in the latter affection, consist simply of a fatty degeneration
and subsequent ulceration, but is considered a genuine diphtheritic
process (Virchow), affecting the mitral valve more frequently than the
tricuspid or pulmonary valves. It begins with hyperaemia and the
exudation of plasma in the cellular elements, so that they appear
larger and darker. The granulations which form are frail and easily
destroyed, so that ulcers form on which fibrin is deposited, and
whence it is conveyed as emboli into the terminal arteries (Cohnheim)
of the spleen, nerves, brain, and eye. Infarctions may also occur in
the valveless veins of these organs, giving rise rather to small
multiple abscesses than to large purulent collections. Suppuration but
rarely takes place in the heart; the granular mass found there resists
the action of aether and alcohol, and spreads throughout the cardiac
parenchyma, so that perforation of the septum and of the right auricle
and aorta has been observed.
[Footnote 36: _Med. Times and Gaz._, ii. p. 204.]
Bouchut and Labadie-Lagrave, out of 15 cases of diphtheria, met in 14
with a plastic endocarditis, which became the source of emboli. Thus,
there were infarctions of the lungs, at times in their centre
colorless, at other times in a state of purulent degeneration;
superficial thrombi of the small veins of the heart, subcutaneous
connective tissue, pia mater, brain, and liver; and in addition,
moderate leucocytosis.
The lungs exhibit (post-mortem) all sorts of inflammatory and
congestive conditions, with their consequences, as oedema, catarrh,
broncho-pneumonia, atelectasis, emphysema, ecchymoses, and large
infarctions.
The spleen (and occasionally the liver) is frequently large,
congested, and friable, and studded with infarctions to a greater or
less extent.
The kidneys are either simply congested or the seat of nephritis or
infarctions. The same forms of inflammation which accompany
scarlatina--to wit, the desquamative and the diffuse--are here
observed. The diffuse form is not of so frequent occurrence as in
scarlatina, but is sometimes extensive and dangerous.
The muscles occasionally exhibit ecchymoses, and are at times the seat
of parenchymatous inflammation, gray degeneration, and atrophy.
The lymphatic glands are frequently inflamed and swollen, either hard
or doughy, oedematous or congested. Large abscesses are rare. It is
more especially the gland tissue, and less the connective tissue of
the glands, which takes part in the pathological process. The
periglandular tissue very soon becomes involved, however. Necrotic
foci have been described by Bizzozero. When the entire surface of the
mucous membrane of the mouth and of the air-passages, from the nose to
the trachea, is the seat of the disease, there is an impregnation of
the mucous membrane, from the epithelial surface to the submucous
tissue, of the entire {688} tongue, borders of the lips, and
frequently of the lips and cheeks, as well as of the tonsils, the
lower portion of the nasal cavities and the upper, and especially the
anterior, portion of the larynx. The fossae Morgagni and the posterior
aspect of the soft palate are more frequently affected in the same way
than the anterior aspect. Small isolated spots are found on the
tonsils and occasionally on the posterior wall of the pharynx. The
so-called croupous form--that is to say, the one in which the
membranes deposited may either be removed in large patches or lie
macerated in the profuse secretion of subjacent mucous glands--is
found partly in the nasal cavities, on the posterior surface of the
soft palate, and also in the trachea and its subdivisions.
The character of the mucous membrane varies with the locality. Its
different elements, as the epithelium, the basement membrane, the
connective tissue mingled with elastic fibres, the blood-vessels, the
nerves from the cerebro-spinal and sympathetic systems, and the
papillae and ducts of numberless glands, all influence the
pathological process going on upon the surface. Their distribution in
the oral cavity and the respiratory organs is a very interesting
study, and in a table already published,[37] I have exhibited it in a
condensed tabular form.
[Footnote 37: _Treatise on Diphtheria_, p. 126.]
Where elastic tissue predominates, diphtheritic impregnation is slow
to take place, and recovery is also slow when the tissue has finally
submitted. Pavement epithelium yields the easiest foothold to
diphtheritic membrane. Thus it is that the tonsils, not from their
prominent situation alone, favor the reception and development of the
infection. But the elastic and connective fibres when once affected
are apt to harbor the disease a long time. Still, there is another
reason why the diphtheritic process should favor the tonsils. For Th.
Hohr has demonstrated that their epithelium exhibits interruptions in
its continuity. Through them round cells may emigrate. Wherever the
epithelial covering of the integuments (skin or mucous membrane) is
intact and unbroken, diphtheria takes hold with difficulty. But where
a defect is established, large or small, diphtheritic formations will
be apt to take place according to the size of the abrasion. This is
one of the modes of the formation of small diphtheritic deposits on
the tonsils, which it has been the tendency of many, both
practitioners and authors, to honor with special names.
Ciliated epithelium is not so liable to be affected. It occupies a
higher rank in the scale of animal formations, has a more complex
function and a greater power of resistance. The presence of a large
number of mucous glands impedes, as a rule, by the presence of the
normal secretion, an extensive destructive action upon the tissues.
The secreted mucus assists in removing epithelial masses, and even
fibrinous exudations, from the surface. Thus it is that the deposits
in the respiratory portion of the nasal cavities are frequently cast
off through the nostrils, and in a similar manner the membranes that
have formed in the trachea are ejected in a semi-solid condition
through the opening made by tracheotomy. The large number of mucous
glands in the larynx and trachea is unquestionably the reason why the
lymphatic vessels of the mucous membrane are not influenced by the
overlying loosened masses, and will not absorb; hence laryngeal and
tracheal diphtheria, when not complicated, have decidedly a local
character, and are usually devoid of constitutional symptoms. For the
{689} same reason the usual form of tonsillar diphtheria is a mild
disease. On the other hand, the large number and size of the lymphatic
ducts of the Schneiderian mucous membrane, as well as their direct
communication with the lymphatic glands of the neck, accounts for the
dangerous character of nasal diphtheria.
Diphtheria of the intestinal canal is characterized by fibrinous
deposits on the surface and in the tissues of the intestine, with
subsequent granular degeneration. It is mostly preceded by a catarrhal
process. The same condition is found in the urinary organs.
There are but few autopsies of cases which have died of, or during,
diphtheritic paralysis. In some instances there was considerable
thickening of the spinal nerves at the junction of the posterior and
anterior roots, with hemorrhages. The superficial connective tissue in
these places exhibited a diphtheritic exudation (Buhl). There was in
the sheath of the nerves of the cerebral and spinal meninges and in
the gray substance of the cord voluminous nuclear infiltration; in one
case there were extensive hemorrhages in the spinal meninges, with
nuclear proliferation in the gray substance of the cord (Oertel).
Disseminated meningitis with perineuritis of the neighboring roots,
characterized by infiltration of nuclei between the nerve-fibrillae
was found by Pierret; and degeneration of the palatine nerves and
fatty degeneration of the palatine muscles by Charcot and Vulpian.
Dejerine, in five autopsies, records an atrophy of the anterior roots
secondary to a myelitic degeneration of the ganglia of the anterior
horns. E. Gaucher found the same in the case of a boy who died with
paralysis of the muscles of deglutition, of the extremities, and of
the trunk. In a child of two years with paralysis of the palate and
extremities the autopsy was negative. In two cases Dejerine reports
finding changes in the intramuscular nerves, such as liquefaction of
myelin and loss of axis cylinders.
Thus, Buhl, Charcot, Vulpian, and Dejerine are unanimous about an
affection of the peripheric nerves and muscles. Oertel, Dejerine, and
Gaucher believe in a disease of the spinal cord. It is true that a
disease of the gray substance would fully explain the symptoms of the
bad cases, but what we know of poliomyelitis anterior, with which this
affection would be identical, precludes the idea of the rapid and
almost certain complete recovery. Therefore, in most cases,
diphtheritic paralysis consists of a trophic affection of the motor
system, almost always seated peripherally in the nerves and muscles,
seldom, if ever, in the centres. This affection must be compared, in
most of its relations, with the degenerative processes taking place in
the muscular tissue after typhoid fever, or in the renal epithelium
after infectious diseases, both of which give rise to serious results,
with usually a favorable termination.
DIAGNOSIS.--The characteristic sign of diphtheria is either the
membrane or the gray infiltration, with more or less injection of the
surrounding parts. In regard to this greater or less injection, I will
say that pharyngeal congestion, when it is uniform, may or may not
point to imminent diphtheria. When it is local, confined to one side
mainly, it is either traumatic or diphtheritic. White spots which are
easily washed away, or which can be removed with a brush, or squeezed
out of the follicles of the tonsils, into which a probe can be
introduced sometimes to the depth of one-half inch, soon announce
their true character--viz. either a {690} simple catarrhal secretion
or suppuration. Even though the superficial deposit contain oidium or
leptothrix in considerable numbers, it can easily be removed; I have
only known the totally inexperienced to mistake muguet (thrush) for
diphtheria. In the larynx muguet is, moreover, very rare indeed, and
always circumscribed. It is sometimes seen on the true vocal cords.
The gray discoloration of superficial follicular ulcerations, as
observed in the ordinary form of stomatitis follicularis, can hardly
fail to be recognized. Such patches are very numerous in the fauces
and on the lips and cheeks--never on the gums, except in ulcerous
stomatitis (which is not follicular). They are accompanied, too, by
vesicles containing more or less serum which have not yet ruptured. It
must be remembered, however, that the mucous membrane, when deprived
of its superficial covering, is liable during an epidemic of
diphtheria to become infected, like every other wound. I have seen
cases in which stomatitis and diphtheria existed side by side, the
latter having invaded the surfaces exposed by the former. The
examination of the entire throat is not always easy. Very young
children vomit frequently and persistently before the whole surface is
exposed to view, and not infrequently repeated examination with the
spatula is absolutely necessary. In general, however, the slight
attempts at vomiting suffice to cause a great part of the swollen
posterior portion of the tonsils to become visible. I have heard that
the pale surface of old hyperplastic tonsils has been mistaken for
diphtheria; I merely mention the fact. When a discoloration happens to
be the result of a deposited flake of mucus, a drink of water will
remove it.
Fever is not always a prominent symptom; as a rule, simple diphtheria
of the tonsils is accompanied by very little fever. Still, there are
plenty of exceptions. But the differences of temperature are not more
striking than in most other infectious diseases, whose either mild or
severe invasion may offer an obstacle to immediate diagnosis. As the
height of the fever does not absolutely determine, or even indicate,
the character of the subsequent course of the disease, but little
importance is to be attached to the temperature unless there be a very
marked elevation. A sudden rise frequently occurs with lymphadenitis.
High fever in the beginning may render the diagnosis difficult or may
postpone it.
The absence of glandular swelling does not exclude the diagnosis of
diphtheria, for when the tonsils are affected by the disease there is
usually little or no swelling of the neighboring glands. Swelling of
the glands enables us to locate the affection in a mucous membrane
richly endowed with lymphatic vessels. It is very marked when the nose
is affected. A few hours' duration of nasal diphtheria suffices for
the development of a severe lymphadenitis, especially at the angles of
the jaw. When the latter condition is found to exist, the throat
should be examined with the idea of finding a membrane extending
upward; nasal diphtheria is very liable to complicate an affection of
the uvula and arches of the palate. The membrane cannot well be seen
by looking through the nostrils; highly serviceable for this purpose
is a very short, broad rhinoscope reaching upward to the bony
structure of the nose. However, nasal diphtheria may frequently be
diagnosticated some days before the membrane becomes visible, by the
rapid development of lymphadenitis; this may be done even where the
sweetish, musty odor of certain forms {691} of diphtheria is absent.
Still, nasal diphtheria may occur without much lymphadenitis; as, for
instance, when the blood-vessels are very numerous and superficial,
and thereby give rise to slight hemorrhages at the very beginning of
the sickness. In such cases the lymphatic vessels are little, if at
all, required to transmit the poison, the open blood-vessels replacing
them in the function of absorbing. Naturally, there are cases in which
an ocular examination cannot be satisfactorily made. In the journals
we read of brilliant results of rhinoscopic and laryngoscopic
examination; in practice we see but few. This holds good especially
for the cases of dyspnoea accompanying laryngeal diphtheria, where the
diagnosis may be doubtful when no membrane can be detected in the
fauces; even if membrane be observed there, symptoms of suffocation
may still arise from a laryngeal stenosis independent of membranous
deposits in the larynx. If aphonia and difficulty of both inspiration
and expiration be present at the same time, there is certainly
membranous occlusion. If aphonia appear late, or even toward the very
last, and only inspiration be impeded while expiration is
comparatively free, there is an oedematous saturation of the
ary-epiglottidean folds and of their copious submucous tissue, and
consequently of the posterior attachment of the vocal cords. Although
a general oedema glottidis in connection with diphtheria is of
exceedingly rare occurrence, the above condition is not at all
uncommon, and has forced me to tracheotomize many times; but, again, a
comprehension of the true condition, where it occurred in not very
severe cases, has on several occasions enabled me to avoid an
operation. This local oedema may sometimes be detected by palpation in
the region of the swollen posterior wall of the pharynx.
One of the diagnostic symptoms of membranous laryngitis, believed in
and referred to by Kronlein, does not exist--viz. the swelling of the
lymphatic glands, which in his opinion is pathognomonic. Not only is
that not the case, but the absence or scarcity of lymphatics on the
vocal cords and in their neighborhood renders the absence of glandular
swellings a necessity, provided the latter do not depend on
complicating diphtheria in other localities. In uncomplicated
diphtheritic laryngitis I expect no lymphadenitis. The character of
the laryngeal pseudo-membrane does not depend at all on the condition
of the pharynx. The latter may have membranes of any description or
consistency without permitting the diagnosis of the condition of the
larynx. I lay stress on this fact because no less a writer than
Kronlein believes that where there is but little or no membrane in the
pharynx, that in the larynx is rather loose and movable.
One of the diagnostic symptoms of diphtheritic laryngitis, or
membranous croup, is the relative absence of fever. Catarrhal
laryngitis, or pseudo-croup, is a feverish disease. A sudden attack of
croup with high temperature, provided there is no pharyngeal or other
diphtheria present, yields a good prognosis; without much fever, a
very doubtful one.
The diagnosis of diphtheritic paralysis offers very little difficulty
in most cases. Its occurrence after an attack of diphtheria, its
beginning in the fauces or in the muscles controlled by the ciliary
nerves, the immunity of the sphincters, the gradual development, the
irregularity of its progress, are good diagnostic points. Examination
by the interrupted or continuous current is not conclusive. Very
frequently in the {692} beginning the response to the interrupted
current is normal, sometimes deficient; to the continuous current,
exaggerated. After some time the power of both to excite contraction
is diminished. When we reflect on the numerous causes which may
underlie diphtheritic paralysis, and that we have not to deal with one
and the same anatomical change in all cases, it becomes apparent that
no reliable conclusions can be based upon electrical examination.
PROGNOSIS.--In general, the prognosis in diphtheria is favorable when
the affected surface is of small extent and where such parts are the
seat of disease as have little communication with the lymphatic
system. To the latter class belongs simple diphtheria of the tonsils.
Marked glandular swelling, particularly if arising suddenly, is always
an unfavorable sign, and calls for the utmost caution in prognosis,
especially if the region of the angles of the jaw be speedily and
markedly infiltrated. This, as we have seen, is particularly apt to
occur with nasal diphtheria, whether developed primarily, (and then
accompanied by a thin fetid discharge), or, as is more commonly the
case, secondarily from an affection of the pharynx and palate which
ascends into the posterior nares. With the appropriate local
disinfection this form of the disease is neither so alarmingly
dangerous as Oertel depicts it, nor so assuredly fatal as Roger but a
few years ago taught in his clinique, or as Kohts appears to
believe,[38] yet it is ever grave. With energetic treatment many cases
will, however, get well. Diphtheria of wounds, complicating diphtheria
of the pharynx, is always an unfavorable sign; that of the mouth and
angles of the mouth, associating itself with a previously existing
diphtheria, having an indolent course, and producing more frequently a
deep impregnation of the tissues than a thick deposit, causes a
painful and serious condition. Diphtheria of the larynx, whether it be
of primary origin or the result of extension from the fauces, is
nearly always fatal. In severe epidemics the mortality is 95 per cent.
Tracheotomy, too, saves but few of those who take the disease at such
a time. In fifty consecutive tracheotomies from 1872 to 1874 I did not
see one recovery. In the last few years I have seen few good results.
In average epidemics tracheotomy will save 20 per cent. A pulse of 140
to 160, and high fever immediately after the operation, render the
prognosis bad; so does absence of complete relief after the operation.
An almost normal temperature the day after the operation is an
agreeable symptom, but does not exclude a downward extension of the
diphtheritic process, and hence cannot be looked upon as assuring a
favorable prognosis. A marked elevation of temperature is apt to
indicate a renewed attack of diphtheria or a rapidly-appearing
pneumonia, and is an unfavorable symptom. A dry character of the
respiratory murmur some time after tracheotomy indicates the approach
of death within from twelve to twenty-four hours from descent of the
membrane; so does cyanosis, whatever be its degree of intensity.
Diphtheria of the trachea, which ascends to the larynx, is positively
fatal. It has a rapid course, and tracheotomy only postpones the end
for a little while, if at all. The general health and strength of the
little sufferer have no influence whatever.
[Footnote 38: Gerhardt, _Handb. d. Kinderkr._, iii., 2, p. 20, 1878.]
Thick, solid deposits need not of themselves render the prognosis so
unfavorable as do septic and gangrenous forms. Even in the nose they
{693} are not of as serious import as the thin, putrid discharge. I
have seen recovery ensue in cases where I was obliged to bore through
the occluded nasal cavities with probes and scoops. Fetid, putrid
discharges are unfavorable, but in no wise fatal; conscientious
disinfection accomplishes a great deal. Slight epistaxis indicates the
possibility of rapid absorption through the blood-vessels; but here,
too, the final result depends on whether the disinfection be equally
rapid and thorough. The same holds true for the sweetish, fetid odor
of the breath, whether of the nose or mouth, which, on the one hand,
demonstrates the significance of the disease, while, on the other
hand, it indicates the possibility of infection by inhalation.
The height of the fever is not in proportion to the danger in any
individual case; some have a favorable, some an unfavorable
termination, without fever of any account. Simple catarrh of the
pharynx and larynx frequently begins with a sudden and marked rise of
temperature; diphtheria in the same parts but rarely. There are cases,
however, in which the height of the fever and the deposited membranes
are in inverse proportion to each other. In these cases the fever may
subside rapidly, owing to a speedy elimination of the poison. Young
children only are in danger of death from convulsions or a rapid
tissue-degeneration due to hyperpyrexia. If the temperature rise
suddenly after some days of sickness, either a complication or a fatal
termination is to be apprehended. Yet, there are as many deaths in
cases with comparatively low as with very high temperatures. Whether
collapse has resulted rapidly or slowly, the patient dies often with
low temperature. Thus, a rapid elevation is hardly a more unfavorable
sign than a rapid fall. The pulse, too, may be very variable. True, a
small, rapid, and irregular pulse is always unfavorable, because it
indicates a weakening of the cardiac function; yet as long as it
retains an approximately normal relation to the frequency of
respiration a rapid pulse gives no cause for alarm. Moreover, the
pulse is not always rapid when the strength gives way. It occasionally
becomes slower, and sometimes very slow, and may then become a
dangerous symptom.
Every complication adds to the danger. Bronchitis and pneumonia are
not infrequent, yet I have seen cases of laryngeal diphtheria recover
in which I had suspected pneumonia before performing tracheotomy, and
was enabled to diagnosticate it after operating. Albuminuria in the
early part of a diphtheritic attack with high fever is of little
significance; nephritis, later in the course of the disease, partakes
of the character of scarlatinous nephritis; cases of acute diffuse
renal disease are fortunately infrequent, and the remainder are very
submissive to treatment. The cases of diphtheria complicated with
endocarditis in my practice have ended fatally. An early affection of
the sensorium, not dependent on pressure upon the jugulars by greatly
swollen glands, is an unfavorable symptom. Purpura, with profuse
hemorrhages and a livid hue of the skin, is ominous; icteric
discoloration, together with marked glandular and periglandular
tumefaction, is absolutely fatal.
Most cases of diphtheria of the pharynx and of the tonsils have a
favorable termination, yet a positive prognosis can in no case be
given with certainty. Still, even in malignant epidemics the mortality
is not very great, for even though there be a large number of severe
cases in {694} any one epidemic, yet it is greatly overbalanced by the
number of moderately severe and mild ones. True, not a few cases end
fatally in several days, owing to the high fever, or to septic
absorption, or nephritis, or croup, but the majority of cases end in
recovery in one or two weeks. Yet diphtheria does not always take so
regular a course; not infrequently, after the pulse has become
stronger, the appetite improved, and the pharynx cleared, and the
patient is apparently on the high road to recovery, another attack
occurs accompanied by fever, as before, and a rapid formation of
membrane. Occasionally two or three such relapses may occur in the
course of three, four, or five weeks; not to speak of the fact that
those who have once suffered from diphtheria are more susceptible to
the action of the poison than those who never suffered before.
TREATMENT.--Every case should be treated on general principles; thus,
it is not possible to lay down a routine treatment for every
individual case. High fever should be reduced by sponging and bathing,
quinia, and sodium salicylate; collapse speedily treated, and severe
reflex symptoms, as vomiting, etc., checked at once. Whether to employ
for this purpose ether, wine, cognac, champagne, or coffee must be
decided by the physician in individual cases. The administration of
the remedy, whether by mouth, by injection into the bowels, or
subcutaneously, as I have employed cognac, ether, alcohol, and camphor
dissolved in ether or alcohol, in some cases with decided and rapid
success, must depend on the condition of the organs and on the urgency
of the case. However, all the above remedies are frequently of no
service, because administered too late and in too small doses. If I
have ever had cause to feel contented with the results of treatment in
diphtheria, it is owing to the fact that I lost no time. No medicines,
however, must be resorted to which are apt to derange the digestion of
the patient; alcoholic stimulants must be given in fair dilution only,
for that reason. The nourishment of the patient is a matter of very
great importance. On general principles it is true that care must be
taken in regard to food administered to febrile patients, but we must
bear in mind that, when the lymphatic vessels are kept empty and no
new and proper material is introduced into them, the absorption of
locally-existing poisonous substances is proportionately increased.
Hungry lymph-vessels are the organism's fiercest enemies.
I dwell particularly on the foregoing remarks for the reason that in
diphtheria, unlike certain diseases having a typical course and those
of a simple inflammatory character, expectant treatment should not be
indulged in. Oertel's advice, that when neither high fever nor
complications are present we should quietly wait, and "act only when
new and most alarming symptoms present themselves," is decidedly
perilous. A mild invasion does not assure a mild course. Never has a
"possibly superfluous" tonic or stimulant done harm in diphtheria, but
many a case has a sad termination because of a sudden change in the
character of the disease, putting the bright hopes of the physician to
shame. Only the philosopher may be a passive spectator; the physician
must be a guardian. When I again read, in the work of the same
meritorious author, "that when in exceptional cases, in children and
young people, death is imminent, not from suffocating symptoms in the
larynx and trachea, but from septic disease and blood-poisoning, it is
necessary to resort to {695} powerful stimulants," it strikes me that
he is frequently too dilatory with his remedies, and, furthermore,
that his experience concerning the terrible septic form of diphtheria
which is so frequently met with in some epidemics must have been very
limited at the time he was writing. In New York, during the past
twenty-five years, for every death from diphtheritic laryngeal
stenosis (membranous croup) there have been three from diphtheritic
sepsis or from exhaustion.[39]
[Footnote 39: We have to improve somewhat on the plan of Thomas
Wilson, though his general instructions be good (as laid down in his
_Tentamen medicum inaugurale de cynanche maliqna_, Edinb., 1790, p.
24): "Cum hactenus nullum inventum est remedium quod contagionem in
corpus receptam suffocare possit; cum medicamenta pleraque quae
putredinem corrigere dicuntur, corpus ejusque functiones manifesto
roborant; et denique cum hunc morbum comitantur virium prostratio, et,
etiam ab initio, summa functionum debilitas, qualis evacuantia
omnigena prohibet, indicationem curandi unicam, scil. debilitatis
effectibus obviam ire, proponam. Hinc corporis conditioni obviam itur
praecipue tonica et stimulantia administrando." (As no remedy has yet
been found which can extinguish the contagion after it has been
received into the body; as most medicines which have the reputation of
correcting putrefaction are roborants for the body and its functions;
and, lastly, as this disease is attended with great prostration and
such debility of functions as to preclude the use of all sorts of
evacuants,--I propose but this one indication for treatment--viz. to
meet the effects of debility. This is fulfilled by the administration
mainly of tonics and stimulants.)]
In regard to the dose of stimulants, it is a fact that there is more
danger in diphtheria from giving too little than too much. When the
pulse barely begins to be small and frequent they must be administered
at once. A three-year-old child can comfortably take thirty to one
hundred and fifty grammes (fl. oz. j-v) of cognac, or one to five
grammes of carbonate of ammonium, or a gramme of musk or camphor (gr.
xv) and more, in twenty-four hours. In the septic form especially the
intoxicating action of alcohol is out of the question; the pulse
becomes stronger and slower, and the patient enjoys rest. In those
cases in which the pulse is slow, together with a weak heart's action,
the dose can hardly be too large. The fear of a bold administration of
stimulants will vanish, as does that of the use of large doses of
opium in peritonitis, of quinia in pneumonia, or of iodide of
potassium in meningitis or syphilis. I know that cases of young
children with general sepsis commenced immediately to improve when
their one hundred grammes (fl. oz. iij) of brandy were increased to
four times that amount in a day.
The remarks I have made in reference to the general treatment of
diphtheria naturally render superfluous a discussion of the value of
abstraction of blood. To be sure, it could only be a question of local
bleeding. For nobody would dare to resort to jugular venesection, as
our predecessors did in the last century. It may be safely asserted of
the latter that it has no influence on the process, but frequently
increases the local swelling and makes the patient more anaemic. There
is no case in which a resort to it would not be criminal. I can
distinctly recall the time when bleeding and calomel formed the
groundwork of the treatment. Until the year 1862 the death-rate in
Rupert, Vermont, from diphtheria was 90 per cent., according to the
reports of the local physicians, and particularly of my pupil, Dr.
Guild, who at that time finished his studies in New York and commenced
practising. When, in the same epidemic, bleeding and calomel were
replaced by stimulants and iron, with the chlorate of potassium, 90
per cent. recovered.
That attention must be paid to the general condition mainly during a
{696} retarded convalescence from previous sickness is self-evident.
Any complications, too, must be subjected to early treatment.
Diarrhoea must be mentioned among these; it reduces the patient's
strength very quickly; likewise, the early appearing nephritis, which
may suddenly end life.
In this connection I must allude to the great danger of
self-infection, which may occur in every variety of cases, severe or
mild. The poison is diffused by expiration and expectoration. Though
care may have been taken to disinfect the linen, towels,
handkerchiefs, the bedstead and bedding, chairs and wall-papers, and
carpets and curtains, even the clothing of the attendants will be
infected. While the patient is getting well he will be infected again,
and have a more serious relapse; and a third one, and succumb. I have
met with such cases often, and with some which went from one attack
into another, and would certainly have perished but for their removal
to a distant part of the town. Where there are vacant rooms the
indication is to change rooms every few days and to thoroughly
disinfect (with sulphurous acid) that which has been used and
infected.
One important axiom must be borne in mind--namely, that prevention is
easier than cure. I do not refer simply to the removal of the healthy
members of the family beyond the danger of infection or to the
isolation of the patient. If the latter becomes necessary, the first
indication is his removal to the top floor of the house. There are, in
addition, however, certain prophylactic measures which will prove
valuable in the hands of every good physician. It is necessary under
all circumstances that the mouth and pharynx of every child be
constantly kept in a healthy condition. Eruptions of the scalp must be
treated at once, and glandular swellings of the neck caused to
disappear. Some cases of laryngeal diphtheria have been traced
directly to the presence of suppurating bronchial glands, with or
without perforation.[40] The same rule applies to nasal and pharyngeal
catarrhs, the treatment of which should be commenced in warm seasons,
when general or local remedies yield better results. Enlarged tonsils
should be resected, or, where that can not be done, scraped out with
Simon's spoon, at a time when no diphtheritic epidemic is raging. It
is important that this take place at a time when, even though sporadic
cases of diphtheria occur, the danger of infection is not great; for
during the height of an epidemic every wound will give rise to general
or local infection. This holds good for any part of the body as well
as of the mouth. I avoid, therefore, an operation at such a time,
provided it can be postponed.
[Footnote 40: Weigert, in _Virch. Arch._, vol. lxxvii., p. 294, 1879.]
Prevention, after all, is not the business of the physician only, but
just as much that of the individual or the complex of
individuals--viz. the town, the state, and the nation. Those sick with
diphtheria must be isolated, though the case appear ever so mild, and,
if possible, the other children must be sent out of the house
altogether. If that be impossible, let them remain outside the house,
in the open air, as long as feasible, with open bedroom windows during
the night, in the most distant part of the house, and let their
throats, and those of their nurses, be examined every day. The
watching eye of a father or mother will discover deviations from the
norm, so that the physician can be notified. Let the temperatures
{697} of the well children be taken once a day, toward evening. Ten
minutes of a mother's time are well paid by the discovery of a slight
anomaly which may require the attention of the physician. Happily,
there are now many mothers who keep and value a self-registering
thermometer as an important addition to their household articles. The
attendant upon a case of diphtheria must not get in contact with the
rest of the family, particularly the children, after his visiting and
handling the patient, for the poison may be carried, though the
carrier remain well or apparently well. Unnecessary petting of the
patient on the part of the well ought to be avoided, and kissing must
be forbidden; the bed-clothing and linen should be changed often and
disinfected, the air of the sick-chamber should be cool and often
changed, and if possible the chamber itself should be changed every
few days.
The well or apparently well children of a family that has diphtheria
at home must not go to school nor to church. The former necessity is
beginning to be recognized by the authorities and teachers, and also,
in consequence of partially enforced habit, by parents; the latter
will be resisted longer. Schools ought to be closed entirely when a
number of cases have occurred. Even when the school-children have not
been affected to a great extent, but an epidemic of diphtheria has
commenced in earnest, it will be better to close the schools for a
time. If that be not advisable, the teacher ought to be taught to
examine throats, and directed to examine every child's throat each
morning, and to send home every one with even suspicious appearances.
In times of an epidemic every public place, theatre, ball-room,
dining-hall, or tavern ought to be subjected to supervision. Where
there is a large conflux of people there are certainly many who carry
the disease with them. Disinfection must be enforced by the
authorities at regular intervals. Public vehicles must be treated in
the same manner. That it should be so when a case of small-pox has
happened to be carried in them appears quite natural. Hardly a
livery-stable keeper would be found who would not be anxious to
destroy the possibility of infection in any of his coaches. He must
learn that diphtheria is, or may be, as dangerous a passenger as
variola. And what is valid in the case of a poor hack is more so in
that of railroad-cars, whether emigrant or Pullman. They ought to be
thoroughly disinfected in times of an epidemic, at regular intervals,
for the highroads of travel have always been those of epidemic
diseases, and railroad officers and their families have often been the
first victims of the imported scourge. Can that be accomplished? Will
not railroad companies resist a plan of regular disinfection because
of its expensiveness? Will there not be an outcry against this as
despotic and as a violation of the rights of the citizen? Certainly
there will be. But so there was also when municipal authorities began
to compel parents to keep their children at home when they had
contagious diseases in the family, and when a small-pox patient was
arrested because of endangering the passengers in a public vehicle. In
such cases it is not society that tyrannizes the individual; it is the
individual that endangers society. And society begins at last, even in
America, to believe in the rights of the commonwealth, and not in the
rights of the democratic person only. The establishment of State and
National Boards of Health proves that the narrow-hearted theories of
the strict constructionists {698} have not only disappeared from our
politics, but also from the conscience and intellect of society.
The sick room must be kept cool, the windows kept open--more or
less--by night as well as by day, the floor frequently washed, the
linen soaked at once, the excrements removed. Dead bodies ought to be
kept moist, for infectious material, chemical or otherwise, will
spread more easily when dry. Attendants must not talk unnecessarily
over the mouth or diphtheritic wounds of the patient, and will do well
to carry a little dry loose cotton--to be changed often--in each of
the nostrils, for it aids in protecting those who are necessarily
exposed to infection.[41]
[Footnote 41: Wernich, in _F. Cohn's Beitr._, iii., 1859, p. 115.]
A very important mode of prevention consists in disinfection. The
experiments of Schotte and Gaertner, and of Sternberg, prove the
inefficiency of small doses of most of the disinfectants in common
use. The popular idea, sometimes even shared by physicians, that the
faint odor of chloride of lime or of carbolic acid in a sick room or
in a foul privy is evidence that the place is disinfected, is entirely
erroneous. Particularly in regard to the latter agent, it may be
stated at once that its employment for disinfecting purposes on a
large scale is impracticable, both on account of the expensiveness of
the pure acid and the enormous quantities required to produce the
desired effect. For in regard to its efficiency it does not rank very
high in comparison with a great many other articles, as may be seen
from a table of the disinfectant properties of different chemicals
published by Miquel in the _Semaine Medicale_.
For practical purposes I know of no better or simpler rules for
disinfection than those published by the National Board of Health. In
its _Bulletin_ No. 10, of September 6, 1879, the following
instructions for disinfection were published: Deodorizers, or
substances which destroy smells, are not necessarily disinfectants,
and disinfectants do not necessarily have an odor.
"Disinfection cannot compensate for want of cleanliness nor of
ventilation.
"I. Disinfectants to be employed:
"1. Roll-sulphur (brimstone) for fumigation.
"2. Sulphate of iron (copperas) dissolved in water in the proportion
of one and a half pounds to the gallon; for soil, sewers, etc.
"3. Sulphate of zinc and common salt, dissolved together in water in
the proportion of four ounces sulphate and two ounces salt to the
gallon; for clothing, bed-linen, etc."
Carbolic acid is not included in the above list, for the following
reasons: It is very difficult to determine the quality of the
commercial article, and the purchaser can never be certain of securing
it of proper strength; it is expensive when of good quality, and
experience has shown that it must be employed in comparatively large
quantities to be of any use; it is liable by its strong odor to give a
false sense of security.
"II. How to use disinfectants:
"1. In the sick-room.--The most available agents are fresh air and
cleanliness. The clothing, towels, bed-linen, etc. should, on removal
from the patient and before they are taken from the room, be placed in
a pail or tub of the zinc solution, boiling hot if possible.
"All discharges should either be received in vessels containing
copperas {699} solution, or, when this is impracticable, should be
immediately covered with copperas solution. All vessels used about the
patient should be cleansed with the same solution.
"Unnecessary furniture--especially that which is stuffed--carpets and
hangings, should, when possible, be removed from the room at the
outset; otherwise they should remain for subsequent fumigation and
treatment.
"2. Fumigation with sulphur is the only practical method for
disinfecting the house. For this purpose the rooms to be disinfected
must be vacated. Heavy clothing, blankets, bedding, and other articles
which cannot be treated with zinc solution should be opened and
exposed during fumigation, as directed below. Close the rooms as
tightly as possible, place the sulphur in iron pans supported upon
bricks placed in wash-tubs containing a little water, set it on fire
by hot coals or with the aid of a spoonful of alcohol, and allow the
room to remain closed for twenty-four hours. For a room about ten feet
square at least two pounds of sulphur should be used; for larger rooms
proportionately increased quantities.
"3. Premises.--Cellars, yards, stables, gutters, privies, cesspools,
water-closets, drains, sewers, etc. should be frequently and liberally
treated with copperas solution. The copperas solution is easily
prepared by hanging a basket containing about sixty pounds of copperas
in a barrel of water.
"4. Body- and bed-clothing, etc.--It is best to burn all articles
which have been in contact with persons sick with contagious or
infectious diseases. Articles too valuable to be destroyed should be
treated as follows:
"A. Cotton, linen, flannel, blankets, etc. should be treated with the
boiling-hot zinc solution; introduce piece by piece; secure thorough
wetting, and boil for at least half an hour.
"B. Heavy woollen clothing, silks, furs, stuffed bed-covers, beds, and
other articles which cannot be treated with the zinc solution, should
be hung in the room during fumigation, their surfaces thoroughly
exposed and pockets turned inside out. Afterward, they should be hung
in the open air, beaten, and shaken. Pillows, beds, stuffed
mattresses, upholstered furniture, etc. should be cut open, the
contents spread out, and thoroughly fumigated. Carpets are best
fumigated on the floor, but should afterward be removed to the open
air and thoroughly beaten.
"5. Corpses should be thoroughly washed with a zinc solution of double
strength; should then be wrapped in a sheet wet with the zinc
solution, and buried at once. Metallic, metal-lined, or air-tight
coffins should be used when possible; certainly when the body is to be
transported for any considerable distance.
"It might have been added here that no public funeral must be
permitted."
In this connection I have to speak of a remedy which I class among the
prophylactic agents--namely, the chlorate of potassium or the chlorate
of sodium. I cannot say that I rely on either of these remedies as
curative agents in diphtheria, and yet I employ them in almost every
case. The reason lies in the fact that the chlorate is useful in most
cases of stomatitis, and thereby acts as a preventive.
There are very few cases of diphtheria which do not exhibit larger
surfaces of either pharyngitis or stomatitis than of diphtheritic
membrane. There are also a number of cases of stomatitis and
pharyngitis, {700} during every epidemic of diphtheria, which must be
referred to the epidemic, sometimes as kindred diseases, and sometimes
as introductory stages only, which, however, do not, or do not in the
beginning, show the characteristic symptoms of the disease.
When, in 1860,[42] I wrote my first paper on diphtheria, I based it
upon two hundred genuine cases, and at the same time enumerated one
hundred and eighty-five cases of pharyngitis, which I considered to be
brought on by epidemic influences, but which, the membrane being
absent, could not be classified as bona fide cases of diphtheria.
[Footnote 42: _Amer. Med. Times_, Aug. 11th and 18th.]
Such cases of pharyngitis and stomatitis, no matter whether influenced
by an epidemic or not, furnish the indication for the use of chlorate
of potassium. They will usually get well with this treatment alone.
The cases of genuine diphtheria, complicated with a great deal of
stomatitis and pharyngitis, also indicate the use of chlorate of
potassium; not, however, as a remedy for the diphtheria, but as a
remedy for the accompanying catarrhal condition in the neighborhood of
the diphtheritic exudation. For it is a fact that, as long as the
parts in the neighborhood of the diphtheritic exudation are in a
healthy condition, there is but little danger of the disease spreading
over the surface. Whenever the neighboring surface is affected with
catarrh or inflammation, or injured so that the epithelium gets loose
or thrown off, the diphtheritic exudation will spread within a very
short time. Thus chlorate of potassium or sodium, the latter of which
is more soluble and more easily digested than the former, will act as
a preventive rather than as a curative remedy. Therefore it is that
common cases of pharyngeal diphtheria will recover under this
treatment alone; and these are the cases which have given its
reputation to chlorate of potassium as a remedy for diphtheria.
The dose of chlorate of potassium for a child two or three years old
should not be larger than half a drachm (2 grammes) in twenty-four
hours. A baby of one year or less should not take more than one
scruple (1.25 grammes) a day. The dose for an adult should not be more
than a drachm and a half, or at most two drachms (6 or 8 grammes), in
the course of twenty-four hours.
The effect of the chlorate of potassium is partly a general and partly
a local one. The general effect may be obtained by the use of
occasional larger doses, but it is better not to strain the
eliminating powers of the system. The local effect, however, cannot be
obtained with occasional doses, but only by doses so frequently
repeated that the remedy is in almost constant contact with the
diseased surface. Thus, the doses, to produce the local effect, should
be very small, but frequently administered. It is better that the
daily quantity of twenty grains should be given in fifty or sixty
doses than in eight or ten; that is, the solution should be weak, and
a drachm or half a drachm of such solution can be given every hour or
every half hour or every fifteen or twenty minutes, care being taken
that no water or other drink is given soon after the remedy has been
administered, for obvious reasons.
I have referred to these facts with so much emphasis because of late
an attempt has been made to introduce chlorate of potassium as the
main remedy in bad cases of diphtheria, and, what is worse, in large
doses (Seeligmuller, Sachse, L. Weigert, C. Kuster, Edlefsen.)
{701} Large doses of chlorate of potassium (2 drachms daily to an
adult I claim to be a large dose, particularly when its use is
persisted in for many days in succession) are dangerous. In several of
my writings I have given instances of its fatal effects.[43] I have
seen fatal cases since, and scores have been published in different
journals. The first effects of a moderately large dose are gastric
and, more especially, renal irritation; the latter it was which I
experienced when I took half an ounce twenty-five years ago. Fountain
of Davenport, Iowa, experienced the same before more serious symptoms
developed, of which he died.[44] The symptoms are those of acute
diffuse nephritis, with suppression of urine, or scanty secretion of a
little black blood, and uraemia deepening toward death in fatal cases.
My earlier cases I considered as primary diffuse nephritis, and I have
even been inclined to attribute the frequent appearance of chronic
nephritis, amongst all classes and ages, in part to the influence of
the chlorates, which have become a popular domestic remedy and are
found in every household. But the experimental researches of
Marchand[45] and others prove that, at least in many instances, the
extensive destruction of blood-cells is the first and immediate result
of the introduction into the circulation of the chlorate, and that the
visceral changes are due to embolic processes.
[Footnote 43: _C. Gerhardt's Handbuch der Kinderkrankheiten_, vol.
ii., 1876; _Med. Record_, March, 1879; _Treatise on Diphtheria_,
1880.]
[Footnote 44: Stille, _Therap. and Mat. Med._, 2d ed., 1874, p. 922.]
[Footnote 45: _Sitzungsber. d. Naturforsch. Ges. h. u. Halle_, Feb. 8,
1879, and _Virch. Arch._, vol. lxxvii.]
Special Treatment.--The first axiom in the treatment of diphtheria is
that there is no specific; the second, that in no other disease the
individualizing powers of the physician are tested more severely.
The treatment is both internal and external. The local remedies are
either such as dissolve the mucous membrane, or such as thoroughly
modify the mucous membrane from which the pseudo-membrane has been
removed, or real antiseptics, with the power of destroying either
chemical or parasitic poisons.
The number of remedies recommended in diphtheria is immense. No other
proof of its dangerous nature is needed. In the following I shall
review those which I consider it worth while either to reject or to
recommend.
Steam is used partly to soften the membranes, but principally to
increase the secretion from the mucous membrane, and thereby throw off
the superjacent membrane. This can be done to advantage only where
there is a natural tendency to it; that is, where there are a great
many muciparous follicles under a cylindrical or fimbriated
epithelium. This is the condition on part of the pharynx, but not on
the tonsils; and in a small portion of the larynx, in the trachea and
bronchi, but not on the vocal cords. Wherever there is pavement
epithelium on the normal surface, and where the membrane is imbedded
into the tissue, steam can hardly be expected to do good. In the other
cases it will. Thus, the locality of the diphtheritic process
determines to a great extent whether steam is indicated or not. If it
be used, the necessity of a full supply of atmospheric air must not be
disregarded. Steam, with an overheated room and without pure air, is
liable to be as injurious as steam in pure air is beneficial in a
number of cases.
{702} There can be no better proof for the necessity of
individualizing, and the impossibility of treating all cases alike,
than the fact that many will do well under steam treatment, and others
are certainly injured by it. I have repeatedly had the joy of seeing
children with croup become less cyanotic after their removal from an
atmosphere of vapor, and I can readily see that pure atmospheric air
would be more agreeable and wholesome to a child with stenosis of the
larynx than an atmosphere laden with steam. Of course this remark does
not apply to cases of pseudo-croup and bronchitis, which are generally
benefited by a warm, moist atmosphere. Those, however, who deem it
judicious to employ steam as a vehicle for carbolic acid, salicylic
acid, chloride of sodium, chlorate of potassium, or lime, had best
resort to the atomizer for applying these remedies. It can be used
without trouble; most children are sufficiently intelligent to allow
the spray to be directed upon the fauces and larynx every ten or
fifteen minutes in case of necessity. When it is deemed advisable to
administer steam, I warn against the use of gas stoves. They require a
great deal more oxygen than an alcohol lamp, which ought to be
preferred when a stove or slaking lime or hot iron or bricks immersed
in water are not available.
Water may be made serviceable in different ways. Its effect on the
skin, when taken in large quantities, under normal or abnormal
circumstances, is a matter of daily experience. Copious perspiration
is its immediate result. The very same effect is produced on the
mucous membranes. In diphtheria, besides professional hydropathists, I
know of but one[46] who favors the plentiful use of water, 100-200
grammes (3-6 ounces) every hour or oftener, either by itself or mixed
with an alcoholic beverage.
[Footnote 46: C. Rauchfuss, in _C. Gerhardt's Handb. d. Kinderkr._,
iii. 2, 1878.]
Severe inflammatory symptoms, such as redness of the throat, great
pain, swelling of the glands, require cold applications, either an
ice-bag or ice-cold cloths well pressed out and frequently changed.
They must, however, be placed where they can do most good--in
laryngeal diphtheria around the neck, in pharyngeal diphtheria with
glandular swelling over the affected part. In the latter, therefore,
the flannel cloth which covers the whole of the application must be
tied over the head, and not behind. When ice-bags are used, care is to
be taken lest they should be too large; if so, they will not affect
the desired spot at all. Small pieces of ice frequently swallowed are
greatly relished by the patient; water-ices in small quantities will
render the same service; ice-cream, in half-teaspoon or teaspoon doses
every five or ten minutes, adds to the necessary nutriment. When the
fever is high and the surface hot, sponging with tepid or cold water,
or water and alcohol, will mitigate both. For the cold bath or the
cold partial pack (trunk and upper part of the thighs) the general
indications hold good. As a rule, I favor the latter, for many cases
have such a tendency to debility and collapse that sometimes the
circulation of the surface of the body is badly interfered with by
cold bathing. Therefore, a contraindication to cold bathing must be
found at once in cold feet, either before or after a bath. When,
unfortunately, the feet do not recover their normal temperature in a
very short time, they ought to be warmed artificially, and the cold
bath not repeated. In such cases the cold pack, however, is still
indicated. A linen or cotton cloth, {703} large enough to cover the
trunk and half of the thighs, is dipped in cold water, well pressed
out, and the body of the patient wrapped tightly in it. The arms
remain outside; the whole body is then wrapped up in a blanket; the
feet may be warmed meanwhile when necessary, and the cold pack
repeated as often as required to reduce the temperature--viz. once
every five minutes, every half hour, every hour.
The contraindications to the use of cold have in part been alluded to.
Very young infants bear it but to a limited extent. The beginning of
recovery contraindicates it, unless for some local cause; for
instance, an inflamed gland. The extensive use of cold water or ice is
also forbidden when there is no fever, where there is perhaps an
abnormally low temperature, where we have to deal with the septic or
gangrenous form of diphtheria, where the vitality is low and the
mucous membranes pale or even cyanotic. In such cases, on the
contrary, while unlimited internal stimulation is required, the hot
bath, or hot pack and hot injections into the bowel, will be found
beneficial.
Lime-water, glycerine, lactic acid, pepsin, neurin, papayotin,
chinolin, and pilocarpine are all solvents of pseudo-membrane, but
whether there is sufficient time and opportunity to produce a curative
effect by every one of them is a question open for discussion. Of
lime-water and glycerine I have employed a mixture of equal parts in
considerably more than a hundred cases after the completion of
tracheotomy, directing the remedy through an atomizer into and below
the canula, but cannot say that the descent of the membrane into the
trachea or bronchi was prevented by it. Lime-water may be used in the
nose and throat as an injection, spray, or gargle, but its solvent
effect is greatly diminished by the action of the carbonic acid of the
breath on the lime. I have no doubt that if water alone was used with
the same persistence as lime-water, its effects would be nearly the
same. Still, what little effect the minute dose of lime (1:800) in the
lime-water may have may just as well be utilized. What I object to is
the omission of more powerful agents. If lime is to be used, slaking
lime frequently in the presence of the patient is attended with vastly
more benefit, inasmuch as by that proceeding a large amount of
powdered lime is projected into the air of the room and the mouth and
respiratory organs.
Lactic acid also, in from ten to twenty-five parts of water, has
yielded no better results in my hands. Those cases of tracheotomy
which I afterward treated with lactic acid spray terminated no better
than such as were treated with lime-water and glycerine. Of the
solvent effect of pepsin I have not been able to convince myself so as
to recommend it. The accounts of neurin have not encouraged me to try
it at all. Chinolin (tartrate) has been used locally by O.
Seifert,[47] Muller, and others. It is said to remove the membranes
and relieve the fever. For a gargle it is dissolved in five hundred
parts of water, or it is mixed with ten parts of water and alcohol
each, and applied by means of a sponge. To relieve the burning
sensation ice is swallowed afterward. The local applications of
alcohol have the same drawback. There are but few patients who do not
suffer intensely from its local contact.
[Footnote 47: _Berl. klin. Woch._, Nos. 36, 37, 1883.]
Papayotin has been recommended by Rossbach for the purpose of
dissolving membranes in a one-half per cent. solution. It peptonizes
{704} albuminoids, and macerates meat, intestinal worms, and croup
membranes in both neutral and feebly alkaline solution. In
concentrated solutions it has a caustic effect. It is recommended, not
as an anti-diphtheritic, but merely as a solvent remedy.[48] Whatever
reliance may have been placed upon it has, however, been jeopardized
by Rossbach's remarks[49] on the variability of the preparations in
the market. Not only are the specimens very unequal, but each of them
is variable, easily spoiled, and particularly affected by moisture.
[Footnote 48: _Berl. klin. Woch._, March 10, 1881.]
[Footnote 49: _Transactions of the Congress for Int. Medicine_, 1883,
p. 162.]
Muriate of pilocarpine was recommended for this purpose three years
ago. It was praised by Juttmann as a specific, and has failed. The
quackish recommendations of the drug have, indeed, earned for it a
certain amount of distrust which it does not deserve in all cases. It
is expected to increase the secretion of the mucous membranes to such
an extent as to float the pseudo-membranes. It sometimes succeeds in
so doing, but only in those cases in which the membrane is deposited
upon the mucous membranes. When the tissue is impregnated the drug
fails. It also fails in septic cases, and mostly for the reason that
it diminishes and paralyzes the heart's action. It ought, therefore,
never to be given unaccompanied with large amounts of stimulants.
Where the patient is strong, and the heart healthy, it may be tried; I
know that a few cases of moderate laryngeal diphtheria improved with
pilocarpine, steam, and turpentine inhalations. The dose is 1/30
grain, dissolved in water, every hour.
Turpentine inhalations were recommended by C. Edel.[50] Fifteen drops
of oil of turpentine are inhaled from a common inhalation apparatus,
which is placed at a distance of three inches from the mouth of the
patient, for a period of ten minutes every hour. He claims recoveries
in from twelve to forty-eight hours. I allow the patient to remain in
his bed, and keep water boiling constantly on an alcohol lamp, on the
stove, or over the gas. A tablespoonful of turpentine, more or less,
is poured on the water, care being taken that nothing is spilled in
the fire. Thus the room is constantly filled with a penetrating odor
of turpentine, which is not at all disagreeable, even when in great
concentration. The effects are very satisfactory indeed. Where
circumstances allowed or required it I have raised a tent over the
bed, large enough not to give inconvenience to the patient and to
admit either the whole apparatus or the tube containing the mixed
vapor of water and turpentine.
[Footnote 50: _Med. Rev._, Jan. 19, 1878.]
Ammonium chloride may sometimes be used to advantage for its softening
and liquefying effects. Its internal administration in bronchial and
tracheo-laryngeal catarrh is so old that it has several times been
obsolete. Of late, more stimulant effects have been attributed to it
than it actually possesses. But its liquefying action, in cases where
the secretion of mucus is defective and expectoration scanty and
viscid, is undoubted. Thus it proves valuable in many cases of simple
catarrh, both when administered internally and inhaled. The latter
mode I have often resorted to, and believe that its macerating
influence has been of service to me in cases of laryngeal diphtheria.
Half a teaspoonful of the pure salt is spread on the stove or burned
over alcohol {705} or gas. It evaporates immediately, and fills the
room or the tent with a white cloud, which, when dense, excites
coughing. But it does not irritate to any uncomfortable degree, and
the process may be repeated in an interval of an hour or more.
Not all cases of diphtheria are septic or gangrenous, nor are all the
cases occurring during an epidemic of the same type. Some have the
well-pronounced character of a local disease, either on the tonsils or
in the larynx. The cases of sporadic croup met with in the intervals
between epidemics present few constitutional symptoms, and assume more
the nature of an active inflammatory disease--very much like the
sporadic cases of fibrinous tracheo-bronchitis. These are the cases in
which mercury deserves to have friends, apologists, and even
eulogists. Calomel, 0.5-0.75 gramme (gr. viij-xij), divided into
thirty or forty doses, of which one is taken every half hour, is apt
to produce a constitutional effect very soon. Such doses, with minute
doses, a milligramme or more (gr. 1/60), of tartar emetic, or ten or
twenty times that amount of oxysulphuret of antimony, have served me
well in fibrinous tracheo-bronchitis. But the mucous membrane of the
trachea and bronchi is more apt to submit to such liquefying and
macerating treatment than the vocal cords. The latter have no
muciparous glands like the former, in which they are very copious. And
while the tracheal membrane, even though recent, is apt to be thrown
out of a tracheal incision at once, the pseudo-membrane of the vocal
cords takes from six days to sixteen or more for complete removal.
Still, a certain effect may even here be accomplished, for maceration
does not depend only on the local secretion of the muciparous glands,
but on the total secretion of the surface, which will be in constant
contact with the whole respiratory tract. Thus, either on theoretical
principles or on the ground of actual experience, men of learning and
judgment have used mercury in such cases as I detailed above, with a
certain confidence.
If ever mercury is expected to do any good in cases of suffocation by
membrane, it must be made to act promptly. That is what the blue
ointment does not. In its place I recommend the oleate, of which ten
or twelve drops may be rubbed into the skin along the inside of the
forearms or thighs (or anywhere when their surface becomes irritated)
every hour or two hours. Or broken doses will be useful, such as given
above, or hypodermic injections of corrosive sublimate in 1/2 or 1 per
cent. solution in distilled water, four or five drops from four to six
times a day, or more, either by itself or in combination with the
extensive use of the oleate, or with calomel internally. Lately, the
cyanide of mercury has been recommended very strongly. I hardly
believe that it will work more wonders than any other equally soluble
preparation. Within the past few years the internal administration of
bichloride of mercury has been resorted to more frequently and with
greater success than ever before. My own recent experience with it has
been encouraging, and so has that of some of my friends. Wm.
Pepper[51] gave 1/32 grain of corrosive sublimate every two hours in a
bad form of diphtheritic croup, with favorable result. But in this
very bad case, desperate though it was--child of five years, resp. 70,
pulse 160--large membranes, "evidently from the larynx," had been
expelled before the treatment was commenced on the {706} seventh day
of the disease. The remedy ought to be given in solution of 1:5000,
and in good doses. A baby a year old may take one-half grain every day
for many days in succession, with very little if any intestinal
disorder and with no stomatitis.[52] A solution of the corrosive
chloride of mercury in water is frequently employed of late as a
disinfectant. It acts as such in a dilution of 1:20,000. As healthy
mucous membranes bear quite well a proportion of 1:2000-3000, any
strength between these extremes maybe utilized. A grain of the
sublimate in a pint or more of water, with a drachm of table-salt,
will be found both mild and efficient. As a gargle or nasal injection
it will be found equally good. But it has appeared to me that frequent
applications give rise to a copious mucous discharge; hourly
injections into a diphtheritic vagina became quite obnoxious by such
over-secretion, which ceased at once when the injections were
discontinued. Thus, when it is desirable not only to disinfect but
also to cleanse the diseased surface, the injections with corrosive
sublimate appear to yield a result inferior to less irritating
applications.
[Footnote 51: _Trans. Am. Med. Ass._, 1881.]
[Footnote 52: _Med. Record_, May 24, 1884.]
Chloride of iron is undoubtedly a valuable remedy in diphtheria, but
in its administration it must by no means be forgotten that small
doses at long intervals are out of the question. I have not the least
doubt but that the failure of the remedy may be attributed in most
cases to the fact that the doses were too small and administered too
seldom. A dose of from five to fifteen drops, properly diluted, every
fifteen minutes, half hour, or hour is indispensable for a proper
estimation of its effects. Gargles are not of much service, for the
simple reason that they do not come into sufficient contact with the
affected parts, and reach at the utmost to the anterior pillars of the
soft palate. A direct application of the remedy to the mucous membrane
of the pharynx may also be desisted from, thereby avoiding any
irritation, the internal administration at short intervals causing the
pharynx to be sufficiently influenced by local contact with the
remedy. It must, of course, not be expected that the chloride will
remove the membrane, but it can frequently be seen to reduce the
hyperaemia and swelling and prevent the reproduction of exuded
material. The chloride of iron exerts a decided influence on the vital
contractility of the blood-vessels. This increased contractility
certainly assists in diminishing the rapidity of absorption of putrid
fluids through the blood-vessels, which constitutes the principal
source of danger from the disease.
It cannot yet be positively asserted that the chloride of iron exerts
a direct effect on the lymphatic vessels. Naturally, this was claimed
when the remedy was recommended, in the treatment of diphtheria, on
account of its therapeutic effects in erysipelas, with the
accompanying inflammation of the lymphatic vessels of the skin.
Although we know of no direct compression of the lymphatic vessels due
to the action of the chloride, yet it may be assumed that perhaps the
compression of the blood-vessels exerts a similar influence upon the
neighboring lymphatics. In consequence of this there would be an
impediment to the absorption and further development of poisonous
substances in the lymph. The chloride, like the sulphate of iron, is a
tolerably powerful disinfecting agent. If this observation be correct,
it may go very far toward explaining the action {707} of the chloride
of iron in septic diseases, which are accompanied by an exalted
activity of the lymphatic vessels and an increase of the white
blood-corpuscles. Furthermore, Saase has endeavored to show that the
ferrous salts possess the power of converting oxygen into ozone. They
share this power with the blood-globules exclusively, and could hence,
to a certain degree, supply a deficiency of the latter. Pokrowsky,
too, has shown that iron increases the process of oxidation in the
body by demonstrating that in health there is an elevation of
temperature and an increase of the percentage of urea in the urine
during its administration. In anaemic persons, to whom iron has been
given for the purpose of increasing the amount of blood, the above
phenomena may be observed before this object is accomplished. Thus
iron appears to replace the blood-corpuscles to a certain extent. Now,
in infectious disorders of the blood, where the red globules are
perpetually menaced with destruction, it seems plausible that the
preparations of iron should exert an antiseptic action.
Finally, it has been found that of all the preparations of iron the
chloride possesses the greatest power of stimulating the nervous
system. Possibly this effect may be traced to an increase of the
arterial pressure in the nerve-centres. It has been said that this
effect has been vividly illustrated in certain forms of chlorosis. If
this be true, iron would be all the more indicated in diphtheria,
since it would act as a prophylactic against a series of nervous
phenomena that so frequently present themselves, both during and
subsequently to the diphtheritic process. Thus it is that for many
years the muriate of iron has constituted the main element, with me,
of internal medication in most cases of diphtheria, both of the mild
and the most dangerous septic type. A common formula is, for a child
of two years,
Rx. Tinct. Ferri Chloridi fl. drachm ij;
Potass. Chlorat. gr. xx;
Aquae fl. oz. v;
Glycerin. Pur. fl. oz. j. M.
S. A teaspoonful every fifteen, twenty, or thirty minutes.
Carbolic acid exerts a powerful influence on the vitality of all
living elements, and hence also on rapidly proliferating epithelium,
which constitutes a part of the diphtheritic membrane. It is of great
advantage for local use. Its local effect, undiluted or diluted with
equal or larger parts of glycerine or alcohol, in shrinking and
removing membranes, is sometimes very useful; in mild solutions in
water (1/2, 1, or 2 per cent.) it is very efficient in nasal
injections or for external applications or mouth-washes. Rothe's
prescription for external use is carbolic acid and alcohol each 2
parts, water 10, tincture of iodine 1. Its internal administration to
the extent of five to twenty grains daily, given largely diluted, in
small and frequent doses, is of less positive value.
Salicylic acid, in a solution of 1:30-50, is caustic. A milder
solution, 1:200-300 relieves or removes foul odor from the nose or
throat, but it does not detach membranes or shorten the duration of
the disease, apparently. Internally, it acts no longer as a
disinfectant, but is changed into a salicylate and is an antipyretic.
It is then better to replace it by the sodium salicylate. With its
administration (for a child of 2 years 3 grains every hour until 20 or
25 grains are taken) it ought not to be {708} forgotten that serious
brain troubles, collapse, and irregular and paralytic breathing, as
well as gastric and intestinal disturbances, may follow its use. It
ought not to be given without careful watching and the simultaneous
free use of alcoholic stimulants.
Binz found, as the result of experiments with solutions of pure quinia
varying from one part in a hundred to one in a thousand, that the
latter sufficed to prevent the development of bacteria in fluids
capable of undergoing putrefaction; but even estimated thus, a patient
with eighteen pounds of blood would require one hundred and
thirty-eight grains of quinia circulating therein in order to satisfy
the conditions of Binz's experiment. If Binz considers two grammes
(half a drachm) of quinia per day sufficient for an individual
weighing one hundred and twenty pounds, his calculation is founded on
experiments with dogs, in which septicaemia was avoided by the
injection of quinia. It is also necessary to bear in mind that Binz
makes a distinction with regard to the preparations of quinia
employed. He warns against the use of the bisulphate as being the most
inactive. No matter which preparations are used--I prefer the
muriate--I have come to look upon quinia as of no great service in
reducing the temperature in infectious fevers. The main indication for
its use can only be found in inflammatory fevers. When it is given,
however, salicylate of sodium may be added for a short time to obtain
a speedier effect.
On the part of bromine Wm. H. Thompson claims the following
advantages: 1. When applied locally, it promptly arrests fetor by
arresting directly the gangrenous process, and thus lessens risk from
absorption. 2. It acts as an anti-putrefactive likewise in the fluids
of the body generally--_i.e._ blood, interstitial circulation, and
secretions--owing to its high rate of diffusibility, equal to that of
sodium chloride itself. 3. It locally destroys the communicable
property of the discharges, shown by the immunity of attendants from
any sore throat when it is used, and from its checking the spread of
the disease in the locality. He orders two solutions to be used: the
first of equal parts of Lawrence Smith's solutio bromini and of
glycerine, applied with a hair pencil to the membrane, as gently as
possible. Sometimes he uses the solution full strength. The brush
should be washed at once in water, and does not last more than one
day, owing to the action of the bromine on the hair. If, however, the
membrane be very extensive and the parts much swollen or difficult to
reach, he resorts instead to douching with a Davidson syringe, using
half a drachm to one drachm of the solution to a pint of warm water.
By beginning gently with the stream directed against the buccal mucous
membrane, the child soon becomes accustomed to the current and allows
it then to play against the deeper parts.
Internally he orders from six to twelve drops of the solution in a
half ounce of sweetened water, every hour, two, or three hours,
according to the urgency of the case, and continuously.
The most convenient way of making Smith's solution is: Take two ounces
of a saturated solution of potassium bromide in water; add to this,
very slowly, in a bottle and with constant shaking, one ounce of
bromine. It is better to add a part, and then let it stand a while
before adding the rest; then fill up gradually, and with constant
shaking with water, until it measures four ounces.
{709} Ozone has been used as an anti-fermentative in inhalation during
three or five minutes every hour or two, by Jochheim.
Boric (boracic) acid, in saturated (1:25) or milder solutions, has
some antiseptic effect. It is mild, and not very injurious when
swallowed by necessity or mistake. In diphtheritic conjunctivitis it
is valued highly, and in nasal injections I have found it very useful.
It is less repugnant than most other substances administered in that
way.
Sodium benzoate cannot be relied on either as an anti-diphtheritic nor
as an anti-febrile. The doses which were recommended were two scruples
or a drachm daily for a child a year old.
Sulphur has been used locally. It gives rise to coughing and vomiting.
Cubebs have been given in incredible doses, two drachms of the powder
to a child a year old. The drug disorders the stomach and kidneys.
Local Treatment.--The mechanical removal of the membranes is not
permissible unless they are almost detached. It is best to avoid their
being cast off, unless partly loosened membranes in the larynx or
trachea afford an indication for an emetic. Scratching and eroding the
mucous membrane of the neighborhood give rise to new deposits. Even
after spontaneous elimination of a membrane a new one may be formed
within a few hours.
To cauterize a diphtheritic membrane or infiltration I consider wrong,
unless I shall be able to do so thoroughly and to limit the action of
the caustic to the diseased surface. Therefore potassa or chromic acid
cannot be utilized, because of the impossibility of limiting their
effect. Nitrate of silver and mineral acids can be restricted in their
effects, but these are not sufficiently thorough, particularly as but
few patients will consent to have the remedy applied properly. When I
do cauterize, I prefer a mixture of equal parts of carbolic acid and
glycerine or the undiluted acid. The membrane crumbles and falls off
in pieces. Force must never be used. Where it would be required in the
case of obstinate children mild washes must be employed instead of the
caustic. Besides, the internal medication detailed above meets every
indication. When there is a slight swelling of the lymphatic glands,
cold water or ice applications are usually all that is needed. The
latter should be made according to general indications. The glandular
and peri-glandular swellings are less the result of an actual filling
up with foreign matter than of secondary irritation. Ice has a happy
effect in such cases, both on internal administration, in the form of
frequent small quantities of ice-water, ice-pills, ice cream, and iced
medicaments, and also externally by ice-cold cloths or india-rubber
bags filled with ice.
In general, the treatment of the swelled glands must be both based on
its causes and adapted to the present condition. The adenitis and
peri-adenitis is of secondary nature, the irritation being in the
mouth, pharynx, and nares. In these localities is where the main
treatment is required. The sooner the primary affection is removed or
relieved or rendered innocuous, the better it is for the secondary
complaint. Frequent doses of chlorate of potassium or sodium, or
biborate of sodium in mild doses frequently repeated, according to the
principles laid down in another part of this article, mouth-washes,
gargles, nasal injections with water, salt water, or solutions of
disinfecting substances, are not only {710} indicated, but highly
successful. When the case is recent, cold applications are required,
but no washes. When it is of older date, stimulant embrocations are in
order. Iodine ointments are absorbed but slowly; mercurial plasters do
good in some cases; iodide of potassium dissolved in glycerine
(1:3-4), frequently applied, iodine in oleic acid (1:8-12), iodoform
in collodion or flexible collodion (1:12-15) applied twice daily, the
latter frequently with very good result, are beneficial. Copious
suppuration is very rare. Cases in which a free incision meets with an
abscess ready to heal are very uncommon. But numerous small abscesses
with gangrenous walls and pus mixed with a sero-sanguinolent or
sero-purulent liquid, are more frequently found. In such cases a probe
introduced into the lancet wound enters easily into the broken-down
tissue in every direction, to a distance even of three to six
centimetres, (several inches), according to the size of the
tumefaction. I have seen fatal hemorrhages from such gangrenous
destructions; therefore the treatment must be both timely and
energetic. The incision must not be delayed too long. When the skin
assumes a purplish hue or is simply discolored, it is time to incise
and to apply concentrated or nearly concentrated carbolic acid to the
interior, unless the neighborhood of very important blood-vessels or
nerves yields a contraindication to concentrated applications. In that
case a milder preparation is advisable, but the application should be
repeated often, until the suppuration becomes more normal. Then mild
disinfectant injections into what has now become a cavity will be
found satisfactory, particularly when meanwhile the general condition
of the patient has been improved.
Treatment of Nasal Diphtheria.--Especially during the prevalence of an
epidemic of diphtheria must we be careful not to allow a nasal catarrh
to have its own way; we must likewise guard against considering the
thin and flocculent discharge in infected cases as a mucous secretion.
Whatever be the origin of nasal diphtheria, whether primary or the
result of a similar affection in the throat, local treatment should at
once be instituted, and if this be done the great majority of cases
will terminate favorably. The danger in this form of disease consists
in an excessive absorption of putrid substances and in the breathing
of contaminated air. The interior of the nasal cavities must be
thoroughly cleaned and disinfected. If this be commenced early, the
original seat of the affection may be reached, and the disinfectant
process will, as a rule, have good results. It is not necessary to
select very energetic disinfectants; a solution of twelve to
twenty-five centigrammes (two to four grains) of carbolic acid in
thirty grammes (an ounce) of water is at once mild and effective, and
hardly gives rise to more discomfort than lukewarm water. Nasal
injections must be made very frequently, until each time the stream of
fluid has a free exit through the other nostril or through the mouth.
They must be made at least every hour, and even oftener if necessary;
at the same time it is advisable to be careful that the fluid does not
enter the Eustachian tube. This can be prevented, to a certain extent,
by compelling the patient to keep the mouth open during the procedure.
I have seldom seen evil or even disagreeable results from the
administration of nasal injections in diphtheria. It is likely that
the mucous membrane of the pharynx is swollen as far as the openings
of the Eustachian tubes to such a degree as to render the entrance of
fluids into the latter improbable. {711} The hardness of hearing,
which is of so frequent occurrence in the course of a severe catarrh
or of a diphtheritic attack, seems to indicate that the mucous
membrane of that part is in a state of swelling. An ordinary syringe
will suffice. However, when administered by parents or nurses the
blunt nozzle of an ear syringe is preferable. Occasionally here, as in
local applications to the mouth and pharynx, the atomizer may be used
to advantage, but the tube must be properly introduced into the
nostrils. There are cases of nasal diphtheria, however, which are far
more troublesome to manage than the foregoing would seem to indicate.
I have seen cases in which the nasal cavities, from the anterior to
the posterior nares, were filled and completely occluded by a dense,
solid membranous mass. I was then compelled to bore a passage with a
silver probe, to gradually introduce a larger-sized one, and then to
apply the pure carbolic acid, in order to remove the densest and
thickest masses, and finally was able to make injections; even in such
cases I have had the gratification of being able to give a favorable
prognosis. The dangerous secondary swelling of the glands will often
subside after a steady employment of disinfectant injections for from
twelve to twenty-four hours. It will be found that children frequently
do not object to this method of treatment; I have even met with some
who, after convincing themselves of the relief afforded thereby, asked
for an injection. When we are about to bring each injection to a close
it is well to press together the nasal cavities for an instant with
the fingers. By this procedure the fluid is forced backward to the
pharynx, and is swallowed or ejected through the mouth, and thus
washes the pharynx and mouth at the same time. Frequently, however,
this latter object is obtained with every injection; for, the palate
being swelled, oedematous, and paretic, the fluid is not prevented
from reaching the pharynx, even in the average case. In regard to the
choice of a disinfecting agent, I have but a few words to say. I
believe that no one of them has important qualifications above the
others. I avoid those which stain or which produce firm coagula. For
the latter reason I do not use the subsulphate and perchloride of
iron; for the former, the permanganate of potassium. I employ, as a
rule, carbolic acid in solution, of the strength above mentioned.
Where there is but a slightly fetid odor I have frequently employed
lime-water or water with glycerine, or a solution (1:100, 1:50) of
chloride of sodium, or of bicarbonate of soda or of borax, or a
saturated solution of boric acid. Disinfecting agents and antiseptics,
whether carbolic acid, salicylic acid, or iron, are of no service when
administered internally only, unless the seat and cause of the septic
infection be attended to previously. Under the local employment of
antiseptics, as described, or by simply washing out with water or salt
water, most cases recover; without them, death will result. Of late,
in many cases, the local applications, injections, etc. of the
corrosive chloride of mercury in water (1:5000-10,000) has proved very
effective. It has this advantage over carbolic acid, that the
swallowing of the former is not so dangerous. This much, after all, my
experience has assured me of, that there is a certain number of cases
which terminate fatally; but it is likewise true that the mortality
need not be excessively great. I cannot grant that it is hard to carry
out the exact and apparently barbarous treatment necessary for a
favorable result, for it is certainly more barbarous to sacrifice than
to save life.
{712} It is a positive fact that when children suffering from nasal
diphtheria, with its peculiarly septic character, are permitted to
sleep much--and they are apt to be drowsy under the influence of the
poison--they will certainly die. To allow them to sleep is to allow
them to die.
The first symptom of improvement is often a rapid diminution of the
glandular swelling wherever it exists. It is not present in all cases,
but chiefly in those in which a bloody serum was discharged in an
early period of the disease. In these the blood-vessels appear to be
very vulnerable, superficial, and apt to absorb; these are also the
most dangerous cases, and require the greatest attention and care, and
also prompt disinfection.
Treatment of Laryngeal Diphtheria.--The severest form of diphtheria is
that located in the larynx, constituting membranous croup. Its general
treatment, whether the disease has originated primarily in the larynx
or trachea or has been communicated from the pharynx, does not differ
from that laid down for diphtheria in general. Naturally the larynx
calls for special treatment on account of the symptoms of suffocation
which result from its stenosis. The main indication of removing viscid
mucus or partly-detached membranes is best met by the administration
of an emetic. Such is their only indication in my experience. The
selection of the emetic, when indicated, is of great importance.
Antimonials ought to be avoided because of their depressing and
purgative effect. Ipecacuanha is but rarely effective. The sulphates
of zinc and copper, and particularly the latter, deserve preference.
Turpeth mineral acts promptly and satisfactorily. When no emesis can
be obtained the prognosis is decidedly bad. Recourse must then be had
to tracheotomy, the good results of which are however only too often
delusive and transient.
When, after the operation, there is scarcely any relief, and
particularly when the case takes a very rapid course, it is probably
one of ascending croup which commenced in the trachea. Mechanical
relief by pushing down a hen's feather or a bundle of them, and
turning it about and twisting, must be tried. It is a much better
instrument than pincers of all sorts and shapes. But what relief will
be accomplished is but of very short duration. When fever sets in
within a few hours it means very much more frequently pneumonia than
diphtheritic fever. It is apt to be soon complicated by that
disproportion between pulse and respiration so characteristic of
inflammatory diseases. Then quinia in larger doses, 0.25 or 0.5 (grs.
iv-viij) every two, four, eight hours, at the same time doses of
sodium salicylate 0.25-0.40 (grs. iv-vj) every hour or two hours until
the temperature goes down, and small doses of digitalis where the
heart requires it, must be given at once. Procrastination is
dangerous; the patients want careful watching; many of them die within
two days after the operation.
Diphtheritic conjunctivitis requires great attention and permits of no
loss of time. Cold applications to the affected eye must be made
constantly. Pieces of linen or lint kept on ice (better than in
ice-water) of little more than the size of the eye, must be changed
every minute or two day and night. The danger to the cornea is so
imminent that constant watchfulness is required. Boric acid in
concentrated solution should be dropped into the eye once every hour.
Care must be taken that the well eye shall not get infected; for that
purpose it is best to cover it {713} with lint and collodion, or with
lint or cotton held in place by adhesive plaster.
Cutaneous diphtheria requires the destruction of the membrane or of
the infected surface by carbolic acid, either concentrated or somewhat
diluted with glycerine, or the application of the actual cautery.
After that the use of ice or iced cloths, or diluted carbolic acid, is
indicated. As soon as the surface is no longer diphtheritic the local
and general treatment is to be continued on general principles.
Diphtheritic paralysis is invariably complicated by anaemia and
debility, and the diet and medical treatment must be regulated
accordingly. However, neither overfeeding nor a sameness of diet are
to be permitted, for not rarely the muscular coat of the stomach
suffers with the rest of the muscular tissue, and the secretion of
gastric juice is very deficient in anaemic individuals. While,
therefore, iron is indicated, we must not neglect to pay particular
attention to nutrition and digestion, and to aid the latter with
pepsin and moderate amounts of muriatic acid, well diluted. Quinia in
small doses and stimulants are appropriate whenever there is no
contraindication to their employment. The treatment of the paralysis
itself will naturally depend on the diagnosis of the condition present
in each individual case, which we have seen to differ considerably.
This alone can explain why various modes of treatment, the electric
current among others, after being recommended by some authors, are
branded by others. Where we have to deal with those rare changes in
the brain and spinal cord, the utmost care is necessary in order not
to make the condition still worse; and in such cases there would be a
contraindication to the use of the faradic current, though this would
not hold true with regard to the use of the galvanic current in short
sittings. Besides, central paralyses are by no means so frequent as
peripheral ones. In most cases there is not the slightest elevation of
temperature during the course of the paralytic phenomena. I lay great
stress upon this point, for I am aware that many cases of central
congestion and even of inflammation exhibit but very insignificant
elevations of temperature. But, as the diagnosis will depend on a
positive knowledge of whether there have been changes of temperature,
I rely on the rectal temperature only, for many a myelitis runs its
course with no greater elevation above the normal than one-half or one
degree. In all cases in which the temperature is normal or subnormal,
I do not hesitate for a moment to employ the faradic or the galvanic
current. In addition to the internal administration of iron I advise
by all means the employment of strychnia. When there is no necessity
for haste, we may give moderate doses, gradually increasing them, and
using iron in combination. When there is danger in delay, recourse
ought to be had to subcutaneous injections of the sulphate of
strychnia, once or twice daily. They are mainly indicated in paralysis
of the muscles of deglutition and of respiration. Of course, where the
former are affected it is necessary to nourish the patient
artificially, partly perhaps by nutrient enemata, but principally by
means of the stomach-tube. In using the latter it is unnecessary to
introduce it into the stomach, as it only requires to be passed a few
inches below the affected parts, when the oesophagus will usually be
found able to undertake the further disposal of the food. In these
cases strychnia should be injected subcutaneously in the neck, {714}
once or twice daily. In a similar manner it should be injected in the
region of the chest, diaphragm, or neck in paralysis of the
respiratory muscles or of the glottis. In paralysis of the muscles of
accommodation (in which Scheby-Buch claims to have seen the process
cut short by the use of the Calabar bean, considered as inert by
Hassner) they may be given in the forehead or temples.
Frictions dry and alcoholic, hot bathing, friction with hot water,
kneading of the affected parts, will be found beneficial and pleasant.
{715}
CHOLERA.
BY ALFRED STILLE, M.D., LL.D.
DEFINITION.--Cholera is an epidemic disease, characterized by the
transudation of serum into the stomach and bowels, and usually by the
profuse discharge by vomiting and purging of a liquid resembling
rice-water, followed by a tendency to collapse. It is endemic in
India, but has been conveyed thence to almost every part of the world.
SYNONYMS.--Cholera algida, C. asiatica, C. asphyxia, C. maligna, C.
spasmodica. In English it is generally spoken of as Asiatic cholera.
HISTORY.--It is sometimes stated that Hippocrates, Galen, Celsus, and
the Greek, Roman, and Arabian medical writers generally record "the
fact of the presence of cholera in the various countries in which they
lived" (Macnamara). Nothing could be more contrary to the truth. All
of these writers describe "cholera morbus" in nearly identical terms;
they all include bilious discharges among its symptoms, and no one of
them speaks of it as a mortal or even as an epidemic disease.
(Compare, especially, Celsus, Aretaeus, Caelius Aurelianus, and Paulus
Aegineta.) Their description of sporadic cholera morbus is very
precise. For example, Caelius Aurelianus says: "Cholericam passionem
aiunt aliqui nominatam a fluore fellis, per os et ventrem effecto."[1]
[Footnote 1: _Acut. Morb._, lib. iii. cap. xix.]
Asiatic epidemic cholera is a very different disease. It seems to have
been known in India from a very remote period, but no detailed account
of it was published until the beginning of the sixteenth century.
During that century many successive descriptions of the disease
exhibited its extreme violence and mortality. It is believed to have
occurred repeatedly, if not annually, in the same localities down to
the present time. The invasion of India by the Portuguese, and
afterward by the English, contributed to spread the disease throughout
the Peninsula, partly by military occupation and partly through
commercial channels, by which it was also carried to the islands in
the Indian Ocean. It prevailed in Batavia in 1629. Between 1768 and
1790 numerous epidemics of cholera occurred. About the former date no
less than 60,000 persons are said to have perished near Pondicherry,
and in 1783 it is reckoned that 20,000 victims to the disease fell in
a single week during the religious gathering at the sacred city of
Hurdwar, where, as will be seen hereafter, it became in later years
more fatal still. The English armies extended their conquests in
Hindostan, and established commerce between that country and Western
Asia and Europe, and by the year 1817 opened new channels of {716}
communication in every direction, both within and beyond the
Peninsula. Along them the disease was carried; it invaded Ceylon and
the Burmese empire, and extended to Batavia, Java, and China on the
east, and advanced westward to Persia in 1821. In that year also it
was carried from Arabia into Africa, and at various later periods
penetrated more and more deeply into the Dark Continent, always
following the track of pilgrims returning from Mecca, the routes of
armies engaged in war, or those of trading caravans.[2]
[Footnote 2: Christie, _Cholera Epidemics in Africa_, 1876.]
In these cases, as in others elsewhere, the spontaneous origin of the
disease has been assumed by certain writers, but at every stage of its
progress careful investigation led uniformly to the conclusion that it
was propagated directly or indirectly from pre-existent cases of
cholera. From Persia it moved northward as far as the shores of the
Caspian Sea, and westward to the Levant in 1823, and there for a time
its ravages were stayed. Meanwhile, it prevailed at various places
throughout Hindostan, and, assuming a greater degree of violence in
1826, it advanced steadily in a north-western direction across
Afghanistan and Persia in the following year. In 1829 it reached
Orenburg, to the north of the Caspian Sea, and was speedily conveyed
into the interior of the Russian empire, where it raged with great
violence in 1830. In 1831 it prevailed at Mecca among the pilgrims,
who had brought it from India, and so virulently that one-half of them
are computed to have perished. Hence it speedily passed with returning
pilgrims to Alexandria and Constantinople, and was carried to St.
Petersburg, to Sweden, to Hamburg, and other places in Northern
continental Europe. From Hamburg and other seaports it was conveyed to
commercial towns on the eastern coast of England, whence it extended
to Edinburgh in the north and London in the south.
In 1832 cholera prevailed in France, and within the year caused
120,000 deaths, 7000 of which occurred in Paris in the space of
eighteen days. In the spring and summer of that year it was reproduced
in England, and extended to Ireland. From Liverpool, Cork, Limerick,
and Dublin five vessels filled with emigrants sailed for Quebec,
Canada, and they, together, lost 179 passengers by cholera during the
voyage.
The immediate results of this importation and first appearance of
cholera on the American continent are described by Dr. Peters as
follows: "All these ships and their passengers were quarantined at
Grosse Isle, a few miles below Quebec. On June 7th the St. Lawrence
steamer Voyageur conveyed a load of these emigrants and their baggage,
some to Quebec, but the majority to Montreal on the 10th. The first
cases of cholera occurred in emigrant boarding-houses in Quebec on the
8th, and the same pest-steamboat, the Voyageur, landed persons dead
and dying of cholera at Montreal, a distance of two hundred miles, in
less than thirty hours. Over this long distance, thickly inhabited on
both shores of the St. Lawrence, cholera made a single leap, without
infecting a single village or a single house between the two cities,
with the following exceptions. A man picked up a mattress thrown from
the Voyageur, and he and his wife died of cholera; another man,
fishing on the St. Lawrence, was requested to bury a dead man from the
Voyageur, and he and his wife and nephew died. The captain of a
passing boat requested an Indian to bury a man from on board; this man
and five other Indians were attacked {717} and died. The town of Three
Rivers, halfway between Quebec and Montreal, forbade steamers to land,
and escaped for a long time. From Montreal the great influx of
emigrants were forwarded away, by the Emigrant Society, as fast as
they arrived, and by them the pestilence was sown at each
stopping-place. Kingston, Toronto, and Niagara soon became affected.
In the end, over 4000 persons died of cholera in Montreal, and more
than an equal number in Quebec. The epidemic reached Detroit in the
same way, ... and continued west along the Great Lakes, until in
September it reached our military posts on the Upper Mississippi....
Fort Dearborn, near Chicago, was temporarily reoccupied in 1832, and
it was here that epidemic cholera displayed its most fatal effects
among our troops. Out of 1000 men, over 200 cases were admitted into
hospitals in the course of seven or eight days.... When these troops
again marched for the Mississippi, they appeared in perfect health,
yet the cholera broke out again on the way, and when the command
reached the Mississippi it had been as fatal as it had been at Fort
Dearborn."
Meanwhile, an emigrant ship with cholera on board reached New York,
whence the disease spread up the Hudson River, and was also carried
southwardly to Philadelphia and the West. The mortality in New York
City from this epidemic is stated at 3500. In 1833 the disease broke
out in the cities of Havana and Matanzas in Cuba, and is said to have
destroyed one-tenth of the entire population. Hence it was carried to
Mexican and American towns on the Gulf of Mexico, and up the
Mississippi and Ohio as far as the western border of Pennsylvania. In
the following year it was again introduced at the port of Quebec by a
vessel filled with emigrants, of whom many had died during the
passage. It prevailed in Canada and the State of New York and spread
over the whole country in 1835 and 1836. In the former of these two
years it was confined to several Southern cities, whither it was
brought, as on a former occasion, directly from Cuba. It then
gradually subsided, and at last disappeared for the space of nearly
ten years.
But in 1845 it was known to be advancing on its former path, which it
steadily pursued, and entered England in October, 1848, at Sunderland,
the very town at which it first appeared in 1831. "During the second
epidemic in Europe, in 1848, two vessels sailed from Havre, where
cholera prevailed--one, the New York, for New York, and the other, the
Swanton, for New Orleans. Both contained large numbers of German
emigrants. On one vessel the cholera appeared when it was sixteen days
out, with fourteen deaths; on the other, in twenty-six days, with
thirteen deaths. The New York arrived at Staten Island Dec. 2, 1848,
and a severe epidemic broke out, but was confined to the quarantine
grounds. The Swanton arrived at New Orleans Dec. 11th; no quarantine
was instituted, and in two days its sick were taken into the Charity
Hospital. This was the beginning of a severe epidemic, which increased
in power all winter, till, in June, 1849, 2500 died of it in New
Orleans. December 20, 1848, it reached Memphis by steamboat from New
Orleans, and for twenty-five days was confined to the landing-place of
the former city, whence it afterward spread. In the spring it was
carried to St. Louis and Cincinnati and the whole Mississippi Valley.
In October it reached Sacramento, Cal., by means of overland
emigrants, and, almost at the same time, San Francisco, by the U.S.
steamer Northerner from {718} Panama. The Chinese of California
suffered most severely" (Peters). In April, 1849, cholera reappeared
in the public stores at the quarantine station, Staten Island, N.Y.,
and in the city of New York, where it was fatal to 5000 persons.
A pause now took place in the ravages of the disease which lasted
until 1853. In that year it destroyed no less than 11,000 persons in
the Persian city of Teheran. At Messina its victims numbered 12,000,
in France 114,000, and in England about 16,000. In 1854 it was
introduced by emigrant ships into New York, causing a mortality of
2000 persons, and was carried to Philadelphia, where its victims
numbered 500. It extended to many towns in New England and westward
along the great channels of emigration. In Montreal the deaths were
1300, and in the then small town of Detroit, 1000.
After an interval of quiescence longer than any previous one the
cholera again broke out among the pilgrims to Mecca in December, 1864.
It appeared in Alexandria during May, 1865, and thence was carried to
many parts of Europe, and from them to North America and the West
Indies. This period of exemption included that of the Civil War in the
United States, when, if ever, the local causes which have been
erroneously assigned to the disease existed in all their forms and in
the most intense degree. It was only when its specific germs were once
more imported that cholera began to prevail again. Official records
show that in 1866 it was introduced from Europe into Halifax, N.S.,
the city of New York, and the military posts of New York harbor.
Thence it was carried in troop-ships to various Southern ports, from
which its progress could be traced to Texas and other Gulf States, and
to the towns on the Mississippi and Missouri Rivers. From New York,
also, the disease travelled westward to Cincinnati and the U.S.
barracks at Newport, on the opposite side of the Ohio River, whence it
advanced in a south-westerly direction to meet the trail that, coming
from the South, followed the great rivers of the Mississippi Valley.
During the summer of 1867 cholera again prevailed, although less
fatally, at most of the points, especially of the Mississippi Valley,
which had been invaded the previous year, and some cases occurred at
the military posts around New York in recruits who had shortly before
arrived from places in the West where cholera prevailed. Thus did the
disease complete the circuit of the United States.
Meanwhile, cholera prevailed to a greater or less extent in the east
of Europe between 1865 and 1874. After the latter date it seems to
have been confined to Syria, Arabia, and the African shore of the
Mediterranean. In 1877-78 it existed to a limited extent among the
pilgrims at Mecca, and since then it has not been known in Europe. The
latest appearance of cholera in the United States was in 1873, when it
occurred at three points far distant from one another. It was
introduced in the effects of immigrants. The vessels that brought them
were in a perfect sanitary condition. The passengers themselves were
healthy, and remained so after landing and until they reached the
distant points of Carthage, Ohio, Crow River, Minn., and Yankton,
Dak., where their goods were unpacked. At each place, "within
twenty-four hours after the poison particles were liberated, the first
cases of the disease appeared, and the unfortunates were almost
literally swept from the face of the earth" (E. McClellan).
{719} In 1881 cholera was brought from Hindostan to Arabia by pilgrims
on their way to Mecca, where it soon afterward broke out and caused
the death of about 8000 persons. In the following year several vessels
from Bombay evaded the quarantine and reached Djeddah, the port of
Mecca, and the pilgrims on reaching the latter city disseminated the
disease. The unusually small number of persons who were there at the
time, and their prompt dispersion before the danger, limited the
mortality, and gradually cases of cholera ceased to appear. In 1882,
the English at that time carrying on war in Egypt, very rigid sanitary
precautions against the importation of cholera were enacted and
successfully enforced, but in the following year, the same urgent
necessity no longer commanding, they were considerably relaxed. At the
end of June, 1883, the cholera made its appearance at Damietta (at one
of the mouths of the Nile), and soon afterward at Rosetta, Port Said,
and Mansourah. During July it spread to various places in direct
communication with those named. At Cairo it was peculiarly fatal, and
on July 20th it was reported to have caused 600 deaths. For several
days the daily mortality varied between 500 and 600. The disease
prevailed somewhat in Alexandria during the height of the epidemic,
and near the end of October it was fatal to numerous European
residents of that city, and some deaths occurred in the British army
of occupation. In all Egypt, during the week ending Aug. 13th, the
total mortality is said to have been 5000, but in the following week
it fell to 2000. It is estimated that the epidemic destroyed at least
20,000 lives. The germ of this epidemic has not been accurately
determined. Some regard it as a survival of the cholera of the
previous year--a supposition which is at least plausible and
sufficient; but certain "sanitarians" have attributed the outbreak to
the ordinary causes of disease intensified by the civil war which had
recently devastated Egypt. It is sufficient here to say that while
such causes have in all ages generated typhus and typhoid fevers and
dysentery, they never produced cholera. Some, more unwise than
judicious, declared that the Egyptian disease of 1883 was not cholera.
It is alleged, on the one hand, that several East Indian merchants
from Bombay arrived at Damietta on June 18th, or three days before the
disease was recognized in that city. It is also said that a stoker
from on board an English steamer from Bombay introduced the cholera
into Damietta. But the judgment of Surgeon-General Murray carries with
it greater weight.[3] He is of the opinion that the Egyptian epidemic
of 1883 was simply a revival of the Arabian epidemic of 1882. He shows
that cholera existed in several villages on the Damietta branch of the
Nile in the latter part of May and during June, and that it broke out
in the capital itself, during a fair which had lasted for eight days,
on the 22d of June, and was spread by the people on their return from
Damietta to their villages. This, adds Mr. Murray, "is a literal
transcript of the accounts of many of the severe epidemics that have
raged over India." It also appears from M. Proust's narrative[4] that
the Ottoman government had already, as early as April, notified the
government of Egypt that certain Indo-Javanese pilgrims were on their
way to Mecca, and that ought not to be allowed to land without
quarantine. The French delegate to the sanitary council also begged
that those of the pilgrims who reached Suez without previous
quarantine should be isolated and kept under {720} surveillance for
three days. But owing to the opposition of the English delegates these
measures were not duly enforced, the council did not meet again, and
no protective system was adopted.
[Footnote 3: _Times and Gazette_, Feb., 1884, p. 209.]
[Footnote 4: _Le Cholera_, 1883.]
ETIOLOGY.--The essential cause of cholera is unknown, unless the
investigations of Koch, described below, may have revealed it. Its
secondary causes, or the conditions of its dissemination, are better
understood. Some general propositions concerning them will here be
laid down, and illustrated so far as the argument requires and the
available space will allow.
Cholera is endemic in no other country than India, and more
particularly in Bengal. When it has occurred elsewhere it has
invariably been carried from India. The cholera poison has been
imagined to be of an aerial nature, but its diffusion has no relation
whatever to the velocity or the direction of the wind. In no instance
whatever has its rate of progress exceeded that of man on land or
water, nor has it ever taken a direction different from that of
commercial or military movements. On land it has usually crept from
place to place, and if sometimes it has seemed to leap across wide
spaces, and even seas and oceans, it has never invaded any inland town
or seaport without having been brought thither from a point already
affected with the disease. Nor, having once entered an inland or
seaboard town, does it spread equally therein in all directions, but
prevails chiefly in the quarter immediately surrounding the place of
its entrance. If appropriate sanitary measures are enforced, it is
sometimes confined to that quarter, and, in the case of quarantine
stations, it has repeatedly been prevented from extending beyond them.
This statement may be illustrated by the fact that of fourteen
epidemics of cholera at Staten Island, the quarantine station of New
York, all but four were prevented from reaching that city.[5] When the
disease does overleap the barrier opposed to it, its origin and
subsequent course can usually be traced.
[Footnote 5: Peters's _Notes, etc._, 2d ed., p. 94.]
A high atmospheric temperature is everywhere associated with the
prevalence of cholera. Its origin in the hot climate of Hindostan and
its general progress prove this conclusively. In nearly all of the
places where a great difference exists between the summer and the
winter temperature the disease has disappeared during the cold season,
and attained its greatest intensity during the hot months of the year.
The only apparent exception to this rule is, that cholera has
prevailed in several Russian, Swedish, and Norwegian cities during the
winter. But these very exceptions confirm the rule; for in the
countries mentioned the intense cold of the winter compels the
inhabitants to seal their houses by every possible means, while the
atmosphere within them is kept at a high temperature by huge stoves,
which hinder ventilation, and indeed render it almost impossible.
Difference of temperature likewise explains the fact that of two
cholera-ships arriving from Havre, the one at New York and the other
at New Orleans, in December, 1848, the former did not disseminate the
disease, but the latter formed the starting-point of an epidemic which
lasted all the winter.
A good deal has been written of the predisposing causes of cholera,
and poverty, crowding, filth, intemperance, and depression of spirits
have been given prominent places in the catalogue. But to any one
familiar {721} with the history of epidemic diseases it will at once
be apparent that every one of these conditions favors the spread of
all communicable infectious diseases. There is not the slightest
evidence that these agencies, singly or combined, can generate cholera
or favor its spread apart from the presence of the specific poison of
the disease and the facility with which it is transmitted from the
sick to the well whenever the population is crowded, poor, of filthy
habits, and weakened by dissipation. Because among such people
intemperance prevails, this vice has been regarded as predisposing to
cholera. Apart from the brutish mode of living of drunkards, there is
nothing to show that they are more liable to cholera than the most
abstemious of water-drinkers. On the contrary, it is notorious that
during cholera epidemics drunkards in the better classes of society
enjoy a certain degree of immunity from the disease; which it is easy
to explain on the ground that they imbibe but little water, which is
the main channel through which the infectious principle of the disease
is spread.
The specific cause of cholera is taken into the alimentary canal, and
acts through it to produce the characteristic symptoms of the disease.
It is conveyed from the sick to the well by means of the
gastro-intestinal discharges, either moist or dry; in the former
state, by means of drinking-water, and in the latter through the air,
whose suspended noxious particles are received into the fauces and
swallowed. There is reason to believe that the poison does not enter
the system through the lungs, or through any other channel than the
gastro-intestinal canal. W. B. Carpenter[6] appears to hold, however,
that the poison may be absorbed through the lungs. To this view there
are two objections: 1, That whatever is taken into the mouth or throat
by inspiration may very well be swallowed; and, 2, that all the
primary lesions of cholera affect the digestive and not the
respiratory apparatus. It is not at all necessary to the propagation
of cholera that its excreta should be furnished by persons laboring
under the fully-formed disease. A specific choleraic diarrhoea is as
infectious as the evacuations which occur in completely developed
cholera. But neither will propagate the disease through the air to a
distance. The tendency to its propagation in this manner depends
chiefly upon the concentration of the poison; thus, it much more
frequently occurs in close than in well-ventilated rooms or than in
the open air. It has been argued that cholera is not contagious,
because so few, comparatively, of the attendants upon cholera patients
contract the disease. On the other hand, as some of them are attacked,
this positive fact outweighs an indefinite number of negative
instances. It should also be noted that different diseases enter the
system and infect it through different channels--some through the
lungs, others through the alimentary canal, etc. Small-pox, the most
contagious of all diseases, is introduced through the air-passages,
and is probably harmless when its virus is taken into the stomach.
That the converse of this proposition applies to cholera is sustained
by the whole history of the disease. Cholera poison may be taken to
considerable distances in either a moist or a dry condition. In the
former state it is mainly conveyed by water, as in rivers,
water-pipes, etc.; in the latter, by fomites and especially by
clothing saturated or merely soiled with cholera discharges, and which
may retain their infectious quality for an indefinite time.
[Footnote 6: _The Nineteenth Century_, Feb., 1884.]
{722} Great stress has been laid upon the humidity and foulness of the
soil, a damp atmosphere, filth, crowding, etc., as elements in the
production of cholera, but in reality they have no more essential
relation to it than to any other disease that occurs epidemically.
Cholera may prevail whether they are present or absent. It is evident
that from the earliest historical periods all of these causes of
disease have existed, and in Europe much more generally and
excessively than during the present century, and that they have never
been removed in Asia Minor, Egypt, Arabia, and Africa. Yet cholera
never was known in any of these countries until it was brought into
them about the end of the first third of the present century.
According to Pettenkoffer, cholera is most prevalent when the subsoil
water is lowest, and least so when the subsoil water is highest. It
would be more descriptive of the fact to say that, so far as cholera
has anything to do with the condition of the soil, it is most apt to
be severe and prevalent when very dry weather follows a very wet
period. Such circumstances are the most favorable to putrefactive
fermentation and the dissemination of its products, which thus reach
wells of drinking-water, and even rivers, especially when sewers empty
into the latter. The identity of this explanation with that which is
generally accepted for the dissemination of typhoid fever is too
evident to be insisted upon. We might go farther, and say that, in
typhoid fever as in cholera, the disease is communicated, although
exceptionally, by the air of the sick room and by the exhalations of
the soiled fomites of the patient. Now, if typhoid fever resembled
cholera not only in being transmitted by means of the dejections, but
also in its poison being derived from one primary source only, the
analogy between the causes of the two diseases would be very striking
indeed. But, in point of fact, the typhoid-fever poison may probably
be generated de novo by fecal fermentation and other forms of
putrefaction, and the disease is only exceptionally communicable;
whereas, the poison of cholera, once received, is conveyed from man to
man and far and wide through various channels; but, so far as is
known, it has but one primary source, and that is in India. Lebert
states that he did not find the localities that are the ordinary seats
of typhoid fever peculiarly liable to invasions of cholera. But it
must be noted that typhoid fever is very far from being exclusively a
disease of the poor, squalid, and vicious. Like death itself, "regum
turres pauperumque tabernas aequo pede pulsat;" while cholera much
more commonly plants itself and disseminates its seeds in the rank
soil of moral and physical degradation.
All morbid causes whatever, derived from race, climate, religion,
dwellings, food, clothing, habits of living, etc., have no more to do
with the development of cholera than with that of the eruptive fevers,
and even less than with the causation of typhus and typhoid fevers and
dysentery. The eruptive fevers are caused, as cholera probably is, by
specific germs which no known combination of natural causes has ever
developed, while the poisons of the other diseases named appear to be
generated anew whenever certain more or less definite physicial
conditions coexist. It would seem that cholera differs radically from
all of these affections by the fact that its cause does not enter the
circulation, but confines its direct operation to the
gastro-intestinal mucous membrane. In this way it becomes intelligible
that while, on the one hand, physicians and nurses of {723} cholera
patients, although often, in fact, yet in relation to their numbers,
are comparatively seldom infected, provided they duly observe proper
sanitary rules, the disease, on the other hand, spreads like wildfire
among those who drink water polluted by cholera excretions, and only a
little less rapidly among people crowded into ill-ventilated
apartments along with cholera patients.
The special fomites of the cholera poison are articles of clothing and
furniture soiled with the discharges of the sick, and the emanations
from privies, sewers, etc. into which these discharges have been cast.
Many considerations render it probable that a very small quantity of
cholera matter may suffice to render infectious a very large quantity
of liquid, and especially of matters in process of putrefactive
fermentation, and that the gaseous or vaporous emanations from them
become diffused in the atmosphere and infect all who imbibe them. But
water contaminated by cholera discharges is the most rapid and
efficient agent in disseminating the disease. Innumerable instances of
this mode of action are furnished by its history in Asia and Africa,
where water is often scarce, and naturally so impure that its
additional defilement by cholera dejections is apt to pass unnoticed.
From the illustrations of this proposition which might be adduced only
a few of the more striking will here be selected.
Hurdwar is a town in Northern India at the base of the Himalayas,
where the Ganges begins its course in the plains. It is the seat of a
great Hindoo pilgrimage, which takes place annually in April, when
sometimes from 2,000,000 to 3,000,000 of people occupy an encampment
of about twenty-two square miles, comprising a low flat island in the
Ganges and the opposite banks of the river. Bathing in the sacred
stream on a certain day is the main object of the devotees; which day,
in the year 1867, fell on the 12th of April. The bath was taken early
in the morning. From noon on that day the pilgrims began to disperse
so rapidly that on the morning of the 15th the encampment was quite
deserted. It appears that up to the former date the health of the
encampment was excellent, and it was the opinion of the reporter (Dr.
Cunningham) that cholera was introduced into the camp by pilgrims from
the neighboring districts going late to the fair. He believed that the
cholera excreta may have been buried in the trenches and carried by a
heavy rain into the river, and there swallowed by the pilgrims; for to
drink of the water of the Ganges as well as to bathe in it is a
religious obligation.
Immediately after the breaking up of the camp cases occurred in the
surrounding districts, the epidemic widening in all directions. The
pilgrims were almost always the first persons attacked in any
locality, and the cholera attended them on their route wherever they
went. In all the districts where the disease prevailed no cases
occurred until ample time had been given for the pilgrims to reach
them. In a word, "the cholera first showed itself among them; it
followed their lines of route only, and did not outrun them; their
progress was its progress, and their limits its limits." The mortality
caused by this epidemic among the whole civil population of the
North-western Provinces of the Punjab has been estimated at about
117,181.[7] The history of the religious festival of 1879 {724} was
identical with that just sketched, except that the number of the
pilgrims was smaller and the deaths proportionally less.[8]
[Footnote 7: _Brit. and For. Med. Chir. Rev._, Jan., 1870, p. 137.]
[Footnote 8: Murray, _Practitioner_, xxvi. 309.]
Out of the numberless illustrations of the manner in which cholera is
disseminated by water the following may be cited: In 1865 about
100,000 pilgrims were assembled at Mecca, of whom from 10,000 to
15,000 fell victims to the disease, two-thirds of them within a period
of six days. Some cause acting simultaneously upon the whole number of
persons must be admitted to account for so extraordinary a fact, and
such a cause is not far to seek. At a certain sacred well "one hundred
thousand people had skinfuls of water poured over them at the side of
the well, and every one of them then drank largely of water drawn from
the well. Much of the water poured over the pilgrims must have found
its way by soakage back into the well, and if any of the pilgrims were
at the time suffering from cholera, or had cholera-tainted garments
about them, the well would be exposed to pollution."[9]
[Footnote 9: Christie, _Cholera Epidemics in East Africa_, p. 488.]
In the cholera epidemics of Zanzibar the disease produced the greatest
havoc among the negroes, the Persians, and the East Indians; very few
Europeans were attacked, and quite as few of the sect of the Banyans,
who drank only water drawn from their own wells. The persons among
whom the disease prevailed so fatally used chiefly the water of a
certain well which was highly prized, but which on this occasion had
become polluted by soakage from an adjacent cesspool into which the
dejections of cholera patients had been thrown. It appears, also, that
in Zanzibar the streams are very rarely bridged, and hundreds of
negroes, in passing backward and forward, wade through them and
pollute them. In these streams, also, the negroes wash their clothes
and all the foul clothing of the contiguous town. While this business
is going on "a gang of negroes may be at work at not many hundred
yards' distance filling water-casks for the shipping." Subsequently to
the watering of the ships in this manner sailors were attacked with
cholera, and others who used water drawn from the stream below the
place where it became polluted were attacked, and many of them died;
while Europeans living on shore, and who drank the water of the same
stream, but drawn from a much higher point in its course and after
having been filtered, escaped the disease.[10]
[Footnote 10: _Ibid._, pp. 320, 492.]
The history of the disease in Europe furnishes a multiplicity of
similar cases, and even more distinctly exhibits the dissemination of
cholera by contaminated water.[11] In Holland not less than five
epidemics of the disease occurred between 1832 and 1869, all of them
causing a great mortality, to which the epidemic of 1866 alone
contributed not less than 20,000 deaths. This was about 55 deaths for
every 10,000 inhabitants. Such exceptional mortality over so wide a
territory has been ascribed to the extreme porosity and humidity of
the soil, which is nearly all below the level of the sea. Such a soil
must necessarily retain longer than other soils whatever it absorbs,
and thus tend to render the well-water habitually impure. If, then, to
the ordinary impurities a specific {725} poison is added, its
characteristic effects may assuredly be looked for. The conditions now
stated explain the conclusions of Ballot of Rotterdam, drawn from a
study of the several epidemics referred to. They are as follows: "1.
Holland is highly affected by the cholera at every epidemic, chiefly
in those parts where they drink water directly from the rivers and
canals or from ground saturated with sewage. 2. In places where
rain-water is generally drunk the disease is far less violent. 3.
Places where there is no other drinkable water but rain-water are not
affected by the epidemic; the single cases occurring there are
imported. 4. When places affected by the cholera were supplied with
pure water instead of the vitiated water the disease disappeared."[12]
In like manner, we find that the cholera epidemic of 1873 in Germany
seemed specially to select those situations where the subsoil was
impregnated with decomposing organic matter; and it is evident that,
in cities especially, such situations would include the most
poverty-stricken districts, while the higher, drier, and at all times
more salubrious localities are inhabited by the classes enjoying the
greatest material prosperity.[13]
[Footnote 11: It is of interest to note that on the first appearance
of cholera in England, at Sunderland, in 1831, a surgeon of that
place, Mr. Ainsworth, collected and published conclusive proofs of the
importation of the disease, of its communication from the sick to the
well, "and of its propagation by clothes, and even by emanations, from
the dead" (_Observations on the Pestilential Cholera_, London, 1832).]
[Footnote 12: _Med. Times and Gaz._, May, 1869, p. 459; June, 1869, p.
626.]
[Footnote 13: "Report of the German Imperial Commission,"
_Practitioner_, xxvi. 153.]
This mode of infection has been traced in numberless individual cases
of cholera. In London there was a certain well into which the liquid
contents of a sewer had been percolating for months. Of the water of
this well hundreds of persons had been drinking without obvious
injury. At last a case of cholera occurred hard by; the discharges
were thrown into a privy which communicated with the sewer and
indirectly with the well, whereupon more than 500 persons who drank
water drawn from that particular well were attacked with cholera
within three days. So in 1856 cholera prevailed in the county jail of
Oxford, Eng., the drain from which emptied into a pool from which the
water was drawn to supply the city prison. In the latter institution
cholera began to prevail, but declined as soon as the pipes conveying
the water were cut off, and soon afterward ceased entirely.[14] Again,
in Constantinople in 1865 the clothes, mattrasses, etc. of cholera
patients were washed at a fountain the basin of which was divided into
two parts by a wall; one part was used for washing clothes and the
other for drinking purposes. Unfortunately, the waste-pipe of the
former being obstructed, the foul water of one side communicated with
the clean water of the other, and in one day 60 people died of cholera
in the small portion of the city which was supplied from the infected
source. The striking case has often been cited which occurred at
Epping, Eng., where a woman brought the disease from a distance into a
perfectly healthy house and neighborhood, and of ten persons affected
with it seven died, including a physician in attendance upon one of
them. An examination of the premises "discovered, below the pipes
leading from the water-closet and from the eye-hole of the sink
through which the choleraic dejections had been passed, a leakage
which extended under the foundations of the building and entered the
well. The sewage was distinctly traceable on the side of the well
corresponding with the leakage in the drain." After this discovery and
the disuse of the foul water not another case occurred.[15] In 1868,
Dr. {726} Farr, in his _History of the London Cholera Epidemic of
1866_, showed that water into which cholera dejections find their way
produces cases of cholera all over the district in which it is
distributed for a certain period of time, and that if the distribution
is in any way cut short the deaths from cholera begin to decline
within about three days of the date at which the distribution is
stopped.[16]
[Footnote 14: _Edinb. Med. Jour._, i. 1122.]
[Footnote 15: _Trans. of the Epidemiological Soc._, ii. 428.]
[Footnote 16: _Lancet_, April, 1868, p. 217.]
Analogous instances are furnished by every cholera epidemic of which
the history has been accurately observed, including that which
extended so widely over the United States in 1873. Most of the
following are cited from the official reports prepared, under the
direction of the Surgeon-General of the army, by Surgeon Ely McClellan
and Dr. John C. Peters. Several of the first cases, however, are
foreign.
In 1861, at a station in India, some fresh cholera dejecta found their
way into a vessel of drinking-water. Early on the following morning a
small quantity of this water was swallowed by nineteen persons, five
of whom were attacked with cholera between the first and the third day
afterward.[17] In 1876 an outbreak of cholera took place in a village
in Hindostan, which followed the arrival of wedding-guests, one of
whom was attacked, and from whom it rapidly spread. The soiled clothes
of one or more of the patients were washed in a pool from which all
the villagers obtained their drinking-water, and on the discontinuance
of this source of water-supply cholera speedily diminished in
frequency and fatality.[18] In the German epidemic of 1873 many cases
occurred where persons deriving their drinking-water from special
sources were attacked with cholera, while their neighbors, supplied
from a different source, remained free. Again, it has frequently
happened that outbreaks of cholera have been checked by the
prohibition of the suspected water and the substitution of a pure
supply.[19] It seems probable that a very small portion of cholera
discharges suffices to infect a very large body of water and maintain
its infectiousness for a considerable time.
[Footnote 17: Macnamara, _op. cit._, p. 196.]
[Footnote 18: Surg.-Major Cornish, _Practitioner_, xxiv. 215.]
[Footnote 19: _Practitioner_, xxvi. 159.]
In December, 1871, an outburst of cholera occurred which was confined
to the inmates of three excellent houses in a fine block of buildings
in Calcutta. There had been no cholera in that neighborhood for four
years. Within forty-eight hours a majority of the lodgers were sick,
and on investigation it was found that the disease was carried in the
drinking-water and in the milk diluted with it.[20] The particular
locality in which Dr. Koch made the discovery of the microscopic
representative of cholera furnishes an example of the same nature: "At
Saheb Ragau, a locality which has repeatedly been visited by cholera
during the last hundred years, numerous cases of the disease were
reported, and these, on inquiry, were found exclusively in the huts
situated round a certain tank. Of the few hundred people who dwelt in
these huts, as many as seventeen died of cholera, though the disease
was not at that time prevalent in the neighborhood, or indeed in the
whole police district of Calcutta. It was proved that, as usual in
such cases, the dwellers around the tank used it for bathing, and drew
thence their drinking-water; it was also elicited that the linen of
the first fatal case, befouled with cholera dejections, had been
washed in the tank."[21] In June, 1873, a new {727} hotel was opened
at Vienna, and many of the guests became affected with diarrhoea that
was attributed to the drinking-water, which was offensive to the taste
and smell. After a fortnight a gentleman died of cholera in the hotel,
and two days later several of the guests were attacked with the
disease, of whom fourteen died. The gentleman who first died was
believed to have brought the poison with him into the hotel, so that
the drinking-water, which previously had been polluted with ordinary
fecal discharges, became specifically affected through him.[22] The
discharges of one ill of cholera were thrown into, and the vessels
used by him were washed near, a well from which all the residents of a
farm-house drank. The wooden curbing of the well had rotted, and the
ground immediately around had sunken; a heavy rain burst the curb,
overflowed the well, and washed into it the entire surface-drainage of
the surrounding ground. No attention was paid to this, and the water
was used as before. It became so offensive that its use was forbidden,
but too late to save the family, nine of whom died of cholera.[23]
[Footnote 20: _U.S. Report_, p. 85.]
[Footnote 21: _Times and Gaz._, April, 1884, p. 527.]
[Footnote 22: _Times and Gaz._, p. 86.]
[Footnote 23: _Ibid._, p. 140.]
At Farmington, Tenn., a man arrived who had contracted the cholera at
Nashville; his illness ran its course at a point just forty paces from
a well. Families that obtained their water from this well suffered in
nearly all their members; where only certain members drank of it, they
alone were affected.[24] At Huntsville, Ala., during an epidemic of
cholera, the city authorities forbade the use of well-water, and
supplied pure water from another source, but only for one week. During
this time no new cases of the disease occurred, and the negroes,
thinking themselves secure, resumed the use of the well-water, and
within four days six fatal cases of cholera occurred in the vicinity.
The use of the well-water was again prohibited, and again the progress
of the disease was arrested.[25]
[Footnote 24: _Ibid._, p. 172.]
[Footnote 25: _Ibid._, p. 408. For other examples of the spread of
cholera by means of drinking-water see Macnamara, p. 149 and seq.]
It has already been intimated that the cholera poison may be diffused
through the air from either moist or dry sources, and especially from
contaminated clothing, and then be taken into the throat and
swallowed. Dr. Richardson refers to a local epidemic in England in
which "the persons most constantly and fatally attacked were the women
who washed the clothes of the sick;" and this circumstance has been
largely confirmed by other observers.[26] In a village not far from
Marseilles, and in an isolated place, a peasant and his wife who had
not left the country sickened and died of the disease. The woman, who
was a laundress, had received a bundle of linen belonging to a person
recently arrived from Egypt, and the husband opened the bundle and
unfolded the pieces. During the Crimean War many of the washermen
attending to the washing of the French hospitals were attacked by
cholera. In the post-office at Marseilles none of the clerks who
handled the outgoing mails were attacked, but of those who sorted the
mails coming from the East, where the disease prevailed, one after
another suffered from cholera.[27]
[Footnote 26: _Trans. Epidem. Soc._, ii. 429.]
[Footnote 27: Read, Boston, 1866.]
The cholera was introduced into Guadaloupe by clothing contained in a
trunk belonging to a person who died on the voyage thither from
Marseilles, where the cholera then prevailed. The woman who washed the
clothing died, with all her family. Attracted by the circumstances of
{728} the case, many came to her house, and of these several died.
From this point the disease spread over the island.[28] A sailor died
at some port in Europe of Asiatic cholera in 1832. A chest containing
his personal effects, clothing, etc. was sent home to his family, who
lived in a small straggling village on the Atlantic coast of the State
of Maine. It reached them about Christmas, and was opened on its
arrival. The inmates of the house were all immediately and suddenly
seized with a disease resembling Asiatic cholera in all its malignity,
and died. There had been no cholera in the State. The last case of
cholera that occurred in the garrison at Malta in the epidemic of 1865
was that of a woman who had stolen a chemise the property of one who
had died of the disease. She put on this fatal garment, probably
soiled with cholera discharges, and certainly unwashed, many days
after the death of its former possessor; she took the disease and
died.[29]
[Footnote 28: _Med. Times and Gaz._, April, 1874, p. 387.]
[Footnote 29: _Lancet_, Feb. 17, 1866.]
It is sometimes said, and oftentimes repeated, that cholera is not
directly contagious--is not communicated by the sick to the well. No
statement could be more unfounded. The whole history of cholera proves
that the physicians and nurses of cholera patients are often affected
by the disease. "In Constantinople no less than twenty-seven
physicians and medical assistants were attacked and died during their
attendance on cholera patients; and in Paris and Toulon similar
results followed. At Halifax, N.S., two of the physicians who
volunteered in aid of the steamer England, which put in there disabled
by the ravages of cholera among the officers and crew, as well as
among the steerage passengers, took the disease, and one died" (Read).
In 1832 the cases of cholera in Edinburgh were in the proportion of 1
to every 1200 of the population of the city, while among those in
attendance upon the sick the proportion was 1 to 5. In 1848-49
one-fourth of the nurses employed in the cholera hospital took the
disease, while in the general hospital, only a few paces distant,
where no cholera patients were received, not a single attendant was
attacked. In the London Hospital, in 1866, none of the medical
officers, volunteer nurses, or sisters were attacked. Of the (regular)
nurses five contracted the disease, and of these four died.[30] In
1849 a severe and fatal epidemic broke out in the Philadelphia
Almshouse. The resident physicians of the hospital were abundantly
occupied with the care of the sick of other diseases, and it was
thought prudent not to allow any, even an indirect, communication
between them and the cholera patients. The latter were therefore
removed to an isolated building in the middle of the quadrangle, and
attended by physicians from the city who had volunteered their aid.
Three or four of these physicians had attacks of cholera, and two of
them died.[31] At this time there was no cholera at all in the city,
and the young physicians could not have become infected outside of the
almshouse. They were attacked while attending the sick of cholera, but
the regular house-physicians, who seldom visited the cholera patients,
escaped altogether.
[Footnote 30: _London Hosp. Rep._, iii. 439.]
[Footnote 31: _Philada. Med. Examiner_, Nov., 1849.]
The importance of recognizing the communicability of cholera is so
great that no apology need be made for introducing the following
additional illustrations of it furnished by Griesinger in his article
on the dangers of cholera to medical men. They are the more important
because {729} in many other instances cholera physicians have suffered
little for their devotion to duty: "At Moscow, in 1840, hospital
attendants contracted the disease to the extent of 30 or 40 per cent.,
while in the general population only 3 per cent. were attacked; at
Berlin, in 1831, in Romberg's hospital, 54 out of 115 persons were
attacked: in 1837 one-fifth of the attendants took the disease, and on
one occasion no less than seven of them fell ill on a single day. In
La Charite Hospital in Paris, in 1849, one-sixth of the attendants had
the disease, while only one-twenty-fifth of the general population of
the city suffered from it; at Mittau, in 1848, one-half of the
physicians took the disease; in 1842, at Toulon, ten health officers
out of thirty-five were ill with cholera, and five of them died, while
of thirty workmen who were employed to carry the dead bodies one-third
succumbed; at Stockholm, in 1853, of 536 attendants one-eighth took
the disease, and half of that number died; at Vienna, in 1854, out of
thirty-six nurses, seven caught the disease, and seven men employed in
removing the dead became affected with a prolonged and exhausting
diarrhoea; in 1849, at Strasburg, five nurses out of ten were
attacked, etc." ... "Physicians, nurses, students, etc. are less
frequently affected, however, than patients ill with other diseases
who are lying in the wards where cholera patients are treated, and are
therefore more constantly exposed to the emanations from the
discharges; and physicians usually suffer less than the attendants who
are constantly waiting on the cholera patients."[32]
[Footnote 32: _Traite des Maladies infectieuses_, 1868, p. 409.]
It may be added that Surgeon-General John Murray, who served
continuously for thirty-eight years in British India, caused upward of
five hundred circulars to be addressed to the local governments and
filled up by the local medical officers. From these returns it
appeared that the belief in the communicability of cholera, in one way
or another, was practically unanimous; for of the whole number, those
who believed that it is conveyed from person to person were 75 per
cent.; from place to place, 85 per cent.; through the atmosphere, 80
per cent.; with the drinking-water, 85 per cent.; by the evacuations,
92 per cent.; and by clothing, 98 per cent.[33] This gentleman has
more recently furnished additional facts supporting the same
conclusion. For example: Out of fourteen cases that occurred at Ramleh
during the Egyptian epidemic, eleven occurred in patients already in
the hospital for other diseases. In 1856, after visiting the
dead-house where the bodies of fourteen cholera patients lay, as he
entered the cholera ward he felt a sudden shock in the epigastrium,
followed by a deadening sensation that rapidly spread over the whole
body. On another occasion he saw a clergyman who was talking to a
cholera patient suddenly seized with vomiting of a watery liquid.
Several analogous instances are related by him.[34]
[Footnote 33: _Practitioner_, xix. 470.]
[Footnote 34: _Med. Times and Gaz._, March, 1884, p. 281.]
It has been objected to the communicability of cholera that its
dissemination does not always follow the deposit of cholera discharges
in privies, wells, etc., and also that when infection does take place,
it may occur between remote extremes as to time, and therefore cannot
be attributed to infectious germs. Such objections are frivolous,
because we know nothing of the nature or vitality of cholera-germs,
and they are, moreover, drawn from exceptional cases. The power of
infected fomites to develop {730} the disease has been preserved, in a
journey from Arabia into Africa, for at least twelve days, and for
even a longer period in passing from Germany to Chicago, as already
related. It is true of every infectious and contagious disease that it
may possess one or both of these qualities in various degrees--that at
one time it is only exceptionally communicated, and that at another
time it appears to propagate itself virulently. So the phenomena of
cholera may consist of little more than a watery diarrhoea, which may
be so mild as hardly to disable the patient from working, while at
other times the attack may include all those terrible and fatal
symptoms which have won for the disease the name of malignant. That a
certain quantity, or "dose," of the cholera poison is required to
develop the disease, but one that varies considerably in different
cases, may be inferred from these facts: 1. Out of a certain number of
persons equally exposed to receive the disease, only a portion may be
attacked at all, and these in very unequal degrees. 2. Persons so
slightly affected as to be ignorant of the nature of their sickness,
and believing it to be an ordinary diarrhoea, may nevertheless become
the innocent, because ignorant, disseminators of cholera. The
explanation of such facts may be manifold: they may depend upon the
dose or upon the energy of the morbid poison, on various possible
conditions of its recipient, and so on; but, however explained, their
reality is none the less certain. The receptivity of persons exposed
to the contagion of cholera is very different. It is well known that
some persons appear to be proof against other contagious diseases,
while others seem never to acquire an immunity from them. On this very
important point the conclusions of Fauvel directly bear.[35] They
include the following propositions: The East Indian ports where
cholera exists as an endemic disease are never the seat of an
extensive epidemic among the native population. But strangers to these
localities are liable to the disease, and such are the Mussulman
pilgrims who come to Bombay to take ship for Mecca. A severe epidemic
of cholera confers upon the locality in which it has taken place an
immunity which in India appears to be of several years' duration. Such
an epidemic in any country is a proof that the cholera is not endemic
there.
[Footnote 35: _Memoire lu a l'Academie des Sciences_, 1883.]
If a contagious disease preserved its virulence undiminished, it might
continue to prevail indefinitely. But we know that all other
contagious epidemics do come to an end sooner or later, and hence we
must conclude that their specific cause progressively loses its
virulent qualities. There is every reason, therefore, to believe that
the same is true of cholera. Its communicability, and therefore its
diffusion, may vary with climatic, seasonal, local, personal, and
other conditions; but of what nature those conditions are, and
especially of the last and most important, the personal, hardly
anything is known. Nor need we too curiously investigate them, so long
as the fact remains that outside of, and independent of them all,
there is but one essential cause of cholera--a morbid poison as
specific in its nature as that of any of the eruptive fevers--a poison
which no determinable conjunction of circumstances has ever
engendered, and which was unknown in Europe and America before it was
carried to them from India. In just such a way did small-pox first
arise in the Western World. It had never appeared in Europe until the
latter part of the {731} sixth century, when for a short time it
prevailed in Marseilles and the neighboring country. Afterward it was
not heard of until it was reintroduced by the Crusaders on their
return from Palestine in the twelfth century, since which period it
has hardly ever ceased. The history of the diffusion of cholera is
closely analogous to this in several particulars, and we may
reasonably expect that what was in the last generation a new disease
will henceforth be liable to prevail again and again as the
intercourse increases between the nations of the West and the
immemorial source of cholera in Hindostan.[36]
[Footnote 36: Additional illustrations of the communicability of
cholera are contained in the _Brit. and For. Med. Chir. Rev._, July,
1872, p. 56.]
In the preceding discussion of the origin and dissemination of cholera
the broad facts of its specific nature and its contagion by means of
excreta have been chiefly insisted upon. Little has been said either
of the nature of the contagium or of the conditions that modify its
activity. These points will be considered hereafter. But it is proper
in this place to state that, in the opinion of most investigators, the
contagious element has the power of multiplying itself, not only
within the body, but wherever it is in contact with decomposing
organic matter, provided that the degree of heat and amount of
moisture present are adapted to promote such a change, which is
certainly analogous to fermentation, if not identical with it. And the
facts already mentioned may be recalled, which show that the contagium
cannot be a light and subtle substance, since, as has been stated, the
immediate attendants upon cholera patients are not as apt as might be
expected, on that hypothesis, to contract the disease, while
washerwomen inhaling, and probably swallowing, the moist fumes from
cholera fomites much more frequently do so; that fomites saturated
with the dried discharges are very infectious; and that water is the
principal vehicle by which cholera-germs are carried into the stomach.
SYMPTOMATOLOGY.--Like other diseases, cholera occurs under very
dissimilar aspects and with various degrees of gravity. Like those
especially which are caused by specific morbid poisons, it may be so
insignificant as to escape recognition, or, on the other hand, it may
give rise to violent and distressing symptoms which come on without
warning and hurry the patient to inevitable death. Whenever epidemic
diseases present such opposite extremes of severity in their symptoms,
it may reasonably be inferred that the differences depend mainly upon
the quantity of the poison that has been received into the system,
precisely as the dose which has been taken of a narcotic or acrid
poison may be estimated by the gravity of its effects. Individual
peculiarities, constitutional or acquired, may modify the
characteristic phenomena, and sometimes a careful inquiry may be
necessary even to detect their existence; but a study of cholera in
all its grades shows that its symptoms are all the effects of one and
the same cause, and that the cholera poison acts primarily upon the
gastro-intestinal mucous membrane. It follows, as a matter of course,
that, being thus applied, it will occasion symptoms differing in
degree and in kind according to the energy of its action, and that
this, again, will depend partly upon the inherent virulence of the
agent and partly upon its quantity. In fact, this feature in the
clinical history of the disease can be explained only by the operation
of a special irritant acting with different degrees of power upon the
gastro-intestinal {732} mucous membrane. In other words, the different
forms under which it is convenient clinically to recognize and
describe cholera are nothing more than different degrees of the
operation of one and the same poison, modified more or less by the
peculiarities of individual patients. In the most typical of the
fully-formed cases of cholera there is a stage of diarrhoea, a stage
of cholera morbus--_i.e._ of vomiting and purging--with more or less
evidence of stagnation of the blood, which is followed either by
reaction and recovery or collapse and death. The phenomena of those
several stages will now be described, after which certain symptoms
will be more particularly considered.
It has more than once been pointed out that, however mild an attack of
cholera may be, the dejections accompanying it are infectious, and may
produce in other persons the gravest types of the disease. Hence the
importance, not only to the patients, but also to others, of
recognizing it in the earliest stage; for while this knowledge may
suggest measures for preventing an extension of the disease, it leads
to the prompt use of remedies at the only period in which their
success can at all be counted upon. The characteristic of this stage,
which has generally been called either choleraic diarrhoea or
cholerine, is a diarrhoea remarkable for its profuseness and the
frequency and serous quality of the stools, which are, however, of a
more or less yellow color. They are preceded by rumbling and gurgling
noises in the abdomen, are voided without colic or tenesmus, and are
followed by a remarkable sense of exhaustion or faintness, which is
sometimes also accompanied with nausea, and, if they are very frequent
and copious, cramps are apt to be felt in the calves of the legs. In
this variety or stage of the attack, as a rule, there is not any
vomiting; there is complete anorexia, but urgent thirst, a white and
clammy tongue, and a peculiar alteration of tone, a huskiness,
faintness, or hoarseness of the voice. The stools vary from six to
twelve a day, and, as above stated, are slightly yellow; they are also
alkaline, and on standing deposit a granular sediment which consists
largely of the debris of intestinal epithelium. Unless the attack is
very severe the temperature is not lowered by much more than 1 degree
F. The symptoms now described, especially in their milder grades, may
last for a week or even longer, and then, according to circumstances,
end either in cure or in fully-developed cholera; but under
appropriate treatment they usually subside in a day or two, and more
or less rapidly according to the degree of damage done to the
digestive mucous membrane.
Between the above, which is the mildest type of epidemic cholera, and
the fully-developed disease must be placed that grade of the disease
which is more appropriately called cholerine, comprising cases in
which vomiting occurs as well as purging, with increased debility and
a tendency, more or less decided, to collapse. The matters vomited,
after the rejection of undigested food, are at first bilious, but they
gradually become less and less so the longer the attack lasts, and,
together with the stools, assume the appearance of rice-water--_i.e._
they consist of a pale grayish, semi-transparent liquid in which white
flocculi are suspended. Its reaction is alkaline, and it has a faint
albuminous or spermatic smell. Along with these symptoms the other
effects of serous depletion arise--debility with pallor, duskiness,
coldness, profuse perspiration, and a sodden condition of the skin,
while the secretion of urine is diminished, {733} and all the symptoms
that belong to the first stage of cholera are present in an aggravated
degree.
A curious feature of this disease is that sometimes the onset even of
its graver forms is not attended by any evacuations, although the
stomach and intestine may be filled with liquid. It is perhaps chiefly
in such cases that the patient experiences a rapid depression of all
the mental and physical faculties. The senses are irritable, the head
aches and is confused, there is a disinclination to sleep, the limbs
totter under the weight of the body, the pulse is frequent and feeble,
occasionally fainting takes place; the skin is cool and bedewed with
perspiration. In other cases, again, the attack is sudden; the patient
is smitten with an unaccountable feebleness, speedily followed by
profuse vomiting and purging and general spasms, and dies without any
suspension of the symptoms or any tendency to reaction.
But more usually the attack begins with the diarrhoea and vomiting
described above, which then assume, more or less rapidly, a high
degree of violence, expressed by their frequency and excess. The
stools with proportionate rapidity lose all their fecal qualities and
acquire the rice-water appearance before mentioned, and the liquid
rejected by vomiting in all respects resembles them. It is poured
forth less by an ordinary act of vomiting than by gushes, as if it
overflowed from the throat and mouth; and it often escapes from the
stomach and the bowels at the same instant. Such profuse evacuations
necessarily occasion an urgent thirst which cannot be satisfied, for
liquids are thrown up immediately on being swallowed. Sometimes a
distressing hiccough accompanies these symptoms. It is indeed only one
of the many spasms which may affect the muscular system. They
generally begin in the fingers and toes, which become bent and stiff;
they seize upon the muscles of the calves of the legs, and render the
muscular wall of the abdomen as hard as a board. The pain they produce
is extremely severe, and unless the patient is exceedingly prostrated
he endeavors to assuage it by a constant change of position.
At this period the debility is very great, and progressively
increases, and the patient is unable to rise, or even to move at all
except under the stimulus of the painful spasms. The features are
shrunken; the nose is sharp and pallid, and bent to one side; the
dusky, lack-lustre, and sunken eyes, the thin lips, the hollow cheeks,
and the contracted muscles that stand out like cords under the tense
and clammy skin, present a physiognomy that belongs to no other
disease in the same degree. The hands and feet grow cold, and steadily
the coldness creeps upward toward the trunk; the temperature falls to
94 degrees or 95 degrees F.; the feeble and even flickering pulse
ranges from 100 to 120. The integuments of the limbs are shrivelled
and damp, and look as if they had been macerated in water; and if a
fold of the skin is pinched up it subsides very slowly indeed. The
eyes grow dull and dry, the tongue has a pasty or sticky feel, and the
urine is almost suppressed. If any of this excretion can be obtained
for examination, it is found to contain both albumen and sugar. As the
attack advances the patient falls into a dull, listless, and
motionless state, which may be mistaken for insensibility or even
unconsciousness but is really due to exhaustion of all the faculties
of mind and body. He may express no interest in anything, and hardly
notice the {734} attention or the distress of his friends, yet he will
generally give clear, although languid, answers to questions, and fall
again into an inert and unobservant state.
As these symptoms continue and the fluids of the body decrease, the
blood accumulates and stagnates in the veins, giving to the hands and
feet, the nose and lips and other features, to the neck, and even to
the entire surface of the body, a bluish, leaden, or violet tint,
precisely like that of cyanotic children. The pulse, that was already
weak and thready, is no longer perceptible; the carotids even and the
impulse of the heart cease to be felt, and the second sound of the
latter becomes inaudible. The skin is everywhere cold; the hands,
feet, and face are sometimes of an icy coldness, and yet the patients
seldom perceive that they are so; indeed, complaint is more apt to be
made of suffering from internal heat. Even the breath as it issues
from the nostrils feels cold. The blood no longer circulates, and the
heart seems still. If a vein is opened a few drops of black and viscid
blood will trickle from the wound, which if it coagulates, yields but
little serum, and in place of a firm clot only a diffluent jelly. The
voice has sunk to a mere whisper or is quite extinct. The features
assume a distorted and frightful expression; the temples and cheeks
are hollowed; the nose is twisted and pointed, and the nostrils are
obstructed with dry and powdery crusts; the eyes are also dry, dull,
and sunken behind the half-closed and purple lids; the conjunctiva is
no longer moistened by its secretion and becomes bloodshot; the
temperature in the mouth may fall to 79 degrees or 80 degrees F.; a
viscid exhalation bedews the icy and marbled skin; and the whole body
is so shrunken from its natural proportions as to lose all the marks
by which its identity has been recognized. From this pulseless,
exhausted, cold, and cyanotic condition there can be but one step to
death. It generally comes on gradually, the patient sinking into the
state of apparent insensibility before mentioned; on the other hand,
he may expire suddenly on attempting to make some unusual effort.
At any period in the progress of cholera, except that of complete
asphyxia, the contest between the system and the disease may be
decided in favor of the former. If this occurs before profuse
evacuations have taken place or blueness of the skin appeared, the
recovery may be gradual and present no special phenomena. The pulse
regains by degrees its natural force; the skin grows warm again, first
upon the trunk and afterward upon the extremities; the breathing
becomes easy, and, the diarrhoea having already ceased, convalescence
is established. But in proportion to the severity of the symptoms, the
intensity and duration of the cold stage, the cramps, and the
evacuations, will there be a tendency to febrile reaction, with more
or less passive congestion of the internal organs, and therefore a
slower return to health. If the attack has been very severe, and
particularly if the algid stage has been prolonged, fever of a low
type is apt to occur, and indeed may terminate fatally. This fever
presents all the characters of the typhoid state, and is marked by
dryness of the tongue, a brown crust upon the teeth and gums, jerking
of the tendons, delirium, and coma. These symptoms are partly
evidences of exhaustion, of inability of the system to resume its
normal action, and perhaps also they denote the retention of the
effete products of nutrition in the blood; but sometimes they appear
to be associated {735} with, and caused by, a local and latent
inflammation of low grade, established usually in the lungs. Again,
the nervous system seems to bear the brunt of the reactionary effort,
and the patient is attacked by convulsions or perishes in an
apoplectic fit. These phenomena appear to be due in most instances, if
not in all, to renal obstruction, and, as it is supposed that their
immediate cause is the retention of urea in the blood, they have
received the title of uraemic. In other cases a wasting diarrhoea, due
probably to the damaged state of the intestinal mucous membrane, is
superadded to the already existing typhoid state. Occasionally the
parotid glands become enlarged and painful, and sometimes a measly or
roseolous eruption appears upon the skin.
It frequently happens that the convalescence from cholera is slow and
irregular. The system seems to be shattered by the trial it has passed
through; the nervous susceptibility is for a long time morbidly
increased, or, what is still more usual, the digestive function is
greatly impaired. The appetite is capricious and the digestion feeble.
The mouth is pasty, the abdomen tympanitic, the bowels are irregular
and alternately confined and relaxed. Finally, patients who leave the
bed too soon or indulge prematurely in their ordinary diet are liable
to a relapse, perhaps fatally, into the original disease. It has
sometimes happened that such a relapse has taken place several days
after an apparent restoration to perfect health.
COMPLICATIONS AND SEQUELAE.--In a small proportion of cases, as above
stated, cutaneous eruptions have been observed during the attack of
cholera, or rather during its decline, for they coincide with the
reaction or follow it, and may be regarded as indications of
increasing vitality. They belong to the exanthematous class, and
comprise roseola, erythema, urticaria, and rarely vesicular
eruptions.[37] But, instead of them, there may occur destructive
tissue-lesions in the form of abscesses or ulcers. These affections
are more usual on the limbs than on the trunk or face, but some of
them may appear even in the mouth or fauces. Profuse sweats have been
noticed elsewhere, and the important fact that they carry off large
quantities of urea, which they deposit upon the skin. Diphtherial
exudation has also been met with upon tender parts of the skin and in
the fauces, as well as in the stomach and intestine. In some epidemics
of cholera suppuration of the parotid gland is occasionally observed,
while in others it may be entirely absent. Instances have been
reported of double parotitis, and in several of them the termination
of the attack was fatal. Still more rarely suppuration of the
submaxillary or the cervical glands has been met with. Another sequela
of cholera is a tetanic contraction of the flexor muscles of the
limbs. Between the tenth and fifteenth days of convalescence the
patient is attacked with a tearing, rending pain in the hands and
forearms, the legs and feet, followed by tonic contraction of the
flexor muscles of these parts. The sensibility is not impaired. The
attack lasts for one or several days, and seems always to end in
recovery (Guterbock).
[Footnote 37: Compare _London Hosp. Reports_, iii. 457.]
* * * * *
Some of the individual symptoms of cholera call for a more detailed
notice than they have received in the foregoing epitome, in which the
continuity of the narrative could not be interrupted by a description
of variations depending upon the stage and grade of the disease.
{736} The first to be considered is the temperature. The animal
temperature in cholera varies according to the part of the body at
which it is taken more than in any other disease. In cases of average
severity it rarely falls below 95 degrees F. in the axilla. The
temperature under the tongue does not furnish trustworthy indications.
In the stage of asphyxia it seldom exceeds 87.8 degrees F., and even
in cases that recover it may fall to about 78.8 degrees F.
(Wunderlich). In the cold stage it is not uncommon for a difference of
temperature to be noted of nearly ten degrees between the axilla and
the rectum. In a female aged thirty-two the temperature in the axilla
was 93 degrees F., and that in the vagina 102.8 degrees F.
(Mackenzie). In other cases a vaginal temperature of 104 degrees F.,
and even of 108.32 degrees F., has been reached (Guterbock). Such high
temperatures furnish an unfavorable prognosis. As Wunderlich has
pointed out, during the algid stage temperatures taken in the mouth do
not give an accurate idea of the general temperature; the rectal and
vaginal temperatures are more nearly correct. The following are some
results of thermometry in 74 cases of cholera: Lorain found the
minimum rectal temperature in 1 case 93.2 degrees F., in 2 cases 95
degrees, and in 10 cases 96.8 degrees. In 47 cases the normal
temperature was preserved; in 27 it rose to 100.4 degrees; in 15 cases
to 102.2 degrees; and in 1 to 104 degrees F. Leubuscher gives the
average temperature in the armpit 92.7 degrees F.; under the tongue,
90.5 degrees; upon the tongue, 81.5 degrees, in the nostrils, 79.2
degrees; and on the palm of the hand, 84 degrees F. These numbers,
however, only represent averages. It should be noted that the low
temperature of the mouth and nostrils is caused not only by the
evaporation from the surface of those cavities, but also by the
relative coldness of the expired air, due to the partial suspension of
the passage of blood through the lungs, and therefore to the heating
of the air contained in them. According to Leubuscher also, the lowest
temperature is found in the nostrils, and next under the tongue, and
at the latter point it may vary from 79 degrees F. to 90.5 degrees F.
In death by asphyxia the vaginal and rectal temperatures may rise to
104 degrees-108 degrees F. The axillary fluctuates less than the
internal temperature. It is remarkable that during the algid stage the
patients, at least before the temperature has reached its minimum, are
not conscious of their coldness, but, on the contrary, complain of
internal heat, precisely as happens in the congestive forms of
periodical fever. When the febrile reaction assumes a typhoid type the
temperature in many cases is normal or only slightly elevated, and it
is of serious import if the temperature then sinks again below the
normal grade (Wunderlich). On the whole, the maintenance of a uniform
temperature, neither much above or below 90 degrees F. in the axilla
or under the tongue, may be regarded as favorable, yet recoveries have
taken place even when the temperature at these points has fallen to 79
degrees F. If the temperature of the parts just mentioned should rise
rapidly to 104 degrees F., it may be regarded as a very unfavorable
sign.
The skin, as has elsewhere been described, is pallid, bluish,
shrunken, and cold, and quite destitute of its natural firmness and
elasticity, so that when it is pinched into folds they subside very
slowly, as if they had been made on the skin of a corpse. It is
curious that, although the drain of liquids through the bowels is so
great, the skin not only remains moist, but generally is bathed in a
profuse cold sweat. Although the secretion of urine is reduced or
quite suspended, that of milk is said to be not {737} always so. Large
quantities of urea have been found in the urine, and in some cases it
has been visible upon the skin in the form of white scales. During
convalescence the skin may be the seat of the various eruptions
already enumerated. Of a graver nature, but, fortunately, of rarer
occurrence, are erysipelas, boils, abscesses, ulcers, and gangrene.
These several affections seem to result from the alternate obstruction
and freedom of the cutaneous circulation. They commonly appear first
upon the limbs, and afterward upon the face or trunk; they may affect
even the cavity of the mouth. Some observers have noted a relatively
frequent occurrence of diphtherial exudations in this disease, while
others do not allude to their existence. The former describe the false
membrane as affecting not only the mouth and fauces, but also the
stomach, the intestine, and the female organs of generation. A case is
reported by Joseph of a young man who, after an attack of cholera, was
affected with a blenorrhoea, due to a diphtherial inflammation of the
urethra.
The character of the heart- and pulse-beats in this disease is quite
peculiar. Their rate does not increase indefinitely, as it does after
hemorrhage; the pulse usually varies from 90 to 110, and indeed seldom
exceeds 120, but its volume, tension, and force progressively decline
until the beats become imperceptible at the wrist, and even in the
brachial and femoral arteries. At the same time, the rhythm of the
heart is interrupted, the energy of its impulse declines until it can
no longer be felt, and its sounds grow weaker and weaker until they
become quite inaudible. Sometimes, it is said, a pericardial friction
sound may be heard, which is attributed to the dryness of the
pericardium. That the decline and suspension of the heart's sounds and
impulse are due not only to the weakness of the cardiac muscle, but
also to the lessened volume of the circulating blood, is proved by the
fact that they persist, sometimes for many hours, after reaction has
commenced, and only become audible again when the arteries have been
replenished with blood.
In the description of the symptoms of cholera it has been mentioned
that the cyanotic color of the skin is produced by an accumulation of
blood in the veins. Many years ago Magendie, and after him
Dieffenbach, on examining the arteries of persons in the advanced
stage of cholera, found those vessels empty of blood. It might be
supposed that, under the circumstances, not only the right side of the
heart, but also the lungs, would be gorged with blood, and that
extreme dyspnoea would result. But, in point of fact, the respiration
in cholera is hurried and shallow rather than oppressed and labored,
while after death the lungs are not engorged with blood, but rather in
a bloodless condition. The pulmonary artery and its branches are also
empty, although the right side of the heart may be filled with dark
and soft coagula. These singular conditions seem to be due, on the one
hand, to the greatly diminished mass of the blood in the vessels, and
to its accumulating and stagnating in various parts of the venous
system, and, on the other hand, to the weakness of the heart, which is
shown by its suppressed impulse and sounds, and which lessens its
power to propel the venous blood into the lungs. The infarction of the
systemic veins and the threatening suspension of the circulation
necessarily impair the activity of all the functions, including those
of nutrition and disintegration, so that the effete detritus of the
economy tends to accumulate in the blood. This tendency is {738}
doubtless counterbalanced not only by the diarrhoea, but also, more or
less, by the almost total suspension of nutrition, due to the
inability of the cholera patient to digest or even to retain food, as
well as by the diminished oxidation of the blood in the lungs. It has
already been observed that, to a certain extent, the impediment to the
passage of the blood from the right side of the heart into the
ramifications of the pulmonary artery tends to prevent congestion and
infarction of the lungs. But this obstruction is precisely what occurs
during the stage of reaction in many cases, which then terminate
fatally by asphyxia, as in the previous stage still more perish by
apnoea.
In the milder attacks of cholera vomiting may not occur, and in the
most severe it not unusually is suspended for some time before death,
although the diarrhoea may continue. In the most malignant cases,
indeed, there may be no vomiting at all, in consequence of the extreme
muscular exhaustion, although the stomach may be distended with
liquid. When rejected, the liquid has the general aspect of
rice-water, which the stools also present. Its reaction is alkaline or
neutral, and it is said to contain a less proportion than the stools
of solid matter, but a larger proportion of urea. The act of vomiting
is strictly one of regurgitation, which is performed without effort or
pain. Sometimes, indeed, it seems to relieve the sense of weight
caused by the accumulated contents of the stomach. It is readily
excited by attempts to drink, and even by slight changes of posture.
The vomited liquid at first contains the various articles of food the
patient may have eaten. Their half-digested remains have sometimes
suggested the announcement of strange specific forms of cholera germs.
The liquid, after ceasing to be colored brownish or greenish, becomes
gray, and subsequently, in favorable cases, more or less green again;
while during the stage of reaction in grave and ultimately fatal cases
it is more or less reddened by an admixture of blood. Its most usual
and characteristic appearance is that of a grayish liquid containing
whitish flocculi. The nature of this liquid, whether discharged by
vomiting or by purging, has been variously estimated. Formerly, some
persons held the white granules to be leucocytes, but the greater
number agree that they are mainly epithelial fragments. When the
vomited liquid is allowed to stand, a sediment forms in it which is
composed almost entirely of epithelial scales, more or less modified
in their appearance by the accidental contents of the stomach, and a
film covers its surface in which globules of fat and phosphatic
crystals may be detected. They are frequently associated with
sarcinae, produced by fermentation in the contents of the stomach, and
after standing for some time the liquid becomes crowded with vibrios
(Lindsay).
Although the propensity of the sick to discover a cause for every
symptom often leads cholera patients to attribute their diarrhoea to
some particular exposure to cold, error of diet, etc., yet, in fact,
this symptom, so far as it belongs to cholera, is primarily an effect
of the cholera poison alone, although it may be aggravated by causes
like those mentioned. It is of great practical importance to bear in
mind that a specific choleraic diarrhoea--that is to say, a diarrhoea
produced by the cholera poison alone--may continue to be very slight
as long as it lasts, which may be for several weeks; and hence, as
elsewhere insisted upon, a person who is not suspected of being
affected with cholera may, quite ignorantly, sow {739} the seeds of a
deadly epidemic of the disease. The danger in cholera is proportioned
to the volume of the discharges rather than to their frequency, just
as a single profuse hemorrhage is more serious than the loss of an
equal amount of blood divided among several successive days. The
special danger, however, is not, as in hemorrhage, from syncope, but
from the progressive loss by drainage of the water of the blood,
rendering it unfit to circulate, and therefore causing it to stagnate
in the veins. The spoliative operation of the diarrhoea has
occasionally been productive of benefit instead of injury, as in the
following case of Barlow: A man suffering from dropsy was attacked
with cholera, "and passed gallons of liquid by stool, had cramps, and
became livid and clammy, but his pulse did not disappear, as in
profound collapse, and he eventually rallied, and left the hospital
apparently well. When he began to recover from cholera his appearance
was almost ludicrous, from the manner in which the integument hung
loosely about him."
The stools pass through a series of changes corresponding to those of
the matters vomited, being fecal at first, and then becoming colorless
and watery. During reaction, if that occurs, they regain more or less
of their proper color, but if typhoid febrile symptoms prevail they
are usually bloody. Decomposed blood sometimes renders them dark,
tarry, and fetid; this condition has caused them sometimes to be
described as being composed of vitiated bile, which is, however, a
product not of the liver, but of the imagination.
In the intestine after death considerable quantities of epithelium are
found floating in the contained liquid or else loosely adherent to the
mucous membrane. It is usually in flocculi, but sometimes in fragments
large enough to form a continuous membrane. A microscopic examination
of cholera stools shows that their turbidness depends chiefly upon
desquamated epithelium, with which is mixed white corpuscles and
bacteria. It is remarkable that although the stools are drained
directly and so rapidly from the blood-vessels, they nevertheless
contain but little albumen, indeed hardly more than a trace of it. If,
however, blood is mixed with the stools, as happens in rare instances,
more albumen is present. Oil-globules are most abundant in cases that
have passed beyond the stage of collapse into that of reaction with
fever. In these it is said that oily matter may be found either in
concrete masses or as a scum of liquid oil. Of inorganic constituents
they contain crystals of the triple phosphate of ammonium and
magnesium and chloride of sodium in greatest abundance, but the
proportion of ammonium and potassium salts is small. Indeed, the total
amount of solids does not exceed 2 per cent. As the quantity of water
in the blood and solids is limited, and as in this disease the stomach
will not receive nor retain any liquid, it follows that the more
profuse the evacuations are, the shorter must be the duration of the
attack, for the sooner then does the blood become too thick to
circulate.
It has several times been stated that in cholera the urine is
diminished, and that, therefore, the blood retains a larger proportion
of effete products than in health. But it has also been remarked that
the amount of these products is abnormally small, on account of the
interference with nutrition of the abnormal state of the circulation.
Doubtless, as in other cases of renal obstruction, an increased
proportion of effete matter is eliminated by the skin, if not by the
bowels. When the amount of {740} urine excreted is only diminished,
its specific gravity may vary between remote extremes, as 1.012 and
1.030. Usually, however, when its quantity is very greatly reduced,
symptoms which are described as uraemic are apt to arise, and the
urine is found to contain the usual products of renal congestion--viz.
albumen, sometimes traces of blood, hyaline and granular casts, and
epithelial scales, with less chloride of sodium and more urea than
normal. It is remarkable that at the beginning of convalescence the
urine, which had been suppressed or greatly diminished, may become for
a time abnormally abundant. Rarely, if ever, does the derangement of
the kidneys now described denote or produce an organic lesion in those
organs. Like the disorders elsewhere, these are due to the loss of
balance between the arterial and the venous sides of the circulation;
both, indeed, have lost their functions more or less, the one by lack
of blood, the other by an excess of blood unfit for circulation.
The occurrence of cramps in cholera, which has bestowed upon the
disease one of its titles, spasmodic, has, however, no distinctive
relation to the Asiatic disease. Spasmodic phenomena occur in many
cases of poisoning by corrosive and irritant agents and in ordinary
cholera morbus, and in cholera infantum they are among the most
alarming symptoms, assuming, as they often do, the character of
general convulsions. In most of these cases they are clonic and
general, and therefore probably of central origin, primary or
reflected; but the spasms of cholera are tonic, and affect the muscles
of the upper and lower limbs, and most frequently the flexor muscles
of these parts, and especially those of the fingers and toes, which
become rigidly bent. The larger muscles contract into hard lumps, and
even those of the chest and abdomen do not escape the terrible spasms.
When they are severe they extort cries from patients who at other
times seem quite apathetic. It is stated by Macnamara that the natives
of Southern Bengal and other people of relatively loose fibre are much
less apt to be attacked by them than the natives of the upper country
or than Europeans. It may be debated whether their immediate cause is
a reflex irritation emanating from the gastro-intestinal mucous
membrane; or whether it is due to the rapid diminution of the supply
of blood to the nervous centres, or to the infarction of those centres
with thick and imperfectly oxygenated blood; or, finally, whether it
is occasioned by a diminished supply of blood, and that blood of bad
quality, to the muscles themselves. Probably all of these factors are
associated causes in producing the spasmodic phenomena of cholera. It
is well worthy of notice, however, that spasms, which are so frequent
in all infantile diseases, and especially in those affecting the
stomach and bowels, rarely attack children suffering from cholera.
This would seem to prove that the spasms in question are not reflex,
but either central and spinal, or else muscular--an inference which is
strengthened by their being tonic and not clonic. As stated, the
spasms, or cramps, frequently affect the limbs, but comparatively
seldom involve the muscles of the chest or abdomen, and those of the
face hardly ever. They are almost the only causes of pain in the
disease, which in not a few instances runs its whole course, even to a
fatal termination, without their occurrence.
As a rule, the abdomen is not so much retracted as might be expected
from the profuse discharges. Probably in some degree its form is
maintained by the constantly recurring accumulation of liquid in the
{741} gastro-intestinal cavity. In protracted cases, however, the
abdomen becomes sunken and hollowed. At all stages of the disease it
is somewhat sore under pressure, especially at the epigastrium, and it
generally has a doughy feel. As to the functions of the digestive
organs, they are completely suspended during a typical attack of the
disease. Not only are these organs incompetent to digest food, but
they cannot even retain it.
Throughout such an attack not only is sleep apt to be prevented by the
pain of the cramps and the frequent evacuations, but, as a rule, the
patient is wakeful, and yet, apart from the restlessness which
accompanies the paroxysms of pain, there is, on the whole, a tendency
to a placid quietness. Mental excitement and delirium are probably
unknown during the primary attack, but sometimes a degree of
somnolence or of apathetic tranquillity exists, which, however, is
quite distinct from coma. When the attack is prolonged, and especially
when it merges into a typhoid state, the eyes become inflamed by their
exposure to the air. The conjunctiva then grows blood-shot, and
occasionally the cornea is ulcerated.
MORBID ANATOMY AND PATHOLOGY.--The appearance after death of a person
who has died in the collapse of cholera is very characteristic. It
comprises a shrunken aspect of the whole body, its prevalent grayish
or leaden pallor contrasting with the livid hue of the abdomen and
back, the fingers and toes, the lips and eyelids, and ears; the eyes
are sunken deeply in their orbits; the nose is sharp and bent, the
temples are hollow, and the skin seems to cling tightly to the bones
beneath it. The connective tissue is very dry, and the muscles are
hard as well as dry, and, owing to the wasting of the softer parts,
stand prominently out. In consequence of the absence of moisture
decomposition takes place very slowly. Cadaveric rigidity is very
marked and persistent. A very notable phenomenon is the occurrence of
muscular contraction after death. It may be excited mechanically or
may occur spontaneously. A case is related (Eichhorst) in which three
hours after death the fibres of the biceps were observed to move
tremulously, and then the entire muscle contracted, causing flexion of
the forearm. Even the fingers performed movements like those made in
piano-playing. The lower jaw has also been observed to move, causing
the mouth to open and shut repeatedly. The late Sir Thomas Watson long
ago described this singular phenomenon as follows: "A quarter or half
an hour, or even longer, after the breathing had ceased, and all other
signs of animation had departed, slight, tremulous, spasmodic
twitchings and quiverings and vermicular motions of the muscles would
take place, and even distinct movements of the limbs, in consequence
of these spasms."[38] It was carefully studied by Barlow, from whose
narrative the following is taken: The patient was a strong man; the
course of his attack was rapid, and he suffered most cruelly from
cramps. "Within two minutes of his ceasing to breathe muscular
contractions began, becoming more and more numerous. The lower
extremities were first affected. Not only were the sartorius, rectus,
vasti, and other muscles thrown into violent spasmodic movements, but
the limbs were rotated forcibly and the toes were frequently bent. The
motions ceased and returned; they varied also: now one muscle moved,
now many. Quite {742} as remarkable were the movements of the arm: the
deltoid and biceps muscles were peculiarly influenced; occasionally
the forearm was flexed upon the arm--flexed completely, and when I
straightened it, which I did several times, its position was recovered
instantly. The fingers and thumbs were now and then contracted, and at
times the thumbs were separately moved. The fibres of the pectoral
muscles were often in full action; distinct bundles of them were seen
at intervals beneath the skin.... After I had taken leave of the body
the nurse was horrified by a movement of the lower jaw, which was
followed by others; and I thought for a moment that the man was alive.
The facial muscles became generally affected, and at length all was
still."[39] These muscular contractions succeed one another in a
regular order, beginning in one lower extremity and extending to the
other, then to the upper limbs, and finally to the face. Their degree
varies from a slight quivering to a powerful contraction, and their
duration from a minute or less to an hour and a quarter. Cases have
occurred in which the legs were so forcibly retracted that they could
with difficulty be straightened again. In one case, six hours after
death movements took place in one leg, and the hand was drawn across
the chest; in another, "the forearms were powerfully flexed, and the
hands, approximating, gave the attitude of praying to the body."[40]
Again, Mr. Ward reports: "I saw the eyes of my dead patient open and
move slowly in a downward direction. This was followed, a minute or
two subsequently, by the movement of the right arm (previously lying
by the side) across the chest." In the same paper Barlow says: "Mr.
Lawrence mentioned to me that a gentleman who died in 1832 of rapid
cholera was turned after death completely on the side by a strange and
forcible combination of muscular contractions."[41] These muscular
phenomena after death form an interesting feature in the history of
cholera, but they are by no means peculiar to that disease. They have
been observed in other diseases, and especially in yellow fever--an
affection in which the pathological condition is quite unlike that of
cholera. In both diseases they have been manifested in robust persons
and when the course of the fatal attack was both rapid and severe.
Thus, Dr. Dowler of New Orleans not only found that they could be
developed in such cases of yellow fever by striking the muscles, but
he observed their spontaneous occurrence in several, of which the
following is a remarkable example: "Not long after the cessation of
the respiration the left hand was carried by a regular motion to the
throat, and then to the crown of the head; the right arm followed the
same route on the right side; the left arm was then carried back to
the throat, and thence to the breast, reversing all its original
motions, and finally the right hand and arm did exactly the same."[42]
In 1860, Drasche alleged that not unusually the skin covering the
contracting muscles became reddish, while the local temperature rose
1/2 degree, and that as soon as the contractions ceased the
temperature fell below the normal and cadaveric rigidity set in.
According to the same observer, analogous contractions affect the
unstriped muscular fibres, in those of the skin producing a projection
of the papillae, and in the genital organs a discharge of semen. This
phenomenon is said to have occurred an hour and a half after death.
[Footnote 38: _Lectures_, Am. ed. of 1872.]
[Footnote 39: _London Med. Gaz._, Nov., 1849, p. 798.]
[Footnote 40: _Ibid._, Jan., 1850, p. 185.]
[Footnote 41: _Ibid._, pp. 185, 186.]
[Footnote 42: _Experimental Researches_, 1846.]
{743} On opening the abdominal cavity of persons who have died in the
collapse of cholera one is struck by the general pink or rose tint of
the peritoneal coat of the intestines. It is produced by a repletion
of the minute branches of the portal venous system. Sometimes the
color is rendered very dark by the pitchy blood contained in the
veins. The surface of the peritoneum, like all the tissues, is
singularly dry, and often has a soapy or sticky feel, caused by a
layer of albuminous matter, which forms a lather when rubbed between
the fingers, and causes the intestinal folds to adhere to one another.
If death takes place during the stage of reaction, these appearances
are less distinct, and the intestines, which in collapse are usually
retracted, are then somewhat distended.
The stomach generally contains a thin, partially transparent liquid of
a greenish or grayish color, and occasionally reddish, holding in
suspension portions of coagulated mucus and an unctuous substance of
an albuminous nature, which adheres to the walls of the cavity. Fatty
globules may be observed floating in the liquid, which under the
microscope reveals epithelial debris, granular corpuscles, and
fragments of gastric glands. Under heat and nitric acid coagulation of
the liquid occurs, and on chemical examination it is found to contain
urea. The gastric mucous membrane is of a dark violet or pale pink
color, according to the stage of the disease; its follicles are
enlarged, and patches of superficial abrasion may be observed on it.
The intestinal canal of those who die during the collapse of cholera
is, in the majority of cases, partially filled with liquid which has
the aspect of turbid serum, more or less mixed with the previous
contents of the bowel if death has taken place very rapidly, but
otherwise it is almost colorless. On the whole, however, it is less
pale and watery than the stools. It contains, like these discharges,
more or less epithelial flocculi, and generally more than were
observed during life in the dejections. The mucus scraped from the
lining membrane of the intestine and mixed with water renders it
turbid with epithelial debris. The same mucus examined microscopically
contains fragments, larger or smaller, of epithelium. These conditions
are said to predominate in the large intestine. Indeed, the proportion
of liquid increases from above downward. Hence in the more prolonged
cases the contents of the bowel at its upper part are less liquid and
are darker in color. There is, indeed, a striking contrast between the
appearance of the intestine in cases which have terminated in collapse
and its aspect in persons who have died during the stage of reaction.
It has been clearly presented by Dr. Sutton.[43] When death took place
in "the cold stage the mucous membrane was unusually pale in three
cases; in two it was healthy-looking; in other two it was pale
throughout, excepting that one or two of Peyer's patches were
congested; and in the remaining three there was more or less
congestion of the mucous membrane. When the mucous membrane was pale
throughout the entire intestine, the valvulae conniventes looked
swollen and oedematous, and the color of the membrane was dead white.
The solitary glands were very distinct and prominent. Those of the
duodenum were remarkably so. In cases of imperfect reaction the mucous
membrane of the intestine was usually found very much congested and
ecchymosed. The congested portions were sometimes {744} granular, and
apparently denuded of epithelium. The mucous surface had often a dark
port-wine color, due to the extravasated blood and the hyperaemia, and
here and there the surface was covered with a dirty gray membranous
substance, likened to a diphtheritic deposit. I have, however, seen no
decided false membrane, such as could be peeled off, as in diphtheria.
The surface was also occasionally bile-stained, and the
greenish-yellow color of the bile and the deep red color of the
congested surface presented a very striking appearance. The solitary
glands were very prominent, and in some cases apparently enlarged."
The general paleness of the intestinal mucous membrane in the stage of
collapse, and its congestive redness whenever the signs of reaction
have existed before death, have a very important bearing upon the
pathology of this disease, for they demonstrate conclusively that the
gastro-intestinal evacuations in cholera have no relation whatever to
inflammation. On the other hand, they render it altogether probable
that the serous flux is in the nature of a sweat, an intestinal
ephidrosis.
[Footnote 43: _London Hosp. Clin. Lect. and Reports_, iv. 497.]
The nature of the exfoliation found in the intestinal canal has been
the subject of much discussion. As long ago as the first American
epidemic of cholera (1832-35) Dr. W. E. Horner, Professor of Anatomy
in the University of Pennsylvania, described an exfoliation of the
epithelial lining of the alimentary canal, whereby the extremities of
the venous system of the part are denuded, as being characteristic of
cholera alone. In 1849, Dr. Samuel Jackson, Professor of the
Institutes of Medicine, and Dr. John Neill, Demonstrator of Anatomy in
the University, in conjunction with Dr. William Pepper and Dr. Paul B.
Goddard, presented a report to the College of Physicians of
Philadelphia, in which they, too, showed that the "epithelial layer of
the intestinal mucous membrane was either entirely removed or was
detached, adhering loosely." This important fact--the most important,
perhaps, in the mechanism of cholera--was confirmed seventeen years
later by the eminent pathologist Dr. Lionel S. Beale,[44] who, when
referring to "the remarkable characters of the matter discharged from
the intestinal tube, and to the fact that the small intestines almost
always contain a considerable quantity of pale almost colorless
gruel-, rice-, or cream-like matter," added: "This has been proved to
consist almost entirely of columnar epithelium, and in very many cases
large flakes can be found, consisting of several uninjured epithelial
sheaths of the villi.... In bad cases it is probable that almost every
villus, from the pylorus to the ilio-caecal valve, has been stripped
of its epithelial coating during life.... These important organs, the
villi, are, in a very bad case, all or nearly all left bare, and a
very essential part of what constitutes the absorbing apparatus is
completely destroyed.... It is probable that the extent of this
process of denudation determines the severity or mildness of the
attack.... It seems probable also that the epithelium may become
detached in consequence of the almost complete cessation of the
circulation in the capillaries beneath, but the death of the cells may
occur in consequence of their being exposed to the influence of
certain matters in the intestine or in the blood, in which case they
would simply fall off."
[Footnote 44: _Med. Times and Gazette_, Aug., 1866, p. 109.]
In this connection, and as complementary of the statements now made,
should be considered the further description by the same author--viz.:
{745} "Remarkable changes have occurred in the smaller vessels,
especially in the capillaries and small veins of the villi and
submucous tissue. The blood-corpuscles appear to have in a great
measure been destroyed in the smaller vessels, and in their place are
seen clots containing blood-coloring matter, minute granules, and
small masses of germinal matter evidently undergoing active
multiplication. Some of the arteries are contracted, but here and
there small clots destitute of blood-corpuscles may be seen at
intervals." Hence, the gastro-intestinal lesions in cholera, according
to their extent and degree, they remove the natural obstacles to
exhalation in the mucous membrane, and also, and in the same degree,
prevent the absorption of the contents of the alimentary canal. It
must not, however, be forgotten that this lesion is not altogether
peculiar to the intestinal mucous membrane. Dr. Beale long ago called
attention to the fact that in this disease there seems to be a
tendency to the removal of epithelium from the surface of all soft,
moist mucous membranes, but not from the follicles of the glands. The
first statement appears to be explicable by the shrinkage of all the
mucous membranes during cholera collapse, for by this merely
mechanical agency the inelastic epithelium must necessarily become
detached. As to the second statement, the remark may be made that the
whole follicular structure furnished with columnar epithelium is an
absorbing and not an eliminating apparatus, and that, since its
functional activity is from the beginning of the disease diminished by
an inadequate blood-supply, it can have but a small and indirect share
in generating the phenomena of the disease.
In 1884, Dr. Koch, during his investigations of cholera in India,
found bacilli in the bowel which he believed to be peculiar to the
disease, and which presented the following characters: they were not
straight, like other bacilli, but curved or comma-shaped; they
proliferated rapidly and displayed very active movements. Bodies of
persons who died of various other diseases did not present them,
although abounding in different bacteria. The bacilli were not found,
or only exceptionally, in the stomach, but abundantly in the
intestine, and most so in the diarrhoeal discharges that occurred at
the height of the disease. As soon as the stools began to be fecal the
specific bacilli disappeared from them. After death at the height of
the disease they were most abundant in the intestinal contents, and
especially in the lower part of the small intestine. When death took
place at a later period none of them might be detected in the liquids
in the bowel, but they would still be present, in considerable
numbers, in the tubular glands. They were not found at all in cases
fatal from some sequela of the disease.[45]
[Footnote 45: _Times and Gaz._, Mar., 1884, p. 398.]
Other abdominal lesions in cholera possess a very subordinate
importance. The isolated and the agminated glands are both prominent,
chiefly because they are swollen by the liquid imbibed from the bowel.
A whitish substance which they sometimes contain may perhaps be the
albumen or fat which they have taken from the intestinal liquid. A
very similar condition of the mesenteric glands is probably due to a
like cause. The liver is pale and flaccid when death takes place in
collapse, and it is also described as presenting a "dirty grayish-red,
homogeneous appearance, and indistinctness of the lobular structure,
as if some glutinous matter had been poured throughout the tissues of
the organ" {746} (Sutton). This appearance would seem to be due to the
total suspension of the blood-supply through the portal vein.
At all stages of the disease the gall-bladder is usually found full of
bile, which is apt to be dark during the collapse and more watery
after reaction has commenced.
The spleen is small, pale, and, as a rule, firm, but occasionally it
is soft.
The kidneys present no marked changes when death has taken place early
in the attack, or at most only exhibit a lighter color than usual of
the cortical substance and a darker one of the pyramids. They show
that the arteries are comparatively empty and that the veins are
congested. Similarly contrasted appearances are met after death from
obstructive disease of the heart and other causes that produce
obstruction of the venae cavae. In the tubules, later on, fatty
degeneration of the epithelium has been observed, and some cylindrical
casts. These alterations, especially of the tubules, are most marked
when death occurs in the stage of reaction, and are then apt to be
accompanied by more or less hemorrhagic transudation. The urinary
bladder is always contracted after death in collapse; after febrile
reaction its mucous membrane may be more or less coated with false
membrane.
The brain and the spinal marrow offer nothing peculiar; their venous
systems are everywhere more or less engorged, and sometimes effused
blood has been found in the spinal canal.
In the state of the respiratory organs the most important facts are
that in algid cholera the lungs are always more or less collapsed,
"shrunk and small, and lying back in the chest, toward the spine," and
that, so far from being congested, they are (with the exception of a
small portion of their posterior part rendered dense by hypostasis)
singularly bloodless, dry, and tough. As might be inferred from these
conditions, they are also lighter in weight than natural. To Dr.
Parkes belongs the credit of having first described this very
important fact in the morbid anatomy of cholera, as follows: "In
fourteen cases the lungs were completely collapsed, appearing in some
cases like the lungs of a foetus. In three cases they were
considerably, in eight slightly, collapsed, and in the remaining
fourteen cases the collapse was in some altogether, and in some
partially, prevented by old adhesions."[46] So Dr. Sutton found that
the average weight of the two lungs during collapse was about twenty
ounces, and after reaction--that is, after the passage of the blood
into the pulmonary artery had become completely re-established--about
forty-five ounces. In the latter condition also the lungs presented
the usual signs of congestion of those organs, being dark-red
throughout or in portions only. Sometimes also they contained masses
or nodules of apparent hepatization, and of these some may have
undergone partial softening.
[Footnote 46: _Med. Times_, 1848, p. 378.]
In absolute conformity with the condition of the lungs that has been
described is that of the heart. If the lungs are bloodless, it follows
necessarily that the left side of the heart must be empty, and almost
as necessarily that the right side of the heart must be distended with
blood. All careful investigators of the subject agree that such is the
condition of the heart when death takes place in cholera during the
stage of {747} asphyxia. All report that the pulmonary artery is
either empty or that it contains a small quantity of dark and usually
of thick blood; that the right side of the heart and the coronary
veins are distended with blood of the same description, while numerous
ecchymoses exist along the course of the coronary veins; that the
venae cavae are filled with half-coagulated blood of a tarry aspect;
and that even the femoral and splenic veins contain similar blood. On
the other hand, the left ventricle of the heart is usually contracted,
and contains a very little semi-fluid blood, with perhaps a small and
pale clot. This engorged condition of the right cavities and emptiness
of the left cavities of the heart diminish very slowly during the
passage from collapse to reaction, during which time the pulmonary
blood-vessels are being gradually replenished. Besides the thick and
tarry aspect of the blood above described, it has been observed that
when the blood is withdrawn by means of a pipette, its globules
rapidly subside and are surmounted by a transparent serum, and that
such blood may remain for a long time uncoagulated. The red corpuscles
are said to be pale and viscous, but not adhesive, and the white
corpuscles abnormally numerous and easily crushed. In the free
intervals are observed "very pale little objects, slightly elongated
and constricted in their middle," which multiplied in blood kept for
one or two days at a temperature of 38 degrees C. (100.4 degrees
F.).[47] If death does not take place until reaction is far advanced
or has merged into a febrile condition, the left ventricle is usually
found not contracted, and it contains a quantity of blood. The term
"usually" is employed to show that even to this rule there are some
exceptions, and that, as in all other diseases, the issue does not
depend absolutely and exclusively upon a definite degree of any
anatomical lesion, but upon the aggregate condition of all the
functions upon which life depends. The pericardium, like the pleura
and the peritoneum, may be covered with a saponaceous film which is
albuminous.
[Footnote 47: _Rapport sur le Cholera d'Egypte en 1883_, par M. le Dr.
Strauss, etc.]
* * * * *
In looking now over the field that has been traversed in the foregoing
pages, and searching for some link that will unite in a consistent
whole the causes, symptoms, and lesions of cholera, it is evident that
only one factor can possibly be so described. That factor is the
gastro-intestinal flux. This it is that produces the vomiting and the
purging; that prostrates the patient and wastes away in a few hours
the fullest and the firmest form; that chills the limbs and afterward
the trunk; that thickens the blood so that the capillary vessels can
no longer convey it, and that spreads a cyanotic shadow over the whole
surface of the body; that cuts off the supply of blood from the lungs
and heart; that paralyzes the nervous system, ganglionic as well as
cerebro-spinal; that obstructs the kidneys and arrests their
secretion; and that, acting through the several links of this
pathological chain, becomes the cause of death. But the question still
recurs, What is the cause of the gastro-intestinal flux? To this also,
in the light of observation, it is possible to give only one answer.
It is a specific poison which originates in Hindostan, and, being
taken into the stomach and bowels, not only produces in the individual
the symptoms and lesions of cholera, but is capable of multiplying
itself and rendering infectious the discharges from the stomach and
bowels of the subjects of the disease, so that it may be transmitted
from {748} one person to another round the whole circumference of the
globe. Regarding the form and nature of that poison little or nothing
is definitely established, beyond what has already been stated as the
result of Koch's observations. As far as they go, they harmonize with
a long-prevalent opinion that the cholera poison consists of certain
microscopic germs, which, on being received into the bowels, propagate
their kind and destroy the epithelium. It is believed by some that
these bodies are products of the rice-plant on the banks of the
Ganges, and that, having once originated the disease, the germs
contained in the discharges become mixed with water or are borne upon
the wind, and enter the system of new victims, who, in their turn,
disseminate the plague. This theory will be further considered below.
Another view, that of B. W. Richardson, is that, "as pus undergoes
changes which convert it into a septic poison, so the excreted matter
from the alimentary canal is equally capable, under peculiar
conditions of oxidation, of producing an alkaloidal organic poison,
which, soluble in water, but admitting of deposit on desiccation,"
becomes the agent for disseminating the disease. In these theories a
false datum and a hypothesis are offered us in place of the fact which
we seek. The cryptogamous nature of the essential cause of the disease
has no positive proof, but only the probability of coincidence in its
favor. There is no proof, because one after another organic form has
been alleged to be the essential generator of the disease, and each
has been proved to be either not peculiar to cholera or has been shown
to be present in other diseases than cholera.
At the present time (1884) it is the fashion to trace every disease to
specific bacteria or analogous organisms. But it may be that the
occurrence of cholera only furnishes the occasion for the development
of these organisms, just as a certain temperature, hygrometric
condition, and deficient light and air will cause mould to form on
bread and other organic substances. The judgment pronounced by Dr.
Beale in this question as long ago as 1866 appears now, as it did
then, to approach the truth upon this point: "There is no good reason
for supposing that the bacteria in such numbers in the alimentary
canal in cholera have anything to do with this disease or with the
falling off of epithelium from the intestinal and other mucous
membranes. Bacteria are developed in organic matter which is not
traversed and protected by the normal fluids of the body, and they
invade the cells and textures in cholera after those cells and
textures have undergone serious prior changes, just as they would
invade textures removed from the body altogether. Nor would it be in
accordance with known facts to infer that cholera was due to the
invasion of some peculiar form or species of bacterium."[48]
[Footnote 48: _Times and Gazette_, Aug., 1866, p. 167.]
We repeat, then, that while nothing can be simpler than the mechanism
of cholera viewed as a gastro-intestinal hyperidrosis, nothing is more
mysterious than the mechanism of the primary cause which gives rise to
it. That its real nature has been correctly described is rendered all
the more probable by the fact, presently to be insisted upon, that
sporadic cholera morbus, which is always the consequence of a direct
irritation of the gastro-intestinal mucous membrane, is often with
difficulty distinguishable from Asiatic cholera, which, indeed,
differs from the former {749} disease chiefly by the intensity of its
cause as measured by the gravity of its symptoms and by the nature of
the special agent that produces it.
The above views regarding the essential cause of cholera were
substantially indited before the Egyptian epidemic of 1883, but they
are in accord with the more definite conclusions arrived at by the
German and French commissions on the subject. Before their reports
appeared, however, a communication was made by Dr. Kartulis of the
Greek hospital in Alexandria, setting forth that the drinking-water
and the stools and blood of the cholera patients contained, the first
a mass of micro-organisms, and the others bacteria and micrococci,
which, however, presented no distinctive characters.[49] The German
report was prepared by Dr. Koch, the French by Dr. Strauss.[50] The
former, alluding to the enormous quantity of micro-organisms found in
the contents of the bowels and in the stools, did not perceive any
connection between them and the phenomena of the disease. On the other
hand, he did assign this relation to a species of bacterium found in
the walls of the intestine, and which he compared to the bacilli of
glanders. They were lodged in great quantities within the intestinal
glands and behind their epithelium, as well as upon the surface of the
villi and within them, and sometimes even in the muscular coat. They
were most numerous at the lower end of the small intestine. Dr. Koch
concluded that although these bacilli, beyond doubt, are in some
manner associated with the development of cholera, they are by no
means shown to be its cause, and may indeed be themselves the product
of the morbid conditions belonging to cholera. All his attempts at
that time to develop cholera in animals by inoculating them with the
organisms gave only negative results. The conclusions of Dr. Strauss
were in entire conformity with those of Dr. Koch, but involved an
additional and very important statement--viz. that the shorter and the
more violent were the fatal attacks of cholera the fewer were the
bacteria found in the intestine. It is evident that this fact is the
very opposite of what should have been found had bacteria been
essential in the causation of cholera. The more recent investigations
conducted in Calcutta by Dr. Koch, which have already been cited, led
him, however, to attribute to bacilli of a specific form the absolute
origination of the disease. He poses the question in the following
manner: Either these "comma bacilli" are a product of the cholera
process, or "the disease only arises when these specific organisms
have found their way into the bowel." The former alternative he
rejects, because, in his judgment, it assumes that the bodies in
question must be pre-existent in every person who becomes affected
with the disease--a hypothesis which he rejects, because they have
never been found except in cholera. He therefore concludes that they
are the cause of cholera. He points out that their first appearance
coincides with the commencement of the disease, that they increase
with it, and that they disappear with its decline.[51] The statement
of Strauss quoted above does not, however, appear to harmonize with
this conclusion, since the bacteria are said by him to have been
fewest in the more violent and fatal attacks of the disease. Another
of Dr. Koch's remarks is also open to criticism. After showing how
rapidly the cholera bacteria multiply when kept moist, he states that
they die after drying more quickly than almost any other form of
bacteria. "As {750} a rule, even after three hours' drying every
vestige of life has disappeared." It is evident that this statement is
not in harmony with the numerous facts, several of which have been
cited, that cholera fomites have preserved their infectious qualities
after several weeks. Dr. Koch endeavored to produce in animals,
artificially, with these bacteria, a disease analogous to cholera, but
without success; and he adds, "If any species of animal whatever could
take the cholera, it would surely have been observed in Bengal, but
all inquiries directed to this point met with a negative result." Dr.
Vincent Edwards, who, however, is of opinion that the cholera poison
is "not an organism, but of the nature of a chemical compound of
comparatively unstable nature," reports that he produced fatal cholera
in pigs by giving them the dejections of cholera patients.[52] But the
_Times and Gazette_ inclines to question that the pigs employed in Dr.
Edwards' experiments were affected with true cholera.
[Footnote 49: _Medical News_, xliii. 377.]
[Footnote 50: _Archives gen._, Dec., 1883, pp. 713, 722.]
[Footnote 51: _Times and Gaz._, Mar., 1884, p. 398.]
[Footnote 52: _Notes on the Poison contained in Choleraic Atomic
Discharges._]
DIAGNOSIS.--The most characteristic symptoms of Asiatic cholera have
repeatedly been mentioned in the foregoing pages. They are rice-water
evacuations by vomiting and purging, rapid emaciation of the whole
body, a cadaverous hollowness of the cheeks and eyes, a livid color of
the face, hands, and feet, a feeble, thready, and at last absent
pulse, an icy coldness of the extremities, face, and even the breath,
a loss of the elasticity of the skin, a thin and feeble voice, and
intense thirst. But every one of these symptoms may occur in cholera
morbus produced by a direct irritation of the stomach and bowels. It
is rather their nature, we repeat, than their phenomena that
distinguishes these two affections from each other. In attempting to
separate Asiatic cholera from other forms of cholera we must endeavor
to dismiss from the mind the erroneous notion that the term cholera
denotes a definite disease identical in its cause, phenomena, and
results. It is no more a disease than dropsy or fever is a disease. It
is a complex group of symptoms which have in common the fact that they
proceed directly from gastro-intestinal irritation, whose degree of
severity--_i.e._ the presence or absence of certain grave
symptoms--and, above all, its issue, depend chiefly upon the nature
and intensity of the cause of the attack, and also, necessarily, upon
the degree of resistance opposed to it by the subjects of the disease.
Nothing has led to more error in regard to epidemic cholera than the
ignorance of this pathological fact by some and the disregard of it by
others.
In the first portion of this article it was shown that the Greek,
Roman, and Arabian conceptions of cholera morbus included a discharge
of bile, the very symptom for the absence of which Asiatic cholera is
notorious; and also that the classical cholera, or cholera morbus,
ended in recovery even more frequently than Asiatic cholera terminates
in death. But local epidemics of cholera morbus sometimes take place
which are of a severe and even of a grave type, and which also appear
to originate in some peculiar atmospheric influence, for they prevail
to a limited extent and in connection with vicissitudes of weather.
Still more circumscribed epidemics have been traced to unwholesome
food and drink, and innumerable instances of individual attacks have
been caused by irritants that are ranked as poisons and others which
are reckoned as food or medicines. Now, under these various
circumstances, which have in common gastro-intestinal irritation,
there may be produced, if the irritation is excessive, {751} a series
of symptoms closely resembling, if not identical with, those of
Asiatic cholera.
In illustration may be cited the comparatively familiar description of
Sydenham.[53] These are his words: "There is vomiting to a great
degree, and there are also _foul_, _difficult_, and _straining
motions_ from the bowels. There is _intense pain_ in the belly, there
is _wind_, and there are _distension_, heartburn, and thirst. The
pulse is quick and frequent, at times small and unequal. The feeling
of sickness is most distressing, and is accompanied with heat and
disquiet. The perspiration sometimes amounts to absolute sweating. The
legs and arms are cramped and the extremities cold. To these symptoms,
and to others of a like stamp, we may add faintness." ... "As the
summer came to a close the cholera morbus raged epidemically, and,
being promoted by the unusual heat of the weather, it brought with it
worse symptoms, in the way of cramps and spasms, than I had ever seen.
Not only, as is generally the case, was the abdomen afflicted with
horrible cramps, but the arms and legs, indeed the muscles in general,
were afflicted also." ... At the risk of repetition an additional
passage may be quoted from Sydenham's later definition of cholera
morbus: "This is _limited_ to the _month of August_ or the first week
or two of _September_. Violent vomiting, accompanied by the dejection
of _depraved humors_, _difficulty on passing them_, _vehement pain_,
_inflation and distension of the bowels_, heartburn, thirst, quick,
frequent, small, and unequal pulse, heat and anxiety, nausea, sweat,
cramps of the legs and arms, faintings, and coldness of the
extremities, constitute the true cholera--and it kills within
twenty-four hours."
[Footnote 53: _Works_, Sydenham Soc. ed., i. 163; ii. 8, 266.]
In spite of the general likeness between this description and the
symptoms of Asiatic cholera, there are differences of considerable
importance which have been italicized in the quotations. These
differences are such as may be attributed to the action of a harsh
irritant in the case of cholera morbus, while in the epidemic
(Asiatic) disease the distinctive phenomena are the result of a sudden
and profuse intestinal flux. Macpherson, who had a long and extensive
experience of epidemic cholera in India, after contrasting in detail
its phenomena with those of cholera nostras, sums up the discussion in
these words: "Cholera indica is essentially a very fatal disease,
while cholera nostras is usually a mild affection and is seldom fatal,
although it was called _atrocissimus et peracutus_, and has
undoubtedly killed in from eight to twenty-four hours."[54] In regard
to the individual symptoms this very competent reporter does not
recognize a single one as being absolutely peculiar to either disease.
Even the ancients, already referred to, after describing bilious
evacuations as being characteristic of cholera nostras, add that
sometimes also they are whitish; and modern writers, both before and
since the advent of Asiatic cholera in Europe, have made a similar
observation. Thus, Quinquaud, in his description of cholera nostras,
of which a slight epidemic occurred in 1869 at the Hospital St.
Antoine in Paris, says: "The principal symptoms were vomiting and
purging, sometimes of a bilious and sometimes of a rice-water liquid;
a shrivelled and cyanotic skin, the latter appearance being sometimes
strongly marked; anxiety, coldness, cramps, altered voice, and
suppression of urine."[55] In 1875 thirty-three cases of this {752}
disease occurred at Valenciennes, near Paris, and its symptoms were
thus summarized by Manouvriez:[56] "Repeated vomiting, first of food,
and then of a dark-green liquid; diarrhoea, which was at first fecal
and then bilious, but afterward serous and like rice-water; painful
tension of the epigastrium and tenderness of this part; headache,
cramps in the legs, suppression of urine; pallor, coldness, and
dryness of the skin, especially of the limbs; pinched features, a blue
circle around the eyes, a small and scarcely perceptible pulse, and a
faltering and whispering voice." Yet of the thirty-three cases only
two were fatal--the one a child of four years and the other an infant
of as many months. The substantial identity of nature of these two
local epidemics, and the almost equally close relation of their
symptoms to those of epidemic cholera, must be quite apparent.
[Footnote 54: _Times and Gaz._, Dec., 1870, p. 725.]
[Footnote 55: _Archives gen._, Mars, 1870, p. 308.]
[Footnote 56: _Archives gen._, Sept., 1877, p. 298.]
Yet the contrasts are neither slight nor unimportant; and the most
striking and significant is the trifling mortality of the European as
compared with the Asiatic disease, notwithstanding the grave symptoms
present in the former. It may be regarded as certain, we think, that
the reason of this difference of danger lies in a corresponding
difference in the nature of the causes of the two forms of disease.
The rapid recovery from cholera morbus produced by changes of weather,
acid fruits, and indigestion renders it certain that no material
lesion of the gastro-intestinal mucous membrane has been produced;
while, on the other hand, inspection after death from epidemic cholera
or by corrosive poisoning renders it equally certain that the damage
to that membrane is substantial and widespread, as well as often
irreparable, and that, therefore, "the powers of life that resist
death" must be engaged in a very unequal and often fruitless struggle.
The cramps in cholera nostras are, as a rule, less severe than in
epidemic cholera, while the colicky, and in general the abdominal,
pains are greater in the former than in the latter disease. The reason
of this difference appears to be that muscular spasm is the natural
result of depletion, whether sanguine or serous, while colic is an
effect of irritation of the surface of the mucous coat of the bowel,
and not of its destruction, such as occurs in epidemic cholera.
It is true only in a limited degree, and indeed only upon a
superficial survey of the symptoms, that the effects of irritant
poisoning are like those produced by Asiatic cholera. The analogy
between the two was pointed out, among others, by Sedgwick in
1867.[57] The resemblance appeared so striking to the vulgar eye that
in Paris, and perhaps elsewhere, a popular tumult followed the first
violent outbreak of epidemic cholera, and it was charged that the
wells had been poisoned. The cases that most resemble cholera are the
following: "Acute poisoning by corrosive sublimate, by arsenic, and by
mineral acids, especially nitric acid; the effects which follow the
eating or drinking of poisonous animal matters, such as tainted or
simply unwholesome meat or fish, and milk which has undergone some
injurious but yet unknown change, decomposing vegetables and some of
the poisonous fungi, and the excessive action of certain drugs, for
the most part belonging to the class of drastic purgatives," as
elaterium and croton oil. The effects produced by these agents
constitute a cholera morbus, and therefore resemble cholera, and have
been occasionally, and almost unavoidably, mistaken for it. It {753}
is remarkable that suppression of urine may occur among them, as well
as vomiting, purging, and collapse. As Griesinger and others have
pointed out, the order in which the symptoms occur is a valuable, and
generally an available, ground of diagnosis. In cholera, diarrhoea
always occurs before vomiting, while in the various irritant
poisonings mentioned vomiting precedes diarrhoea. In irritant
poisoning also there is generally severe abdominal pain--not so much
colicky and paroxysmal as constant and burning; the stools are not so
copious as in cholera, and they do not possess the rice-water aspect,
but are rather dark, bloody, and fetid, and are voided with tenesmus
or with heat in the anus; and even when the urine is suppressed it is
less persistently and completely so than in cholera, and attempts to
void it are attended with vesical tenesmus and strangury. In a
doubtful case it is important to ascertain whether a metallic or other
unpleasant taste is perceived in the mouth, whether this cavity or the
throat bears marks of corrosion, whether any unusual article of food
has been used, etc. Moreover, it is of extreme importance to learn
whether Asiatic cholera prevails, not merely in the immediate
neighborhood, but at any place from which diseased persons or infected
goods may have arrived. The instances should not be forgotten in which
cholera-infected clothing from Europe has developed the disease in the
valley of the Mississippi. Nor should those still more numerous cases
be overlooked in which travellers affected with choleraic diarrhoea
have disseminated the disease at great distances from their
starting-point, although unconscious of the nature of their own
ailment, whose seed they were sowing along their route.
[Footnote 57: _Med.-Chir. Trans._, li. 1.]
PROGNOSIS.--Like the diseases called septic, of which the eruptive
fevers may be taken as examples, and also like the effects of irritant
poisons, the gravity of cholera must mainly depend upon the amount and
the activity of the specific poison that is received into the system.
It is most probable that the cholera poison is organic, and that it
has a limited power of reproduction and term of existence, a period
also of intense activity and a period of exhaustion; in a word, that
either by progressive dilution as an inorganic substance or by organic
senescence it finally ceases to exist. By no other theory is it
possible to explain the numerous degrees of severity which cholera
exhibits, from a mild indisposition to a malignant and rapidly fatal
disease. On the one hand, the patients, if they may so be called, are
hardly prevented from attending to their customary occupations. They
may even be able to travel and carry the disease to distant places,
and so appear to justify the erroneous and irrational doctrine of the
atmospheric or spontaneous origin of cholera. On the other hand, the
entire apparent duration of an attack may not exceed two or three
hours, during which all the distinctive symptoms of the disease may be
crowded together in the most appalling forms. Such grave cases are
always most numerous at the commencement of an epidemic. These
statements are true not only in regard to individual cases in the
greater number of epidemics, but they represent the distinctive
character of particular epidemics, some of which are as remarkable for
their benignity as others are for their extreme malignity. For such
contrasts no plausible reason can be suggested, unless it be a
difference either in the essential virulence of the morbid poison or
in the dose of it imbibed. That they are due to the activity rather
than to the quantity of the poison seems to {754} be proved by the
progressive weakening in the gravity of the cases; for if the quantity
of the poison remained the same some malignant cases might be expected
to occur even during the decline of an epidemic.
These considerations help to explain the extreme diversities of
mortality in different epidemics. The extremes may be stated at 10 and
90 per cent., and they would perhaps be still wider apart if all the
mild cases, which are never reported--many of which, indeed, do not
even fall under medical observation--were included in the reckoning.
The general or average mortality of cholera is about 50 per cent.
According to Allbu, the epidemics in Berlin from 1831 to 1873 gave a
total of 28,753 cases and 18,916 deaths; that is, a mortality of 65.8
per cent. (Eichhorst). It should be noted that, as in other epidemic
diseases, there is no uniform proportion between the extent and the
mortality of cholera epidemics. Some of very limited extent have been
proportionally the most destructive. It should also be remembered that
the disease is far more fatal in infancy and old age than at any other
period of life, and for a similar reason it is very dangerous to all
who are weakened by any cause, such as an inherited morbid diathesis,
a chronic debilitating disease, etc. There seems to be a doubt whether
its male or female victims are the more numerous. In this connection
it may be suggested that while males are more likely to contract the
disease by drinking contaminated water, etc., more women are exposed
to its contagion by their intimate relations with the sick, by their
handling and washing infected fomites, by carrying away the cholera
discharges, etc.
Undoubtedly, the class of society to which cholera patients belong is
not without influence on its prognosis. Not only is the total
mortality greater among the laboring classes, but the individual
belonging to those classes has a less chance of recovery, because he
is not apt to resort to treatment on the appearance of the premonitory
signs of the disease, and because the treatment he receives is less
intelligently and sedulously pursued by his physicians and friends.
In regard to the particular symptoms which are favorable or
unfavorable, nothing need be added to what has already been stated in
detail, unless it be that during the height of the attack the danger
is to be measured by the degree of prostration and of the stasis of
the blood, and, during reaction, by the grade of the typhoid state.
Gradual reaction, as denoted by the state of the skin and the pulse
and a more natural aspect of the stools, is generally indicative of
improvement.
Finally, a word of caution may be given to those who are apt to
attribute all the favorable changes in the conditions of an epidemic
to the sanitary or medicinal measures they have instituted. Cholera
epidemics are remarkable for the comparatively short period of their
duration, which may be stated at less than a month in the same place.
Doubtless, judicious sanitation and timely treatment save a great many
lives, but the qualifying fact, already insisted upon, must not be
overlooked, that the mortality occasioned by the disease in a given
place is greatest during the first period of its prevalence, and that
thenceforth it gradually declines. Yet it is of essential significance
that the disease rarely attacks a large number of persons
simultaneously; the epidemic proper is usually preceded by a few
scattering cases which are apt to become foci of ignition that
presently unite to form a widespread conflagration. The recognition
{755} of these cases, their isolation, and the proper treatment of the
localities where they occurred have frequently stamped out what might
have been the commencement of a deadly epidemic.
PREVENTION.--The history of cholera demonstrates conclusively that
since the disease, outside of India, never arises spontaneously, it
must be more or less preventible, partly by excluding its seeds and
partly by rendering the soil in which they are planted more or less
unfit for their development; in other words, by quarantines and
sanitary cordons and by various measures of local sanitation.
In regard to the former there would be comparatively little difference
of opinion, at least theoretically, if both measures were alike
efficacious. But there would seem to have prevailed a tendency in
official quarters to undervalue the efficiency of both. Those who made
and administered the sanitary laws relating to cholera seem to have
forgotten the emphatic question, "What will not a man give for his
life?" or at least to have considered that whatever value some men may
set upon their own lives, the lives of other men become of no account
when balanced against the needs, or even the conveniences, of
commerce. The ethics which justified the introduction of opium into
China by the English and the American gift of alcohol to the Indian to
gratify a lust for lucre or for land is only paralleled by those
contained in the official protests against cholera quarantines. At the
International Medical Congress held in 1873 at Constantinople, it was
almost unanimously resolved that "the practice of (land) quarantine as
now carried out ought not to be maintained, because, on the one hand,
it does not constitute a real protection, and, on the other hand, _it
is directly opposed to the interests of commerce and industry._" A
leading critic, in commenting upon this, remarks that if a quarantine
were possible it would give no real security, because it would be
evaded, just as customs laws are evaded by smuggling.[58] A logical
deduction from this curious argument would be that customs laws should
be abrogated. In 1880 was published the report of the German Imperial
Commission on the cholera epidemic of 1873 in Germany, edited by
Hirsch, from which we learn that "all the German medical experts agree
in condemning the employment of quarantine, for, while largely
detrimental to the _interests_, _welfare_, _convenience_, and
_happiness_ of a community, it is _quite inert_ and _inefficient_ as a
safeguard against the further diffusion of cholera."[59] Whether this
opinion refers only to land quarantine or not is left in doubt, but
the spirit of subordinating the lives of the people to the commercial
interests of a country is just the same as, and is not less worthy of
condemnation than, the spirit which has more than once blinded customs
officials to the disease on board of vessels from which it has
afterward issued to destroy thousands of lives.
[Footnote 58: _Practitioner_, xii. 226.]
[Footnote 59: _Ibid._, xxvi. 159.]
It seems to be overlooked that in national as well as in personal
affairs "honesty is the best policy," and that if, instead of
concealment or false statements regarding the sanitary state of ships,
their passengers, and cargoes, and equally false assertions respecting
the contagiousness of cholera, and a contemptuous neglect of
well-tried preventive measures,--if, instead of this delusive and
disastrous policy, all nations had honestly carried out the rules
prescribed by experience for the exclusion of the disease, and for its
management after it had passed the frontiers of a country, {756} there
can be little doubt that its ravages would ere this have been confined
to the region in which it originated. As we have seen, there is urged
against the enforcement of a rigid quarantine by land or sea the
singular argument that it has not always excluded the disease. A more
logical inference would seem to be that since it succeeded, not
completely, but yet partially, its inefficiency should be charged to
its imperfect execution; or, even granting that the absolute exclusion
of cholera is impracticable in every instance, including cases of
choleraic diarrhoea, contaminated clothing and merchandise, does it
therefore follow that the transit of men and things should be
unimpeded? As well might it be maintained that because one or more
houses cannot escape destruction by fire, therefore no effort should
be made to save the remainder of a threatened city; as well might it
be argued that because some men must be killed in battle, no
precautions should therefore be used to preserve the rest of the army;
as well abstain from all local sanitation intended to mitigate the
ravages of the disease, because, do what we may, some victims it will
surely have. This is taking counsel from despair; is a stupid fatalism
which one might imagine to have been imported with the disease from
the East; or it may be a sign of the unconscious blindness of
Mammon-worshippers, who, neither fearing God nor regarding man, have
as little pity for the victims of cholera, permitted, if not invited,
by them to scourge the nations, as devout Christians once felt for the
negroes who were bought or kidnapped in Africa to toil and die under
the lash of the slave-driver.
Probably no sanitary cordon nor any quarantine will invariably and
completely exclude cholera, since it is transmissible by living men
and by water and by fomites of various descriptions, and, worst of
all, by men who neither exhibit its characteristic symptoms nor are
conscious of the poison which they conceal and disseminate. But, as
has already been urged, it is no argument against preventive measures
that they are not absolutely perfect in their efficiency. If they
sometimes succeed in arresting the progress of cholera, and if they
always, when honestly executed, lessen the number of channels through
which the infection can be conveyed, and thereby reduce to a minimum
its fatal effects, they ought to be maintained and perfected, and not
decried or abolished. It is difficult to characterize that state of
mind which concludes against the use of a salutary measure because its
efficiency is not absolute, the more so when it is admitted that its
inefficiency is not intrinsic, but due to negligent, and even
fraudulent, administration. The preponderance of official and personal
authority is altogether on the side of the necessity of a quarantine,
not in its literal, but in its technical, sense. The International
Medical Congress of 1874 declared as follows: "Quarantine ought to be
limited to the time requisite for the examination and disinfection of
the ship, the crew, and the passengers; and if there be no disease on
board the latter should be released immediately after disinfection.
But if there be cholera or sickness of a doubtful nature on board, it
will be necessary to isolate and disinfect the ship also." The same
congress, however, wholly condemned land quarantines, apparently upon
the sole ground of the extreme difficulty of rendering them
efficient--an argument, as before remarked, that touches not the
principle of the measure, but only the manner of its execution. In
this respect the congress occupied a lower position than its
predecessor of 1866, which held that the futility of {757} quarantine
in "arresting the march of cholera" arose "rather from the
unintelligent application of the measure than from any fallacy in its
principle."[60]
[Footnote 60: _Practitioner_, xxviii. 393.]
It would burden this narrative even to enumerate the instances in
which a strict quarantine has protected places to which cholera has
been carried by sea. In the United States numerous examples might be
given of seaports into which cholera was brought from foreign
countries, and within whose quarantine stations it was confined by
rigid sanitary regulations; but it is sufficient to cite the case of
New York, through whose quarantine at Staten Island nine-tenths of all
emigrants to America have passed. Writing in 1867, Dr. Peters said:
"There have been fourteen epidemics of cholera at Staten Island, and
only four have reached New York." A large number of illustrations has
been collected by Dr. Smart, Inspector-General, R. N.,[61] who sums up
the matter as follows: "Believing that cholera has frequently been
excluded from islands by quarantine, and as often introduced by its
non-observance, I regard it as a truly preventive measure; but,
recognizing the impracticability of exacting it under many
circumstances, I would insist on the most strict isolation of all the
first cases or units of disease, whether introduced from without or
originating from relationship to introduced cases, or persons or goods
imported from infected countries."
[Footnote 61: _Lancet_, April, 1873, pp. 555, 659; _Times and
Gazette_, April, 1874, p. 387. Compare also Colin, _Brit. and For.
Med.-Chir. Rev._, July, 1874, pp. 42-44.]
While experience demonstrates the efficacy, and therefore the
necessity, of quarantine against cholera in seaports, it has also
shown that the same agent of prevention need not be invariably and
rigidly applied. When quarantine meant literally a detention, and
almost an incarceration, for forty days, it often failed through its
very rigor at a time when proper methods of disinfecting ships,
cargoes, crews, and passengers were either unknown or inefficiently
applied. It is now certain that quarantine may be reduced to a
fraction of its original duration, and yet possess a much greater
degree of efficiency, its length depending upon the number and the
sanitary condition of the crew, etc., the nature of the cargo, etc. It
is evident that a ship carrying only cabin passengers is less open to
suspicion than one crowded with filthy emigrants, although both may
have sailed from the same cholera-infected port. A more liberal rule
may govern the one than the other; and in the second case a rigid
inspection and cleansing of luggage may be imperative which would be
superfluous as well as vexatious in the first case. The importance of
such a treatment of emigrants' effects has already been illustrated by
cases in which they caused an outbreak of cholera after having been
carried from a seaport into an interior town many hundreds of miles
distant.
In regard to the time during which a vessel that has had cholera on
board within a week or ten days should be detained under sanitary
inspection and treatment, including a thorough cleansing of the
passengers and their effects, no absolute rule can be laid down; but
it would appear that if no suspicious cases arise within a week, there
need be little apprehension that any will occur.
The sanitary measures which should be undertaken wherever there is
reason to fear an invasion of cholera are, in the first place, such as
are {758} equally appropriate in anticipation of any infectious and
contagious epidemic disease, and relate especially to the removal of
all sources of putrid emanations, whether in stagnant ponds, in
streets, markets, shambles, sewers, privies, cellars, or inhabited
rooms; for these influences, although they do not cause cholera, yet,
by lowering the vitality of persons exposed to them, create an
abnormal susceptibility to disease. Many instances in Europe might be
cited to prove that whole cities, which in the earlier epidemics were
devastated by cholera, were either spared entirely in the later ones
or suffered in a far less degree. The measures which proved most
efficient were an improved water-supply and a better system of
sewerage; and this fact strongly corroborates the belief that
contaminated water and fecal emanations are the principal agents in
propagating this disease. Cleanliness is the best disinfectant, but
during epidemics of cholera, as of other diseases, the popular faith
is very strong in numerous articles called by that name. The real
value of these preparations is commercial rather than sanitary, but,
indirectly, they are useful by prompting those who use them to be more
diligent in searching out and removing many sources of
air-contamination that perhaps invite and intensify attacks of
cholera.
The disinfectants in common use comprise chlorine gas, chlorinated
soda, chloride of zinc, sulphate of iron, permanganate of potassium,
carbolic acid, and the fumes of burning sulphur. Some of them--and
especially the chloride of zinc, sulphate of iron, the permanganate of
potassium, and carbolic acid--are supposed to be capable of destroying
the infectious principle of the vomit and stools. Another method is to
receive such matters in vessels containing saw-dust, which, after
being dried, is consumed by fire; and still another is to mix them
with dry earth and bury them. If they are thrown into water-closets or
privies, they should have added to them a portion of sulphate of iron.
Whatever has been used by cholera patients should be destroyed, unless
of value, and in that case it should be thoroughly purified by hot air
or boiling water and long exposure to the sun. The importance of
having large and well-ventilated rooms for cholera patients is very
great, but less, perhaps, for the patients themselves than for their
medical attendants and nurses. All persons should be excluded from
them who are not required by the duties of the sick chamber, and in
case of death funeral assemblages ought not to be allowed; nor, during
a cholera epidemic, ought crowded assemblies for any purpose to be
permitted.
During epidemics of cholera, as of some other diseases, the liability
to be attacked is greatest when the vital powers are depressed by
mental or by physical causes. Hence it is desirable that one's courage
and confidence should repose upon a consciousness of having done
whatever is recognized as proper to ward off the disease--not by a
minute, watchful, and anxious attention to rules at every step, but by
such a general care of the health as good sense and experience enjoin.
Undoubtedly, other things being equal, the weak, sickly, careless, and
imprudent are more liable to suffer than the strong and cautious, and
therefore it is incumbent upon all to maintain as high a degree of
health as possible, avoiding not only all probable sources of
contagion, direct or indirect, but excessive fatigue, catching cold,
depressing emotions, sexual excesses, etc. During the first cholera
epidemics in this country it was considered so dangerous {759} to eat
fruit and fresh vegetables that many persons lived entirely upon meat,
rice, and bread. Such a regimen intensified choleraphobia, and was
also an unsuitable midsummer diet. There is no reason to believe that
any intrinsically wholesome food need be prohibited during the
prevalence of cholera.
The one article of diet about which the greatest and most peculiar
care should be taken is water. It is the first duty of towns supplied
with water from a common source to be sure that it is, and continues
to be, uncontaminated. Well-water should be used as little as possible
after the disease has made its appearance, and, as an additional
precaution, no water should be drunken that has not previously been
boiled. Where ice can be procured it may be used to restore the boiled
water to an agreeable temperature for drinking. Filtered water,
provided that it be properly filtered, may likewise be regarded as
innocuous.
TREATMENT.--If regard be had to the various methods and particular
medicines which have been used in the treatment of cholera, it will
appear that in hardly any other acute disease has a greater number or
variety been employed. If, on the other hand, we endeavor to learn
what measures have been really and generally curative in cholera, and
what are they to which, on the occurrence of an epidemic of the
disease, we may turn with confidence in their power to cure, the
result of the investigation is disheartening, and adds to the
accumulated proofs that the power of medical art is exceedingly
restricted. To this conclusion we must assent at whatever cost to a
faith which is strong in proportion to the ignorance out of which it
grows. Nor, if we consider the matter rationally, ought we to be
surprised or humiliated on account of the comparative helplessness of
medicine in this disease, since, if we reflect upon it, the case is by
no means peculiar or exceptional. Every disease that may become mortal
occurs more or less frequently with phenomena which place it beyond
the resources of therapeutics as completely as cholera is in its most
malignant forms; and yet no one lays it to the charge of medicine that
the various fevers, for example, are at times utterly uninfluenced by
the most rational and judicious treatment. Nor does any one bring a
railing accusation against medicine when accident fatally damages a
part essential to life.
One accident of frequent occurrence presents a certain analogy to
cholera in its effects, and that is a burn or scald involving a very
large portion of the skin. In cases of this sort experience assures us
that death is almost inevitable, and that the duty of the physician is
to avoid officious and meddlesome treatment, and address himself to
soothe the patient's suffering and maintain his strength, if haply the
powers of nature may triumph over the effects of the injury. This,
too, is the lesson, substantially, which experience has taught
respecting cholera. It is certain that in this disease the function of
the whole gastro-intestinal mucous membrane is reversed, and that it
is no longer a secreting and absorbing organ, but one almost
exclusively exhaling, and that through it the liquid which is
essential to carrying on the functions is rapidly running away. If the
lesion on which this symptom depends is complete, if the
gastro-intestinal mucous membrane has entirely lost its natural
function, evidently it is quite futile to address any treatment to
this organ. But if, as probably happens in a great majority of the
cases, the {760} disorganization takes place gradually, it is evident
that there is more to hope from remedies when the disease is gradually
developed than when it reaches its acme at a single bound and leaves
no time for medical intervention. The one unmistakable lesson that
experience teaches respecting the treatment of cholera is, that its
success depends upon its prompt and early application. Almost as
distinctly does observation teach that subsequently to the first (or
diarrhoeal) stage the comparative value of different methods and
individual medicines is very uncertain. And, finally, it would seem
that in this, as in other acute diseases, intelligent and careful
nursing and regimen are quite as important as any medicinal treatment
whatever. However a false notion of the power of medicine may blind us
to the fact, it is none the less a fact, that if different methods of
treatment are compared, that method gives the best results which is
least perturbative. For example, in England, on board of a hospital
ship, were 85 cases, of which 19 treated by quinine gave 12 deaths, 12
by calomel gave 2 deaths, 12 by carbolic acid gave 3 deaths, and 37 by
"Nil" gave 1 death.[62] Or, again, in 1865, at the London Hospital,
159 patients were treated--48 with a mixture containing logwood,
ether, aromatic sulphuric acid, camphor, and capsicum, of whom 31
died; 56 with sweetened water, of whom 28 died; 21 with castor oil, of
whom 14 died; and 20 with "saline lemonade," of whom 6 died.[63] In
the last example the deaths during the use of the astringent mixture
were twice as great as under sugar and water, and under castor oil
twice as great as under "saline lemonade."
[Footnote 62: _Times and Gaz._, Dec., 1866, p. 590.]
[Footnote 63: _London Hosp. Reports_, iii. 444.]
We shall first give an account of the management of cholera in
general, and then consider some of the particular medicines used in
its treatment.
The essential elements of all plans of treatment for this disease, as
for so many others, are rest and abstinence. Whatever else may be
done, nothing avails without them. This remark applies emphatically to
the premonitory diarrhoea; if it is neglected it may readily be
converted into the full-formed disease. It is therefore essential,
during the prevalence of cholera, that whoever is attacked with
diarrhoea should at once give up all active occupation, and confine
himself to a recumbent posture and to the use of food of the blandest
quality, such as mucilages and similar preparations, especially of
rice, which, less than any other vegetable food, is liable to
fermentation during digestion. It is prudent to drink no water that
has not been boiled. If there is reason to believe that the bowels
retain feces from before the attack, it is generally thought advisable
to administer a laxative dose of castor oil, to procure the discharge
of matters which would act as irritants. Except for this purpose
purgatives are neither indicated nor expedient. In a large number of
cases nothing more is necessary than the use of means to check the
action of the bowels, and which should consist of absorbents or
antacids, astringents, and opiates as they are contained in the
officinal chalk mixture, with the addition of tincture of kino or
catechu and a small proportion of laudanum. This medicine should be
given in dessertspoonful doses at intervals of not more than an hour.
If, instead of a diarrhoea which differs from ordinary dyspeptic
diarrhoea chiefly by its watery character, there should also be colic
and profuse discharges, it is proper to add to the medicines just
suggested some which are of a decidedly stimulant character, such as
the essential oils of {761} cajeput, cloves, cinnamon, peppermint,
etc., with which chloroform, ether, or Hoffman's anodyne may be
associated. At the same time rubefacient embrocations may be applied
to the abdomen, which should also be compressed slightly with a broad
flannel bandage. Instead of these stimulants, and perhaps more
efficiently, may be used a simple epithem made by dipping a large
towel several times folded in cold or cool water, applying it so as to
cover the whole abdomen, and then enveloping it and the body with a
dry towel. This application is more soothing than any liniment and its
action is more constant. Instead of any of these agents dry heat may
be used, obtained from bags of hot salt or sand, or moist heat from
thick poultices of flaxseed meal or Indian corn meal or similar
substances enclosed in flannel bags and applied to the abdomen while
they are as hot as can be borne. It is difficult to determine which of
these applications is the most useful. But, on the whole, heat is
preferable to rubefacients, and moist to dry heat. The cold-water
dressing is probably best suited to young and robust persons.
It must be remembered that between choleraic diarrhoea and cholera in
its complete form there are several grades, in one of the most common
of which a tendency to vomit, and even a certain amount of vomiting,
accompanies the diarrhoea. Anti-emetic remedies are then indicated.
They may consist externally of rubefacient and aromatic applications
to the epigastrium (especially the spice poultice); and it is claimed
that a hypodermic injection of morphia in this part is very efficient.
Internally, the best remedies are ice swallowed in small pieces and
small but frequent draughts of iced carbonated water or iced
champagne. Where these liquids cannot be procured, effervescing
powders used in the same way form a very good substitute for them. If,
notwithstanding such remedies, the diarrhoea continues or if it tends
to increase, astringent and absorbent medicines may be substituted for
them; for example, bismuth may be given instead of chalk, and if this
also fails acetate of lead may be prescribed. The last may be used by
the rectum as well as by the mouth, but with very questionable
advantage. Meanwhile, especial care should be taken to avoid giving so
much of any opiate as will induce sopor or excite nausea.
Whoever has had the care of cholera patients has probably, at first,
felt sanguine of success in their treatment, even after the
characteristic discharges and the symptoms of collapse had set in; but
a little more experience has proved their hope to be deceptive, and
revealed the reason of it in the absolute suspension of the
sensibility and absorbent function of the digestive canal. Hence the
dismal unanimity of all medical authors, who from actual observation
of cholera have declared that no treatment avails to arrest the
fully-developed disease. And yet there is some encouragement in the
fact that recoveries sometimes occur from even the most desperate
state of collapse and under the most dissimilar methods of treatment;
so that the physician is warranted in not yielding to discouragement
and in cheering his patients with hope even to the end of life. The
popular dread of this, and indeed of all epidemics, is sure to be
exaggerated, and it therefore behooves the physician to combat the
fears of his patients, and by a cheerful manner as well as encouraging
words administer the cordial of hope, which often proves stronger than
pharmaceutic elixirs.
{762} It may be well to enumerate, as many do, the indications of
treatment in the active stage of cholera, but they really need no such
specification. It is evident that they consist in combating the
symptoms--the vomiting, the purging, the debility, the cyanosis, the
cramps, etc.; and the only means by which the carrying out of such
indications can even be attempted are neither more nor less than would
be used to relieve the same symptoms in other affections. If the
evacuations could be controlled, evidently the cramps and the collapse
would not occur; but this essential and preliminary step cannot be
secured. The medicines introduced into the stomach or rectum are not
absorbed, but are speedily rejected; those which are administered
subcutaneously are not taken up by the stagnant blood as freely as in
other diseases; the nervous system gives little or no response to the
mechanical and physiological stimulants applied to the skin. Yet, in
spite of these obstacles, the physician must persist in the use of
rational methods, in the hope, however faint it may be, that he may
succeed in restraining, and possibly in arresting, the fatal course of
the attack. For this end he has hardly any means at command except
those, or such as those, which were recommended in the first stage of
the disease--the anti-emetic and anti-diarrhoeal medicines, which he
is only too likely to see rejected as soon as administered. Yet he
must not cease to allay the thirst by the repeated administration of
small quantities of carbonated and cold liquids, water, or champagne
wine, or morsels of ice swallowed whole. The application of pounded
ice in a bladder to the epigastrium is a measure of an analogous sort,
and is sometimes as efficient as generally it is soothing. In other
cases the aromatic poultice seems to answer better. Of irritants
little can be said that is favorable, but the combined irritant and
anaesthetic action of chloroform is useful, and morphia should be
applied to the epigastrium as well as given hypodermically.
If the vomiting tends to become less frequent, acetate of lead may be
prescribed, in the hope that it will exert some constringing action
upon the gastro-intestinal mucous membrane. The distressing symptom,
hiccough, cannot with any certainty be controlled by medicine, but
perhaps the inhalation of chloroform is more efficient than any other
remedy, as it also is for the cramps in the limbs. For the latter
purpose it is preferable to the frictions with flannel or with
stimulating liniments which are generally employed. If such liniments
are used, care should be taken that they do not contain ingredients
that may disorganize the skin either immediately or subsequently. A
dangerous compound of the latter sort introduced during the first
epidemic of cholera in this country became officinal under the name of
liniment of cantharides.
The loss of the water and of the salts it holds in solution in the
blood is, as has now been frequently repeated, the chief pathological
element of the disease, next after the conjectural cause which injures
the mucous membrane of the stomach and bowels. It was rationally
indicated, and therefore a method was early practised, to supply this
loss by injecting into the veins a solution of sodium salts. The
method was seductive as well as rational, for its primary effects were
extremely encouraging; it nevertheless failed, and probably for the
very reason that suggested its use. Indeed, there is no more reason,
if there is as much, to suppose that a liquid artificially introduced
into the blood-vessels will be retained when {763} the natural liquor
sanguinis cannot be so. Necessarily, the one will escape where the
other has escaped.
Certain systematic writers prescribe a method intended, on the one
hand, for reviving the animal heat, and on the other for restoring the
movement of the circulation. It need hardly be remarked that the two
form essentially but one and the same indication. If the circulation
is restored the animal heat will revive, but not otherwise. The same
treatment leads to both ends, and it consists partly, as already
stated, in the use of stimulants, such as alcohol, camphor, coffee,
ether, etc.; but their efficacy depends upon their being taken into
the blood, and with it reaching the various nervous centres upon which
the renewal of functional activity depends. Little, therefore, can be
expected from them at the height of the disease--that is, in the stage
of collapse--but as soon as any signs of reaction are manifested they
tend to promote it, and hence may enable the functions to revive. For
this reason they are adapted to persons who are feeble by reason of
their tender or their advanced age, or who have previously suffered
from ill-health. But if they act at all, and the more they tend to
act, they must be employed with circumspection, lest they outrun the
purpose of their administration and produce a violent or excessive
reaction. Instead of, or in conjunction with, these internal remedies
the local stimulants of the skin, already enumerated, may be used with
the due precautions, and, in addition, baths at a temperature of 105
degrees F. of water alone or with the addition of salt or mustard; but
all such remedies are of little avail until reaction has commenced.
Before that event there is reason to believe that the cold bath is
preferable, or, still better, frictions of the whole body with cold
water, or even with ice, after which the patient should be wrapped in
dry and warm blankets. Yet the efficacy of this powerful agency is by
no means comparable to that which it produces in the algid forms of
malarial fever. The two conditions, although apparently analogous,
are, in reality, very different. In the cold stage of fever the
mechanism is indeed paralyzed, but none of its mechanical elements are
wanting; but in algid cholera there is an actual subtraction of water
from the blood, that turns it from a liquid capable of circulating
through the narrowest channels into one that stagnates even in the
largest vessels. In the one case force is wanting to circulate the
blood; in the other there is no normal blood to circulate.
The treatment of the stage of reaction when it does not exceed a
moderate degree, consists simply in strictly enforcing the rules for
the patient's repose; that is to say, in intelligent nursing. Mental
excitement must be forbidden, and neither medicine nor food allowed
that is likely to interfere with the gradual and steady progress of
convalescence. Of all articles of food, cool water is not only the
most urgently desired, but is the most imperatively necessary for
replenishing the emptied blood-vessels and restoring the normal
functions. But unless great caution is observed it will be taken too
freely and provoke a renewal of the discharges. If any food besides
water is allowed, it should be of the simplest sort--of whey first,
and then of milk in small quantities at a time, with lime-water if it
provokes nausea or retching. Afterward thin broths may be given, also
in great moderation, and by degrees farinacea in milk and in animal
broths. Only when the strength is much improved should even the most
{764} digestible meats be permitted. In proportion as convalescence is
marked or interrupted by symptoms of undue reaction is it necessary to
prolong and render stringent this regimen; and if those symptoms
unfortunately arise which oftener, perhaps, depend upon an
over-zealous stimulant treatment than upon the natural reaction of the
system, they must be combated by measures which will lessen the local
congestions, especially of the brain and the lungs, and also by such
as will tend to prevent the system from falling into a typhoid state.
For the former dry cups applied to the back of the neck, and cold
lotions and affusions upon the scalp, are to be recommended, and for
the latter dry cups and warm stimulating poultices upon the chest near
the affected region. It is probable that the general warm bath, with
cold affusion upon the head at the same time, would prove as efficient
as it does in analogous states of typhoid affections. If the urinary
secretion is suspended or remains scanty, there is not usually an
urgent need of using means for its restoration; for that will
generally occur when the blood-vessels become replenished. It should,
however, be mentioned that, according to Macnamara, if the patient
does not pass any urine within thirty-six hours of reaction coming on,
ten minims of the tincture of cantharides in an ounce of water should
be given every half hour until six doses have been taken, and the
patient encouraged to drink freely of water. If this treatment does
not cause urine to pass, we must, after the sixth dose, discontinue
the medicine for twelve hours, and then repeat it in precisely the
same way. The dose here referred to is of the British preparation, and
if the use of it were not recommended by so competent an authority its
propriety might very properly be challenged.
After the cholera patient has become convalescent his restoration is
very apt to be retarded by dyspeptic disorders, for which, perhaps,
the best remedy is a judicious use of condiments with the food and of
bitter tonics, especially quinine, colombo, quassia, etc., before
meals. If there is constipation, it should be corrected by the
cautious use of fruits, and, if these prove insufficient, of mild
saline laxatives or small doses of castor oil or rhubarb. On the other
hand, if there is a tendency to diarrhoea, it should be met by the use
of a mild laxative, such as castor oil, magnesia, or rhubarb, followed
by chalk or bismuth, and the use for a time of simpler food and in
less than the usual quantities.
Having thus furnished a sketch of the plan of treatment of cholera
which we regard as dictated by experience, it may be not without some
interest to consider certain elements of the method a little more
fully, and criticise, in passing, some other remedies which have from
time to time been proposed. The first of these is venesection. There
was a time when certain physicians, carried away by conceptions of the
disease evolved from their inner consciousness, maintained that it
consisted essentially of a spasm of the blood-vessels, and that the
natural and legitimate cure for it was to be found in bleeding. No
theory is so gratuitous or absurd but cases may be found which appear
to justify it, and in this instance also examples were not wanting to
illustrate at once the truth of the theory and its successful
application. Longer experience, however, and a more correct conception
of the disease, have long since condemned this method, which was
almost as dangerous as it was irrational. If any additional argument
against it were required, it would be found in the condition of the
lungs after death. These organs, we have seen, are not {765} only not
engorged, but they are empty of blood, and death is due not to
asphyxia, but to apnoea, when it takes place in collapse.
If ever there existed any reason for the administration of an
emetic--and ipecacuanha has generally been used at the commencement of
an attack of cholera--it must be looked for, not in any clinical
experience of its virtues, but simply in the deplorable routine that
required the administration of an emetic at the commencement of nearly
all acute diseases, so that, whatever else was prescribed, the lancet
and an emetic seldom failed to be so. In this case also the proofs of
the successful administration of ipecacuanha were not wanting, and one
might be tempted to suppose, in view of the alleged facts in its
favor, that it was useful by causing an evacuation of the material
cause of the disease. Physicians were even to be found, of high
station and character, who contended that cholera is a species of
fever, and to be treated by an emeto-cathartic composed of tartar
emetic and epsom salts. If the treatment had been efficient, the
absurdity of the reasons for it might have been overlooked; but the
one was as disastrous as the other was false. But, as usual, the facts
had been misstated or misinterpreted, and emetics ceased to form a
part of the systematic treatment of cholera. The idea which possessed
those who advocated the use of evacuants was that there was either a
poison to be eliminated from the blood or one to be expelled from the
bowels. Apparently, the method was not efficacious, for the latest
phase of it, the use of castor oil in acute stage of cholera, was of
short duration.
When cholera first appeared in Europe the tendency naturally arose to
follow in its treatment the example of the British practitioners in
India. It then appeared that one of the most eminent among them,
Annesley, gave a scruple of calomel, with two grains of opium, at the
commencement of the attack, and repeated the dose in six or eight
hours, and again upon the following day. In the decline of the disease
he ordered scruple doses of calomel for the removal of a
"cream-colored, thick, viscid, and tenacious matter exactly like old
cream cheese, which glues the gut together and obstructs its passage."
Three, four, and even five, scruples of calomel were usually taken
before this effect was produced. When it is added that this
practitioner held depletion to be the capital element of the
treatment, and that he was equally lavish of his patient's blood and
of his own drugs, we can only wonder that any subjects of his heroic
method survived. It is now conceded by all enlightened physicians that
mercurials in large or in ordinary doses are worse than worthless in
epidemic cholera. In 1832, Dr. Ayre of Hull, Eng., proposed another
method of using calomel, to which he adhered in treating this disease.
It consisted in the administration of very small doses of calomel at
short intervals, and with each of the first doses a few drops of
laudanum. Such a method, if not carried too far, certainly has the
merit of sparing the patient a great deal of the perturbative
treatment against which we have, in the preceding pages, protested.
But that was not at all the notion of its proposer. He claimed for it
positive and active virtues. He stated, as the fundamental ground of
his plan, that "the primary and leading object of the treatment must
be to restore the secretion of the liver." He did not in the least
doubt that he was able to do this by the administration of
mercury--not, indeed, by a direct action upon the liver {766} itself,
but indirectly and sympathetically through the stomach, and by the
healthy and specific stimulus imparted to it, by which the due
secretion of the bile is promoted. It is, indeed, difficult to
conceive of any stimulus that calomel could impart to the stomach that
would not be equally given by any other non-irritant and insoluble
powder--subnitrate of bismuth, for example. Indeed, Ayre himself
relates the case of a man who in an attack of cholera took during
three days no less than five hundred and eighty grains of calomel, and
recovered without any soreness of the mouth. But the plan which he
finally elaborated was different. It was to give small doses of
calomel repeatedly--in the premonitory stage one grain every half hour
or hour for six or eight successive times, or, if this failed, every
five or ten minutes--and in the stage of collapse one grain and a half
every five minutes. In a few cases of extreme severity two grains of
calomel were given every five minutes for an hour or two, and then the
ordinary dose of one grain was resumed. But this was not all: with
every dose of calomel was associated one, two, or three drops of
laudanum, so that if these doses were repeated frequently the patient
received a very efficient amount of the narcotic during the attack.
Indeed, Ayre attributed to it the virtue of sustaining the vital
powers under the depressing influence of the disease, and of removing
or abating the cramps, as well as of detaining the calomel in the
stomach.[64] From the preceding account it follows that the treatment
of cholera by small doses of calomel with laudanum is founded on an
erroneous assumption of the mode of action of calomel, and that
whatever efficacy the plan of treatment may possess may with more
justice be attributed to the opium, whose effects we know, than to the
calomel, whose action, so far as it is known at all, has no
conceivable relation to the disease for which it was given. However
this may be, if the results of Ayre's treatment are compared with
those of other plans, it exhibits very little if any superiority. In
the report of the cholera committee of the College of Physicians,
London, made in 1853, we find the statement that in 725 unequivocal
cases treated on Ayre's plan the deaths were 365, or about 50 per
cent., and also the following commentary: "In general, no appreciable
effects followed the administration of calomel, even after a large
amount in small and frequently-repeated doses had been administered.
For the most part, it was quickly evacuated by vomiting or purging,
or, when retained for a longer period, was passed from the bowels
unchanged. Salivation but very rarely occurred, and then only in the
milder cases. We conclude that calomel was inert when administered in
collapse, and that the cases of recovery following its employment at
this period were due to the natural course of the disease, as they did
not surpass the ordinary average obtained when the treatment consisted
in the use of cold water only."[65] It is of interest to compare the
mortality of 50 per cent. above stated to have occurred under this
sort of calomel treatment with the mortality noted at the London
Hospital under various kinds of treatment, including the
administration of calomel in doses varying "from five to ten and
twenty grains every quarter, half, one hour, two, four, etc." Out of
509 cases, 281 were fatal, or 54.9 per cent.[66]
[Footnote 64: _A Report on the Treatment of the Malignant Cholera_,
Lond., 1833.]
[Footnote 65: Dr. Gull's _Report_, p. 177.]
[Footnote 66: _Lond. Hosp. Reports_, iii. 437, 441.]
Every disease in which exhaustion and coldness occur is sure to be
{767} treated more or less actively with alcohol, but in the collapse
of cholera, as in the cold stage of fevers, it is generally useless,
and sometimes hurtful. We believe that the following protest of
Macnamara is sustained by almost universal experience: "I would here
enter an earnest protest against the use of brandy or any alcoholic
stimulant in this [the second] stage of cholera. I believe these, both
theoretically and practically, to be the cause of unmitigated evil. I
simply, therefore, mention brandy, champagne, and the like in order to
condemn their use most emphatically in cholera; according to my ideas
and experience, it is almost impossible to hit on a more detrimental
plan of treatment than that usually known as 'the stimulant' in this
form of disease."[67] It is true that apparent dissidents from this
judgment may be found, like Playfair, a deputy inspector of hospitals
in Bengal, who even circulated printed directions for the treatment of
the first stage of the disease by means of brandy or strong rum,
cayenne pepper, and laudanum, and had entire confidence in the
efficacy of the method.[68] Dr. Macpherson, inspector-general of
hospitals, also, after comparing the results of a stimulant treatment
with those of other methods, reaches the conclusion that the
mortality-rate of cholera is affected neither by the moderate nor by
the excessive use of alcohol.[69]
[Footnote 67: _Op. cit._, p. 456.]
[Footnote 68: _Edinburgh Med. Jour._, xix. 471.]
[Footnote 69: _Med. Times and Gaz._, Jan., 1870, p. 62.]
Upon no other point in the treatment of cholera is the agreement of
physicians more complete than upon the use of opiates in the early
stage of the disease. The premonitory diarrhoea has always been
treated by opiates alone or associated with astringents. Probably the
best rule is to give from twenty to thirty drops of laudanum, or an
equivalent dose of some other liquid preparation of opium, in a little
brandy and water, and repeat the dose as often as a stool is voided.
Opiates have also been generally employed to mitigate the symptoms of
the fully-developed disease. But, like all other medicines introduced
into the stomach or rectum, they are apt to be rejected, and even if
they are not, their absorption is very doubtful, so that at the height
of the attack they must be considered as nearly if not quite useless.
When the vomiting and purging begin to subside and reaction is about
to commence, small and repeated doses of opiates undoubtedly tend to
lessen the evacuations; but great caution must be observed not to
exceed the due degree of stimulation, lest a dangerous state of
narcotism or collapse be induced. It might be supposed that the
hypodermic use of morphia would be less open to objection than its
administration by the stomach; but it is to be remembered that the
suspension of gastric absorption is only a part of the similar
condition affecting the whole circulatory system, and that the
stagnation of the blood in the systemic veins prevents the absorption
of medicines administered subcutaneously perhaps as completely as the
state of the gastric blood-vessels interferes with their absorption
from the stomach itself. In point of fact, the utility of opiates at
any stage of cholera after the first is not easily determined, for
nearly always they are associated with other medicines, and especially
with astringents. In this disease, as in others that involve life, we
are seldom at liberty to test the powers of individual medicines, but
are bound to endeavor to save life by associating those which seem to
be required for the purpose. Opiates, then, are nearly always given in
conjunction with astringents or stimulants {768} during the first (or
diarrhoeal) stage of the attack, but after vomiting is added to
diarrhoea and a tendency to collapse is manifested they are at least
useless.
The patient, it has already been said, should be disturbed as little
as possible, and hence, if he becomes restless, and especially if he
is rendered so by pain, he should be tranquilized by means of
anaesthetics. Chloroform has generally been employed, and is best
administered on the first accession of cramps. Much pain, with
muscular fatigue and depression, is thus saved, and the inhalation of
the medicine may be repeated as often as the pain threatens to return.
No doubt other anaesthetics, and especially ether, would answer the
same purpose.
Camphor has been claimed to be a valuable medicine in cholera, but
there is no clinical evidence that it is so. Indeed, the only series
of cases in which it was mainly depended upon gave a large mortality.
Acids have been employed in cholera, but chiefly on theoretical
grounds, "in the hope of destroying the specific cholera process going
on in the intestinal canal" (Macnamara). It is hardly necessary to
discuss so vague a reason. What specific process is going on? What
relation to it has the administration of acids? And, after all, only
the hope is held out of destroying the hypothetical morbid process.
The reaction of normal stools is usually acid, but sometimes it is
neutral or even alkaline. In other acute bowel complaints with profuse
diarrhoea they are acid, as in cholera infantum, but in epidemic
cholera they are alkaline, because they consist chiefly of the water
of the blood. It is far from proven that mineral acids can be useful
merely by reversing the reaction of the stools. Far more probable is
it that, in so far as they are of use, it is because they act as
astringents upon the digestive mucous membrane. This may be inferred
from the fact that, according to the advocates of these medicines, it
is always difficult, and is often impossible, to acidify the stools in
cholera. Moreover, it must be remembered that, like other medicines,
the greater part of them are rejected by vomiting. If, then, mineral
acids tend to lessen the diarrhoea of cholera, they act by their
astringency and not by their acidity. Diluted or aromatic sulphuric
acid may be given in the dose of from two to thirty minims, at
intervals of an hour, in acid water or carbonated water, or diluted
nitric acid, in doses of from twenty to fifty minims, at the same or
somewhat longer intervals.
Intravenous injections were used in England during the first epidemic
of cholera in 1832-33, but their results were regarded as unfavorable;
subsequently, in 1849, they were tried with somewhat better success,
and in 1867 the effects were still more encouraging. The liquid
employed on the last-mentioned trial consisted of chloride of sodium
60 gr., chloride of potassium 6 gr., phosphate of sodium 3 gr.,
carbonate of sodium 20 gr., alcohol 2 drachms, and distilled water 20
ounces. The alcohol was added only when the liquid was about to be
used, and the temperature of the latter was not allowed to exceed 110
degrees F. or fall below 100 degrees F. The liquid was contained in a
zinc vessel holding about eighty ounces, with a lamp underneath, a
thermometer hanging within, and a tap near the bottom, from which
proceeded an india-rubber tube four feet long, with a silver nozzle at
its end. The fluid was allowed to enter the vein by the force of
gravity. If difficulty was experienced in introducing the nozzle, the
vein was freely exposed, supported on a probe, and incised
longitudinally. It was found that the success of the operation
depended greatly {769} upon having an ample supply of the solution
prepared, so as to repeat the injection as often as might be found
necessary. Mr. Little, who practised this method in numerous cases,
stated as follows: "When a patient has been long pulseless clots form
in the heart, and, as I have seen, extend into the larger veins. In
one case the fluid would not flow in, and only distended the veins of
the arm injected. After death clots were found extending from the
heart into the axillary vein."[70] Five out of twenty apparently
hopeless cases recovered under this treatment. The first effect of the
injection was to revive the pulse, which had ceased to be felt; the
voice also was restored, the color and expression improved, the cramps
were relieved, the temperature rose, and the patients became convinced
that their recovery was assured. A profuse perspiration and a severe
rigor accompanied these symptoms. The rigor was evidently a nervous
phenomenon, and not a chill, for it occurred when the temperature was
rising. Other cases might be cited which unquestionably owed their
recovery to this mode of treatment. It is true, however, that much
more frequently it failed of success; and probably not only because
the injection could not reach the heart, but because, having permeated
the blood-vessels of the whole body, it escaped, as the serum of the
blood had done, from the damaged intestine. Nevertheless, it would
seem that an expedient which in a certain proportion of cases has been
quite successful might yet be rendered more certain in its results if
the operative procedure were perfected.
[Footnote 70: _London Hosp. Reports_, iii. 470.]
Cramps in the limbs may be lessened by active friction and shampooing,
but there is no clinical reason for believing that these measures tend
to restore the circulation. Equally ineffectual are other means used
for communicating heat to the algid body and thereby reviving its
functions. It is true that some physicians found that warm baths, at
from 90 degrees to 104 degrees F., gave relief to the cramps and
restored the failing pulse. In most cases the calming influence of the
bath was noted, but it does not seem to have been curative or to have
diminished the mortality-rate.[71] It should not be forgotten that the
patient has no perception of his coldness. In all analogous
conditions, as has already been remarked, such as frostbite and the
cold stage of periodical fevers, cold, and not heat, promotes
reaction. Still more injurious, if possible, than hot applications are
irritants and stimulants after the stage of collapse has set in. Not
only are they absolutely futile for restoring the animal temperature,
but they are liable, unless very cautiously used, to produce
intractable sores upon the skin if recovery ensues. It should also be
remembered that the cholera patient's exhaustion is exceptionally
great, and is apt to be increased by the officiousness implied in the
use of many stimulating agents.
[Footnote 71: _Ibid._, iii. 445; _St. Bartholomew's Reports_, iii.
190.]
As early as 1832 a marked advantage was ascribed to the use of cold
affusions in cholera.[72] One of the physicians of the cholera
hospital of Berlin said: "In these living corpses which are struck
with asphyxia, lying cold and powerless, external and internal
medicines cease to stimulate; no steam apparatus, no warm bathing, no
friction, no irritant, avails." The condition is comparable to that in
approaching death by cold, in which friction with snow is well known
to be the proper remedy. Cold affusions were employed in the second
stage of the disease. If the pulse revived, the affusions were
continued in a tepid bath, after which the patient was {770} put to
bed and gently rubbed with cold flannels. Internally, ice-water was
freely administered. Labadie-Lagrave[73] refers to forty cases treated
in this manner, with only seven deaths. Yet the cold-water treatment
does not appear to have commended itself to physicians generally.
Evidently it does not meet the prime indication, which is to restore
the wasted waters of the blood and retain it in the blood-vessels.
[Footnote 72: Ainsworth, _Pestilential Cholera_, 1832.]
[Footnote 73: _Du Froid en Therapeutique_, 1878.]
Cold water ought to be given as freely as possible to assuage the
thirst that exists in every stage of cholera, and especially in
collapse. Nor should it be withheld because it will presently be
rejected, for not only does it produce a grateful sensation in the
mouth and throat, but it renders the act of vomiting easier. Yet, to
some extent at least, the thirst may be allayed by rinsing the mouth
and throat with cold water. Iced water is preferable to ice used for
the same purpose, for the latter, by its relatively intense coldness,
irritates and dries the mouth. Fragments of ice swallowed whole allay
the burning heat in the stomach.
On the hypothesis that the cholera poison consists of organic germs
various antiseptics have been employed in this disease. Permanganate
of potassium was fortunately excluded from the list, on account of its
corrosive action, but, unfortunately, carbolic acid was conceived to
possess virtues that rendered it an eminently suitable remedy, and
creasote, which resembles it very closely, was presumed to possess
corresponding virtues. Then sulphurous acid and the sulphites, which
for a time were warranted to destroy every species of germ, were
confidently appealed to to stay the progress of cholera, and it was at
one time even a matter of dispute whether sulphite of sodium or
sulphite of potassium was the more efficacious. In truth, all of these
medicines were useless, even when they were not mischievous.
Cholera has never prevailed in any country without giving rise to
extraordinary theoretical and practical divagations. One physician in
the earliest American epidemic gravely proposed, as the best mode of
checking the diarrhoea, to plug the anus with a soft velvet cork.
Another, in England, suggested that the "blood may be kept circulating
by putting the patient on his back on a board and keeping up a
rocking, see-saw, to-and-fro movement from eighty to one hundred times
a minute." Another had the revelation that the disease is essentially
a "paralysis of the sympathetic nerve and want of performance of the
organic functions, with deficient vitality of the mucous membranes,"
and that its proper remedies are "bleeding, turpentine, and cool
drinks, without heat and stimulants;" and to this remarkable doctrine
a well-known physician gives his adhesion, thus: "The cause, I firmly
believe, is an union of the poison with the sympathetic."[74] Still
another discovered that the disease is a spinal disorder, and is to be
treated by the application of ice-bags to the spine. Were not the
evidence so palpable, it would hardly be believed that such irrational
ideas should have been published concerning a disease which had then
been under observation by the whole medical profession in Europe and
America for more than thirty years, and in Asia for a much longer
period.
[Footnote 74: _Times and Gazette_, Aug., 1866, p. 209; _ibid._, Nov.,
1866, p. 555.]
The most important lesson to be drawn from this history of the
treatment of epidemic cholera is, that the arrest of the disease in
the diarrhoeal stage is comparatively easy, and that in the stage of
collapse its cure by any means whatever is altogether an exceptional
occurrence.
{771}
THE PLAGUE.
BY JAMES C. WILSON, M.D.
DEFINITION.--An acute specific fever of short duration and very fatal,
endemic in certain Oriental countries, and frequently epidemic; it is
characterized by buboes, carbuncles, and petechiae.
SYNONYMS.--([Greek: plege], _plaga_, a stroke); the Pest; Pestilence;
the Bubonic, Glandular, Inguinal Plague; the Oriental, Levantine,
Levant Plague; the Indian, Pali Plague; Mahamari; Septic or Glandular
Pestilence; Pestilential Fever, Adeno-nervous Fever; Typhus
Pestilentialis, Gravissimus, Bubonicus, Anthracicus, etc. _Gr._
[Greek: ho loimos]; _Lat._ Pestis; _Fr._ La Peste; _Ger._ die Pest,
Beulenpest.
CLASSIFICATION.--The plague, pest, pestilence, and their equivalents
in various tongues, are terms that have been used from the earliest
historical times to designate every epidemic disease attended by great
mortality. As knowledge of diseases becomes clearer the terms by which
they are designated become more definite; those which did service for
a class are restricted to particular groups, and new names are found
for other maladies only allied to such groups by superficial
resemblances. Hence by degrees the term plague has become more
restricted in its use. To-day it is understood as designating
exclusively the specific affection defined above, the bubo plague.
The student of medical history meets with insurmountable difficulties
in attempting to classify the recorded epidemics which have been
described under this term. Even when used in its more restricted
signification, difficulties as to the propriety of its application to
certain epidemics arise. Thus, nosologists are not in agreement as to
whether the great plague--the black death--which swept over Europe in
the fourteenth century and destroyed in three years twenty-five
millions of inhabitants, was a modification of the bubo plague or an
essentially different disease. A like difference of opinion exists in
regard to the relationship between the Indian or Pali plague which has
from time to time prevailed in North-western India during the present
century and the true plague.
The black death of the fourteenth century and the Pali plague, though
presenting many of the characteristics of bubo plague, differ from it,
while they resemble each other, in one important particular. Among the
earlier and more common symptoms of note are those dependent upon
gangrenous inflammation of the lungs, a lesion, according to
Hirsch,[1] extremely rare in bubo plague. This author informs us that
recent observations have fully confirmed the early opinion that the
Pali plague {772} differs from that of the Levant chiefly in this
modification, and cites Pearson and Francis as saying of the former
disease that "the collective symptoms are more like those of plague
than of any other known disease.... We believe it to be in all
essential particulars identical with the plague of Egypt."
[Footnote 1: _Handbuch der historisch-geographischen Pathologie_, Dr.
August Hirsch, 1860.]
The three forms of plague--(_a_) the grave (or ordinary), (_b_) the
fulminant (pestis siderans), and (_c_) the larval or abortive,
observed in epidemics and hereafter to be described--do not represent
distinct varieties of the disease, but are merely expressions of
differences in the intensity of the action of the infecting principle
upon different groups of individuals in given communities--differences
to be explained here, as in the other infectious diseases, in part by
variations in the activity of the poison itself, in part by the
individual peculiarities and susceptibilities of those exposed to it.
HISTORICAL SKETCH.--Upon the authority of Rufus of Ephesus, quoted by
Oribasius,[2] it is stated that the bubo plague prevailed as an
endemic, and at times as an epidemic disease, in Libya, Egypt, and
Syria prior to the beginning of the Christian era.
[Footnote 2: _Medicinalia Collecta_.]
In the year 542 A.D., according to Procopius,[3] the plague appeared
in Egypt, at Pelusium; extended westward to Alexandria; eastward to
Palestine, Syria, and Persia; passed from Asia Minor to Europe, where
it first invaded Constantinople, whence it spread in all directions
with such fury that before the close of the sixth century one-half the
inhabitants of the Eastern empire had perished, either of the plague
itself or of the universal destitution that followed in its train.
[Footnote 3: See Hirsch.]
With this epidemic, known in history as the Justinian plague, this
disease established itself for the first time in Europe, where it
maintained foothold for more than a thousand years.
About the middle of the seventeenth century the wide prevalence of the
plague in Europe began to draw to an end. In Spain it was epidemic for
the last time from 1677 to 1681; in Italy the last general epidemic
came to a close in 1656, although local outbreaks continued to occur
till the beginning of the following century. In France it still
prevailed in several provinces in 1668, although it had for the most
part disappeared some years before. In Switzerland we encounter it for
the last time in 1667-68; in the Netherlands in 1677; from England the
plague disappeared with the great outbreak of 1665. In the early part
of the eighteenth century two important epidemics occurred within the
boundaries of Europe. The first spread from Turkey, through Hungary
and Poland, to Russia, thence to Norway and Sweden, and along the
shores of the Baltic Sea to the Low Countries. This epidemic came to
an end in 1714. Six years later the last great outbreak of the plague
on European soil took place. It prevailed with great fury in
Marseilles in 1720-21, and overran the whole of Provence. From this
date till the close of the century Europe remained free from the
plague, with the exception of Turkey and the contiguous countries.
During the second and third decades of the present century repeated
epidemics occurred in the Balkan Peninsula and the regions bordering
on the Lower Danube and the Black Sea. The plague appeared also in
Malta in 1813, and prevailed till 1815, and in 1816 it reached certain
of the Ionian Islands. {773} Only twice has this pest shown itself
during the present century in Western Europe--once, during the
epidemic at Malta in 1815, at Noja, a town of the Neapolitan province
of Bari; the second time, in 1820, at Majorca, whither it was carried
over from the coast of Barbary.
Between 1552 and 1784 the plague prevailed twenty-six times in Tunis
and Algiers. Some idea of the importance assumed by this scourge in
the countries of North-western Africa may be found from the fact that
many of these epidemics lasted continuously for years, that which came
in 1784 not ceasing for fifteen years. Between 1816 and 1821 the
plague again prevailed in Tunis and Algiers, and again in 1836-37.
During the first half of the present century a change took place in
the prevalence of the disease elsewhere. Shortly before its complete
disappearance from Europe it ceased to prevail in Western Africa (with
the exception of the Nile countries), in Mesopotamia, and in Persia.
It disappeared from Asia Minor, Syria, and Palestine in 1843, from
Egypt in 1844.
For a short period the plague seemed to have disappeared altogether.
Those who cherished this hope were, however, destined to
disappointment. In 1853 an outbreak occurred in the Assyr country,
Western Arabia; and from that time till the present unmistakable local
epidemics of the bubo plague have occurred in isolated regions of
Africa and Asia; thus, in 1858 at Benghazi in Tripoli; in 1857 in
Mesopotamia; in 1863 in the district of Maku, Persian Kurdistan; in
1867 in the marsh district on the right bank of the Euphrates; in 1870
in Persian Kurdistan; in 1871-73 in the Yunnan province, Western
China; in 1873 in the marsh district on the left bank of the
Euphrates. During four years following the outbreak of 1873 the
disease continued to prevail over an extensive area in the countries
bordering on the northern banks of the Persian Gulf. In 1874 it
reappeared also in the Assyr district, Western Arabia, and in
Benghazi, Northern Africa. In 1876, whilst still infesting the regions
about the Lower Euphrates, the plague appeared in South-eastern
Persia, and during this and the following years it appeared at several
isolated points on the borders of the Caspian Sea. Early in 1878 the
disease was reported as prevailing in the district of Souj-Bulak,
Persian Kurdistan, and it appeared in October of the same year at the
Cossack village Vetlanka, on the Lower Volga, district of Astrakhan,
Russia, after an absence from Europe of thirty-seven years. It has
more recently prevailed in the Assyr district, Western Arabia, and
there have been rumors of its reappearances in Persian Kurdistan.
The Indian or Pali plague (Mahamari) has prevailed in local epidemics
of great severity on several occasions during the present century in
the North-western provinces of India. This fever was first recognized
in Kutch in May, 1815, after a season of great scarcity of food. It
spread rapidly over an extensive territory, and appeared in the spring
of the following year at various points in Guzerat, next in Merawi,
later in Rhadenpur, spreading thence westward to Sindh. Not until the
following year (1817) did the pest reach the British possessions. This
epidemic continued to prevail until 1821. The disease did not reappear
until July 6, 1836, when it broke out in Pali, the principal depot of
traffic between the coast and North-western India. It spread with
great rapidity to the {774} adjoining provinces. Toward the close of
the year 1837 the disease broke out anew in Pali, and raged until the
spring of the following year. In 1834-35, again in 1837, there were
outbreaks of this pest in Gurwal, and in 1846 and 1847 in Karmoun,
provinces of the southern slopes of the Himalayas. This destructive
pest has raged at an altitude of 10,300 feet, and we learn from Hirsch
that it has never wholly disappeared from the mountain-districts of
the Himalayas since 1823, and that its ravages in these regions have
been so great that certain settlements have been wholly destroyed.
The fever was remittent in type, with a great tendency to become
continued; it was characterized by rapidly developing extreme
prostration, and was very fatal. In most cases there were glandular
swellings in the groins, armpits, and neck. Carbuncles and petechiae
are not mentioned as having been observed. Dyspnoea, cough, and bloody
expectoration were frequent symptoms. Vomiting, at first of bilious
matter, later of dark, coffee-colored fluid, was likewise common.
The plague has never appeared in the western hemisphere.
ETIOLOGY.--1. Predisposing Influences.--Whilst the present views as to
the causation of the specific diseases compel us to assume a specific
infecting principle as the real cause of every outbreak of the plague,
there are certain circumstances which are recognized as so favoring
the development and action of that principle that they have come to be
looked upon as indirect or auxiliary causes of particular epidemics.
It is more in accordance with the facts to speak of them as
predisposing influences. Chief among these circumstances is that
combination of physical and social wretchedness which goes hand in
hand with poverty and overcrowding. The plague has been termed by a
recent observer (Cabiadis) miseriae morbus, and he has thus reproduced
in 1878 a name applied to the great plague of London in 1665--the
poor's plague. All observers of recent epidemics unite in ascribing to
poverty the foremost rank among the predisposing influences of plague
epidemics. It is only necessary to enumerate the evils which form the
train of poverty, whether in cities or in villages, to complete the
list.
With poverty come ignorance and neglect of all sanitary laws;
overcrowding and ill ventilation; personal filthiness; improper as
well as insufficient diet; indifference as to the location of
dwellings and their surroundings. The condition of the villages which
have been the scene of some of the recent epidemics beggars
description. All observers unite in testifying to such accumulations
of filth in and around the houses as requires to be seen to be
believed. In these communities latrines are unknown, and no such thing
as organized scavenging has ever existed.
The accumulation of unburied or imperfectly buried corpses has been
looked upon as the real cause of the plague, and some of the recent
epidemics have followed the prevalence of distinctive epizootics.
Whilst it is not difficult to disprove that under ordinary
circumstances the effluvia from exposed and rotting carcasses can give
rise to outbreaks of the plague, it is more than probable that an
atmosphere charged with such emanations (together with other causes)
can so unfavorably influence a community as to increase its
susceptibility to the specific cause of this or any other infective
disease. There can be but little doubt that the {775} dead bodies of
the victims of the plague are capable of disseminating the disease,
and that the reopening of graves containing such bodies, even after a
long period of time, has given rise to fresh outbreaks of the disease.
The season of the year does not appear to exert any very marked
influence upon the development of epidemics, if we base our deductions
upon observations made in different countries. In northern countries
the disease has prevailed as severely in mid-winter as in summer. The
epidemics of London showed a rise during July and August, their
furious prevalence in September, and a gradual decline during October
and November. In Constantinople the disease has commonly remained
dormant during the winter months, and become active as the weather
grew hotter. In Egypt, on the contrary, the activity of the outbreaks
has developed in winter, increased with the advance of spring, and
suddenly abated upon the advent of the summer. Such also has been the
case with the three general epidemics in Mesopotamia studied by
Tholozan.[4] "Their beginning took place in winter, their development
during the spring, their decline and their extinction in summer. Their
recrudescences obeyed the same laws: after an incubation during the
summer season ... revivification took place in winter and in spring."
It is added in this writer's account that the exceptional hot weather
of summer in that country, and especially that of the shores of the
Persian Gulf, has always moderated or directed the course of epidemics
of this pest. In Cairo the epidemics have usually ceased upon the
recurrence of intense summer heat in June. Dampness, and particularly
a thoroughly wet soil, are favorable to the development and spread of
the disease. The marshy regions of the Lower Euphrates, the shores of
the Caspian and the Black Seas, the valley of the Nile, have been the
scenes of repeated visitations. On the other hand, the plague has
maintained its foothold in the mountainous districts of Western
Arabia, in Yunnan, on the slopes of the Himalayas at a great
elevation, and upon a dry, non-alluvial soil even more firmly than in
the low and humid plains of Mesopotamia.[5]
[Footnote 4: _Histoire de la Peste Bubonique en Mesopotamie_, 2d
Memoire, Paris, 1874.]
[Footnote 5: Tholozan, _Histoire de la Peste Bubonique en Perse_, 1st
Memoire, Paris, 1874.]
Individual predisposition to contract the disease seems to be
increased by all depressing influences, among which may be mentioned
excessive bodily or mental exertion, intense and prolonged anxiety,
fear, and the like. Previous debilitating disease also increases the
liability to the attack. Neither sex nor age exerts an influence in
this respect, save that after the age of fifty few contract the
disease. Occupation confers no immunity. Physicians, nurses, and
others occupied in the care of the sick, and those who bury the dead,
have especially suffered in recent[6] as well as in the older
outbreaks. Oil-carriers and dealers in oils and fats, and to a less
degree water-carriers and the attendants at baths, are said to enjoy a
comparative immunity from attack. Those who have suffered from the
disease and recovered also enjoy a relative immunity. Second attacks
are usually of less intensity than the first.
[Footnote 6: See summary of a report addressed by Dr. G. Cabiadis to
the Constantinople Board of Health on the outbreak in Astrakhan in
Russia, 1878-79, by E. D. Dickson, M.D., _Medical Times and Gazette_,
1881, vol. i. pp. 4, 32, 119.]
2. The Exciting Cause.--The exciting cause of the plague must, in
{776} the present state of our knowledge, be assumed to be a specific
infecting principle. Upon no other hypothesis can the continued
existence of a disease so specific in its characters, unchanged
through the course of centuries, disappearing when the influences
favorable to its presence cease, reappearing in certain regions when
they again arise, be explained. Capable of being transmitted by the
vehicles of commercial intercourse, of control by quarantine and
cordons sanitaires, of spreading from limited foci of contagion into
overwhelming epidemics, the plague is the very type of the infective
diseases. The nature of this infecting principle is wholly unknown. It
is probably a microphyte capable of development within the human
organism--capable also of a prolonged independent existence under
favorable circumstances outside of the body, and of again giving rise
to the disease. The plague is properly to be classed as a
contagious-miasmatic disease (Liebermeister) with cholera, dysentery,
and enteric fever. It continues to exist by the continuous propagation
of its cause, and it spreads by the transportation of that cause.
It is conceded on all hands that the plague has never arisen
autochthonously in Europe, but has in every instance been conveyed
thither. Those who regard its reappearance after long intervals of
time in those countries where it still occasionally prevails as
spontaneous are compelled to ignore difficulties in reasoning far
greater than the supposition of an equally prolonged condition of
quiescence or an inexplicable or unsuspected reintroduction of the
cause.
As to the disputed question of the contagiousness of the plague, to
set forth the arguments and examples adduced in favor of either view
would far exceed the limits of the present article. All the facts are
to be explained upon the theory that the exciting cause of the plague,
like that of cholera and enteric fever, consists of a miasm that must
undergo certain changes outside the body before acquiring its virulent
properties, and that the time required for these changes is
exceedingly brief. But what the physical properties of this miasm are,
or how it finds access to the body, or how it is eliminated, are alike
utterly unknown to us.
It is certain, however, that it is incapable of being freely
transmitted to great distances in the air. Whether or not it is
conveyed or retained by the discharges from the bowel is not known.
The history of recently observed outbreaks, from which alone definite
and trustworthy facts are to be obtained, goes to show that the
exciting cause of the plague clings closely to the patients and their
immediate belongings. The closer the relation between those sick and
the healthy, the greater the risk that the latter will contract the
disease. Those in the house with the patients are more liable to fall
sick than those in the adjoining houses--those who are constantly in
their presence than those who occasionally see them. Thus, nurses much
more frequently contract the plague than doctors, though the latter
have in all epidemics been largely numbered among the victims. Among
357 deaths in the outbreak in Vetlanka, already referred to, were a
priest, his wife and mother, three doctors, six assistant medical
officers, and two Sisters of Mercy. Dr. Cabiadis remarks that the
information obtained "shows that the malady propagated itself, in the
first instance, from the sick to their relatives and to those who
lived with them or who assisted them during their illness. If, on the
one hand, these facts showed its contagious character, on the other
hand evidence is {777} still wanting to prove whether this
transmission of the malady was caused by contact with the sick and
their clothing, or by breathing an atmosphere impregnated with the
deleterious particles emanating from their morbid bodies."
The period of incubation is from two to seven days. In the report of
the commission of the French Academy of Medicine, drawn up by Prus in
1844, the statement appears that the plague has never shown itself
among compromised persons after an isolation of eight days. The recent
outbreaks tend to confirm this conclusion. L. Arnaud concluded from
observations made at Benghazi in 1874 that the mean duration of this
period was five or six days, and that the maximum did not exceed eight
days. Cabiadis sets this stage down as three days as the rule, but as
occasionally not exceeding twenty-four hours. He found no data,
however, to show the longest period to which it could extend. Hirsch,
from information collected in his investigation of the same epidemic
(that of Astrakhan), concluded that the minimum period of incubation
observed was from two to three days, the maximum more than eight, and
that the average was five days. He states that very short or very long
periods were seldom observed.
SYMPTOMATOLOGY.--Individual cases of the plague, as of other epidemic
diseases, differ in their onset and progress under different
circumstances and at different periods of particular outbreaks.
Besides the ordinary form, to which as a type the greater number of
the cases more or less closely conform, there are, on the one hand,
others so severe that death takes place before the characteristic
manifestations have time to appear, and, on the other hand, cases so
light that such manifestations are but partly developed, and the
nature of the malady is only to be recognized in the light of the
prevalent epidemic influence.
Hence among the cases three forms are recognized: (_a_) The grave or
ordinary form; (_b_) the fulminant form; and (_c_) the larval or
abortive form.
(_a_) Grave or Ordinary Form.--The plague in typical cases is a
febrile malady of the most acute kind, with localizations in the form
of buboes or carbuncles.
The course of the attack may, for convenience of description, be
divided into four stages: 1, the stage of invasion; 2, the stage of
intense fever; 3, the stage of fully-developed localizations; and 4,
the stage of convalescence.[7]
[Footnote 7: This formal division of the description is suggested in
some of the older accounts. (See "_Loimologia; or, An Historical
Account of the Plague in London in 1665_, by Nathan Hodges, M.D., and
Fellow of the College of Physicians, who resided in the City all that
Time, Lond., 1721.")
The appearance of the plague in France in 1720 was the occasion of a
great number of curious and interesting publications on this subject.]
1. The stage of invasion is marked by a feeling of lassitude, by pains
in the loins and extremities. There is extreme bodily and mental
weakness, headache, fulness and throbbing of the head, dizziness. The
patient's expression is dull, stupid; he replies to questions slowly
or awkwardly, his face is pale, his eyes languid, his gait feeble and
staggering. The appearance in this stage has been compared by several
observers to that of a drunken man. Shivering occurs, but if fever be
present it is slight. Nausea, vomiting, and diarrhoea are symptoms
sometimes {778} observed. This stage begins suddenly. It is often
imperfectly developed, and it may last only a few hours or a day or
two.
2. The second stage is characterized by fever of the most intense
kind. It is ushered in by a chill, sometimes slight, commonly severe.
The lassitude continues, the headache increases, the dulness deepens
to stupor or gives way to delirium. The temperature rises to 102
degrees-104 degrees F., or even to 107.6 degrees F. The pulse quickly
mounts to 120 or 130. The skin is hot and dry; the patient complains
of burning inward heat and of great, sometimes unbearable, thirst. The
eyes are sunken and injected; the tongue moist, pale, and thickly
covered with a chalk-white or grayish pasty coating; the vomiting
often continues. The delirium is commonly active or noisy, and
accompanied by great restlessness; it may, however, be mild, tending
to sopor or coma. The progress of the disease now rapidly advances.
The patient falls into the so-called typhoid state. His tongue becomes
dry, hard, and fissured; sordes collect upon the teeth and lips,
bloody crusts about the nostrils. At this time the evidences of
failure of the forces of the circulation become conspicuous. The pulse
grows feeble, small, often irregular--sometimes it can scarcely be
felt; the lips become bluish, the extremities cold. There is tendency
to collapse. During the course of this stage buboes begin to make
their appearance. Sometimes the enlargement of the superficial
lymphatics is preceded by tenderness or pain of more or less
intensity; often the glands are found to be enlarged only upon search.
The termination of this stage is marked by a sudden fall of the
temperature to subnormal ranges (93.2 degrees F. has been observed);
at the same time copious strong-smelling sweat not infrequently
occurs. The pulse grows feebler, and falls to 100 or below it, and the
mind becomes clearer.
3. These changes lead up to the stage of fully-developed local
manifestations. The enlarged lymphatics are most commonly situated in
the groins or on the upper part of the thighs at a point below that
commonly the seat of venereal buboes; less often they are to be found
in the armpits or the region of the angle of the jaw; as a rule, they
occupy only one or two of these positions in the same patient. They
vary in size from a little mass or kernel, only to be discovered after
careful search, to the bulk of a hen's egg or a mandarin orange. The
swelling of the gland takes place at times with great rapidity.
Suppuration is followed by the discharge of an ichorous pus, and not
rarely by ulcerative destruction of the surrounding tissues.
Suppuration occurs more frequently than resolution, but is
comparatively rare in fatal cases. Hence it has come to be popularly
regarded as a favorable prognostic sign, whilst the early subsidence
of the swelling has been looked upon as an omen of grave import.
The time of the appearance of the buboes varies greatly. In the
greater number of cases they have shown themselves on the second,
third, or fourth day of the attack, occasionally within six or eight
hours of the beginning of the attack, and occasionally they have been
observed to precede the general manifestation of the disease; rarely
they have appeared as late as the fifth day. In many cases they are
absent altogether.
Carbuncles demand attention as being among the characteristic local
manifestations of this stage. They are less common than buboes. Their
usual position is upon the lower extremities, the buttocks, or the
back of {779} the neck. In favorable cases the gangrene after a few
days becomes limited and the slough separates. Boils also occasionally
appear.
Petechiae occur in the worst cases, and often at an early period in
the course of the disease. Their appearance usually indicates a fatal
issue. They occupy at times extensive areas of the body or the greater
part of its surface; at times they appear only in the neighborhood of
the buboes. They vary in size from a mere speck to spots several lines
in diameter. When very numerous they give a livid hue to the skin, and
that appearance to the cadaver to which, together with the high
mortality, was doubtless due the term black death by which severe
epidemics were known in the Middle Ages.
Vibices and extensive ecchymoses sometimes appear shortly before
death.
4. The stage of convalescence sets in between the sixth and tenth
days. It is often protracted by prolonged suppuration of the bubonic
enlargements. Both relapses and distinct second attacks have been
noted by recent as well as the older observers.
In addition to the foregoing sketch of the course of the disease in
its ordinary form it is necessary to describe certain other symptoms.
The attack has sometimes begun with a convulsive tremor, at other
times with a prolonged shaking, which has lasted from six hours to
three days, the patient remaining free from fever and not complaining
of cold. This condition has terminated in coma, followed speedily by
death.
Sometimes the attack has come upon the patient with great confusion of
mind, so that he appears dazed, or else a curious distraction has
befallen him in the midst of his ordinary avocations. If absent from
home, such patients commonly at once set out to return, either
trembling and staggering as though tipsy, or else rushing wildly
through the streets with frantic gestures and outcries.
The vomited matters are usually at first gastric mucus with bile,
afterward dark coffee-colored fluid; in certain cases blood is
vomited. Bleeding from the nose, lungs, bowels, vagina, and urethra
have also been observed. Cases attended by hemorrhages have in almost
all instances terminated fatally.
Constipation has been, as a rule, present during the acute stages;
later in the attack diarrhoea has occasionally occurred. It has been
looked upon as a favorable symptom.
The urine has been diminished and suppressed in grave cases.
Trustworthy observations, both as to its quantity and its chemical
composition, are wanting. It has been observed to contain blood.
As has been already pointed out, the Mahamari of North-western India
has been especially characterized by lung symptoms. Other regions also
have been visited by epidemics in which acute pulmonary lesions formed
a prominent part of the morbid complexus.
(_b_) The Fulminant Form.--Chiefly in the early days or weeks of
epidemics, but to some extent also later, cases occur in which the
intensity of the sickness is so great that the patient dies before its
usual manifestations have time to develop. The duration of the whole
attack, which ends fatally, is often not more than a few hours; its
symptoms, which differ but little if at all from those of similar
cases of other epidemic diseases--such, for example, as epidemic
cerebro-spinal fever in its fulminant {780} form--are of the most
aggravated character, and the patient perishes overwhelmed by the
infection as though struck by a thunderbolt. Profound disturbance of
the nervous centres, convulsions, coma, the rapid formation of vibices
and petechiae, collapse, are the speedy forerunners of the fatal
issue.
(_c_) The Larval or Abortive Form.--Toward the close of an epidemic
the character of the disease usually undergoes a change. It becomes
less malignant. The cases present the essential symptoms, but in
diminished intensity. Some cases terminate in an early defervescence
with rapid subsidence of beginning local manifestations; others
present merely the evidences of a slight disturbance of the general
health, without any characteristic symptoms of the prevalent disorder;
others, again, are characterized by the appearance of buboes without
pain or fever. These swellings undergo resolution in fourteen days or
thereabout. Exceptionally they suppurate.
The duration of the plague is from six to ten days in typical cases
running a favorable course; those of fatal cases from one to twenty
days. Clot Bey[8] found the duration of the worst cases two or three
days, of those next in point of severity five or six days, whilst in
milder cases death did not occur until the second or third week. Of
534 fatal cases noted by W. H. Colvill, 126 occurred one day after the
attack, 80 two days after it, 105 three days, 76 four days, 60 five
days, 26 six days after the attack. After six days the number of
deaths rapidly declined; on the nineteenth day 1 death, and on the
twentieth day after the attack 11 deaths, occurred. It is said that
death after the seventh day is commonly not in consequence of the
disease itself, but of sequels. Of 16 fatal cases in the village
Prischib in Astrakhan, noted in the report of Dr. Cabiadis, and of
whom the names, as well as the day of their exposure, their falling
sick, and their death are given, 1 died in one day, 4 in two days, 6
in three days, 3 in four days, and 2 in six days.
[Footnote 8: _De la Peste observee en Egypte_, Paris, 1840.]
The mortality of the plague is greater than that of any other epidemic
disease. In all epidemics a large majority of those who contract the
disease die. This is especially true of epidemics at their beginning,
when it has often happened that for a time all the cases have
perished. Of this, as of other epidemic diseases, it is true that the
death-rate has varied in different outbreaks and at different periods
of the same outbreak. Colvill states that in the epidemic of 1874 in
Mesopotamia the mortality of stricken villages during the first half
of the time was 93 to 95 per cent. of those attacked, but that
afterward the majority of those attacked recovered. The same authority
states that in Bagdad in 1876 the mortality was 55.7 per cent. of
persons attacked. Arnauld gives the mortality at Benghazi in 1874 as
39 per cent. of attacks. The death-rate at Vetlanka was 82 per cent.
of those attacked. In Toulon in 1721, of a population of about 26,000
human beings, about 20,000 were attacked, and of these 16,000 died. It
has been by no means of rare occurrence that nearly half the
population of towns have perished in an epidemic, or that small
villages have been completely depopulated by this scourge.
COMPLICATIONS AND SEQUELS.--The appalling mortality of the plague on
its approach, the rapidity of its spread, the popular commotion upon
its appearance, its brief course, and the fact that its recent
outbreaks have {781} taken place in regions where trained European
physicians have been, with a few exceptions, beyond reach, all unite
in maintaining the gloom that has since the Middle Ages enveloped the
clinical facts of this disease.
Of its clinical course, beyond the brief outline already given, little
is accurately known, of its complications still less. In some of the
recent epidemics, and particularly in the outbreaks of plague in
India, the evidences of pulmonary lesions have been so conspicuous
that they deserve to be classed among the essential manifestations of
the disease rather than as complications; in others pulmonary
congestion, haemoptysis, the evidences of croupous or catarrhal
pneumonia, have occurred in a small proportion of the cases. Aside
from this, there is nothing to be said as to the complications.
Among the known sequels are protracted ulceration of the enlarged
lymphatics, boils, superficial or deep abscesses, catarrhal pneumonia,
pertussis, mental troubles, and the like. Extensive and deep
cicatrices are not infrequently found in the site of the ulcerating
local manifestations.
MORBID ANATOMY.--The existing knowledge of the morbid anatomy of the
plague is but scanty. The observers of the early outbreaks contributed
nothing; the recent outbreaks have taken place under circumstances in
which anatomical investigations were impracticable. The knowledge
which we possess is almost wholly due to the investigations conducted
by the French in Egypt at the close of the last and the beginning of
the present century, and again during the years 1833 to 1838.
The descriptions of Bulant,[9] Clot Bey, and others point to gross
lesions, such as are found after death in the acute stages of the
infectious diseases in general. The viscera were engorged with dark
fluid blood; ecchymoses were often found in the mucous and the serous
membranes, in the substance of the different organs, and into the
connective tissue. The spleen was in almost all cases enlarged,
softened, and of a dark color. Not rarely the kidneys were deeply
engorged, and extravasations of blood into their substance, their
pelves, and into the surrounding connective tissues were often
encountered.
[Footnote 9: _De la peste oriental d'apres les maternaux recuilles a
Alexandrie, a Smyrne, etc., pendant les Annees 1833 a 1838_, Paris,
1839.]
The only constant and characteristic changes relate to the lymphatic
system. The lymphatic glands were, as a rule, enlarged and deeply
injected with blood. Where no buboes existed the glands of the various
cavities of the body showed evidences of acute inflammatory processes.
In some instances the affection of the glands appeared to be general;
less frequently it was most conspicuous in, or apparently limited to,
one or more great groups. Thus, the bronchial, the mediastinal, the
mesenteric, the lumbar, etc. were severally the seat of marked changes
with or without enlargement of superficial groups, or several of these
groups were at the same time implicated.
In no instance were symmetrical enlargements of the inguinal regions,
the axillae, or the throat met with.
According to Runnel,[10] in 2700 cases there were inguinal buboes in
1841, axillary in 569, maxillary in 231; inguinal buboes occurred 175
times on both sides, 729 times on the right only, 589 times on the
left only; the axillary buboes were double 9 times, right only 185,
left only {782} 163. Buboes of the neck only occurred 130 times, and
of them 67 cases were children.
[Footnote 10: _A Treatise on the Plague_, London, 1791.]
The connective tissue surrounding the affected glands was the seat of
an infiltration sometimes serous, sometimes cellular; it also very
commonly contained more or less extensive extravasations of blood.
Even where no buboes appeared on the surface of the body the glands
were enlarged to twice their usual size or more. The substance of the
glands in the larger swellings was at times uniformly red or violet,
again whitish or marbled or pulpy or denser, or of the consistence of
fat. It was also sometimes soft like jelly, and rarely it contained
minute collections of pus. Some observers speak of dilatation of the
lymph-vessels in the neighborhood of the enlarged glands.
DIAGNOSIS.--The difficulties attending the recognition of the plague
at the beginning of an outbreak speedily subside. The rapid spread of
the disease, its frightful mortality, the overwhelming intensity of
the symptoms, the prompt occurrence of cases characterized by buboes,
carbuncles, or petechiae, are collectively considered diagnostic of
this, and of no other disease whatever. In regions subject to the
repeated visitations of this pest there exists a universal
unwillingness to mention even the name of a disease whose suspected
presence alone is followed by consequences of the most serious nature
to the freedom of personal and commercial intercourse. To this
unwillingness, rather than to any real likeness between the plague and
other diseases with which it has been compared, are to be traced most
of the difficulties as to the differential diagnosis that have been
raised, especially in the regions bordering on the Mediterranean Sea.
It is not, therefore, necessary in this place to discuss the diagnosis
between the plague and malarial and other pernicious fevers, malignant
typhus, epidemic dysentery, lymphadenitis, syphilitic buboes,
parotitis, and so forth.
TREATMENT.--Preventive.--The efficient treatment consists in
prophylaxis. The history of this disease indicates with singular
clearness the measures which, properly carried out, are capable of
controlling the spread of the epidemic diseases. These measures
arrange themselves into two groups, of which the first has to do with
the removal of the conditions familiar to the development of the
disease, the predisposing influences; and the second with the
restriction of the disease to the locality in which it shows
itself--isolation, quarantine.
The conditions favorable to the development of the plague have already
been set forth under the heading Etiology. They relate to poverty and
ignorance, and their attendant evils, in communities. They are those
conditions which tend to disappear under the influences of
civilization, and in truth it may be said that at the present time the
plague occurs only in half-civilized countries.
Preventive medicine has achieved no other work comparing in magnitude
and importance with the extinction of the plague in Europe. This was,
to use the words of Hirsch, "a gradual process, and kept pace in great
measure with the development and perfection of the quarantine system
with reference to the Orient and the different countries of Europe."
This author continues: "I cannot, in fact, understand how any one
criticising the facts without prejudice, and having regard to the
{783} state of the plague in the East, can for a moment hesitate to
attribute the chief cause of the disappearance of the plague from
European soil to a well-regulated quarantine system." The European has
by no means lost his susceptibility to the disease. He is liable to
attack in the East. His protection at home lies in the restriction of
the exciting cause of the disease to its present haunts.
Any extended notice of quarantine and quarantine laws is beyond the
scope of this article. It may be said, however, that with reference to
the plague measures quite unnecessary under ordinary circumstances
assume the greatest importance when this disease makes its appearance
in countries bordering upon Europe, and that no amount of hardship to
individuals necessary to avert so great a calamity as a plague
epidemic could be looked upon as excessive. Indeed, we can with
difficulty realize the severity with which measures of isolation have
been carried into effect at times when the devastation produced by the
plague was still vividly remembered. Violation of the orders issued
during an epidemic has been punished with no less a penalty than
death. It is related that upon the appearance of the plague in the
little town of Noja in Lower Italy in 1815, troops were despatched
immediately to surround the place with a cordon. The town was
encircled by two deep ditches, and opposite the gates three ditches
were spanned by drawbridges, which served as a means for the
introduction of provisions, but no other communication was allowed.
Only letters were allowed to leave the city, and these were first
dipped in vinegar. Cannons were posted at the city gates. The ditches
were occupied by sentinels, who were ordered to shoot down any one who
approached and failed to stand still the moment he was hailed. A
plague patient who escaped while delirious and attempted to pass the
lines was, in fact, shot dead. Outside this cordon two others were
established. Those who disobeyed the orders were treated with the
greatest severity. An inhabitant of Noja, who had thrown a pack of
cards to the soldiers, together with the soldier who picked it up, was
tried by court-martial and shot.[11]
[Footnote 11: _Ueber die Pest zu Noja_, Nurnberg, 1818, quoted by
Liebermeister in _Ziemssen's Encyclopedia_, article "Plague."]
Lower Italy, possibly Europe also, owed its escape to the rigorous
measures carried out in this instance; nor can it be doubted that the
measures of isolation practised during the outbreak on the Volga
1878-79 restricted the disease to the district in which it appeared
and brought it to a speedy end. On this occasion three efficient
cordons were established to isolate the infected places. The first
cordon was put around every place where plague prevailed, to prevent
persons from entering or quitting that locality until forty-two days
had elapsed after the last attack of the malady there. The second
cordon was formed around the infected area, encircling all the
infected localities. Its circumference extended 800 kilometres, and
was guarded by pickets of soldiers stationed at intervals of five
kilometres. This cordon had four quarantine stations. The third and
outermost cordon was established round the whole province of
Astrakhan. It served to control the functions of the inner cordons,
inasmuch as all persons coming from within its area, who could not
prove that they had undergone quarantine at the stations of the middle
cordon, were stopped.
{784} The complete disinfection of all clothing and other articles
used in the service of the sick is to be included among measures of
prophylaxis. It is no uncommon thing to destroy by fire the houses in
which cases have occurred, along with their contents.
No efficient means of protection are known for those who during an
outbreak cannot escape from the infected neighborhood. It would be
without purpose other than to amuse the reader to reproduce the quaint
fancies of the older physicians in this matter, or to dwell upon the
amulets and incantations, the absurd costumes, the protective power of
tobacco, according to Diemerhoeck, or the disbelief in its virtues on
the part of Hodges, who preferred "canary, of the best sort, of which
he frequently drank while he attended the sick."
Clinical.--"The treatment of individual cases must in the present
state of knowledge be expectant and symptomatic. Notwithstanding our
acquaintance with the symptoms that characterize plague, we are
utterly ignorant of the treatment best suited to its cases"
(Cabiadis).
Physicians who have written from personal observation unite in
advising a treatment of the simplest kind. Ventilation, cleanliness, a
liquid diet, abundant cool drinks, are to be ordered. The initial
collapse and the evidences of failure of the circulation call for the
use of stimulants, and especially of alcohol. Cold or tepid sponging,
in accordance with the sensations of the patient, may be resorted to.
If there be high fever an energetic antipyretic treatment might be
carried out. Cold effusion is said to have been of use in many
instances.
Purging, bloodletting, mercurials, blistering, emetics, have proved
either positively injurious or altogether without effect upon the
course of the disease.
Of drugs, ammonium chloride, salicylic acid, carbolic acid, quinine,
have been administered without positive effect.
It is stated that the free inunction of oil from the very beginning of
the attack was affirmed to exert a favorable influence.[12]
[Footnote 12: See Griesinger, _Virchow's Handbuch der Speciellen
Pathologie und Therapie_, ii. 2, s. 316.]
In early times the buboes were often incised, or even excised, as soon
as they began to swell. More recently they have been treated with
leeches or inunctions of mercurial ointment. The treatment by
poultices and the evacuation of pus as soon as it can be detected is
at present regarded with greater favor. Carbuncles are likewise to be
treated in accordance with accepted surgical procedures.
{785}
LEPROSY.
BY JAMES C. WHITE, M.D.
DEFINITION.--Leprosy is a constitutional disease of chronic course and
fatal termination, characterized by peculiar changes in the tissues of
skin, mucous membrane, nerves, and most organs of the body.
SYNONYMS.--Elephantiasis of Greek writers; Lepra of Arabian authors;
Anssatz (Germany); Spedalskhed (Norway). The local names in use among
the numerous races in which it prevails are too numerous to be given
here.
HISTORY.--Although great confusion has existed among the most ancient
as well as later medical writers with regard to the definition of this
disease, it having been confounded with several other affections
(elephantiasis arabum, syphilis, psoriasis, morphoea, etc.), leprosy
has prevailed in certain parts of the world from the time of the
earliest records. The biblical accounts show that it existed among the
Jews in Egypt, although it was not accurately distinguished from other
diseases resembling it in some respects. It was recognized in Greece
before the Christian era, and in the early centuries after Christ it
had extended widely over Europe. In the seventh and eighth centuries
special leper-houses were founded in Italy, France, and Germany. The
disease reached its height in Europe in the twelfth and thirteenth
centuries, when 19,000 lazarettos are said to have been in existence.
Its spread was greatly increased by the constant intercourse kept up
between Europe and the East during the Crusades. In the fifteenth
century it began to diminish, and in the course of the seventeenth it
had almost wholly disappeared from the most civilized states. It has
lingered, however, in other parts, and exists to-day in France and
Spain and Portugal, in Norway and Sweden, and in Italy, Greece, and
Southern Russia. As in ancient times, it is widely spread along the
coasts of Africa and prevails largely throughout Asia. It is found in
many of the islands of the Indian and Pacific Oceans, in Japan, New
Zealand, Madeira, the West Indies, extensively in some of the states
of Central and South America and Mexico and the Hawaiian Islands.
It may be interesting to trace its history in the United States and
adjacent districts more minutely. It is not known just when leprosy
was introduced into North America. According to the Louisiana
historian, Gayarre, the Spaniards established leper hospitals in
several of their colonies on the Gulf of Mexico during the last
century. One existed in New Orleans as late as 1785. In 1776 the
disease was reported as existing among the blacks in Florida. It seems
to have died out, and with {786} it all remembrance of its former
existence amongst us, until within the last few years, when its
occurrence in the Southern States has again attracted attention. In
Louisiana the first case was discovered in 1866 in an old woman whose
father came from the south of France; she died in 1870. In 1871 it
appeared in one of her sons, in 1872 in two others, and in 1876 in a
nephew. A sixth case developed in a young woman who was in constant
attendance upon the first case. In addition to this group, other cases
have been observed in several parishes, amounting to twenty-one in
all, as collected by Salomon of New Orleans in 1878.[1] Two other
cases, brother and sister, in Louisiana are known to the writer, one
of whom has recently died under his care. In South Carolina the
disease is reported by J. F. M. Geddings[2] to have been observed in
sixteen cases since the year 1846; four were Jews, four negroes, and
eight whites. In none was any hereditary taint to be traced. No new
cases have developed since that report.[3]
[Footnote 1: _New Orleans Med. and Surg. Journal_, March, 1878.]
[Footnote 2: _Trans. Intern. Med. Congress_, Philadelphia, 1876.]
[Footnote 3: See article on "Contagiousness of Leprosy" by writer, in
_Amer. Journ. of Med. Sciences_, Oct., 1882.]
In Minnesota and other North-western States leprosy has been known to
exist for a considerable time among the Norwegian immigrants who have
settled in them in large numbers. Holmboe in 1863 and Prof. Boeck
later made visits to these colonies while in this country, and
published reports concerning them after their return.[4] The latter
found eighteen cases among his countrymen, most of which were leprous
before emigration; in others the disease developed after arrival in
America. It had not manifested itself in any person born in this
country. The character and progress of the affection seem to have been
little influenced by residence here. Since these observations other
cases have been collected by the committee on statistics of the
American Dermatological Association,[5] showing the continuance of the
disease in these States. In 1879 there were fifteen cases in
Minnesota. Its spread in this portion of our country is slow.
[Footnote 4: _British and For. Med.-Chir. Review_, Jan., 1870, and
_Nord. Medic. Ark._, Bd. iii.]
[Footnote 5: See _Transactions_.]
Since 1871, 52 cases of the disease have been inmates of the hospital
for lepers in San Francisco, California. Of these, all, with one
exception, were Chinese, and forty-five of them had been sent back to
China. It is presumed to have shown itself after arrival in this
country, as "unproductive labor would not be imported by the Six
Companies."[6] No case of the disease known to have been acquired in
this country has yet been reported upon the Pacific Coast. One case
has developed in San Francisco after residence in the Hawaiian
Islands.
[Footnote 6: _Trans. Am. Derm. Assoc._, 1881.]
In Oregon, too, the disease has appeared among the Chinese immigrants,
steps having been recently taken to re-ship five lepers from the
poor-farm at Portland to China.
Since 1815, possibly earlier, leprosy has prevailed among the poor
French settlements along the Miramichi River, near the Bay of
Chaleurs, New Brunswick. It was first noticed in a woman whose mother
came from Normandy, and has continued mainly in her descendants since.
No measures were taken to control the disease until 1844, when a
hospital was erected on Sheldrake Island. In 1849 the present
lazaretto at {787} Tracadie was established. During the first five
years (1844-49) there were admitted 32 patients; from 1849 to 1863, 67
additional patients were received; and from the latter date to 1879,
30 more, making a total number of 129 up to the last report. The
greatest number present at any one time was 37. In 1878 there were 16
patients in the lazaretto--6 men and 10 women. The total number of
deaths in the hospital has been, up to 1878, 123. A. C. Smith, who
resides near Tracadie, states that at the latter date but three cases
were known to exist outside the lazaretto. Residence is not
compulsory, and no sufficient measures are taken to remove patients
from their homes before they may have inoculated other members of the
family. The disease is more restricted in locality than formerly.
Within the last two years two or three small groups of the disease
have been discovered in the island of Cape Breton, which are described
in the _Canadian Journal of Med. Science_, Sept., 1881.
These are all the places north of Mexico where the disease exists in
an endemic form. A considerable number of cases have been reported
within the past few years from other parts of the United States, where
it has manifested itself in persons who have formerly resided in
leprous countries or in those who have wandered from the above
infected districts. A very few instances have been recorded in which
it has appeared in those who have never visited any infected locality
or have been in apparent contact with lepers. Such cases, if
authentic, establish the possibility of a sporadic origin of the
affection. The fact of so many foci already established, and the
penetration of a race so prone to the disease as the Chinese into all
parts of the country, give the study of leprosy in America a special
importance.
ETIOLOGY.--The study of the etiology of leprosy is intimately
connected with that of its history and geographical distribution. From
the earliest times it was regarded in all parts of the world as a
contagious affection, and efforts were made by the sternest laws of
Church and State to control its spread by segregation, by interdiction
of marriage, etc. No disease has ever been regarded with an equal
degree of abhorrence by mankind; none has received greater attention
from physicians of every age. Within the present century it has come
to be regarded, almost without exception, by the profession as
non-contagious. Peculiarities of climate, soil, and modes of life have
been looked upon as predisposing, exciting, or even essential
influences in its causation; but the widespread distribution of the
disease, with the consequent diversity of diet and customs of living,
its prevalence upon the coast and in interior regions, in high
altitudes as well as at the sea-level, in Iceland as in the tropics,
show that these conditions, however they may affect the course of the
affection, have no direct relation to its causation. The theory of
heredity, as the most plausible explanation, has received its
strongest support in the investigations of Boeck and Danielssen in
Norway, where the disease can be traced for several generations in
families. The same conclusions readily present themselves where the
disease is studied in restricted localities, as in Louisiana and New
Brunswick at the present time, where, as we have seen, it manifests
itself closely in families in different generations. But this is a
narrow point of view from which to study the etiology of leprosy. It
often fails to manifest itself in the descendants of lepers in {788}
such communities, and affects persons in whose families it has never
previously existed. Moreover, in countries where it does not prevail
it not infrequently attacks individuals who have at some time visited
regions where it was endemic, and in the latter places may develop in
immigrants from parts of the world where it has never existed.
The same class of facts which seem to demonstrate its hereditary
nature may be used in support of its infectious character. The proper
field for observation in this regard would be a virgin region where
its natural course could be studied independently of theories.
Fortunately for science, such an opportunity is afforded in the
history of the disease in the Hawaiian Islands. The exact date and
mode of its introduction there are not definitely known. The islands
have for years been the resort of the whaling-fleets manned by sailors
coming from leprous regions. The natives also shipped as sailors, and
after visiting such ports returned home. The absence of any restraint
in the intercourse of crews and native women is well known. Isolated
cases may have occurred as far back as 1830, but the disease made slow
headway until about 1860, when it increased so rapidly that the
government took stringent measures to control it, all cases discovered
being sent to the leper segregation upon an island from which there is
no escape. Since 1866, 2000 cases have been received there, and at
last report the asylum contained 750 inmates. This by no means
represents the extent of its prevalence in the islands, however. As
the native population by recent census was only 44,000, it will be
seen that the proportion affected is very large. This unwonted
rapidity of spread cannot be accounted for on the ground of heredity.
Transference from individual to individual by inoculation seems to be
the only possible explanation, and all resident physicians believe
that the disease is contagious in this sense. It affects almost
exclusively those of native descent, and their habits of life are such
as would greatly facilitate its wide dissemination in this way--viz.
their great licentiousness and absence of all fear of the disease,
which affords no bar to ordinary association or cohabitation; the
crowding of large families in small huts and sharing the same mats and
blankets; the eating of poi with the fingers from the same dish;
passing a common drinking-vessel or pipe from mouth to mouth, etc.[7]
Promiscuous and compulsory vaccination with impure virus, too, has
been generally practised during recent epidemics of small-pox. It is
evident that abundant opportunity has in many ways been presented for
the inoculation of pus or blood into the circulation from infected to
healthy persons. Where immunity from contraction has followed marriage
with a leper, it may be assumed that the conditions of an abraded
surface and the contact with pus or blood have not been fulfilled. The
wide spread of syphilis among the natives, and a consequent cachexia,
have no doubt contributed to these conditions and established a
national lack of resistance to the ravages of the disease. Nor can we
overlook the proclivity of all endemic diseases to extraordinary
manifestations of virulence in insular nations not previously
protected by gradual inoculation. Many reliable cases are cited by
resident physicians where the evidence of direct communication of the
disease seems to be reliable. Facts of the same nature may be
collected in the study of the history of {789} the disease in New
Brunswick and in Louisiana, where, as above stated, much better fields
for investigating this question exist than in the Old-World regions
where the affection has been rife for centuries.
[Footnote 7: Dr. G. W. Woods, U.S.N., in _Hygienic and Med. Reports_
of Navy Department, vol. iv., 1879.]
If we admit the fact of transference by inoculation in a single
instance, there is no reason why we should not regard this as the
principal if not the only means of extension of the disease, whether
we accept or not the theory of its parasitic nature. It is not
inconsistent with our knowledge of its laws and history to believe
that leprosy is an affection communicated with difficulty, and after a
prolonged period of incubation, from one person to another by contact
with certain products of the diseased tissue; that it has in past and
present time in this way spread from nation to nation; and that its
progress as an endemic affection has been checked only by laws based
upon this theory. All the negative facts so frequently urged against
this doctrine of contagion apply as strongly to that of heredity, and
may be interpreted in support of the former. The latest investigations
into its pathology afford tangible evidence in its favor. It may at
least be claimed that the question of contagion through inoculation
must be reopened.[8]
[Footnote 8: See article on the question of contagion in leprosy in
the _American Journal of Med. Sciences_, Oct., 1882, by the writer.]
Leprosy affects both sexes in about equal degree, and may first show
itself in early childhood. It is apt to produce sterility, so that
marriages between lepers are rarely fruitful. This result seems to
limit the extension of the disease under the law of heredity if we
admit its action. There can be no doubt that cohabitation may take
place for years without communication of the disease where one party
alone is leprous; and such immunity may be explained by the failure of
favorable conditions for sexual inoculation, just as in syphilis. The
disease would naturally be most dangerous in its ulcerative tubercular
form.
SYMPTOMATOLOGY.--There are two well-marked forms of leprosy--viz. the
tubercular and the anaesthetic--which are characterized by certain
easily recognized external manifestations, and which are accompanied
by symptoms indicative of disturbances of the general economy as well
as of special organs. These forms are not always sharply defined, and
often occur simultaneously or in succession in individual cases. Both
are generally preceded by premonitory symptoms, consisting of
unaccountable languor of mind and body, tingling sensations in the
skin, rise of temperature in the evening, and various disturbances of
digestion, or by the occasional outbreak of single or several blebs.
This prodromal stage affords no indication of the type of disease to
follow, and may last for days, months, or even years, with greater or
less intervals and intensity.
TUBERCULAR LEPROSY.--This form may declare itself at once by the
characteristic tubercles, but frequently an earlier manifestation is
the appearance of macules or dull red spots, varying in size from a
pea to two or three inches in diameter. They have an indistinct
margin, a glazed and smooth surface, and become paler on pressure. The
patches, although not at all or but slightly elevated above the
general surface, are firmer, and penetrate more or less deeply into
the cutaneous tissues. They may increase in size peripherally and
undergo involution in the older central portions simultaneously.
During the latter process the color changes from a more or less dull
red to a brown, yellow, or grayish tint, and {790} finally may become
quite white. The spots also become thinner or even slightly depressed.
Their seat is principally the trunk, but also the limbs, and less
frequently the face. This condition of the skin may precede any other
changes in its tissues for months or years, the patches appearing and
disappearing or remaining as permanent stains. At last well-defined
tubercular elevations show themselves, varying in size from a small
shot to a filbert, flattened or semi-globular in form, generally
smooth and firm to the touch, and of a dull red or brown color. They
occur upon any part of the surface, but are especially abundant upon
the face, where they may cause great deformity of the features. The
forehead and eyebrows may become very greatly thickened by general
infiltration, or thrown out into very prominent folds and
protuberances by the massing of individual tubercles. The lips
thicken, the nose broadens, and the ears stand out conspicuously with
their increased bulk. All these changes in form, with the great
darkening in tint which is often present, give at times a most
repulsive expression to the face. The tubercles are sometimes to be
felt imbedded in the skin, or considerable areas are found to be
uniformly thickened and scarcely at all prominent. All forms are
capable of involution after an existence of months, and may leave
dark-colored atrophic patches to mark their seat. They are rarely
painful, and occasionally slightly sensitive. They may be transformed
into ulcers, especially upon prominent positions, as the knuckles,
elbows, knees, as the result of pressure or injury, which are
extremely indolent, although shallow, and may heal and break down
repeatedly. Occasionally they give rise to serious
complications--inflammation of the lymph-vessels, suppuration of the
joints with loss of the attendant members, as the fingers and toes.
Tubercles appear also upon the mucous membrane of the nasal cavities,
the mouth, and larynx, often in great abundance, causing a very
characteristic hoarseness or loss of voice. With these changes in the
cutaneous tissues, which may be accompanied in their periods of
greatest activity by febrile disturbances, there are developed after
months or years, with gradual failure of strength, manifestations of
changes in the internal organs, the lungs, intestines, and brain,
which may prove fatal at any time, or the patient may die of slowly
progressive marasmus. The course of the tubercular form is on the
average between eight and ten years. At any period there may supervene
manifestations of the anaesthetic type, which makes the so-called
mixed variety, in which either form may predominate.
ANAESTHETIC LEPROSY.--This variety is characterized by the loss of
sensation in the skin over areas of varying extent, which occupy no
definite positions in relation to nerve-distribution. The anaesthetic
patches may appear upon the seat of old maculae or former tubercles or
of a preceding bullous efflorescence, or upon parts not previously
affected in any way. They may follow a reddened and hyperaesthetic
condition of the cutaneous tissues, or they may be surrounded by a
serpiginous border of this character. The degree of anaesthesia in the
affected parts is sometimes so complete that the skin and underlying
tissues may be deeply pricked or cut or burned without the patient
being aware of the injury. Such patches may possibly regain their
sensibility. Their surface appears in later stages dry, wrinkled,
shrunken, and of a brownish color, and atrophy, not only of the skin
but of the muscles, is gradually developed, {791} in consequence of
which the expression of the face undergoes a marked change. The
eyelids and lips droop, the hair falls, the hands contract, and the
joints of the fingers and toes are laid bare, so that the phalanges,
or even the whole hands and feet, drop off. Ulceration or gangrene of
the parts may develop, and whole extremities may shrivel up. With
these manifestations of local derangements of nerve-action the
functions of the brain fail, the patient becoming stupid and incapable
of action or motion, the temperature and pulse are lowered, and death
comes slowly by marasmus or the most various complications--tetanus,
disease of the lungs, pyaemia, etc. The average duration of this form
is from eighteen to twenty years.
PATHOLOGICAL ANATOMY.--The structural changes which take place in the
tissues of parts which are the seat of the appearances above described
have received the special study of many excellent observers[9] in
recent times, and are now well understood. A section through the
thickened skin or a tubercle shows the corium and underlying
connective tissue infiltrated with round cells, as in lupus and
syphilis; in other words, converted into "granulation tissue." This
change first takes place along the course of the cutaneous vessels and
glands, penetrating more deeply and forming a firmer cell new-growth
in proportion to duration, the cells being enclosed in a coarse
meshwork of fibrous tissue, and encroaching upon the various
structures of the skin, so as to produce atrophy and finally
destruction of all its characteristic tissues. This cell-infiltration
may of itself undergo later changes, as fatty degeneration and
softening (ulceration). The lymph-glands and corpuscles assume a
special fatty metamorphosis. An examination of the tubercles upon the
mucous membrane reveals the same small-celled new-growth. In the
nerve-tissues also marked structural changes are found, both in the
central and peripheral systems, in the anaesthetic form of the
disease. In many cases the posterior segments of the gray cornua and
the fibres of the commissure, as well as the nerves of the
extremities, have been found altered by inflammation, which will
account for the disordered sensibility and the subsequent disturbances
of nutrition, muscular atrophy, etc. The nerve-trunks are often to be
felt beneath the skin, thickened and sensitive on pressure. The
chronic cell-infiltration affects the fibrous structure of the outer
sheath, the neurilemma, and the septa between the nerve-bundles,
producing fatty metamorphosis and atrophy of the nerve-bundles.
Similar cell-infiltrations are found also in the connective tissue of
all the internal organs of the body, which lead to destructive
processes in their respective structures.
[Footnote 9: Boeck and Danielssen, _Traite de la Spedalskhed_, Paris,
1848; Virchow, _Die Krankhaften Geschwulste_; Kaposi in _Hebra's
Lehrbuch der Hautkrankheiten_; Monasterski, _Vierteljahressch. fur
Derm. u. Syph._, 1879, p. 203; Hansen, _Virchow's Archiv_, Band 79,
1880; Neisser, _Virchow's Archiv_, Band 84, 1881; Cornil et Souchard,
_Annales de Derm. et de Syph._, 1881, No. 4.]
Within the last two years repeated observations have been made which
confirm the statement published by Hansen in 1873, that a peculiar
bacterium occurs in leprous tissues, which, it is claimed, establishes
the parasitic nature of the affection. These examinations have been
carried on with leprous material derived from many parts of the world,
and the results have been uniform. Within the round cells which
characterize the cutaneous neoplasms, both in the distinct tubercles
and the diffused {792} infiltrations, small agglomerations of minute
rod- or staff-like bodies (bacilli) are found, arranged in parallel
rows or placed end to end. Their length is one-half or three-fourths
the diameter of a red blood-globule, and their breadth is one-fourth
their length. With them minute granular particles are seen in the
cells. They occur in greatest numbers in the cells of the upper layers
of the true skin, which are considerably swollen by their presence.
They never penetrate the epithelial layer, nor are they found in
epithelial cells in any position. When the protoplasm of the cell is
interfered with by the later tissue-changes of the disease, the
bacillus perishes. They are found not only in the leprous cells, but
also in those of the connective tissue running between the
agglomerated masses of the former. Between the leprous cells and the
filaments of connective tissue but few free bacilli are seen. The
neoplasms of the mucous membrane and of many organs of the body have
been found to contain them also. In the blood they have been detected
by some observers. Their presence in the nerve-tissues is of
importance as throwing light upon the question of the specific or
inflammatory nature of the morbid processes above described as
affecting them. If we regard the bacteria as pathognomonic of leprous
tissue-changes, their occurrence, recognized in the cells penetrating
between the fibres of the peripheral nerves, would seem to make all
primary structural changes identical, and the anaesthetic as much as
the tubercular form the direct result of their presence. Neisser draws
the following conclusions from his investigations: "Leprosy is a real
bacterial disease, caused by a special kind of bacterium. The bacilli
appear in the tissues as such, or more probably as spores, and remain
for a longer or shorter time in a state of incubation, according to
circumstances, in depots, perhaps in the lymph-glands. This period,
much longer than in other infective diseases, is in proportion to the
physiological resistance of the human organism compared with the
feeble developing power of the bacilli. It, as well as the course of
the disease, is more rapid in tropical countries than in Europe. From
these depots the disease extends throughout the body in those portions
of the skin most exposed, the face, hands, elbows, knees, and into the
peripheral nerves. The other organs are less freely invaded. The
bacilli excite inflammation, and by a specific action transform the
migrating cell into the leprous cell. Leprosy is probably an
infectious disease, and its specific products are contagious--viz. the
leprous cells of the tubercles, the tissue-fluids, and the pus
containing bacilli or viable spores. On the other hand, the pus may
not always be infectious, as the fluid contained in the bullae is
not."
It must be said that the bacterial nature of leprosy, if established
in accordance with the above observations, furnishes a satisfactory
basis of explanation of all facts, historical, clinical, and
pathological, which have so long been awaiting solution. The inability
of the parasite to penetrate the epithelial layer of the skin and
mucous membrane explains why contagion is so difficult, and why the
ulcerative tubercular form would be more favorable to such
transference than the anaesthetic variety.
DIAGNOSIS.--Leprosy in some of its early appearances may be readily
confounded with vitiligo, morphoea, pemphigus, lupus, and syphilis. In
some cases its prodromal manifestations cannot be positively
diagnosticated until other symptoms have developed, which by
concurrence establish their true significance. Such are the
pemphigus-like bullae, the {793} pigment-changes, and the smaller
tubercular efflorescences. In regions where the disease occurs only by
importation, and in the so-called sporadic cases, it is not at all
strange that it should fail of recognition, even in well-advanced
forms, unless the observer is acquainted with its whole
symptomatology. On the other hand, there is no disease which presents
more strikingly characteristic features in its advanced stages.
PROGNOSIS.--Leprosy is almost uniformly a fatal affection, and its
course toward this termination varies but slightly under the most
diverse conditions of life. Its development and progress are naturally
more rapid under circumstances of least individual resistance, where
food is poor and scanty, where extremes of climate are most felt,
where the constitution of the individual or nation is debilitated by
previous disease, as that of the Hawaiians by syphilis, or where no
proper professional care is employed. It has been believed that a
change of residence from infected to non-leprous regions would retard
its advance or avert its appearance in those supposed to be
hereditarily disposed; but the former effect follows probably only so
far as the general condition of the patient is affected by the change,
as in other constitutional disorders, and the latter is necessarily a
matter wholly of conjecture. No case of leprosy in the Norwegian
colony in our North-western States has ceased to progress after
arrival toward its fatal ending, even if this has been somewhat
delayed in individual cases under more generous ways of living. If it
could be known that a child born in Norway had escaped leprosy by
removal to America, we should not, if we accept the bacterial origin
of the disease, consider that climate or other mysterious influences
had overcome its inherited tendencies, but that it had been taken away
from the chance of direct inoculation. It is stated that very rarely
cases cease to progress beyond certain stages even in countries where
the disease is endemic. The course, as has been stated, varies
according to the clinical form, the duration of the tubercular variety
being on an average but one-half that of the purely anaesthetic type.
Leprosy may be called the slow disease, its period of incubation, so
far as this can be determined, extending from one to several years,
its prodromal stage lasting often several more years, and its
well-developed forms requiring at times more than twenty years to
destroy the patient. Cases sometimes prove fatal, however, in a single
year.
TREATMENT.--In a disease which affects so many of the races and such
great numbers of mankind, which has been for centuries the object of
special attention on the part of physicians, and of late years of
government commissions and of eminent pathologists, it is evident that
every remedy which the materia medica includes, as well as those of
merely popular reputation in the widely-diverse geographical regions
in which it prevails, must have been employed in its treatment. None
of them exert any specific action upon it; it remains incurable. Every
year some new article is employed with the usual claims of success
which accompany the introduction of new remedies, but they merely
swell the long list of failures in the therapeutics of the affection.
Still, leprosy is influenced somewhat by medical care; life may be
prolonged and made more comfortable. To this end we may employ
remedies which are capable of improving and maintaining the
constitutional powers of resistance to the disease, such as are found
of service in other chronic wasting affections. {794} The patient is
to be put in as healthy ways of living as possible, removed from
debilitating localities, and given generous diet and tonics, as iron
and quinia. Several new drugs which seem to stimulate the nutrition
and produce temporary improvement in the local and general symptoms
have lately been widely employed, as Gurjun balsam and chaulmoogra
oil, but they have wrought no cure. Digestion is to be aided,
diarrhoea to be checked, and disturbances of respiration to be
alleviated. Local treatment is also of service. The tubercles may
sometimes be made to disappear--partly, at least--by stimulating
applications, and ulcers made to heal by cauterization and other
well-known methods of dressing. These ulcers and their secretions
should be regarded as possible sources of infection by attendants and
members of the patient's household. For the anaesthetic alterations in
the tissues but little can be done locally. If the bacterial origin
and causation of the disease be eventually established, its future
extinction must be based upon studies directed to the nature and mode
of protection against this organism. Collectively, the disease should
be treated by every nation by thorough segregation, and importation
should be prevented by the most rigid quarantine laws.
{795}
EPIDEMIC CEREBRO-SPINAL MENINGITIS.
BY ALFRED STILLE, M.D., LL.D.
DEFINITION.--A febrile, and often malignant, but non-contagious
disease of unknown origin; usually occurring as a local epidemic;
confined hitherto to the North American and European continents, and
to the vicinity of the latter; characterized by its rapid and
irregular course, and usually by a tetanic rigidity or retraction of
the neck, a tendency to disorganization of the blood, and the
formation of inflammatory exudates beneath the membranes of the brain
and spinal cord.
SYNONYMS.--Spotted fever; petechial fever; malignant purpuric fever;
malignant purpura; pestilential purpura; black death; typhus
petechialis; typhus syncopalis; febris nigra; febbre
soporoso-convulsivo; tifo apoplettico tetanico; fievre
cerebro-spinale; typhus cerebro-spinale; phrenitis typhodes; epidemic
meningitis; epidemic cerebro-spinal meningitis; malignant meningitis;
typhoid meningitis; meningite cerebro-spinale epidemique; meningite
cerebro-rachidienne; Genickkrampf; Genickstarre.
The names which have been given to this disease convey more or less
distinctly one or the other of two ideas: 1st, that the disease is
essentially a blood-disorder; and 2d, that it is an inflammation of
the cerebro-spinal meninges. Under the first head belong the following
names: Malignant purpuric fever; malignant purpura; pestilential
purpura; petechial fever; spotted fever; febris nigra; black death,
etc. Under the second head belong epidemic cerebro-spinal meningitis;
epidemic meningitis; malignant meningitis; typhoid meningitis, etc. As
partaking of the qualities of both categories may be cited the names
cerebro-spinal fever and fever with cerebro-spinal meningitis. In
regard to all those of the first class it is sufficient to repeat the
criticism made by the early American writers who described this
disease after having largely studied it. One only of them need be
cited, because he expresses the opinion of all. Miner, writing in
1822, said: "It is quite unfortunate that a single symptom
(petechiae), and one, too, that is wanting in a great majority of
cases, should have been seized upon to give it the odious and
deceptive name of spotted fever, as that name has been applied by
European writers to a very different kind of fever." Among the names
given to the disease, cerebro-spinal fever is perhaps the least
suitable and the least in harmony with the principles of scientific
nomenclature. It is one of those terms which may be pardoned when used
by the laity, but which educated physicians ought not tolerate.
Parallel examples may be found in such compounds as brain-fever,
lung-fever, gastric-fever, and, most unfortunate of all, enteric
fever. The first three of these are {796} inflammations, pure and
simple, of the brain, lung, and stomach; and, after their example,
cerebro-spinal meningitis would be, what it is not, merely an
inflammation of the membranes of the brain and spinal marrow. The name
of the remaining disease has only to be turned into English and called
intestinal fever to demonstrate its defects. It is evident that other
diseases--and dysentery in particular--are equally entitled to be
called enteric fever. Moreover, there are cases of enteric fever in
which death takes place so early that the intestinal lesion is
undeveloped, and the fatal issue must be attributed to the
fever-poison in the blood or else to the changes it has wrought in
that fluid. Analogous illustrations abound in the history of the
eruptive fevers. The disease we are studying presents another
affection in which the septic element sometimes so far overrides the
inflammatory as to destroy life before the latter has developed
characteristic tissue-changes. There may be no valid objection against
classing it among the fevers, but there can be no excuse for
denominating it cerebro-spinal fever. The very reasons that militate
against its being regarded as a meningitis forbid its being considered
as a meningeal fever. But if it is a meningitis, inchoate or complete,
then the prefix epidemic denotes its constitutional nature and its
probable blood origin, and a term is employed which is descriptive and
accurate, and not misleading. Moreover, the term epidemic indicates,
or at least implies, the characteristic type of the disease, which is
asthenic and sometimes more or less typhoidal, just as other
inflammatory diseases become so in their epidemic form--_e.g._
pneumonia, bronchitis (influenza), dysentery, etc.
There ought to be no doubt whether epidemic meningitis should be
classed with general diseases or with inflammations. It is excluded
from the latter class by the total absence of any tangible external
cause from its causation, as well as by its frequent fatal termination
before the characteristic signs of inflammation have had time to form,
or because the peculiar type of the disease prevents their
development. It belongs to the former class because it is epidemic in
the largest sense, its outbreaks occurring simultaneously in remote
parts of the earth and independently of all cognizable celestial or
terrestrial influences. In this as in other elements of its pathology
the disease stands absolutely alone. While the acute affections of the
pulmonary and digestive organs, which were just now alluded to, affect
large districts, and even sweep over a whole continent, epidemic
meningitis breaks out in limited localities, and may for years prevail
in a populous city within a hundred miles of another still more
populous which during that time may altogether escape its ravages. Of
this curious fact the cities of Philadelphia and New York present a
striking illustration. Since, then, we are ignorant of the
circumstances under which the disease arises, and since, as will more
distinctly appear later on, its several forms really include quite
various morbid conditions, we are compelled to consider it as
occupying a peculiar and exceptional nosological position.
HISTORY.--Previous to the present century the existence of this
disease can hardly be demonstrated. And yet Dr. B. W. Richardson
believed that some faint traces of it could be discovered, as in the
following statement:[1] "The great plague which visited Constantinople
in 543, and which Procopius and Enagrius described, the plague of
{797} hallucination, drowsiness, slumbering, distraction, and ardent
fever, with eruption on the skin of black pimples the size of a
lentil,--this plague, which usually killed in five days, and left many
who recovered with withered limbs, wasted tongues, stammering speech
or such utterance of sound that their words could not be
distinguished,--this plague, which had passed into mythical learning
under the name of cerebro-spinal meningitis, has also in our time
reappeared." The concluding statement in regard to the name of the
plague is quite erroneous, and there is nothing in the description
which distinctively applies to the disease we are examining. On the
other hand, we know that Procopius wrote a history of the Oriental
plague, which invaded Europe for the first time at the very date above
given. It had as a distinctive symptom the well-known inguinal bubo,
and there is no mention whatever, in the descriptions of it that have
survived, of the tetanoid symptoms belonging to epidemic meningitis.
In 1802 an epidemic occurred at Roetlingen in Franconia which had a
certain resemblance to the subject of this article, for it was
characterized by lacerating pains in the back of the neck. According
to Hecker, this was the sweating sickness which had ravaged various
parts of Europe during the Middle Ages, and of which limited outbreaks
still recur. In 1880 such a one took place at l'Ile d'Oleron in
France, and many of the patients were affected with tonic or clonic
spasms, both general and local, but not, apparently, opisthotonic.[2]
[Footnote 1: _Diseases of Modern Life_, p. 16.]
[Footnote 2: Pineau, _Archives gen. de med._, tom. i., 1882, pp. 25,
169.]
If epidemic meningitis occurred before the nineteenth century, it must
have been confounded with other affections, but when we consider its
characteristic symptoms such an error seems improbable. The
comparatively rare resort at that time to post-mortem examinations,
particularly of the cranial and spinal cavities, may in part account
for such a confusion of ideas; and even when dissections were made,
the skill to interpret the discovered lesions was possessed by few. It
has been thought that in the latter part of the last century some
cases of this disease were seen and described, although their
nosological value was unrecognized. Thus, Stoll[3] speaks of a young
soldier who was seized with a pain in the back of the head and neck,
and who was affected with opisthotonos before he died. On examination
pus was found between the arachnoid and the pia mater. The first clear
and unquestionable description of epidemic meningitis was published in
1805, first by Vieusseux and directly afterward by Mathey.[4] The
disease appeared at Geneva in the spring of the year, in a family
composed of a woman and three children, of whom two of the latter died
within twenty-four hours. A fortnight later four children in a
neighboring family died of it after fourteen or fifteen hours'
illness, and a young man in an adjoining house, being attacked, died
the same night, with his whole body of a violet color. The disease
ceased during the spring, after having destroyed thirty-three lives.
Its distinctive features were an abrupt attack during the night,
bilious vomiting, excruciating headache, rigidity of the spine,
difficult deglutition, convulsions, nocturnal paroxysms, petechiae,
and death in from twelve hours to five days. Vieusseux calls it "a
malignant non-contagious fever," and Mathey gives as the lesions
revealed by dissection a gelatinous {798} exudation covering the
convex surface of the brain, and a yellow puriform matter upon its
posterior aspect, upon the optic commissure, the inferior surface of
the cerebellum, and the medulla oblongata.
[Footnote 3: Quoted by Boudin, _Hist. du typhus cerebro-spinal_, p.
5.]
[Footnote 4: _Journ. de Med., Chirurg. et Pharm., etc._, an. xiv.,
tom. xi, pp. 163, 243.]
After its first appearance at Geneva the disease does not seem to have
extended in any direction from that place as a centre, but we next
hear of it at two points remote from it and from one another--Germany
and the United States. From the former it extended to the conterminous
countries, Bavaria, Holland, and the east of France, where, however,
it prevailed neither extensively nor fatally, and soon died out; while
in America it first appeared at Medfield, Mass., in 1806. The European
epidemic was faintly felt in England the following year, and between
that time and 1816 it prevailed at several places in the east of
France, and slightly at Paris, while during the corresponding period
it had extended through New England into Canada, New York,
Pennsylvania, and several Western and South-western States. It is a
noteworthy fact that on both sides of the Atlantic it ceased in the
same year (1816). During the six following years we can discover no
trace of its existence, but in 1822-23 it reappeared at Vesoul in
France, and at Middletown, Connecticut, and does not seem to have
extended beyond those places. Again, after an interval of five years,
in 1828 it was heard of in Trumbull co., Ohio, two years later at
Sunderland in England, and three years afterward (in 1833) at Naples.
After four years of quiescence the disease entered upon a wider and
more destructive career than ever before, which was almost
uninterrupted from 1837 to 1850. During the first two years of its
recurrence in Europe it was confined almost wholly to France. It began
in the southern departments, with Bayonne as a centre, and extended
gradually westward and northward, in some places attacking only
military garrisons and in others only civilians. Elsewhere the
predilection was reversed, or, again, civilians and soldiers were
equally affected. As Boudin has pointed out, "it located itself in
certain districts; in garrison-towns it seemed to affect certain
barracks only, and in them only certain rooms. In one place it broke
out in a prison and spared the soldiers; in another its victims were
among the soldiers and the citizens, while the prisoners were
untouched." Thus the disease spread over the whole of France, and was
more fatal almost everywhere else than in Paris itself. Almost at the
gates of the capital, at Versailles, and among the garrison, it was
very destructive in 1839, causing a mortality among those attacked of
from 50 to 75 per cent. About the same time it occasioned a great
mortality at other military posts, especially at Rochefort and Metz,
and in 1840-41 at Strasbourg. In 1843 the disease had almost ceased to
prevail in France, but in 1846 it reappeared at Lyons, and in the
following years, and until 1849, affected the garrisons of Orleans,
Cambrai, Saint-Etienne, Metz again, Luneville, Dijon, Bourges, and
Toulon. In some of these places the military experienced five, and
even seven, successive epidemics. Meanwhile, the disease spread to
Algeria (1839-47), and to Italy in the former year--not, however, on
the confines of France, but at Naples and in the Romagna, whence it
extended to Sicily and Gibraltar, and did not cease there until 1845.
In 1839 it first showed itself in Denmark, and remained for about
three years, while in 1846 it "appeared in the {799} majority of the
workhouses of Ireland," and in the spring of the same year it occurred
in England, at Liverpool and Rochester.
While the disease was thus spreading throughout Europe, it again, in
1842, appeared in the United States, but at places as remote as
possible from Transatlantic communication and hundreds of miles
distant from one another--_e.g._ in Louisville, Kentucky, in
Rutherford co., Tennessee, and in Montgomery, Alabama. In the
following year it prevailed in Arkansas, Mississippi, and Illinois. In
1848 it occurred again at Montgomery, Ala., and simultaneously, in
Beaver co., Pa.; in 1849 it existed in Massachusetts and in Cayuga
co., N.Y., and in 1850 at New Orleans.
Between 1850 and 1854 epidemic meningitis ceased to be heard of, but
in the spring of the latter year it began to appear in the southern
provinces of Sweden, whence it rapidly spread over the greater part of
the kingdom, reaching an extreme degree of fatality in 1858, and not
finally disappearing until 1861. It is said to have caused more than
four thousand deaths. It was not until the height of the Swedish
epidemic in 1858 that it invaded Norway, where it seems to have been
even more malignant and extensive. Between 1850 and 1860 local
outbreaks of the disease took place in Ireland, and isolated cases
were observed in various parts of England, but in that country it has
never prevailed as a general epidemic. This fact alone is sufficient
to defeat all the attempts that have been made to trace the origin of
the disease to any of the conditions associated with a crowded
population. In Scotland, where such conditions exist in their greatest
intensity and fulness of development, it has never occurred as an
epidemic. During the decade under consideration (in 1856 and 1857)
epidemic meningitis again appeared in the United States, and, as
before, at points very remote from one another. In the former year it
occurred for the first time in North Carolina, and in the latter year
in the central portions of New York and Massachusetts.
Hardly had the disease subsided in the Scandinavian peninsula and in
the United Kingdom when it reappeared in Holland during the winter of
1860-61. In the following year and at the same season it occupied a
large extent of Portuguese territory, including the cities of Oporto
and Lisbon, and now for the first time it spread over Germany.
Beginning slightly during the summer of 1863 in Prussia, it acquired
new vigor during the succeeding winter, and in the two following years
it devastated almost every part of Northern Germany, and in 1864-65
extended throughout Bavaria except in its southern and western
provinces. Strange to relate, the disease appears to have passed
almost wholly by Austria proper, and to have prevailed, although not
extensively nor fatally, in Hungary, and in the latter part of the
decade in Istria, Greece, Turkey, and Asia Minor.
The American counterpart of this epidemic first appeared in Livingston
co., Missouri, in the winter of 1861-62, and during the same season it
invaded Indiana and Kentucky in the West and Connecticut in the East.
From about the same date, and until 1864, it prevailed in Ohio, and
during the last-named year in Illinois. Cases occurred at Newport,
Rhode Island, in 1863, and in Vermont in 1864. In the winter and
spring of the latter year it broke out at Carbondale, Pa., and in a
population of 6000 caused the death of 400, principally among children
and {800} very young persons.[5] In the winters of 1863-64 and of
1864-65 it prevailed in the U.S. army, and in the early part of this
period in the Confederate army which at the time was stationed near
Fredericksburg, Va. In North Carolina also, from 1862 to 1864, the
disease assumed a very malignant type, and affected citizens and
soldiers equally, and the latter in the Union and Confederate armies
alike. During the winter of 1864-65 a limited but very fatal epidemic
of the disease prevailed at Little Rock, Arkansas. About the same time
it existed as an epidemic in Maryland, Alabama, and other Southern
States, and throughout the Civil War affected both whites and negroes,
but showed, as in France, an exceptional gravity among the military.
[Footnote 5: Burr, _Trans. Med. Soc. State of N. York_, 1865, p. 40.]
The first appearance of the disease in Philadelphia took place in
1863, and from that date until the present (1884) it has never failed
to appear among the causes of death in the reports of the Health
Office. A table compiled by Dr. C. F. Clark, and printed in a paper on
the subject by Dr. James C. Wilson,[6] exhibits the difficulties of
obtaining accurate statistics, even from official reports, on this
subject. The medical profession of the city, having had but little
knowledge of the disease either by reading or observation, reported
deaths from it which occurred in their practice under various
denominations. At first it was spotted fever, which continued to be
used by many for a year or two, when it was superseded almost entirely
by cerebro-spinal meningitis. There can be no doubt that both of these
terms were used to designate the same disease, and therefore no error
will be committed in merging the deaths charged to each of them, and
in estimating by their annual totals at least the relative mortality
of the disease in the successive years of the period. But in the
Health Office reports there are at least three other rubrics that
suggest doubt. One is typhus fever, which seems to have presented a
sudden and remarkable increase of mortality during the first years,
and the most fatal, of the existence of cerebro-spinal meningitis. It
should also be observed that typhus fever is applied by many German
physicians in this country, as in their native land, to typhoid fever.
A second is malignant fever, and a third is congestive fever, neither
of which has claimed many victims in the health reports of
Philadelphia except while meningitis was epidemic. It seems probable,
therefore, that nearly all of the deaths charged under these heads
belong to the disease under consideration.
[Footnote 6: _Phila. Med. Times_, xiii. 88.]
_Deaths in Philadelphia from Cerebro-Spinal Meningitis from 1863-82._
| Brought over 1136
1863 49 | 1873 246
1864 384 | 1874 82
1865 192 | 1875 83
1866 92 | 1876 85
1867 109 | 1877 56
1868 55 | 1878 90
1869 37 | 1879 62
1870 36 | 1880 78
1871 49 | 1881 90
1872 133 | 1882 41 to Sept. 23d.
---- ----
1136 Total 2049
If to these deaths are added those charged to malignant fever, 111,
and to {801} congestive fever, 279, we obtain a total of 2439 deaths,
nearly all of which may be set to the account of epidemic meningitis.
It may also be remarked that up to the date at which this computation
was made (May, 1883) hardly a week passed in which the Health Office
did not register several deaths from this cause. Hence it would appear
that the disease continues to linger in this locality longer than has
been reported of any other place from which information has been
obtained.
In the city of New York it appears to have been much more limited both
in extent and duration. The first recorded death from it was in 1861;
in 1866 the deaths were 18; in 1867 the deaths were 32; in 1868 they
were 34; in 1869, 42; in 1870, 32; in 1871, 48. In 1872 the disease
became epidemic, and "from January 6 to May 31, inclusive, 632 cases
were reported to the City Sanitary Inspector, and 469 deaths to the
Bureau of Records of Vital Statistics" (Clymer). After this period the
disease seems to have declined very rapidly, and not to have
reappeared, since no notice is taken of its recurrence by the medical
journals of New York.
It was mentioned above that about 1870 some traces of the disease were
observed in Asia Minor, and in 1872 several cases are said to have
occurred at Jerusalem,[7] but beyond that time and place it does not
appear to have extended as an epidemic. In 1879, Cheevers said: "I am
not aware of the existence of any report of an outbreak of the disease
in India." He refers, however, to several cases occurring in Calcutta
as possibly representing this affection.[8]
[Footnote 7: _Berlin klin. Wochensch._, May, 1872.]
[Footnote 8: _Times and Gazette_, Aug., 1879, p. 121.]
In 1867-68 sporadic cases occurred at Little Rock, Ark., and in the
former year in Madison co., N.Y., thirty-three cases were reported.[9]
In Chicago, between February and April, 1872, Dr. Davis reported forty
cases observed in his own practice in seventy-two days. In the same
year the disease occurred at Elizabethtown, Ky.,[10] and at
Louisville, Ky., in December of the same year. It existed in Michigan
between 1868 and 1874, but only in the latter year epidemically, and
not to a very great extent.
[Footnote 9: _Trans. Med. Soc. State of N.Y._, 1868, p. 251.]
[Footnote 10: _Richmond and Louisville Journ._, Nov., 1872, p. 555.]
Of later occurrences of the disease the following may be mentioned:
Several cases were reported in London in 1867, 1871, 1876, and
1878.[11] In 1870 four cases were observed in Providence, R.I.[12] In
1882 cases were met with in Boston, New York, Philadelphia, Pittsburg,
Western Ohio, Indianapolis, Detroit, Louisville, Memphis, New Orleans,
Richmond, Milwaukee, St. Louis, Salt Lake City, San Francisco, etc.,
but in none of these places did the disease become epidemic.
[Footnote 11: _Times and Gazette_, July, 1867, pp. 58, 59; Nov., 1867,
p. 511; _Guy's Hospital Rep._, 3d Ser., xvii. 440; _St. Bart's
Reports_, xii. 267; _Times and Gaz._, Aug., 1878, p. 167.]
[Footnote 12: _Boston M. and S. Jour._, Oct., 1870, p. 261.]
ETIOLOGY.--Epidemic meningitis has occurred in Europe and America in
every portion of the temperate zone, but its greatest prevalence and
mortality have undoubtedly been in the northern rather than in the
southern portions of that region. One of its most interesting features
consists in its appearing simultaneously at points very remote from
one another and having no connection with each other save through the
atmosphere. Of this statement several illustrations have already been
presented. Another {802} peculiarity of the disease consists in its
occurring with hardly any relation to external natural conditions or
to those of its victims. It affects localities as diverse as possible
in their geological, meteorological, and sanitary states, the rich and
the poor, the old and the young, and both sexes, and (as it is
certainly not in a strict sense contagious) its rise and spread must
necessarily be attributed to some occult cause pervading the
atmosphere.
It is evident that the prevalence of the disease has some relation to
meteorological agencies, for not only is it greater, on the whole, in
_cold_ than in warm climates, but it is also greater in cold than in
warm seasons. Thus, if we examine the epidemics in Europe and America
we shall find that they almost invariably were most severe in the
winter and spring. Yet the rule presents several exceptions on both
continents. In France, out of 216 local epidemics, more than
one-fourth took place during the warm months of the year, and in
Sweden the proportion was about the same. It is evident, therefore,
that cold is not an essential cause of the disease. Among the problems
that remain unsolved in regard to this disease none is more obscure
than the apparent immunity of Russia from its ravages, although the
climate seems adapted to favor it, and the domestic habits of no
people are fitter to intensify it if individual conditions entered
into the etiology of the disease; but, in truth, no such causes are
related to epidemic meningitis. Localities of every sort, high and
low, dry and moist, those saturated with marsh miasmata and those
fanned by pure mountain-breezes, have been alike visited by this
disease. It has passed by large cities reeking with all the
corruptions of a soil saturated with ordure and populations begrimed
with filth, as Vienna, Berlin, Paris, London, and New York, to
devastate clean and salubrious villages and the families of
substantial farmers inhabiting isolated spots.
By far the greatest number of the subjects of epidemic meningitis are
young persons. In Sweden, according to Hirsch, of 1267 fatal cases of
the disease, 889 occurred in persons under fifteen years of age, 328
between sixteen and forty years, and 50 in persons of forty years and
upward. In 1866, in the Kronach district (Germany), of 115 cases, 75
occurred under the seventh year, 22 between the seventh and twelfth
years, and 10 between the thirteenth and twentieth years (Schweitzer).
During 1865 a local outbreak of the disease in Bavaria affected 53
persons, of whom 22 were children under ten years of age, 18 between
ten and twenty years, and 11 between twenty and thirty years. Under
the fifth year few were attacked (Orth). Dr. J. L. Smith[13] found
that, according to the reports of the Board of Health of the city of
New York, out of 975 cases, 771 occurred in persons under fifteen
years of age, the greatest number for any quiquennial period being 336
in children under five years. Of the 469 deaths occurring in this
epidemic, 216 were of children under five years of age, and the next
largest number for an equal period was 99, which represented the
deaths between the ages of five and ten years. Of adults or persons
beyond the age of twenty, the whole number was but 39. The peculiar
liability to the disease of the young recruits in the French army has
already been alluded to. The proportion of male victims to this
affection is rather larger than that of females in the civil
population, but in France especially the excess was greatly on the
side of males, owing to the prevalence of the disease in the army. In
other places, as {803} in Sweden and Germany, the number of deaths
among females equalled, or even exceeded, that of males, and in
Leipsic the garrison remained exempt while the disease prevailed among
the citizens. In 1847 a fatal epidemic of it affected the second
regiment of the Mississippi Rifles, and was entirely confined to that
corps (Love). During the Civil War of the United States the disease
affected particular corps or regiments in the South or in the North,
yet it never became epidemic in the army, even when the disease
prevailed among the adjacent civil population.
[Footnote 13: _Amer. Jour. of Med. Sci._, Oct., 1873, p. 320.]
Various depressing or debilitating causes, such as lowness of spirits,
home-sickness, mental or bodily strain, over-eating, drinking alcohol,
the action of excessive cold or heat, checking perspiration, etc.,
have been enumerated as causes of this disease. It is unnecessary to
dwell upon such gratuitous assumptions. All of these influences are
constant, but epidemic meningitis is the rarest of epidemic diseases,
and the agencies referred to have no further operation than to lessen
the resistance of the body to morbid influences of every description.
If there be one peculiarity about this disease which is more
surprising and inexplicable than another, it is that its peculiar
victims are not the feeble and delicate, but the vigorous and
active--not the old and decaying, but the young and stalwart.
No one of authority has claimed that this disease can be propagated by
_contagion_. All of its early American historians are of the same
opinion upon this question, and nearly all European authorities are in
perfect accord with them. The apparent exceptions to this all but
universal judgment are so insignificant in number and weight as not in
the least to diminish its validity. A case has been published in which
a pregnant woman at full term died of the disease after giving birth
to an apparently healthy child. "Two hours later the infant presented
symptoms of meningitis, followed rapidly by death."[14] Supposing the
concluding statement to be accurate, the case only shows that the
cause of the disease which destroyed the mother's life infected the
system of the child also. If there is one point in the history of the
disease established by the concurring testimony of American and
European writers, it is the extreme rarity of its attacking either the
physicians and nurses in attendance upon patients affected with it, or
those laboring under other diseases and occupying beds adjacent to
persons ill with epidemic meningitis. That, nevertheless, there is a
material morbific principle which inheres in certain localities, so
that those who occupy them successively are liable to suffer from this
disease, and that also this principle may be carried from place to
place so as to render certain houses (barracks) infectious, seems to
be demonstrated by the history of the disease in the French army.
Between 1837 and 1850, when the disease prevailed in various parts of
France, it did so not indiscriminately, but it usually followed the
ordinary routes of communication, and especially the movements of the
military in their transfers from one post to another, and the course
of navigable streams. Strangely, also, it attacked soldiers much
oftener than civilians. The most curious fact of all is one already
referred to--viz. that although the disease prevailed in almost every
part of the provinces, and although then as ever an incessant stream
from them was flowing into the capital, neither its civil nor its
military population was generally affected, nor, {804} indeed, at all
so, until near the close of the period mentioned. Meanwhile, however,
the disease extended to several countries conterminous with France or
in close and frequent intercourse with it--to Italy (1839-45), Algeria
(1839-47), England, Ireland, and Denmark (1845-48). These events seem
to point to a certain transmissibility of the disease until we examine
the negative facts that bear upon the question. They are such as
these: The epidemic did not spread at all from France into two of the
adjacent countries, Belgium and Switzerland, with which the
first-named country maintained an incessant intercourse by travel and
traffic, but, on the other hand, it broke out at an early date within
the period mentioned at places very remote and absolutely independent
of all influence emanating from France or any other European
source--in the south-western portions of the United States. It is by
numerous facts of this description that we are compelled to remove the
disease from the category of endemic and even epidemic diseases, and
relegate it, along with influenza, to that of pandemic affections.
[Footnote 14: _Med. Record_, xxii. 547.]
There seems to be some reason for thinking that the epidemic cause of
this disease may affect the lower animals as well as man. It was
stated by Gallup in 1811 that during the epidemic of meningitis in
Vermont "even the foxes seemed to be affected, so that they were
killed in numbers near the dwellings of the inhabitants;" and of the
epidemic in 1871 in New York, Dr. Smith relates that "it was common
and fatal in the large stables of the city car and stage lines, while
among the people the epidemic did not properly commence until January,
1872." It would be desirable to learn more precisely the characters of
these vulpine and equine epidemics before associating them with the
disease we are studying, the more so that we have been unable to
discover a similar relation between any epizootic and other epidemics
of meningitis. In this connection may be recalled the statement of Dr.
Law of Dublin, that while he was attending a lady suffering from
cerebro-spinal meningitis "nine rabbits, out of eleven which her son
had, died, all in the same way: their limbs seemed to fail them, they
fell on their side, and then worked in convulsions, and died." On
examination of the bodies of several of them congestion of the vessels
of the base of the brain was found, and also "vascularity of the
membranes of the spinal marrow, indicating inflammation."[15]
[Footnote 15: _Dublin Quarterly Journ._, May, 1866, p. 298.]
TYPES.--No disease presents a greater variety--and, indeed,
dissimilarity--of symptoms than epidemic meningitis. Some of its
epidemics are sthenic and even inflammatory in their type, while
others have the malignant aspect of rapid blood-poisoning. These
contrasts have been exhibited on a large scale, for while upon the
continent of Europe the disease for the most part has presented
sthenic phenomena, it has been more generally asthenic and adynamic in
Ireland. One might be inclined to attribute the latter peculiarity to
the permanent prevalence of typhus fever in the latter country, or
rather to the special causes producing typhus, were it not that in the
United States both types of the disease have been observed at
different times and in different places. Such contrasts of type are,
however, not unusual in other diseases that occur as epidemics,
including not only the eruptive fevers, but inflammations, or
affections involving inflammation, such as pneumonia, dysentery, {805}
diphtheria, etc. Hence it is evident that certain epidemics, and
certain cases in each epidemic, may exhibit on the one hand a
predominance of inflammatory, or on the other of adynamic or ataxic,
symptoms, and each of them in every conceivable degree and
combination. It is this variation of type that has led to such
different conceptions of the nature of epidemic meningitis, many
physicians regarding it as a fever, and many others as an
inflammation, while, as we believe, it is both the one and the other,
and acquires from either element, according to its ascendency, the
typical character of the particular epidemic under observation.
As illustrative of these statements we may mention in this place the
several _forms_ of the disease as they have been seen and interpreted
by different observers. Forget classified them as follows: (_A_)
CEREBRO-SPINAL; 1, _Explosive_ (_foudroyante_); 2,
_Comatose-convulsive_; 3, _Inflammatory_; 4, _Typhoid_; 5,
_Neuralgic_; 6, _Hectic_; 7, _Paralytic_. (_B_) CEREBRAL: 1,
_Cephalalgic_; 2, _Cephalalgic-delirious_; 3, _Delirious_; 4,
_Comatose_. In the first of these divisions three-sevenths belong to
the first and fourth varieties. But "there were slight and severe
cases; violent and hectic forms; cerebral symptoms predominant in some
and spinal in others, etc."
In his excellent paper on the epidemic of 1848 in New Orleans, Ames
arranged his cases in two categories--the _Congestive_ and the
_Inflammatory_, subdividing the former into the _Malignant_ and the
_Mild_. Malignant congestive cases were distinguished by prostration,
coma or delirium, or both; opisthotonos; and a pulse varying extremely
in its degree of frequency. In _mild congestive_ cases a good degree
of strength was preserved; the pulse was below 90; there were marked
pain in the head and tenderness of the spine, but no coma, delirium,
or stiffness of any muscles besides those of the neck. The purely
_inflammatory_ cases were, in general, distinguished by a temperature
of the skin above that of health and a full, firm pulse, but the
_malignant inflammatory_ were marked by the early occurrence of
delirium or coma, great irregularity of pulse, opisthotonos,
convulsive spasm, strabismus, and occasional amaurosis, with vomiting
and a rapid and fatal course; the _grave_, by a slighter development
of the same symptoms, except coma and delirium; and the _mild_, by a
lower grade of febrile excitement, the preservation of a good degree
of strength, a tendency to become chronic, and by the absence of coma,
drowsiness, delirium, and a cold stage.
Wunderlich adopted the simple plan of arranging the cases in three
categories: 1, the _gravest_ and most rapidly fatal cases; 2, the
_less grave_; and 3, the _lightest_. The arrangement of Hirsch had
more significance, as well as a clinical foundation--viz. 1, the
_abortive_; 2, the _explosive_ (_m. siderans_, the same as _m.
foudroyante_ of Tourdes); 3, the _intermittent_; 4, the _typhoid_.
Dr. Bedford Brown,[16] who observed the epidemics in North Carolina
from 1862 to 1864, arranged the cases under the following heads: 1,
the _inflammatory_ form, in which the fever is high, the pain very
acute, and the delirium furious, but which is exceedingly rare; 2, the
_neuralgic_ form, which is stated to be the most frequent and
protracted, with moderate fever and a pulse but slightly accelerated,
and giving a favorable prognosis; 3, the _ataxic_ form, in which great
nervous depression is {806} associated with a low and busy delirium,
and the temperature "is generally much reduced below the natural
standard.... This is always a dangerous form;" 4, the _paralytic_
form, in which stupor and insensibility are early and prominent
features, with a very slow and feeble pulse, blanched skin, and death
by syncope.
[Footnote 16: _Richmond Med. Jour._, ii. 1.]
Dr. Purcell of Cork[17] furnished a classification which is one of the
best for practical and clinical purposes--viz. 1, the _rapid_ variety,
attended with purple blotches, embarrassed respiration and
circulation, followed by sopor, insensibility, and coma; 2, the
_cerebro-spinal_ form, with retraction of the head, pain and cramps of
the muscles, hyperaesthesia of the skin, delirium, etc., accompanied
by fever, herpetic eruptions, etc. These two forms are apt to be more
or less associated in the same case.
[Footnote 17: _Dublin Quarterly Jour._, Aug., 1870, p. 243.]
Of the various forms admitted by different authors, and of which we
have seen examples, we would class together--(_a_.) The abortive, in
which the characteristic phenomena are often faintly defined, and yet
to the practised eye distinctive. (_b_.) The malignant, in which the
symptoms, of whatever kind, are exaggerated, the attack sudden, the
course short, and the issue fatal. (_c_.) The nervous, including 1,
the _Ataxic_--viz.--1, the _delirious_; 2, the _cephalalgic_; 3, the
_neuralgic_; 4, the _convulsive_; 5, the _paralytic_; and 6, the
_adynamic_ (_comatose_ and _typhoid_). (_d_.) The inflammatory. (_e_.)
The intermittent. Of these the _abortive_ and _intermittent_ call for
a brief explanation. Abortive meningitis is observed only during the
prevalence of the disease in a more characteristic form. Thus, the
mother of a boy who had died of the fully-developed disease
"complained of the head and back and limbs, and of chilliness, and
presented a petechial eruption. After active purgative and
counter-irritant treatment she was about her work on the second
day."[18] The late Dr. Burns of Frankford, Philadelphia, while
attending patients affected with the disease suffered from headache,
severe pains along the spine and in every joint of the body, and a
general languid feeling.[19] Kempf during the decline of an epidemic
observed "a great number of individuals, especially adults, who
complained of headache, malaise, neuralgic pains in various parts of
the body, and pain in the nape of the neck or other parts of the
spine."[20] In a case observed by the writer (June, 1867) most of the
characteristic symptoms were present in a mitigated form, and the
pulse was at 60. Within five days restoration was complete.[21] The
_intermittent_ and _remittent_ types are apt to be quotidian or
tertian, and in fatal cases the former has been taken for malignant
intermittent fever, which it resembles by a periodical febrile
movement, with pains, cramps, delirium, etc. This type sometimes first
manifests itself during the decline of an attack.
[Footnote 18: Sargent, _Amer. Jour. of Med. Sci._, July, 1849, p. 35.]
[Footnote 19: _Amer. Jour. of Med. Sci._, April, 1865, p. 339.]
[Footnote 20: _Ibid._, July, 1866, p. 55.]
[Footnote 21: _Epidemic Meningitis_, p. 42.]
SUMMARY OF THE SYMPTOMS.--Like other fatal epidemic diseases,
meningitis is sometimes sudden and sometimes gradual in its
development. In the former case the patient, who has gone to bed
apparently in perfect health, awakes suddenly from a sound sleep about
the small hours of the night to find himself in a severe chill. In the
case of young children a convulsion attends the awakening. Or the
patient, while {807} pursuing his ordinary avocations, may be seized
with a chill, prostration, vomiting, and headache, of which symptoms
the last is often intensely distressing. In this, as in other epidemic
diseases, such violent seizures are most common during the earlier
periods of its prevalence, but later in its course premonitory
symptoms are more frequently observed. They may last for an hour or
two, or may extend to several days; and, in general, it may be stated
that the longer their duration the milder will be the subsequent
attack. But the symptoms in either case are essentially the
same--prostration, chilliness, feverishness, and sometimes vomiting
and sharp pains in the head, back, and limbs. The character of the
vomiting, as well as the absence of all gastric lesions in fatal
cases, proves that it is occasioned by an irritation of the central
nervous system.
In the cases which are regularly developed these phenomena more or
less gradually assume a graver aspect or usher in a heavy chill, which
in its turn is followed by alarming symptoms, and especially by an
excruciating pain in the head, a livid or pale and sunken countenance,
and extreme restlessness. The pulse is as often slow as frequent, and
the skin is rarely hot, and, indeed, is generally but little, if at
all, warmer than natural. The vague pains that began with the attack
are now concentrated, and seem to dart in every direction from the
spine, which is also, at its upper part, the seat of severe aching;
and in some cases hyperaesthesia of the skin is very marked. In a
large proportion of cases the spinal muscles become more or less
rigidly contracted, so that the head is drawn backward or the whole
trunk is arched as in tetanus. Trismus is not uncommon, and clonic
spasms frequently affect the limbs. Even general convulsions are
occasionally observed. As these phenomena grow more decided delirium
of various degrees is often manifested, from mere wanderings and
hallucinations during the sleepless watches of the night to violent
maniacal ravings or incoherent mutterings, or the stertor of coma.
Frey and others have noted a remission of the symptoms occurring on or
about the third day in cases of a regular type. The rigidity of the
cervical muscles becomes relaxed, the headache subsides, and the
mental condition improves. But this amelioration lasts but a short
time, and then the normal course of the symptoms is resumed.
As the attack advances the pulse gradually or rapidly rises above the
normal rate, and sometimes becomes very frequent, and the skin,
although it grows warmer, does not often acquire the temperature
observed in idiopathic fevers or sustain it as they do. In many cases
eruptions appear upon the skin. During some epidemics the only one
observed is herpes labialis; in others the eruption resembles roseola,
measles, or the mulberry rash of typhus, or from the first it consists
of petechiae, vibices, or extensive ecchymoses. The tongue presents
the characters which belong generally to the typhoid state. At first
moist and coated with a whitish fur or a mucous secretion, it
afterward, if life is prolonged, grows red and shining or brown and
fuliginous. There is usually a complete loss of appetite, and the
thirst is not commonly urgent. One or two liquid stools at the
commencement are generally followed by constipation, which continues
throughout the attack, although in very grave and protracted cases
diarrhoea may persist, and even become colliquative. When the attack
tends to a fatal issue the patient generally, but by no means always,
sinks into a soporose condition, in which {808} muscular relaxation,
debility, and tremulousness, such as are common in the typhoid state
of fevers, are associated with paralysis of the sphincters and of
other muscles. But we have seen rigid opisthotonos continue until
within a few hours of death in a case of more than the average
duration.
In cases that tend toward recovery the typhoid condition is rarely so
grave, but patients have often survived very severe nervous symptoms.
It is true that the return to health may be tedious and uncertain, and
not unusually a perfect restoration of all the functions is very long
delayed, or, it may be, is never attained.
INDIVIDUAL SYMPTOMS.--Pain in the head is one of the most
characteristic symptoms of epidemic meningitis. It is always present,
except in those malignant cases in which the morbid poison seems to
spend its fatal power upon the blood. In some, however, of a less
rapid but still malignant type, in which after death no exudation is
found, but only an extreme venous congestion of the membranes, or it
may be an effusion of blood beneath them, this symptom may be more or
less marked. It is generally an excruciating pain, sometimes darting
apparently through the head from the nuchae to the forehead, extorting
cries and groans, and is variously described by the sufferers as
throbbing, boring, lancinating, sharp, or crushing, "as if the head
were in a vice or nails or screws were being forced into the brain."
Its paroxysms arouse the patient from his apathetic stupor or his
coma, and cause him to become restless or violent or to shriek with
agony. Even when this evidence of anguish is wanting the patient often
attests his suffering by contortions or cries, or by frequently
carrying his hands to his head. That it depends upon mechanical
pressure upon the sensitive ganglia within the cranium and upper part
of the spine is shown by the relief which revulsive and
counter-irritant measures afford when applied to the occipital region
and the back of the neck. Identical in cause and quality with this
pain is the spinal pain proper. No better description of it has been
given than that of Fiske in 1810. It is in these words: "Its bold and
prominent features defy comparison.... In some a pain resembling the
sensation felt from the stinging of a bee seizes the extremity of a
finger or toe; from thence it darts to the foot or hand or some other
part of the limbs, sometimes in the joints and sometimes in the
muscles, carrying a numbness or prickling sensation in its progress.
After traversing the extremities, generally of one side only, it
seizes the head, and flies with the rapidity and sensation of
electricity over the whole body, occasioning blindness, faintings,
sickness at the stomach, with indescribable distress about the
praecordia--a numbness or partial loss of motion in one or both limbs
on one side, with great prostration of strength. The horrible
sensation of this process no language can describe."[22] These spinal
pains are always aggravated by pressure made on either side of the
spinous processes of the vertebrae, and, like the cephalic pains, are
more or less mitigated by revulsive applications. Accompanying the
pains is a hyperaesthesia or morbid sensibility of the skin, rendering
it painfully sensitive to the slightest touch; in the advanced stages
of the disease, when the spinal phenomena predominate, the irritation
of the nerves by the pressure of the exudation on their roots is
exchanged for numbness or {809} absolute insensibility, due to the
increase and continuance of that pressure. Moving the limbs or
separating the closed eyelids will sometimes provoke resistance, and
even extort cries; and especially is this true of attempts to
straighten the rigidly bent spine or the flexed extremities. Lewis
states that such outcries were so often excited by slowly introducing
the thermometer into the rectum that he was forced to believe that the
anal and perhaps the rectal surface was hypersensitive.
[Footnote 22: North, on _Spotted Fever_, p. 176.]
The physical causes that give rise to the pains which have just been
described likewise occasion the spasmodic and tetanoid phenomena that
are so peculiar to this disease. In general terms, they are most
marked in cases attended with inflammatory exudation, and least so
when, instead of this lesion, there is only vascular congestion of the
meninges of the spinal cord. But the rule is, of course, not absolute,
for individuals are so differently constituted that one will remain
impassive under an irritation that will throw another into
convulsions. There is no doubt that spinal rigidity may be produced by
mere congestion of the cord, and, on the other hand, that it may be
absent even when plastic exudation is abundant. This symptom is,
however, more than any other one, characteristic of the disease. It
existed in the original epidemic at Geneva, attracted the attention of
the earliest American observers of the disease, and elsewhere has
marked a greater or a smaller proportion of the cases in every
epidemic. It was described by such terms as these: "a drawing-back of
the head;" "a corpse-like rigidity of the limbs;" "the form of tetanus
called opisthotonos;" "spastic rigidity of the muscles of the lower
jaw and the posterior muscles of the neck;" "rigidity of the posterior
cervical muscles, retracting the head considerably backward." The
historians of the disease in Europe are, if possible, still more
emphatic in their elaborate descriptions of this phenomenon, and, on
the Continent at least, it seems to have been more uniformly present
than it was in Ireland or in this country. Tourdes, in describing the
epidemic of 1842 at Strasburg, said: "The decubitus of the sick was
distinguished by a backward flexion of the head and spine; most
frequently the neck alone was affected, but sometimes the whole trunk
was arched." And again: "The contraction often involved all of the
extensor muscles of the spine, and the trunk formed an arch opening
backward and resting upon the occiput and sacrum." In Ireland, Gordon
says of a patient, "Her spine presented a most wonderful uniform curve
concave backward; her head was also curved backward on the spine of
the neck." During an epidemic at Birmingham in 1875 in one case "the
retraction was so marked that a slough formed from the occiput
pressing between the scapulae."[23] In some cases rigid flexion of the
body forward or laterally has been noticed. The rigidity persists, as
a rule, until death, but sometimes ceases a short time before that
event. If recovery takes place, this symptom gradually subsides, and
disappears within a few days; but, on the other hand, more or less
stiffness of the spine may last for several weeks. In one case it
continued for more than two months, and in another until death on the
forty-ninth day.
[Footnote 23: Hart, _St. Bart's Rep._, iv. 141.]
The same physical cause that occasions rigidity, when acting less
intensely or when a special susceptibility of the nervous system
exists, also excites clonic convulsions. They are oftenest observed in
patients of the {810} age especially liable to spasmodic
affections--in children before the completion of the first dentition.
They vary in degree from twitching or subsultus affecting particular
muscles, as of the eyes, the face, a limb, etc., to general
epileptiform convulsions with loss of consciousness. They may be
associated with paralysis, as where the two halves of the body are,
the one convulsed and the other paralyzed. A case occurred in Dublin
which "presented the very striking phenomenon of continued and violent
convulsions during the whole of the brief course of the illness."[24]
These convulsions, like others occurring at the commencement of acute
diseases, are by no means always fatal, even when they are general. In
the case of a robust adult convulsions occurred repeatedly during the
first two days, and less frequently during the two following days, but
the patient ultimately recovered.[25]
[Footnote 24: _Dublin Quart. Jour._, xlvi. 187.]
[Footnote 25: _Boston Med. and Surg. Jour._, Feb., 1884, p. 121.]
Paralysis, it may be inferred from the statements already made, is an
incident of this disease, for an excess of the action causing tonic or
clonic spasm must induce paralysis. Paralysis of an arm or leg or of
the muscles of deglutition was long ago noticed among even the initial
symptoms of the attack. In Dublin (1865) it was said of a patient,
"All his members seemed to be paralyzed; he could move neither arms
nor legs." Wunderlich describes the case of a man who "on the second
day of the disease lost both sensibility and motility in the lower
limbs and over the greater part of the trunk, while his left arm also
was partially paralyzed." In another case complete paralysis of the
right side occurred on the third day, the left side being rigid.[26]
Baxa relates the case of a soldier in whom paralysis of the left side
persisted after recovery from the disease,[27] and that of a woman in
whom paralysis of the left lower limb continued along with right
ciliary paralysis. Ptosis, strabismus, paralysis of the bladder and
rectum, of the muscles of deglutition, and even general paralysis,
have been observed. Aphasia also has been recorded by Hirsch and by
Hayden.[28]
[Footnote 26: _Dublin Quart. Jour._, 1867, p. 431.]
[Footnote 27: _Wiener med. Presse_, No. 29, p. 715.]
[Footnote 28: _Dublin Quart. Jour._, xlvi. 187.]
The condition of the eyes and of vision in this disease is directly
due to pressure of the exudation at the base of the brain upon the
nerves and blood-vessels that supply these organs. One of the most
striking peculiarities of the countenance of a patient at the
beginning of an attack is the diffused and uniform redness of the
conjunctivae. In children it has a light tint, but a darker one in
adults, and in some cases the eye becomes suffused with an
extravasation of blood. The conditions of the pupil are also very
peculiar. Very long ago it was observed to undergo sudden changes from
contraction to dilatation, or the reverse. Dilatation is, however, its
ordinary condition, especially in the fully-formed attack. Very often
the pupils of the two eyes are in opposite states. In cases of long
duration, with great exhaustion, they are almost invariably dilated.
Photophobia is not uncommon, and oscillation of the pupils and
spasmodic movements of the eyeball have frequently been observed.
Strabismus is a symptom of very ordinary occurrence, particularly when
other paralytic or spasmodic phenomena exist. It may be convergent or
divergent, but most commonly is the former, and may be either a
transient or a {811} permanent symptom. Like other individual
symptoms, it may be present rarely or frequently in a particular
epidemic.
Blindness has been repeatedly observed. At first it seemed to be
noticed as a transient symptom only. Fish (1809) states that it was
sometimes the first deviation from health, and then was followed by
paralytic spinal symptoms. He also observed that sight was sometimes
restored in a few hours, and in no case did he know it to be
permanently lost. American as well as European physicians, however,
have met with many cases in which the sight was seriously and
permanently impaired or altogether destroyed. In 1873 the changes
affecting the eye were more fully and accurately described, especially
those which tend to the structural injury of the organ. The abnormal
appearances included cloudiness of the media, discoloration of the
iris, irregularity of the pupils, and their obstruction with exudate.
In exceptional cases the cornea ulcerated, and the globe collapsed
after losing its contents. Ordinarily, however, says Lewis, "no
ulceration occurs, and as the patient convalesces the oedema of the
lids, the hyperaemia of the conjunctiva, the cloudiness of the cornea
and of the humors gradually abate, and the exudation in the pupils is
absorbed. The iris bulges forward, and the deep tissues of the eye,
viewed through the vitreous humor, which had a dusky color from
hyperaemia, now present a dull white color. The lens itself, at first
transparent, after a while becomes cataractous, and sight is lost
totally and for ever."
Impairment or loss of hearing has been occasionally observed during
the successive epidemics of this disease, even from the beginning of
its history, and it was early noticed that the symptom was often quite
independent of any cognizable lesion of the ear itself. It was also
observed that the sense of smell sometimes became impaired or was lost
at the same time with that of hearing. More recently, Collins reported
a case in which the patient lost the sight of one eye and became
permanently deaf in both ears. Knapp states that in all of thirty-one
cases examined by him the deafness was bilateral, and, with two
exceptions of faint perception of sound, complete. Among twenty-nine
cases of total deafness only one seemed to give some evidence of
hearing afterward.[29] This surgeon holds that the deafness results
from a purulent inflammation of the labyrinth, and his judgment has
been confirmed by Keller and Lucas. When the impairment of hearing
occurs simultaneously, or nearly so, in both ears, it is probable that
the chief cause of the deafness is the pressure of the plastic
exudation in which the auditory nerve is imbedded. Such deafness is
rarely permanent. When the loss of hearing, whether complete or
partial, does not improve, there is reason to believe that the
internal ear has suffered great and incurable changes of structure.
Sometimes this follows a distinct attack of suppurative inflammation
of the middle ear; but as complete and permanent deafness sometimes
occurs without being preceded by any such affection, it must be
inferred that atrophic changes have taken place in some portion of the
nervous apparatus of hearing. It is stated by Moos that of sixty-four
cases of recovery from cerebro-spinal meningitis, which showed
disturbance of hearing as a sequel, one-half manifested in addition a
more less disordered equilibrium. Of these twenty-nine were totally
deaf on both sides, two totally deaf on one and hard of hearing on the
other side, and one case had merely {812} impaired hearing in both
ears. The disturbance of locomotion had existed for periods varying
from three weeks to five years from the inception of the disease, and
was chiefly characterized by a staggering or waddling gait.[30] In the
deaf-mute institutions at Bamberg and Nurnberg it is said that out of
91 pupils, 80 owed their infirmity to this disease (Ziemssen). Salamo
states that some awake out of sleep totally deaf, and remain so for a
long time, or, it may be, permanently (Moos).
[Footnote 29: Smith, _loc. cit._]
[Footnote 30: _Mening. Cerebro-spinal epid._, p. 11.]
The expression of countenance in this disease is peculiar. When the
pain in the head is severe and paroxysmal the features are apt to be
violently distorted; when it is more persistent the face assumes a
fixed or rigid expression, or is at the same time dull, particularly
after a long continuance of the pain. In the apoplectic form the
expression may be set and stupid, but the features have neither the
dark, dull, swollen, and duskily-flushed aspect of typhus, nor the
languid, sleepy expression, and circumscribed flush on the cheek which
are so characteristic of typhoid fever. Except during absolute
insensibility in rapidly fatal cases there is a look of greater
intelligence than belongs to either of the diseases mentioned. Indeed,
in the beginning of the attack in regular cases the distinctive facies
presents pale and sunken features, with paleness of the skin over the
whole body.
Delirium in this disease exhibits a great many degrees and varieties.
It may occur among the earliest symptoms in certain rapid cases not of
the congestive type, but is more apt to arise on the second or third
day in those more typically developed. It may be mild, reasoning,
hysterical, or maniacal, or it may change from one to another of these
forms during the same attack. Fish states that it is apt to be violent
if it comes on at the commencement of the illness, but that when it
begins at a later period it is milder, and sometimes playful, the
patient being sociable and humorous. All good observers have furnished
similar descriptions of this symptom; some have added that the mental
condition is often desponding and apprehensive, and others that
certain patients remain sombre and silent; and it sometimes happens
that the delirium comes on abruptly, as when a patient "woke suddenly
in the middle of the night and began to hum tunes, to fancy that
people were conversing with him," etc. (Gordon).
Coma is met with sooner or later in nearly all fatal cases, but rarely
in a marked degree until the approach of death. If anything is
surprising in epidemic meningitis, it is the absence of that deep and
prolonged stupor that characterizes the typhoid state, notwithstanding
the pressure of the exudation upon the brain in most cases, and in
others such a profound alteration of the blood that it exudes through
the tissues as water passes through a porous body. Another striking
phenomenon of the disease is that the patient after recovery has
generally a complete oblivion of all that happened to him between the
beginning of the attack and convalescence. This is true even of cases
in which the brain symptoms are far from being conspicuous.
Another symptom closely related to the local lesion and the
blood-change in this disease is vertigo. As originally described by
Miner in 1823, it occurred from the very commencement of the attack,
and was even then regarded as denoting a deficient supply of the blood
to the {813} brain, so that when the patient rose to an erect posture
it was felt along with uneasiness in the stomach, acceleration of the
pulse, dimness of sight, nausea, and fainting. Tourdes, speaking of it
as it occurred in the Strasburg epidemic, says that it confused the
mind and rendered walking impossible. In two cases patients were
seized with a giddiness which compelled them to whirl around, when
they fell and did not rise again. According to Moos (1881) unilateral
affections of the labyrinth give rise to vertigo, and bilateral
lesions to a staggering gait. Bilateral hemorrhage or acute
suppuration of the ampullar terminations of the auditory nerve
occasions paralysis and staggering. Children, and those who at the
same time have the sight impaired, are apt to remain affected for a
long time. Otherwise, prolonged and systematic muscular exercise may
remove the tottering walk.
To the same causes must doubtless be attributed the debility which is
so early and so conspicuous a symptom in this disease, and which gave
it one of the names, typhus syncopalis, by which it was first known in
this country. It was manifested by the vertigo already noticed, by a
sense of sinking in the epigastrium, by a quick, frequent, feeble, and
irregular pulse, and by a sudden and extreme loss of muscular power,
so that the patient found himself unable to raise his hand before he
was sensible of being ill. This state of asthenia is conspicuous
throughout the whole of the disease, and is the immediate cause of the
slow and irregular convalescence which is characteristic of it.
Of the symptoms peculiar to the digestive apparatus hardly any belong
to it directly. They are nearly all the effect of reflex influences.
The condition of the tongue is for the most part quite unlike that
which belongs to the typhoid state. The fuliginous condition of the
tongue, gums, cheeks, and lips which characterizes that state is
seldom met with in epidemic meningitis. The older writers agreed that
even when the tongue does grow dry and brown the condition is not of
long continuance, and later observers have confirmed their statements.
Thus, J. L. Smith (1872) says, "Occasionally, in cases attended with
great prostration, the fur of the tongue is dry and brown, but only
for a few days, when the moist whitish fur succeeds." We have
generally found it moist, whitish in the centre and at the tip and
edges.
Nausea and vomiting are very constant among the initial symptoms of
the disease, and, as already pointed out, are due to irritation of the
cerebro-spinal ganglia. Very often the vomiting is not preceded by
nausea, and is brought on by the patient's raising himself, etc. The
stomach itself undergoes no change. Both symptoms are usually
accompanied by faintness or giddiness, and are more decided in the
initial than in the later stages of the attack. The matters vomited,
varying with the contents of the stomach and the urgency and duration
of the symptom, consist of ingesta, mucus, serum, or bile, and in some
grave cases of a dark grumous matter taken to be altered blood. In
some epidemics, apparently, more than in others, this symptom is very
distressing, as it was at Birmingham in 1875.[31] The inability of the
stomach to retain food necessarily leads to a rapid wasting of the
flesh, which is aggravated by the patient's suffering, restlessness,
and want of sleep. Nevertheless, no sooner is the vomiting appeased
than a desire for food is felt, and when {814} it is retained it
generally undergoes digestion. Indeed, in no other disease is the
return of a good appetite and digestion so prompt and complete. It is
true that the recovery of flesh and strength is not always in
proportion to the appetite. As might be expected in a disease in which
fever plays so subordinate a part, there is seldom urgent thirst. But
epidemics differ in this as in so many other respects. In that which
we witnessed in the Philadelphia Hospital in 1866-67 the patients were
clamorous for liquids. Constipation is the rule among patients with
this disease, as, indeed, might naturally be expected, for no lesion
affects the bowels and little or no food is retained by the stomach.
Yet in a few cases diarrhoea accompanies persistent vomiting.
[Footnote 31: Hart, _St. Bart's Rep._, xii. 112.]
The fauces appear to have been more or less inflamed in some
epidemics; swelling of the parotid glands is an occasional occurrence,
and sometimes they undergo suppuration. Aphthae have also been met
with.
The secretion of urine is not affected in any uniform manner.
Sometimes it is diminished and sometimes increased in quantity. The
latter symptom has occasionally long survived the disease. It retains
its normal acidity. In rare cases either albumen or sugar has been
detected; the former may have been due to the action of blisters of
cantharides used in the treatment of the disease.
One of the most curious and unintelligible phenomena occasionally met
with in this disease is a peculiar affection of the joints, which
first was observed in this country. Jackson (1810 and 1813) wrote: "In
some cases swellings have occurred in the joints and limbs. They have
been very sore to the touch, and their appearance has been compared to
that of the gout. The parts so affected feel as if they had been
bruised. These swellings arise on the smaller as well as on the larger
joints, and are often of a purple color." So Collins[32] reports: "The
joints sometimes become swollen, red, and tender; at other times red
and painful without any swelling; while, again, intense pain and rapid
enlargement from effusion have occurred unattended with redness. The
joints most usually attacked are the knee, elbow, wrist, and the
smaller articulations of the fingers and toes." In an epidemic which
occurred in Greece in 1869 articular swellings similar to those of
inflammatory rheumatism were observed.[33] These descriptions, which
apply to some cases in most epidemics, are of more than casual
interest, for they demonstrate conclusively, as we think, the truth
which the whole history of the disease confirms--viz. that it is a
systemic and not a local affection, and is dependent for its existence
upon a specific poison which is absolutely unlike every other morbid
poison known to pathology.
[Footnote 32: _Dublin Quart. Jour._, Aug., 1868, p. 170.]
[Footnote 33: _Archives generales de med._, Mai, 1883, p. 622.]
The act of respiration is variously modified in this disease, as
might, indeed, be expected from the seat and nature of the
cerebro-spinal lesions. It is sighing, labored, and interrupted.
Burdon-Sanderson describes its differences from the so-called
Cheyne-Stokes respiration; it is, he says, "marked by a slow, labored
inspiration, followed by a quick expiration and a long pause." When
opisthotonos is very great and persistent, it necessarily interferes
with the dilatation of the lungs, and leads to oedema of those organs,
and even to sanguineous effusions into them. {815} Pneumonia is not an
unusual complication of the disease when it prevails in cold weather.
The distinguishing characters of the pulse are diminished force and
volume, and a tone so much impaired that slight causes produce extreme
variations in its rate and rhythm. If the disease be a fever, as is by
some maintained, then it is the only fever in which the pulse-rate is
often far below the normal, and at the same time neither full nor
tense, unless transiently and in altogether exceptional cases. In no
other disease attended with inflammation do the rate and quality of
the pulse vary so greatly within short intervals. It may be said, in
general terms, to be variable in rate and strength even in the most
sthenic cases of the disease, and in those which tend to a fatal issue
to be small, thready, weak, intermittent, or imperceptible for a
longer or shorter time before death. It is no uncommon thing for the
pulse-rate at the beginning of an attack to fall as low as 40, or even
27, and afterward rise to 120 or even more, in a minute, without
necessarily indicating a fatal issue. Muscular exertion, rising from a
recumbent posture, etc., will sometimes double its frequency, besides
producing irregularity. Read, describing the pulse as he observed it
in Boston in 1873-74, speaks of cases in which "both the rhythm and
the force of the beats are entirely destroyed; ... one moment, while
beating very fast, it will suddenly drop to a much lower rate....
These conditions also may outlast apparent convalescence." Some fatal
cases are attended by distressing palpitations of the heart.
Nothing is more remarkable in the early histories of this affection
than their unanimous statement that it is not distinguished by a
febrile temperature. It is true that the observers of those days had
not the advantage of using clinical thermometers, but they were too
nearly agreed in their judgments and harmonious in their descriptions
to permit any serious doubt of the substantial accuracy of their
conclusions, which were expressed in such terms as these: "A
diminution of heat may be considered as among this most striking
symptoms of this disease" (Strong); or, "the temperature never
exceeded the standard of health in more than three or four cases, ...
and a great majority of the patients had no fever at all" (Miner); or,
again, "A high febrile movement took place only in a limited number"
(Gilchrist); or, "The heat of the surface was less in all cases than
is usually observed in acute diseases" (Jenks). It will be observed
that these statements, and very many others which agree with them,
were founded upon the perception of the patients' temperature by the
hand, which was of course applied to the most accessible parts of the
body--the face, neck, arms, and hands--but they have more real value
and significance than the more recent measurements taken in the mouth,
axilla, rectum, or vagina, for we know that, however valuable the
temperatures of these parts may be for comparative studies, they do
not really indicate the condition of the individual who presents them.
It is a familiar fact that the difference of temperature in cholera
when taken in the rectum and the axilla may be 4 degrees F., or even
more than this.
Since the thermometer has been used in the study of epidemic
meningitis greater accuracy of results has been attained, and yet the
general statements of the earlier observers have been confirmed. Thus,
Githens has shown that the temperature of the body in this disease is
lower than that recorded of any other fever or inflammatory affection;
the average, {816} indeed, of his cases was lower by four or five
degrees than that of typhus or typhoid fever, pneumonia, etc. In 2
cases only did the thermometer in the axilla reach 105 degrees. The
highest temperature in 15 cases was between 104 degrees and 105
degrees; in 12, between 103 degrees and 104 degrees; in 7, between 102
degrees and 103 degrees; in 6, between 101 degrees and 102 degrees;
and in 2 it was below 100 degrees.[34] Tourdes, Niemeyer, and others
have noted the slight rise of temperature during the first and second
days of the attack, and Wunderlich found fever of very unequal degrees
and with very variable maxima, but the highest temperatures were
observed by him as well as others in fatal cases and immediately
before death. In one instance it reached 107.5 degrees F.
Burdon-Sanderson and others have found that an increased temperature
always attended exacerbations of pain. Von Ziemssen gives the average
temperature as varying from 100.4 degrees to 103 degrees F., but with
variations between higher and lower points, and particularly notes the
persistence of a normal temperature while the other symptoms are
undergoing a variety of changes, as well as the fact that, unlike
other febrile affections, this disease has no representative
temperature curve. In his clinical observations Hart found for several
successive days as much as six degrees of difference between the
morning and evening temperatures. A morning rise for several days was
noticed in four cases, and usually there was no relation between the
pulse and the temperature, nor any uniformly between the temperature
and the gravity of the attack.[35] But not rarely it has been noticed
that the daily exacerbations, if any, did not occur in the afternoon,
but with great irregularity, so that the maxima and minima might occur
on successive days and at the same hour of the day. Dr. J. L. Smith,
whose thermometric observations in this disease seem to have been
carefully made, used the thermometer in the rectum, and thus obtained
temperatures higher that the average of other observations, such as
105.4/6 degrees to 107.2/6 degrees in several cases. Yet he found the
fluctuations of rectal temperature remarkable, though less so than the
surface temperature, of which he states that sometimes it rose above
or fell below the normal standard several times in the course of the
same day.
[Footnote 34: _Amer. Jour. of Med. Sci._, July, 1867, p. 38.]
[Footnote 35: _St. Bart's Reports_, xii. 112.]
Nothing can be more irregular, uncertain, or various than the
eruptions and other cutaneous symptoms that have been met with in this
disease. When it first appeared in New England a large proportion of
the cases, and especially of the grave cases, exhibited petechial
eruptions and ecchymotic spots, whence the disease presently received
the name of spotted fever. Yet even then, North and the other
historians of its epidemics were careful to state that spots on the
skin were by no means characteristic of the disease, and very often
were not present at all, especially in cases that terminated
favorably. Woodward, for example, wrote (1808): "An eruption on the
skin so seldom appeared that it could no longer be considered a
characteristic symptom of the disease." In various American local
epidemics an eruption of some kind seems to have existed in about
one-half of the cases. In one that we observed in the Philadelphia
Hospital no eruption whatever was observed in thirty-seven out of
ninety-eight cases. In the epidemic at Chicago in 1872, N. S. Davis
says:[36] "About one-third of the cases presented some red
erythematous spots" between the third and the seventh day. In mild
cases they were few and {817} bright red; in grave cases, darker and
larger, with some swelling of the skin; and in the worst cases, purple
spots one or two or more inches in diameter. In that of
Louisville,[37] Larrabie states that the eruption "was generally
herpetic in its character, and accompanied by sudamina; but in several
instances an urticarious eruption suddenly appeared and disappeared."
Nothing is said of petechiae or ecchymoses. In the New York epidemic
of 1873[38] the skin in grave cases presented dusky mottlings,
especially when the animal temperature was reduced; also a punctated
red eruption, bluish spots a few lines in diameter, and large patches
of the same color. Herpes also was common. It is chiefly in cases of a
malignant type and rapid and fatal course that ecchymoses have been
observed. Of this statement illustrations will be given in the
paragraph relating to the duration of the disease.
[Footnote 36: _Louisville Med. Jour._, June, 1872, p. 705.]
[Footnote 37: _Louisville Med. Jour._, Dec., 1872, p. 782.]
[Footnote 38: _Amer. Jour. of Med. Sci._, Oct., 1873, p. 329.]
In continental European epidemics of meningitis the proportion of
cases in which a general eruption existed seems to have been smaller
than it was in this country. In the Geneva epidemic of 1805 a
considerable number of cases at the point of death presented purplish
spots, some earlier than this, and some after death only. In the
Neapolitan epidemic of 1833, and in that which occurred in Dublin in
1867-68, ecchymoses were often present, and in a very marked degree.
Stokes and Banks mention that in some rare instances the spots ran
together and coalesced over some portions of the body, so as to cover
a large extent of the skin and render it completely black, as though
it were wrapped in some dark shroud. The entire right arm and half of
the right side of the chest in one case, and in the other the whole of
the lower portion of one leg and foot, were thus affected.[39] In
Strasburg, on the other hand, only three cases of petechiae were
observed by Tourdes; at Rochefort and Versailles, in 1839, they were
rarely noticed; at Gibraltar, in 1844, they do not seem to have been
observed; in 1848-49, at the Val de Grace Hospital (Paris), they
appear not to have attracted attention; and at Petit Bourg they were
not noticed, although the state of the skin was fully described. In
Prussia, in 1865, neither Burdon-Sanderson nor Wunderlich mentions
petechiae or vibices as occurring during life; and Hirsch, after
noting their occasional presence, is obliged to draw upon American
authors for an account of them.
[Footnote 39: _Dublin Quart. Jour._, xlvi. 199.]
Of the eruptions other than petechiae and ecchymoses, several of which
have already been mentioned, it is necessary to take some notice here.
They are, chiefly, and in general terms, exanthems, including
erythema, roseola, and urticaria, and in addition herpes, particularly
of the lips. The last has no special relation to this affection, as it
is met with in almost every febrile disease, but it has sometimes
extended to the whole face in this one. The former may be connected
pathologically either with the altered condition of the blood or with
the irritation produced by the exudation in the spinal nervous
centres. They have frequently been compared to measles and to
scarlatina, but sometimes they have assumed the form of bullae. Thus,
in the case of a child four years old, described by Grimshaw,[40] an
eruption of pemphigus occurred over the whole body. Jackson long
before had mentioned, as one of the eruptions belonging to this
disease, "large bullae, as if produced by cantharides." Jenks {818}
described "large elevated spots of a very dark color, presenting
outside of the dark color a blistered appearance." In some cases
gangrene of the skin has been observed when the spots have been
exceptionally dark, and occasionally has been produced by pressure.
[Footnote 40: _Jour. of Cutaneous Med._, ii. 37.]
The cause of death in many of the more rapid cases is coma, which is
often preceded by convulsions, especially in children; but in many
others, even when attended with all the marks of dissolution of the
blood, consciousness may be but slightly impaired until the actual
imminence of death. In many other cases, which are fatal in the midst
of an attack with spinal symptoms, death is due to asphyxia, partly
owing to pressure on the medulla oblongata, and partly to the
interference with the respiratory act due to this pressure, and
occasioning excessive bronchial secretion. Again, death may occur
through a gradual exhaustion of the powers of life, without marked
spasm, blood-change, or complication. In these cases also the
intelligence remains unimpaired almost until the moment of
dissolution. Death is not very rarely due to pneumonia, and when the
disease is greatly prolonged or the convalescence from it is imperfect
a fatal termination by dropsy of the brain is still among its dangers.
Hirsch once declared that the duration of epidemic meningitis "is
between a few hours and several months," and, however hyperbolical the
phrase may seem, it is quite accurate. Such inequalities are more
characteristic of acute blood diseases than of inflammations, and in
this case the coexistence of elements of both kinds doubtless accounts
for the extreme irregularity of the symptoms and duration of the
attack. The early American writers insisted strongly on this as a
characteristic feature of the disease. They record an unusually large
proportion of cases that were fatal within the first day, and even
after an illness of five hours, although they agree that the most
usual date of death was between the fourth and seventh days--a result
that has been confirmed by subsequent observation. Dr. N. S. Davis
gives the duration of the disease, as seen by him, as between twenty
hours and twenty-eight days. Out of 469 fatal cases in the city of New
York in 1872, 334 are said to have terminated within eleven days, and
of this number 270 were fatal in the first six days of the attack,
including 52 who died on the first day, and 51 in from one to two
days. It is perhaps worthy of note that while from the eleventh to the
fourteenth day only 11 deaths occurred, 20 took place on the
fourteenth and fifteenth; and while from the fifteenth to the
twenty-first day only 16 died, yet from the twenty-first to the
twenty-second 12 deaths were reported. This would seem to indicate a
peculiar danger on the days represented by multiples of seven. Of
cases that recover, the duration is even more indefinite than that of
fatal cases, owing to complications that occur in many, and especially
such as involve the cerebro-spinal centres. When death takes place
within a few hours it usually, if not always, is attended with
symptoms that denote a disorganization of the blood. In 1864 we
attended a young man previously in perfect health, but who died in
twenty-one hours after the first seizure. His mind was unclouded
throughout his brief but fatal illness. Within seven hours of death a
purpurous discoloration of the skin began, and about an hour before
that event the surface everywhere assumed a dusky hue. The forearms
and hands were almost uniformly purple and the face turgid; many
ecchymotic spots on the trunk and lower limbs were nearly black and
measured {819} one or two inches in diameter.[41] In the case of a
child of five years death in convulsions took place after an illness
of ten hours, the skin presenting purpurous spots, some of them very
large and of a deep bluish livid hue. On post-mortem examination there
was not the slightest appearance of any meningeal lesion, except a few
dark spots like sanguineous effusion under the arachnoid. The heart
was full of dark blood in a semi-coagulated state, and the white
corpuscles were three times as numerous as the red.[42] A case is
reported by Gordon[43] in which the entire duration of the illness
until death was five hours. This is probably the shortest case on
record. A lady aged twenty-two years died in sixteen hours, the skin
covered with livid ecchymoses, some of them measuring an inch or an
inch and a half in diameter.[44]
[Footnote 41: _Amer. Jour. of Med. Sci._, July, 1864, p. 133.]
[Footnote 42: _Dublin Quart. Jour._, 1867, ii. 441.]
[Footnote 43: _Loc. cit._]
[Footnote 44: _Med. Press and Circular_, May, 1866. For other cases
see _ibid._, pp. 296, 298-300.]
The character of the convalescence from epidemic meningitis must
evidently be affected by the causes that determine its duration, the
grade of the disease, the development and extent of the lesions, etc.;
but it is certain that, except in those imperfect and, as it were,
shadowy cases which denote a very slight action of the morbid cause,
its subjects do not recover rapidly. The essential lesion of the
fully-formed disease requires time for its removal, just as in typhoid
fever the intestinal ulcers are often slow of healing, and hence
become a cause of tardy recovery and even of unlooked-for death. The
convalescence, then, from the disease we are now studying is slow and
irregular, is attended often with debility and emaciation, and
sometimes with persistent headache, neuralgia, convulsions, stiffness
of the neck and pain in moving it, hyperaesthesia of portions of the
skin, palpitation of the heart, dyspepsia, etc. Relapses are very far
from being uncommon.
Among the causes of tardy convalescence in this disease are those
lesions and disorders which may be embraced by the term sequelae.
Impaired vision, due to various affections of the eyes, has already
been considered among the symptoms proper of the disease, but they are
not infrequently developed after the acute attack has subsided. Thus,
in a case reported by Larrabie:[45] "Just as convalescence seemed
beginning the left eye became affected in all its parts, with entire
loss of vision and also complete deafness. After a short remission
hydrencephaloid symptoms appeared, followed by the same changes in the
hitherto sound eye, complete blindness and deafness, general cachexia
and marasmus, rigid flexion of the right limbs, and death by
exhaustion at the end of sixteen weeks." The impairment of hearing,
which also was described as a symptom of the acute attack, is apt to
become more marked after the acute stage has passed by, and, as before
stated, is very often permanent. Occurring in young children, it then
involves deaf-mutism. It is in many cases associated with defective
vision, weakness or loss of memory, mania, impairment of intelligence,
persistent pains in the head or chronic hydrocephalus. Sometimes to
one or more of these symptoms is added more or less general paresis or
complete paralysis. Southhall[46] mentions the case of a child two
years old whose attack was followed by incomplete paralysis, and death
at the end of eight months with softening {820} of the brain. Gordon
thus describes the conclusion of a case: "The man has gradually passed
into a state of almost organic life; he eats, drinks, and sleeps well;
he passes solid feces and urine without giving any notice, yet,
evidently, not unconsciously; ... he seems to understand, but cannot
answer; ... he can draw up his legs and arms, but he cannot use his
hands at all." Hirsch has remarked that disorders of speech are met
with, due apparently to an inability to articulate certain sounds. Von
Ziemssen regards chronic hydrocephalus as not a rare consequence of
epidemic meningitis, and as one not absolutely or immediately fatal.
Its symptoms include severe paroxysmal pain in the head or neck or
extremities, with vomiting, loss of consciousness, convulsions, and
involuntary evacuation of excrements. Between the paroxysms, which
sometimes occur periodically, the patient generally suffers from
neuralgic pains, hyperaesthesia, and various motor and even mental
disorders; but in other cases the intervals are free, or nearly so,
from all morbid manifestations. Davis (1872) and many others speak of
severe neuralgic pains following this disease; according to Dr. D.,
they are most frequent at the heads of the gastrocnemii muscles, in
the abdomen, and the head; a very fretful disposition, variable
appetite, and disturbed sleep are often observed. Relapses have been
noticed in almost all the epidemics, and it seems probable that they
are often due to the influence of accidental exciting causes, mental
or physical, in renewing the inflammation around the cerebro-spinal
lesions. Miner (1825) remarked that they were most apt to occur within
the first week, but that when the disease had once run its course
there were very few relapses during convalescence. But, he adds, there
were several repeated attacks after the most perfect recovery, and
several of the patients had had the disease the preceding year.
[Footnote 45: _Richmond Journal of Med._, Dec., 1872, p. 779.]
[Footnote 46: _Ibid._, Aug., 1872, p. 141.]
Like other epidemic diseases, meningitis presents itself with every
possible degree of gravity between that of a slight indisposition and
that of a malignant and deadly malady. The mortality in a number of
epidemics compared by Hirsch varied between 20 per cent. and 75 per
cent. It changes with the locality. Thus, nearly at the same time that
the death-rate from this disease in Massachusetts was 61 per cent., it
was but 33 per cent. in the Philadelphia Hospital. In 1872 the whole
number of deaths caused by it in Philadelphia was 133, while at St.
John's College, Little Rock, Ark., 21 cases out of 29 were fatal
(Southhall). It differs, also, at different periods; for while ten
epidemics in various places, occurring between 1838 and 1848,
presented an average mortality of 70 per cent., a similar number,
occurring between 1855 and 1865, gave an average mortality of only 30
per cent. It must, however, be confessed that such statistics cannot
be relied upon as accurate, for in private practice many cases occur
that are never reported unless they end fatally.
MORBID ANATOMY.--The lesions found after death from epidemic
meningitis consist essentially of congestion or inflammation of the
cerebro-spinal meninges, but they also include in many cases
hemorrhage, serous effusion, plastic exudation, and tissue-changes in
the brain and spinal marrow, and in many other cases an impaired
constitution of the blood. As the signs of the latter, and not the
former, alterations are met with in the more malignant cases, it is
evident that, looking at the disease as a {821} whole, it must involve
a toxic element of whose operation the various post-mortem lesions are
only effects. These lesions, on the whole, vary with the type of the
disease, and also with its duration, but some are chiefly met with in
cases of a malignant and others in cases of an inflammatory type.
The exterior of the body after death in the early stages of this
disease almost always presents the marks of transudation of the
contents of the blood-vessels. The dependent parts of the body exhibit
large livid patches or a uniform discoloration of the same hue. In
acute cases the muscles are more deeply colored than natural, and when
the attack is prolonged they are said to have their cohesion impaired
by fatty degeneration. Congestion of the brain is an unfailing
accompaniment of the first stage of the disease; its blood-vessels are
all distended with dark blood; the sinuses of the dura mater are
usually filled with coagula of the same hue, though sometimes very
dense. Serum abounds in the arachnoid cavity and in the ventricles of
the brain; it may be clear or milky, and sometimes it is quite
purulent. It is alleged by one reporter that no less than three pints
of turbid serum escaped in a case in which, however, death did not
occur until the thirty-fifth day. Craig found eight and twelve ounces
of a limpid fluid in two cases; and Tourdes found pus in more than
one-half of his cases, either unmixed or forming a milky liquid. J. L.
Smith refers to the case of an infant who had the disease at the age
of five months, and two months subsequently great prominence of the
anterior fontanelle, and other symptoms which indicated the presence
of a considerable amount of effusion within the cranium. In a case in
Dublin,[47] there was no meningeal lesion except in a "few dark spots
like sanguineous effusion under the arachnoid." White[48] mentions the
case of an adult that terminated fatally in thirty-six hours, in which
the vessels of the pia mater were very much congested, and sanguineous
effusions existed above and below the cerebellum, and a clot of blood
three inches long and external to the theca extended downward from the
lowest portion of the medulla oblongata. In all of these instances,
then, congestion, the first stage of inflammation, existed. That such
was its real nature is proved by what follows.
[Footnote 47: _Dublin Jour._, July, 1867, p. 441.]
[Footnote 48: _Med. Record_, iii. 198.]
The most characteristic lesion is a fibrinous or purulent exudation in
the meshes of the pia mater. American physicians described it as early
as 1806 in such terms as these: "The dura mater and pia mater in
several places adhered together and to the substance of the brain; ...
between the dura mater and the pia mater was a fluid resembling pus"
(Danielson and Mann). In 1810, Bartlett and Wilson found "an
extravasation of lymph on the surface of the brain;" and in the same
year Jackson and his colleagues, after describing the congestion and
serous effusion found within the cranium "in those who perished within
twelve hours of the first invasion," state that the arachnoid and pia
mater present an effusion between them of "coagulated lymph or
semi-purulent lymph" both on the convexity and at the base of the
brain. These descriptions correspond in all respects with those of
Mathey relating to the epidemic at Geneva in 1805, for he says: "The
meningeal blood-vessels were strongly injected. A jelly-like exudation
tinged with blood covered the surface of the brain; ... on its lower
surface and in the ventricles a {822} yellowish puriform matter was
found." Such lesions have been described by a long line of
observers--by Wilson in 1813, Gamage in 1818, Ames and Sargent in
1848; by Squire, Upham, and a host of others since 1860 in the United
States, and by Tourdes, Gilchrist, Ferrus, Wilks, Gordon, Banks,
Gaskoin, Niemeyer, Burdon-Sanderson, and many more in Europe.
It is evident, therefore, that in a certain number of fatal cases only
sanguineous congestion of the membranes of the brain and spinal cord
are found, and in certain others--constituting, it may be added,
nine-tenths of the whole number--evidences exist of cerebro-spinal
meningitis. Hence the natural conclusion is that the congestive
lesions represent the first stage of a process which if prolonged and
perfected occasions the lesions peculiar to inflammation. For the
development of the latter two factors would seem to be essential--not
only a fibrinous condition of the blood, but also sufficient time for
exudation to occur. But when we come to study the actual results of
examinations post-mortem, it is found that the duration of the attack
does not determine absolutely the nature of the lesions. On the one
hand, in a case which terminated fatally after a week's illness there
was found reddish serum between the arachnoid and the pia mater and in
the lateral ventricles, with intense injection of the pia mater of the
base, medulla oblongata, and upper part of the spinal cord, but no
exudation of lymph.[49] And, on the other hand, numerous cases have
been published in which, although death occurred within twenty-four
hours from the onset of the attack, coagulated lymph and also pus were
found upon the brain and spinal marrow. For example, during the winter
of 1861-62, in the army, that then lay near Washington, D.C., a
soldier was attacked with a chill, severe fever, and headache,
followed by opisthotonos and repeated convulsions before his death,
which occurred in about twenty-four hours. No eruption or
discoloration of the skin is mentioned in the history. On examination
there was found beneath the arachnoid a thin layer of lymph and
abundant exudation over the posterior lobes of the cerebrum, and also
at the base of the brain and on the medulla oblongata.[50] In a case
reported by Gordon[51] the entire duration of the illness was under
five hours, and after death the cerebral arachnoid was more or less
opaque, and in some spots had a layer of very thin purulent matter
beneath it. And, again, not only may the symptoms belonging to
blood-dissolution be consistent with a certain prolongation of life,
but also with decidedly inflammatory tissue-changes. Thus, in another
case of Gordon's the duration of the illness was at least six days,
and the patient presented all the characteristic symptoms of the
disease, including "a most wonderful and uniform curve of the spine
and head backward," "spots black as ink," "bullae which rapidly became
opaque and dusky," "herpetic eruption, etc." After death the body had
a very frightful appearance. It was still prominently arched forward.
It was of a dusky blue color, with a copious eruption of black spots
of various sizes, and one or two of them were gangrenous.... When the
theca vertebralis was opened purulent matter flowed out, and a
purulent effusion was found in patches on the brain. {823} The
cerebral arachnoid was all opaque, the lateral ventricles were filled
with serum, and the blood in all the cavities was very fluid and dark
colored. From all that precedes, therefore, it must be inferred that
the nature of the lesions in this disease depends not on the type
alone, nor on the duration merely, of the attack--that a very brief
course is compatible with marked inflammatory lesions, and a prolonged
one with profound alterations in the condition of the blood. In other
words, it seems that there must be something besides the appreciable
lesions that influences, if it does not determine, the issue of an
attack of this affection. While bringing forward prominently this
proposition, and the facts on which it rests, we have no intention of
under-estimating the relative significance of the two most conspicuous
types of the disease, the purely inflammatory and the adynamic, or
calling in question the fact that the evolution of the former is most
usually comparatively slow and regular, and of the latter rapid and
irregular. In the one, when death takes place early, congestive
changes are found, and when later these have merged into exudative
lesions; in the other or adynamic cases congestion and liquid
transudation prevail, and the results of complete inflammation are
seldom seen. When the disease has been very much prolonged the
exudation becomes tough, adherent, and shrivelled.
[Footnote 49: Davis, _Richmond Med. Jour._, June, 1872, p. 709.]
[Footnote 50: Frothingham, _Amer. Med. Times_, Apr., 1864, p. 207.]
[Footnote 51: _Dublin Quart. Jour._, May, 1867, p. 409.]
The brain-tissue has generally been found softer than natural, and,
although in some cases this diminished consistence might be attributed
to post-mortem changes, yet on the whole it must be associated with
the inflammatory lesions of the meninges. As a rule, it is greater the
longer the attack has lasted, and is by no means equally diffused, but
is more marked where the meningeal alterations are greatest. Ames
found softening in nine out of eleven cases, and chiefly in the
cortical substance, but also in the fornix and septum lucidum; and
Chauffard states that in protracted cases "the interior surface of the
ventricles, the fornix, and septum lucidum, were reduced to a
pultaceous and creamy consistence." But it is by no means true that
softening is met with in all cases of long duration.
The lesions of the spinal marrow and its membranes correspond with
those of the brain. The dura mater is often very dark, its
blood-vessels engorged, its arachnoid cavity distended with serum more
or less bloody, turbid, or purulent. Two ounces of pus have been
removed from it through a puncture. Fibrinous and purulent exudation
fills the meshes of the pia mater, and is usually most abundant in the
cervical and dorsal portions, and generally upon the posterior rather
than upon the anterior surface of the organ; but sometimes large
accumulations of lymph and pus are found at the lower end of the cord.
Gordon[52] relates of a case that "when an opening was made into the
lower part of the theca vertebralis purulent matter flowed out, and
the entire surface of the pia mater was covered with a coating of thin
purulent matter, which, like a thin layer of butter, remained adherent
to it." Occasionally the cavity of the spinal arachnoid contains
blood. Softening of the spinal cord has been often noticed. Chauffard
states that in some cases of particularly long duration it was reduced
to a mere pulp, and he adds, "in the place of portions of the spinal
marrow, completely destroyed, was found only a yellowish liquid, or
the empty membranes fell into contact where it was {824} wanting."
Similar disorganization has been described by Ames, Klebs, and others.
Fronmuller reports the case of a girl aged fourteen years in whom the
central canal of the spinal cord was distended with pure pus.
[Footnote 52: _Dublin Quart. Jour._, xliii. 414.]
The lesions of the internal auditory apparatus consist of softening in
the fourth ventricle and of the root of the auditory nerve, yet such
lesions are said to have been found even when no defect of hearing had
existed. In other cases in which deafness did occur the lesions
consisted of inflammatory changes in the cavity of the tympanum and
suppuration of the labyrinth. They probably arose from an extension of
inflammation from the pia mater along the trunk of the auditory nerve
(Von Ziemssen). In like manner, the inflammatory and destructive
changes in the eye which have been elsewhere described arise from an
analogous cause affecting the optic nerves.
It is unnecessary to dwell upon the condition in which other organs
are found after death from epidemic meningitis. In cases that present
a typhoid type, and even in such as are rapidly fatal with ecchymotic
discoloration of the skin, the various organs present no distinctive
tissue-change, but only such engorgement as is common to all diseases
of a similar type. It deserves to be particularly mentioned that in
this affection the spleen is not enlarged, as it always is in a
greater or less degree in diseases whose primary stage involves an
altered condition of the blood. This fact becomes all the more
important in view of the remarkable contrast which the constitution of
the blood presents in epidemic meningitis and in various typhous
affections.
The state of the blood in this disease is one of peculiar interest,
dominating as it does its whole pathology and determining its
nosological position. It is the blood of a phlegmasia rather than of a
pyrexia. This fact was early established by American physicians who
observed the disease, and the opportunities for doing so were not
wanting, since venesection was used by every one who treated it. In
1807-09 a rapidly fatal case or two was found in which the "blood was
darker and had a larger proportion of serum than usual," but in others
"it did not present any uncommon appearance, and no inflammatory buff,
nor was it dissolved" (Fish). In 1811, Arnell stated that "the blood
drawn in the early stage appeared like that of a person in full
health; there was no unusual buffy coat, neither was the crassamentum
broken down or destroyed." In the epidemic studied by Mannkopff (1866)
he found that blood obtained by venesection gave a clot with a thick
buffy coat. Andral, seeking to establish the law that in every acute
inflammation there is an increase in the fibrin of the blood, remarks
that in a case of cerebro-spinal meningitis it was very marked.[53]
Ames states that "the blood taken from the arm and by cups from the
back of the neck" "coagulated with great rapidity." "Its color was
generally bright--in a few cases nearly approaching to that of
arterial blood; it was seldom buffed; in thirty-seven cases in which
its appearance was noted it was buffed in only four." Analyses were
made in four cases, "the blood being taken early in the disease from
the arm, and was the first bleeding in each case. They furnished the
following results: {825}
Fibrin. Corpuscles.
I 6.40 140.29
II 5.20 112.79
III 3.64 123.45
IV 4.56 129.50
The first was from a laboring man thirty-five years old; the second
from a boy twelve years old, while comatose; and the two others from
stout women between thirty and thirty-five."[54] Tourdes, whose
analyses follow, states that "blood drawn from a vein was rarely
buffed; if a buffy coat existed, it was thin, and generally a mere
iridization upon the surface of the clot."[55]
Fibrin. Corpuscles.
I 4.60 134.00
II 3.90 135.54
III 3.70 143.00
IV 5.63 137.84
Maillot gives, as the result of an analysis of six cases, an increase
of fibrin to six parts and more in a thousand. This summary
represents, as far as is known, all of the analyses of blood taken
from living patients in this disease, and it shows that in every case
the proportion of fibrin exceeded that of healthy blood, and
corresponded exactly to that observed in the blood of inflammatory
diseases, while the proportion of red corpuscles varied within the
normal limits. How different is this condition of the blood from that
of typhus fever, in which there is a marked diminution of fibrin, and
a falling off in the red corpuscles as well, or from that of typhoid
fever, in which neither element declines until the disease affects the
body by inanition! (Murchison).
[Footnote 53: _Path. Haematology_, p. 73.]
[Footnote 54: _New Orleans Med. and Surg. Jour._, Nov., 1848.]
[Footnote 55: _Epidemie de Strasbourg_, p. 160.]
* * * * *
In regard to the condition of the blood after death the historians of
the disease are not so well agreed; nevertheless, the preponderance of
the testimony is in favor of the statement that the blood presents
appearances resembling those belonging to the continued fevers rather
than to the inflammations. It is true that even in this the agreement
is neither general nor complete. Tourdes, for example, states that in
an autopsy "the blood was remarkable for the abundance and toughness
of the fibrinous clots," but the greater number have reported it as
being dark and liquid. Such was its condition in the epidemic which we
studied at the Philadelphia Hospital in 1866-67, and it has been
correctly described by Dr. Githens as follows: "The blood was fluid,
of the color and appearance of port-wine lees; under the microscope
the corpuscles were shrivelled and crenated, and there was a space
apparent between them as they were arranged in rouleaux. There were in
two cases white, firm, fibrinous heart-clots extending through both
ventricles and auricles and into the vessels leading to and from the
heart."[56] It may be added that the red corpuscles are often crenated
and shrivelled when the case has been protracted, and it has been
stated--from limited observation, indeed--that "the white corpuscles
are three times more numerous than the red."[57] The blood has been
scrutinized to discover, if possible, some of those bodies which are
judged by Koch and his disciples to differentiate {826} general
diseases, but it is stated that the investigation has been without
definite result.[58]
[Footnote 56: _Amer. Jour. of Med. Sci._, July, 1867, p. 23.]
[Footnote 57: _Dublin Quart. Jour._, May, 1867, p. 441.]
[Footnote 58: Jaffe, _Phila. Med. Times_, xii. 599.]
It does not seem difficult to reconcile the conflicting statements now
given of the condition of the blood in epidemic meningitis. One of
them points to an excess and the other to a loss of the spontaneously
coagulable element of the blood. It is evident that venesection, which
was necessary for procuring the living blood for analysis, would only
be performed when the type of the disease authorized it--that is, when
the type was sthenic; whereas the blood examined after death had
necessarily undergone changes which tended to, if they did not
actually, occasion death. Hence we find among the former cases, when
fatal, the most extensive and massive exudation, and always among the
latter less evidence of inflammation, but, on the other hand, a
greater or less manifestation of those appearances which denote a loss
of the vitality and organization of the blood. In the one case death
may fairly be attributed, above all other causes, to the pressure
upon, and the disorganization of, the cerebro-spinal organs essential
to life; in the other, primarily, to the death of the vital elements
of the blood produced by the specific cause of the disease. It is
probable that the post-mortem fluidity of the blood exists under two
conditions. In the one the morbid cause is powerful enough from the
very commencement rapidly to destroy the life of that fluid, and in
the other it acts less violently, but continuously, to exhaust the
powers of life.
Our conception of the pathology of epidemic meningitis is implicitly
contained in the foregoing discussion. Of its essential cause and of
the conditions that call it into existence nothing whatever is known.
The disease is most probably due to some atmospheric agency that is
capable of acting at the same time upon widely separated localities.
Its specific cause appears to enter the blood first of all, and
doubtless through the lungs, and to be capable of destroying life by
its action upon the blood alone. Failing this effect, its force is
spent upon the cerebro-spinal pia mater, and it may become fatal by
the mechanical interference of the products of inflammation with the
nutrition of those parts of the central nervous system which are
essential to life. An inflammatory and a septic element together
constitute the fully-developed disease; either may be in excess and
overshadow the other. According to the relative predominance of one or
the other, the disease assumes more of a typhoid or more of an
inflammatory type, and it is doubtless this diversity in its
physiognomy, as well as in the lesions that attend it, which has led
to the most opposite doctrines respecting its nature and its
nosological affinities.
DIAGNOSIS.--The most distinctive phenomena of epidemic meningitis are
suddenness of attack and rapidity of development of the following
symptoms: acute pain in the head, neck, spine, and limbs; faintness,
vomiting; stiffness or spasm of the cervical or spinal muscles;
hyperaesthesia of the skin; delirium, alternating with intelligence
and merging afterward into dulness or coma; occasional convulsive
spasms; paralysis of the face or of one side of the body. The
evidences of associated blood-poisoning are, the epidemic prevalence
of the disease, various eruptions upon the skin (herpes, roseola,
petechiae, etc.), ecchymoses, debility out of proportion to the
evidences of local disease, redness of the eyes, {827} foulness of the
tongue and mouth, and more or less of the other conditions which
characterize the typhoid state. To these features must be added the
rate of mortality, which is greater in most epidemics of meningitis
than that of any disease with which it is liable to be confounded.
It is distinguished from sporadic meningitis by the fact that the
latter disease is never primary, but is always either an epiphenomenon
of some other and previous malady (various fevers and chronic blood
diseases) or is traumatic in its origin. The thermometer readily
distinguishes it from various functional nervous affections, chiefly
hysterical, in which the temperature remains normal.
From typhoid fever it differs as widely as possible by its rapid
onset, the exquisite pain in the head, the neuralgic pains, the
opisthotonos, and the convulsions. The alternate delirium or coma and
clearness of mind in meningitis contrast with the persistent hebetude,
stupor, or muttering delirium and the muscular relaxation in typhoid
fever. The sordes on the tongue, the diarrhoea, the meteorism, the
intestinal hemorrhage of the latter, instead of the moist or merely
dry tongue and the transient vomiting and torpid bowels of the former;
high or continuous fever on the one hand, slight or variable increase
of temperature on the other; diffluence of blood in the one and an
increase in the proportion of its fibrin in the other; in the one
suppurative inflammation of the cerebro-spinal meninges, in the other
specific lesions of the intestinal and mesenteric glands,--these, as
well as the very different modes of origin of the two affections, draw
a broad and manifest line of distinction between them.
It would scarcely be necessary to point out the contrasts between
epidemic meningitis and typhus fever were it not that, notwithstanding
the abundance of instruction on the subject in medical treatises and
lectures, a large number of physicians confound typhus fever, typhoid
fever, and the typhoid state of inflammatory diseases with one
another. The confusion was intensified at one time by designating the
disease we are studying as spotted fever--a term originally applied
and properly belonging to typhus fever (typhus petechialis). It is
true that New England physicians soon became aware of their error,
which was distinctly pointed out and condemned by North, Strong,
Miner, Foot, Fish, and others in the early part of this century. A
similar error was at first committed both in Ireland and England, but
was corrected by maturer experience. In order to contrast the two
diseases as strongly as possible, we place their distinctive features
side by side in the following table:
EPIDEMIC MENINGITIS. | TYPHUS FEVER.
|
A pandemic disease. Occurs | An endemic disease, due to local
simultaneously in places remote | causes and spreading by
from one another and without | intercommunication.
intercommunication. |
|
Attacks all classes of society. | Attacks the poor, filthy, and
Is never primarily developed by | crowded alone.
destitution, squalor, or |
defective ventilation. |
|
Is not contagious. | Contagious in a high degree.
|
Attacks more males than females.| Both sexes equally affected.
|
Attacks more young persons than | More adults than young persons.
adults. |
|
Generally occurs in winter. | Epidemics irrespective of season.
|
Eruptions are absent in at least| Eruption rarely absent, and
half of the cases; they occur | appears about the fifth day.
within the first day or two. | {828}
|
The eruptions are various; they | Eruption always roseolous, and
include erythema, roseola, | then petechial. Ecchymoses are
urticaria, herpes, etc. | rare.
Ecchymoses are common. |
|
Headache is acute, agonizing, | Headache dull and heavy.
tensive. |
|
Delirium often absent; often | Delirium rarely absent; usually
hysterical, sometimes vivacious,| muttering. Rarely begins before
sometimes maniacal. Generally | the end of the first week.
begins on the first or second |
day. |
|
Pulse very often not above the | A slow pulse exceedingly rare.
natural rate; often | Its rate usually between 90 and
preternaturally frequent or | 120.
infrequent. Is subject to sudden|
and great variations. |
|
"The temperature is lower than | The temperature is always
that recorded in any other | elevated, and does not fall until
typhoid or inflammatory | the close of the attack. "The
disease." It is also very | skin is hot, burning, and pungent
fluctuating. | to the feel."
|
The body has no peculiar smell. | The mouse-like smell is
| characteristic.
|
The tongue is generally moist | The tongue is generally dry,
and soft, and if dry is not | hard, and brown, and the teeth
foul. Sordes on teeth rare. | and gums fuliginous.
|
Vomiting is an almost constant | Vomiting is rare and not urgent.
and urgent symptom, especially |
in the first stage. |
|
Pains in the spine and limbs of | The pains, if any, are dull, and
a sharp and lancinating | apparently muscular.
character are usual. |
|
Tetanic spasms occur in a large | Tetanic spasms are unknown in
proportion of cases and within | typhus. Convulsions sometimes
the first two or three days. | occur, due to pyaemia.
They are due to an exudation on |
the medulla oblongata and |
spinalis. |
|
Cutaneous hyperaesthesia is a | The sensibility of the skin is
prominent symptom. | generally blunted.
|
Strabismus is common. | Strabismus is rare.
|
The eyes, if injected, have a | The blood in the conjunctival
light red or pinkish color. | vessels is dark.
|
The pupils are often variable | The pupils are equal and
and unequal. | contracted.
|
Deafness and blindness are often| Deafness almost always ceases
complete and permanent. | with convalescence. Blindness
| never follows typhus.
|
Duration very indefinite, but | Duration from twelve to fourteen
generally from four to seven | days.
days. |
|
Relapses are common. | Relapses are rare.
|
The blood is often fibrinous. | The blood is never fibrinous.
|
The lesions, except in the most | In typhus no inflammatory lesions
rapid cases, consist of a | exist.
plastic or purulent exudation in|
the meshes of the cerebro-spinal|
pia mater. |
|
Mortality from 20 to 75 per | Mortality from 8 to 40 per cent.
cent. |
PROGNOSIS.--In the section relating to the mortality of epidemic
meningitis it has been seen that its death-rate varies at different
times and places between widely remote extremes. This fact must be
borne in mind in estimating the influence of various circumstances in
controlling the issue of the disease. The relative as well as the
aggregate mortality is far greater in childhood than in adult life.
After the age of thirty or thirty-five it decreases rapidly until old
age, when recovery from the disease is quite exceptional. A sudden or
rapidly developed attack is generally unfavorable, especially when the
symptoms are adynamic and there is a purplish discoloration of the
skin. Indeed, even apart from evidences {829} of blood-change,
cerebral are, on the whole, of graver importance than spinal
phenomena, and the more so the more typhoidal their type. Of still
more serious significance is a want of perception of the gravity of
the situation or unconcern about its issue. A preternaturally slow and
compressible pulse implies danger, and so does coolness of the skin,
especially if it grows purplish from a diffusion of blood beneath it
or even from venous stasis. The various eruptions that have been
described including petechiae, are not necessarily dangerous signs.
Profuse sweats during a soporose state, bullae and gangrenous spots,
obstruction of the bronchia with mucus or serum, pneumonia or
pericarditis,--these are all grave indications. So, too, are a dry,
fissured, shrivelled, and pale tongue or a fuliginous state of the
mouth, swelling of the parotids, obstinate vomiting, and profuse
diarrhoea at an advanced stage of the disease. Among the most
unfavorable nervous symptoms are great restlessness, rigid retraction
of the head, spasms of other than the spinal muscles, general
convulsions, extensive hyperaesthesia, deep coma, dilatation and
insensibility of the pupils or their rapid change from a dilated to a
contracted state, retention or incontinence of urine, and all cerebral
paralyses, including that of the muscles of deglutition. The favorable
indications comprise a general mildness of the symptoms, a moderate
loss of strength, a slight degree of pain and muscular stiffness, the
absence of petechiae or vibices (although in many grave epidemics they
are of rare occurrence), a desire for food and the ability to digest
it. Yet it is imprudent to make an absolute prognosis in any grave
case of this disease. Recovery has sometimes occurred when it appeared
impossible, and some have died when the period of danger seemed to
have passed on the sudden accession of cerebral or spinal nervous
symptoms.
TREATMENT.--The difficulties that attend the solution of therapeutical
questions regarding diseases which are comparatively regular in their
evolution, and are produced by definite causes acting in an
intelligible manner, are very numerous and often insuperable. They
become multiplied in relation to a disease which, like this one,
stands alone in many respects; whose causes, phenomena, and
lesions--in a word, whose laws--are specific; and whose varieties of
type are as numerous as can be formed by the combination, in a
constantly varying proportion, of a special (hypothetical) alteration
of the blood, deranging the molecular actions of the economy, and at
the same time of an inflammation of the cerebro-spinal meninges, and
even of the substance of the great nervous centres. These reasons are
sufficient to account for the diverse and often opposite methods of
treatment that have been applied to the disease. As in almost all
other cases, the methods have consisted in using remedies to
counteract certain symptoms--now a stimulant or tonic regimen to
combat the debility which conferred the name of "sinking typhus" on
the disease; now an antiphlogistic course to allay the inflammation of
the brain and spinal marrow denoted by the neuralgic pain and the
tetanoid phenomena; and, again, large doses of narcotics to blunt the
pain and subdue the spasm. Still other medications have been used with
a similar purpose, and some, as we shall see, with more or less
theoretical views. It may be said, with Von Ziemssen, "that we are far
from having it in our power to decide whether a rational treatment of
the symptoms has cured the disease or lessened its mortality;" but a
review of the methods {830} that have been employed and their results
leads to no doubtful conclusion that some are mischievous and others
more or less salutary.
Emetics were among the first medicines used in the treatment of this
affection, and were probably suggested by the vomiting which is one of
its most constant initial symptoms. But we can readily understand why
they failed to afford relief. The vomiting and retching are not
gastric symptoms at all, but, as already stated, are due to the
irritation of the congestive or inflammatory process at the base of
the brain. These medicines may therefore be omitted. The employment of
purgatives is even less rational; they debilitate without affording
any relief.
Venesection was probably employed as a part of a routine treatment
which neither sound reason nor clinical experience justified. It was
generally found to fail of its curative purpose, and often induced,
especially in young persons, dangerous exhaustion. No better
illustration is needed to show that the disease we have been studying
is far more than a local inflammation of the cerebro-spinal meninges.
On the other hand, local depletion is often of marked utility. Our own
experience would lead us to conclude that in the more sthenic cases
scarified cups, applied to the nape of the neck and along the cervical
vertebrae, are of essential service in mitigating--and generally,
indeed, in wholly removing--the neuralgic pains which form so
prominent and severe a symptom in many cases of this disease. When any
abstraction of blood appears to be contraindicated by the patient's
debility, even dry cups will afford him signal relief. Leeches have
been applied to the parts mentioned, and over the mastoid processes
have sometimes been used with advantage, but their depletory surpasses
their revulsive action, and is, so far, injurious. Cold to the head
and spine is among the most efficient means of relieving certain
symptoms. In the Massachusetts Medical Society's Report of 1810 we
read: "Cold water, snow, and ice have been applied to the head when
there was violent pain in that part with heat and flushed face, and
when there was violent delirium. They afforded great comfort to the
patient, and mitigated or removed those important symptoms." It is
probable, however, that the value of the remedy is almost entirely
restricted to the forming--or at least the early--stage of the attack,
when the pain in the head is most intense. Its soothing influence is
then very marked, as well as its indirect action in promoting sleep.
Heat of head is not an essential condition for its use, for even in
the most violent cases it is rarely extreme, and is often entirely
wanting. Pain calls more distinctly for the application, and when that
symptom has subsided cold is apt to be more annoying than grateful to
the patient. Cold is best applied to the head in the form of pounded
ice enclosed in a bladder or rubber bag; but cold affusions are also
very valuable, especially for children. For the application of cold to
the spine the most efficient apparatus is the long, flat rubber bag,
either single or double.
From the earliest history of epidemic meningitis in this country
blisters formed a conspicuous element in the treatment. They were
used, as they had been in other forms of meningitis, to relieve the
pain and diminish the congestion in the cerebro-spinal centres. The
results of their use were by no means uniform, for not only were they
employed in many of the cases which must almost necessarily have been
fatal before inflammation could be established, but even in the
inflammatory cases {831} they were often applied when time enough had
elapsed to allow the exudation to be fully formed, and when,
therefore, they were too late to be useful. Again, they were sometimes
used so as to vesicate too deeply, and thus by the pain they caused at
first, and by the exhaustion that resulted from the excessive
discharges they maintained, the patient was more injured than
benefited. Our own experience proves that in the early stage of the
inflammatory form of the disease blisters applied below the occipital
ridge and upon the back of the neck, and only allowed to vesicate
superficially, not only remove the pain in the head, but diminish the
delirium, spasms, and coma, and therefore contribute as directly as
other remedies, if not more so, to the favorable issue of the attack.
But such salutary effects are not to be looked for when the disease
assumes a malignant type nor after its constitution has become
definitely fixed. The application of stimulant and even vesicating
agents to the spine below the neck has not been generally practised
because, probably, the seat of the spinal lesions was known to be
chiefly at the upper part of the organ. Still, the neuralgic pains
felt in the spinal nerves may be mitigated by stimulant and anodyne
liniments applied with friction to the spinal column.
American physicians early recognized coolness of the skin among the
most striking phenomena of the disease; and this probably suggested
their use of diaphoretic remedies, among which were the external
application of moist heat in baths and warm wrappings, as well as
"bottles of hot water or billets of wood heated in boiling water and
wrapped in flannel," or the patient "was wrapped in flannel wrung out
of boiling water, sinapisms were applied to the feet, while hot
infusions were administered, made from the leaves of mint, pennyroyal,
and other similar plants, and also wine-whey, wine and water, wine,
brandy, and other ardent spirits more or less diluted, camphor,
sulphuric ether, and opium. It was not generally thought useful to
excite profuse sweating, but important to maintain the activity of the
skin from twenty to forty hours, and even longer in some instances.
Soup and cordials were at the same time administered. Under this
treatment most commonly the violent symptoms, and not very rarely all
the appearances of disease, have subsided" (Jackson). Beyond all
doubt, this method was a rational one, for it tended to promote an
elimination of the morbid poison, while it depleted the blood-vessels
and acted revulsively upon the local inflammation of the
cerebro-spinal meninges. Yet it seems not to have been revived during
the more recent epidemics of the disease, unless, partially, by Gordon
(1867), who says: "What I have seen most useful in the stage of
collapse is external warmth applied to the entire surface by means of
flannel bags containing roasted salt, applied along the spine, along
the chest, inside the arms, and to the feet and legs and between
them."
Except typhus fever, there is no disease in which a due administration
of alcoholic stimulants may become more important. In cases of the
inflammatory type they are rarely needful, and are frequently hurtful,
but in those which exhibit signs of blood disorder with nervous
exhaustion they are often indispensable. Nothing demonstrates their
necessity more clearly than the extraordinary tolerance of alcohol
exhibited in some cases of the disease. Among the earlier American
authorities may be found many illustrations of this statement.
Woodward (1808) {832} observed that very large quantities of wine or
ardent spirits may be given without injury. Arnell said: "In some
cases I have given a quart of brandy in six or eight hours with the
happiest effect." Haskell maintained that "the bold and liberal use of
diffusible stimuli is the only safe and efficacious mode of
treatment." In Ireland the habitual use of alcohol in the treatment of
typhus fever no doubt suggested its liberal employment in this
disease, but such stimulants have never been in vogue among the
physicians of France or Germany. This difference may in part be
accounted for by the generally asthenic type of the disease in the
first-named country and its more inflammatory character in the others.
Similar contrasts of type mark different epidemics, and individual
cases during the same epidemic. We have no doubt that while these
agents are indispensable in the treatment of cases of the former type,
they must even then be exhibited discreetly, for their too lavish
exhibition entails the gravest peril by intoxicating the patients and
oppressing instead of arousing their vital energies. In 1866, on
taking charge of the medical wards in the Philadelphia Hospital, we
found that the patients were using as large quantities of alcohol as
are given in typhus fever, but a very short period of observation
showed that this use of the stimulant was excessive; consequently the
dose of it was first reduced, and finally it was omitted altogether
unless special indications for it arose. This change was followed by a
manifest improvement in the general aspect of the sick and the
subsidence of symptoms which, it then became evident, were due to a
lavish use of stimulants rather than to the gravity of the disease.
Alcohol is no more essential to the treatment of epidemic meningitis
than of any other acute affection; it is a cordial to be held in
reserve to meet those signs of failure of the heart and nervous system
which may arise in all acute diseases attended with changes in the
condition of the blood.
The use of opium in the treatment of this disease was strongly
advocated by nearly all of the early American writers upon the
subject, and by many of them enormous doses were given. It was
observed not to produce narcotic effects in ordinary doses. In one
case, marked by excruciating pain in the head and maniacal delirium,
sixty drops of laudanum were given every hour until nearly half an
ounce had been taken within eight hours (Strong). Haskell states: "We
have been obliged frequently to exhibit ten grains of opium for a dose
in some of the violent cases attended with strong spasms, and have
never known it to produce stupor in a single instance." Miner relates
that "a few cases imperiously required half an ounce of the tincture
of opium in an hour, or half a drachm [of opium] in substance in the
course of twelve hours, before the urgent symptoms could be
controlled, and even some cases required a drachm in the same time.
All these patients recovered." In Europe, Chauffard administered opium
in doses of from three to fifteen grains, and Boudin frequently
prescribed from seven to fifteen grains at a single dose at the
commencement of the attack, and subsequently one or two grains every
half hour, until the patient grew sleepy or his symptoms subsided.
This tolerance of the drug is remarkable, and so is the fact that it
does not cause constipation. These and many similar statements agree
entirely with our personal experience. We were in the habit, during
the epidemic above referred to, of prescribing one grain {833} of
opium every hour in very severe and every two hours in moderately
severe cases, and in no instance was narcotism induced, or even an
approach to that condition. Under the influence of the medicine the
pain and spasm subsided, the skin grew warmer and the pulse fuller,
and the entire condition of the patient more hopeful. It seemed
probable, however, that the benefit of the opium treatment was most
decided in the early stages of the attack, and hence in those in which
the inflammatory and spasmodic elements predominated. The hypodermic
injection of morphia is to be preferred before the internal
administration of other preparations of opium, not only on account of
its prompter action, but because it avoids the rejection of the
medicine by vomiting. On the whole, Von Ziemssen is within the bounds
of truth when he says, "Beyond all doubt morphia may be considered the
most indispensable medicine in the treatment of epidemic meningitis."
There is no evidence sufficient to show that epidemic meningitis has
ever been cured by quinia alone. In the early prevalence of the
disease it was treated by large doses of cinchona, but unavailingly,
and subsequently smaller doses were given during the convalescence, as
it was in that of other acute diseases. In some parts of this country
where miasmatic diseases prevail, and epidemic meningitis, like all
other acute, and especially febrile, disorders, displayed more or less
of a periodical or paroxysmal type, quinia was used in large doses,
but the expected result was not realized. Upham states that in some
instances it was given to the extent of sixty, or even eighty, grains
within twelve hours from the beginning of the attack, but without
effect. In Europe it was extensively tried and unanimously condemned.
It may very properly be left out of the list of medicines suitable for
this disease, particularly since it is no longer probable that any
physician would be rash enough to employ it in the so-called
antipyretic doses with or without their usual associates, cold baths.
According to Karl Jaffe, the medicinal antipyretics (quinia, salicylic
acid, and also sodium benzoate) may be entirely discarded, because
they ruin the already weakened digestion.[59]
[Footnote 59: _Phila. Med. Times_, xii. 600.]
Common sense has also proved stronger than theory in excluding
mercurials from the treatment of epidemic meningitis. At one time they
were extensively used, especially when it was learned that the disease
in its full development included a paramount inflammatory element. But
it was soon found that the results of their use were far from uniform,
and farther still from being demonstrably beneficial. In this, as in
many other similar cases, it is quite impossible to reach a definite
judgment unless it were known what was the type of the cases in which
the medicine was given, whether they were asthenic or inflammatory,
and again whether it was used during the active or during the
declining stage and toward convalescence. In the absence of any
trustworthy testimony upon the subject it is only possible at present
to state that in the treatment of this disease mercurials should not
be used. This conclusion is all the more imperative because the
medicine is not an indifferent one. If it is not necessary--and it
certainly is not--it is too dangerous in its immediate and ultimate
effects for its employment to be warranted.
Since belladonna and ergot were shown to diminish vascular action in
the cerebro-spinal axis by contracting its capillary blood-vessels,
they have {834} been put forward as having a specific virtue in this
disease. If the fact be so, how is that other fact--a clinical one,
moreover--to be disposed of, which is that opium, the physiological
antagonist of belladonna and ergot, is more efficient than they are in
curing the disease? It is possible, indeed, that they may have that
curative power, and that opium possesses it also, and that the
explanation given of the action of all of these agents is erroneous.
Upham states that, in 1863, Haddock recommended ergot upon theoretical
grounds, and that during an epidemic at Newbern, N.C., several cases
treated by it recovered. Three cases recovered in which it was
prescribed by Borland. Read used it in 1873-74 at Boston, Mass., and
out of 19 cases 16 recovered and 3 died.[60] This mortality of about
15 per cent. is not more than half of that which has generally been
met with, and if it can be attributed to the treatment would go far to
prove the efficacy of the latter. One grain of ergotine, with
one-tenth of a grain of extract of belladonna, was administered every
three hours. Considering the exiguity of the dose of belladonna, it is
not surprising that, except in one case, it did not dilate the pupil;
and the dose of ergotine is likewise far smaller than the average
medicinal dose of that preparation. Moreover, all of the cases except
the fatal ones appear to have presented the disease in a subacute, and
certainly not in an aggravated, form.
[Footnote 60: _Philadelphia Med. and Surg. Reporter_, Jan., 1875, p.
68.]
In 1872, Dr. S. N. Davis,[61] moved by the success of Calabar bean in
tetanus, employed it in this disease. A mixture of one ounce of
tincture of Calabar bean with one and a half ounces of fluid extract
of ergot was administered in doses of half a teaspoonful every two
hours, and with better results than had followed other remedies. Here,
again, it is to be noticed that the analogy suggesting the use of
physostigma is not a logical one. That drug indeed relieves the spinal
spasms of tetanus--a disease in which there is an irritation of the
spinal axis, but no exudation from its meningeal vessels, as in the
affection we are studying. Moreover, it is a disease of extraordinary
power, as shown not only by the spasms, but by the exceptionally high
temperature, and thus again is in direct contrast to epidemic
meningitis. If, therefore, Calabar bean benefits that disease, it
cannot do so in the manner suggested by the author.
[Footnote 61: _Richmond and Louisville Med. Jour._, xiii. 711.]
Bromide of potassium and hydrate of chloral have also been employed to
allay the spasmodic symptoms; but the former is too feeble for the
purpose, and the depressing action of the latter upon the heart
renders it dangerous. Bromide of potassium has been given to children
of two and five years in doses of four and six grains every two hours;
but these doses appear to be quite too small even for the purpose in
view--viz. to prevent convulsive attacks. Whatever remedies may be
suggested hereafter, none should be employed that tend to reduce the
power of the heart, which, as we have seen, is dangerously depressed
by the disease.
During the decline and convalescence of the affection it is probable
that iodide of potassium may be advantageously used to promote the
removal of the exudation-matter on the brain and spinal marrow, and
probably to prevent the hydrocephalus which sometimes follows the
attack, and is attributable to the pressure of effused lymph upon the
cerebral veins.
DIET.--The mildly febrile character of epidemic meningitis, and the
{835} remarkable debility which characterizes so many cases of the
disease, and which, as was before pointed out, conferred upon it the
name typhus syncopalis, plainly justify what experience has taught,
that appropriate food for the subjects of this affection is at once
the most digestible and nutritious that can be taken. It is true that
this regimen is interfered with by the vomiting, but, as that symptom
is of cerebral and not of gastric origin, it is more apt to be allayed
by suitable food than by abstinence. It has been our custom to observe
in this disease the same rules respecting diet that are recognized as
the most suitable in typhus fever. In doing so, indeed, we did,
without at the time knowing it, follow the example of the early
American physicians. Strong, who wrote in 1811, advised "soup made
from chicken, veal, mutton, and beef, richly seasoned with pepper and
savory herbs." These articles were prescribed by him during the height
of the disease. Later on he says: "The stomach soon begins to crave
something more solid than soup; oysters, beefsteak, cold ham, or
neat's tongue are received with peculiar relish. Often I have seen
convalescents, when they had hardly strength enough to raise
themselves in bed, make a hearty meal of the above-mentioned articles,
which were received with great satisfaction, sat well upon the
stomach, and were well digested and assimilated." This method is
substantially the same that was found successful in the earlier, as it
has been in the later, epidemics in this country, and we have no
hesitation in attributing to it and the appropriate use of opium and
blisters the degree of success we enjoyed in the treatment of the
disease in the Philadelphia Hospital and elsewhere.
During convalescence from epidemic meningitis the patient should
carefully abstain from physical exertion and mental excitement, and
before this state is fully established he should even very cautiously
change his position from a recumbent to an erect posture. And,
finally, he should return to his ordinary occupations, mental or
physical, as late as possible, on account of the danger of a relapse,
which has already been described.
{836}
PERTUSSIS.
BY JOHN M. KEATING, M.D.
HISTORY.--A careful study of this disease from the various writings
since the time of Hippocrates leaves little doubt in the mind of the
reader as to its antiquity, so little indeed has it changed in its
various characteristics. Whether the affection passed to continental
Europe from Africa, or whether its starting-point was India, are
questions difficult to solve, and, except for the medical historian,
of little import. Desruelles probably truthfully asserts that the many
differences which mark the descriptions of the disease, especially by
the early Grecian writers, may be due, not to the non-existence of the
disease as we know it, but to the influence which climate exerted then
as now, and to the unrecognized fact that it is only fatal in its
complications. The writings of Hippocrates, Galen, and Avicenna,
though undoubtedly referring to the many affections in which
paroxysmal cough is a prominent symptom, contain many expressions that
would point clearly to the existence of a specific disease. Dr. Watt
believed that the disease was not known to the Greeks, and other
writers claim that it came from the north and spread southward over
Europe about the sixth century; nevertheless, it first appears on
record as a distinct affection, disentangled from the confused mass
with which it was involved for centuries, about the middle of the
seventeenth century. Steffen mentions the first well-established
accounts as coming from Baillou in the year 1600, and Schenck in 1650,
and Ettmuller in 1685. Sydenham casually mentions it in 1670. Since
the time of Willis the definition of the disease has remained
unaltered, and so accurate was the description then given of it that
we can but naturally conclude that for many centuries at least it has
varied but little.
In studying affections of this kind, occurring in epidemic form
especially, and which are increased in intensity by whatever means the
contagious element, whether gaseous or parasitic, is made more
virulent, much allowance is to be made for the climate, customs, and
habits of the people whence our data are derived. Thus, most of the
diseases of antiquity, the descriptions of which have reached us, have
been drawn from types modified by mild climates where the people have
led an out-door life, and though the disease we see at the present day
is one and the same so far as its causation is concerned, the indoor
life and close confinement, the bad ventilation, and the artificial
existence in our large cities must weaken the individual, intensify
the poison, and exert an influence on the disease.
DEFINITION AND DESCRIPTION.--Whooping cough has been {837}
characterized as an acute contagious affection, occurring usually in
childhood, though it may occur at any age, and lasting several weeks.
It is manifested usually by malaise, catarrh of the respiratory tract,
and subsequently by a convulsive cough occurring in paroxysms, the
peculiarity of which consists of a series of forcible expirations,
followed by a sonorous inspiration or whoop, which may be repeated
several times.
At the beginning of these paroxysms of coughing, there are evidences
of slight laryngeal irritation, attended by an effort at suppressing
the cough; then follow gradually increasing and more audible
inspirations, which become more and more difficult. The child is
agitated, the face becomes pale, and the countenance has a mingled
expression of supplication and fear. If it is old enough it will seize
the nearest object for support. As the spell advances, the eyes become
suffused and prominent and the loose tissue surrounding the orbits
appears puffy and congested. Finally, the paroxysm reaches its height;
the child, with a livid countenance, with veins standing out like
cords, gives a succession of violent expiratory efforts, followed by a
long inspiratory whoop. The same is repeated several times, until
finally almost complete cyanosis takes place; the spasm relaxes, a
glairy, tenacious mucus runs from the mouth, the contents of the
stomach are vomited, and the child falls back exhausted. The lividity
of the countenance is succeeded by a deathly pallor; the face still
appears swollen and puffy beneath the eyes; the tears course down the
cheeks, and frequently hemorrhage occurs from the eyes, nose, ears, or
throat, owing to the terrific strain upon the circulation. As soon as
the child has recovered from the fatigue of the paroxysm all is
apparently over, and were it not for the characteristic expression of
the eye, which is pathognomonic in a well-advanced case, nothing would
be noticed to even suggest the disease when uncomplicated. The voice
is clear; there is little or no elevation of temperature.
The paroxysms which have given the name to this disease can only be
likened to an epileptic convulsion, which by gradually increasing
cyanosis is self-curable, the carbonized blood finally bringing about
an anaesthetic effect. The severity of the paroxysms is by no means in
proportion to the local catarrh, which latter may be superficial and
slight, not to be detected during life by the most careful laryngeal
examinations, and only after death by the aid of the microscope. The
frequency and intensity of the paroxysms are dependent in a measure
upon the degree of excitability of the nervous system, which of course
differs in individuals. It is evident that the success of treatment
must be powerfully influenced by this circumstance, and it is partly
owing to it that there are so many opinions as to the value of
remedies in this disease.
The complications are usually dependent upon outside causes, and have
nothing to do with the poison proper of whooping cough, as far as we
can tell. There are some which depend on an inflammation of the mucous
membrane, which may be limited to any portion of the respiratory tract
or may extend throughout it. Complications may arise from mechanical
obstruction to inspiration by the swollen mucous membrane or from
plugs of tenacious mucus, which may cause pulmonary collapse and favor
the development of catarrhal pneumonia, and later even of phthisis; or
from impediments to free and easy expiration, whether from spasm of
the bronchioles, from forcible compression of the thorax through
reflex {838} nervous irritation, or from other obstructions, all of
which tend to produce emphysema. Disturbances of the circulation, in
the brain or elsewhere, may proceed from thrombi or emboli and give
rise to complications which will render fatal an otherwise mild form
of the disease. The invariable disturbance of nutrition which
accompanies every disease affecting the nervous system is apt to show
itself in the breaking down of products which are simply inflammatory.
Vomiting may be a most serious complication, both from its immediate
and remote effects. It may be due to gastric catarrh, or more
frequently to irritation of the pneumogastric nerve.
ETIOLOGY.--Very numerous theories have been advanced as to the nature
of this interesting disease. Hufeland, Lebenstein, Pinel, Jahn, Todd,
Cullen and a host of others have regarded it as essentially a
neurosis. By many others it has been supposed to be due to a lesion of
the brain or of its membranes, but careful investigation has
established the fact that there is no lesion in whooping cough at all
constant or characteristic. By still others, and especially by Gueneau
de Mussy, it has been regarded as essentially an affection of the
tracheo-bronchial glands, a bronchial adenopathy, causing irritation
of the pneumogastrics and of their bronchial branches by pressure of
the enlarged glands. We have, however, seen many post-mortem
examinations of the bodies of children who have died of measles, where
marked enlargement of these glands was constantly found, but where no
symptoms of whooping cough had been present. There are indeed many
features of the disease which seem inexplicable on any other theory
than that the essential cause of whooping cough is a specific poison,
and such is the view now generally adopted. This poison is capable of
being carried by fomites, though as it is highly infectious it is
often communicated through the atmosphere, and is most frequently
conveyed from individual to individual. Dolan,[1] who has recently
published a very interesting and valuable monograph on this affection,
quotes Linnaeus, who ascribed it to the irritation of insects, as the
author of the modern view that whooping cough is due to the presence
of a peculiar microbe, though it must be conceded that as yet it has
not been discovered. Most observers hold that the contagium is not in
the blood, but that it resides in the secretions of the respiratory
passages, and is most virulent during that stage of the disease when
the secretion is abundant. Letzerich states that he has {839}
succeeded in producing whooping cough in rabbits by inoculating the
trachea with the sputa of the human subject. Dolan obtained similar
results by injecting the nasal secretions, and also by compelling
rabbits to inhale air impregnated with decomposing sputa and vomit of
patients suffering with the disease.
[Footnote 1: Dolan, Thos. M., _Whooping Cough_, London, 1882.
The following brief statement of his conclusions may be quoted as
presenting the most important facts concerning the pathology of the
disease:
1st. Pertussis depends on a specific poison or contagion; this is
universally admitted.
2d. This contagion is active and highly infectious; this is also
granted.
3d. The contagion is analogous to the contagia which produce splenic
fever, measles, scarlatina, variola, etc.
4th. It has a peculiar determination to the lungs.
5th. Like all other contagia, it has its period of activity and
decline.
6th. The period of greatest activity is in the first and second
stages.
7th. Pertussis runs a regular course like measles, scarlatina,
variola, etc., and rarely attacks a person but once.
8th. It may thus be classed among zymotic diseases.
9th. The fact that there is no primary pathognomonic morbid change
supports this view.
10th. There are various secondary lesions which are characteristic, as
ulcerations of the fraenum linguae.
11th. The mode of death harmonizes with this view.]
I do not, however, feel entirely satisfied in adopting the view that
the contagium of whooping cough resides alone in the mucous membranes
of the air-passages.[2] Children have been known to be born with the
disease, the mother having suffered from it some time previous to
confinement. The following case occurred under my own observation:
Mrs. F----, the mother of two children, was in her eighth month of
pregnancy; the two children had at the time a very severe attack of
whooping cough, which required the constant attendance of the mother.
She, though an extremely intelligent woman, belonged to the poorer
classes, and had no one to assist her at this trying time. One day she
complained that the movements of her child in utero had entirely
changed. Suddenly, without any previous motion, the child would become
very active; the force of its movements was such as to make hazardous
any attempt on her part to walk in the street. The suddenness with
which the movement would come on would oblige her to seize the nearest
object for support. This continued until the child was born. Shortly
after labor my attention was called to the infant, which had a curious
attack, it became deeply cyanosed, seemed asphyxiated, as it were, for
a moment, had no convulsions, and within a few seconds resumed its
normal breathing and the circulation seemed once more established. I
saw the child in several of these attacks; its health did not seem to
be impaired, and without treatment, within a few weeks they
disappeared altogether. The mother insisted upon the fact that the
child had whooping cough, and the absence of the characteristic whoop
was the only thing that prevented the diagnosis from being positive.
This would show--and there are enough cases on record to warrant our
basing an opinion upon them--that the contagium of whooping cough is
found not alone in the matters expectorated, notwithstanding the
statement of Dolan and others that their experiments failed to show
its existence in the blood.
[Footnote 2: Colson, _Lancet_, July 2d.]
It must not be forgotten, in reference to cases which seem to have
arisen without any exposure to the specific poison, that the
characteristic whoop is not always present, and that consequently the
true nature of mild cases of the disease which may infect other
individuals may have been overlooked. Childhood probably acts as a
predisposing cause, though the disease occurs at all periods of life,
and as it usually occurs but once in the same individual, it is clear
that the apparent diminution of susceptibility in later years may be
largely due to the fact that most persons have had the disease in
childhood. More children are attacked from one to five years, and the
disease is more prevalent in summer and fall months. Causes which,
like exposure to inclement weather, give rise to irritation of the
bronchial mucous membrane, or diseases which, as measles, are
accompanied with catarrhal symptoms and susceptibility of the
bronchial mucous membrane, also may serve as predisposing causes. Sex
appears to exert some positive influence. Of 360 cases of pertussis by
Dessau,[3] the total number of males were 154, that of females 206.
Girls are more {840} frequently attacked than boys, in proportion of 2
to 1.50; this seems true at all ages; this statement is substantiated
by Unruh of Dresden, based on an analysis of 1952 cases.
[Footnote 3: _N.Y. Jour. of Obst._, 1881, xiv. 490-503.]
SYMPTOMS.--The disease begins usually with an ordinary catarrh,
preceded by malaise and slight laryngeal irritation, which may be
overlooked; in fact, during the first stage there is nothing to
attract special attention, unless a direct history of exposure be
known and suspicion be aroused on that account. Meigs and Pepper state
that the earliest period at which they have known the distinctive
whoop of the disease was three days, though in a great many instances
it was delayed as late as three weeks. The same authors state that the
ordinary duration of a paroxysm or kink is from one-fourth to
three-fourths of a minute. They mention a case where the paroxysm
lasted fifty-five minutes. Ordinarily they number about thirty-five or
forty during the twenty-four hours at the height of the disease,
differing greatly in individuals. Their number is most frequent in the
course of the third or fourth week, after which they remain
stationary, and then gradually decline. The paroxysms may occur
spontaneously, or they may follow some irritation, either direct or
reflex, or they may be induced by nervous excitement. Toward the end
of the attack, after the catarrhal irritation has greatly subsided, or
in fact has entirely disappeared, the paroxysmal kinks may be provoked
by irritation of the fauces, and also by nervous excitement; and there
is no question but that at this time they can be controlled by
will-power. In many cases a distinct relapse occurs after the disease
has been apparently cured.
Dolan believes the phenomena of the cough or kinks to be due, as
suggested by Laennec, to a "spasmodic condition of the muscular or
contractile fibres of the bronchi and their branches." He remarks that
the lungs are supplied from the anterior and posterior pulmonary
plexuses, formed chiefly of branches from the sympathetic and
pneumogastrics. The filaments from these accompany the bronchial tubes
upon which they are lost. Irritation of these nerves is said to have
the effect of producing contractions of the bronchial canals
sufficient to expel a certain quantity of air. If this theory is true,
it helps us in explaining why the large, mediate, and smaller bronchi
are closed during the expiratory stage of the paroxysmal cough of
pertussis. The general opinion seems to be that the pneumogastric
nerve is not inflamed, as has been asserted by some.
The highly sensitive condition of the nervous system, which is
probably in a great measure intensified by the anaemia, and by the
interference with nutrition due to the disturbance of the circulation
by the cough, will show itself in many ways, and even when no
secondary nervous affections complicate the attack or follow it. Some
time will elapse after the disease has passed away before the child
will recover its self-control, or its nutrition will show the
influence of a healthy nervous system. The total duration of the
affection is said to vary from six weeks to three months in ordinary
cases; though probably, if active treatment could be instituted early
enough and kept up with thoroughness, there is no specific disease
more capable of being shortened in its course than the one under
consideration; this remains, however, for future statistics to decide.
During the second stage of the disease the symptoms are sufficiently
{841} marked to attract attention and render a diagnosis easy to make.
Frequently the catarrh seems to extend to the bronchioles, and gives
rise to symptoms that are alarming; and the intensity of the paroxysm
will cause the engorgement of the blood-vessels to get relief in
profuse hemorrhage; this is the period for caution. Complications may
arise, the strength may fail, the secretions may become too abundant,
and asphyxia may ensue; emphysema may show itself, or catarrhal
pneumonia may gradually supervene.
The period of decline is very gradual; the secretions become less in
quantity and more viscid, the paroxysmal cough is less frequent, but
may at times be equally severe, the child's strength is usually
exhausted, and its nutrition is greatly impaired. The expected
paroxysm throws it into a state of intense nervous excitement; it is
sleepless--in fact, worn out. Probably at this period of the disease
treatment will show the most marked results, and the long lists of
sedatives, tonics, etc. which are presented to us by their zealous
advocates owe much of their popularity to their value at this stage of
the disease. The catarrhal symptoms are the first to subside; the
nervous disturbances remain for some time, and gradually fade, and the
constitutional symptoms, or those from exhaustion, are the last to
leave the patient.
Strange as it may seem, the heart appears to suffer but little in the
long run from the great strain upon it; the palpitation and
irregularity of its actions are not followed by structural changes as
a rule, though we may state that feebleness of the circulation has
remained in most of our bad cases for some months after recovery.
As regards the ulceration of the fraenum linguae, which has given rise
to so much discussion as to its exact value as a symptom of this
disease, our own experience leads us to believe that though it is
nearly always present in the severe cases, its almost invariable
absence before dentition and in milder cases shows it to be of
traumatic origin. Roger's exhaustive report before the French Academy
supported this view, and showed how clearly it is caused by the
violent rubbing of the fraenum on the free border of the incisors. On
the other hand, Delthil of Paris and Blake of England believe that it
is a pathological feature of the disease. The former reported cases in
which it occurred before dentition. The ulcer is not always found on
the fraenum linguae, but is found on either side of it. Bouffier noted
severe cases of ulceration in children who had no teeth, but he
attributed it to the injury produced by the mother in detaching the
mucus with the finger.
Examinations of the urine have been carefully made by many observers.
The appearance of sugar, about which so much has been said, does not
seem to be constant, or even very frequent. Out of 50 cases, Dolan
found traces of it in but 13. This coincides with our experience also,
for we have frequently tested the urine in seven cases with negative
results. Since, as is well known, irritation of the pneumogastric
centre may cause glycosuria, it was at one time attempted to show that
the paroxysms in whooping cough were due to congestion of the
pneumogastric nerves, a condition which is said to have been
occasionally found in this disease. Dolan says he has never seen
hemorrhage from the kidneys during the course of whooping cough, nor
blood in the urine.
MORTALITY.--It is an extremely difficult matter to reach, with any
{842} degree of certainty, the true mortality of this affection. Meigs
and Pepper say: "Of the 208 cases observed by ourselves, 143 were
simple, all of which recovered;" and, again, "Some form of
complication occurred in the 65 of the 208 cases observed by
ourselves; of these 65, 12 died." The mortality seems greater under
five years; thus: Of the 9008 deaths attributed to it in the United
States during the census year ending June 1, 1870, the number of
persons under one year of age was 4424, and 8396 were under five
years. There were 1784 deaths from it recorded in Philadelphia from
1860 to 1876; of this number, 1724 were under five years of age. The
census of the United States for 1880 gives a return of 11,102 deaths
from this disease.
Females seem more liable to die of it than males; of the 1784 deaths
in this city, 766 were males and 1018 females. As we have already
seen, females are more liable to the disease than males.
Robt. J. Lee, M.D.,[4] says that from the Registrar-General's report
of 1876 it is seen that in a total mortality in England of 510,315,
whooping cough was returned as the cause of death in 10,554 cases, or
nearly 2 per cent.
[Footnote 4: In a paper in the _British Med. Jour._, 1879, vol. i. p.
307.]
As for the time of year, we quote the following: "Thus, according to
the census statistics, most deaths occur in the spring, there being a
rise up to the middle of May. From the middle of May the number
lessens largely until August, when a rise occurs and continues until
October, when a decline sets in and continues until December, when a
rise begins and goes on increasing until the middle of May. This rise
in mortality from August to October is attributed to the wear and tear
of a hot summer and the intestinal troubles then so prevalent."
The mortality statistics of this disease are uncertain. It is fatal in
its complications or by inducing a debilitated condition which invites
degenerative processes. The severity of the symptoms is no guide for
prognosis as far as uncomplicated cases are concerned, and there is no
doubt but that at present we are able to greatly reduce the
mortality-rate by care and medical treatment, as well as to shorten
the attack. Sporadic cases are apt to be neglected until they become
complicated. When the disease occurs in epidemic form, measles is
often prevalent simultaneously, and in consequence children who become
affected by both diseases have a greater tendency, from debility, to
become the victims of those affections of the respiratory organs which
are such frequent and fatal complications of both maladies.
Instead of surprise at the mortality of this affection, the marvel is
that so large a percentage of recoveries take place, when we consider
that we are dealing with a disease whose lesion is a catarrh of the
air-passages which seldom lasts less than two months, with a tendency
to involve the lungs in one way or another, and then witness the
carelessness with which, among the lower classes, the child is often
treated--exposed to all weathers, under-clothed, under-fed, and
probably allowed to pass through the whole attack without medical
treatment. Taking this into consideration, the probability is that the
mortality of this disease could be reduced to a very small figure by
careful management, even if the investigations of those now seeking
the microbe of pertussis do not lead to any plan, in accordance with
Pasteur's teachings, which will still further lessen the gravity of
the disease. Until {843} then, we can but insist upon a rigid
quarantine of schools, a registration of all cases, and the seclusion
of them, as we have done to-day in the case of variola and scarlatina.
MORBID ANATOMY.--Although whooping cough is a serious disease, the
cause of death is generally found to be dependent upon its
complications, and there is no lesion at all characteristic of it. The
chief complications and sequelae are--bronchitis, which may become
capillary; lobular collapse, which, according to Alderson,[5] is
frequently found; emphysema, usually marginal, probably due, as
suggested by Jenner, to violent expiratory exertions; rupture of
air-vesicles, with subcutaneous emphysema; catarrhal pneumonia,
pleurisy, phthisis, acute tuberculosis, croup, cerebral apoplexy,
meningitis, etc. As any of these complications, and others which may
arise from debility, may be the cause of death, independent of the
action of the specific poison itself, it is usual to divide the
post-mortem appearances into those that are the result of the
extension of the catarrh itself and those produced by the interference
with the circulation and with nutrition from mechanical violence. Of
the former, the usual causes of death are pneumonia, gastritis and
enteritis. Of the latter, we have thrombosis of the cerebral sinuses,
hemorrhages, emphysema, and exhaustion following constant vomiting.
[Footnote 5: _Medico-Chir. Trans._, pp. 90, 91, 1830.]
Tubercular disease of the lungs or of the brain is apt to be a cause
of death. Convulsions carried off 5 of the 12 fatal cases reported out
of 208 by Meigs and Pepper. This may be due to congestion of the
brain, especially in teething children. Spasm of the glottis with
sudden death is occasionally found. In such cases there is found
intense congestion of the brain, also of the liver and kidneys, and at
times of the mucous membrane of the stomach and intestines, as well as
of that of the respiratory tract.
In all cases, especially at the teething age, sudden death may occur
because effusion into the ventricles of the brain or the formation of
heart-clot has taken place. It is important to know this, that active
treatment applied early enough may save the patient.
PROPHYLAXIS.--Should the interesting and seemingly conclusive
statements of Dolan and the microscopic investigations of Carl
Bruger[6] receive the endorsement of future workers, the subject of
prophylaxis will assume a degree of importance which hitherto it has
only maintained with the medical profession. No one has doubted that
the disease was contagious, and yet there is no affection which has
attached to it a corresponding fatality that is so carelessly dealt
with as pertussis.
[Footnote 6: Bruger of Bonn, in the _Berliner klinische Wochen._,
describes at length the special micro-organisms of pertussis. They
appear as small elongated elliptical bodies of unequal length, the
smallest being double as long as broad. High powers show subdivisions
in the largest specimens. They are generally isolated, but may appear
in groups. They bear some resemblance to _Leptothrix buccalis_, the
spores of which are often found in whooping-cough sputa. Occasionally
the bacillus is seen inside the mucous corpuscle in the sputum. They
stain in the usual way, fuschin and methyl violet. This bacillus is
not found in any other kind of sputum, is very abundant in pertussis,
and increases in direct proportion to the severity of the disease.]
Within the past few days we have heard on two occasions in crowded
railway-cars the characteristic paroxysm of the third stage of the
disease, and yet people will endeavor to convince themselves that
unless contact with the child takes place the danger is little.
{844} The atmosphere in school-rooms, railway-cars, and places of
amusement which are badly ventilated, is an excellent medium for the
propagation of the contagious matter, and many extraordinary cases are
on record of momentary exposure being sufficient to contract the
disease. Believing that the contagium or virus resides in the mucus
and air thrown off by the child, and also in the vomited matters,
which contain a large amount of ropy mucus, and also that it gains
entrance by means of the respiratory organs, protection from contagion
divides itself as follows: thorough disinfection of the exhaled air,
of the mucus remaining within the bronchial tubes and air-passages,
and of the clothing, together with exposure to fresh air and thorough
cleansing of all furniture and household utensils, including cups,
silverware, and toys, used by the child. Oxygen is said to have this
effect, and thorough, constant ventilation, with the breathing of
fresh air by the child, the thorough washing of its surface, and
disinfection of its clothing, are the first indications; while the
impregnation of the atmosphere with the spray of well-known germicides
by means of the steam or other atomizer and the frequent inhalation of
such materials by the patient are no less important. Every case of
whooping cough should be compelled to use two or three times daily the
spray impregnated with a substance of this sort, either carbolic acid,
the oil of eucalyptus, a solution of quinia, or thymol. Chlorine (from
chloride of lime) used thus has of late been followed by excellent
results, and the spray of a solution of corrosive sublimate or of
ammonium chloride has been found very useful. The protective treatment
should be applied to those exposed to contagion. Such children should
be guarded from exposure to colds; their diet should be simple and
nourishing, their clothing warm; they should be kept as much as
possible in the open air. The breathing of air impregnated with such
substances as above mentioned will no doubt act upon the virus before
it comes in contact with the mucous membranes so as to be absorbed,
and probably the severity of the attack might be mitigated by
modifying the germ of the disease.
TREATMENT.--As can be readily imagined, a disease which is so
universal, so distressing, and at the same time so obscure in its
pathology, as the one under consideration, would have in its
literature a mass of recommendations for treatment from zealous
advocates, based upon theory or experience, as numerous as the authors
themselves. It would be impossible for us to dwell at length upon all
of these, but we will confine ourselves especially to the
consideration of a few of the most important. It will be convenient to
consider first those remedies which have been used with the view of
relieving the congestion and irritability of the respiratory mucous
membrane and of promoting more free secretion. It will also be
observed that many of these remedies may now be regarded as of value
for destroying the special germ which is thought to be the essential
cause and real virus of pertussis. Allusion has been made above to the
importance of inhalations as a prophylactic for those who have been
exposed to the contagion, as well as for the purpose of rendering the
secretions less contagious; and so too we find that the inhalation of
various substances has received favor with many as a method of
treatment. Thus, hyoscyamus, belladonna, ammonium bromide have been
used. Helenke and Serbaud say that bromide of {845} potassium is best
for inhalation. Letzerich recommended the insufflation of quinia twice
daily, using the quinia muriate with potassium bicarbonate and
gum-arabic. Forchheimer[7] reports 97 cases of whooping cough treated
by the insufflation of the quinia muriate; of the 97 cases, 52 were
females, 45 males--the youngest three weeks, the oldest nine years
old. Five cases gave no results, while in the others benefit was shown
by a shortening or amelioration of the disease. The vapor of benzole
has been used with good results. The vapor of carbolic acid has of
late been highly recommended, either administered with the atomizer
several times daily, or used by saturating flannels in carbolic acid
solution and placed around the child's bed at night. It is said that
the inhalation of the vapor of a few drops of carbolic acid on some
hot coals will ensure a night of freedom from violent coughing.
Probably in this way we may account for the belief that proximity to
gas-works is beneficial to a child with this disease. As is well
known, Niemeyer and others in the north of Germany believed in the
value of the inhalation of oxygen, and the experience of every one who
has had much to do with this disease favors an out-door life. We may
here also mention the value of a small quantity of chloroform or
ether, by inhalation, in allaying the severity of the paroxysms of
cough. We have also tried the nitrate of amyl, but without marked
result.
[Footnote 7: _New York Jour. Obstet._, 1882.]
Others have recommended the use of solutions of various substances,
applied directly by a brush to the interior of the larynx. Quinia has
been used in this way also by Hagenbach; but the most satisfactory
results have been obtained by the application of very weak solutions
of nitrate of silver, as first recommended by Watson in 1849.
After the secretions have been fully established and the
characteristic whoop has appeared, the indications in the treatment
are to relieve the respiratory tract of its burden by occasional
emesis with alum or ipecacuanha, to give freely antispasmodics and
sedatives, as belladonna, chloral, the bromides, hydrobromic acid, or,
as recommended by some, digitalis; to give quinia freely, and to use
counter-irritants to the neck and chest with liniments composed of oil
of amber, croton oil, or turpentine.
The value of emetics has been long recognized in this affection,
although we are told by Vogel that the continuous use of emetics in
the early stage for several days causes harm. Copeland ordered an
emetic every third day in ordinary cases. All writers agree that the
milder emetics should be used by preference; that tartar emetic should
be avoided, except as an external application where a counter-irritant
is desired; and that ipecacuanha is the safest, though alum is also
safe and as an astringent useful. Trousseau preferred the sulphate of
copper. In the earlier stages of the disease emetics are not, as a
rule, indicated; it is only when the secretion has become extremely
tenacious, and the paroxysms so frequent and severe as to greatly
strain the patient and endanger his lungs, that they are of value.
There seems to be a close connection between the amount and tenacity
of the secretion and the severity of the paroxysm. The potassium
carbonate has been recommended as an active agent in the amelioration
of this affection; it is probably valuable in rendering the secretion
less tenacious. Alum has been used with success, as has tannin,
probably owing to their local action on the mucous membrane.
Macartan[8] says that in the East {846} Indies the disease is treated
in the first stages by astringent and tonic gargles.
[Footnote 8: _Dictionnaire des Sciences Med._, 1813, vol. vi.]
Belladonna certainly receives the endorsement of the greatest number
of writers. Vogel considers it superior to all other drugs, and
regards dilatation of the pupil as the only sure guide in its
administration. He says it does not cut short the attack, but
mitigates the paroxysm. Trousseau was also an advocate of this form of
treatment. When combined with alum[9] it is considered by Meigs and
Pepper to be one of the most valuable drugs recommended. They also
advise the use of potassium carbonate. Seiner trusted belladonna more
than any other remedy; so also Rilliet and Barthez. William Lee, in an
interesting paper in the _New York Medical Journal_, 1883, advocates
the use of atropia hypodermically; he believes that atropia chiefly
acts in these cases on the laryngeal branches of the pneumogastric
nerves, and that it is probable that it has a decided effect also on
the medulla oblongata itself, and renders it less capable of exciting
reflex action. Kroon's experiments led him to conclude that the
valerianate of atropia was the most useful. Evans[10] gave the 1/120
of a grain of atropia to a child aged three years until the pupils
were dilated, then reduced the dose; this stopped the paroxysm in
twenty-one days. At the commencement of the treatment the child had
twenty-three paroxysms in the day, and twenty-seven at night. Case No.
2 under same circumstances recovered in fourteen days. In case No. 3
the paroxysms were reduced from twenty-six to two or three a day.
Arthur Wiglesworth[11] used a solution of sulphate of atropia,
administered in the morning fasting; the dose he advises for children
from one to four years is gr. 1/120, given only once a day except in
some cases. The results are as follows: There is a steady diminution
in the number of paroxysms; a change in the character of the whoop as
if the vocal cords were not so closely approximated. If atropia is
withheld, the beneficent effect derived from it subsides.
[Footnote 9: Golding Bird, _Guy's Hosp. Rep._, April, 1845.]
[Footnote 10: _Glasgow Med. Jour._, 1880.]
[Footnote 11: _Lancet_, April 12, 1879.]
West advises dilute hydrocyanic acid, and many writers agree with him,
ranking it next to belladonna.
Harley and others are strong advocates for the bromide of ammonium; it
is supposed to have a local anaesthetic action on the pharyngeal and
laryngeal mucous membrane. Fordyce Grinnell[12] during four months
treated 223 cases with this remedy, and highly recommends it. The
doses were in accordance with those of Dr. Kormann--3/4 to 4 grains,
as indicated by age, three or four times a day and at night when the
paroxysms were severe. No other treatment was used in these 223 cases,
except camphorated oil to the throat and chest in some cases.
Potassium bromide has been recommended by Helenke, Beaufort,
Erlenmeyer, and others. Henry Field[13] recommends sodium bromide.
[Footnote 12: _Med. News_, 1882.]
[Footnote 13: _Brit. Med. Jour._]
Probably next to belladonna in the treatment of this disease we should
place chloral hydrate.
Hebner, after an elaborate study of the relative value of potassium
bromide, quinia, salicylic acid, chloral, and belladonna, says:
"Salicylic acid and chloral tend to relieve the paroxysms--belladonna
and quinia to shorten the disease." Kennedy[14] writes: "I cannot
doubt {847} its specific effects on the cough. Chloral seems to me to
yield the best and most constant results. The advantage of chloral
hydrate seems to exist in producing sleep; it should be given in from
2- to 5-gr. doses, at night." If there is much irritability or
fretfulness, or any premonition of eclampsia, it should be associated
with potassium bromide.
[Footnote 14: _Dublin Jour. M. S._, 1881.]
Croton chloral has received much praise from those who have used it;
we have had no experience with it.
We have already alluded to the value of quinia, which has been used
largely in this disease, both internally and as a local application.
Originally recommended in the latter manner on account of its power of
controlling the development of low organisms, it has not proved so
satisfactory or valuable as when given internally. Binz in 1870 was
perhaps the first to recommend quinia given frequently and in
solution, and Dawson in 1873[15] reports excellent results from the
sulphate or muriate of quinia given in full and frequent doses, and in
such solutions as will not prevent its acting on the mucous membrane
in its passage through the pharynx. Breidenbach[16] gives the quinia
muriate in larger doses--one and a half to fifteen and a half grains
per diem. The effects were surprising as soon as the proper dose for
each person had been determined; this, he says, is the keynote of
success. To prevent complications he continued it for a long time in
small doses.
[Footnote 15: _Am. Jour. Obstetrics._]
[Footnote 16: _Practitioner_, Feb., 1871.]
Our own experience favors the view that quinia, when given in solution
or suspended in mixture, is valuable in many cases of this disease; it
can be ordered in powder, and given in a spoonful of simple syrup or
of the preparation known as the syrup of yerba santa, which makes an
excellent vehicle. Liquorice also disguises the taste of quinia
admirably for children.
Albrecht[17] has found from an experience of ten cases of whooping
cough in children between the ages of one and a half and nine years,
all of a marked scrofulous type, much benefit from the muriate of
pilocarpine, given in small doses after every fit of coughing. To
prevent collapse, he advises that it should be given in a mixture
containing a little brandy. After twenty-four hours of its
administration an obvious change for the better takes place in the
appearance of the mucous membrane of the throat, velum palati, and
uvula, which becomes paler, less swollen, and more moist;
laryngoscopic examination shows a similar improvement. During the
catarrhal period cold compresses to the neck and sweetened milk
containing potassium chlorate are used instead of the pilocarpine,
which is to be resumed as soon as a whoop recurs.
[Footnote 17: _London Med. Rec._, March 15, 1882, p. 110.]
Dr. Tordeus, of the Hospice des Enfants Assistes, Brussels, states
that he has found the sodium benzoate useful in whooping cough,
diminishing the frequency and violence of the paroxysms, and by its
action on the pulmonary mucous membrane preventing those pulmonary
complications which so frequently supervene and constitute the danger
of the disease.
Sulphur has been largely used by the Germans in two- or three-grain
doses, and is said to be greatly esteemed by them. Cantharides has
been recommended, and it is stated that when strangury is produced the
whoop will cease; we should consider this rather severe treatment. The
{848} fluid extract of castanea is used by many with undoubtedly good
results, though this also has been somewhat of a disappointment in the
way of treatment, as at one time it was looked upon almost as a
specific. Many claim that an infusion of the fresh leaves gives a
better result. Dewar[18] regards ergot with great favor in the
treatment of pertussis. Certainly in those cases where, from violent
straining, hemorrhages have taken place we have found it to be highly
valuable. We have had no experience with it in the treatment of
ordinary cases, though Dewar claims that it shortens the attack. The
ammonium picrate, and recently resorcine, have been used with success.
[Footnote 18: _The Practitioner_, London, May, 1882.]
Counter-irritation to the neck and chest has always been found useful
in the treatment of this disease. Autenreith[19] recommends tartar
emetic to the epigastrium till vesicles appear and even ulcerate.
Milder forms of counter-irritation over the chest seem equally
efficacious if continued for some time. The oil of amber, when used in
liniment with camphor or turpentine, is by some considered almost a
specific. Great care should also be observed in the dress of children
with whooping cough. Warmth about the chest is always indicated, while
there should be nothing close or tight about the throat allowed.
[Footnote 19: _Dict. des Sciences Med._, 1813.]
In the third stage, when there is the nervous element remaining,
tonics, such as cod-liver oil, iron, the phosphates and
hypophosphites, are required.
The diet should be nutritious, easy of digestion, and abundant, and
the bowels should be kept regular by fruits or laxatives. Over-feeding
should of course always be avoided, and the attempt at weaning a babe
with this disease would certainly meet with unfavorable results.
Bicarbonate of soda or lime-water should be given freely with the milk
taken by children with this disease. Milk certainly should form the
basis of the diet of children with pertussis, and reliable
meat-extracts are to be recommended in this disease even for older
children, who from the severity of the attack would vomit more solid
food. If the vomiting be so severe as to affect nutrition, the child
should be sustained by peptonized milk, soup, or gruel, given by the
bowel.
The importance of a proper regulation of the temperature of the air
which the patient breathes is especially recognized in France. If the
attack occurs in mid-winter and the seashore be inaccessible or
inexpedient, the child should be restricted to a well-ventilated
nursery or suite of rooms, the temperature of which should be kept
uniform.
Salt air is recognized to be of great value in advanced cases of this
disease; this has been attributed partly to the effects of stimulation
of the mucous membrane in rendering less viscid and more copious the
bronchial secretions, and also to the balmy softness and great purity
of the atmosphere at the sea-shore. But probably there is another
element in the local action of the chloride of sodium, either in
establishing a resistance on the part of the patient or in modifying
the germ of the disease.
The most serious complication of whooping cough is pneumonia. It
occasionally happens that an attack of croupous pneumonia may develop
during the course of whooping cough, but in the vast majority of cases
the disease is of the catarrhal type. When, indeed, it is remembered
that a bronchial catarrh, which is the invariable precursor or
accompaniment {849} of catarrhal pneumonia, is a constant factor in
whooping cough, and, further, that all conditions of debility, and
especially of enfeebled or embarrassed respiration, dispose to this
form of pneumonia, it is not surprising that this complication should
be of such frequent occurrence. It is not impossible that in aiming at
securing sufficient fresh air and out-door exercise to maintain the
general health, an injudicious degree of exposure may be permitted
which will aggravate the existing bronchitis and induce an extension
of inflammation to the alveoli. But usually the catarrhal pneumonia
develops in a subacute and more or less insidious manner, and without
being traceable to any such exposure. It may happen occasionally that
in the violent inspiratory efforts at the close of the paroxysms
irritating secretions may be sucked from the bronchioles into the
alveoli, and there excite inflammation. Or, again, it doubtless
happens frequently that, with the existence of swelling of the
bronchial mucous membrane and of viscid secretions in the bronchial
tubes, collapse of portions of lung tissue is developed by the
forcible expulsion of air during the paroxysms of cough, which cannot
be replaced owing to the relative weakness of inspiration and to the
ball-valve action of the plugs of mucus in the obstructed bronchioles.
The intimate relation between pulmonary collapse and catarrhal
pneumonia is familiarly known. It is not to be considered that the
mere occurrence of collapse will induce pneumonia in the areas
affected, but certainly it will aid in rendering effective the other
irritating causes. As a consequence, it usually happens that when
catarrhal pneumonia occurs in whooping cough it is associated with
more or less collapse. When, then, especially in children of
debilitated or rachitic constitution, or in those who are subjected to
unfavorable hygienic influences, such as overcrowding, bad air, and
the like, there is a rather gradual development of dyspnoea, with
increasing debility, emaciation, and evidences of impaired oxygenation
of the blood, it is to be feared that this serious complication has
developed. The physical signs are often difficult of interpretation,
but if careful examination of the chest be conducted, together with
thermometric observations, the approach of this danger or its actual
presence may be detected. The result is fatal in a large proportion of
cases, so that suitable treatment--for the details of which reference
is made to the appropriate section--must be instituted without delay.
* * * * *
Our investigations of this disease have led us to the conclusion that
we have to deal with an affection caused by a specific germ, which is
usually, after a period of incubation, made manifest by a catarrh of a
portion of the air-passages; that this catarrh, existing for an
indefinite period, is capable of being influenced by medication,
applied either by means of inhalation or by acting on the mucous
membrane after absorption by the stomach. In this way we have known
the administration of quinia and of alum diminish the number of
paroxysms, to all appearance checking the excessive secretion to a
marvellous extent. The other element of the disease, the neurosis,
which soon follows the initial catarrh, and seems to last for an
indefinite time after the mucous membrane has regained its normal
appearance, is also capable of being controlled by the use of drugs,
especially belladonna, chloral, the bromides, and hydrocyanic acid,
not to speak of the other antispasmodics and sedatives, and by the
{850} analgesic effect of carbonic acid gas, or by the spray of
bromide of ammonium, carbolic acid, and other substances upon the
larynx.
Vogel tells us in his classical work on children, "If now, as a
resume, I would give an explanation of my views, it would go to show
that there never has been, and most probably never will be, a remedy
by which whooping cough may be abridged, any more than we are able to
cut short the acute exanthemata or typhus fever or pneumonia." And yet
the experience of many whom we have quoted in this article tends to
support the view that by a form of treatment calculated to act on the
two elements of the disease which we have just noted, the affection
can be greatly modified in its intensity, and probably the attack be
somewhat shortened. Certain it is that the recent studies of this
disease give us hope that the day is not far distant when the cause,
whatever it is, will be definitely known, and if it is found to reside
in the secretions from the larynx, that treatment by inhalation or
atomization will modify or destroy it, and prevent its dissemination.
{851}
INFLUENZA.
BY JAMES C. WILSON, M.D.
DEFINITION.--A continued fever, occurring in widely-extended
epidemics, and due to a specific cause; it is characterized by early
catarrh of the mucous membrane of the respiratory tract, and in many
cases also of the digestive tract; by quickly oncoming debility out of
proportion to the intensity of the fever and the catarrhal processes;
and by nervous symptoms. There is a strong tendency to inflammatory
complications, especially of the lungs. Uncomplicated cases are rarely
fatal except in feeble and aged persons. An attack does not confer
immunity from the disease in future epidemics.
SYNONYMS.--Febris catarrhalis; Defluxio catarrhalis epidemicus;
Catarrhus a contagio; Rheuma epidemicum; Cephalalgia contagiosa;
Epidemic catarrhal fever; Tac; Horion; Quinte; Coqueluche; Ladendo,
also written La Dando; Baraquette; Generale; Coquette; Cocotte;
Allure; Follette; Petite poste; Petit courier; Grenade; La Grippe;
Ziep; Schaffhusten and Schaffkrankheit; Huhner-Weh; Blitz-Katarrh;
Modefieber; Mal del Castrone. There are also several names indicating
its supposed origin; thus it has been called in Russia, Chinese
catarrh; in Germany and Italy, the Russian disease; in France, Italian
fever, Spanish catarrh, and so forth.
It is a remarkable fact that in two instances at least the popular
name for the disease under consideration has found its way widely into
medicine and medical literature, almost to the exclusion of the
studied terms by which science has sought to designate it; these are
influenza and la grippe.
Such obsolete and now meaningless terms as Peripneumonia notha
(Sydenham, Boerhaave), Peripneumonia catarrhalis (Huxham), Pleuritis
humida (Stoll), have been omitted from this list of synonyms as being
of interest rather to the student of medical history than to the
student of medicine.
Febris catarrhalis, Defluxio catarrhalis epidemicus, Rheuma epidemicus
are terms which no longer retain the place given them in the
literature of influenza by the older medical authorities.
Catarrhis a contagio (Cullen) and Cephalalgia contagiosa are derived
from a view of the nature of the disease, which has been the cause of
no little controversy.
Epidemic catarrhal fever is, with its Latin equivalent, the most
satisfactory of the so-called scientific names by which the disease is
at present known.
In the popular names for the affection there is to be noted an {852}
indication of the national character of some of the peoples who have
suffered from its frequent visitations.
Among the English it is known as cold or epidemic cold, or, in
deference to medical authority, as catarrh or epidemic catarrh; and at
present, both among the folk and the doctors, as influenza. Englishmen
are neither quick to see in the disease a resemblance to some common
circumstance or thing, nor are they disposed to make a joke about it.
The Germans find obvious resemblances. In the labored respiration and
the character of the cough they find a suggestion of a common
epizootic affecting the sheep, hence Schaffhusten and Shaffkrankheit;
or, because the cough is like the crowing of a cock and the
disturbance of respiration and rapid prostration suggest some
resemblance to a common disease of the domestic fowl, it has been
called Huhner-Weh (chicken disease, whooping cough), and Ziep, which
is about equivalent to pip. They call it also, from its rapid
invasion, Blitz-Katarrh, and from its diffusion, Modefieber.
The French are disposed to make a jest of everything, and the more
serious the subject the better the joke. Hence they have found a new
name for almost every great epidemic, and each more trivial than the
last. Thus, tac (rot); horion (in jest, a blow); quinte, because the
spells occur at intervals of five hours (sic); coqueluche (a hood or
cowl), from the cap worn by those suffering from the malady; and so on
through the long list given above.
La grippe is said to be derived from the Polish Chrypka (Raucedo); it
may, however, be derived from agripper (to seize).
Influenza is of Italian derivation. It is said that the disease
received this name because it was attributed to the influence of the
stars, or from a secondary signification of the word indicating
something fluid, transient, or fashionable.
HISTORICAL SKETCH.[1]--Epidemics of influenza have been clearly
recorded only since the beginning of the sixteenth century. There are
numerous accounts of earlier epidemic diseases resembling it, but they
are not sufficiently particular to warrant us in inferring its
undoubted existence. It is supposed to be referred to in the writings
of Hippocrates, who, however, gives no exact description.[2] An
outbreak in the Athenian army in Sicily (415 B.C.), recorded by
Diodorus Siculus, has been supposed to have been influenza. Despite
these statements, and those of others to the effect that it is a
disease known from a remote antiquity, it may be said that no accounts
can be confidently established, as referring to the disease now known
as influenza, in the writings of classical antiquity.[3]
[Footnote 1: See also _The Continued Fevers_, by the author of this
paper, New York, 1881.]
[Footnote 2: Parkes, _Reynolds's System of Medicine_, vol. i., 1868.]
[Footnote 3: Zuelzer, _Ziemssen's Cyclopaedia of Medicine_, vol. ii.,
1875.]
As early as the ninth century several epidemics of catarrhal fever,
Italian fever, and the like, which were probably influenza, were made
matter of history. In the year A.D. 827 a cough which spread like the
plague was recorded. In 876 there appeared in Italy a similar
epidemic, which spread with great rapidity over all Europe. It is
related that dogs and birds suffered with symptoms not unlike those
characterizing the affection in man. In 976, Germany and all France
suffered from a fever of which the chief {853} symptom was cough. No
further epidemic is noted until two centuries later, when, in 1173, a
widespread malady, of which the symptoms were chiefly catarrhal, raged
throughout Europe; while less important epidemics of a like character
are recorded as having occurred during the following century
(1239-99).
In the medical writings of the fourteenth century there are to be
found records of six epidemics, and in the fifteenth seven great
visitations of influenza are described (Parkes).
Aitken[4] speaks of a very fatal prevalence of influenza throughout
France in 1311, and of an epidemic in 1403 in which the mortality was
so great that the courts of law in Paris were closed in consequence of
the deaths.
[Footnote 4: Aitken's _Practice of Medicine_, vol. i., 1872.]
Influenza is mentioned in the _Annals of the Four Masters_ as having
prevailed in Ireland in the fourteenth century, and a disease
characterized by similar symptoms is alluded to in early Gaelic
manuscripts under the name of Creatan (creat, the chest). The disease
is described also in an Irish manuscript of the fifteenth century
under the terms Fuacht and Slaodan.[5]
[Footnote 5: Theophilus Thompson, _Annals of Influenza_, 1852.]
The earliest epidemic that prevailed in the British Isles of which any
accurate description remains is that of the year 1510. The disease
came from Malta, and invaded first Sicily, then Italy and Spain and
Portugal, whence it crossed the Alps into Hungary and Germany as far
as the Baltic Sea, extending westward into France and Britain. Its
track widened over the whole of Europe from the south-east to the
extreme north-west, and it is said that not a single family and scarce
a person escaped it. It was attended by a "grievous pain in the head,
heaviness, difficulty of breathing, hoarseness, loss of strength and
appetite, restlessness, retchings from a terrible tearing cough.
Presently succeeded a chilliness, and so violent a cough that many
were in danger of suffocation. The first day it was without spitting,
but about the seventh or eighth day much viscid phlegm was spit up.
Others (though fewer) spat only water and froth. When they began to
spit, cough and shortness of breath were easier. None died except some
children. In some it went off with a looseness, in others by sweating.
Bleeding and purging did hurt."[6] Blisters were commonly
employed--two each upon the arms and legs, and one to the back of the
head. The description is sufficiently clear to place the nature of
this epidemic beyond all doubt.
[Footnote 6: Thomas Short, _A General Chronological History of the
Air, Weather, Meteors, etc._, London, 1749; quoted in the _Annals of
Influenza_.]
The epidemic of 1557, starting westward from Asia, spread over Europe,
and then crossed the Atlantic to America. The malady broke out in
England, after a season of unusual rain and great scarcity of corn, in
the month of September. "Presently after were many catarrhs, quickly
followed by a more severe cough, pain of the side, difficulty of
breathing, and a fever. The pain was neither violent nor pricking, but
mild. The third day they expectorated freely. The sixth, seventh, or
at the farthest the eighth day, all who had that pain of the side
died, but such as were blooded on the first or second day recovered on
the fourth or fifth; but bleeding on the last two days did no
service." "Some, but very few, had continual fevers along with it;
many had {854} double tertians; others simply slight intermittent. All
were worse by night than by day; such as recovered were long
valetudinary, had a weak stomach, and hypped." Gravid women either
aborted or died. This epidemic spread with frightful rapidity.
Thousands were attacked at the same time. The entire population of
Nismes, with scarcely an exception, fell ill of it upon the same day.
It was extremely fatal. In Mantua Carpentaria, a small town near
Madrid, it broke out in August, and so fatal were the bloodletting and
purging which constituted the treatment at first, that, of the two
thousand persons who were bled, all died. The disease raged in some
parts till the middle of the following year (1558), and carried off,
in Delft alone, five thousand of the poor. In all cases mild treatment
was called for, with warm broths and speedy immersals, "to recall the
appetite and keep the vessels of the throat open."
In 1580 a great epidemic of influenza spread from the south-east
toward the north-west over Asia, Africa, and Europe. From
Constantinople and Venice it overran Hungary and Germany, and reached
the farthest regions of Norway, Sweden, and Russia. It spread into
England, and has been described by Dr. Short. In Italy it prevailed
during August and September, in England from the middle of August to
the end of September, and in Spain during the whole summer. In most
places its duration was about six weeks. As a rule, the termination
was favorable, although the disease ran a somewhat protracted course.
In the account of Dr. Short it is stated that "few died except those
that were let blood of or had unsound viscera." In some places, on the
contrary, the course of the disease was very severe. In Rome two
thousand died of it, according to the author just cited, but Zuelzer
informs us that the victims of this epidemic in the Eternal City were
not less than nine thousand, and adds that Madrid must have been
almost depopulated by it. This high mortality has been attributed to
the bloodletting practised in the treatment of the disease. The
symptoms were similar to those of the previous epidemics, with a
greater shortness of breath, which continued in many cases for some
time after the disappearance of the catarrhal trouble. There was great
sweating at the end of the attack. The plague, measles, and small-pox
prevailed also, and with considerable violence, during the year 1580.
Influenza, unfelt for several years, reappeared in Germany in 1591; an
epidemic extending from Holland through France and into Italy occurred
in 1593. In 1610 catarrh is said to have prevailed throughout Europe.
In 1626-27 epidemic catarrhal fever made its appearance in Italy and
France; in 1642-43 in Holland; in 1647 in Spain and in the colonies of
the Western World; and again, in 1655 in North America. According to
Webster,[7] this epidemic of 1647 was the first catarrh mentioned in
American annals.
[Footnote 7: Noah Webster, _A Brief History of Epidemic and
Pestilential Diseases_, London, 1800.]
In 1658 and 1675 it again visited Austria, Germany, England, etc. The
first of these two epidemics is described by Willis,[8] and the second
by Sydenham,[9] as they occurred in England, and the accounts are to
be {855} found in the _Annals of Influenza_. It is about this period
that the disease began to be known as influenza, and it is not without
interest to observe that the influence of the stars suggested itself,
in connection with its sudden appearance and wide prevalence, to the
minds of the physicians of this date. Willis writes that "about the
end of April (1658), suddenly a distemper arose, as if sent by some
blast of the stars, which laid hold on very many together; that in
some towns in the space of a week above a thousand people fell sick
together."
[Footnote 8: Dr. Willis, _The Description of a Catarrhal Fever
Epidemical in the Middle of the Spring in the Year 1658: Practice of
Physick_, 1684.]
[Footnote 9: _The Epidemic Coughs of the Year 1675, with the Pleurisy
and Peripneumony that supervened_: from the _Works_ of Thomas
Sydenham, M.D.]
Epidemics are recorded as having occurred in Great Britain and Europe
in 1688, 1693, and in 1709. The disease raged in 1712 widely over
Europe from Denmark to Italy.
In 1729-30 a widespread epidemic swept over Europe. In five months it
extended over Russia, Poland, Germany, Sweden, and Denmark. In Vienna
sixty thousand persons fell ill of it. In the autumn it spread to
England, and reached France and Switzerland; from there it extended to
Italy, and by February it had reached Rome and Naples. Spain did not
escape its ravages, and it is said to have found its way to Mexico.
The symptoms did not differ in any important respect from those
already described as characterizing previous epidemics. Pains in the
limbs and fever marked the onset of the attack; catarrh, oppression,
hoarseness, cough followed. In some cases delirium, drowsiness, and
faintings occurred. A petechial eruption was observed, in some
instances, between the fourth and seventh days. This renders it
probable that typhus or cerebro-spinal fever prevailed at the same
time. Turbid urine, copious sweats, bilious stools, and nose-bleeding
were often noted. In Switzerland only children and old persons died.
The disease was not very fatal.
Two years later (1732-33) an epidemic, starting from Saxony and
Poland, overran Germany, Switzerland, and Holland, and invaded Great
Britain in the month of December. Toward the end of January it spread
in a south-easterly direction to France, Italy, Spain, and westward to
North America, thence southward to the islands of the West Indies, and
on to South America. The course of the disease in this epidemic was
favorable. The attack terminated in from three to fourteen days, with
sweating, bleeding from the nose, or an abundant discharge from the
nasal passages. The aged and those suffering from chronic pulmonary
diseases mostly perished. In Scotland three forms of the affection
were described--namely, the cephalic, the thoracic, and the abdominal.
The epidemic slowly spread over Eastern Europe and in a south-easterly
direction, and may be said to have lasted till 1737.
Concerning this epidemic John Huxham of Plymouth wrote as follows:[10]
"About this time a disease invaded these parts which was the most
completely epidemic of any I remember to have met with; not a house
was free from it; the beggar's hut and the nobleman's palace were
alike subject to its attacks, scarce a person escaping either in town
or country; old and young, strong and infirm, shared the same fate."
The malady had raged in Cornwall and the western parts of Devonshire
from the beginning of February; it reached Plymouth on the 10th, which
was on a Saturday, and that day numbers were suddenly seized. The next
day multitudes were taken ill, and by the 18th or 20th of March
scarcely {856} any one had escaped it. "The disorder began at first
with a slight shivering; this was presently followed by a transient
erratic heat and headache and a violent and troublesome sneezing; then
the back and lungs were seized with flying pains, which sometimes
attacked the heart likewise, and though they did not long remain
there, yet were very troublesome, being greatly irritated by the
violent cough which accompanied the disorder, in the fits of which a
great quantity of a thin, sharp mucus was thrown out from the nose and
mouth. These complaints were like those arising from what is called
catching cold, but presently a slight fever came on, which afterward
grew more violent; the pulse was now very quick, but not in the least
hard and tense like that in a pleurisy; nor was the urine remarkably
red, but very thick, and inclining to a whitish color; the tongue,
instead of being dry, was thickly covered with a whitish mucus or
slime; there was an universal complaint of want of rest and a great
giddiness. Several likewise were seized with a most racking pain in
the head, often accompanied by a slight delirium. Many were troubled
with a tinnitus aurium, or singing in the ears; and numbers suffered
from violent earaches or pains in the meatus auditorius, which in some
turned to an abscess. Exulcerations and swellings of the fauces were
likwise very common. The sick were in general very much given to
sweat, which, when it broke out of its own accord, was very plentiful
and continued without striking in again, and did often in the space of
two or three days wholly carry off the fever. You have here a
description of this epidemic disease such as it prevailed hereabouts,
attacking every one more or less; but still, considering the great
multitude that were seized by it, it was fatal to but few, and that
chiefly infants and consumptive old people. It generally went off
about the fourth day, leaving behind a troublesome cough, which was
very often of long duration, and such a dejection of strength as one
would hardly have suspected from the shortness of the time.
"On the whole, this disorder was rarely mortal, unless by some very
great error arising in the treatment of it; however, this very
circumstance proved fatal to some, who, making too slight of it,
either on account of its being so common or not thinking it very
dangerous, often found asthmas, hectics, or even consumptions
themselves, the forfeitures of their inconsiderate rashness."
[Footnote 10: _Observations on the Air and Epidemical Diseases,
translated from the Latin_, London, 1758.]
Arbuthnot also described this visitation of the disease.[11] He
regarded the uniformity of the symptoms in every place as most
remarkable, and tells us that during the whole season in which it
prevailed there was "a great run of hysterical, hypochondriacal, and
nervous distempers; in short, all the symptoms of relaxation."
[Footnote 11: _An Essay concerning the Effects of Air on Human
Bodies_, London, 1751.]
During the years 1737-38 influenza again swept over England, North
America, the islands of the West Indies, and France; in 1742-43 it
prevailed in Western Europe and the British Isles; in 1757-58 in North
America, the West Indies, France, and Scotland. In 1761 it overran the
North American colonies and the West Indies.
The epidemic of 1762 extended very generally over Europe and Great
Britain. In Germany nine-tenths of the population were attacked by the
disease.
Widely extended epidemics prevailed in Europe and America in 1767
{857} and 1775; in 1772 it raged in North America; in 1778-80, in
France, Germany and Russia. Noah Webster found influenza prevalent in
North America in 1781; the next year one of the most remarkable
epidemics of this disease (described as the epidemic of 1782) appeared
in Europe. It came from the East, from Asia into Russia. From St.
Petersburg it spread during the winter and spring over Sweden,
Germany, Holland, and France. In the autumn it was in Italy, Spain,
and Portugal. The crews of Dutch and English ships were taken ill with
the disease upon the high seas.
In Vienna three-fourths of the population fell ill of it with such
suddenness that it got here for the first time its name of "Blitz
Katarrh" (lightning catarrh). It was characterized by great pain in
the back, breast, and throat, and by extraordinary enfeeblement.
Relapses occurred, and inflammation of the lungs and bowels was
common. Children remained relatively exempt from its seizure. This
epidemic broke out in England about the end of April and raged until
the end of June. "The duration of the malady in some was not above a
day or two, but it usually lasted near a week or longer. In a few the
symptoms seemed to abate in two or three days, but some returned and
raged with more violence than at first."[12] The disease was not
regarded as in itself fatal, and few could be said to have died of it
"but those who were old, asthmatic, or who had been debilitated by
some previous indisposition."
[Footnote 12: _An Account of the Epidemic Disease called the Influenza
of the Year 1782. Collected from the Observations of several
Physicians in London and in the Country, by a Committee of the Fellows
of the Royal College of Physicians in London. Read at the College,
June 25, 1783._]
Numerous recurring outbreaks took place in Europe and America during
the years 1788-90. One of these, as it occurred in America, is well
described by Dr. John Warren[13] of Boston in a letter to Lettsom.
This letter is dated May 30, 1790, and among other matters of great
interest respecting the disease it is stated that "Our beloved
President Washington is but now on the recovery from a very severe and
dangerous attack of it in that city" (New York).
[Footnote 13: _Memoirs of the Life and Writings of J. Coakley
Lettsom_, Thomas Joseph Pettigrew, 1817.]
Webster mentions an epidemic in America in 1790, one in Europe in
1795, and another in Europe in 1797, but there seems to have been no
general epidemic of sufficient importance to attract the attention of
other writers upon the subject until 1798, when the malady again broke
out in Russia and spread over the greater part of Europe, continuing
to prevail in various regions till 1803, when it again appeared in
England, and is described by several writers of that country.
From 1805 to 1827 influenza prevailed (according to Zuelzer, who tells
us that few years during this interval were free from it) in
frequently-recurring epidemics in Europe and America. Thompson
mentions no visitation in England between 1803 and 1831.
In the year 1830 began a series of epidemics remarkable for their wide
diffusion and the rapid succession with which they followed one upon
another. The disease began in China; in September it reached the
Indian Archipelago; it swept into Russia, and invaded Moscow in
November; in January, 1831, it was raging in St. Petersburg; March
found it in Warsaw; April in Eastern Prussia and Silesia; in May it
prevailed in Denmark, Finland, and a great part of Germany, and in
{858} the same month it fell upon Paris; in June it affected England
and Sweden; it was still creeping about Middle Europe and lingering in
Great Britain at the end of July; in the early winter it swept
southward into Italy, and westward across the Atlantic to North
America, and was still harassing the inhabitants of certain regions of
the United States in January and February, 1832. Meanwhile it
continued in the East, spreading to Java, Farther India, and the
Indian Archipelago. It continued in Hindostan after it had died out in
Europe. But in January, 1833, it again visited Russia, and rolled
thence southward and eastward over the most of Europe. It is recorded
that by February it had reached Galicia and Eastern Prussia; in March
it was in Prussia, Bohemia, and Warsaw, and had extended to Syria and
Egypt; in April to many parts of Germany and Austria and to France and
Great Britain. Midsummer found the disease yet prevailing in some
districts of Germany and Northern Italy, and in the early autumn it
was in Switzerland and Eastern France; in November it visited Naples.
Epidemics so frequent, so widespread, and so unsparing of individuals
wherever the disease appeared could not fail to excite a deep and
general interest. From this period the literature of the subject has
been voluminous.
A brief period of repose ensued. For three years no epidemic occurred
which was of sufficient importance to attract the attention of medical
historians.
In December, 1837, influenza reappeared, and first, as so often
before, in Russia; Sweden and Denmark were almost simultaneously
affected; in January, 1837, it broke out in London, and rapidly swept
over all England and into France and Germany. In January it appeared
in Berlin, and shortly afterward in Dresden, Munich, and Vienna. The
disease spread by February into Switzerland, and into Spain as far as
Madrid by the end of March. In London almost the whole population was
attacked, and the mortality was enormous. It is stated that the deaths
were quadrupled during the prevalence of the disease. Large
populations suffered most. This epidemic spread into the southern
hemisphere, and prevailed at the same time, and consequently at
exactly the opposite season that it prevailed north of the equator, in
Sydney and at the Cape of Good Hope.
From 1837 to 1850-51 numerous epidemics of influenza occurred. Few
years were exempt from them. The epidemic of 1847-48 has been
described by many writers, and more particularly, as it occurred in
London, by Peacock[14] with great exactitude. It is estimated that
one-fourth of the entire population of that city were more or less
affected by the disease. The epidemic prevailed in London for six
months, and, although the deaths registered for the entire period as
from influenza amounted to only 1739, it is stated in the report of
the registrar-general that during the six weeks the epidemic was at
its height not less than five thousand persons died, in the
metropolitan districts, in excess of the average mortality of the
period, the excess showing itself in nearly every class of disease,
the local maladies which had been the predominant affections being
doubtless in many cases assigned as the cause of death. This {859}
epidemic affected between one-fourth and one-half of the population of
Paris, and in Geneva the proportion of those attacked was not less
than one-third of the entire population.
[Footnote 14: _On the Influenza, or Epidemic Catarrhal Fever of
1847-48_, Thomas Berill Peacock. M.D., 1848.]
More or less widespread epidemics of influenza are recorded as having
occurred in 1857-58 and 1860; in 1864 in Switzerland; in 1867 in Paris
in the spring; and at various times in the United States and Canada.
A mild epidemic occurred in 1874 in Berlin.
Influenza prevailed over a wide area in the United States during the
early months of 1879. The characteristics of this visitation have been
well described by Da Costa.[15]
[Footnote 15: "The Prevailing Epidemic of Influenza--Its
Characteristic Phenomena--Pulmonary, Gastro-intestinal, Cerebral, and
Nervous--Its Wide Distribution, Mortality, and Treatment," _Medical
and Surgical Reporter_, Philadelphia, March 8, 1879.]
The disease, since the great epidemic of 1847-48, has affected a
smaller proportion of the inhabitants of the localities visited, and
has run a less dangerous course, than in the earlier epidemics. It has
for this reason occupied a less conspicuous place in the medical
literature of recent years. It is nevertheless true that even in the
mildest epidemics, when a relatively small number of persons are
seized and the symptoms are in most cases almost insignificant, cases
do here and there occur which are of a serious or even fatal
character, and that the death-rate from other diseases is for the time
considerably increased.
Catarrhal affections have often prevailed among the domestic animals
when influenza has been epidemic. Horses, dogs, and cats are subject
to these disorders; neat cattle, goats, and sheep have been less
commonly affected; chickens and pheasants have suffered, and it is
stated by some of the older writers that birds, and particularly the
sparrow, have deserted localities in which influenza was prevailing,
and that migratory birds have taken flight earlier than usual.
These epizootics have sometimes preceded the appearance of influenza
among men by a period of some weeks or days; in other instances they
have appeared at the same time; and in a widespread outbreak among
horses in the United States in 1872, in which the symptoms and morbid
anatomy, accurately observed, were undoubtedly those of influenza, the
disease did not affect man except to a very limited extent. A want of
fulness of description, and the inaccuracy of diagnosis too common in
the consideration of the general diseases of the lower animals, leave
the precise nature of most of the epizootics described by the earlier
writers doubtful.
An extensive influenza of moderate intensity prevailed as an
epizootic, chiefly affecting horses, during the latter part of the
summer and the autumn of 1880 in Canada and the United States east of
the Mississippi River. Dogs were also affected, but less generally,
and human beings to a still slighter extent. In several localities
where this invasion was observed by the writer the horses were first
affected, the dogs next, and after the lapse of some weeks, as the
animals were recovering, the disease became epidemic; but those
persons who took care of horses and were much in contact with them
neither suffered earlier nor more severely than others not so exposed.
ETIOLOGY.--1. Predisposing Influences.--There are no {860}
well-established facts pointing to the existence of individual
peculiarities that can be regarded as predisposing influences. When
the disease appears a large proportion of the population is attacked
without distinction of age, sex, social condition, or occupation.
Previous illness, whether acute or chronic, local or constitutional,
affords no protection. Aged and infirm persons and those of nervous
temperament are peculiarly liable to attack, but the robust possess no
immunity. All races and dwellers in every climate are the victims of
influenza. In a community invaded by the disease females are apt to be
the first attacked, adult males next, and children last. It has been
observed that in some epidemics children are but little liable to
contract the disease.
An attack confers no exemption from the disease in another epidemic,
and independently of relapses, which are not infrequent, persons have
been known to experience a second attack during the prevalence of the
same epidemic.
Persons dwelling in overcrowded and ill-ventilated habitations and in
low, damp and unhealthy situations have, in certain epidemics,
especially suffered, and the increase of deaths by influenza is
proportionately much greater in districts in which there is ordinarily
a high mortality than in healthier places.
Influenza appears at all seasons of the year and affects the
inhabitants of every latitude. It has no connection with known
atmospheric conditions. Many of the earlier writers sought to
establish a relation between low temperatures and sudden variations of
temperature and influenza, and by reason of the confusion among the
people between these diseases and common "colds" there has always
existed an opinion that such a relation obtains. There is, however, no
evidence to sustain this view; neither low temperature nor abrupt
changes give rise to the affection. It has prevailed in hot and dry
seasons, in the West Indies, on the coast of Java, in India, in Egypt,
at the Cape of Good Hope, on the Riviera in summer.
The condition of the air as regards moisture, or dryness, does not
influence the spread of the disease. It has occurred at sea, on low
sea-coasts, and in the dryest climates, as, for example, in Upper
Egypt.
Its spread is not much influenced by local winds. It does not travel
with the same velocity, and even sometimes advances against them. In
several well-authenticated instances a dense and foul fog has preceded
and attended the local outbreak of epidemics. The much greater number
of epidemics that have occurred altogether without such manifestations
make it in a high degree probable that this has been a coincidence.
Ozone in large quantities artificially produced may give rise to the
symptoms of ordinary catarrh, but it is not a cause of influenza. The
disease is not in any way connected with the condition of the soil,
elevation, volcanic eruption, or any other local cause. The history of
every epidemic may be adduced in proof of this statement.
Before taking up the consideration of the exciting causes of
influenza, it is important to review the known facts concerning the
march of epidemics and the spread of the disease in affected
localities. It has prevailed with greater or less frequency in almost
every region of the globe. Epidemics recur at irregular periods. It
was at one time supposed that the course of the disease was cyclical,
with a return at intervals of about one hundred years. This view was
long ago proved to be unfounded. About every {861} twenty-five or
thirty-five years great epidemics have swept over vast areas of the
globe, and influenza may be said to be, at such times, pandemic.
Less-widely extended epidemics have taken place with greater or less
frequency in the intervals between the great outbreaks. But it is not
possible to establish anything like a regular periodicity in the
returns of the disease.
It has been supposed in some instances to prevail within restricted
localities, as, for example, in a single city. Such local epidemics
are without doubt due to local causes, and are of the nature of simple
ordinary catarrhal fever, rather than true influenza.
The epidemics have extended over great areas, usually in a direction
from the east or north-east toward the west and south. At other times
they take the opposite course, and in some years they have appeared to
radiate in various directions from several centres. It is in
consequence of these facts that two views have arisen concerning the
origin of the affection. The first of these is, that each epidemic
starts out from some single unknown source, and spreads thence from
point to point, invading more distant localities successfully as it
advances, until at length it dies out in regions remote from the
starting-point. This opinion is in accord with the popular belief.
Thus, the Italians have called it the German disease; the Germans, the
Russian pest; the Russians, the Chinese catarrh. The geographical
relation of these nations indicates the usual track of the great
epidemics, as shown in the foregoing historical sketch. The other
opinion is, that it arises not from some single particular place, but
that it may start anywhere, and that widespread epidemics are due to
the successive outbreaks of the disease at many distinct points of
origin.
The evidence that the great epidemics of influenza are due to some
general and pandemic influence is conclusive. The point of origin of
the great epidemics has not yet been indicated with precision, and
must remain beyond conjecture until further facts bearing upon the
question of their source are brought to light. When it has prevailed
over a large portion of the earth's surface its progress from place to
place has usually been rapid. In this respect, however, the epidemics
show a great diversity. It sometimes travels exceedingly slowly. It is
said to have overrun Europe in six weeks, and it has again taken six
months to do so. It sometimes attacks places widely remote from each
other within short intervals of time, and it has appeared at the same
time in different quarters of the globe. It does not follow the great
lines of travel and commercial intercourse.
When influenza enters a city it continues to prevail, as a rule, from
four weeks to two months, but exceptionally it remains a longer time;
for example, the epidemic of 1831 was prevalent in Paris for the
greater part of the year. It in all instances finally disappears, and
sporadic cases do not occur in the intervals between the epidemics.
In rare instances the epidemics are heralded by scattered cases. But
as a rule this disease attacks simultaneously great numbers of the
inhabitants of affected districts, so that, when the epidemic is
severe, the sick are in a short time to be counted by thousands and
business is paralyzed as by a blow. Epidemics rapidly reach their
height, and subside almost as suddenly as they began. In a large city
the disease frequently, perhaps always, makes its appearance nearly at
the same time in several {862} different localities, affecting certain
streets and quarters solely or more generally than others for a time,
and spreading thus from several centres through the entire community.
Large towns and cities are generally affected earlier than the
villages around them, and the latter, though closely adjacent,
sometimes escape for weeks. The crews of ships upon the high seas, not
sailing from an infected port, are said to have suffered from the
seizure, and epidemics have many times crossed the Atlantic from the
Old World to the New, and more than once in the opposite direction.
2. The Exciting Cause.--Large as has been the place in medical
literature occupied by the histories of epidemics of influenza, the
nature of the "epidemic influence" which gives rise to the disease is
still unknown.
The question of the contagiousness of influenza is one of grave
interest, and has been the subject of much controversy. The great
rapidity of the spread of epidemics, the vast area they overrun, the
fact that they do not follow the lines of human intercourse, the
suddenness with which great numbers of the inhabitants of an invaded
district or city are seized, the fact that the most complete seclusion
from intercourse with affected persons, or even the shutting up of
houses, affords in most instances no protection whatever,--all go to
show that the disease spreads, in the main, independently of direct
contact. This opinion has been almost universally entertained. There
is evidence, however, to show that the disease is to some extent
contagious; and so convincing have the facts bearing upon this point
appeared to some that they have believed it to be propagated entirely
by human intercourse. Haygarth[16] declares, as the result of his
observations during the epidemics of 1775 and 1782, that the influenza
spreads "by the contagion of patients in the distemper;" and
Falconer,[17] writing of the epidemic of 1803, says, "I have no doubt
that it is contagious in the strictest sense of the word." Watson[18]
regards the instances in which the complaint has first broken out in
those particular houses of a town at which travellers have arrived
from infected places as too numerous to be attributed to mere chance.
Very often those dwelling near the invalids are attacked next in the
order of time, and when the disease affects a household all do not
usually manifest the symptoms at the same time, but one member after
another is stricken down with it.
[Footnote 16: John Haygarth, M.D., F.R.S., _On the Manner in which the
Influenza of 1775 and 1782 spread by Contagion in Chester and its
Neighborhood._]
[Footnote 17: William Falconer, M.D., F.R.S., _An Account of the
Epidemic Catarrhal Fever, commonly called the Influenza, as it
appeared at Bath in the Winter and Spring of the Year 1803_, Bath,
1803.]
[Footnote 18: _Principles and Practice of Medicine_.]
In a few rare cases the isolation or seclusion of a community has
appeared to give protection, as in cloisters, prisons, garrisons, and
the like; at all events, there are instances on record where
segregated communities of this kind have escaped attack.
The following observation, conducted under unusual circumstances,
establishes the fact that influenza may be brought from an infected
city in such a way as to give rise to a localized outbreak in a remote
community. Drs. Guiteras and White[19] narrate that, influenza
prevailing in Europe, and particularly in Paris and London, an
American gentleman in bad health contracted the disease in London,
improved, suffered a relapse {863} shortly afterward in Paris, and
died there at the end of December, 1879. His body was embalmed and
sent home. Following the exposure of the remains of this person to the
view of his family in Philadelphia there was an outbreak of influenza
with characteristic symptoms, which affected, in the first place,
members of that family; afterward, friends living in close intercourse
with them; next, the medical attendant of some of them; and finally,
the housekeeper and a patient or two of one of the physicians who
wrote the paper, the whole number affected in Philadelphia being
eighteen at the time of the publication of the account. Subsequently
two or three other cases were developed, but the disease did not
extend beyond the immediate circle of those in direct communication
with the invalids.
[Footnote 19: John Guiteras, M.D., and J. W. White, M.D., "A
Contribution to the History of Influenza, being a Study of a Series of
Cases," _Philadelphia Medical Times_, April 10, 1880.]
It was at one time thought that influenza developed at once, without a
period of incubation, persons in perfect health being struck down with
it as by lightning-stroke. It is, however, now known that a period of
incubation, varying from a few hours to several days, and usually
without subjective symptoms, exists. Many instances are recorded in
which persons coming into an infected city have remained well for one,
two, or three days, but have eventually shared the sufferings of those
into whose midst they have come. There are cases also in which the
period of incubation could not have been less than two or three weeks.
There is no sufficient evidence of a causal relation between influenza
and any other epidemic disease. The statement that other prevalent
diseases abate in frequency and intensity upon its outbreak is not
sustained by well-observed facts. Graves[20] holds that those
suffering with acute diseases are less liable during the febrile
stage, but that they are attacked as convalescence sets in.
[Footnote 20: _Clinical Medicine_.]
The facts in reference to the spread of epidemics of influenza and the
course of the disease in infected localities are comprehensible upon
no other theory than that of a specific infecting principle as its
exciting cause. What this principle may be is not yet known; where it
originates is equally unknown; and our knowledge of the influences
that from time to time call it into activity and send it forth in
definite directions over the earth is no less negative.
So general a disease can only be disseminated by the most general
medium, the atmosphere, and its exciting cause must be capable of
reproducing itself in that medium, otherwise it would be lost by
dispersion in traversing distances measured by the boundaries of
continents and oceans. The rapid diffusion of influenza, sweeping over
continents in a few weeks at one time, its slow migration, creeping
about a city and its environs for months, at another, are to be most
easily explained upon the theory of a living miasm capable of being
transmitted by the air, and possessing at the same time an independent
existence. Such an entity would find certain localities more favorable
to its growth, reproduction, and prolonged existence than others. From
this point of view influenza is a miasmatic disease. The infecting
principle of this disease is also, to a slight extent, capable of
being reproduced in or about the human body and transmitted by
personal intercourse, as well as conveyed from place to place by the
persons or clothing of those affected or those travelling from
localities in which the disease prevails. We are thus led to the
conclusion that it is also contagious, though feebly so.
{864} CLINICAL HISTORY.--Influenza, in individual cases, presents the
greatest variation as regards intensity, from the most trifling
indisposition to an illness of the gravest kind, terminating in death.
These variations are dependent upon--1st, the previous health of the
individual, his age, and the power of resisting depressing influences
which he possesses; 2d, the energy and the amount of the specific
cause of the disease to which he has been exposed--in other words, the
dose of the fever-producing poison; and 3d, the character of the
prevailing epidemic.
It is important to observe that cases of very great severity are
occasionally encountered during the prevalence of mild epidemics. In
every epidemic, on the contrary, a considerable part of the community
suffers from influenza in the mildest, or what has been called the
rudimentary, form. This is characterized by general malaise, an easily
oncoming weariness upon bodily and mental effort, a disinclination for
business, some inability to fix the attention, and slight mental
confusion; to these nervous disturbances are added catarrhal symptoms,
as coryza, sore throat, a tickling cough, and the like; but the
indisposition is subfebrile--it does not amount to a fully-developed
fever. Other cases present the symptoms of an ordinary attack of acute
coryza, laryngitis, bronchitis, pharyngitis, with unusual
constitutional disturbance, distressing headache, and pains in the
back and limbs. The fever in this class of cases does not range high,
yet the patients are ill enough to betake themselves to bed.
In severe cases the onset is usually abrupt. The attack begins with
shivering or a chill, or with fits of chilliness alternating with
heat. Fever is rapidly established. It is usually moderate; sometimes
it reaches a high grade. It shows a tendency to morning remissions.
Sensations of chilliness occur; they are called forth by slight
changes in the external temperature. They are often followed by
flushes of heat, and are, in many cases, attended by annoying sweats.
The febrile outbreak is sometimes preceded by intense frontal
headache, with pain in the orbits and at the root of the nose. In
other cases these pains quickly follow the chill. Sneezing, redness of
the eyes and edges of the nostrils, a more or less abundant thin
discharge from the nose, and lachrymation, now occur. In some
instances there is bleeding from the nose. The throat becomes sore;
there is a tickling sensation in the upper air-passages; a dry cough
sets in, attended by more or less hoarseness and shortness of breath.
The cough is paroxysmal, hard, distressing. It sometimes causes
vomiting, like that which occurs in the paroxysms of whooping cough.
Chest-pains, stitches in the side, frequent sneezing, loss of the
sense of smell and of taste, attend the development of the general
catarrhal manifestations.
The fever is attended by great depression, pains in the limbs, loss of
appetite, thirst, constipation, and diminished secretion of urine. The
pulse is full, but, as a rule, only moderately increased in frequency.
There is in many cases slight, or even decided, blueness of the lips
and finger-tips. The patient is distressed by restlessness and want of
sleep. At the end of four or five days the febrile symptoms decline,
at times gradually, oftener rapidly, with copious sweats or
spontaneous flux from the bowels. The fever continues, however, when
severe complications have taken place, ten or twelve days. The
defervescence is marked by {865} an increased flow of sedimentary
urine and considerable amelioration of the subjective symptoms. The
catarrhal symptoms outlast the fever two or three days, but cough and
expectoration may not disappear for some time.
With these symptoms are associated the evidences of functional
disturbance of the nervous system. There is remarkable nervous
depression; loss of strength and lowness of spirits are combined with
mental weakness, or even stupor and delirium. In some cases slight
convulsions take place. Cutaneous hyperaesthesia occasionally occurs,
and areas of burning pain in the skin are to be met with. Neuralgia,
muscle-pain, and aching referred to the bones are very common and
often severe.
In other cases abdominal symptoms are prominent, while those referable
to the head and chest are less urgent. The disease assumes the guise
of a more or less severe catarrh of the gastro-enteric mucous
membrane, with disturbance of the functions of the liver. The fever
and the peculiar nervous depression are, however, the same. Cases
likewise present themselves in which but little of the usual tendency
to localization of the catarrhal processes is to be observed; there is
fever of varying intensity, with great depression, and simultaneous
and equal implication of the head and the organs of the chest and
abdomen.
Many writers have sought to arrange the foregoing different forms of
influenza in definite categories. It would be a useless task to
reproduce their views upon the subject, or even to enumerate the
varieties that have been described. In practice, the various described
types merge so gradually into each other, and are so modified by the
individual peculiarities of the sick, and by the complications which
arise in the course of the attack in consequence of such peculiarities
or of previously existing diseases or tendencies to special forms of
disease, that, in point of fact, particular cases cannot usually be
referred to theoretical categories. Hysterical persons and those of a
nervous constitution are prone to suffer especially from the peculiar
nervous symptoms of influenza. The disease is also modified by the age
of the subject of the attack; children manifest in a high degree the
signs of cerebral congestion, while old persons are subject in a
peculiar manner to dangerous pulmonary complications, and those of a
gouty or rheumatic constitution suffer more than others from muscular
pains.
The duration of the mildest form of influenza is from two to three
days; in well-developed cases without complications convalescence sets
in between the fourth and tenth days; while severe cases with
complications last much longer, several weeks often elapsing before
recovery is complete.
SYMPTOMATOLOGY.--ANALYSIS OF THE SYMPTOMS.--For the purpose of
separate consideration it is convenient to take up the symptoms
belonging to the fever first, then those of the special catarrh, and
finally those more particularly referable to the nervous system; but
we encounter in the present state of our knowledge of the pathology of
influenza--or our ignorance of its pathology--no little difficulty in
deciding under which of these headings particular symptoms are
properly to be classed, by reason of the close interdependence of the
chief processes of the disease and the anomalies of its phenomena
viewed as a whole.
The Fever.--The fever is of the sub-continuous or remittent type,
{866} but its range is very irregular. Irregularity of temperature is
characteristic of influenza and may assume diagnostic importance.
The intensity of the fever is variable. As a rule, it is moderate or
slight; occasionally it is severe. I observed in several cases during
the epidemic of 1879 in Philadelphia an evening temperature of only 39
degrees C. (102.2 degrees F.). Da Costa in the same outbreak found the
febrile movement not high; the highest temperature he observed was 40
degrees C. (104 degrees F.). Biermer found a temperature of over 39
degrees C. in moderate cases of catarrhal fever, and does not doubt
that under certain transient conditions the temperature may reach the
height of that of pneumonia or typhus. In weakly persons and the aged
the fever is adynamic.
The pulse has no constant characters. Its frequency is moderately
increased; it is apt to be less forcible than in health, is generally
compressible, sometimes full, often irregular, changing in character
in the course of a few hours.
The urine is usually diminished; sometimes its secretion is
temporarily suppressed; as a rule, it shows little change, and is
rarely, as in other fevers, concentrated and high-colored. It deposits
on cooling a sediment of urates, which toward the close of the fever
is often very abundant. The defervescence is in many instances
attended by a copious secretion of urine. Albumen is not present
except as a result of some complication.
At first the skin is hot and dry; later, frequent sweats occur;
sweating generally attends the febrile remissions and the
defervescence not rarely sets in with copious, acid, ill-smelling
sweats. In some cases a tendency to sweat shows itself early and
continuous throughout the attack. Sudamina occur in great numbers.
The face is often flushed, and irregular mottlings of the skin,
especially upon the neck and chest, have been frequent in some of the
epidemics. An outbreak of herpes about the lips is occasionally seen.
Disturbances of the digestive tract are more or less prominent in
almost all cases. Only in a rudimentary and sub-febrile form are they
absent. In many cases they are such as are usually seen in febrile
disorders--namely, loss of appetite, thirst, impaired taste, pasty
tongue, tenderness in the epigastrium, and constipation. Nausea and
vomiting sometimes usher in the attack. In other cases (the so-called
abdominal form) all the above symptoms are more severe, and diarrhoea,
colicky pains, and vomiting are superadded. In certain epidemics the
intestinal catarrh has shown a tendency to run into dysentery.
The expression of the countenance is changed, in part by the
appearance characterizing an ordinary attack of coryza of considerable
or great severity, and in part by anxiety and depression. It is pale.
Where the pulmonary catarrh is excessive and dyspnoea great the lips
become bluish. The facies sometimes suggests that of typhoid fever.
The Catarrh.--A more or less extensive hyperaemia of the mucous
membrane of the respiratory tract is invariably present, and may be
said to characterize the disease.
There is cold in the head, more severe in most cases than ordinary
simple coryza. The eyelids are swollen and reddened, there is
lachrymation, sneezing is frequent, and the discharge from the nose is
abundant. Epistaxis is not rare. Sore throat, with tickling sensations
and difficulty {867} in swallowing, is due to inflammation of the
pharynx and neighboring parts. In many instances the catarrhal
symptoms are due to a pharyngitis and tonsillitis only, the lower
air-passages escaping. Hoarseness is common.
Cough is a prominent symptom. It is apt to be frequent and
distressing--sometimes paroxysmal from the beginning of the sickness,
almost always so at some period of its course. Its spasmodic character
in some of the older epidemics led to the confounding of epidemic
catarrhal fever with whooping cough. It is apt to be worse toward
evening and at night, but the sick are often tormented day and night
by the loud racking cough. It often leads to vomiting, and by its
violence and persistence gives rise to pain and soreness in the
muscles of respiration (myalgia), and occasionally to hernia. It is at
first dry or attended with a scanty muco-serous expectoration; later
on the sputa become opaque and muco-purulent, and in consumptive or
full-blooded persons or those having mitral disease they are sometimes
streaked or mingled with blood. Toward the close of the attack the
cough becomes less urgent and loses its spasmodic character. In some
epidemics cough is not a prominent symptom, and a few cases are
encountered in most epidemics in which well-developed influenza runs
its course without unusual, peculiar, or excessive cough. If the cough
be due to bronchitis, we find on auscultation the physical signs of
that affection. They are of course wanting when it is due simply to
laryngo-tracheal irritation. Hence we frequently detect sonorous and
sibillant or mucous and subcrepitant rales upon both sides of the
chest in the course of the attack, as in non-epidemic acute
bronchitis; and, on the other hand, cases occur where the auscultatory
signs are but little or not at all altered from those of health. It is
scarcely necessary to add that there are no special physical signs
that can be regarded as diagnostic of influenza.
Many patients suffer from dyspnoea. Although due in some instances to
complications, it occurs with remarkable frequency in those in whom
none of the objective signs of any pulmonary lesion can be discovered.
It is here of nervous origin. Graves assumes a direct disturbance in
the function of the vagus as its cause. This view is sustained by the
observation that the dyspnoea is now and then intermittent, or shows
rhythmically recurring remissions, which are unattended by alteration
of the physical signs. To Biermer it appears more probable that the
congestions so common in influenza, not attended by marked physical
signs until they lead to oedema, are to be regarded as the cause of
the dyspnoea. It varies greatly in intensity. In many patients it goes
on to marked oppression, great shortness of breath, precordial pain,
and the like. In certain epidemics orthopnoea and suffocative attacks
were very common. Stitches in the side and pain under the sternum are
observed without appreciable physical signs.
Symptoms Referable to the Nervous System.--Great prostration of
muscular strength is a very early symptom, and constitutes, in most
epidemics, one of the remarkable features of the disease. Patients
from the onset feel extremely weak, and are exhausted by the slightest
bodily effort. The ordinary strength is not regained until
convalescence is far advanced.
Headache is a constant symptom. Severe frontal pains are scarcely
{868} ever absent. They extend across the brow and deeply about the
orbits and at the root of the nose, having their seat in the
Schneiderian mucous membrane and its prolongations lining the frontal
sinuses and the nasal ducts. Sometimes the pain is referred also to
the region of the antrum of Highmore and to the Eustachian tube and
the middle ear. It occasionally extends over the whole head. Cutaneous
hyperaesthesia of the head and neck and stiffness of the neck-muscles
are also met with. The headache is often most intense; it lasts
commonly till the end of the attack, and may even outlast it. It
increases in severity with the fever and mental agitation toward
evening. The occurrence of epistaxis affords some relief.
Among the more constant symptoms of influenza are very severe pains in
the limbs. Patients experience sensations of soreness and bruising,
such as follow the most severe and unaccustomed muscular effort. Dull,
tearing, and burning pains are felt sometimes in particular muscles or
tendons; sometimes they are diffused over the whole body. Distressing
pains of a dragging or boring character in the loins and calves of the
legs are complained of. These pains are neither relieved nor
aggravated by gentle movement or by moderate pressure. A sense of
contraction of the chest and precordial distress also occurs, and
stitches in the side (pleurodynia), substernal pain, and pains in the
throat and nape of the neck are common. When the attack is severe the
patient is usually restless, sleepless, and anxious. Dizziness and a
tendency to faint occur on rising, particularly in women. Mild
delirium is not uncommon, but the more intense forms are occasionally
observed. Active delirium was thought to be a mortal symptom in some
of the older epidemics.
The inability to sleep bears no direct relation to the intensity of
the fever. It is seen in some cases where fever is slight or even
absent.
Somnolent states also occur. Great hebetude and torpor have marked
some epidemics. That of 1712 was called the sleepy sickness, by reason
of the prevalence of these symptoms.
In grave cases painful muscle-cramps, subsultus tendinum, twitchings
of particular muscles, and tremblings of the hands occur.
The mental power is enfeebled, and the acuteness of the special senses
is diminished.
COMPLICATIONS AND SEQUELS.--The most important complications of
influenza are inflammatory diseases of the lungs. The hyperaemia and
intense bronchitis already described as occurring in the severer cases
cannot properly be looked upon as complications. They constitute
rather essential processes of particular forms of the disease. But
capillary bronchitis, catarrhal pneumonia, and less frequently
croupous pneumonia, arise as complications in the course of the
disease. Satisfactory statistics are wanting, but Biermer estimates
that from 5 to 10 per cent. of the whole number of patients suffer
from inflammatory lung-complications, and holds that the bloodletting
so frequently practised by the older physicians was due to a desire to
combat inflammation. The comparative frequency of chest complications
in different epidemics varies greatly, but the estimate of Biermer may
be accepted as an approximate average.
Owing to the masking of the physical signs in the early stages and the
pre-existing pulmonary oedema, it is not always easy to recognize at
once {869} the occurrence of capillary bronchitis. This complication
is attended with increasing dyspnoea, decided lividity of the face and
extremities, and great prostration. Crepitant and subcrepitant rales
at the lower portions of the posterior dorsal regions, rapidly
spreading to all parts of the chest, without dulness at first and with
increased resonance later, instead of the signs of consolidation which
are met with in pneumonia, are the signs which attend its appearance.
Catarrhal pneumonia occurs insidiously, with gradual intensification
of the bronchitic symptoms about the fourth or fifth day, but it may
set in as early as the second day, or much later, during
convalescence. It is, as a rule, developed without chill or great
increase in the fever.
Old persons and those of feeble constitutions are most liable to the
foregoing complications.
Lobar pneumonia is less common. It is a late complication, occurring
toward the close of the attack or even when the patient is beginning
to get about. It is easily recognized, and differs in no wise from
acute lobar pneumonia occurring under other circumstances.
In October, 1880, influenza being prevalent in Philadelphia, both
epizootic and epidemic, but very mild both among horses and men, I
attended a medical student who, having had what he regarded as a cold
for about a week, had kept at his work without treatment, until, upon
the occurrence of a chill followed by grave thoracic symptoms, he was
obliged to betake himself to bed. I first saw him the following day in
the hospital of the Jefferson College. There were the symptoms of
acute lobar pneumonia, with the signs of extensive consolidation of
the left lung and pleurisy of the right side. Moreover, there were
delirium and jaundice. The urine was non-albuminous. The next evening
he died. At the same time many members of the class suffered from
influenza, and a careful inquiry into the history of the case of this
young gentleman satisfied me that the pneumonia had arisen as a
complication in a neglected and moderate severe catarrhal fever. Until
the eighth day before his death he was in excellent health. No
examination of the body was permitted.
Graves[21] thought that a kind of paralysis of the lungs, with great
oedema, takes place in some cases, and attributed it to an affection
of the vagus. It was his conviction "that the poison which produced
influenza acted on the nervous system in general, and on the pulmonary
nerves in particular, in such a way as to produce symptoms of
bronchial irritation and dyspnoea, to which bronchial congestion and
inflammation were often superadded."
[Footnote 21: _Annals of Influenza_.]
It is certain that localized collapse of the lung often occurs. White
and Guiteras attributed the consolidations of the lung to congestive
collapse due to enlargement of the tracheal and bronchial glands and
"disturbance of the great nervous tract about the root of the lung."
They were enabled to satisfy themselves of the existence of glandular
enlargement--adenopathie bronchique--in nine of their eighteen cases
by percussion practised in the method of M. Geneau de Mussy,[22] who
was the first to call attention to the importance of percussing the
spinous processes of the vertebrae over the course of the trachea.
Following this line in the healthy subject, a distinct tubular
(high-pitched and slightly {870} tympanitic) sound is elicited by
percussion down to the point of bifurcation of the trachea on the
level of the fourth dorsal vertebra. Opposite the fifth and downward
we get the lower-pitched pulmonary resonance. When the tracheal and
bronchial glands are enlarged, the tubular sound over the upper dorsal
vertebrae is replaced by dulness, which may contrast sharply, above
with the tracheal, and below with the vesicular resonance.
[Footnote 22: _Chirurgie medicale_, Paris, 1874.]
Some well-recognized peculiarities of the so-called pneumonias of
influenza give weight to the view that the consolidations are not, in
the beginning, pneumonic at all. Thus, we have at first weakness of
the vesicular murmur, then its absence; the respiration soon becomes
bronchial, without being preceded by dulness or the crepitant rale;
the extension of those consolidations from one part of the lung to
another is very irregular; the process is more apt to involve both
sides than one; the disappearance of the consolidation is frequently
very rapid.
The relations of cause and effect between collapse and catarrhal
pneumonia are so close that it is not difficult to see how the
condition spoken of may lead to secondary lobular or catarrhal
pneumonia. In truth, this is a frequent result of collapse from any
cause.
White and Guiteras do not adduce any post-mortem facts in support of
their theory. Peacock, however, observed in the epidemic of 1847
softening and enlargement of the bronchial glands in several cases,
and in one instance where there was no antecedent disease of the
lungs, and where the physical signs corresponded to some extent with
those of the cases upon which White and Guiteras base their views.
Gangrene of the lungs must be named as one of the less common
complications.
These complications are the chief cause of the danger of influenza in
the aged, the debilitated, and those suffering from previous disease
of the thoracic organs.
Pleurisy is rare except where there is coexisting inflammation of the
lungs. It may be associated with pericarditis. In old persons serous
effusions into the pleural sac are now and then encountered.
Troublesome laryngitis and chronic bronchitis may follow the attack.
In consequence of the extension of the catarrhal processes along the
Eustachian tube an actual inflammation of the middle ear is, in rare
instances, set up. Parotitis with salivation sometimes occurs,
likewise aphthous inflammations of the mouth.
Herpes labialis occasionally occurs toward the end of the attack; it
is then a favorable indication.
Phthisis may be developed in consequence of an attack of influenza,
and if phthisis be already established it is apt to run a more rapid
course. Emphysematous affections are aggravated; diseases of the heart
are unfavorably influenced; chronic nervous affections are made worse,
and, in particular, neuralgias are aggravated. Old neuralgias, that
have long ceased to give trouble, occasionally reappear during the
convalescence.
Persons subject to latent or chronic Bright's disease are especially
liable to the more serious manifestations of influenza. The fatal
termination of such cases not unfrequently occurs in consequence of an
attack.
Many of the older observers speak of the intermittent character of
{871} influenza in certain epidemics, and its tendency to run into
intermittents, particularly of a certain type, during convalescence.
This has not been observed in the outbreaks of later years, and it is
probable that in such instances an endemic malaria has modified the
epidemic catarrhal fever, or the former has broken out as the latter
passed away.
Pregnant women are in danger of aborting.
PATHOLOGY.--Our knowledge of the pathology of influenza is as yet very
imperfect. Biermer has described it as the sum of a series of
catarrhal manifestations developed under a common epidemic influence.
The close association of the various local affections arises from
their almost simultaneous occurrence as results of primary
pathological processes common to them all. Each of the three groups of
symptoms which make up the clinical picture of the disease--namely,
the fever, the catarrh, and the symptoms referable to the nervous
system--constitutes a distinct factor of influenza, and is a direct
outcome of the action of the infecting principle. There is no constant
interdependence among these groups, either in the order of their
succession or in their intensity. Thus, while all three groups are
commonly present from the beginning of the attack, any one of them may
be the first to appear or have an intensity out of all proportion to
each of the others. The fever is not a result of the catarrhal
inflammation, nor are the nervous symptoms the result of both the
others. They all spring directly from the action of the same cause.
This view is at variance with the opinion--based upon the fact that
ordinary acute local inflammatory diseases, tonsillitis, bronchitis,
and the like, sometimes run their course in a similar way to
influenza, with fever, nervous depression, and a serious sense of
illness--that influenza is a simple epidemic catarrhal inflammation.
The sudden onset of influenza, its not infrequent abrupt termination,
which suggests crisis, its unsparing seizure of great numbers of the
population, the severity of the nervous symptoms, and the amount of
laryngo-bronchial irritation, often out of measure with the lesions of
the mucous membranes,--all point to the action of a morbid agent
affecting the body at large. The severity of the symptoms also, in
many cases, is much greater than in similar acute non-specific local
affections, while the complications, and in particular the
recrudescence of fading neuralgias and the tendency to abortion, and
the sequels, as cough, weakness, headaches, flying pains, which often
remain long after convalescence, are evidences of its belonging to the
group of infectious diseases rather than to that of simple acute
inflammatory diseases.
In conclusion, it must be urged that the similarity of the symptoms in
many epidemics, occurring during the course of several centuries and
under different social conditions, and even different degrees of
civilization, forcibly demonstrates the specific and definite
character of the causes which give rise to influenza.
Very little light is thrown upon the pathology of the disease by the
anatomical changes found after death. Uncomplicated influenza is
rarely fatal. As a rule, the unfavorable termination is due to lung
complications. The essential lesions are congestion and catarrhal
swelling of the mucous membrane of the upper air-passages and the
bronchial tubes. These changes may be restricted, in the lungs, to the
trachea and larger {872} bronchi, or they may extend to the finest
twigs. They may amount to great thickening and deep capillary
injections of the mucous lining of the tubes, which contain clear,
frothy mucus or thick, viscid masses of muco-purulent secretion
unmixed with air.
More or less congestion of the gastric mucous membrane, and more
rarely of that of the intestine, is also met with. The solitary and
agminate glands of the intestine are not affected, save as the result
of special complications. A few observations relate to the finding of
enlarged and softened bronchial glands. More extended researches are
needed, not only upon this point, but also in the whole domain of the
pathological anatomy of the disease.
Hyperaemia, oedema, hypostatic congestions, splenization, catarrhal
pneumonia, and hepatization affect the lung-tissue in cases fatal by
the complications which are associated with such changes. The
tissue-changes of diseases existing prior to the attack of influenza,
such as old consolidations, tubercle, brown induration, emphysema, and
so forth, are of course frequently discovered.
DIAGNOSIS.--The discrimination of influenza from other affections
having some points of resemblance to it is, under ordinary
circumstances, unattended with difficulty. The march of the epidemic,
the number of persons attacked, the prominence of the nervous
symptoms, the rapidly developed debility, and the character of the
cough, usually severe out of proportion to the physical signs,
distinguish it from all other epidemic diseases.
It is to be differentiated from non-specific catarrhal affections
attended by fever, malaise, weakness, severe headache, and pain in the
extremities by a due regard to the causative relations of the two
affections. Simple catarrhs not rarely present the group of symptoms
which characterize epidemic catarrhal fever, but they occur almost
constantly as the result of great and sudden changes in the weather,
and are therefore met with in greatest frequency in bad seasons, and
are particularly common at the end of winter and in the spring.
Influenza is not in any way dependent upon the vicissitudes of the
seasons, and may occur, as has been shown, at all times of the year,
in wet or dry, mild or cold seasons equally, and in every variety of
climate. It is of course diagnosticated without difficulty from the
sporadic catarrhal fevers, which lack the characteristic depression,
neuralgic and rheumatoid pains, the irritative cough, dyspnoea, and so
on.
Cases of influenza are met with that bear a strong resemblance to
beginning enteric fever. The malaise, headache, obtunded hearing,
mental depression, high fever, coated tongue, tender belly, diarrhoea,
are symptoms to be observed in both affections. But influenza lacks
the temperature curve, the splenic enlargement, and the eruption of
enteric fever, and the progress of the disease will in a few days
clear up the most doubtful case.
PROGNOSIS AND MORTALITY.--Death is rare in uncomplicated cases. The
very young bear influenza badly; the old bear it more badly still.
Nevertheless, children have in some epidemics enjoyed a considerable
proportionate immunity. Healthy persons in the middle periods of life
bear it well. Certain pre-existing diseases modify its course
unfavorably; among these are chronic bronchitis, emphysema, fatty
heart, and Bright's disease. {873} The debility of advanced phthisis
and other exhausting diseases renders influenza dangerous. Death takes
place, in by far the greater number of cases, as the result of the
complication of the attack, either by some pre-existing affection or
by an acute disease arising in its course. The commonest of the latter
are inflammations of the parenchyma of the lungs.
Patients presenting very severe symptoms generally recover if they be
not the subjects of complicating maladies or very young or very old.
Relapses are not uncommon; independently of relapses, second attacks
have been known to occur during the continuance of an epidemic; it is
often the case that an individual in the course of his life passes
through several epidemics of influenza, and is the subject of the
disease in each of them.
The prognosis is greatly modified by the character of the prevailing
epidemic. In some epidemics the deaths are few, and the mortality from
other diseases does not appear to be greatly augmented. In others many
die of the epidemic disease, and the death-rate of certain endemic
affections is much increased. In some of the older epidemics the high
mortality was doubtless due to injudicious measures of treatment,
among which bloodletting and other depressing agencies were
conspicuous. Some of the older accounts also warrant the suspicion
that a coexisting typhus had to do with the high death-rate. It is
estimated that in the epidemic of 1837, which was a very severe one, 2
per cent. of those attacked died. The proportion of fatal cases in
particular epidemics varies in different countries, and even in
different quarters of the same city.
TREATMENT.--Efficient measures of prophylaxis are as yet unknown.
Unfavorable hygienic surroundings, overcrowding, a damp, unhealthy
locality, appear to increase the prevalence and severity of influenza.
The opposite conditions of living do not, however, secure immunity
from the attack. During an epidemic aged persons, those enfeebled by
chronic diseases, and in particular those subject to chronic
bronchitis, consumption, emphysema, fatty heart, and Bright's disease
should be cared for with unusual diligence and solicitude, since they
constitute the classes most prone to the graver complications of the
disease, and from which its fatal cases are almost wholly derived.
Such individuals should be warmly clad; they should shun, so far as
possible, the vicissitudes of the weather, even, if practicable,
keeping within warmed and well-ventilated apartments; they should
exercise unusual prudence in diet and lead a carefully regulated life,
with long hours of sleep. It is true that these measures are not
preventive of the attack. Families not quitting the house, living in
the greatest seclusion, even the bedridden, do not always, or even as
a rule, escape. Yet it has frequently been observed that those whose
occupations are carried on in the open air are attacked earliest and
in greatest numbers. On the other hand, in rare instances, persons
isolated from the community with strictness--in prisons, cloisters,
hospitals--have remained free from the disease prevailing around them.
It therefore appears probable that, under certain favorable
circumstances not as yet perfectly understood, the avoidance of the
open air and of the direct influences of the weather may confer some
degree of immunity from the attack, and it is desirable that the class
of persons most liable to the graver consequences of the disease
should avail themselves of even the most uncertain precautions.
{874} The treatment of influenza is expectant and supporting. Not only
is the epidemic self-limiting, tending to exhaust the susceptibility
of a community, in most instances, in the space of a few weeks, but
the attack is also of definite duration, and the perturbations set up
by the action of the influenza-poison upon the individual subside
spontaneously in three or four, or at most ten or twelve, days. The
susceptibility of the individual is also, for the time being,
exhausted, for second attacks in the same epidemic are not very
common. In cases where the duration of the attack is prolonged beyond
the period indicated, it is kept up by complications, and we have to
do not so much with the pathological processes of influenza as with
secondary diseases that the influenza has excited either by the
intensity of its action or by reason of some peculiarity of the
subject of the attack.
By far the greatest number of cases are light and unattended by
danger. The treatment is therefore, for the most part, an extremely
simple one. These lighter cases seldom require medical measures. The
patients are uncomfortable and anxious, easily fatigued, and unfitted
for business. It is best that they keep the house, and, if willing,
the bed or sofa, for the space of two or three days. The diet should
be restricted to a few simple and easily-digested dishes. Meat should
be avoided. The common custom of taking hot beef-tea is an extremely
bad one; it often increases the headache and languor. Moderate
quantities of cold drinks may be taken. The fruit-syrups, lemonade,
raspberry vinegar, a weak solution of citrate of potash or of cream of
tartar, and barley-water with lemon, are useful. Very weak wine-whey
is often liked. The effervescing mineral waters or Apollinaris are
preferred by many persons. The best of such drinks is a mixture of
equal parts of Seltzer-water and milk, iced. If the stomach be
irritable, koumiss will be found an excellent beverage and food. In
the mild cases stimulants are not necessary. Sound claret, with or
without Seltzer-water, is not contraindicated. In all cases the amount
of fluid taken should be moderate.
Quinine in moderate doses should be taken from the onset. The
head-pains are not increased by it. Dover's powder, if well borne,
should be administered at night. Some form of opiate may be required,
even in mild cases, to counteract wakefulness. A compressed pill,
containing extract of opium 0.030 gramme (gr. 1/2), camphor 0.15 (gr.
ij), and ammonium carbonate 0.15 (gr. ij), will be found useful when
Dover's powder cannot be employed. During convalescence iron and barks
are often requisite.
The coryza, tonsillitis, laryngitis, bronchitis are to be treated
according to general principles, if they require treatment at all. In
most mild cases the catarrhal symptoms call for no special measures of
treatment.
Free inunctions of fatty substances about the brow and over the bridge
of the nose are of use as regards the coryza. For this purpose animal
fats, washed lard, simple cerate, cold cream, and the like are to be
preferred to cosmoline and vaseline.
Morphine dissolved in cherry-laurel water, one part in fifty or sixty,
is useful for the relief of the head-pains associated with the coryza.
A few drops may be snuffed up from time to time. These pains are
mitigated to some degree by wearing a flannel cap or wrapping the head
in a silk handkerchief. Warm applications sometimes give comfort,
while cold almost invariably add to the distress.
{875} Distress in the upper air-passages and the tickling cough call
for steam inhalations, and the air of the apartment may be rendered
moist by the evaporation of water kept boiling in a broad, shallow
vessel. Gargles of potassium chlorate, or potassium chlorate with
sumac, exert a soothing influence upon the congested tonsils.
Severe cases call for more energetic measures of treatment. The most
prominent indications are the control of the fever; the diminution of
the hyperaemic fluxion to the mucous tracts; measures of support; the
mitigation of pain and the induction of sleep; and, finally, the
prevention of the pulmonary congestion, to which the depression leads
by enfeeblement of the circulation. The last indication is especially
urgent in infants, the very old, and those previously debilitated from
any cause.
Inflammatory complications require special treatment or modifications
of treatment.
The febrile movement is not, as a rule, high; grave nervous symptoms
and serious catarrh may be associated with moderate fever.
An anti-febrile regimen is to be observed. The moderate duration of
this fever, as compared with enteric fever, renders it less important
that large amounts of fever-food should be given, while the tendency
to depression makes it of the utmost importance that the
administration of food be systematic and carefully looked after by the
medical attendant. The disinclination to take food is so great that it
is often with difficulty that a sufficient quantity can be given in
the early days of the attack, and it is to be doubted whether benefit
follows anything in excess of the most moderate amount. It is
necessary to observe regular hours, as in the management of all the
low fevers. As soon as convalescence begins the patient should be
urged to eat; the quantity of food taken at one time is to be
augmented, and the intervals between the meals may be longer.
A favorable action upon the excretory function of the skin and kidneys
will result from the moderate drinking of water or of the beverages
already spoken of. At least enough fluid should be taken to relieve
thirst.
Diaphoretics have been much used, upon the theory that by
determination to the skin they correspondingly diminish the tendency
to hyperaemia of the affected mucous tracts. Dover's powder, solution
of the acetate of ammonia, and other mild diaphoretics are to be
selected. Jaborandi should be employed with caution. The wet pack and
other hydrotherapeutic measures have been employed to act upon the
skin and to effect a direct reduction of temperature in influenza. For
old and feeble persons warm packs are employed. A profuse sweating at
the onset of the attack is said to occasionally cut it short. Early
diaphoresis often brings about a rapid and lasting amelioration of the
symptoms. It is to be borne in mind that the fever is rarely
excessive, and that sweating is not infrequently a troublesome
symptom. In some epidemics it has been a very troublesome one.
General bloodletting is not to be resorted to in influenza. Its danger
was apparent to some of the early writers. As has been pointed out,
the high mortality of some of the older epidemics is to be explained
by the venesections practised at the beginning, and even during the
course, of the attack. It has no favorable effect upon the catarrhal
processes, and but little upon the subjective symptoms. The fever is
not relieved by it; the {876} nervous depression is increased and the
risk of lung-congestion is augmented. Bleeding is not likely to be
practised in epidemic catarrhal fever while the present views of its
place in therapeutics continue to influence practice. Cautious local
bloodletting for the relief of local inflammatory trouble is spoken of
in most of the modern books. The occasions for its employment are so
rare in the treatment of this disease that even this statement should
be henceforth omitted. In influenza, as it is known to medical men of
the present from the descriptions of the old and personal experience
of the few recent and milder epidemics, bloodletting, either general
or local, is clearly uncalled for.
Emetics hold a high historical place. It was of old customary to begin
the treatment with a vomit. As late as the epidemic of 1837, Lombard
of Geneva believed that they shortened the attack and lessened the
intensity of the symptoms when administered at the beginning. In cases
attended by early gastric disturbance and nausea they are said to be
especially of use. They sometimes set up great irritability of the
stomach, with vomiting that it is difficult to control. On the whole,
the cases in which an emetic would do good are extremely rare.
Purgatives were formerly regarded as important in the treatment. This
view no longer prevails. In case of constipation gentle purgation, ex
indicatione symptomatica, is a necessary part of the proper management
of the case. For this purpose the laxative mineral waters, as
Friederichshalle, Hunyadi, Pullna, are excellent. Castor oil may be
given, and calomel is in some cases, and particularly in childhood, of
great service. Simple enemata of warm water or soap and water will
often suffice. The tendency in some cases to exhausting and
troublesome diarrhoea, and the fact that diarrhoea occurs
spontaneously some time in the course of most cases, should inspire
caution in the use of purgatives. Repeated purgation during the
progress of the attack is not only useless--it is also positively
injurious.
In the severe cases quinine is to be given early and in full doses. It
exerts at the same time a powerful influence upon the temperature,
upon the tendency to local hyperaemias, and upon the nervous symptoms,
and in particular the headache. Rawlins,[23] as early as 1833, found
that excellent results followed its administration, the effect being
the better the earlier it was given. It has even been lauded as a
specific for influenza.
[Footnote 23: _London Medical Gazette_, May, 1833.]
The mineral acids may be given with a view to realizing their tonic
effects.
For the most part, the foregoing measures, directed against the fever,
will exert a favorable influence upon the catarrhal processes.
Expectorants are of advantage; ipecac is useful. The preparations of
antimony are inadmissible by reason of their tendency to depress.
Ammonium chloride is indicated in the earlier stages of the
bronchitis. Among recent drugs, yerba santa (Eryodiction glutinosum)
and the oil of eucalyptus are of use in mitigating the symptoms in
epidemic catarrh, as they do in certain forms of simple sporadic
catarrh.
The peculiar dry, racking cough so often present in the early days of
the attack should be relieved. It is not useful in removing bronchial
accumulations, being, as has been shown, in most instances out of
proportion to the lesions of the bronchial mucous membrane; on the
other {877} hand, it tends to increase the hyperaemia of the upper
air-passages by the mechanical violence of the cough-paroxysms.
Further, it is distressing and exhausting, and contributes to the
muscular and nervous prostration. Benefit will be derived from keeping
the air of the apartment moist, and from the occasional inhalation of
the steam from hot water, either used alone or poured upon the
compound tincture of benzoin, a pint to the teaspoonful, or upon
paregoric, a pint to the tablespoonful, in a proper vessel or inhaler.
No drugs are more potent to this end than opium and its derivatives,
and in particular morphia and codeia. The hypodermic use of the
morphia salts, judiciously resorted to, constitutes our most valuable
therapeutic resource in fulfilling the threefold indication of
relieving cough, alleviating both the head-pain and the pains in the
extremities, and in procuring sleep. The old-time dread of opium in
influenza was not well founded. The administration of this drug in
moderate doses is attended with advantages that far outweigh any
danger of increasing the tightness across the chest and retarding
expectoration. It is necessary to observe the same caution in giving
it to infants and aged persons in influenza that is necessary under
other circumstances. The influence of carbolic acid in restraining
cough makes it a useful addition to soothing draughts in this disease.
The substernal and other chest-pains may be combated with sinapisms,
turpentine stupes, repeated inunctions of fatty substances containing
extract of belladonna, and the like. Pleurodynic stitches call for
similar measures; a long strip of machine-spread belladonna plaster,
about five centimetres (two inches) in width, applied very firmly to
the side of the chest from the spine in a direction downward and
forward parallel with the ribs, and reaching to the median line in
front, affords great relief to the lateral chest-pains.
The control of the debility must be regarded as the most important
indication in old and feeble persons. Wine, spirits, milk-punch,
ammonia, spirits of chloroform, are to be used, not in accordance with
fixed rules, but as occasion may require. In many cases wine or
whiskey will be indicated from the beginning, the quantity being
determined rather by the effect upon the circulation and the general
condition of the case than by rule. Women and others unaccustomed to
the use of alcoholic drinks often take wine and brandy in considerable
quantities, with striking benefit and without flushing or other
evidences of its disagreeing.
Chloral is inadmissible as a hypnotic by reason of its depressing
effect upon the heart. Paraldehyde may be used, or the bromides in
connection with opium if the latter alone is not well borne.
Diarrhoea must be managed in accordance with general principles. If
slight, it does not require special treatment. It is apt to occur at
one period or another in the course of most cases, and not
infrequently marks the beginning of convalescence. Colic may be
treated with warm fomentations and carminatives; if it be due to
constipation, mild laxatives are to be combined with them.
Severe cases of influenza demand the careful attention of the
physician, who must be on the alert to detect the inflammatory lung
complications which so often lead up to the fatal issue as early as
possible. Their treatment must be regulated by the circumstances of
the case, the nature {878} of the particular complication, the age of
the patient, and so on, in accordance with general therapeutical
indications.
Finally, all measures, of whatever kind, that tend to depress the
general nervous system or the functional activity of the respiration,
and especially the heart-power, are to be sedulously avoided in the
management of influenza. During the convalescence unfavorable
influences of the weather are to be guarded against. It is important
to warn the patient that a severe attack of influenza renders him
liable for some time afterward to pulmonary disorders. The sequels,
and in particular those implicating the respiratory tract, are to be
appropriately treated. After severe cases a course of tonics is
commonly of advantage, and a change of climate often necessary to
re-establish the health.
As bearing on what is stated in the foregoing pages on the causation
of influenza, reference may be made to the investigations of
Seifert,[24] who claims to have found in the mucus expectorated by
patients with influenza numbers of a peculiar micrococcus. It is
evident, however, that no conclusions can be based upon these
observations until the results have been subjected to careful
examination in other epidemics.
[Footnote 24: _Volkmann's klinische Vortrage_, No. 240, June 20,
1884.]
{879}
DENGUE.
BY H. D. SCHMIDT, M.D.
SYNONYMS.--Break-bone fever, Dandy fever.
HISTORY.--The history of this disease dates only from the second half
of the last century, though it appears very probable that previous to
this time dengue existed in the tropical regions of Africa and Asia,
whence it was carried to Europe and America.
In Spain the disease has been known since 1764, when, up to 1768, it
prevailed in Cadiz and Seville under the name of la piadosa or la
pantomina.[1] In 1780 it appeared in the form of an epidemic in
Philadelphia, where it was first noticed and described by Rush under
the name of bilious remitting fever, commonly called break-bone fever
on account of the violent pains attending it. Next it prevailed in
Calcutta in 1824, and two years afterward it made its first appearance
on the southern coast of the United States, in Charleston and
Savannah, where it prevailed to 1827. Toward the close of 1827 another
dengue epidemic broke out in the West Indies, whence the disease
proceeded to the American continent, reaching New Orleans in the
spring, and visiting Charleston and Savannah in the summer and autumn
of 1828.[2] In 1844 it showed itself in Mobile, and in 1848 in
Natchez, whilst in 1850 it reappeared along the Southern seacoast,
particularly in Charleston, from which it proceeded even to inland
towns, such as Augusta, Ga.[3] In 1865 dengue appeared in Teneriffe
and other Canary Islands, whilst at the same time and through the
years 1866 and 1867 it prevailed in Andalusia and in some other
Spanish provinces.[4]
[Footnote 1: R. H. Poggio, _La calentura roja observada in sus
apariciones epidemicas de los anos 1865 y 1867_, Madrid (reported in
_Virchow und Hirsch's Jahresbericht fur das Jahr 1871_, vol. ii. p.
200).]
[Footnote 2: G. B. Wood, _Practice of Medicine_, 4th ed., vol. i. p.
444.]
[Footnote 3: S. H. Dickson, _Elements of Medicine_, 2d. ed., p. 747.]
[Footnote 4: R. H. Poggio, _Virchow und Hirsch's Jahresbericht fur das
Jahr 1871_, vol. ii. p. 200.]
One of the most extensive epidemics of dengue prevailed from July,
1870, to January, 1871, in Zanzibar,[5] on the East Coast of Africa,
whence it extended to Aden in Arabia and Port Said in Egypt. In
December, 1871, the disease appeared simultaneously at Bombay and
Calcutta,[6] to which place it had been carried by transport-ships
from Aden. Proceeding from Bombay in a northern direction along the
railroad, it spread {880} over the central regions of the
North-western Provinces, the Rajputana states, Cashmir, and the
Punjaub. From Calcutta it passed over Assam and Bhotan to Thibet, and
thence downward into Burmah and to all the large cities along the
coast; while it also extended along the coast of Malabar over
Visigapatam to Madras and Pondichery, finally arriving at Mysore. Thus
the disease had actually spread over the whole Peninsula from Cape
Tutikorin to the foot of the Himalayas, attacking equally all races or
nationalities without regard to age, occupation, or position. Forty
years previously, however, an epidemic of dengue had prevailed in
Burmah. In 1873 it appeared on the island of Mauritius, to which it
had been carried from India by an emigrant ship. In the same year a
considerable number of cases of dengue were observed in New Orleans.
In 1877 it appeared again in Egypt, where it prevailed in Ismailia.
[Footnote 5: J. Christie, "Remarks on Kidniga Pepo, a peculiar form of
exanthematous disease epidemic in Zanzibar, East Coast of Africa, from
July, 1870, to January, 1871," _Brit. Med. Journal_, July 1, 1872, p.
577 (reported in _Virchow und Hirsch's Jahresbericht fur das Jahr
1872_, vol. ii. p. 203).]
[Footnote 6: _Virchow und Hirsch's Jahresbericht fur das Jahr 1873_,
vol. ii. p. 208.]
Finally, in 1880, dengue, in the form of a very extensive epidemic,
prevailed once more along the Southern coast, visiting equally
Charleston, Savannah, and New Orleans. A number of valuable
observations concerning the nature and symptoms of the disease were
made during this epidemic by Drs. D. C. Holliday of New Orleans, J. G.
Thomas of Savannah, and F. T. Porcher and J. Forrest of Charleston.[7]
At the same time it prevailed at Alexandria[8] (Egypt) to such an
extent as to affect nearly the whole population.
[Footnote 7: The papers of Drs. Holliday, Thomas, and Porcher were
read before the American Public Health Association at its annual
meeting, December, 1880, and published in the _Proceedings_ of the
Association. Dr. Forrest's paper was published in the _American
Journal of Med. Science_, April, 1881.]
[Footnote 8: A. Vernoni, "Le Dengue a Alexandrie d'Egypte en 1880,"
_Gaz. hebd. de med. et de chir._, 41, 42 (reported in _Virchow und
Hirsch's Jahresbericht fur das Jahr 1880_, vol. ii. p. 5).]
Dengue has been known under various popular names which it received
from the people of the particular localities where it appeared in
epidemic form. Even the designation, dengue, itself, by which the
disease is at present generally known to the medical profession of the
leading civilized nations, is of popular origin,[9] for it is supposed
to be a Spanish corruption of the word dandy, the name of dandy-fever
having been jocosely conferred on the disease by the negroes of St.
Thomas from the stiff carriage of those affected with it. At Zanzibar
it received the popular name of kidniga pepo, signifying spasmodic
pains.
[Footnote 9: G. B. Wood, _Practice of Medicine_, 4th edit., vol. i. p.
444.]
DEFINITION.--Dengue is a peculiar febrile disease, generally appearing
epidemically in tropical or semi-tropical regions, and characterized
by a single paroxysm with or without remissions, severe pains, and
stiffness in the joints and muscles, a peculiar exanthematous
eruption, and almost never terminating fatally.
SYMPTOMS, COURSE, AND DURATION.[10]--Dengue never commences with a
decided chill, though in many cases the attack of the disease is
preceded by a feeling of general uneasiness and depression, vertigo,
and headache, or even by a slight chilliness--a condition which may
last from a few to twelve or even eighteen hours. In the majority of
cases, however, the disease appears suddenly, very frequently at
night, and announces itself at once by pains and a feeling of
stiffness in the muscles, joints, back, and loins; in severe cases the
pain may even extend to the {881} bones.[11] The larger and smaller
joints are equally affected, either simultaneously or successively,
and frequently swollen, those of the hands and feet generally before
the others. The pain in the joints is increased by motion, and is
therefore justly regarded by most authors as rheumatic in nature. The
same may be said of the muscles. Sheriff even observed redness of the
skin covering the joints. According to the degree of severity of the
case these pains may be more or less intense. In some cases
hyperaesthesia of the skin of the palms of the hands and of the soles
of the feet has been observed.
[Footnote 10: Judging from the various accounts rendered by a
considerable number of observers, it appears that the clinical
symptoms of dengue had been the same in all the different localities
on the globe where it has hitherto prevailed epidemically.]
[Footnote 11: M. Sheriff, "History of the Epidemic of Dengue in Madras
in 1872," _Med. Times and Gazette_, Nov. 15, p. 543 (reported in
_Virchow und Hirsch's Jahresbericht fur das Jahr 1873_).]
Simultaneously with the affection of the joints and muscles the fever
commences; its duration is from four to five days on the average, with
one or, in exceptional cases, even more remissions. The temperature of
the body during the first and second days of the fever rises to 102,
103, or even to 105 degrees F; it then declines, to return to the
normal standard on the fifth day. According to the measurements made
by the late Dr. D'Aquin[12] of New Orleans, the temperature curves of
dengue showed a continuous and steady rise until the highest point was
reached on the first, second, or third day of the attack; then comes a
short stadium of a few hours, and then a remission, soon to be
followed by another rise of temperature, which, however, never reaches
the maximum point of the first. The pulse rises with the temperature
of the body, generally to from 80 to 120 beats a minute, and
subsequently declines with the temperature. Delirium is very rarely
observed in adults, but frequently in children, though without
aggravation of the other symptoms. The face is generally flushed, the
eyelids swollen, and the eyes injected and watery. The tongue in the
beginning of the disease is covered with a white fur; its edges are
red and its body swollen. As the disease advances the coating
increases in thickness and assumes a dirty yellow color. The appetite
is lost, without excessive thirst. In many cases there is slight
irritability of the stomach, accompanied sometimes with nausea, though
vomiting rarely takes place. The condition of the bowels is variable.
The urine is small in quantity, and highly colored in some cases,
whilst in others it has been reported to be pale and copious, and rich
in phosphates in the beginning of the disease; it seldom shows any
sediments and very rarely contains albumen. The disease generally
reaches its acme on the third or fourth day, when the fever commences
to subside, and an amelioration of the other symptoms takes place, so
that the patient feels greatly relieved. This, however, is only of
short duration, for not many hours afterward the fever rises again,
while the other symptoms also increase in severity. At this time an
exanthematous eruption appears upon the upper part of the body, the
face, neck, breast, and shoulders, which in the course of two days
extends over the whole body. Simultaneously with the appearance of the
eruption the lymphatic glands of the back of the head and those of the
neck, axillae, and groins commence to swell; in severe cases the
mucous membranes of the nose, mouth, and pharynx also become
congested. The eruption, which is attended with much heat, itching, or
even pain, is not uniform in character; for while in some cases it may
{882} represent a simple rash or erythema, it resembles in others the
eruptions of scarlatina, rubeola, lichen, or urticaria. Frequently it
is very light and evanescent, showing itself only for a few hours, and
perhaps in the majority of cases it does not appear at all. In the
severer cases it generally remains two days, when it commences to fade
and disappear with desquamation, while at the same time the fever
subsides and disappears entirely, though the stiffness and soreness in
the joints and muscles, together with the inflammatory condition of
the superficial lymphatic glands, may persist for many weeks. In
exceptional cases the eruption, after an intermission of a few days,
reappears, generally with greater intensity and with an aggravation of
the other symptoms. In others, again, it has been observed to remain a
whole week.
[Footnote 12: D. C. Holliday, "Dengue or Dandy Fever," read before the
Amer. Publ. Health Assoc. at New Orleans, December, 1880.]
Hemorrhages from the nose and gums are also occasionally observed.
Holliday even observed the occurrence of black vomit in the cases of
two female children, aged respectively six and twelve, in the same
family, who had suffered from yellow fever in 1878; they both
recovered from the attack of dengue, though they were extremely ill
and much prostrated. In female patients an attack of dengue not
unfrequently causes the reappearance of the menstrual flow, while the
pains attending the disease equally predispose to premature labor in
pregnant women.
In severe cases of dengue the prostration following upon the
subsidence of the fever is very great, for the patient is affected
with a general weakness both of body and mind, indicating a great loss
of nervous energy. In some cases observed by Slaughter the memory for
names and words, as well as the ability for correctly writing even
short sentences, was lost for one or two weeks after the commencement
of convalescence. In children also cases are reported in which the
mind remained affected for a short time after the attack. The
convalescence in dengue, therefore, is comparatively slow,
particularly as the pains in the muscles and joints, as already
mentioned, pass away only gradually.
The duration of the disease, including the stage of convalescence, of
course depends upon the degree of intensity of the attack, and
accordingly varies in different cases. In a great number of cases
dengue manifests itself only in its milder form. The average duration
of the disease is from three to six days.
PATHOLOGY.--The pathological changes taking place in the different
organs during the course of dengue are unknown, on account of the
almost constantly favorable termination of the disease. From the
peculiar features of some of the clinical symptoms accompanying the
disease, however, we may speculate to a certain extent upon the nature
of the pathological processes to which they are due. The sudden
appearance of the characteristic pains in the muscles and joints, but
particularly those in the head, neck, and loins, accompanied by a
comparatively high fever, evidently point to the presence of an
infectious poison in the system, though the question whether the
noxious influence of this poison primarily affects the blood or the
nervous system will be difficult to answer. But, judging from the
early appearance of the pains, as well as from the physical and mental
depression of the patient, we may presume that the nervous system is
involved from the very beginning of the disease, and that the pains
depend upon a hyperaemic condition of the affected parts, probably
caused by a vaso-motor paralysis. The great resemblance of the painful
{883} affection of the muscles and joints in dengue to that of acute
articular rheumatism leads to the supposition that the pathological
condition in these joints is the same in both diseases; this view
appears to be held by the majority of medical observers. In dengue, as
in rheumatism, the pain due to the pressure of the hyperaemic and
swollen tissues upon the irritated sensory nervous filaments is
increased by motion--a phenomenon generally absent in neuralgia. The
persistent headache, restlessness, and want of sleep, as well as the
delirium and loss of memory observed in the severer cases, furthermore
indicate a hyperaemic condition not only of the pia mater, but even of
the brain-substance.
It is to be regretted that the literature of dengue within our reach
shows no record of a quantitative analysis of the urine, from which we
might have learned the quantity of urea secreted during the different
stages of the disease, and which might have enabled us to form some
idea of the extent of the destruction of the albuminous substances
during the febrile stage, though, judging from the high grade of fever
observed in the severer cases, we may well presume that the
interchanges of matter are considerably augmented during this stage;
while, on the other hand, the great nervous prostration of the patient
directly after the subsidence of the fever, as well as the tardy
convalescence, sufficiently shows that a large part of this waste is
derived from the nervous tissues. The exanthematous eruption,
representing a hyperaemia, or even an inflammation, of the skin,
furthermore contributes to depress the nervous system by the pain and
itching which it causes. This eruption, together with the inflammation
and swelling of the superficial lymphatic glands, we are inclined to
associate with the final elimination of the infectious poison from the
organism.
Very little also is definitely known about the condition of the
remaining organs, such as the kidneys, liver, and alimentary canal.
The examinations of the urine in dengue recorded in literature are
very few in number, and appear too unreliable for drawing any definite
conclusions from them with regard to the condition of the kidneys. As
albuminuria is met with in other infectious diseases, it is not
impossible that it has also occurred in severe cases of dengue; though
from the favorable termination of the disease it appears quite
improbable that organic changes take place in these organs. In the
same way may the liver be functionally deranged, or, judging from the
destruction of matter during the febrile stage, a slight fatty
infiltration of the organ may even occur--conditions which are apt to
pass away with the exciting cause. The gastric irritability, whenever
present, may be of nervous origin, though the vomiting, and
particularly that of black hemorrhagic matters, observed in
exceptional cases, evidently depends upon a hyperaemia of the stomach.
ETIOLOGY.--There is nothing positively known of the origin of dengue,
but in perusing the accounts given by a number of medical observers
from the different localities of the globe where it prevailed, we may
presume that it existed in some parts of Asia and Africa long before
it appeared in Europe and America. Perhaps the earliest record of
dengue is the one dating from Cadiz and Seville, and concerning the
epidemics prevailing in the cities in 1764 and 1768, when it was
believed by the people that the disease had been imported from Africa.
In Zanzibar (Christie), during the epidemic of 1870, the older native
inhabitants {884} remembered that fifty years before the disease had
prevailed in this place. The Arabians living at this island also had
known the disease in their own country, while the inhabitants hailing
from the East Indies had never seen it. From the accounts of other
writers we may presume that dengue has been known in Arabia for many
generations. But, leaving aside its origin, it is authentically known
that wherever dengue has appeared it has almost always been in the
form of an epidemic, spreading from place to place and from family to
family, without respect to race or nationality, to age, occupation or
position, until every one susceptible to the disease was affected.
Slaughter reports from India that even domestic animals, especially
dogs and cats, were not exempt, as they appeared to suffer from
rheumatoid affections of the joints.
Although toward the end of the last century dengue once prevailed
epidemically in the temperate zone, at Philadelphia, it must
nevertheless be considered as a disease especially at home in the
tropical and semi-tropical regions, where it prefers to haunt low
lands, particularly along the sea-coast, leaving almost untouched more
elevated places. Though nothing definite is known about its special
cause, its history and symptoms evidently show that it is not only
infectious, but also highly contagious, in its nature, and in
consequence must be caused by the entrance of a specific poison into
the system. This view is held by the great majority of physicians
residing in the various localities of the globe where the disease has
prevailed. But, contagious as it may be, it greatly distinguishes
itself from other contagious diseases by almost never proving fatal.
As dengue generally prevails in the summer season and disappears with
the approach of cold and rainy weather, its cause is apparently
subject to the influence of certain meteorological conditions.
DIAGNOSIS.--When dengue appears epidemically, it is distinguished from
other diseases without difficulty. The only disease with which it
might be confounded when appearing in a sporadic form is acute
articular rheumatism. But even from this affection it may be
distinguished in its earlier stage by the pains not being limited to
the joints, as is generally the case in articular rheumatism, but
being also present in the head, back, and loins. Dengue is, moreover,
characterized by a general physical and mental nervous depression,
while in rheumatism the mind almost always remains clear. In the
latter stage the peculiar eruption and painful swelling of the
superficial lymphatic glands in dengue decides the question.
It has frequently been stated that dengue resembles yellow fever, and
some physicians have even regarded it as a mild form of this disease.
In examining attentively, however, the temperature of the patient
during the febrile stage, it will be found that while it steadily
rises in yellow fever, it is remittent in dengue. There is,
furthermore, a difference observed in the state of the pulse, which in
yellow fever generally falls on the third day, while the temperature
continues to rise; in dengue, on the contrary, the pulse rises with
the temperature. In the condition of the stomach also dengue
considerably differs from yellow fever, for while in the latter
disease this organ is almost always irritable, and vomiting is very
frequently present, it is but rarely affected in dengue. The urine in
yellow fever very frequently contains albumen as soon as the third
day; in dengue, almost never, so far as the analyses recorded enable
us {885} to judge. Finally, the absence of jaundice and the appearance
of the eruption on the fourth or fifth day remove all doubt about the
nature of the disease. There are a number of other points by which
dengue may be distinguished from yellow fever, which we, however,
forbear to enumerate, for the reason that those already mentioned will
suffice for a correct differential diagnosis.
PROGNOSIS.--Dengue, as has been stated before, scarcely ever
terminates fatally unless it is complicated by some intercurrent
disease. The prognosis, therefore, is highly favorable.
TREATMENT.--Nearly all authors recommend a symptomatic treatment in
dengue, beginning with a mild cathartic, mercurial or not, and
followed by a mild diaphoretic. To relieve pain and procure sleep
opium--either uncombined or in the form of Dover's powder--belladonna,
camphor, assafoetida, valerian, etc. have been recommended by
different physicians; liniments containing camphor or chloroform have
also been used with advantage for the same purpose. Foot-baths have
been recommended to relieve the headache. To relieve the stiffness of
the muscles and the articular pains after the subsidence of the fever
iodide of potassium appears to be a favorite remedy in the East.
Colchicum combined with aconite is also recommended for this purpose,
as well as artificial sulphur baths and massage. The nervous
depression during convalescence is to be combated with tonics and with
regulation of the diet. Quinia appears to be generally discarded as a
remedy in dengue.
{886}
RABIES AND HYDROPHOBIA.
BY JAMES LAW, F.R.C.V.S.
SYNONYMS.--Canine Madness, Rabidus Canis, Canis Rabiosa. _Greek_,
Lyssa, Lytta, Lyssa Canina, Cynolyssa, Hydrophobia, Pantephobia,
Aerophobia, Phobodipsia, Erethismus Hydrophobia, Clonos Hydrophobia,
Dyscataposis. _French_, Tetanus Rabien, La Rage, Toxicose Rabique.
_German_, Wuth, Hundswuth, Tollwuth, Wuthkrankheit, Hundtollheit.
_Italian_, Rabbia, Arabiata. _Spanish_, Rabia, Rabiosa. _Swedish_,
Hundsjuka. _Roumanian_, Turbarea.
DEFINITION.--Canine madness is an acute infectious disease, supposed
to arise spontaneously in the genus Canis (dog, wolf, fox, etc.) and
Felis (cat, etc.), but transmissible by inoculation to the other
Mammalia and to birds. It is characterized by a long period of
incubation, by exaggerated reflex excitability, by disorder of the
intellectual, emotional, and other nervous functions, by change of
habits, by extreme irritability of temper, by optical and other
delusions, by spasms of the muscles of the eyeballs and throat, by
paralysis, and by more or less fever. The disease runs a short and
almost without exception fatal course.
HISTORY.--Plutarch claims that hydrophobia was first recognized by the
Asclepiadae, and Homer's allusions to the malign dog-star and to
Hector's acting like a raging dog have been quoted as implying a
knowledge of rabies. We find no certain reference to the affection,
however, until we come to Democritus and Aristotle, in the fourth
century B.C. The latter clearly describes the disease and uses the
name lytta, but, singularly enough, claims for man an exemption from
the general susceptibility to the infection by inoculation.[1] From
that date to this the successive outbreaks, sufficiently noteworthy to
secure a place in history, are so numerous and widespread as to show a
continuous prevalence of the malady in the Old World, and, since the
early part of the eighteenth century, in the New.
[Footnote 1: _Historia Animalium_, lib. viii. cap. 22.]
GEOGRAPHICAL DISTRIBUTION.--Rabies is more prevalent in temperate
regions than in the tropics and Arctic Circle, but this is common to
all animal plagues propagated solely or mainly by contagion, and is
manifestly due chiefly to the density of population, the activity of
commerce, and the free movement of men and animals in the temperate
zone. That a hot or cold climate is incompatible with rabies is
disproved by its prevalence under the tropics in Southern China,
India, Abyssinia, the West Indies, Peru, Chili, and Brazil, and in the
Arctic Circle in Northern Greenland, Lapland, Siberia, and Kamtchatka.
On the other hand, many {887} islands and secluded regions in the
temperate zones maintain a continued immunity or have been invaded
only recently by the introduction of infected dogs. We may instance
the Hebrides, Australia, Tasmania, New Zealand, South Africa, West
Africa, the Azores, St. Helena, and, until the last half century, La
Plata, Malta, and Hong-Kong. The disease is well known throughout
North Africa, Arabia, Syria, Turkey, and Asia generally, in Ceylon and
other of the East Indian islands. It is also notorious that even when
unusually prevalent its progress is often abruptly arrested by a
considerable river, and Schrader and Virchow both notice that though
it ravaged both banks of a river, yet the islands in the river
escaped, as was notorious of the islands in the Elbe during the great
Hamburg epizootic in 1852-53. While, therefore, rabies prevails most
extensively in the more civilized countries and in large cities, yet
we can point to no geographical area in which the contagion has failed
to spread among those bitten by rabid animals, nor to any locality in
which the disease has been shown to arise spontaneously from
unwholesome conditions of climate, soil, or general environment.
ETIOLOGY.--We know of but one efficient cause of rabies--namely,
infection. Yet as many conditions are believed to favor its extension,
or even to determine its spontaneous eruption, it is necessary to
speak of them shortly.
As shown above, climate cannot be charged with the generation nor
diffusion of rabies. Many countries formerly thought exempt are now
known to suffer. The following may be named: The East and West Indies,
Syria, Egypt, Cyprus, Siberia, the lands north of the Baltic, and
South America. Others manifestly maintain their exemption only because
the morbid germ has not yet been introduced.
Certain seasons undeniably show a far wider extension of the disease
than others, but such epizootics are not limited to a particular
season or year, and, unless cut short by human intervention, cover a
succession of years of the most varied climatic character, spare
inaccessible or secluded islands in the very centre of the outbreak,
and the cycles of prevalence will succeed each other, in place of
occurring simultaneously, in closely adjacent countries subject to the
same climatic vicissitudes, but separated by narrow seas. Even a broad
river destitute of bridges usually abruptly arrests an epizootic, and
protects the land beyond lying under precisely the same general
influences. In this connection may be quoted the recent great
epizootic of 1856-72 in England, which succeeded, but did not
accompany, that of 1851-56 in Germany. Prof. Roll reports the
extraordinary prevalence of rabies at Vienna in 1814, 1815, 1830,
1838, 1842, and 1862--years remarkable for diversity rather than
uniformity of climatic characters.
Popular opinion refers rabies to the extreme heats of summer, and each
year dogs are muzzled or otherwise confined by order of municipal
authorities during the dog days, though left at liberty throughout the
rest of the year. In 1780, Andry observed that the coldest and hottest
months furnished the least number of cases, and later Hurtrel
D'Arboval claimed that in France dogs suffered most in May and
September, and wolves in March and April. Bouley claims that the
majority of dogs suffer in March, April, and May. The following
statistics are interesting in this connection: {888}
_Cases of Rabies in_
WINTER. SPRING. SUMMER. AUTUMN.
Dec., Jan., March, April, June, July, Sept., Oct.,
Feb. May. Aug. Nov.
Dogs 755 857 788 696 (Bouley).
Men 17 25 42 13 (Boudin).
The increase of cases of rabies canina in the spring and summer
months, as shown by the above statistics (7-15 per cent.), cannot
reasonably be attributed to the influence of the weather, since even
the strongest advocates for spontaneity would at once decline to claim
any such ratio of spontaneous developments. The increase must
therefore be mainly, if not altogether, due to the increased number of
inoculations; and these latter are provided for in the jealousies and
quarrels in the troops of males that follow each rutting bitch in
spring, the principal period of oestrum in the canine female. The
infection spread in this way in early spring tends to remain more
prevalent throughout the hot summer months.
With regard to the greatly enhanced mortality in man during the summer
months, as shown in Boudin's statistics for France, in the absence of
any genuine hydrophobia in man apart from inoculation from a rabid
animal, it may be attributed to three principal causes: 1st. The bites
sustained from rabid dogs in spring and early summer, when the disease
is most widely spread among these animals, will give rise to
hydrophobia weeks or months later. 2d. In the warm season the body is
more thinly clad and the hands and other portions are more frequently
left bare, so that the teeth are less likely to be cleansed of the
virulent saliva by passing through the clothes before entering the
skin. 3d. The languor, fever, and nervousness attendant on extreme
heat tend not only to hasten the activity of any disease-germs
actually present in the system, but also strongly favor the increase
of that nervous fear which so often generates a fatal
pseudo-hydrophobia (lyssophobia) in persons that have been bitten by
dogs.
Hunger, thirst, and spoiled food are invoked as causes of rabies, yet
in the East, where the dogs are the scavengers of the cities and often
suffer severely from hunger and thirst, eat the most offensive
carrion, and drink the foulest water, the disease has a very
restricted prevalence, while in South Africa and Australia the outcast
and sheep-dogs, often the victims of starvation and thirst, entirely
escape. Bourgelat, Dupuytren, Majendie, Breschet, and others have
cruelly destroyed dogs by privation of food and water and by exposure
under a broiling sun, but no rabies, nor anything resembling it, was
produced. Dogs perspire little and suffer severely from heat, but
there is no evidence that this can develop canine madness. It is
claimed that Rossi of Turin developed rabies in cats by withholding
food and drink, but, as he furnishes no inoculation-tests confirmatory
of its virulence, the claim cannot be endorsed. Experiments with an
exclusive diet of salt meat, putrid meat, and water only have failed
to produce rabies.
The large preponderance of male dogs attacked with rabies has been
constantly remarked by writers. Of 1990 rabid dogs reported by
different authors, 1746 were males and 244 females--a ratio of more
than 7 to 1. This excess of males attacked is much higher than the
ratio of males in the dogs of the districts drawn upon. Thus, Bourrel
found a {889} ratio of 6 rabid males to 1 rabid female, while in his
patients generally the proportion was 4 to 1. Leblanc found that 14
per cent. of the male dogs went mad, while but 1 per cent. of the
females suffered. That sex is no protection against inoculated virus
is shown by the frequent inoculation of castrated dogs of both sexes.
The excess of male subjects may be attributed mainly to the frequency
with which these bite each other when following a female in heat, and
the respect of all alike for the latter sex. Even in the rabid dog the
sexual instinct rises above the propensity to bite in the early stages
of the malady.
Toffoli claims that he has caused spontaneous rabies by shutting up
several dogs in a loose box with a bitch in heat and allowing them to
fight for the prize. Weber and Leblanc have noticed similar
occurrences. But Greve and Menecier have repeated the experiments with
a contrary result; so that it remains probable that when successful
the victims had already been inoculated before they were shut up.
Moreover, the seclusion of male canine animals for a lifetime in
menagerie cages, often adjoining those of their corresponding females,
has never been known to induce rabies.
The bite of the violently enraged dog, and the bites mutually given
when following a rutting bitch, are popularly supposed to cause
rabies; but if this were the case, the disease must have been
universally prevalent. The idea that the bite of a dog will cause
hydrophobia should that dog at any subsequent period go mad is a
similar delusion. Men doubtless occasionally develop lyssophobia under
such an influence, but animals do not contract genuine rabies.
Dogs are alleged to have gone mad from violent suffering after an
operation, and cats from being scalded or robbed of their kittens, but
all such causes are continually operating without such effect, and
when in a solitary case rabies develops, it can only be looked on as a
coincidence.
Much popular prejudice exists against certain breeds, and the
Pomeranian has been virtually ostracised on account of its supposed
liability to rabies; but statistics show that the liability to
contract the affection bears a relation to the exposure rather than
the special breed. Eckel, Pillwax, and Hertwig found that dogs kept as
house- or watch-dogs, and most pampered and confined, are the most
liable, while St. Cyr and Peuch found the greatest number of cases
among those running at large and allowed the freest exercise.
There is a popular belief that the bite of the skunk (_Mephitis
mephitica_) is always rabific. Rev. H. C. Hovey describes a number of
cases of infection from this animal,[2] and John G. Janeway has
reported other instances.[3] Both claim that the disease is
spontaneous in the skunk, and Mr. Hovey holds, on very insufficient
grounds, that the affection is a distinct variety of rabies (rabies
mephitica). The facts seem to warrant only the conclusion that skunks
in certain districts of Michigan and Kansas have had rabies
communicated to them, and follow the rabid impulse to bite other
animals and men. The Mephitinae abound in the Eastern States, but we
never hear of them stealing up and biting men or dogs, nor of the
latter contracting rabies from skunk-bite. Eastern dogs frequently
kill skunks and sustain bites, but do not thereby contract rabies.
Even in Kansas this evil {890} influence of the skunk-bite was unknown
until 1870, showing that it is not inherent in the climate nor soil,
but has been presumably imported. The spontaneity of the affection is
assumed, not proved.
[Footnote 2: _Amer. Jour. of Science and Art_, May, 1874.]
[Footnote 3: _New York Medical Record_, March 13, 1875.]
In the above epitome of alleged causes we find nothing proving the
spontaneous evolution of rabies. The prevalence of the affection in
wolves, foxes, jackals, cats, skunks, etc. proves nothing for
spontaneity, more than its existence in the dog. In all these species
of animals the malady develops the dread propensity to bite, and thus
in all alike provision is made for the perpetuation and propagation of
the malady. Unless a previous attack by a rabid animal has been
observed, owners usually insist that their dogs have contracted the
malady spontaneously, yet a rigid scrutiny will almost always reveal a
strong probability, at least, of inoculation. The rabid dog wanders
far from home, and sometimes accomplishes wonderful feats of leaping
to reach his victim, so that his presence in a district is not even
suspected, and animals thought to be safely secluded inside high walls
suffer from his fangs. He is more inclined to bite and rush on than to
stay and devour, and thus small animals, like the skunk, when bitten
may survive to propagate the disease in places to which a dog could
not possibly find access. Much circumstantial evidence makes strongly
against the theory of spontaneity. Thus, the immunity of the islands
of the Elbe in the very midst of a severe and protracted epizootic,
the continued immunity of the Hebrides and of Malta, each famed for
its indigenous race of dogs, for long centuries, during which the
malady prevailed at frequent intervals on the adjacent mainlands, and
the continued exemption of South Africa and of the Australasian and
other islands, in the face of the counter-fact that the affection
persisted after importation in the West Indies and South America,
speak strongly for the doctrine that the introduction of a
pre-existing germ is an essential condition of the evolution of the
disease. The following statistics of cases which entered the Berlin
Veterinary College furnish further corroborative evidence. There
entered the college,
In 9 years, 1845-53, inclusive, 278 rabid dogs.
" 1854 4 " "
" 1855 1 " dog.
" 1856 1 " "
" 5 years, 1857-61, inclusive, 0 " "
The average for each of the first nine years was a fraction less than
31. In the two last of the nine the cases rose to 68 and 82, and this
led early in 1854 to an order for the muzzling of all dogs, which was
rigidly enforced by the police. The disease was promptly suppressed,
the two cases in the two succeeding years being probably due to
infected kennels or to importation from without. The results in Eldena
(Fuertenberg) and Holland (Van Capelle) are equally conclusive. The
inefficiency of some orders for the muzzling of dogs makes nothing
against these facts. A law on the statute-book is not always a law in
force, as I saw in Alfort and Lyons in 1863; the dogs wore their
muzzles only in honor of the periodic visits of the commissionnaire of
police, and rabies prevailed.
The great majority of competent observers of to-day deny, or at least
strongly doubt, the occurrence of the disease apart from inoculation.
Without assuming to decide the question for all times and places, it
may {891} be safely asserted that there is no sufficient proof of such
an occurrence in any recent time.[4]
[Footnote 4: Mr. Saze, a former student, informed me that boys in
Japan produce what is believed to be canine rabies by administering to
dogs a fungus (bukeryo) found growing on a coniferous tree. The dogs
do not all seem to die, but are usually killed by way of precaution.
The symptoms are those of delirium, with a propensity to bite, and the
disease is assumed to be communicable, though no facts are given to
show that it is so. This popular fancy has all the air of a popular
fallacy, but as the counterfeit attests the genuine, it shows the
familiarity of the Japanese with true rabies.]
The contagion of rabies is usually resident in the saliva, but is by
no means confined to that product. Paul Bert found the bronchial mucus
virulent in dogs in which the saliva was non-virulent. The flesh has
conveyed the disease when eaten, though probably only because of sores
or abrasions on the alimentary tract. Smith records the death of
negroes in Peru from eating rabid cows;[5] Schenkius, that of persons
who ate of a rabid pig; and Gohier and Lafosse have infected dogs by
feeding the flesh of rabid dogs and ruminants; Rossi and Hertwig have
separately induced rabies by inoculating sound animals with portions
of nerves from rabid ones. No absolute proof can be adduced that the
disease has been conveyed through consumption of the milk. Cases
quoted to show its virulence are open to the objection that the dam
probably licked the offspring. A similar uncertainty attaches to the
spermatic fluid. Women are alleged to have acquired hydrophobia by
coitus, but no such case can be adduced among animals, though rabid
males have often had connection with healthy females. The alleged
cases in women were therefore probably the result of an excited
imagination or caused by virus introduced through some other channel.
The breath and perspiration seem incapable of becoming media for the
transmission of the disease. The blood was supposed to be non-virulent
by Breschet, Majendie, Dupuytren, Blaine, Youatt, etc., but has been
shown by Eckel and Lafosse to be rabific. Eckel successfully
inoculated the blood of a rabid he-goat on a sheep and that of a rabid
man on a dog. Lafosse accomplished the same in one of three attempts
by inoculation from dog to dog. The blood is probably only virulent in
the advanced stages of the disease, and its virulence implies the
virulence of all vascular tissues.
[Footnote 5: _Peru as it Is_.]
The saliva of rabid Herbivora and Omnivora, long held to be harmless,
is now known to be virulent. Berndt has successfully inoculated it
from an ox to four sheep; Eckel from a goat to a sheep; Rey from sheep
to sheep; Lessona from an ox to two horses and a sheep; Tombaro from a
heifer to a sheep, a horse, and two dogs; Youatt from horse and ox
respectively to dogs; Ashburner from an ox to fowls; King from a cow
to fowls; and Majendie, Breschet, Eckel, Hertwig, and Renault from man
to dog; and Earle from man to rabbits. Besides these are a series of
accidental cases, as from horse to man (Youatt), from a sheep to its
shepherd (Tardieu), and from man to man (Aurelianus, Enaux,
Chaussier).
Experiments by Hertwig and Eckel seem to show that saliva loses its
virulence on the supervention of cadaveric rigidity or putrefaction in
the dead body. Haubner even believed dried saliva to be innocuous. Yet
Count Salm successfully inoculated the dried saliva of a rabid dog,
and Schenkius reports a case of hydrophobia produced by a scratch of a
hunting-knife that had been used to kill a mad dog some years before.
A veterinary student at Copenhagen cut his finger while dissecting
{892} the body of a rabid dog twelve hours after death, and died of
hydrophobia six weeks later. These cases in man may, it is true, have
resulted from fear, but the same cannot be said of the infection of
hound after hound placed in empty infected kennels, as recorded by
Blaine, Youatt, and others. In the face of this it would require very
strong negative testimony, indeed, to prove that the virus of rabies
is devitalized in drying--a process which prolongs the vitality of
other virulent matters.
Up to the present time the germ of rabies has not been demonstrated.
That it is a particulate living organism may be reasonably deduced
from its power of indefinite increase--a quality possessed by no mere
chemical nor mechanical agent, also from the saliva proving
non-virulent after filtration through plaster, while the solid residue
left on the filter was virulent (Bert). But, although bacteria have
been found in the saliva, those demonstrated up to the present are
manifestly ordinary aerial bacteria, such as in Pasteur's experiments
produced septicaemia rather than rabies. It still remains, therefore,
for some future observer to discover that germ of which we cannot
doubt the existence.
The point of election of this germ appears to be mainly the nervous
tissue. Pasteur found the brain-matter of rabid animals invariably
infectious, and has preserved the moist brain in an infecting
condition for three weeks at a temperature of 12 degrees C. He found
that by direct inoculation in the brain-substance the period of
incubation was abridged, rabies often showing itself in six, eight, or
ten days. In the face of Rossi's successful inoculation of nerves and
Pasteur's results with brain-matter it is difficult to account for the
unsuccessful inoculation of nerve-tissue in six successive experiments
by Hertwig. It seems to show that though the virus is concentrated in
the brain, and especially in the medulla and pons, yet it does not
equally permeate the entire nervous system. This election of the
poison for the nervous tissue led Dr. Douboue in 1851 to advance the
theory that it is propagated from the seat of inoculation to the brain
through the medium of the nerves--a position now assumed by Pasteur.
This, we fear, is not well founded. The poison, advancing for a month
or more along the lines of the nerves, would probably derange and
abolish their functions, as it does so speedily and effectually that
of the nerve-centres after it has gained a seat in them, whereas, in
reality, the local paralysis only appears in the last stages and after
the symptoms of cerebral disorder are well established. Furthermore, a
common premonitory symptom of rabies is congestion, swelling, and
irritation of the inoculation wound, showing a sudden extraordinary
activity at that point as a herald, if not a condition, of the general
infection, whereas under a slow propagation along the nerves from the
first this irritation would probably have been greatest in the wound
at the outset, and would have thereafter kept pace with the progress
of the virus along the nerves. Again, the blood is not always
infecting. Blaine, Youatt, and others of the older observers had no
fear of the blood. Hertwig obtained rabies in two cases only out of
eleven inoculations with the blood of rabid subjects. The blood in
this, as in some other diseases (variola equina, v. ovina, lung plague
of cattle), proves to a certain extent inimical and destructive to the
poison. Galtier inoculated nine sheep and one goat by intravenous
injection of the saliva of mad dogs, in no case with fatal results nor
indeed with any manifestation of rabies, but with the effect of
fortifying the system so, {893} that subsequent inoculation into the
tissues of the saliva of rabid animals was harmless. Test inoculations
made in the tissues of other animals with the same virus used in his
intravenous injections, and his subsequent inoculations of the animals
so treated, invariably determined rabies. Pasteur repeated these
intravenous injections in dogs with the result of rapidly inducing
rabies in a fair proportion of cases. One of his cases produced in
this way recovered, and thenceforward resisted all further inoculation
with the virus. Others that did not perish from intravenous injection
afterward died of rabies after inoculation in the brain.
Unfortunately, neither Galtier nor Pasteur have reported how much
virulent saliva was injected in any one case, so that we have no data
as to whether the difference was due to the varying quantity of the
virus introduced in the various cases. Lussana, an Italian physician,
had already in 1878 experimented on two dogs by injecting into their
veins the blood of a physician who died of hydrophobia. The blood was
drawn by leeches and cupping-glasses, and five grammes were injected
into each dog. One died on the twenty-fourth day, presenting the
symptoms and post-mortem appearances of rabies. The second at the end
of one hundred and forty days developed symptoms of rabies which
lasted a month, when the animal was sacrificed, and nothing special
found at the autopsy. The data do not warrant a very positive
conclusion, yet they seem to imply that the receptivity on the part of
the dog is greater than that of the small ruminants. They suggest,
further, a greater relative potency in the battle for life of the
blood-globules of the small ruminants with this unknown rabific germ.
This antagonism between the blood of the ruminant and the germ of
rabies finds a parallel in the case of other disease-poisons in their
relations to the nuclei of the tissues. Thus animals may prove
refractory to a small dose of the poison of anthrax, yet Chauveau has
shown that this virus will overcome all native or acquired
insusceptibility when administered in excess. The same is true of the
poison of chicken cholera, which Salmon dilutes until it is non-fatal,
though still affecting the system and conferring an immunity from its
attacks in the future. So with the lymph of variola ovina, which Peuch
diluted to 1/50 and injected with the effect of producing slight fever
and immunity without vesiculation.
This view would imply that in ordinary cases (inoculation with a
moderate amount of the poison) the virus is for a time localized in
the vicinity of the wound; and this is further supported by the fact
that thorough excision and cauterization of the wound some time after
it has been received is still often protective. It is weakened by the
fact that bites of dogs in the stage of incubation sometimes produce
rabies, but it must be borne in mind that there is still a period
between the passage of the living germ to the salivary glands and
brain and the growth of the germ in the nerve-centres, so as to
produce pathognomonic symptoms, during which both blood and saliva
must be virulent.
The ratio of successful inoculations to the bites is very varied.
Thus, out of 555 dogs reported to have been bitten by rabid dogs, 188
contracted rabies; out of 183 experimentally exposed till bitten or
inoculated, 91 became mad; out of 73 cattle bitten, 45 became rabid;
out of 121 sheep bitten, 51 succumbed; and of 890 persons bitten, 428
took hydrophobia (48 per cent.). Of 440 bitten by rabid wolves, 291,
or 66 per cent., took the disease. Such statistics are, however, far
from satisfactory. Of dogs {894} reported mad, some have only suffered
from epilepsy, convulsions, or colic, while of those bitten by the
really mad dog, some have sustained simple bruises without any real
abrasion; in other cases the teeth have been wiped clean by passing
through thick wool, hair, or clothing, or even the flesh of other
animals just bitten; in other cases the bite has been inflicted at a
time when the virulence of the saliva was at its minimum, or in a
subject which was naturally insusceptible. The protective effect of
clothing was well illustrated in a case which came under my notice in
London. Six animals bitten by a rabid dog all contracted rabies,
whilst a man bitten a few hours before through the coat-sleeve, and
who did not have the wound cauterized for a full hour after the bite,
escaped. Bouley found that in 32 persons bitten in the face, 29 died
of rabies (90 per cent.); of 73 bitten on the hands, 46 died (63 per
cent.); of 28 bitten on the arms, 8 died (28 per cent.); of 24 bitten
on the lower limbs, 7 died (29 per cent.); of 19 bitten on the body
(usually multiple wounds), 12 died (63 per cent.). The high mortality
from the bites of rabid wolves and skunks is mainly due to this habit
of attacking the face and hands. As illustrative of insusceptibility
may be quoted the poodle of Hertwig, which was inoculated nine times
with unquestionably rabic virus without effect; also the pointer of
Rey, which was seventeen times bitten by rabid dogs without harm; also
the acquired immunity of Galtier's sheep and rabbits, above referred
to.
INCUBATION.--In the dog this varies from 6 days (Pasteur) to 240 days
(Bollinger). In the majority of cases it ends in from 20 to 50 days.
Pasteur, by inoculating into the brain substance direct, reduced the
incubation from 20 days to 6 days. In the horse the limits of reported
cases are from 15 days to 92 days. In the ox incubation varies from 20
to 30 days; in sheep, from 20 to 74 days; and in swine, from 20 to 49
days in recorded cases.
In man incubation is believed to be often much more prolonged. In 6
per cent. of all cases it is from 3 to 18 days; in 60 per cent., from
18 to 64 days; and in 34 per cent. it exceeds 64 days (Hamilton,
Thamhayn). Quite frequently symptoms of hydrophobia appear from three
to six months after the bite; in a few the period is prolonged to one
or two years, and in rare instances to seven (Schule), and even twelve
years (Chabert). But all such cases of prolonged incubation in man are
at the least extremely doubtful. Man often contracts a
pseudo-hydrophobia as the result of fear, and is curable by moral
suasion alone; and as no such protracted incubations are noticed in
the lower animals, and as no one of these abnormally deferred attacks
in man has been verified by successful inoculation on animals, it is
prudent to reserve a full assent until they are supported by better
testimony. A specimen of such cases is that recorded by Chirac, in
which a cadet bitten at Montpellier afterward spent ten years in
Holland, and then, returning and hearing that his fellow-cadet bitten
by the same dog had died of hydrophobia, he also manifested the
disease and died. Another is the case of a man who, after having been
bitten, spent two years in prison, and then developed hydrophobia and
died. A mind naturally erratic and rendered weaker and more
susceptible by prolonged confinement would prey upon itself and
exaggerate the danger when the subject had been forcibly presented. In
all such cases the attending physician should feel bound in the
interests of humanity to {895} inoculate a dog or other animal and
ascertain whether or not the disease is virulent. The value of such
results in dealing with future cases of the same kind cannot be
overestimated.
The period of incubation appears to be relatively shorter in the young
(average 45 days) than the old (average 70 days), and is believed to
be shortened by constitutional excitement from violent passion, fever,
the heat of the weather, or electrical disturbances.
During incubation no sign of the disease can be detected; it is even
said that the wounds heal with unusual rapidity; but it is certain
that toward the end of the latency the cicatrix, alike in man and
animals, tends to become sensitive, itchy, congested, and even the
seat of papular eruptions. The vesicles (lyssi) which, according to
Xanthos, Marochetti, and Magistel, appear near the opening of the
sublingual glands within a few days (6 to 20) after inoculation, have
not been found by any recent observer.
SYMPTOMATOLOGY.--Three forms of rabies in the dog are recognized--the
furious, the paralytic, and the lethargic. The prodromata are,
however, the same in all, so that these may be conveniently considered
before the different types are noticed.
The premonitory symptoms are by far the most important, as if these
are recognized the dog may be safely secluded or destroyed before
there is any disposition to bite. Any sudden change in a dog's habits
or instincts is ground for suspicion. Bouley well says that a sick dog
is always to be suspected. In some cases there is unusual dulness and
apathy, in others great restlessness, watchfulness, and nervousness. A
morbid appetite, in house-dogs a tendency to pick up and swallow
straws, thread, paper, pins, and other objects, or to devour their own
dung and urine, is highly characteristic. A desire to lick cold smooth
objects, as a stone, a boot, a piece of metal, or the nose of another
dog, is often seen. Smelling and licking the anus or generative organs
of another dog and the exhibition of sexual desire are frequent
manifestations. An increased fondness for the owner, shown by fawning
and licking, is occasionally seen, though more commonly there is a
change from a formerly amiable temper to a morose, sullen, retiring,
and resentful disposition. If a naturally quiet dog flies into a
violent passion at the sight of another dog or a cat, and attempts to
bite it, he should be carefully watched. If a social dog seeks
seclusion and darkness, or if while crouching and shrinking from a
blow (hyperaesthesia) he yet bears it without howl or whine, he is to
be strongly suspected. Barking without object, constant moving,
searching, and scraping, a disposition to tear wood, clothing, etc. to
pieces, and, above all, an absence from home for a day or two, should
beget grave apprehensions. The rabid bark or howl which is often heard
early in the disease is hoarse, low, and muffled, partaking of the
nature of both bark and howl, the first running into the second, and
consists of one loud howl followed by three or four others
progressively diminished in force and uttered without closing the
mouth. Some rub the chaps with the forepaws as if to dislodge an
offending body from the mouth; others reject bloody matter by
vomiting; and others turn the head and eyes as if following imaginary
objects, and snap at them. Finally, a tendency to bite, rub, or gnaw
the wound is significant, and usually draws attention to the fact that
the wound, long healed, is still red, sensitive, and swollen, {896} or
even papular. The conjunctivae are usually congested, there is an
increased nasal defluxion, and the skin of the forehead and over the
eyes is drawn into wrinkles. This stage lasts from a half to two or
three days.
Following one or more of the above symptoms, paroxysms of wicked fury
come on, alternating still with periods of quiet, in which prodromata
only are observed. The red congested eyes assume a fixed stare, often
squint or roll as if following an imaginary object, at which the dog
presently snaps. A paroxysm is ushered in by increasing uneasiness,
frequent change of position, and a desire to escape, shown in rushing
at the door, tugging at the chain, or gnawing the post and walls of
the kennel. The tendency to bite and gnaw is further shown by seizing
the straw or tearing to pieces wooden and other articles within reach,
or even by the victim lacerating its own body.
The rabid howl becomes more frequent, and the rage and disposition to
bite strange animals and persons merge into a mischievous desire to
worry all that come in the way, the respect for former companions and
friends being steadily lost as the paroxysm increases in violence. Yet
for a considerable time the voice of a loved master recalls the
suffering animal to some degree of self-control. If free to escape
during such paroxysms, the dog expends his excitement in wandering,
making long journeys of five, ten, or twenty miles, and flying at
every animal or man he meets, especially if they increase his
excitement by any noise or outcry. If the victim escapes destruction
during one of these wanderings, he returns during a lucid interval
exceedingly dangerous, for, though he may recognize or even fawn upon
his friends, yet the demon of mischief is even more potent within him,
and may be roused to sudden violence by any noise or excitement. The
intervals of quiet are attended by a prostration proportionate to the
violence of the previous paroxysm, and the animal usually seeks
seclusion and darkness, where he may lie dull and torpid, but he may
be roused at any time to a renewed paroxysm by any noise, disturbance,
the presentation of a stick, or, above all, by the approach of another
animal. During the paroxysm the animal is manifestly the subject of
acute delirium, has hallucinations, snatches and bites at unreal
objects, turns on his best friends, even his master, seizes and holds
on to a stick or iron bar until the teeth are detached and the gums
lacerated, bites his own body, even amputating tail, testicles, or
toes with his teeth; a bitch deserts her puppies or worries them, and
all follow the unconquerable impulse to wander and to wound living
beings. The victim will sometimes manifest incredible strength in
breaking his chain and scaling high walls. Twitchings of the muscles
of the face, and even general convulsions, are sometimes seen. Food is
usually rejected, or if swallowed is soon vomited. In the course of
two or three days the furious stage merges into the paralytic one,
first shown by paresis of the hind extremities and a swaying motion in
walking, then by paralysis of the lower jaw, which hangs pendent and
allows the escape of a viscid saliva. The palsy gradually extends over
the whole body--a sure precursor of approaching death, which is rarely
delayed beyond eight days, and never more than ten, from the onset. In
this last stage the animal has become extremely emaciated, with dry
withered hair, hollow flanks, and small weak pulse; he may at first
rise on his fore limbs when {897} disturbed, and even attempt to snap,
but there is now little danger of a bite. Convulsions may alternate
with the paralysis. The result is invariably fatal.
The peculiarity of dumb or paralytic rabies in dogs is that the last
or paralytic stage supervenes at once on the prodromata, without any
intervening period of acute delirium and fury. The animal is
throughout dull, quiet, and depressed, and shows little tendency to
bite, to wander, or to restless movement. The excitement of the sexual
passion is the same as in the furious forms, and the howl is still
emitted, though much more rarely. Soon the lower jaw drops from
paralysis, allowing the saliva to drivel from the mouth, and the
animal can only succeed in closing it momentarily under the greatest
provocation to bite. Paralysis of the hind limbs and of the whole body
speedily follows, and death ensues in from two to three days. As soon
as the jaw is paralyzed the subject is unable to drink, eat, bite, or
bark, and emaciation advances with extraordinary rapidity.
The lethargic or tranquil form of rabies in dogs is manifested neither
by furious madness nor by palsy of the jaws, but the nervous
prostration is shown in a profound lethargy and apathy. The patient
curls himself up, and will not be roused by his master's voice, by any
noise, disturbance, or even punishment; he makes no response to the
caresses of his friends, and pays no attention to the food or drink
they bring him, but remains in his place, growing daily more emaciated
and lethargic, until relieved by death toward the tenth or fifteenth
day of the illness.
Besides the three typical forms there are intermediate varieties,
which are classed with one or other according as the symptoms of that
type seem to predominate. The same virus, inoculated, will produce
different types in separate individuals, the result seeming to depend
more on the susceptibility of the subject than any special quality in
the poison. With many notable exceptions it may be stated that, on the
whole, furious rabies predominates in hounds, bull-dogs, and other
less domesticated or naturally vicious and courageous breeds, while
the paralytic and tranquil types attack especially house and pet dogs.
POPULAR FALLACIES.--It is a dangerous delusion to suppose that mad
dogs have a dread of water and polished surfaces, that they will not
eat or drink, that they froth abundantly from the mouth, and that they
run with the tail drooping between the hind limbs. There is no
hydrophobia in the dog or other domestic animal. The rabid dog drinks
freely in the early stages of the disease, lapping even his own urine;
later, he still laps, and even plunges his nose in water, though often
unable to swallow; and in his wanderings he swims rivers without the
slightest reluctance. The appetite is not entirely lost, though
greatly impaired and usually depraved, all sorts of unsuitable,
noxious, and disgusting objects being picked up and swallowed with
avidity. Frothing from the mouth is exceptional in rabies, and the
flow of saliva is rarely seen unless when the jaw is paralyzed and
pendent. Carrying the tail between the legs is a symptom of all
diseases attended by abdominal pain, and is by no means constant in
rabies. During the paroxysms the tail is usually carried erect.
Foxes, jackals, and badgers attacked by rabies lose their natural
{898} shyness, enter villages, follow and bite other animals and men,
and, like rabid dogs, die in an unconscious and paralytic condition.
Wolves are affected like foxes, but are more dangerous because of
their power, the ferocity of their attack, and their habit of flying
at the face and hands. Rabid cats are more retiring than dogs, and
show less disposition to attack, but when they do, use both claws and
teeth, and especially on bare portions of the body. The cry is hoarse
like that emitted during the period of rut. They usually die about the
third or fourth day.
The rabid horse is the subject of violent excitement, nervousness, and
fear. There are trembling, loss of appetite, rubbing and eversion of
the upper lip, neighing, sexual excitement, and inclination to bite
and kick. Delirium may be suspected, but during the paroxysms the true
nature of the disease is betrayed by the unconquerable desire to bite,
kick, and otherwise injure those about him. He will even gnaw the
manger and kick the stall to pieces, or lacerate his fore limbs and
flanks with his teeth. In the early stages there is the same tendency
to lick and rub the wound, which becomes red and irritable, the same
red glaring or squinting eyes, and the same jerking of the muscles, as
seen in the dog, and the affection winds up in the same way, in
paralysis and death in four or five days.
Rabid cattle lose appetite, become very restless and excitable, grind
the teeth, lick the cicatrix, evert the upper lip, and otherwise show
sexual excitement, bellow often in a loud, terrified manner, as if
still apprehensive of the attack of the dog, paw and scrape the ground
with the fore feet, butt and kick viciously, have twitching of the
muscles, and finally paralysis and death in from four to seven days.
When paralysis is coming on the hind feet are often drawn forward as
in inflammation of the feet. The pulse and breathing are accelerated
during the paroxysms, but I have not found the temperature raised.
Rabid sheep and goats present the same general symptoms, bleat
hoarsely, but viciously, have sexual excitement, nibble the cicatrix,
have muscular weakness, emaciation, and paralysis, and die in from
five to eight days.
Rabid swine show much fear, restlessness, and excitability, hide under
the litter, start violently at noises, grunt hoarsely, champ the jaws,
show a great disposition to bite and to gnaw and tear objects to
pieces, have dark red, glaring eyes, gape and yawn, and become weak
and paralytic. Breathing is often labored, and the mucosae and white
skin assume a dull red or leaden hue. Death ensues as early as the
fourth or fifth day.
In Herbivora and Omnivora a paroxysm is usually induced by the sight
of a dog--a fact of importance in diagnosis.
Rabid skunks have naturally received but little study. They tend,
however, to steal up to men and animals and bite some exposed part of
the body, like the finger, ear, or nose, and as stealthily retire. It
is claimed that their odorous secretion is suppressed.
Symptoms of Hydrophobia in Man.
In some cases the prodromata are altogether omitted, the disease
setting in suddenly with spasms of the pharynx and inability to
swallow. More commonly, the premonitory symptoms last from one to
three days. The first symptom is often an itching, prickling, or more
or less violent {899} aching in the seat of the bite, and even of an
aura, a numbness, or shooting pain extending from that point toward
the heart. In such cases the wound is red or bluish, and even swollen.
In other cases there is chilliness, a general feeling of headache,
malaise, and prostration, with lack of appetite or nausea, gloomy
forebodings, taciturnity, nervous excitability, and restlessness. That
restlessness which in patients cognizant of the consequence of the
bite often induces insomnia during incubation, now often shows itself
in an inability to keep quiet or to remain in one position or
place--the exact counterpart of the initial restless stage shown in
the canine patient. The sleep is now even more broken and unrefreshing
and disturbed by fearful dreams. The restlessness soon merges into
intense nervous irritability. Though devoured by thirst, the patient
is afraid of water, and the attempt to drink will cause slight spasms
with a sensation of filling of the throat and difficulty of
deglutition. Even the air blowing upon his surface produces nervous
irritation and apprehension, and a sudden glare of sunshine or other
strong light is still more injurious. The pulse is increased in
frequency, hard, and small; the breathing accelerated, oppressed, with
at times yawning, sighing, or sobbing; there is some redness of the
fauces, vascular injection of face and eyes, with, in some cases,
dilated pupils; nausea or oppression at the epigastrium, sometimes
vomiting; and usually constipation, which cannot, as in dogs, be
referred to the earth, sand, and unsuitable materials swallowed.
Intelligence is unimpaired.
With or without some or all of the premonitory symptoms above
described the patient is sooner or later seized with constrictive
spasms of the pharynx and respiratory muscles, the immediate occasion
being an attempt to swallow liquid or some sudden fright or
excitement. So great is the agony produced by this attack that, though
consumed by thirst, the patient will rarely afterward attempt to
drink, and the mere sight or offer of water, the noise of liquid
flowing from one vessel to another, or even the sight of the vessel in
which liquid was contained, suffices to bring on a violent paroxysm.
This hydrophobia is peculiar to the human being suffering from this
disease, being rarely seen in rabid animals; and it serves to
enormously enhance the agony and horror of the affection. During a
paroxysm the dyspnoea is usually extreme; there is a gasping or
sighing respiration, and shrill, inarticulate sounds or screams are
emitted which have been likened to the bark of a dog. These are
manifestly due to the threatened suffocation rather than to an attempt
to bark. The sensations have been described as a rising of the stomach
into the throat, while others felt as if the throat had turned into
bone and could not admit nor pass on the liquid. The abdominal
contractions are often well marked, and retching and vomiting ensue.
This reflex irritability of the nerves of deglutition and respiration
is followed or attended by a condition of the most intense
hyperaesthesia and a great exaltation of the special senses. A deaf
and dumb child is said to have heard distinctly at this stage. There
are, besides, during a paroxysm, general muscular trembling and clonic
spasms of the muscles of the trunk and extremities. The facial muscles
are contracted, the nostrils dilated, the face and eyes red and
injected, and the pupils dilated, producing a spectacle of the most
intense agony. Even in the intervals the hyperaesthesia is so extreme
that the slightest touch of an attendant, a {900} current of air, the
approach of a candle, or even the ordinary tones of conversation,
produce extreme agitation and may precipitate a violent convulsive
paroxysm. The duration of the paroxysms and of the intervals varies
much, but in general terms the former increase rapidly in number and
severity, while the latter are correspondingly shortened. Restraint
serves to aggravate the paroxysm, while, according to Hunter, the
earlier and lighter ones may be relieved by running. The intense
excitement sometimes becomes manifest in the persistent talking, and
it is noticeable that the patient is free from mental delusions. As it
is impossible to swallow, the patient spits out the now viscid saliva
on all sides--a feature, like the fear of water, peculiar to man. As
the disease advances the paroxysms are marked by the most perfect
hallucinations and delirium, which impel the victim to acts of insane
violence toward every one and every thing about him. In these fits he
will use every available means of offence, even to the snapping of the
jaws, though on the subsidence of the fit he will often express the
greatest regret and warn his victims to be on their guard when he
finds another paroxysm coming on. In some few instances the delusions
continue even during the remissions, and the patient remains possessed
of a sense of suspicion and horror of all about him, and yet the fear
of being left alone is usually greater still. The convulsions may
become tetanic (as opisthotonos). They are habitually more severe in
men than in women and children. During a convulsion the victim will at
times become black in the face, and may die from suffocation,
apoplexy, or nervous exhaustion.
Should he survive this danger the final paralytic stage sets in. The
spasms gradually become weaker, reflex irritability is lessened, and a
period of quiet, and even comparative composure, may ensue, during
which the former sights and sounds fail to produce a paroxysm, and
some patients even recover the power of deglutition; but muscular
weakness and prostration become more extreme, the lower jaw may even
drop, and the viscid saliva drivel from the lips; finally, stupor
supervenes, and the patient dies in a state of profound coma or
complete exhaustion. This last stage lasts from one to eighteen hours.
Cases are met with in the human subject, as in the dog, in which the
paroxysmal stage is omitted in greater part or entirely. The patient
complains only of oppressed breathing, and sighs deeply when he
attempts to swallow, and paroxysms, if they occur at all, are very
mild. Decroix indeed claims that if a person suffering from
hydrophobia is kept in a dark room and perfectly quiet, no paroxysms
appear. The malady is, however, none the less fatal.
DIAGNOSIS.--The diagnosis of rabies and hydrophobia is not usually
difficult if the disease has progressed to its paroxysmal stage. The
most pathognomonic features are the fact of a bite by a rabid animal
and the evidence of lesions and an extraordinary irritability of the
medulla oblongata, inducing severe reflex spasms of the muscles of
deglutition and respiration under the influence of any peripheral
irritation. The clonic nature of the spasms and the entire absence of
trismus serve to distinguish it from tetanus. From pharyngeal anthrax
and diphtheria attended with spasm it is diagnosed by the extreme
exaltation of the special senses and the absence of any marked febrile
reaction; from acute mania by the difficulty of breathing and
deglutition, the more rapid heart-beats during {901} a paroxysm, and
by the marked hyperaesthesia and exalted reflex susceptibility, as
well as by the perfectly lucid intermissions; and from epilepsy, in
that the latter is not associated with the same hyperaesthesia, that
the paroxysm is not developed by noise, movement, attempts to swallow,
sight of water, etc., that the spasms are more universal, and that
they do not recur often, nor can they be roused by the causes
immediately producing those of hydrophobia. Hysterical cases can
usually be recognized by the imperfection of the symptoms; the
subject, not knowing all the manifestations of hydrophobia, naturally
fails to produce them.
The most difficult to distinguish from the genuine disease are those
cases in which hydrophobia occurs as a disease of the imagination, the
result of fear--the lyssophobia or hydrophobie non-rabique of the
writers. In these there is always the history of a bite; the cicatrix
even may have become the seat of congestive redness, itching, or
neuralgic pains, and these, acting on a susceptible brain, develop a
disease which is hardly distinguishable from true hydrophobia, and
which is quite as fatal if left to run its course. These cases have
usually less reflex susceptibility than genuine hydrophobia; the
attack mostly occurs shortly after some conversation on the subject,
and especially about the effects of the bites on others; and the
victim is seen to have a nervous organization, and may even be known
to have been subject to hysteria or other nervous disorder. At the
same time, the concentration of the mind on this subject sometimes
produces even structural changes in the medulla, and the reflex
susceptibility in co-ordination with the other symptoms may be almost
perfect. In a case reported a few years ago by Hammond the symptoms
appeared perfectly characteristic, and at the necropsy circumscribed
points of congestion were found near the roots of the vagus; yet the
dog that bit this man was said to be alive and well, and in the
absence of any successful inoculation from biter or bitten the case
must be presumed to have been lyssophobia.
Many cases with a more favorable issue are recorded. Bellenger had a
patient who had been bitten by his cat, and manifested violent
paroxysms of hydrophobia, but was instantly cured by the sight of the
animal in good health. Bouardel records that a man was bitten by his
dog, which afterward disappeared. He was seized with severe
hydrophobia, which continued for two days, when the lost dog was found
and presented to him, and the symptoms disappeared. Trousseau speaks
of a magistrate whose hand had been licked by his hound, which
immediately after attacked a flock of sheep, so that many of them died
of rabies. The master then manifested hydrophobia, but as death was
deferred beyond the usual time, he concluded it was not genuine and
recovered. Prof. Dick was called to visit a man who had been bitten by
a favorite dog while suffering from distemper, had manifested severe
hydrophobic symptoms, and had been given up by the attending
physicians. He succeeded in convincing the subject that as the dog had
had distemper, and as no two great diseases could coexist in the same
system, it could not have had rabies. In spite of the false premises,
this reasoning had the desired effect and the patient recovered. A few
years ago a boy twelve years old in Ithaca, N.Y., was bitten by a dog
supposed to be rabid, and in due time manifested hydrophobia, which
advanced rapidly until he was having a violent paroxysm every half
hour, and it was pronounced impossible for him to survive another day.
At this time I saw him, observed that he {902} had a nervous
organization, and was somewhat lacking in the hyperaesthesia of
rabies, learned that he had recently been gorging himself with
Christmas delicacies, and was now very costive; and, as there was no
satisfactory history of the dog, I at once suspected lyssophobia. The
friends and strangers who had come to condole with the parents and
feast on the horror were excluded, and the boy's attention fully
engaged in amusing pictures and conversation; the paroxysms were
omitted, and in two hours the patient, overcome by weariness, went to
sleep. Next morning he was still kept secluded and quiet, and two
enthusiastic students took up the role of keeping his attention
constantly engaged on whatever would interest him. The prima viae was
relieved by medicine, and under a course of tonics the boy quickly
recruited, and at the end of a week went back to school.
In doubtful cases the test by inoculation may be tried. Inoculation
with the saliva of a man suffering from hydrophobia is manifestly
useless, since he must die before we can hope for the development of
the disease. But in the case of a dog having bitten one or more people
the inoculation of the virus on the brain of one or two other dogs
would ensure the development of the affection in the course of one or
two weeks, provided the first was rabid. The non-success of this
operation when practised on two dogs would provide the best possible
medicine for the diseased mind of the person bitten.
PATHOLOGICAL ANATOMY.--Post-mortem lesions are rather remarkable for
their inconstancy than for their specific characters. Hardly a single
lesion can be specified which may not be absent in particular cases,
yet some are so characteristic that, when taken along with the
symptoms during life, they very materially assist in diagnosing the
disease. Of the pathological appearances common to man, dog, and other
animals the following may be named: The body is greatly emaciated; the
rigor mortis is normal or nearly so; decomposition usually sets in
early; a white skin is livid, cyanotic, or petechial; the cicatrix is
often hardly noticeable even after the animal has been shaved; the
superficial veins, especially those of the neck and head, are filled
with black inspissated blood; the external mucous membranes are of a
dark livid hue, those of the mouth and nose being covered by a
tenacious mucous or muco-purulent secretion (in dogs they are usually
covered with earth or dust); the fauces, pharynx, and tonsils are
usually of a dark livid hue, and sometimes swollen; in other cases the
dark red hue and manifest swelling that obtained during life disappear
after death; similar lesions are found in the larynx, and I have seen
extensive erosions; the bronchial mucous membrane is reddened and
coated with a muco-purulent secretion (and in dogs with earth and
foreign bodies); the lungs are usually congested, often to the extent
of showing death by asphyxia; the heart and large blood-vessels are
filled with a black thick, venous blood, and the muscles, charged with
the same blood, have a dark reddish-brown hue; the stomach is usually
congested, sometimes to a port-wine hue, and is the seat of
blood-extravasations and even erosions; this congestion is often
present, though to a less degree, in the intestines; the mesenteric
glands and those in the vicinity of the pharynx are not unfrequently
enlarged and congested; a very constant feature is the entire absence
of proper food in the stomach and of chyme in the small intestine; the
liver is usually hyperaemic, {903} exuding on pressure the
characteristic dark blood, and it may be the seat of some granular
degeneration, but it usually retains its normal consistency; the
spleen is normal; the kidneys are hyperaemic and leaden or bluish
gray, and slightly cloudy on the surface (in dogs fatty degeneration
of the inner cortical layer is common even in health); the urinary
bladder is usually empty or contains a little turbid, yellowish,
slightly albuminous urine, while the mucous membrane is often covered
with dark reddish-brown petechial spots; the brain is usually
hyperaemic, and, together with its membranes, slightly oedematous, yet
the lesions are not constant either in kind or degree; the medulla
oblongata usually shows a similar condition, and even minute points of
acute congestion, but neither these nor the hyperaemia and oedema of
the spinal cord can be found in every case.
Some conditions are especially pathognomonic in the dog. In nearly all
cases of furious rabies the stomach is gorged with foreign bodies,
such as hay, straw, wood, coal, leather, portions of textile fabrics,
faeces, earth, sand, stones, pieces of iron, lead, etc., and the same
materials are usually found in the small intestine, while the large
intestines are empty. Portions of these foreign bodies are often found
in the bronchia as well, giving rise to circumscribed lobular
pneumonia. The significance of such matters when found in large amount
in the stomach of a dog which has been given to biting or other
symptom of rabies is very great, and if the stomach contains none of
the natural food of the animal and the duodenum no chyme, it may be
held pathognomonic of rabies. If, however, the materials are small in
quantity and mingled with natural food, and if the duodenum contains
chyme, the dog was probably not rabid. Dogs frequently chew and
swallow fresh leaves of grass, and those in detention gnaw and swallow
pieces of wood, cloth, horn, etc.; but these are used either as an
emetic or a teething-ring, and virtually imply that digestion is not
entirely abolished. Their presence, therefore, along with food does
not indicate rabies.
PROPHYLAXIS.--In view of the almost or quite constantly fatal issue of
rabies in man and animals, the main attention should be given to the
question of prevention. As the disease is perhaps never in our time
developed except as the result of contagion, we have the most perfect
guarantee that by suitably devised measures it may be absolutely
suppressed and excluded from any country. Even if we allow that a rare
case is at long intervals developed spontaneously, it is none the less
certain that the disease can be practically abolished, as nothing can
be easier than to nip the disease in the bud in the locality where it
first shows itself. Thus in Australia, Tasmania, and New Zealand
rabies has not yet appeared, though prevailing in the same latitude
and climate in both hemispheres. It reached Mauritius in 1813, and has
prevailed uninterruptedly since, while in Bourbon, immediately
adjacent and almost identical in geology, climate, flora, and fauna,
it is still unknown. The same truth is told in the entire extinction
of rabies in Berlin by the universal muzzling of dogs, as recorded
above. The immunity lasted for nine years, during which muzzling was
enforced. A more recent example of the same kind is found in Holland.
In 1875 universal muzzling was made obligatory in all communes where
rabid animals had been and in adjoining communes. From 1877 on the
disease was unknown save on the borders of {904} Belgium and Prussia
and in a very few dogs recently imported. Nearly all cases of
hydrophobia in man and animals being due to bites by rabid members of
the canine fraternity, a fundamental condition of all success in
prevention is the prohibition of its diffusion by dogs. For this
reason the following measures are requisite: 1st. All dogs should be
registered and heavily taxed. The number of useless dogs kept in every
community affords the greatest opportunity for the speedy diffusion of
the rabid germ whenever that has been introduced. Whatever tends to
reduce this number directly tends to the restriction and extinction of
rabies. 2d. Every dog should be made to wear a collar with plate
bearing the name and residence of his owner. All stray dogs without
such badge should be summarily shot by the police. This will secure
the payment of the taxes and the destruction of superfluous and
dangerous dogs. 3d. In all cities and counties where rabies has
existed within a year, and in the counties adjoining them, every dog
should be muzzled except when securely shut up or tied. All dogs found
at large without a muzzle should be promptly shot by the police. The
objection to muzzles is satisfactorily met by the use of the wire
muzzle, which impedes neither breathing nor drinking. 4th. Dogs and
cats suspected or known to have been bitten by rabid animals should be
at once destroyed, or if considered sufficiently valuable may be
confined in a secure cage for six months under veterinary supervision.
5th. Dogs which have bitten and are supposed to be rabid should be
similarly caged and placed under veterinary supervision. If rabid, the
symptoms will be fully developed in a few days, whereas if destroyed
at once the bitten party is liable to develop lyssophobia. 6th. Dogs
imported from countries where hydrophobia is known to exist should be
subjected to a period of quarantine of six months. 7th. Foxes, wolves,
badgers, martens, skunks, must be indiscriminately destroyed in
localities where they have become infected with rabies. 8th. The
disinfection or burning of the kennels where rabid dogs have been is a
natural corollary of the above.
Other measures less thorough and efficient are often advocated and
resorted to, but should be discarded whenever it is possible to
practise a method of absolute extermination. Among these may be named
the flattening of the teeth, and especially of the canines, with a
file, as advocated by Bourrel, and later by Fleming. While this is a
measure of protection, it does not remove the desire to bite, nor the
power of wounding the skin when that is delicate or tender. Another
method is to hang a block of wood from the neck, so that it may impede
the movements of the forelegs and prevent a rush and sudden attack.
The futility of such a resort need hardly be remarked upon. The
emasculation of dogs is another preventive measure advocated. The
single advantage of this is that it does away with the host of suitors
that follow a rutting bitch, and the mutual worrying and biting that
ensue. But it is not yet proved that the disease is produced by
privation of the generative act, while if it were it is still certain
that cases of spontaneous rabies are extremely rare; that the rabid
dog bites the castrated one as readily as the perfect male; that the
emasculated one contracts rabies as readily as others when bitten, and
that he communicates it no less persistently. Galtier's method of
intravenous injection of the rabic saliva, which seems to have proved
effectual in sheep and rabbits, utterly failed in the hands of Lussana
and {905} Pasteur in dogs. Besides this objection, that it is useless
for the animal which is beyond all comparison the main propagator of
rabies, it has the serious disadvantages that its practice would
necessitate the maintenance of a constant succession of cases of
rabies, that great danger attends this production and handling of the
virus, and the expense and risk of a general application of the
measure must absolutely forbid it.
More recently Pasteur has found that the virus when transmitted
through several monkeys in succession becomes so weak as to be
harmless to the animal inoculated, and yet protects the animal against
the more virulent poison. This fact he utilizes by inoculating this
mitigated ape-virus on the brain of the animal just bitten, so as to
render that refractory to the disease when the poison from the bitten
wound shall reach it by its ordinary slow channel. At the time of
writing, the method is being attempted on a man bitten by a mad dog.
Another precautionary measure which is always in place is the
diffusion among dog-owners of correct information as to the
premonitory symptoms of rabies, and the necessity for careful
seclusion when any such symptoms are manifested.
TREATMENT OF BITES.--The treatment of bites by animals supposed to be
rabid consists mainly in seeking the elimination of the poison or its
destruction by caustic. The first object should be to prevent
absorption of the poison. If the bite has been on a limb, a tourniquet
should be instantly placed above it. A stout cord or handkerchief is
always at hand, and may be tied around the limb and twisted with a
piece of wood until circulation is arrested. Sucking the wound is
usually effective in withdrawing the poison, and can convey no
additional danger to the person bitten. If the patient cannot reach
the wound with his own mouth, another may volunteer to suck it, though
in these days of diseased teeth and gums the act is pregnant of
danger. This may be largely obviated by alternately sucking and
rinsing the mouth with a solution of carbolic acid, or, better, by
applying such a solution to the wound before sucking, or finally by
sucking through a tube. Cupping over the wound is highly commendable,
though less effective than sucking. When cupping can be combined with
wringing of the wound, there is an approximation to sucking. Cupping
is especially valuable in wounds of the trunk, where a tourniquet
cannot be applied. Intermittent squeezing and wringing of the part and
steeping in warm water is an excellent resort when no better measure
can be had. Cutting the wound open to its depth, while it may in
certain cases be necessary to allow of the thorough application of a
caustic, is objectionable as multiplying the points of infection and
absorption. Drinking of liquids to excess temporarily retards
absorption by overfilling the vascular system. Ammoniacal, alcoholic,
and other stimulants are resorted to for the same purpose, being held
to cause plenitude, not only by quantity, but by rarefying the animal
fluids.
No such measures should, however, be allowed to delay for an instant
the use of caustics. This is the one effectual means of destroying the
poison, and the choice of caustic is of less consequence than its
thorough application. The hot iron in the form of a skewer, nail,
poker, or other available instrument, at a white heat, may be brought
in contact with all parts of the wound to its utmost recesses.
Of chemical caustics, solid sticks of nitrate of silver, chloride of
zinc, {906} and potassa, or the crystals of cupric or ferric sulphate,
are to be preferred to the liquid forms (mineral acids, butter of
antimony, etc.), because of the greater thoroughness with which they
can be brought into contact with all parts of the wound. Lastly, the
galvano-cautery may be used if within reach. If the liquid caustics
are employed, they may be introduced into the depth of the wound by
means of a pipette, a piece of porous wood, or a pledget of tow. For a
great number of small wounds a bath of corrosive sublimate has been
recommended.
In some cases the amputation of a badly-lacerated member or one with a
compound fracture offers the only measure of protection.
But although nothing should be allowed to delay cauterization, yet the
impossibility of an immediate application should not be accepted as a
reason for its neglect at a later date. On the presumption that the
virus is localized in the seat of inoculation until it has increased
largely and is poured into the blood in sufficient quantity to
subjugate the blood-globules to its influence, it is logical to excise
the cicatrix and cauterize the wound, though days or even weeks have
elapsed.
If it should be shown by further experiment that Galtier's intravenous
injection of virulent saliva is harmless and protective to sheep,
rabbits, and it may be other Herbivora, it would be logical to employ
this in these animals just after they have been bitten, as there will
be ample time to establish the systemic influence of the intravenous
injection before the poison shall have accomplished its recrudescence
in the cicatrix. The constantly fatal result of rabid bites in these
animals would at least warrant such an attempt, the main precaution
being that the liquid shall be most carefully preserved from contact
with any of the tissues, including even the coats of the injected
vein.
In addition to the local treatment of the sore, certain general
medication has usually been resorted to, though its real value may
well be questioned. Thus, the elimination of the poison has been
sought by profuse perspiration induced by warm, Turkish, and Roman
baths, and by the use of medicinal agents, sudorifics, sialogogues
(mercury), laxatives, and diuretics (cantharides). The neutralization
of the poison has been attempted by ammonia, the sulphites and
hyposulphites, chlorine, etc. Besides these are used nerve-sedatives
and tonics, such as venesection, belladonna, prussic acid, tartar
emetic, sulphates of copper and zinc, arsenic, strychnia, etc.
What is probably of greater importance is a sound hygiene. Stimulating
food eaten to excess is injurious alike to man and beast, and by
inducing digestive disorder and cerebral congestion will tend at least
to precipitate the attack. Costiveness or biliousness from sedentary
habits and lack of exercise in the outer air and sunshine, exposure to
intense heat or cold and over-exertion, are all to be guarded against.
Finally, psychical treatment is of the highest importance. Those about
the person who has been bitten should preserve a calm, equable, and
cheerful demeanor and avoid all allusion to the occurrence. The
patient should be protected against all sources of excitement, and
should not be allowed to see that he is an object of solicitude. If
the matter is referred to incidentally, he should be impressed with a
conviction of the efficacy of the treatment adopted.
THERAPEUTIC TREATMENT.--Almost every agent in the {907} Pharmacopoeia
has been employed as a remedy for hydrophobia, but, up to the present,
it must be acknowledged, with no measure of success. The agents
supposed to be prophylactics are those also resorted to as therapeutic
remedies. To these may be added the potent nerve-sedatives and
anti-spasmodics--chloroform, chloral hydrate, ether, bromides of
potassium, sodium, and ammonium, curare, Calabar bean, and the
sialogogue diaphoretic pilocarpine.
Chloroform is one of the most appropriate, as it may be taken by
inhalation, though with much excitement to the patient, and it at once
relieves the oppressed breathing and pharyngeal and other spasms,
while it acts as a cerebral sedative and anaesthetic; and if it cannot
be held up as a curative agent, it at least secures euthanasia.
Chloral given as an injection, so as to induce its soporific action,
is equally soothing, though nothing more. Curare injected
hypodermically overcomes the spasms, but does not usually, if ever,
retard death. Three cases of hydrophobia in man treated in this way
recovered, but we have no proof that even these exceptional cases were
rabies. Pilocarpine has been used in a number of cases, but, with the
exceptional case of a young man reported by Denis Dumont, all
terminated fatally. The committee of the Paris Academy of Medicine
reported in 1874 that in three experimental cases "it hastened death
by the fits it brought on." Morphia is often of great value in calming
the excitement and giving rest and sleep during the intervals of the
paroxysms. Daturia and atropia, administered hypodermically, are
somewhat less effectual. Inhalation of oxygen is said to arrest the
convulsions and delirium, but not to retard death. Vaccine virus and
the venom of the viper have each been tried, but with no good effect.
Of non-medicinal therapeutic measures the following are among the most
promising: Perfect seclusion, quiet, and darkness serve to abate the
hyperaesthesia, the painful acuteness of the senses, and the
convulsive and delirious paroxysms. It can no longer be doubted that a
very few cases of genuine rabies recover, but those that do so have
almost all had special advantages in the way of quiet and seclusion,
and few have had the excitement of medicinal treatment. Eight cases of
the recovery of rabid dogs are reported by Menecier, Decroix,
Laquerriere, Rey, Harold Leiney, and Pasteur. The two first were
attested by successful inoculation on other animals; Decroix's second
case was caused by inoculation with the saliva of a hydrophobous man;
the next three had been bitten by dogs undoubtedly mad; while
Pasteur's was inoculated with the brain-matter of a rabid cow. All in
due time presented the characteristic symptoms of rabies, yet all
recovered, without any record of medicinal treatment. Pasteur's case,
when again inoculated, resisted the disease. A certain number of
recoveries of men from pronounced hydrophobia under medicine and
without it are on record, but in the absence of successful
inoculations it is impossible to tell how many were cases of infecting
rabies. The parallel between rabies and tetanus in the intensity of
the reflex excitability would demand darkness and quiet as a sine qua
non of any rational treatment. Faradization has produced a temporary
relief, but no permanent improvement. Warm baths, steam baths, and
hot-air baths serve to abate excitability and spasm, and have been
lauded as specific in hydrophobia, but have proved useless in the
lower animals.
{908} Intravenous injection of warm water (two pints) in a
hydrophobous man reduced the pulse from 150 to 86 and restored the
power of deglutition. Life was prolonged for nine days, but in great
agony, from the supervention of suppurative arthritis (Majendie). In
another case the dread of water disappeared, but death ensued in
fifty-four hours. In the hands of Youatt and Mayo it proved equally
unsuccessful in dogs. A cold bath with submersion to unconsciousness
is an old remedy now abandoned. Venesection to fainting, with or
without mercury, mitigated the symptoms, but seemed to hasten
paralysis and death. The excision and cauterization of the cicatrix,
or the cutting of the nerves proceeding from it, has been useful in
delaying, or even absolutely preventing, the paroxysms. When,
therefore, the premonitory symptoms of hydrophobia have set in, and
when an aura or shooting pain is felt proceeding from the seat of the
wound toward the heart, one or other of these measures may serve to
prevent the immediate occurrence of reflex convulsions. When the
poison has actually invaded the brain, this can be looked on as a
palliative measure only, but in the many cases of lyssophobia it may
put an instant stop to the affection.
{909}
GLANDERS (EQUINIA GRAVIOR, FARCY).
BY JAMES LAW, F.R.C.V.S.
SYNONYMS.--_Greek_, [Greek: malis]. _Latin_, Malleus, Equinia Nasalis,
E. Apostimatos, Farcinia. _French_, Morve, Farcin. _German_, Rotz,
Lungenrotz, Hautrotz, Wurm, Hautwurm. _Italian_, Morva, Moccis,
Cimurro. _Spanish_, Cimorro, Lamparones.
DEFINITION.--An infectious, bacteridian disease occurring in the
horse, ass, or mule, and communicated by inoculation to various other
animals, including man. It is usually ushered in by rigors, followed
by articular pains, lameness, and the formation of a specific deposit
in the lymphatic system of some part of the body, with a tendency to
destructive degeneration and ulceration. In the form known as glanders
these deposits and ulcers take place mainly in the nasal mucosa, in
the lungs, and in adjacent glands, while in that known as farcy the
deposits occur in the cutaneous and subcutaneous lymphatic plexuses
and the dependent glands.
HISTORY AND GEOGRAPHICAL DISTRIBUTION.--Under the name of malis
Aristotle describes a fatal disease of asses, supposed to have been
identical with the malleus humidus of Vegetius Renatus and other
writers of early Christian times, and with the cymoira of other early
Roman writers. This malady was characterized by swelling of the
submaxillary glands and discharge from nose and mouth. From the
fourteenth century onward glanders is reported from different parts of
Europe at frequent intervals; thus in 1320 in England (Rogers); in
1640 in Badajoz, brought by Portugese horses (Villalba); in 1686 at
Treves (Eggerdes); again in 1776 in Southern France (Lafosse); in 1794
in Bavaria (Plank); in 1796 in Franconia (Laubender); and in 1798 in
Piedmont (Toggia). At the beginning of the present century this
affection was very widely prevalent in Great Britain, the chronic
cases being habitually worked in stage-coaches, but of recent years,
when it has been made criminal to expose or use a glandered horse, the
malady has to a great extent disappeared. To-day glanders is almost
coexistent with the distribution of the domesticated equine family,
yet its prevalence bears a direct relation to the facilities for
infection (horse-traffic, war, preservation of the diseased,
confinement in close stables, ships, etc.), and some countries appear
to be entirely free from the affection. Thus, Krabbe gives the yearly
losses per 100,000 horses for the principal countries of Europe and
Algiers as follows: Norway, 6; Denmark, 8.5; England, 14; Sweden, 57;
Wurtenberg, 77; Prussia, 78; Saxony, 95; Belgium, 138; {910} France
(army), 1130; Algeria (army), 1548. The losses in Prussia more than
doubled after the Franco-German War; thus, in 1869-70 they were 966,
and in 1873-74, 2058. In Bavaria they rose in the same period from 173
to 390 (Hahn). In Lisbon, Portugal, glanders was unknown for the
thirty years preceding the Peninsular War, whereas after the war it
proved a veritable scourge (Saunier). Charles Percivall, during an
eight years' residence at Meerut and Cawnpore, Hindostan, saw not a
single case of glanders, and so late as 1275, Fleming claims an entire
immunity for India; yet in 1877 complaints were numerous of the very
general prevalence of the disease in Upper India especially, while in
1879 the campaign in Afghanistan was seriously affected by its
ravages. Climate appears to have little influence. The disease is
virtually unknown in the island of Bornholm with 7000 horses, and in
the Faroes and Iceland with 35,000, while it is quite frequent in
Sweden. It is unknown in Australia, but is very prevalent in China,
South Africa, Abyssinia, and Algiers, and but little known in Asia
Minor, Arabia, and Egypt.
In the United States as in Europe the disease has mainly concentrated
itself in the large cities in times of peace, and spread widely on the
advent of war. It is alleged that it first entered Mexico in 1847 with
the American cavalry, though with the horses kept in the open air it
failed to gain a wide extension. The horses and mules drawn into the
Union armies in 1861 brought infection with them, and soon the disease
was most prevalent and destructive, not only in the ranks, but in
every State in which the armies operated. John R. Page says the first
case he saw in the Confederate army was a captured Federal troop-horse
on the retreat from Manassas, and that the breaking down of the
Confederate cavalry in the last two years of the war was mainly due to
glanders. At the close of the war the sale of army horses distributed
the infection widely through all the States, North as well as South.
Every year in a country district in Western New York I see several
cases of glanders, and occasionally a whole stud is carried off
through an infected purchase. In other States the case is no better.
In Pennsylvania, Ohio, Illinois, and Michigan cases are constantly
seen in the country districts, and in the three last-named States five
human victims have been reported within a short period. In Connecticut
the same is true, and the disease made one human victim in Waterbury
in 1879. In the large cities the case is still worse. Liautard of New
York in 1878, in a single visit to one car-stable, condemned 8 horses,
in another stable 18, and in a third, at two visits, 45, while a
fourth had lost no fewer than 200 horses in the course of one year
from glanders. In the Troy (N.Y.) car-stables the malady prevailed
from 1875-77, most of the subjects suffering from chronic farcy, until
in the latter year, by my advice, these propagators of contagion were
destroyed. In Springfield, Mass., in 1879, the disease assumed such
alarming proportions that it was vigorously suppressed by a city
ordinance enjoining summary slaughter. These are but indications of
what is happening all over the country, entailing losses of many
hundreds of thousands yearly as well as an enormous risk to humanity.
The following table gives the number of cases occurring in the equine
family in two of the principal countries of Europe in the last few
years: {911}
Cases of Glanders in-- Great Britain. Germany.
1878 888 2753
1879 1367
1880 2048 1941
1881 1710 1774
1882 1389 1838
As both countries systematically suppress this disease through their
veterinary sanitary officials, it cannot be doubted that the figures
for America, if obtainable, would be relatively higher.
Glanders prevails especially in horses, asses, mules, and other
solipedes, and is communicated by inoculation to all domestic animals
except the genus Bovis. In the sheep and goat the receptivity is
considerable, and the disease may prove fatal in fifteen days
(Gerlach) or it may be delayed for seven weeks (Bollinger). The
Carnivora (dogs, cats, lions, polar bears) contract the affection by
eating diseased flesh, as do some rodents (prairie-dogs, rabbits,
guinea-pigs, mice), and, by administration, solipedes. Swine contract
the disease by inoculation (Gerlach, Spinola), though in these and in
the dog the constitutional symptoms are usually slight and recovery
may follow the local affection.
The susceptibility of man is doubtless less than that of the
solipedes, judging from the few cases of glanders compared with the
frequent exposures, yet when once established in the system it can
hardly be said to be less malignant or fatal.
ETIOLOGY.--The one known cause of glanders is contagion, and the
recent experiments of Capitan and Charrin in France and of Schutz and
Lofler in Germany, demonstrating that the bacillus of the glanderous
deposits is the one essential cause of the disease, effectually
dispose of any claim of its spontaneous origin. Glanders can no longer
be considered spontaneous, further than that its germ is now proved
capable, like that of anthrax, of survival and multiplication out of
the animal economy, so that infection may come from other objects than
a sick animal; and it may even yet appear that the bacillus, living at
times as a harmless saprophyte out of the animal body, may acquire
deadly properties under certain conditions of the environment. At the
same time, the most extensive acquaintance with glanders and the
broadest generalizations from known facts do not warrant the
assumption of the extension of the disease by the growth of the
bacillus out of the living body, unless it be on the rarest possible
occasions, while the soundness of extensive countries (Australia, New
Zealand) for a century or more speaks strongly against any frequent
development from a harmless saprophyte.
To the same effect speak the experiences of the English army. At the
beginning of the century, under the teaching of Coleman, most cases
were attributed to lack of stable care, and extensive experiments were
made in the treatment of the disease, with the result of a very high
mortality from this cause. Now, when contagion is looked on as the
main or sole cause, and all suspected horses in the army are promptly
destroyed, the disease is only seen in recently-purchased animals or
after the inevitable exposures of a campaign.[1] In the French army
the doctrine of the {912} non-contagiousness of chronic glanders led
to a greater prevalence of this disease than in any other country of
Europe. Prior to 1836 it was about 90 per 1000 per annum, whereas now,
under the doctrine of contagion and a corresponding practice, glanders
kills but 2 per 1000 per annum (Rossignol).
[Footnote 1: Wilkinson, _Jour. of Roy. Agr. Soc._, No. 50.]
But while the essential cause of glanders is the specific bacillus, an
individual susceptibility is no less requisite to an attack. This may
be innate or acquired. As we have seen, it varies according to the
genus, being greatest in the solipede. But many solipedes show a
strong power of resistance. Of 138 horses similarly exposed by
cohabitation with glandered horses, but 29 (21 per cent.) suffered. Of
28 inoculated with glanders virus, but 9 (32 per cent.) succumbed
(Lamirault, Bagge, Tscherning). The accessory causes which predispose
the system to the reception of glanders may be included under one
general term--low condition and ill health. Three of these causes,
however, deserve especial mention: 1st. Impure and rebreathed air.
Prior to 1836 the yearly losses per 1000 of the French army horses
were from 180 to 197. At the date named the ventilation of the stables
was greatly improved, and the mortality fell to 68 per 1000 per annum,
one-half from glanders. Later improvements have reduced the 34 cases
to 2. During the Italian War, in 1859, 10,000 of these horses were
kept for nine months in open sheds, with but one case of glanders.[2]
In the expedition to Quiberon during the Napoleonic wars, a cavalry
contingent, believed to be healthy, shipped on new transports,
encountered a storm, and had the hatches fastened down, so that
several horses were suffocated. Among the survivors, landed at
Southampton and placed in stables hitherto unchallenged, many soon
developed glanders in its worst form. Similar results followed the
English expeditions to Varna in 1854, and that to Abyssinia in 1867.
In badly-ventilated mines and stables, especially cellar stables,
glanders, once started, is always most virulent.
[Footnote 2: Larrey, _Hyg. des Hop. Mil._, 1862, p. 63.]
2d. Cold, damp, draughty stables greatly favor the progress of
glanders. Leblanc reports the case of a stud of 240 horses that had
had no glanders for eight years, but which lost half their number in
three months after removal into a new stable, very lofty, but dark and
damp, and subject to cold draughts. It is worthy of notice that they
had also been subjected to double work, and were consequently
emaciated, but there was not known to be any unusual exposure to
contagion. In a Boston street-car stable, where glanders had long
prevailed, Thayer cut it short by destroying the infected animals and
by improving the ventilation by windows hung at the bottom and opening
inward, so that the air entered in an upward direction, and cold
draughts on the horses were avoided.
3d. Debility from ill-health, low feeding, or overwork.--The nervous
and nutritive debility consequent on chronic disease, overwork, and
exhaustion lessens the power of resistance to specific poisons, but in
such circumstances there is always the added predisposition of an
excess of waste material in the blood, a specially abundant food for
the disease-germ. So notorious is this that it used to be held that
the specific poison of glanders was generated in connection with the
excess of creatine, creatinine, and lactic acid resulting from
muscular action. Of the effect of {913} low diet we have a striking
example, furnished by Bouley, of a stud of 120 horses, 60 of which
were attacked within a year after they had been placed on a food
insufficient to repair the body-waste, and from which the disease
disappeared after the slaughter of the infected and improvement of the
ration. So long as glandered horses were preserved for work, the then
nearly ubiquitous germ attacked nearly all that were run down by
chronic diseases; hence glanders was looked upon as the natural
winding up of exhausting diseases in the horse, as tuberculosis was
thought to be in the human subject. Modern discovery shows that
without the germ all such debilitating causes are impotent, but it can
never disprove the great potency of these in laying the system open to
attack, nor the value of vigorous health and sound hygiene in
fortifying the system against it.
The channel of infection manifestly varies in different cases. In
direct inoculations the morbid process develops first at the point of
insertion, and secondly in the nearest lymphatic glands and internal
organs. When contracted in the ordinary way, the lesions are usually
first seen in the posterior nasal passages, the larynx or the lungs,
or in the superficial lymphatics, especially of the hind limbs. This
susceptibility of the deeper portions of the air-passages seems to
imply that the bacillus, borne on the air, is lodged on different
parts of the respiratory mucous membrane, and first sets up the morbid
process in the thinnest or most susceptible portion. That it can be
thus borne on the air is shown by the experiments of Viborg and
Gerlach, who separately collected the particulate elements from the
exhalations of glandered horses and successfully inoculated them. That
the virus is not usually carried far on the air in a virulent form is
attested by the many instances in which horses have stood for months
in the same stable with a glandered animal without becoming infected.
That infection may also take place through the ingestion of infected
matters is undoubted, as glanderous products mixed with food, or even
made into balls and enclosed in paper and administered to horses in
this form, have produced the disease. The virulence is said to be lost
by passing through the digestive canal of man (Decroix), dog, pig, and
fowl (Renault), but even to Carnivora the infection may be conveyed in
the food.
While the virus is concentrated in the material of the special
glanderous deposits and the discharges from these, yet no part of the
body can be considered as free from the poison. Viborg, Coleman,
Hering, and Chauveau have communicated the disease by transfusion of
blood from a glandered horse to a healthy one; hence every vascular
organ must be liable to infect. The secretions of the diseased body
(tears, saliva, mucus, sweat, urine, and milk) have each been
successfully inoculated, and the conveyance of the disease to the
foetus in utero and to the female by coition imply that even the
generative secretions are virulent. Failures to convey the disease by
inoculation with the blood and secretions have often occurred,
however, and they must be held as less virulent than the products of
the local disease-processes.
The claims that inoculation with pus, ichor, and other irritants have
produced glanders must be entirely discredited. The deposits and
ulcers in the lungs and elsewhere resulting from such inoculations
have been either septicaemia, mistaken for glanders in the earlier
days of pathological anatomy; or the septic and other inflammations
set up by these {914} inoculations have merely served as fertile spots
for the planting and growth of the glanders bacillus accidentally
present, and which to a healthy system might have proved harmless.
In 1882, Chauveau had demonstrated the particulate nature of the
glander germ by his unsuccessful inoculations with the liquids
filtered from dilutions of pus taken from a pulmonary glanderous
ulcer. The filtrate and the liquid mixture formed by mixing the pus
with five hundred times its own weight of water retained their
virulence undiminished. In 1868, Christol and Kiener discovered in
glanderous products a bacillus which they figured as made up of a
chain of nearly globular elements apparently enclosed in a common
sheath. In 1881-82, Bouchard, Capitan, and Charrin cultivated these
microphytes in a neutralized extract of meat through five successive
cultures, using in each case a milligramme of the previous culture, or
less than 1/1000 part of the culture-liquid. Counting that the
milligramme of pus would give to each centigramme of the first
culture-liquid 1,000,000,000 bacilli, it follows that the second
culture would, on the principle of dilution, contain 1,000,000, the
third 1000, the fourth 1, while for the fifth it was as 999 to 1 that
it would receive nothing unless the germ were multiplied in the
culture-liquid. Inoculation of a cat with this fifth culture, started
originally from a nasal ulcer of a glandered horse, led to a fatal
result in twenty-five days, with suppurating tumor of the left
testicle and inguinal glands. The products of the first cat were
inoculated on a second, those of the last on a third, those of the
third on a guinea-pig, and those of the guinea-pig on an ass,
producing in every case specific lesions of glanders, including
miliary nodules and abscesses, and death respectively on the following
days: 16, 7, 31, and 10.
In September, 1882, and the two succeeding months, a similar course of
experiments was conducted by Schutz and Lofler at Berlin. The virulent
matter used for starting the culture was procured from a pulmonary
deposit and spleen of a glandered horse; the cultivation was continued
through eight successive culture-fluids. One horse was successfully
inoculated with the product of the eighth culture, and a second with
both the fifth and eighth. The first died on the fifty-eighth day, and
the second, now very weak, was sacrificed on the fifty-ninth. Both
showed the most extensive lesions of glanders alike in the skin, the
lymphatic glands, the pituitary and laryngeal mucous membrane, and the
lungs. To demonstrate the bacillus they take a thin layer of the
infecting liquid on a cover glass, dry it, stain with methyl violet,
wash with dilute acetic acid, dehydrated by absolute alcohol, and
clear by oil of cedar. Like other pathogenic microphytes this may be
preserved for months or years if thoroughly dried, but in the moist
condition it is easily destroyed by heat (133 degrees F.; Viborg,
Hofacker, Renault), chlorine, and the disinfectant chlorides and
sulphites.
SYMPTOMS.--Acute nasal glanders in horses has a period of incubation
lasting from three to five days in inoculated cases. Where in infected
subjects the incubation appears to have extended over months or a
year, there have usually (or always) been deposits in internal organs
which passed without recognition until the lesions appeared in the
nose. At the outset there is fever, which appears before any local
lesions are recognizable, even post-mortem (Chauveau), and soon with
languor, {915} and loss of appetite, there is a serous nasal
discharge, often from one side only. By the sixth day this has become
yellowish, the margin of the nostril is often swollen, and upon the
pituitary membrane may be detected elevations of various sizes of a
general yellowish tinge, dotted with minute red points and surrounded
by a bright-red or purple and slightly elevated areola. These may be
simple, pea-like nodules or more or less extensive patches, which in
certain cases extend over nearly the whole pituitary membrane. At the
same time the submaxillary lymphatic glands on the same side become
the seat of a hard nodular painless enlargement, feeling like a
conglomerate mass of peas, and often showing a tendency to become more
closely adherent to some adjacent part (bone, skin, base of tongue);
but they only ulcerate exceptionally. Extensive hot, painful
engorgements also often appear on other parts of the body, and if on
the limbs or joints cause lameness. Soon the swellings on the mucosa
become eroded and are gradually destroyed, forming large unhealthy,
chancrous-looking ulcers, tending to become confluent and to eat
deeply through the mucosa into the subjacent tissues. These are mostly
reddish gray or yellowish gray, with raised ragged red or
yellowish-red margins. They bleed readily, and may be black from
hemorrhage, or greenish or of some other shade from decomposition. The
discharge is always somewhat glutinous and sticky, but it may vary in
color from simple white to yellowish, greenish, brownish, or red,
according to the destruction of tissue, the septic changes, or the
effusion of blood.
By the sixth to the fifteenth day the acme has been reached. The alae
of the nostrils are glued together by the drying discharge, and this,
with the general swelling of the nasal passages, renders the breathing
snuffling and difficult. The lymphatics on the side of the face are
usually inflamed and corded, and the same is true of the cutaneous
lymphatics of the hind limbs of some other part of the body (farcy).
Death usually ensues from suffocation, preceded by the most painful
dyspnoea.
Chronic glanders in horses often sets in insidiously, but frequently
also it first shows itself by constitutional disturbance, which
gradually subsides as the local lesions are formed. Among frequent
premonitory symptoms may be mentioned intermittent or continued
lameness, oedema of one or more limbs, infiltration of the testicle,
cough, and bleeding from the nose. The general health may appear good,
and if in good hygienic condition the digestion and nutrition may be
sufficient, the body plump, and the skin shining; but there is usually
some dulness of the eye, dryness of the coat, lack of endurance, and a
tendency to sweat easily and to run down rapidly under hard work or
debilitating conditions. The discharge, at first clear, becomes
turbid, grayish, sticky, and purulent, tending to agglutinate the
hairs and edges of the alae nasi, and is expelled by snorting in
masses. The nasal mucosa, and especially over the septum, is the seat
of the peculiar elevations, ulcers, and firm white, condensed deposits
resembling cicatrices, usually low enough down to be seen or felt. The
submaxillary lymphatic glands are the seat of the nodular enlargement
described in acute glanders, and, as in that affection, there may be
pulmonary or skin deposits shown by cough or oedema, with swelling and
cording of the cutaneous lymphatics with nodules and ulcers.
These cases often maintain this indolent type for years, spreading the
{916} infection widely, but they tend sooner or later to develop the
acute type, especially under some debilitating conditions.
When the mucous membrane of the larynx and bronchi is first attacked
the nasal lesions may be delayed for a time, but the cough, the
variously colored tenacious expectoration, the excessive tenderness of
the larynx, and the nodular enlargement of the adjacent lymphatic
glands, with the general ill-condition, suggest that which is later
confirmed by the specific lesions in nose and skin.
When the affection is confined to the bronchia and pulmonary
parenchyma, there are the usual signs of bronchitis, disturbed
breathing, with hard, soft, mucous, or dry husky cough, and blowing,
mucous or sibilant rale, at points crepitation, and at others some
diminution of murmur and resonance. The breath is mawkish or fetid,
and expectoration more or less sticky and charged with bacilli; but
all these symptoms are at times equivocal, and inoculation alone can
attest the true nature of the disease. This should be practised by
preference on a donkey or an old horse in poor condition but with
general good health. Then the disease shows itself in the acute form
in six days. If solipedes are not available, rabbits or guinea-pigs
may be used for inoculation.
In acute cutaneous glanders or farcy, premonitory symptoms resemble
those of ordinary acute glanders, which indeed is usually present as
well, and always supervenes before farcy terminates in death. The
local lesions consist in inflammation of the lymphatic vessels, which
become like firm cords, the appearance at intervals along these cords
of rounded glanderous nodules varying in size from a pea to a
hickory-nut, and with a marked tendency to ulceration and the
formation of hot, painful oedematous swellings. The swelling of the
lymphatics appears by preference in the lower part of a hind limb, and
the first nodules may be near the fetlock or tarsus. The ulcers
forming about the sixth day have a yellowish-white appearance with red
points and raised irregular borders, and the discharge is grumous and
viscous, with a yellowish or reddish tinge. The disease extends toward
the body, the upper air-passages become involved, and death speedily
follows.
Chronic cutaneous glanders, chronic farcy, usually begins by a local
swelling, mostly of the fetlock, in the midst of which a careful
examination detects a small glanderous nodule. This tardily softens,
ulcerates, and discharges the characteristic ichor, the lymphatics
leading up from it become thick and rigid (corded), and new nodules
appear. Though very indolent, these finally tend to ulcerate, and in
time oedematous swellings appear in the vicinity or at distant parts
of the body, with nodules at intervals. This will go on for months, or
even for years, and recoveries occasionally take place, while in other
cases, and especially when the conditions of life are bad, acute
glanders supervene.
MORBID ANATOMY.--The lesions consist essentially in a cellular growth
in the connective tissue, determined by the presence of the specific
poison, and in destructive changes in the elements of such
growth--softening, fatty degeneration, ulceration, and discharge. In
certain cases of nasal glanders at the earliest stage there is merely
an increased proliferation of the mucous corpuscles, which become more
granular or purulent. Soon, however, the fibro-vascular layer is
involved, the affected part being the seat of dark bluish congestion,
and {917} of the proliferation of small rounded lymphoid cells,
comparable to those of the early stage of tubercle, and enclosed in
more or less dense fibrous areolae. The common nasal nodule or patch
has a soft velvety surface, dirty gray or grayish yellow, and the
lymphoid cells are so circumscribed in nests that when soaked in water
the cells are washed out and the fibrous reticulum is left hollowed
out like a honeycomb. In this fibrous reticulum are many
spindle-shaped and a few rounded cells. Its vascularity is easily
demonstrated by injection. The centre of each nest is the palest part
of the mass, and unless stained by extravasation it contrasts with the
reddish areola. These islets of lymphoid cells, at first isolated and
each the size of a pin's head, may enlarge and become confluent,
forming the larger nodules. With this increase the centre of each
becomes turbid, and the cells are found to have become granular and
fatty, and to have in part broken up into a granular debris. This
characterizes the period of ulceration, and erosions and ulcers follow
in ratio with the extent of the neoplasm and the rapidity of its
growth. If the growth is tardy, the ulcer, with irregular eroded and
everted edges, may remain for some time stationary or even recede,
while if rapid, new tubercles form around the margin of the first, and
by the disintegration of their elements the ulcer is continuously
extended. The lesions are especially common on the septum nasi and
turbinated bones. Similar lesions may be found in the nasal sinuses or
larynx.
The nodules found in the lungs strongly resemble miliary tubercles,
but are usually less numerous. As in the nose, they have a punctiform,
central, grayish, turbid portion, encircled by a more translucent
ring, surrounded in its turn by a vascular area. They are also
composed of the same granular rounded cells, though they may,
especially in the chronic forms, have undergone caseous, fibrous, or
calcareous degeneration. The acute tubercles are often surrounded by
circumscribed pneumonia with considerable exudation. They are
distinguished from genuine tubercle by their vascularity and by the
absence of giant-cells.
The cutaneous deposits are composed of the same histological products
imbedded in the dermis or in the subcutaneous connective tissue, and
extending in some cases deeply between the muscles, with no clear line
of demarcation from the sound tissue. Not only the chains of nodules
(farcy-buds), but the connecting lymphatic trunks, are the seat of the
characteristic cellular product, and in chronic cases there is the
enlargement of the adjacent lymphatic glands as well. In these there
is a special tendency to early disintegration and ulceration.
In the diffuse glanderous swellings (infiltrated glanders,
inflammatory glanders) the affected tissues are the seat of an
inflammatory process with profuse exudation throughout, while in the
interstices of the connective tissue are numerous granular
glander-cells. The same tendency to necrobiosis is shown as in the
other forms of glanderous neoplasms, and such diffuse swellings become
the seats of very extensive, deep, and irregular ulcers, or frequently
of fibroid growth and induration, forming the so-called cicatricial
deposits. These are hard, firm, and resistant, and histologically
consist of a dense fibrous stroma interspersed with the spindle-shaped
cells. They are especially common in chronic cases, and such an
appearance on the nasal mucous membrane is always suspicious, as this
dense fibroid appearance rarely follows a simple traumatic lesion.
{918} Diffuse glanderous infiltrations in the nose may implicate the
entire mucosa of one or both nasal chambers, and the ulcers are liable
to be greater than from the nodular form of the disease. They are also
especially associated with thrombosis of the veins, which occurs to a
less extent in the nodular form and conduces to the dark-blue tint of
the mucosa.
Glanderous infiltration of the lungs is inflammatory in its nature
(pneumonia malleosa), attacking an area of two or three inches in
diameter at or near the margin of the lungs, and proceeds to caseous
necrobiosis, suppuration, calcification, or fibroid induration. In the
skin such infiltrations also frequently terminate in induration, while
ulceration and abscess tend to appear when the proliferation of
glander-cells is most abundant (farcy-buds).
The glander-nodules are not uncommon in muscles, intermuscular
connective tissue, spleen, liver, kidneys, and testicles. Leukaemia is
also a constant feature, the irritation of the lymphatic glands
manifestly stimulating the production of the lymph-cells.
DIAGNOSIS.--The diagnosis of glanders usually rests on the viscid
nature of the discharge, the painless nodular swelling of the
submaxillary glands and the indisposition to suppurate, the
characteristic appearance of the nodules, elevations, ulcers, and
indurations of the nasal mucosa, and the presence of the specific
bacillus. The diagnosis of farcy rests mainly on the nature of the
nodules and corded lymphatics, of the ulcers and their discharges, on
the extension of the affection toward the trunk, and the tendency to
implicate the respiratory organs. Usually, there are several victims,
the earlier ones chronic cases, the later ones acute, or there is a
history or presumption of exposure. Yet in many cases, and especially
in the more chronic internal forms (laryngeal, pulmonary, etc.), the
diagnosis is difficult, and inoculation of a horse, goat, sheep, or
rabbit may be the only available means of reaching a decision.
Auto-inoculations are unreliable, as parts not yet the seat of active
disease will often resist inoculation.
PROGNOSIS.--This is always unfavorable. The constancy of internal
deposits and the viability of the germ in such products render it
impossible to eliminate the poison from the system in the great
majority of cases. In external glanders only is there any reasonably
good hope, and even this is confined to the chronic cases. In stating
this much, it is not denied that recoveries even of chronic nasal
glanders do occur, yet these are few, and the majority of those that
do apparently recover usually succumb as soon as they are subjected to
hard work or specially trying conditions of life, so that but little
faith can be placed in most of the alleged recoveries.
TREATMENT.--Considering the great danger of multiplying and preserving
the germs of a disease so fatal alike to man and beast, the treatment
of glanders is never commendable. The danger is least in the case of
chronic farcy, not only because the processes are less active, but
because the virus is not being thrown out and diffused with the tidal
air of respiration, sneezing, and coughing. The unbroken farcy-buds
and swollen lymphatics may be actively treated by compound iodine
ointment, and the ulcerous nodules freely cauterized with corrosive
sublimate, biniodide of mercury, chloride of zinc, sulphate of copper,
or iodized {919} phenol. Local inflammations may demand fomentations
and astringent antiseptic lotions. Meanwhile, the system must be
supported by a tonic regimen and medication, abundance of pure air, a
liberal and wholesome diet, and the maintenance of the various bodily
functions in a healthy condition. Of medicinal agents the most
pronounced tonics have the best reputation--sulphate of copper and
iron, biniodide of copper, arsenic, and, above all, arsenite of
strychnia. Next to these the sulphites rank, and a combination of the
two last named is perhaps to be preferred.
PREVENTION.--The glandered horses and all animals attacked with acute
or obstinate farcy should be destroyed and their bodies be burned or
deeply buried. Every State should legally interdict the use of a
glandered horse or his exposure in any public or other place where
infection is likely to reach other animals by contact or through
fodder, litter, stable utensils, or any other objects employed about
animals. No less imperative should be the perfect disinfection of all
stables, harness, and other objects with which glandered animals have
come in contact. The value of such measures is sufficiently attested
by what has been stated above as to the prevalence of this disease in
the French army so long as the doctrines of non-contagion dominated in
its management, and the comparative disappearance of the disease so
soon as a change of theory and method had been inaugurated; the
absence of the disease in the English army, where the doctrine of
contagion and its extinction has long prevailed; and the entire
absence of the disease from Australia, New Zealand, etc., into which
it has never been imported, though prevailing in a corresponding
latitude and climate at the Cape of Good Hope.
Glanders in Man.
Up to 1812 the communication of glanders to man failed to be
recognized. Then Lorin, a French surgeon, published a case of the kind
in which inflammation of the hand was induced by inoculation from a
horse suffering from farcy, and Waldinger and Weith drew attention to
the dangers of infection about the same time. In 1821, Muscroft in
England and Schilling in Germany simultaneously reported cases of
infection from the horse in which the true symptoms of glanders in man
were recognized. Rust, Sedow, and Weiss soon followed with additional
cases; then Forozzi (1822), Seidler (1823), Wolff, Grossheim, Eck,
Brunslow, Lesser, Travers (1826), Kries, Grubb, Brown (1829), Neumann
(1830), Vogeli (1831), Alexander (1832), and Elliotson (1833). Though
the disease was now well recognized, yet its nature has been
elucidated by a series of later writers, including especially Rayer,
Tardieu, Virchow, Leisering, Gerlach, and Koranyi.
ETIOLOGY.--Man is rarely infected from any other source than the
horse. In a very few instances the contagion has been derived from
infected men. The modes of infection, immediate and mediate, are the
main points to notice in this connection. Those employed about horses
are usually infected by direct contact of the poisonous discharges,
blood, or tissues with abrasions on the skin or mucous membranes. The
inoculation received in giving medicine, examining the nose,
performing operations with effusion of blood, dressing cutaneous
ulcers, slaughtering, {920} skinning, making a necropsy, burying,
etc., is not uncommon. Again, direct infection is sustained through
snorting of the horse, so that particles of the virulent discharge are
lodged on the mucous membrane of the eye or nose. Closely allied to
this is infection by inhaling the exhalations of glandered horses, and
this doubtless accounts for some few cases which have been recorded as
communicated through the unbroken skin. The bite of the glandered
horse is a rare means of infection. From infection by eating glandered
animals man is usually saved by the cooking of his food and by his
inherent power of resistance, yet with instances of this kind on
record, as recorded by Ringheim, and the well-known conveyance of the
disease to animals in this way, it would be folly to ignore the risk
to man from eating the flesh of glandered horses, sheep, goats, and
rabbits.
Among the mediate forms of contagion may be named drinking from the
same pail or trough after a glandered horse, using a knife that has
been employed to open a glanderous abscess, wiping a wound with an
infected blanket or handkerchief, handling infected harness,
wagon-pole, or manger with wounded hands, sleeping over glandered
horses or in a stall or on litter previously used by such horses.
Conveyance of glanders from man to man has taken place through using
or handling the same dishes, towels, or handkerchiefs, through
dressing the wounds, or, as in the case of the veterinarian Gerard,
through making an autopsy of a victim of the disease.
Fortunately, the susceptibility of man is slight, but few out of the
multitudes handling glandered horses becoming infected. It is
essentially an industrial disease, 114 cases being distributed as
follows among the different occupations: hostlers, 42; farmers and
horse-owners, 19; horse-butchers, 13; coachmen and drivers, 11;
veterinary surgeons and students, 10; soldiers, 5; surgeons, 4;
gardeners, 3; horse-dealers, 2; policemen, shepherds, blacksmiths,
employes at veterinary school, and washerwomen, 1 of each.
A condition of ill-health doubtless predisposes to this as to other
invasions of infectious disease, yet men in apparently the most
vigorous health have succumbed to the poison.
SYMPTOMS.--The incubation of acute glanders in inoculated cases
usually varies from one to four days. In cases in which the mode of
entrance is not so manifest it may apparently extend over one, two, or
even three weeks. If the disease has occurred by external inoculation,
the seat of the wound shows the first symptoms, consisting of tense
swelling, pain, and a dark or yellowish erysipelatoid redness, while
the edges of the wound are puffy and everted, the matter escaping is
sanious, and the surrounding lymphatics are swollen and red and the
lymphatic glands enlarged and tender. After a few days constitutional
disorder sets in--languor, extreme weakness and prostration, aching in
the limbs (muscles and joints) and in the head, rigors alternating
with fever or a continued fever after the first violent chill, and in
some cases nausea, vomiting, and even diarrhoea. In cases not
resulting from external inoculation the febrile symptoms are the
earliest to be noticed, and the muscular and articular pains may be at
first mistaken for acute rheumatism. In other cases, in which the
gastric and intestinal disorders are the most prominent and the
prostration and weariness extreme, the symptoms at first strongly
{921} suggest typhoid fever. Soon, however, with a sense of
formication a local yellowish or livid erysipelatoid inflammation
appears, by preference on the softer parts of the face, the nose,
eyelids, cheeks, or on one of the principal joints, the shoulder,
elbow, or knee. In the midst of the phlegmonous swelling, or even
antecedent to it, there appear small firm red spots or nodules,
sometimes as small as those of variola, at others like a pea or as
large as a walnut or larger. These gradually blanch in the centre,
soften, and change into pustules or abscesses, and, bursting,
discharge a slimy, thick, sanguineous pus, often emitting a mawkish or
fetid odor. The sores thus formed are ulcerous and unhealthy, with
puffy, ragged, everted borders and a grayish or yellowish red base,
which often extends deeply between the muscles and exposes tendons and
bones. When several deposits of this kind are closely aggregated, they
tend to combine in one slough, which may involve a great extent of
tissue. In all cases there are the swollen, reddened, tender condition
of the connecting lymphatics and the tumefaction of the lymphatic
glands. At times the deposits and abscesses are deeply seated in the
interstices of the muscles, and at other times the joints are enlarged
by exudation.
In nearly one-half of the cases glanders supervenes on the cutaneous
symptoms. At first a viscid, whitish nasal catarrh appears from one or
both nostrils, mixed with striae of blood; then upon the pituitary
membrane appear ulcers like those already described in the horse; the
same form on the buccal, pharyngeal, and laryngeal mucous membranes,
and by physical examination they may even be found to have invaded the
lungs. The margins of the nostrils become adherent through the drying
of the tenacious mucus; the meati are blocked or narrowed by the
swelling of the mucosa, the detachment of sloughs, and the
accumulation of the discharges; the breathing becomes snuffling and
difficult; the voice altered or lost; the cough weak, with a mucous
and bloody expectoration, and the breath offensively fetid. The
submaxillary lymphatic glands are inflamed and enlarged, and may even
go on to suppuration and ulceration. The conjunctiva is usually
involved, and at times the specific formation and ulceration extend to
the stomach and intestines, and nausea, vomiting, indigestion,
irregularity of the bowels, and fetid diarrhoea ensue. There is
complete anorexia, but thirst is ardent, especially with diarrhoea.
With the advance of the disease dyspnoea supervenes, and nervous
disorder is shown by the extreme weakness, anxiety, sleeplessness,
troubled dreams, nocturnal delirium, dilated pupils, and even coma.
The temperature, though at first unaltered, may later rise to 104
degrees F., and the pulse to 110 to 120 beats per minute. The
diagnosis is confirmed by detection of the bacillus in the discharges,
and, above all, in the liquids of freshly-opened pustules
(Wassilieff).
The duration of acute glanders in man may be no more than three days,
though usually it is protracted to fourteen or twenty-one, and
exceptionally to twenty-nine days. The almost constant termination of
this form of the disease is in death.
Chronic glanders occasionally appears in man, and is in most respects
the counterpart of that of the horse. The morbid process shows itself
in the integumental or other tissues of the body, and only attacks the
nose and air-passages later, when the constitutional symptoms become
more intense. The general malaise, languor, prostration, aching of
{922} limbs and joints, and inappetence are usually present,
complicated by a local swelling in the seat of inoculation (face,
hands, etc.), with small nodules progressing to pustules, congestion
of the lymphatics, and swelling of the lymphatic glands. These lesions
may subside even before suppuration, and the disease is manifested for
a week or two only by a general feeling of weariness and ill-health;
but sooner or later the local symptoms reappear in the same or another
seat, and the neoplasms, though indolent for an indefinite length of
time, finally degenerate, soften, burst, and form ulcers. These ulcers
have the general characters already described--a livid grayish or
yellowish hue, with red, puffy, irregular edges, and a viscid
greenish, yellowish, dirty white, or bloody discharge. They tend to
increase, or they may appear to heal by the peculiar firm cicatricial
formation, but on the swollen margins new deposits, abscesses, and
ulcers tend continually to form. Sometimes these are of considerable
size and seated deeply among the muscles, but when opened they show
the same unhealthy serous or bloody pus, and manifest a tendency to
extension rather than to healing. When the disease extends to the
respiratory organs, often two or three months after the onset, there
is cough and sore throat, blocking of the nose by the tenacious
discharges and swollen mucosa, and in the pharynx, fauces, and nose
the characteristic ulcer may be detected. The attendant constitutional
symptoms are also much more marked--indigestion, nausea, vomiting,
diarrhoea, rigors, profuse perspiration, high temperature, excited
breathing and pulse, a yellowish or earthy hue of the skin, rapid
emaciation, and great prostration. Though great emaciation, debility,
and hectic ensue on the indolent chronic processes, yet the disease
usually assumes all the characters of the acute type before
terminating fatally.
In cases that recover the fever diminishes, exacerbations cease,
ulcers granulate and cicatrize, vesicles dry up, the nodules and
enlarged glands diminish, the erysipelatoid swellings of skin and nose
subside, and a very tardy and imperfect convalescence is established.
The duration of chronic glanders, nasal or cutaneous (farcy), is
exceedingly indefinite, varying from three months to ten or eleven
years. One of the most protracted cases is that recorded by Bollinger
of a veterinarian who, after an eleven years' illness, recovered with
cicatricial contraction of the nose and larynx and a decided cachectic
appearance.
MORBID ANATOMY.--Besides the lesions above mentioned as occurring in
the skin and mucous membranes of the nose, mouth, and pharynx, the
frontal sinuses, the larynx, and less frequently the lungs, are the
seats of the specific glanderous processes. In the lungs there are
then the nodules, hard, caseous, or purulent according to their age,
and varying in size from a millet-seed and pea upward to the involving
of the greater part of a lobe. Beneath the pleurae may be seen
ecchymoses, hard, fibrous nodules, and yellow elevations, which on
being incised furnish grumous pus. The spleen is usually enlarged,
gorged with blood, gray or black, and is the seat of suppuration. The
liver is enlarged, softened, and may be the seat of glanderous
processes, with ulcers in the bile-duct or gall-bladder. The joints,
like other serous cavities, become the seat of specific suppuration.
The bones are often implicated in adjacent deposits, especially in the
face, cranium, and hands, so that the compact tissue may become
reduced to the merest shell, while the medulla and periosteum {923}
abound in the specific products. The cerebral meninges and
brain-tissue are frequently the seat of specific growths and minute
abscesses. It is noticeable that the enlargement of the lymphatic
glands is usually less than it is in the horse, though they are never
entirely free from lesions. Indeed, the tendency in man to the
formation of considerable glanderous neoplasms is much less than in
the solipede.
The microscopy of the lesions is essentially the same as in the horse.
O. Wyss describes the cutaneous nodules as formed by a great
proliferation of round cells (like pus-cells) in the upper layer of
the corium just beneath the papillary layer. In a more advanced stage
the corium and papillae are filled with pus-cells, and, becoming
disorganized, give rise to the formation of pustules and small
abscesses. Lagrange describes in a chronic ulcer of the palm, a layer
about 2 mm. in thickness of embryonic cells closely packed with an
amorphous intercellular substance. The nuclei appeared larger than in
ordinary ulcers or tubercles. Extending into this layer were capillary
vessels packed with red globules and with blind extremities, or in
some instances minute ruptures and hemorrhages. Beneath this
superficial cellular layer was a stratum of striated muscle,
especially noticeable for the excess of condensed connective tissue
making up the intermuscular septa, and the great multiplication of
nuclei with large, clearly-defined nucleoli, not only inside the
sarcolemma, but also between the fibrillae and separating them widely.
At some points the muscular tissue had undergone a vitreous
degeneration, while at others were many fusiform cells. At one point,
where the ulcer extended to the phalanx, the compact layer of the bone
was attenuated to the thinnest shell and perforated, so that the
medulla was continuous with the ulcer. The medulla contained a great
number of white globules, medulla-cells, and minute embryonic nuclei.
The vessels were remarkable by the extensive fibroid thickening of
their coats. On section of the ulcer many orifices stood widely open
because of the rigidity of their walls. The internal coat was
plicated, as if too large for the lumen. The external fibrous layers
were at points abundantly interspersed with, and even replaced by,
groups of embryonic cells, the active proliferation of which meant the
destruction of the perivascular fibrous layer. These embryonic cells
even invaded the lumen of the vessel and partly blocked it, so that
the remnant of the tube remained as the centre of a disintegrating
mass, or later a caseous or purulent focus.
DIAGNOSIS.--Acute glanders, when well developed, is unmistakable. The
presence on or near the skin of the characteristic nodules, pustules,
phlyctenae, and ulcers, the oedema or erysipelatoid condition of the
adjacent skin, the redness of the lymphatics, the presence of the
neoplasms and ulcers in the nose, and the sticky, fetid, variously
colored nasal discharge, with the acute fever, prostration, and pains
in the limbs and joints, make a tout ensemble that is pathognomonic.
In the initial stage only it may be confounded with rheumatism, but
the arthritic pains are not usually attended by the same amount of
redness and swelling of the joints, the prostration is far more
profound, and there are in most cases an irritable, unhealthy-looking
wound and a history of exposure to infection from glandered horses.
In chronic glanders, and especially in the external form (farcy), the
diagnosis is often more difficult. From pyaemia and septicaemia it is
{924} usually to be distinguished by the comparative absence or the
slightness of the chills, by the less healthy character of the pus,
and by the implication of the nasal mucosa, the larynx, and lungs.
When the nose, larynx, or lungs are but slightly affected, there may
be a strong resemblance to syphilis or miliary tuberculosis, but a
close attention to the character of the lesions, the absence of any
concomitant history or symptoms of syphilis, and deductions drawn from
the occupation of the patient and the presumptive exposure, will
greatly assist in reaching a diagnosis.
The detection of the bacillus is not conclusive, as in tuberculosis
and some forms of septicaemia there are similar organisms, agreeing
with the microbe of glanders even in the matter of size. In cases of
doubt a little delay will usually allow the development of new and
more characteristic symptoms.
The final resort, however, is to inoculation. Auto-inoculation, as
practised by Poland, is rarely satisfactory, as the system has
acquired a partial tolerance of the disease and local lesions are not
so certainly developed as in the healthy subject (St. Cyr).
Inoculation on a healthy goat, sheep, or rabbit can always be availed
of, and if practised on more than one subject can be relied upon, as
the virus loses nothing of its power in passing through the human
system, but usually determines an acute form of the disease in the
animal inoculated.
PROGNOSIS.--Acute glanders is almost constantly fatal to man. Of
chronic cases, and especially the external form (farcy), from
one-third to one-half of the subjects recover. When both internal and
external (farcy--glanders), the issue is usually fatal. Kutner claims
that cases caused by external inoculation are more favorable than
those caused by the inhaled poison. This accords with the general
principle, that a poison viable in the comparatively vitiated air of
the lungs or on the surface of the intestinal canal is better fitted
by its habit of life for survival in the blood and plasma, and is
consequently more redoubtable. The greater the duration of the disease
in any particular case, the more favorable is the prognosis.
TREATMENT.--In the treatment of glanders in man the same principles
must guide as in animals. In external, inoculated cases the wounded
tissues should be early destroyed by potent caustics--fuming nitric
acid, corrosive sublimate, iodized phenol, chlorine, sulphate of
copper, carbolic acid, or the hot iron. The erysipelatoid swellings
may be treated by leeching, followed by solutions of carbolic acid,
iodine, or chlorine-water, by ice, and internally by laxatives and
iodide of potassium. The first two antiseptics may be freely used by
hypodermic injection. Abscesses and tumors should be laid open and
cauterized as above, and then treated by weaker solutions of the same
agents. Nasal ulcers may be treated by insufflation of iodoform and
injections of creasote, carbolic acid, nitrate of silver, or
permanganate of potash solutions. Of the greatest importance is a
general tonic and stimulating regimen. A nutritious diet (including
beef-tea), abundance of pure air, alcoholic stimulants, quinia,
tincture of the chloride of iron, and, above all, arseniate of
strychnia, have been used with advantage. Various anti-ferments, such
as the bisulphites in full doses, carbolic acid, and iodide of
potassium, have apparently proved beneficial, and deserve a further
trial. As in the horse, a great {925} variety of other agents, mostly
of a tonic nature, have been employed, but with very variable results.
PREVENTION.--The first step toward the prevention of glanders in man
is the systematic restriction and extinction of the affection in
animals. This has been already sufficiently referred to above. Further
measures of prophylaxis embrace the following: the avoidance of
contact with glandered and suspected horses by all persons having any
wounds, abrasions, or ulcers on their skins; the cauterization with
nitrate of silver of all such sores on persons necessarily brought in
contact with glandered or suspected animals or their products; the
general diffusion of information as to the danger from glandered
animals; washing of hands and face in a solution of carbolic acid or
chloride of lime after handling infected or suspected animals or their
carcases or products; the thorough disinfection or destruction
(preferably by fire) of harness, clothing, racks, mangers,
wagon-poles, buckets, troughs, brushes, combs, litter, and fodder that
have been exposed to infection; and, finally, the exclusion from the
markets of all meat derived from suspected or infected animals. It is
generally held that the flesh of the horse alone demands inspection,
but with the known susceptibility of sheep, goats, and rabbits it can
easily be conceived how the infection may reach man through his food,
though horse-flesh is never consumed. That glanders has never been
recognized as arising from the consumption of diseased sheep or
rabbits does not prove that it has never reached man by this channel,
any more than the absence of all recognition of the infection of man
from the horse would prove the non-occurrence of such infection until
the beginning of the present century. The knowledge that the animals
used for food in this country are liable to contract and convey this
disease is an additional reason for the systematic and universal
suppression of the disease among the equine population.
{926}
ANTHRAX (MALIGNANT PUSTULE).
BY JAMES LAW, F.R.C.V.S.
SYNONYMS.--_Latin_, Ignis Sacer, Anthrax Epizooticus, Pustula Maligna,
Pustula Pestifera, Erysipelas Carbunculosum, Carbunculo Contagioso,
Glossanthrax, Angina Carbunculosa, Anthrax Haemorrhoidalis, Mycosis
Intestinalis, Apoplexia Splenitis, etc. _English_, Black Erysipelas,
Malignant Vesicle, Anthrax Fever, Splenic Apoplexy, Splenic Fever,
Inflammatory Fever, Carbuncular Fever, Black Quarter, Blood-Striking,
Bloody Murrain, Blain, etc. _French_, Pustule maligne, Charbon, Fievre
putride, Typhohemie, Pelohemie, Mal de Rate, Splenite Gangreneuse,
etc. _German_, Karbunkelkrankheit, Contagiose Karbunkel, Milzbrand,
Milzseuche, Milzbrandfieber, Brandbeulenseuche, Rothlauf, etc.
_Russian_, Jaswa (boil-plague). _Italian_, Antrace. _Spanish_,
Carbunculo, Lobado. _Swedish_, Boskapssjukan. _Mexican_, Calentura del
piojo.
DEFINITION.--Anthrax is an acute, infectious, bacteridian disease,
occurring mostly in the Herbivora and Omnivora, but communicable to
other mammals (including man), to birds, and even fishes. Its local
manifestations are exceedingly varied in kind, but the malady is
characterized by the presence in the tissues or blood, or both, of
specific spherical and linear bacteria (micrococcus and bacillus
anthracis), leading to arrest of haematosis, to disintegration of the
blood-globules, to sanguineous engorgement of the spleen, to capillary
embolism, and to a spreading gangrenous inflammation.
HISTORY AND GEOGRAPHICAL DISTRIBUTION.--While ancient history is not
clear as to the specific diseases of animals, yet there is the
strongest presumption that nearly all great plagues that attacked
indiscriminately animals and man were of this nature. Thus, the plague
of murrain, with boils and blains breaking out on man and beast, in
the days of Moses, was probably of this kind (Gen. ix. 3.); also that
which at the siege of Troy extended from animals to man, and many
later epizootics in all parts of the world. No infectious disease of
man and animals, with the single exception of tuberculosis, has been
more widely diffused, and none can be considered as more cosmopolitan.
Heusinger, in his classic work on _Milzbrandkrankheit_, traces the
ravages of the disease from the highest to the lowest latitudes in the
northern and southern hemispheres and in the Old World and the New. He
adduces outbreaks in Siberia, Astrakan, Lapland, and Finland, in
Russia, Prussia, Poland, Silesia, Bavaria, Holland, Belgium, France,
Spain, Portugal, Italy, Switzerland, Austria, Hungary, Greece, Turkey,
Egypt, East and West Indies, {927} North and South America, etc. We
can now add all the great English, French, and other European colonies
not included in the above (South Africa, Australia, New Zealand,
Algeria, etc.), together with China and Japan. We find, moreover, that
the disease is always most prevalent where agriculture is in its most
primitive condition, so that there can be little doubt of the
prevalence of the affection in the less-civilized countries as well.
But while the disease is prevalent in all parts of the world, its
ravages are largely subordinate to the nature of the soil. Wherever
this is close, impervious, marshy, or charged with an excess of
organic matters, the gaseous emanations of which drive out most of the
oxygen, the anthrax-germs, once introduced, tend to be preserved
indefinitely. Thus, in drying up basins with no natural drainage, on
lake and river margins, on deltas, in forests, in mucky, mossy, or
peaty soils, and on those that are habitually over-manured, the germs
of anthrax are especially liable to be perpetuated. It has long been
noticed that herbivorous animals are the most susceptible to anthrax,
while the purely carnivorous, and to a less extent the omnivorous,
have relatively a far higher resisting power. That the immunity is
largely due to the food is manifest from the experiments of Feser on
rats. Those fed on vegetable aliment contracted anthrax readily from
inoculation, while those kept on an exclusive diet of flesh
successfully resisted. The same rats that escaped while on a flesh
diet were afterward placed on a vegetable diet, and then perished
after inoculation.[1] Davaine found the same to be true of foxes kept
on meat and vegetables respectively, and inoculated with the virulent
blood of the allied disease, septicaemia. He found, moreover, that
guinea-pigs were much more susceptible to anthrax than rabbits.
One-thousandth of a drop of virulent anthrax blood invariably killed
the guinea-pig, while it left the rabbit unharmed.[2] Klein has never
found a rabbit insusceptible. It has recently been claimed that pigs
are insusceptible, but I have known of many instances in which the
offal of anthrax cattle, when devoured by pigs, has determined fatal
anthrax in the latter. Chickens too prove much less susceptible to
anthrax than the Herbivora. Inoculations made by Cohn and others
proved invariably unsuccessful, while Pasteur has showed that they can
be infected easily after the body has been cooled by partial immersion
in cold water.[3] Pasteur attributes this immunity to their normally
high temperature, yet rabbits, sheep, pigs, wolves, and foxes, though
maintaining a correspondingly high temperature, are still subject to
anthrax. Even the herbivorous mammal suffering from acute anthrax
fever has its temperature raised to that of the chicken, yet the
disease progresses none the less surely to a fatal result. Again,
anthrax liquids inoculated under the skin of a fox proved harmless,
while if thrown into the warmer peritoneal cavity they proved fatal.
It may well be suspected that the relative insusceptibility of
chickens is in part due to the large amount of animal food consumed by
them, and that the chilling process increases the receptivity by
deranging sanguinification and nutrition.
[Footnote 1: _Wochenschrift f. Thierheilkunde und Thiersucht_, Nos. 24
and 25, 1879.]
[Footnote 2: _Rec. de Med. Vet._, Mar. 15, 1879.]
[Footnote 3: _Ibid._, Mar. 15, 1880.]
The insusceptibility to anthrax is often characteristic of certain
individuals or families or of the animals living in a particular
district. Thus, Chauveau found that some French sheep, and nearly all
Algerian ones, {928} resisted inoculation with a moderate amount of
anthrax virus, while the introduction of a maximum amount proved fatal
to these as to others. In the same way, it is often noticed that
animals living in an anthrax region escape the evil effects of the
poison, while strange animals brought in either fall ready victims or
for a time do badly until they have become habituated to the locality.
In view of the subsequent protective effect on the system of a first
and non-fatal attack of anthrax, it is probable that all these
examples of immunity in the Herbivora depend on a previous mild attack
of the same disease or on the extinction of the more susceptible
races. Even in the case of the animals that do badly on first coming
into an anthrax district, and recover better health with immunity
later, we may well infer that a mild form of the anthrax infection has
been passed through.
ETIOLOGY.--The one essential cause of anthrax is the introduction into
the system of a specific bacteridian germ (bacillus anthracis or its
spores). This is not, as a rule, carried far on the atmosphere, but
demands for its propagation contagion, immediate or mediate. Unless,
therefore, it meets in the soil the conditions necessary to the
preservation and propagation of the germ, it is transmitted with some
uncertainty from animal to animal, and thus the disease does not
spread widely and rapidly, like an ordinary plague, but tends to
become localized in particular districts as an enzootic.
But its dangers are none the less real nor its existence less to be
dreaded. In predisposed localities, where the disease-germ has gained
a footing, the animal mortality may exceed that caused by the great
plagues, while the risk to human beings is incomparably greater than
from any other acute infectious disease of the lower animals. Thus, in
San Domingo, in 1770, 15,000 people perished in six weeks from eating
the carcases of anthrax animals, and the mortality was only arrested
when the meat was legally interdicted. In the worst anthrax years on
some of the Siberian steppes as many as one-fourth of the whole human
population suffer from the malady. The prevalence and death-rate,
however, vary greatly in different localities and seasons. Sometimes
only one or two solitary cases of the affection are observed; at other
times the disease becomes moderately prevalent, but a lack of
virulence in the poison or a previously acquired insusceptibility of
the individual protects the great majority of the animals exposed,
while at others, still, the poison attacks nearly all exposed to its
contagion.
The animal products that mainly convey the disease are the blood, the
liquid exudations, portions of the diseased carcase, and the bowel
dejections. The virus is most potent when derived from an animal still
living or only recently dead, yet under certain conditions (with
spore-formation) it may long retain its virulence under the most
extreme changes of climate, temperature, dryness, and humidity.
Russian hides tanned in England or America frequently convey anthrax,
which is known especially as a tanner's malady, and wool and hair sent
from Buenos Ayres have repeatedly produced malignant pustule
(woolsorter's disease) in Britain and the United States. The preserved
scabs of malignant pustule have been often successfully inoculated on
the lower animals, so that, like other forms of poison, this seems to
be preserved indefinitely by desiccation.
The simple contact of the virus with the slightest abrasion will
suffice {929} to convey the disease. It has often been communicated
where no lesion of the epidermis could be found, yet the presumption
is that even in such cases the cuticle had been in some way wounded.
Eating the flesh of animals killed while suffering from anthrax has
often conveyed the disease. In an outbreak in Swineshead,
Lincolnshire, England, in 1863, I found a dog and a number of swine
suffering from eating the bodies of dead bullocks. In 1864 an East
Lothian (Scotland) farmer fed his pigs with the offal of a slaughtered
anthrax bullock, and lost nearly the whole herd. The carcase of the
bullock had been sent to market. About 1860 cattle, and even horses,
died yearly on a swampy meadow at Brighton, Mass. On one occasion the
owner, John Zoller, fed the offal of a dead bullock to his pigs, which
were speedily attacked with anthrax, and as speedily killed to save
their bacon (Dr. Thayer). Even when cooked the flesh is not always
safe. Of this we have the undoubted case in San Domingo above noticed,
the alleged death of 60,000 people in the vicinity of Naples from the
same cause in 1617 (Kircher), and the thousands that die on the
Russian steppes every anthrax year from eating the sick horses
(Rawitch). But in all these, and in the ever-recurring cases in which
families suffer from eating anthrax meat, there is the possibility, if
not the probability, of the contamination of the meat subsequently to
cooking by the knives, forks, tables, and dishes used. The San Domingo
slaves had few appliances for cleanliness, much less disinfection, and
the Tartars eat their meat from the same board on which it has been
chopped up raw.
In accurate experiments it has been found that the bacilli are
destroyed by a temperature of 145 degrees F. maintained for five
minutes, but the spores are capable of surviving the boiling
temperature for five or even ten minutes. The varying power of
resistance may be compared to that of the green stalk of the pea and
the dry flinty seed. The first is destroyed by a very moderate heat,
while the second will sprout after having had boiling water poured
over it. The resisting bacillus-spores are never found in the living
animal, but may be developed in the blood and tissues after death, and
may account for the occasional extraordinary viability of the poison
when exposed to a boiling temperature.
Milk, though often used with impunity, conveyed the disease when
inoculated by Bollinger, and the same was true of the vaginal mucus.
Innocent in the early stages of the disease while the germs are still
localized, they become virulent after the bacilli swarm into the
blood.
Healthy men and animals often carry the poison, though themselves
insusceptible. The question of its conveyance by insects has been much
debated, but the constant occurrence of malignant pustule on the
uncovered parts of the body goes far to settle the question. Bourgeois
long ago noticed that it was most frequent on the face, hands, neck,
and arms, and rare on the trunk. In sixty cases recorded by A. W. Bell
of Brooklyn, all occurred on the face except two on the hands, one on
the wrist, and one on the forearm. The bite of a fly or mosquito had
in many of these cases proved the starting-point of the malady.
Bollinger has shown the presence of the bacillus in the stomach of
such flies as fed on flesh and blood (horse-flies, bluebottles, etc.),
and, together with Raimbert and Davaine, has produced anthrax by
inoculations with the stomachs, legs, and proboscides of these
insects.
{930} Surgical instruments occasionally convey anthrax. At
Cockburnspath, East Lothian, Scotland, a yearling heifer contracted
anthrax, and the whole herd was bled, commencing with the sick one.
Next morning seven were found dead, the disease in each case extending
around the fleam-wound. At Brunt, in the same county, a shepherd
skinned an anthrax bullock, and after washing and taking a turn among
his sheep, on the same day castrated several litters of pigs, all of
which perished. In St. Lawrence Co., N.Y., in 1870, a surgeon
inoculated himself while opening a vesicle on the hand of a farmer.
Harness, stables, stable utensils, vehicles, fodder, and litter are
frequent bearers of contagion. At Geneseo, N.Y., in 1877, three horses
and a cat died in midwinter after licking the blood from a stone-boat
which had conveyed the skin of an anthrax bullock to market. Green
fodder or hay harvested from ground formerly occupied by anthrax
victims or from their graves often convey the poison, but probably
only by the adherent earth and dust containing the anthrax-germ.
That the anthrax bacillus and its spores may be long preserved in
earth is abundantly proved. At Avon, N.Y., nine months after any cases
of the disease, the liquid leaking out on the river-bank near to the
grave of a victim of the year before was licked by six cattle, and in
two days they all perished. On the same pasture victims were seized
yearly for seven years, but with a rigid seclusion of these, their
products, and their graves the malady has finally disappeared. The
persistent deadly effect of some soils on animal life, apart from the
presence of the carcases, seems to show that in certain soils we find
the normal home of the anthrax bacillus, while the migration into the
animal economy is but an accident of its existence. The soils that are
especially subject to anthrax are the dense clays, the limestones, and
the rich alluvials. Among the essential conditions are the exclusion
of oxygen, excepting a limited amount bearing some relation to what is
found in the animal fluids, and the abundance of some alkaline agent
(lime, potash, soda, ammonia), so that the earth is either neutral or
only very slightly alkaline or acid. An acid vegetable infusion is
inimical to the germ, which soon disappears from such a medium. The
requisite paucity of air is found in all the dense, less pervious
soils (clays, etc.), in soils habitually waterlogged (swamps, deltas,
river-bottoms, low meadows, natural basins, drying lakes and ponds),
and in soils rich in decomposing organic matter (peat, alluvial,
over-manured). The antacid is often found present as lime or potash,
or is constantly being produced in the form of ammonia, etc. by
organic decomposition. Such places are known to farmers as "dead
lots," because no stock will live on them. The bacillus in the buried
carcase does not produce spores (Bollinger), though it may in the soil
at any temperature between 59 degrees and 110 degrees F. In the
graves, therefore, at a lower temperature, the poison can only be
preserved by a continuous generation of the bacillus.
Pasteur, who successfully inoculated the casts of earth-worms taken
from anthrax graves, attributes to these an important role in bringing
the germs to the surface. A more important agent, however, is probably
the rise and fall of water in the soil. By this means the bacilli and
spores are washed up toward the surface, and when the superficial
layers dry out they are easily carried by the winds. Hence it is that
anthrax is usually prevalent in late summer and when the soil is dried
and heated to its {931} greatest depth. Thus it is, too, that wet
seasons followed by specially dry and hot ones are, above all,
productive of anthrax in herds. Wet seasons fulfil the further purpose
of carrying off the germs into rivers and depositing them on the banks
or on inundated meadows, where after the subsidence of the flood the
disease appears, for the first time perhaps.
There is, however, good reason to believe that the effect of a warm
season is not confined to its influence on the soil and its germs. The
high temperature deranges the vital functions of the animal economy,
and, inducing a febrile disturbance, lessens the power of resistance
to the anthrax virus, just as the cooling of the warm-blooded bird
lays it open to infection. On this account, and because of the
frequently recurring electric storms, the hot dry season is especially
the season of anthrax. The hottest, driest autumns of Siberia always
coincide with the anthrax years, and in the last fifteen years in the
United States I have noticed the wide extension of anthrax whenever
the season has been unusually hot and dry. In Corsica the herdsmen
confidently pasture their stock in the close still valleys throughout
spring and early summer, but whenever the surface soil is dried out
they make all haste to remove it to the hills, well knowing that delay
means devastation and ruin.
Plethora is undoubtedly an important predisposing cause of anthrax,
and so is the alternation of cold nights with hot days. The febrile
condition induced in the animal economy is perhaps the main factor at
work in each case. Finally, youth is on the whole more liable than
age, but whether because of the greater receptivity of the growing
system and its tissues, or because it has not yet acquired some
immunity by exposure to the milder effects of the poison, is not
certainly determined. Sex is without influence.
It is not a little remarkable that the bacillus germ has not yet been
found in the placental liquids nor foetal blood of sheep, goats, or
rabbits, though swarming in that of the mother. Bollinger attributes
this to the action of the placenta as a "physiological filter"--a
conclusion seemingly at variance with the passage of the bacillus
through all the other animal membranes, including those lining the
mammary glands and the vagina. Two other possible explanations remain:
first, that the secretions of the uterine glands are inimical to the
bacillus; and, second, that the foetus, being in some sense a
carnivorous animal, possesses the immunity characteristic of
Carnivora. Bacilli have recently been found in the foetal guinea-pig.
The bacillus anthracis was first observed by Pollender and Branel in
1849 (Birch-Hirschfeld), but it was only publicly claimed as the cause
of the disease in 1855 by Davaine. Branel discarded Davaine's theory,
because blood in which he had failed to find bacillus produced anthrax
with bacillus in the blood of two foals inoculated. Later observations
by Bollinger and others have shown that cultures of bacillus can
always be made from such infecting blood, and that in most cases the
presence in the infecting blood of spherical bacteria can be
demonstrated by the microscope. That the bacillus is the true
pathogenic element is proved by the following facts: 1st. That the
bacillus is the only ectogenous, particulate, organized structure
constantly found in the anthrax blood and fluids; in cases in which it
is apparently absent cultures show its actual presence. 2d. After
cultivation in pork or beef infusion to the {932} hundredth generation
the virulence is unimpaired, though it must be assumed that all
non-organized poisons derived from the infected animal body must have
been diluted or decomposed to extinction. 3d. That filtration of the
anthrax liquids through a plaster or other efficient filter renders
the filtrate innocuous, while the solids retained in the filter remain
infecting (Chauveau, Bert, Toussaint). 4th. That the clear filtrate
injected to excess killed by virtue of its contained chemical products
in twelve hours, while the solids filtered out and containing the
bacillus or its spores only killed after thirty hours.[4] 5th. Anthrax
blood from the living animal or one just dead, and destitute of
spores, when subjected to compressed oxygen (50 atmospheres), is
non-infecting (Bert). 6th. The same anthrax liquid, destitute of
spores, after boiling is completely innocuous. 7th. The same liquid,
if kept in a closed tube apart from oxygen for eight days, shows the
bacilli broken down by granular degeneration, and proves absolutely
harmless when inoculated in small quantity. 8th. The same sporeless
anthrax fluid when treated with absolute alcohol loses its virulence.
9th. The anthrax liquid which has been cultivated with free access of
air in a temperature varying from 25 degrees C. (77 degrees F.)
(Klein, Loffler) to 41 degrees C. (105.5 degrees F.) forms spores, and
then remains infecting, though it may have been subjected to
compressed oxygen, boiling for several minutes, absolute alcohol,
dilution with water, putrefaction, or the exclusion of oxygen.
[Footnote 4: Bert, _Compt. Rend. de la Societe Biol._, p. 355, 1879.]
The bacillus anthracis, as found in the blood and animal fluids, is in
the form of fine rods, straight (rarely bent or angular), motionless,
and 0.007 to 0.012 Mm. in length. Smaller forms are seen to be minute
ovoid or oblong bodies, and the smallest absolutely spherical
(micrococcus); but in all cases, as seen under the highest powers of
the microscope, they have clear-cut, even margins, linear or curved,
which easily distinguish them from the irregular normal granules of
the blood and tissues. Under the highest powers of the microscope the
bacillus is seen to be made up of a series of oblong (Koch) or cubical
(Klein) cells enclosed in one common sheath. This is rendered more
manifest if they are first swollen by the addition of water. The
motionless form of the anthrax bacillus is of especial value in
distinguishing it from the motile bacteria of putrefaction
(saprophytes).
Within the living animal body the development never goes aside from
these forms. The growth appears limited to micrococcus and bacillus
rods, while spores or bacillus threads are never found. This finds its
counterpart in the micrococcus poisoning caused by the inoculation
with the spores of common moulds (Grawitz); and in septicaemia also
micrococcus and bacillus forms only are found, the filamentous never.
When grown in organic infusions out of the animal body the
anthrax-germ develops from micrococcus or bacillus into a long,
branching, filamentous product, which in the presence of oxygen
develops into spores. Apart from oxygen or when the proper nourishment
of the bacillus is exhausted the protoplasmic elements within the
filamentous sheath undergo granular degeneration, and finally the
empty envelope disintegrates and disappears. The spores appear at
intervals in the protoplasm of the filament as clear, brightly
refrangent bodies, at first spheroidal, afterward larger and oblong.
Unlike the micrococcus and bacillus, {933} they do not stain. Under
favorable circumstances the primary cell is capable of forming one, or
if extra long, two spores (Koch, Klein). Cossar-Ewart claims to have
seen the formation of motile flagellate organisms aggregating
themselves into zooglaea masses, but as these were not found in the
carefully-conducted cultures of Koch and Klein, they are supposed to
have been aerial microphytes accidentally introduced.
The great tenacity of life in the spores in heat and cold, dryness and
wet, excluded from air and under several atmospheres of oxygen, in the
midst of putrefaction and in pure watery fluids, well accounts for the
persistence of infection in buildings and localities where the poison
has gained a foothold. In order to their destruction in a natural
manner it seems necessary that they should germinate and develop into
the anthrax micrococcus, bacillus, or mycelium. This germination may
take place in the presence of moisture, oxygen, and suitable
nourishment, whether in the soil, the animal body, or elsewhere, and
then the exhaustion of the aliment, the exclusion of the oxygen by
putrefaction, the submergence in a medium unfavorable to development,
or exposure to a very high temperature, may suddenly destroy the
poison.
There is reason to believe that a too free exposure to oxygen proves
destructive to the virulence, if not to the life, of the poison, and
thus in all porous, well-drained soils the anthrax poison, even when
introduced from without and concentrated by the death and burial of
many victims, soon disappears. This feature, which is common to many
zymotic diseases the germs of which live and multiply outside the
animal body (typhoid, yellow fever, tuberculosis, swine plague,
chicken cholera, diphtheria, etc.), offers countenance to the claims
of Buchner that he had by prolonged culture, in the presence of air,
metamorphosed the bacillus anthracis into a harmless mycrophyte, and
that, conversely, by continuous cultivation under the surface of a
suitable beef infusion he had changed the harmless bacillus subtilis
of hay into the deadly bacillus anthracis. Koch, Klein, and others
have discredited Buchner's results, on the ground that he had not, in
their opinion, taken due precautions against impure cultures, and that
his alleged transitions took place too abruptly; yet further
observation must determine whether he has been condemned too hastily.
The diminished virulence of Pasteur's attenuated virus, which is
unaffected by the next subsequent culture or by the formation of
spores, shows plainly enough that the bacillus anthracis is capable of
physiological changes under the influence of varying conditions of
growth, and that such changes are not at once undone by a return of
the former conditions.
How anthrax-germs enter the body is partly known and partly
conjectured. Direct inoculation on a sore by contact, by insects, by
harness, by accidents, etc. is an undoubted method. The sound cuticle
is probably an efficient barrier, since bacteria habitually inhabit,
without hurt, the surface and gland-ducts of the skin; yet the
entrance of these saprophytes through the shell and membranes of the
egg leaves a doubt as to the efficiency of the cuticular obstacle. The
mucous membranes are manifestly frequently penetrated by the parasite.
Hence the local affections in the mouth and throat (glossanthrax,
anthrax angina) and in the lungs (pulmonary anthrax). Cohn claims that
the gastric juice of Carnivora especially is destructive to the
anthrax poison, yet the constant recurrence of intestinal anthrax
(mycosis) seems to imply that the germs often escape destruction {934}
in the stomach. Pasteur supposes that anthrax-infected food is only
injurious when there are inoculable sores in the mouth or pharynx, but
it seems as if in that case the disease would be first shown at these
points and in the nearest lymphatic glands rather than in the bowels,
the rule for the inoculated anthrax being to develop first in the
tissues and thence to reach the blood-vessels through the lymphatics.
The anthrax poison expends its fatal energy especially on the blood
and blood-vessels. The bacilli in the blood use up the available
oxygen, so that the circulating liquid becomes venous, dark, and
unfitted for the maintenance of the normal functions of life. What is
even worse, the ability of the blood to absorb oxygen is greatly
impaired. In men and dogs suffering from anthrax the consumption of
oxygen was found to be reduced in one instance even by two-thirds,
probably in part by reason of the action of the chemical products of
the bacillus. A third condition constantly found is embolism of the
capillaries by the bacillus and the occurrence of local gangrene.
SYMPTOMS.--Anthrax shows itself in three principal forms: 1st, the
apoplectiform; 2d, anthrax fever without local external lesions; and
3d, external localized anthrax. The two last forms correspond in the
main to the acute and subacute forms.
The period of incubation varies according to the dose of the poison
and the receptivity of the animal. In some cases infection is at once
followed by illness. In these it is probably the chemical products
that produce the first effect, while the disease caused by the
propagation of the bacillus appears later should the animal survive.
Such incubation is shortest for the smaller animals (mice, rabbits,
guinea-pigs, cats), in which illness usually sets in in from
twenty-four to forty-eight hours. In sheep and goats incubation may be
extended to three or four days, while in horses and cattle it may last
a day longer.
The apoplectiform type attacks animals which a few minutes before
seemed in fine health, appetite, and spirits, striking them down as if
by lightning, and the victims struggle convulsively for some minutes,
expel blood perhaps by the nose or anus, and expire. In the less
suddenly fatal cases there may be muscular trembling, unsteady gait,
excited breathing, accelerated pulse, tumultuous heart's action,
bleeding from some natural orifice, and death in from one to several
hours. Occurring as these cases often do in summer, the sudden death
is probably hastened by insolation.
In anthrax fever or acute internal anthrax there is loss of appetite,
and, in ruminants, of rumination, suppression of milk, dulness,
languor, staring coat, or even a rigor, and thirst. Then follows the
hot stage, in which the temperature may rise to 106 degrees or 107
degrees F.; there are acceleration of pulse and breathing, petechiae
or a brown or yellowish tinge of the mucous membranes and white parts
of the skin, tenderness of the spine, often jerking or clonic spasms
of the muscles of the extremities, and much prostration and weakness,
the patient hanging back on the halter, leaning against a wall, or
swaying when made to move. The feces are usually more or less mingled
with blood-clots, or may be at once liquid and bloody. Bloody urine
and the discharge of blood from other natural channels are frequent.
Some cases are manifestly delirious, and in others the skin crackles
on being handled. Remissions are not uncommon, {935} during which the
animal remains dull and prostrate. As the disease advances and the
blood is robbed of its oxygen, the temperature descends below the
natural standard, great weakness and stupor set in, the pupils are
widely dilated, and death from asphyxia occurs in one or two days from
the onset.
In localized external anthrax the local swellings may be first seen.
There are usually some tenderness of the skin, erection of the hair,
and the formation of a little nodule, like a hazel-nut or walnut,
adherent to the deeper parts of the skin, firm and comparatively
painless even when cut. Sometimes the swelling is diffuse, with a
dropsical or erysipelatoid aspect, and crackles like parchment when
handled. Whether the affection attacks the tongue, the throat, or some
part of the head, body, or limbs, the tendency is to gangrene of the
part, and, if the subject survives long enough, to an extensive
sloughing and unhealthy sore. The sloughs and sores have either a
black sanguineous appearance or they are lardaceous and intermixed
with streaks of dark red. If fever is not present at the outset, it
sets in early, and passes through the same stages as in the acute
internal anthrax, the animals being suddenly plunged in prostration
and stupor, with dusky yellow or blood-stained mucous membranes,
dyspnoea, dilated pupils, convulsions, and death. On the mucous
membranes (gloss-anthrax, anthrax angina) the engorgement is usually
complicated with bullae with red or yellow contents, and which on
bursting leave unsightly gangrenous ulcers. In all such cases the
morbid liquids of the swellings teem with bacilli.
MORBID ANATOMY.--The most characteristic changes are usually met with
in the blood. This is black, thick, tarry, uncoagulable or coagulates
only in loose diffluent clots, which are redissolved before squeezing
out the serum; the fibrin is diminished (often by two-thirds), the red
globules are not adherent in rouleaux, and are crenated and broken
down and the haematin diffused through the liquid, so that it stains
the hands or paper deeply; the white globules are increased, probably
by reason of the early irritation of the lymphatic glands and spleen
by the poison; and it reddens slowly and but slightly on exposure to
the air, and speedily passes into decomposition. The blood can
scarcely be made to flow in a full stream, but often trickles down the
hair and skin by reason of its thick, consistent character. The
microphytes above described are usually found in the blood, and always
in the affected tissues if examined just after death.
Next to the blood, the spleen presents the most constant lesions,
being enlarged (by one-third, one-half, or to double, triple or
quadruple its normal size) and gorged with blood (sometimes even to
rupture). The lymphatic glands, and especially those adjoining the
local anthrax swellings of the tissues, are always enlarged, marked
with petechiae, friable, easily reduced to a pulp, and swarming with
bacilli and micrococci. Next to the glands of the affected parts the
central ones, the axillary, prepectoral, thoracic, sublumbar, and
abdominal, are the most constantly affected. The lymph is reddish and
opaque.
Decomposition sets in early, and the resulting gases cause a puffy,
emphysematous condition of the connective tissue. The fat and other
white tissues are dusky brown or yellow, and petechiated; the muscles
are soft, flabby, and dark red or brown, with occasional blood {936}
extravasations; the blood-vessels, especially the veins, and the right
heart are gorged with black, uncoagulable blood, and have their inner
coats blood-stained. The serous membranes present numerous petechiae,
and contain more or less of a reddish serum. The intestines, and
sometimes the stomach, are dark red throughout, marked by petechiae,
and are often the seat of thickening from sanguineous or transparent
colloid infiltration. The lesions are especially extensive on the
small intestines and rectum. The vagina and womb are also the frequent
seats of sanguineous infiltration. The liver and kidneys are enlarged,
congested, softened, and friable, and the ganglia of the sympathetic
are enlarged, congested, and softened. The swellings are of two kinds,
sanguineous and colloid. The former, when cut into, present one or
more loose clots of black blood or a grumous mass of blood-elements,
separating the tissues and often mixed with fetid gases. The colloid
exudations are glairy, semi-solid, jelly-like masses, infiltrating the
tissues. The tissues affected and the skin covering them are the seat
of bacterial embolism and gangrene, and there is no tendency to
suppuration. These products swarm with the specific microphytae.
DIAGNOSIS.--The differential diagnosis of anthrax from other
affections due to the propagation of microzymes in the system is not
always easy--so much so that a variety of bacteridian and allied
diseases (septicaemia in its various forms, erysipelas, swine plague,
chicken cholera, poisoning by the micrococci of fungi, black quarter
from bacteria, milk sickness, and Texas fever) have been erroneously
confounded with this affection. These all show the same dusky or
cyanosed mucous membranes, disintegrating blood-globules, loose
blood-clots, petechiae, blood-extravasations, sudden and great
prostration, and enlargement and congestion of the lymphatic glands or
spleen. In some of these the duration of incubation (in swine plague
six to fourteen days and in Texas fever one month) serves to
distinguish, while in the majority the microzyme is globular (Texas
fever, micrococcus of fungi-poisoning, chicken cholera); in swine
plague the cocci are arranged in pairs; in black quarter the microbe
is a refrangent ovoid, single or in chains of two or three and a
motile linear body with a refrangent nucleus in one end; and in milk
sickness the germ is a spirillum. The germs are far more likely to be
detected in the local lesions and lymphatic glands than in the blood.
The specific nature of the symptoms and lesions can usually be relied
on, but in cases of doubt the inoculation of a small animal (rabbit,
guinea-pig, sheep) will be a material guide.
PROGNOSIS.--True anthrax leads to a very high mortality. The
apoplectiform cases are fatal almost without exception; the acute
cases of anthrax fever in many outbreaks perish to the extent of 75 or
80 per cent., and the more tardy ones to the number of 50 per cent. In
a general outbreak the earlier cases are usually the most fatal, while
later, when the less susceptible animals are attacked, the mortality
is often decreased. Again, the mortality is often at once arrested by
the emigration of the herd to a more healthy soil, a large proportion
of those already attacked recovering.
PROPHYLAXIS.--In prophylaxis the soil demands the first attention. If
this is damp and calcareous or rich in organic matter, the remainder
of the herd should be at once removed to a drier and more porous soil,
where the germ is less likely to be preserved and increased. In an
{937} enzootic in Livingston County, N.Y., in 1875, 40 bullocks out of
200 had perished in ten days, yet after removal to an adjacent dry
pasture and the use of antiseptics with the food and water the attacks
abruptly ceased and 48 out of 50 head already sick recovered. The
drainage of anthrax soils leads to a steady reduction of the poison,
favoring as it does the germination of the spores and the destruction
or modification of the germ. When drainage is impossible, the
mortality may be reduced by driving the stock to drier grounds during
the hot, dry season, by stabling them morning and night when the dews
are on the grass, also in wet times, when they are likely to pull up
the plants by the roots, or, better still, by cutting the fodder and
soiling the stock in stables or yards. Yet in all these cases the
germs will at intervals find access to the animals in the green food
or hay, so that badly infected soils must be secluded from live-stock,
and either be abandoned or devoted to other cultures. A point of the
very first importance is the safe disposal of the products and
carcases of the sick. These should be thoroughly burned, or, failing
this, deeply buried (4 feet) and the graves covered with coal tar and
fenced in from all other stock for from five to ten years.
Contaminated litter and fodder should share the same fate. Stables and
yards where the sick have been, and all vehicles and implements used
for them or their products, should be thoroughly disinfected. In the
epizootic in Livingston County, above referred to, these measures seem
to have eradicated the disease in the course of six years, though the
land was neither drained nor subjected to cultivation, and the
dangerous meadows are now again pastured with impunity.
In the case of sick animals the greatest care is requisite to keep
them from common drinking- or feeding-troughs; to exclude all other
animals, even the smaller quadrupeds and birds, which may become the
bearers of the poison; to avoid the chance of the drainage of infected
excreta into other yards and pastures, and to carefully disinfect and
guard the human attendants against contamination. The sale of animals
out of an infected herd, and, above all, for the meat-market, and the
use of the milk or other products of such animals, until attested
sound, are highly reprehensible.
Finally, there are the different methods of protecting the system by
inoculation with modified virus. The first of these is that of
Burdon-Sanderson, Dugnid, and Greenfield, who in 1878 and 1879
inoculated six cattle with the blood of guinea-pigs dead of anthrax,
all of which survived except an old, emaciated, worn-out, and pregnant
cow, and all the survivors would only afterward contract anthrax in a
mild form. The anthrax blood of the guinea-pig inoculated on the sheep
proved fatal. The second mode is that of Pasteur, who cultivated the
anthrax-germ artificially in flasks of meat-infusion, and after the
nourishment in the latter had been used up left the bacilli to
degenerate until their virulence had been so far decreased that the
liquid could be safely inoculated on animals, so as to produce a mild
anthrax infection and thereafter secure immunity from this poison. For
all the larger domestic animals he found that the eighth day of the
culture sufficed, provided there had been no formation of spores; and
the method has now been applied on many scores of thousands of
domestic animals. Klein, however, has found that cultures in
pork-broth of the same age are invariably fatal to rodents, {938} and
that a guinea-pig which survived inoculation with culture a month old
did not possess immunity against fresh virus. The third method, that
of Toussaint, consists in heating the fresh virus, so as to lessen its
activity, and then inoculating it on the animals to be protected. He
found that a temperature of 55 degrees C. (131 degrees F.) maintained
for one hour rendered the virus non-fatal, without impairing its
prophylactic powers on animals inoculated. In spite of a partial
failure at Alfort from insufficient heating of the virus, the method
has now been firmly established as at once easy and effective.
The great value of these discoveries can hardly be overestimated, yet
it is to be feared that the eclat of their reception has led to a far
too general adoption of the methods. No one of the methods professes
to destroy the life of the bacillus nor to impair its power of
self-propagation. The bacillus, therefore, is likely to be planted in
the localities where it is being employed, and, if the soil is
favorable, to be perpetuated there. It follows also, from the
susceptibility of the bacillus to change under varying conditions of
life, that the modification impressed on it by the methods of Pasteur
and Toussaint may be reversed under a reverse state of the
environment, and that the harmless virus sown by our inoculators may
in favorable soils produce the more deadly types. The methods secure
the safety of the individual herd inoculated, at the expense of
planting in the pasture a seed most perilous to all future
uninoculated herds that may roam there. The only place for such
protective inoculations is on pastures already charged with the
anthrax bacillus, and from which that cannot be eradicated. On the
dry, healthful soils where the bacillus cannot survive the inoculation
is useless, while on the dense, damp, rich soils favorable to its
preservation, but as yet uninfected or nearly so, this inoculation is
but sowing deadly seed to secure a very temporary and questionable
advantage.
TREATMENT.--Bloodletting and laxatives have been largely used in the
treatment of anthrax, though both are mostly useless in acute cases,
their possible good effects being anticipated by the early death. When
of service at all, it is probably mainly in reducing that plethora
which serves often to enhance the virulence and severity of the
malady. Apart from these, the agents resorted to are more or less of
an antiseptic nature, and probably exert their action mainly on the
bacilli undergoing development near the surface of the skin or
intestinal mucous membrane. In extensive outbreaks I have had the best
results with the administration thrice daily of carbolic acid,
nitro-muriatic acid, or bichromate of potassium, and hypodermically of
iodide of potassium and sulphate of quinia. Alcoholic stimulants,
chlorate of potassium, and muriate of iron are equally indicated,
especially when the period of prostration has set in. If the local
anthrax can be detected when there is as yet but a hard nodule, there
should be no hesitation in cauterizing it to its depth and treating
the resulting sore and surrounding parts with tincture of iodine or
iodized phenol. After crucial incision the nodule may be treated with
powerful caustics (potassa, nitric acid, chloride of zinc), to be
followed by iodized phenol, with or without poultices or fomentations.
{939} Anthrax in Man (Malignant Pustule or Vesicle, Anthrax
Intestinalis, Mycosis Intestinalis).
Fournier in 1769 first traced the communicated anthrax of man to the
consumption of the flesh of diseased animals and the handling of their
wool. Until quite recently, however, the form which originated as a
local external affection was the only type recognized, while internal
anthrax was confounded with a multitude of other affections.
ETIOLOGY.--That anthrax in man is almost invariably derived from the
lower animals by infection is now undoubted, while for the direct
infection of man, as of animals, by the germs propagated in the soil,
there is no absolute proof. The latter mode of propagation has only
been recognized in the Herbivora, which are so much more exposed to
contamination from the soil; yet, abstractly, there is no reason to
suppose that man is less susceptible to the earth-grown bacillus than
to that produced in the animal, if only he were as frequently exposed
to its infection. The spontaneous development of anthrax apart from
the pre-existent bacillus in animals or soil is a chimera. The
principal modes of infection may be considered as direct and mediate.
Among the direct are included infection from handling the sick
animals, their carcases, their wool, hair, bristles, hides, fat, and
guts; the inoculation of physicians, surgeons, and nurses from their
patients; and the infection of men by the meat, milk, and cheese
eaten. As attested modes of mediate infection may be cited the
inoculation by insects (mosquitoes, bluebottles, and other
bloodsuckers), and the introduction by water into which anthrax
products have drained or been washed; there are also hypothetical
cases in which anthrax-germs from the earth have entered the system in
the air, drink, or food (raw vegetables). The direct inoculations are
especially common in certain classes (shepherds, farmers, butchers,
knackers, tanners, veterinarians, and workers in hides, hoofs,
glue-factories, fat-rendering works, in hair, wool, bristles, and
catgut, and in felting and paper-making). In such cases the disease
usually begins as a local one, and occurs on uncovered portions of the
body. Three such cases occurred in 1875 on one farm at Avon, N.Y.,
where the victims had assisted in burying forty dead cattle, and a
number of other similar instances can be adduced in different parts of
the same State, in one of which a physician was accidentally
inoculated in dressing a farmer's hand. Physicians whose practice
includes large tanneries become very familiar with the disease and
recognize it very readily.
Infection through food is much less frequent in men than in animals,
the process of cooking combining with the action of the gastric juice
in destroying the poison. Yet it is by no means unknown. The records
above given of infection in St. Domingo, Naples, and the Russian
steppes can be easily supplemented. Dr. Keith of Aberdeen, Scotland,
records the case of a family that suffered, two of them fatally, after
partaking of broth and meat which had been boiled for hours, one
member of the family (a vegetarian) having alone escaped. Infection
through milk, butter, and cheese is less common, the gravity of the
disease in animals leading to an early suppression of the mammary
secretion. In all such cases the infection enters through sores in the
mouth or from the bowels.
Those cases in which the bacillus enters the system with the inspired
{940} air are probably the least numerous. Yet the germ may reach the
lungs in fine dust, and then find in the delicate respiratory mucous
membrane the most accessible of all channels into the system.
The proportion of men affected is much greater than that of women and
children, doubtless by reason of their greater exposure to infection,
and, as in the lower animals, the summer months are most productive of
anthrax. The susceptibility of the human race appears to be less than
that of the Herbivora, and doubtless varies, as in these animals, with
the nature of the food. It is at least temporarily exhausted by a
first attack, though in exceptional cases and under a strong dose of
the poison a man may be affected a second time.
SYMPTOMS.--Symptoms usually set in within twenty-four hours after
inoculation of the poison, though it is alleged that the incubation
may be extended to twelve or fourteen days. Itching draws attention to
a small red spot like a mosquito bite, but with a black central point.
This speedily increases to a small rounded swelling (papule), and in
fifteen hours is surmounted by a minute vesicle with dark-red or
bluish contents. From the size of a millet-seed this increases to that
of a pea, and in thirty hours bursts spontaneously or under friction
and forms a dark-red, indurated, comparatively painless nodule (parent
nucleus, Virchow). The adjacent skin shows a swollen areola livid and
red, on which there appear vesicles similar to the first, which pass
through the same stages, burst, and leave a livid, hard, or doughy
gangrenous surface. By this time the surrounding skin is red, shining,
and puffy, and the disease continues to spread by the same method of
extension. The diseased part now becomes the centre of an oedematous
swelling which may invade the entire arm, face, or neck, and is
attended with more or less constitutional symptoms. The affected part
may be cold or hot, and it may show the red lines of lymphangitis and
the swelling of the adjacent lymphatic glands.
The pyrexia, at first slight, often reaches a high grade, attended
with occasional chilliness, pains in the back and loins, great
prostration, languor, dulness, and even delirium, with cold sweats,
anxiety, dyspnoea, and at times muscular spasms. As in beasts, there
are the dusky skin and mucous membranes, petechiae, and cyanosis, and
in bad cases there may be sudden collapse and death. The symptoms vary
much, however, according to the extent of the local lesion, to the
amount of poisonous chemical products thrown into the blood, to the
degree of the invasion of the blood by the bacillus, and to the
complication (not infrequent) of the affection with septicaemia. In
the very mildest cases the affection never proceeds beyond a local
slough, the size of a quarter or half dollar, the germs do not enter
the blood in sufficient numbers to survive, the constitutional
symptoms are few or absent, and the sore heals by granulation.
The disease usually lasts from six to ten days, and for the first
forty-eight hours the symptoms are generally purely local.
Malignant anthrax oedema (oedeme maligne) was first observed by
Bourgeois as occurring in the eyelid, and has since been recognized in
other parts of the body (arm, forearm, head). It differs mainly from
malignant pustule in the absence of the preliminary vesicle, of the
hard nodule (parent nucleus), and of the early circumscribed gangrene.
It has this further peculiarity, that the local disease often appears
as a {941} sequel rather than a precursor of the constitutional
disturbance. It corresponds in the main to the diffuse erysipelatoid
anthrax of the lower animals, and has been attributed to the anthrax
poison introduced by inhalation. It has been observed to follow eating
of anthrax flesh (Leube, Muller). Inasmuch as the active disease is
often delayed a week or ten days after exposure to infection, it may
reasonably be supposed that the bacillus has been imprisoned on the
mucous membrane, or, entering the blood in small quantity only, has
been held in check by the antagonism of the blood-globules until some
elements, escaping into the connective tissue, have started the local
disease. The symptoms are usually first languor, sleeplessness,
restlessness, with some sense of chill, debility, and headache, and
finally, after a few days, the formation of the specific oedema at one
point or more. This has a pale, semi-translucent, slightly yellowish
or greenish aspect, pits on pressure nearly equally at all points, and
tends to a rapid extension, with concomitant aggravation of the
constitutional symptoms, and in many cases nausea and vomiting.
Gangrene sets in--not progressively, as in malignant pustule, but
simultaneously over a more extensive surface--and is followed by great
prostration, stupor, dyspnoea, cyanosis, collapse, and death.
Anthrax intestinalis may be looked upon as the counterpart of the
internal anthrax or anthrax fever of animals, described above. As in
animals, the constitutional symptoms may result early in a fatal
issue, with scarcely any local lesion save in the blood and spleen
(Carganico, Leube, Muller, Winkler, Lorinser). As in animals too, the
sanguineous engorgement of the spleen and the intestinal anthrax are
often complicated by external anthrax oedema or malignant pustule
(Heussinger, Virchow, Buhl, Waldeyer, etc.). In this form pyrexia and
other constitutional disturbances are first seen. There is a general
feeling of languor and depression, with some chilliness, fever, pains
in the limbs, back, and head, vertigo, and ringing in the ears. Even
at this early stage there is noticed a dusky hue of the skin and
visible mucous membranes, which goes on increasing to a brown or
yellow tinge, to petechiae, or, with the supervention of dyspnoea, to
cyanosis. Digestive derangement is early shown in abdominal pain,
nausea, vomiting, tenderness, some swelling, and finally diarrhoea,
often bloody and sometimes profuse and exhausting. In acute cases the
symptoms become rapidly worse, and then follow discharge from the
mouth and nose of uncoagulable blood, dyspnoea, cyanosis, small pulse,
dilated pupils, great anxiety or drowsiness, and stupor, or there may
be tonic spasms of the trunk or extremities. Death usually results
from asphyxia or collapse, as in animals. These cases are almost
invariably fatal within a period of thirty-six hours, though some
linger six or seven days.
Allied to the intestinal anthrax is anthrax angina, a not unknown
occurrence in man. This begins as a bad sore throat, with an
especially dark-red hue of the pharyngeal mucous membrane. As it
advances the shade becomes increasingly darker, the power of
deglutition is lost, serous phlyctenae with gangrene and deep
ulceration set in, but without any tendency to the formation of false
membrane as in diphtheria. There are early superadded the
constitutional symptoms above described, and the patient dies in a
state of collapse or asphyxia.
MORBID ANATOMY.--The lesions closely agree with those already {942}
described for animals in general. The blood presents the same dark-red
or black, tarry, incoagulable, or only slightly coagulable condition
in the worst cases, yet this is less constant in man, as the bacteria
are less constant or numerous in the blood, in keeping with the more
prolonged localization of the external anthrax in man, and the more
pronounced antagonism between the blood and the bacillus which results
from feeding exclusively or largely on flesh. The red globules do not
tend to adhere together, and the white globules are in excess and very
granular. The spleen is less extensively enlarged than in animals, but
is highly charged with blood, bacilli, and micrococci. The lymphatic
glands too are enlarged, hyperaemic, cloudy, hemorrhagic at points, of
a dark grayish, deep red, or blackish color, and highly charged with
the bacillus. The surface of the skin and mucous membranes (mouth)
presents hemorrhagic spots and patches, with serous vesicles and
eschars. The malignant pustule when cut into presents a central slough
and a surrounding hard indurated mass, both of a dark blood-red, with
similar prolongations downward into the adipose tissue, and around all
the characteristic oedematous infiltration, often streaked with blood.
The bacillus is found in tufts or dense groups at intervals in the
rete mucosum, the dermis, and the subcutaneous connective tissue. The
serous membranes present the same general lesions as in animals. The
walls of the stomach and bowels are the seat of cloudy red
infiltration, with at intervals small hemorrhagic foci, and on the
mucous surface distinct sloughs. Jelly-like exudations are also found
in these membranes in the mesentery and in the retro-peritoneal
tissue. The liver and kidneys are usually congested or are infiltrated
with an oedematous exudate, and in these, as in all the local anthrax
lesions, the characteristic bacilli are found.
DIAGNOSIS.--Malignant pustule is distinguished by its commencing from
a minute red point with dark centre, and by its progressive extension
from this point by a dark-red, puffy, and vesicular areola, with
steadily advancing induration and gangrene. The bites of insects have
a yellowish central point with red areola. A boil lacks the dark
centre and the rapidly rising elevated red areola. Carbuncles and
plague-boils tend to appear on clothed parts of the body, respectively
on the back of the neck and shoulders and on the trunk and
extremities. In carbuncle several boils rise and burst simultaneously,
though they may finally slough into one sore, while in anthrax the
extension is from one point. The plague-boil is usually multiple and
much more painful than anthrax. The glanderous nodule is usually
multiple, situated at intervals on the course of a lymphatic, the
intervening portion of which is inflamed, hard, and cord-like. It is
also usually associated with the specific glairy discharge from the
nose, the nasal ulcers and nodules, and the enlarged painless,
nodular, and indolent submaxillary lymphatic glands. As a last resort
the detection of the bacillus in the indurated nucleus and the
inoculability of the disease on the lower animals (rabbit,
guinea-pig), may be appealed to.
Malignant anthrax oedema is less easily recognized, but may be
inferred from the sudden swelling with a dusky yellow or greenish hue
and a tendency to vesiculation and gangrene, the whole preceded and
attended by the constitutional symptoms of anthrax, and, above all,
from the presence of the bacillus in the exudate.
{943} In both of these forms much may be deduced from the known
liability of the district to anthrax, from the occupation of the
subject as being exposed to infection (worker in hair, wool, bristles,
hides, catgut, etc.), or from his having eaten meat which was open to
suspicion.
Internal anthrax is less certainly diagnosed because of the absence of
local symptoms until the constitutional disorder is well advanced. Yet
the reasonable suspicion of infection and the sudden and violent
eruption of the disease (headache, nausea, vomiting, bloody diarrhoea,
extreme anxiety, debility, dyspnoea, cyanosis, convulsions, collapse,
with petechiae, and local discharges of diffluent blood) serve to
identify it. The bacillus is not always to be detected in the blood
under the microscope, but its presence can usually be demonstrated by
inoculation.
PROGNOSIS.--The prognosis of malignant pustule energetically treated
in its early stages is good. The disease is as yet a local one, and
the germs can be extinguished by local treatment. In anthrax
districts, where the disease is feared and early recognized, the
mortality may be from 5 per cent. (Nicolai) to 9 per cent. (Lengyel,
Koranyi). Even this mortality is mainly due to delay in treatment. In
districts, on the other hand, where the malady is infrequent, and
where efficient measures are applied too late, the mortality is often
30, 40, or even 50 per cent. After internal infection, and where local
symptoms only appear after general infection, the case is very
hopeless.
PROPHYLAXIS AND TREATMENT.--The prophylaxis of anthrax in man is to a
large extent identical with that for animals. All considerations as
regards soil, culture, drainage, sick and dead stock, cremation,
burial, disinfection, etc. have a most important if only a secondary
bearing on the protection of man. Still more important is the free use
of carbolic acid, chloride of lime, or tincture of iodine for the
hands of those dressing unhealthy sores in animals or handling
suspicious cases of sickness or cadavers, and of those working in
hides, wool, hair, horns, hoofs, guts, etc. Similarly, all products of
animals with anthrax should be withheld from general use.
In external anthrax of man, before the system has been contaminated,
the thorough destruction by caustic of the diseased part with its
contained poison is most effectual. Where there is as yet but the
preliminary papule it may be incised and thoroughly destroyed by a
stick of chloride of zinc, caustic potassa, or nitrate of silver, or,
if more convenient, by fuming nitric acid, muriatic or sulphuric acid,
or, perhaps preferably to all others, iodized phenol. Should the
parent nucleus have already formed, it should be excised with the
knife or deeply incised in a crucial direction, and then thoroughly
cauterized with one of the more potent escharotics (caustic potassa,
strong nitric acid) or with the iodized phenol. The latter agent may
be further applied on the sound skin adjacent, especially if there is
the slightest swelling or redness. Should the peripheral oedema
persist or reappear after the cauterization, the latter should be
repeated until this tendency is overcome. Hypodermic injections of a
solution of iodine and iodide of potassium may be made into the entire
swelling. After the caustic has done its work the eschar may be
softened and its separation favored by a warm poultice containing a
small amount of carbolic acid or iodized phenol. This treatment is
often highly beneficial, even after constitutional symptoms have set
in, by arresting the {944} propagation of the bacillus and checking
its introduction and that of its chemical products into the
circulation.
Constitutional treatment is not to be forgotten. Carbolic acid may be
profitably given to the extent of fifteen drops daily, iodide of
potassium ten to twenty grains thrice a day, and sulphate of quinia
ten grains at the same intervals. The strength should be sustained by
iron (tincture of the chloride) and wine or other alcoholic beverage,
both being, like the agents already named, calculated to retard if not
to limit the propagation of the bacillus. The diet throughout should
be nutritious and easily digested.
When a person is known to have eaten anthrax meat an emetic will be
indicated, followed by a smart oleaginous purgative combined with five
drops of carbolic acid, and subsequently by the constitutional
treatment above recommended. In case of extensive anthrax oedema,
incisions may be made into the part as far as the yellow exudate
extends, and a poultice containing carbolic acid may be applied. Or,
preferably, the swelling may be freely injected with a weak solution
of iodized phenol (1:100 water), and then painted with the same agent
or with tincture of iodine.
{945}
PYAEMIA AND SEPTICAEMIA.
BY B. A. WATSON, M.D.
HISTORY.--There is little to be learned from existing literature of
the views which were maintained by the ancients, prior to the birth of
Christ, in regard to the morbid conditions now designated pyaemia and
septicaemia; although it is certain they were recognized by the
"Father of Medicine," who reports a well-marked case of puerperal
fever terminating fatally on the twentieth day of the disease, and
also a case in which death was unquestionably caused by septic
poisoning, as is clearly shown in the following:[1] "Criton, in
Thasno, while still on foot and going about, was seized with a violent
pain in the great toe; he took to his bed the same day, had rigors and
nausea, recovered his heat slightly; at night was delirious. On the
second, swelling of the whole foot, and about the ankle, erythema with
distension and small bullae (phlyctaenae); acute fever; he became
furiously deranged; alvine discharges, bilious, unmixed, and rather
frequent. He died on the second day from commencement." Additional
confirmation of the fact that Hippocrates was familiar with the
phenomena of these diseases may be found in his dissertation on
empyema and fevers. Prof. C. Heuter says, under the head of septic
fever,[2] "Hippocrates and Celsus observed the fever in cases of
injuries which proved so dangerous that this danger could not have
originated from the inflammation or from the wound alone." Jacotius, a
commentator of Hippocrates, has even mentioned putrid fevers, the same
as Adrianus Spigelius, who spoke of fevers which arise from
putrefaction; but both authors, as well as their followers, did not
discriminate between septicaemia arising from the putrescence of
wounds and pyaemia. In the mean time both varieties were regarded as
intermittent fever.
[Footnote 1: _Works of Hippocrates_, trans. by Adams, vol. i. p. 377.]
[Footnote 2: Pitha und Billroth, _Handbuch der Chirurgie_, 1 Band, 2
Abth., 1 Heft, 1 Liefg., S. 6.]
"Aretaeus lived during the middle of the second century of the
Christian era. In his remarks on pneumonia he observes that the
subjects of this disease die mostly on the seventh day. 'In certain
cases,' he says, 'much pus is formed in the lungs, or there is a
metastasis from the side if a greater symptom of convalescence be at
hand. But if, indeed, the matter be translated from the side to the
intestine or bladder, the patients immediately recover from the
peripneumony.' He speaks of a metastasis to the kidneys and bladder
being peculiarly favorable in empyema. He ascribes suppuration of the
liver to intemperance and protracted disease, {946} especially
dysentery and colliquative wasting. The symptoms described by him
resemble those of chronic pyaemia."[3]
[Footnote 3: Braidwood on _Pyaemia_, p. 2.]
Galen and some of the other ancient physicians recognized the
existence of septic poisoning, as is shown by the opinions expressed
on the subject of putrid fevers. According to Galen, putrid fevers may
either arise from the conversion of ephemerals, or originally from
putrefaction of the fluids within the vessels.
Aetius states that they arise from constriction of the skin or
viscidity of the humors, whereby the perspiration is stopped, and the
quantity of vital heat so altered as to give rise to putrefaction,
first of the fluids, and afterward of the fat and solid parts. When
these corrupted fluids are contained within the vessels they occasion
synochous fevers, but when distributed over the body they give rise to
intermittents. Synesius and Constantinus Africanus give a similar
account. Alexander gives an interesting and ingenious disquisition on
the origin and nature of putrid fevers, one of the most common causes
of which he holds to be the conversion of ephemeral fevers, and the
inseparable symptoms being want of concoction in the urine and
quickness of the pulse with systoles. This is the account of them
given by most of the other authorities, both Greek and Arabian, so
that we need not enter into any circumstantial exposition of their
views. We shall merely give the brief account of those furnished by
Palladius. There are, he says, two kinds of synochous fevers, the one
being occasioned by effervescence, and the other by putrefaction of
the blood; of these the latter are the more protracted and dangerous.
In them the pulse is contracted, the heat pungent, and the urine white
and putrid.[4]
[Footnote 4: Paulus Aegineta, trans. by Adams, vol. i. p. 236
(Sydenham Soc., 1844).]
A new era in the literature of this subject dawned during the
sixteenth century. Ambrose Pare and Bartholomew Maggi each published a
work in which they pointed out the old errors and announced new
truths. Pare's _Treatise on Gunshot Wounds_ was published in Paris in
1551, while Maggi's treatise appeared a year later at Bologna. Pare
gained his first experience in the treatment of gunshot wounds in
1536, which is described as follows: "The storming of the small
mountain-fortress Villane, near Susa, probably gave him for the first
time full occupation, and he followed in all things the example of
older colleagues. Like them, although hesitatingly, he poured into the
gunshot wounds boiling oil of elder to destroy the poison, but the oil
fell short, and then he was compelled to dress the other wounded men
with an ointment of oil of roses and turpentine. Fearing that the
latter would soon become victims of the wound-poison, he passed a
sleepless night, got up early to see the ill consequences, but was
greatly surprised to find those that he had half given up free from
pain and without inflammation or swelling, while those who had been
treated with boiling oil lay in a state of fever, with great pain and
much swelling. He therefore determined, as he tells us, never again to
burn the poor subjects of gunshot wounds so cruelly."[5] It will be
seen that Pare's treatise on gunshot wounds was published fifteen
years after this impressive experience at the fortress of Villane. In
this work he sought to correct the prevailing idea that {947} gunshot
wounds were poisonous, and was ably supported in his effort by
Bartholomew Maggi; but it required all the respect which Pare enjoyed
in riper years to gradually obtain consideration for the new view. The
idea that gunshot wounds were poisonous is supposed to have originated
in the fact that in every war there are cases of acute sepsis,
developed after the infliction of these injuries, which agree in all
their essential points with the results of the bites of poisonous
snakes. We are even informed that during the late Franco-Prussian War
there were cases which even excited suspicion among the laymen that
the enemy had used poisoned missiles.
[Footnote 5: _German Clinical Lectures_, 2d series (New Sydenham Soc.,
1877), p. 65 _et seq._]
The nature of the error which Pare and Maggi endeavored to correct is
shown by the declaration made by Johannes de Vigo at the commencement
of the sixteenth century, who expressed in dogmatic form the views
then firmly held by physicians. "A gunshot wound is a contused wound,
he says, for the bullet is round; it is burnt, for the bullet is
heated; it is poisoned, for the powder is poisonous. The poisoning is
the essential condition; therefore the treatment must be directed
above all to counteract this."
The next step was that a poisonous substance may develop itself or
settle in the wound, and especially in gunshot wounds--a substance
which has nothing to do with powder or lead. Pare himself adopted this
view. When he took part in the siege of Rouen many wounds sloughed and
had a cadaverous smell, and on opening the bodies of those who died
numerous collections of pus were found in different parts full of
greenish ill-smelling ichor. Besiegers and besieged believed
themselves to be wounded with poisoned bullets. Pare looked for the
cause in a deterioration of the air by the large quantity of
decomposing substances, and he appears to have assumed, as is done at
this day, a direct action of the so-called deteriorated air upon the
wound itself.
The evil influence of air vitiated by the products of decomposition,
not upon wounds only, but upon the organism generally, has never been
lost sight of by physicians since that time. That rotten straw,
decomposing bodies of men and animals, surfaces saturated with
excrement, and overcrowding of badly-ventilated hospitals give rise to
infectious fevers and unhealthy state of wounds is not a result of
modern observation only. That it was a question of the processes of
fermentation which became communicated to the body by means of the
exciters of fermentation contained in the air was a view frequently
adopted. "To quote one only out of many; John Pringle, in his
_Observations on the Diseases of the Army_, published in 1775, devotes
a chapter especially to 'Diseases resulting from Bad Air,' and his
forty-eight experiments on septic and antiseptic substances contain
numerous hints at attempts resembling those made at the present day to
determine the antiseptic power of certain things. No advance was made,
however, beyond vague surmises concerning the nature of the exciters
of putrefaction, and they were for the most part looked for amongst
the volatile, ill-smelling products of decomposition, and were
believed to be extremely subtle gaseous matters."[6]
[Footnote 6: _German Clinical Lectures_, Second Series (New Sydenham
Soc., 1877), p. 67 _et seq._]
Ambrose Pare (1582) first taught that secondary abscesses in surgical
cases, "which he had observed in the spleen, lungs, liver, and other
viscera, were due to a changed condition of the fluids produced by
some {948} unknown alteration in the atmosphere and determining a
purulent diathesis."[7] The following quotations force the conclusion
that in the early history of medicine there was supposed to be some
important relation between wounds of the head and multiple abscesses.
"Nicholas Massa (1553) mentions a case of abscess of the left lung,
following an injury of the head."[8] "Valsalva (1707) was induced by
his own observation to say that the viscera of the thorax were
sometimes affected in wounds of the head." "Desault (1794) considered
abscesses of the liver to be a very frequent sequence of head
injuries."[9] The fact that wounds of the head were frequently
followed by abscesses of the lungs, liver, and other organs probably
led to the opinion expressed by Desault, Barthez, Brodie, W. Phillips,
Copeland, and others, that the disease had its origin in a nervous
agency.[10] "Bertrandi and Audouille (1819) sought for a mechanical
explanation of the occurrence of hepatic abscesses after head injuries
and in cases of apoplexy." Morgagni (1740) somewhat obscurely hinted
at the doctrine of the reabsorption of pus--a doctrine which was
afterward elaborated by Quesnay in 1819. Morgagni, after quoting a
great number of instances of wounds of the head followed by visceral
abscesses, opposes the idea of a mechanical transportation of pus
thither, and states that abscesses are not confined to the liver and
that they may follow wounds and ulcers of other parts besides the
head. He ascribes their formation to particles of pus (not always
deposited in the form of pus) resulting from the softening and
suppuration of small tubercles, which, having been mixed with the
blood and disseminated, are arrested in some of the narrow passages,
perhaps of the lymphatic glands, and by obstructing and irritating
these, as happens in the production of venereal buboes, and by
retaining the humors therein, distend them and give origin to the
generation of a much more copious pus than what is carried thither;
and by this means, he says, we may also conceive how it is that much
more pus is frequently formed in the viscera and cavities of the
bodies than a small wound could have produced.[11]
[Footnote 7: Braidwood on _Pyaemia_, p. 2 _et seq._]
[Footnote 8: _Ibid._, p. 2.]
[Footnote 9: _Ibid._, p. 3.]
[Footnote 10: _Ibid._, p. 10.]
[Footnote 11: _Ibid._, p. 3 _et seq._]
Cheston (1766) believed that the translation of matter from one point
to another was a frequent occurrence after amputations of the larger
limbs. John Hunter (1793), and after him Velpeau, demonstrated the
existence of pus in the blood. Hunter believed that the pus was
derived from the interior of the inflamed veins. He described three
forms of inflammation of these vessels--viz. adhesive, suppurative,
and ulcerative. Pyaemia he considered to be an aggravated form of
phlebitis. Arnott (1829) concluded from his observations--1, That
death does not result from the extension of the inflammation of the
veins to the heart; 2, that the dangerous consequences of phlebitis
have no direct relation to the extent of the vein which is inflamed;
and, 3, that the presence of pus in the veins, though the principal,
is not the sole, cause of the secondary affection. He accordingly
opposes the idea of Abernethy, Carmichael, and others that the
constitutional affection is owing to the extension of the inflammation
to the heart. The publication of Arnott's and Dance's treatises led to
the general opinion being held in England and in France that phlebitis
and purulent infection were identical affections, or, at least, that
the latter was invariably caused by the former.[12]
[Footnote 12: _Ibid._, p. 14.]
{949} Cruveilhier (1829), admitting the doctrine of the formation of
secondary abscesses being due to capillary phlebitis, further laid
down an axiom, since proved untenable, that the foreign body
introduced into the veins, whose elimination by the emunctories is
impossible, will produce visceral abscesses similar to those which
occur after wounds and operations, and that these abscesses are the
result of capillary phlebitis of those viscera.[13]
[Footnote 13: Braidwood on _Pyaemia_, p. 14 _et seq._]
During the early part of the present century it was generally admitted
by the best authorities that the symptoms and lesions in pyaemia were
entirely due to the presence of pus in the blood, but whether absorbed
from the wound or developed by an inflammation of the veins was at
that time a disputed question.
Haller made the first experiments on animals with putrefying
substances in the latter part of the eighteenth century, and was
convinced that nothing destroys the animal fluids more powerfully than
putrefaction. Gaspard (1822) published a complete work based upon his
experimental research in regard to the action of putrefying substances
on living organisms. He, having produced septic infection in animals
by injecting into their blood pus or other putrefying substances, thus
prepared the way for other experimenters, by whom he was quickly
followed. Ernst R. Virchow repeated the experiments of Gaspard, and
discriminated with greater precision between the surgical
diseases--septicaemia with its sharply-defined group of symptoms, the
opposite of pyaemia. Furthermore, "he showed that the changes in the
veins which had been regarded as due to phlebitis were caused by the
coagulation of the blood and by subsequent degenerative changes in the
thrombi thus formed; that the infarctions and abscesses seen in the
viscera were due to emboli which had become detached from softened
thrombi; that, as the white blood-globules and pus-globules were
identical in appearance, they could not be distinguished; and that it
was improbable that pus-globules made their way into the blood."[14]
[Footnote 14: _The International Encyclopaedia of Surgery_, ed. by
Ashhurst, vol. i. p. 204.]
Panum (1855) conducted a series of important experiments, and
endeavored to separate the infectious substance and determine its real
nature. He concludes that the real poison is not identical with any of
the chemical combinations or any of the single substances which have
until now been isolated by chemical analysis from the products of
nitrogenous decomposition, but adds that it is probably a concealed
ferment belonging to the so-called extractive matters--carbonate of
ammonium, leucin, tyrosin, fatty acids, acetic acid, etc. Furthermore,
that the putrid poison is stable, fixed, and non-volatile; that it is
neither decomposed by boiling nor by evaporation to dryness; that it
is insoluble in absolute alcohol, but soluble in water; that the
albuminous substances found in putrefying liquids become venomous only
because they are impregnated with the septic poison; and that washing
these substances in a large quantity of water renders them innocuous;
and that the energy of these putrid poisons can only be compared to
the venom of serpents, curare, and other vegetable alkaloids.
The prize offered by the Faculty of Medicine at Munich for the best
essay on the action of putrefying substances in the animal organism
was awarded to Hemmer in 1866. His essay was distinguished for its
{950} accurate delineation of the pertaining literature and for the
number of experiments reported, while his conclusions bear a striking
resemblance to those of Panum.
Bergmann in 1868 sought to determine the poisonous element contained
in decomposing animal substances, and for this purpose chemically
treated putrid fluids, hoping to find the agent that would excite all
symptoms of septic poisoning. He obtained a body of this nature from
decomposing yeast, which he called sepsin, although we have no proof
that either he or any one else has ever found the same in pus or any
decomposing animal matters; and even if it had been found in these, it
would then become necessary to demonstrate the fact that no other
substance contained in the putrefying liquids could produce septic
poisoning. Many other experiments, similar to those which have just
been mentioned, were made in the mean while by Magendie, Stich,
Billroth and Hufschmidt, O. Weber, Duprey, Learet, Urfrey, Saltzman,
Fischer, Frese, Muller, and others. Bergmann had extracted the sepsin
from yeast, but Schmidt and Petersen (1869) were able to obtain it
from putrefied blood. In 1869, Zuelzer and Sonnenschein claimed, on
the contrary, to have separated a new, unnamed septic alkaloid, which
was not the sepsin, and the action of which resembled that of atropine
and hyoscyamine. Nevertheless, the separation of the sepsin or of the
alkaloid of Zuelzer seemed to demand a talent in the manipulator which
is not possessed by everybody, and rare are the chemists who possess
it--so rare that these substances are not yet either officinally
recognized or classified. The attention of the medical profession had
now become thoroughly fixed on the chemical character and the
physiological action of these newly-discovered substances. It is
therefore only natural that we should find during the next few months
that the medical societies were much occupied with discussions on
these subjects, although no important progress seems to have been
made.
Political events now gave a new direction to thought, and the
Franco-Prussian War filled the hospitals of both nations with wounded
in which there was opened a grand field for the practical study of
purulent infection in all its various forms. Humanity now demanded the
best efforts of the medical profession. Neither the mechanical nor
chemical theories had ever yielded practically any beneficial results;
consequently, something better was demanded in this emergency. It was
during this important epoch that the germ theory began to assume form
and to attract some general attention in the medical profession,
although Schroeder and Dusch had shown in 1854 that the filtration of
the air through cotton was sufficient to prevent the putrefaction of
albuminous substances which had been previously boiled. Pasteur also
demonstrated the existence of germs in the air in 1863, and likewise
showed their agency in the process of fermentation.
Lister began the antiseptic treatment of compound fractures in 1865,
although he did not publish his report until 1867. The cotton-wadding
treatment of wounds, which is based on the fact that the air passed
through cotton is freed by it from all germs, was first employed by
Alphonse Guerin, who refers to it in the following language: "In the
latter part of 1870 I had the idea that the cause of purulent
infection existed in the germs or ferments which Pasteur had
discovered in the air. It was at the end of the war; all the cases of
{951} amputation had succumbed to the purulent infection, and not a
single large wound escaped the scourge. The studies which I had made
from the month of September to the end of December in 1870 had
confirmed me in the opinion that purulent infection is neither due to
phlebitis nor to the absorption of pus. I believed more firmly than
ever that the miasms emanating from the pus of the wounds were the
real cause of this frightful malady to which I had been compelled to
see the wounded succumb, whether they were treated with charpie or
cerate, whether with the lotions of alcohol or of carbolic acid
applied several times a day, and which was soaked up by the linen
which remained in contact with the wounds. But this miasmatic theory
remained, nevertheless, useless, since from 1847, when I professed it,
the cases of amputation in my service succumbed to purulent infection
in about the same proportion as those who were cared for by my
partisan colleagues did from the absorption of pus or the inflammation
of the veins. In my despair, seeking constantly a means to prevent
this terrible complication of wounds, I had thought of the miasm of
which I had admitted the existence, because I was not otherwise able
to explain the production of the purulent infection, and which was not
only known to me by its deleterious influence, but which appeared to
consist of living corpuscles of the nature of those that Pasteur had
seen in the air; and then the history of the miasmatic poison
possessed for me a new clearness. So, said I then, the miasms are the
ferments. I am able to protect the wounded against their fatal
influence by filtering the air, as Pasteur had done, while
maintaining, in opposition to Pouchet of Rouen, that there is no
spontaneous generation. I thought then of the cotton-wadding
treatment, and had the satisfaction of seeing my anticipation
realized. It was from this time that dates in reality the theory of
germs or of ferments as a cause of purulent infection."[15]
[Footnote 15: _Nouveau Dictionnaire de Medicine et de Chirurgie
pratiques_, t. xxx. p. 265.]
A series of important experiments were made in 1872 by Coze and Feltz,
which consisted in injecting into the jugular vein and the
subcutaneous cellular tissue putrid liquids; and they record, among
other interesting results observed by them, that the blood of the
animal thus destroyed always contained infusoria. These experiments
have been repeated and their results confirmed by several observers,
and in particular by Davine in 1872.
Another series of experiments were made by Behier and Lionville, which
absolutely confirmed those of Coze and Feltz; they likewise found in
the blood rounded and rod-shaped corpuscles possessed of movements
more or less energetic. Vulpian also confirmed the results obtained by
Davine and Behier. He says: "It will not do to deny to the immovable
or movable vibriones and corpuscles found by Coze, Behier, and Davine
a very important role, because they are not the essential contagion of
the poisonous blood; it is at least necessary that they should be
there in order to produce the alterations which have occurred in this
fluid." Chauveau has experimented extensively, and likewise admits the
action of the septic vibriones of Pasteur.
Pasteur has made known the result of his investigation in
communications to the Academy of Medicine in 1877, 1878, and 1879.
There exist, according to him, two principal vibriones--the pyogenic,
or the {952} producer of pus, and the septic, the producer of the
properly so-called septicaemia. But the latter is not a unique
disease, and, as we have seen from the outset, there are confounded
under this name different states, light or grave, corresponding with
as many forms of vibriones.
The questions of greatest practical importance in regard to this whole
group of diseases seem to us to be, as expressed by Dr. Budd, where
and how the specific poisons which cause them breed and multiply; and
all who have closely followed the scientific investigations bearing on
these points which Prof. Tyndall has conducted during the past few
years, and who have repeated even a portion of his experiments, cannot
fail to be powerfully impressed with the value of the views which he
embodied in his work entitled _Floating Matter of the Air_.
NOMENCLATURE.--The want of a systematic classification of the various
morbid conditions arising from septic infection has long embarrassed
alike authors and students, and even at the present time the vague
manner in which the terms pyaemia and septicaemia are used leads to
much confusion. The Pathological Society of London appointed, in 1869,
a committee to investigate the nature and causes of those infectious
diseases known as pyaemia, septicaemia, and purulent infection. This
committee, having spent ten years in the study of these affections in
connection with nearly all the large hospitals of London, report the
following: "Summary.--It would seem, from a careful study of all the
cases here collected, that it is probable that the diseases commonly
known clinically as pyaemia and septicaemia may be grouped as follows:
1. Septic intoxication.--The effects of poisoning by the chemical
products of putrefaction. A non-infective disease. 2. Septic
infection.--A general infective process arising from the introduction
of some peculiar constituent of putrid matter into the blood-stream.
It is supposed by some to be due to the multiplication of living
organisms in the blood, and by others to the effect of a non-organized
ferment. It terminates fatally without secondary inflammations. 3.
Pyaemia (for want of a better name).--An infective process probably,
similar in nature to septic infection, but differing from it by giving
rise to local inflammation and suppurations, often complicated by
thrombosis and embolism, probably due to the blood condition. 4.
Thrombosis with softening and decomposition of the thrombus and
embolism, causing local abscesses in the viscera wherever the septic
emboli lodge, but without the development of any general infective
process. 5. Various combinations of one or more of the foregoing
conditions in the same subject. 6. Infective periostitis or acute
necrosis. 7. Infective endocarditis or ulcerative endocarditis. 8.
Infective myositis. 9. A group of obscure cases in which it is
impossible to form any idea as to the exact nature, often called
spontaneous septicaemia or pyaemia."[16]
[Footnote 16: _Trans. Pathological Soc. of London_, vol. xxx. p. 38.]
It will be observed that the earlier writers on medicine, although
aware of the existence of septic diseases, wholly failed to
discriminate between pyaemia and septicaemia until 1848, and even
since that date these terms have been only partially adopted by
authors, by whom frequently the meaning of the same word has been so
modified as to refer to essentially different conditions. Custom
having fully sanctioned the use of these terms, it is now thought that
a separate consideration of their {953} nomenclature may be
advantageous, and consequently we shall pursue this course.
NOMENCLATURE OF PYAEMIA.--In Dunglison's _Medical Dictionary_ the
definition given to pyaemia is, "Pyohaemia," and the latter word is
defined as follows: "Pyohaemia, Pyaemia, Pyohemie (F.), from _pyo_,
and [Greek: haema], 'blood;' alteration of the blood by pus, giving
occasion to the diathesis seu infectio purulentia."
The committee appointed by the Pathological Society of London in 1869
report on this subject as follows: "The most common definition of
pyaemia is, no doubt, that adopted by the College of Physicians in the
nomenclature of diseases. It is as follows: 'A febrile affection
resulting in the formation of abscesses in the viscera and other
parts.'"
Birch-Hirschfeld includes under the name pyaemia "all cases in which
any general infective process is set up as a secondary consequence of
a wound."[17] Virchow has proposed the name ichorrhaemia. O. Weber
uses the name embolhaemia for the condition in which emboli are found
in the blood. Hueter in pure cases of purulent infection without
metastasis calls the disease pyohaemia simplex; in cases with
metastasis, pyohaemia multiplex; and when complicated with septicaemia
he designates it as septo-pyohaemia. The term hospitalism has been
applied to this disease by Erichsen and Sir James Y. Simpson, and the
former remarks that "the term pyaemia is used in a very wide and
elastic manner, and by many is made to include various forms of
blood-poisoning."[18] Billroth says: "Pyaemia is a disease which we
believe to arise from the taking up of pus, or of the constituent
parts of pus, into the blood." Koch employs the term pyaemia merely to
denote a general affection accompanied by metastatic inflammation and
suppuration.
[Footnote 17: _Trans. Pathological Soc. of London_, vol. xxx. p. 22.]
[Footnote 18: _On Hospitalism_, p. 73.]
The French definition and nomenclature of pyaemia, according to
Guerin, is as follows: "Purulent infection, or pyohaemia, purulent
fever, surgical typhus." The purulent infection is a poisoning of the
blood, which terminates by the formation of multiple abscesses, which
have been improperly known under the name of metastatic abscesses.
From 1820 to 1870 surgeons admitted that these abscesses were the
result of a phlebitis having its origin in a wound exposed to the air.
Therefore, this disease was variously designated under the name of
phlebitis, pyohaemia, or purulent infection. Tessier called it
purulent diathesis; "in 1847, I compared it to the typhus, and, as the
poison is absorbed from the surface of the wound in the purulent
infection, I gave it the name of surgical typhus or purulent
fever."[19]
[Footnote 19: _Nouveau Dict. de Med. et de Chir. pratiques_, t. xxx.
p. 222.]
Having given enough on this subject to answer our purpose, we will
consider the nomenclature of another septic complication.
NOMENCLATURE OF SEPTICAEMIA. The term septicaemia was first employed
by Piorry, and was applied for a considerable time to all those
diseases in which the blood was submitted to a septic influence.
Therefore, the term was made applicable to the morbid conditions
existing in anthrax, glanders, typhus and typhoid fevers, variola, and
also all forms of purulent and putrid infections. Guerin now adds:
"Fortunately, for several years the most competent authors seem to
have wished to {954} reserve the name of septicaemia for what surgeons
call putrid infection, and for the morbid state that the experimenters
produce by the injection of putrid material into healthy animal
tissues; it is consequently the experimental septicaemia which we aim
at first and foremost."[20]
[Footnote 20: _Nouveau Dict. de Med. et de Chir. pratiques_, t. xxx.]
Dunglison defines septicaemia with a single word, septaemia. The same
authority gives the following derivation and definition to septaemia:
"From [Greek: septos], 'rotten,' and [Greek: haema], 'blood.' A morbid
condition of the blood produced by septic or putrid matters."
Sanderson says: "What I mean by septicaemia is a constitutional
disorder of limited duration, produced by the entrance into the
blood-stream of a certain quantity of septic material. It must,
therefore, be regarded less as a disease than as a complication,
differing from pyaemia not only in the fact that it has no necessary
connection with any local process, either primary or secondary, but
also in the important particular that it has no development."[21]
[Footnote 21: _British Medical Journal_, Dec. 22, 1877.]
Both Davine and Koch designate as septicaemic all cases of general
infection from wounds in which no metastatic changes occur.
"Birch-Hirschfeld limits the term septicaemia much in the same way as
Sanderson. He describes as septicaemia those cases in which the
disease results merely from the absorption of the products of
putrefaction, and regards it merely as a process of poisoning, such as
might arise from the injection of any other noxious chemical substance
into the blood. Pyaemia, on the other hand, he considers a truly
infective process, probably due to the entrance of specific organisms
into the body. He would therefore include many of the cases described
by Koch as septicaemia under pyaemia."[22]
[Footnote 22: _Trans. Pathological Soc. of London_, vol. xxx. p. 9.]
Billroth defines septicaemia as an "acute general affection which
arises from the taking up of various kinds of putrid substances into
the blood, and it is believed that these putrid substances so change
the quality of the blood that it can no longer fulfil its
physiological functions."[23]
[Footnote 23: _Lectures on Surgical Pathology and Therapeutics_
(trans. from 8th ed.), vol. ii. p. 41.]
Heuter defines septicaemia as a fever caused by the entrance into the
circulation of the products of putrefaction from local centres of
decomposition. He draws no clear distinction between an infective and
a non-infective form, but the affection he describes as pyaemia
simplex or pyaemia without metastasis seems to include many cases
which Davine, Koch, and others would include under septicaemia.[24]
[Footnote 24: _Trans. Path. Soc. of London_, vol. xxx. p. 9, 1879.]
Having before us the views of some of the prominent authors who have
written upon the nomenclature of pyaemia and septicaemia, we observe
that the use of these terms is based either on known or imaginary
morbid conditions of the body, more especially of the blood. It
therefore seems that the first step toward determining the proper
limit within which these terms can be employed consists in learning
their accurate meaning, which is fortunately clearly shown by their
derivation. The next step consists in the application of these terms
to the morbid conditions which are described more or less completely
by these words. It may be here added that there will be frequently
required for a full and definite expression certain modifying words,
and consequently we may {955} properly employ such phrases as
puerperal septicaemia, spontaneous pyaemia, etc.
Having carefully examined the terms employed by various authors in
connection with the morbid changes which are known to occur in certain
cases of septic contamination, we give our preference to the following
nomenclature: Septicaemia, septo-pyaemia, pyaemia simplex, and pyaemia
multiplex.
The term septo-pyaemia is applied to a morbid condition possessing
certain peculiarities of both septicaemia and pyaemia, and it is
supposed to arise from the absorption of both poisons; the term
pyaemia simplex is applied to a pyaemic condition in which there is no
metastasis; while the name pyaemia multiplex is given to that form of
disease which is characterized by the existence of metastatic
abscesses. It may be well to add here that this nomenclature is not
intended to cover all cases of septic poisoning, but to be applied to
those cases only in which the morbid changes give to the terms a
certain degree of appropriateness.
Septic poisoning may be justly regarded as a single chain composed of
many links. Take, for example, a case of amputation of the thigh,
followed within a few hours by traumatic fever, later by septicaemia;
afterward there may be developed secondary fever; formation of
ichorous pus, with absorption and its concomitants; pyaemia,
accompanied by embolism, thrombosis, abscess in the lungs, liver, etc.
To these may also occasionally be added phlebitis and inflammation of
the joints, terminating speedily in suppuration. This chain may in
this case be further lengthened or varied with traumatic erysipelas or
with hospital gangrene. In fact, the variations in these cases are
very numerous, and all these conditions, together with many others,
are due to septic blood-poisoning.
ETIOLOGY OF PYAEMIA.--Four theories have been advanced at different
times to explain the etiology of pyaemia, and they have been
designated as follows: the mechanical, the nervous, the chemical, and
the germ theories respectively; and their action is based on the
following hypotheses: 1, that pus enters the blood, circulates in it,
and acts as a poison; 2, that an irritation is excited in certain
visceral organs in sympathy with inflammation of the fibrous membranes
of the cranium or the bones of the upper or lower extremity, and there
is thus produced a metastasis to these organs of an ichorous miasm or
of a fluid which is more or less acrid; 3, that a chemical poison is
generated from the pus in the wound, and when it is absorbed produces
pyaemic manifestations; 4, that the putrefaction of pus in wounds is
caused by a microscopic organism which enters the circulation and
produces pyaemia.
The first hypothesis was somewhat modified, as we have already
mentioned, by John Hunter and others, who advanced the idea that
pyaemia consisted essentially of a phlebitis, and that the pus found
in the circulation had its origin within the veins. However, it has
since been shown conclusively that pyaemia cannot be produced by the
injection of healthy pus into the cellular tissue or veins. This fact
having been generally admitted by the profession, it is thought
unnecessary to adduce here either the experiments or the arguments
which have been accepted as conclusive on this important point. It is
not even necessary to bring forward the disputed question of the
possibility of the entrance of pus into the blood, since laudable pus
does not produce pyaemia. In fact, we have reached a point in the
{956} progress of medicine when the discussion of either the first or
second hypothesis ceases to be interesting to medical men.
Consequently, our chief interest in the study of the etiology of
pyaemia centres in the third and fourth hypotheses; and we believe
that it may be safely asserted that the origin of this disease has
been fully demonstrated by an almost unlimited number of experiments.
The injection of pus into living animals produces local, remote, and
constitutional symptoms. The character of these symptoms depends
principally on the kind of pus, laudable or ichorous, the quantity
injected, and the site of the injection. It will be readily perceived
that in cases where the pus is thrown directly into a vein the local
symptoms would be unimportant, while the danger of remote
trouble--metastatic abscesses in the lungs, liver, etc.--would be very
great; but should the injection be made into the connective tissue,
then the relations would be reversed. Constitutional symptoms may
exist in both cases, but will differ in character and degree.
In regard to the character of the pus, and its agency in the
production of this disease, Billroth says: "The old view, that pyaemia
is only induced when decomposed pus (ichor) is reabsorbed, is entirely
erroneous. There are cases where decomposed, putrid pus enters the
blood, and which present a combination of the symptoms of septicaemia
and pyaemia (septo-pyaemia of Hueter)."[25] Dupuytren failed to
produce metastasis by injections of pus into the veins of dogs; these
results were confirmed by Boyer, who only obtained metastasis when he
used ichorous pus in his experiments. The same results are recorded in
the works of Gunther and Sedillot, based on numerous experiments. Beck
made fourteen experiments very carefully, but did not succeed in
producing metastasis in a single case. The same results are recorded
by a commission of the Physiological Society of Edinburgh. O. Weber
has recently shown by extended experiments that carefully filtered pus
will not produce metastatic abscesses in the lungs. Therefore, it may
be considered as proved that fluid pus injected into the veins of an
animal produces no metastatic points of inflammation.
[Footnote 25: _Surgical Pathology_, p. 344.]
It should not be supposed, however, that because injection of fresh
(non-ichorous) pus failed to produce metastatic abscesses, it was
therefore without results, as the earlier experimenters thought.
Billroth and O. Weber have shown by their recent experiments that
these injections are uniformly followed by fever, and, if
subcutaneous, by abscess; and further, that injections of fresh pus
produce even a higher temperature than do those of ichorous pus; but
the pus taken from cold abscesses has apparently very slight effect.
The fresh non-ichorous dried pus was found to possess in a similar
degree the power to excite inflammation and suppuration; even the
removal of the albumen did not change its character or power. It will
be observed that these injections caused not only local inflammations,
but severe constitutional symptoms, as high temperature, etc.
Experiments have thus far completely failed to show the agent that
excites the inflammation, although it is generally admitted that it at
least exists in the molecular bodies.
Virchow and Panum have shown conclusively by their experiments on
living animals that the introduction of foreign bodies into the {957}
veins--as powdered coal, wax balls, and quicksilver--fail in all cases
to produce metastatic abscesses in the visceral organs or symptoms of
pyaemia. These foreign bodies were frequently found blocking up the
terminal branches of the pulmonary artery, in some cases encapsulated,
frequently resembling miliary tubercles, and occasionally surrounded
by evidences of slight local inflammation, but in every instance
without suppuration. The same experimenters, however, observed that
the introduction of ichorous pus and decomposing animal tissue into
the veins was attended with the formation of metastatic abscesses and
other symptoms of pyaemia. They therefore conclude that the
introduction of putrid animal substances into the veins, and the
further transport of the same to the branches of the pulmonary artery,
produce metastatic abscesses, and that the origin of these deposits is
independent of the mere stopping up of the branches of this artery.
The occlusion of the blood-vessels in this diseased condition is a
subject which has given rise to much discussion. Some of the earlier
writers supposed this phenomenon constituted the disease pyaemia,
while others believed it to be the essential cause. Roser says: "But
the thrombus is, as can be easily proved, not the cause, but only a
symptom, of pyaemia. If a surgical patient--_e.g._ one suffering with
an injury of the head--is attacked by inflammation, and occlusion of a
large vein, as of the common iliac vein, for instance, then there are
three different theories for the inflammation of the occluded
vessel--viz. Hunter's, Rokitansky's, and Virchow's. According to the
old Hunterian phlebitic theory, the coagulation of the blood should be
the result of the inflammation of the vein. On account of the
circumstances under which the coagulation of the blood in the vein has
occurred, one might suppose that the cause must be the oozing of
coagulable exudation from the inflamed wall of the vein, but
pathological dissections, especially Rokitansky's, would not accord
with it. Large veins were found plugged up without the existence of
corresponding indications of inflammation, and perfectly clear
indications were often present that occlusion had preceded the
inflammation. Consequently, the occlusion of the vein was the primary
condition, and this must be explained in some other way than by its
inflammation. Rokitansky in his theory recognized an independent
disease of the blood. Yet it does not appear, on examination of the
morbid conditions, that this theory can account for them. If it is
recognized as correct that a primary disease of the blood is to be
admitted, yet the coagulation of the blood in a large vein has not
been traced back to it. It remained wholly unexplained why a single
vein, especially one so large and strong as the common iliac, should
become the seat of the local coagulation. The necessity of finding a
local basis for the local coagulation could not be denied. For that
reason it was greeted as a highly desirable advance when Virchow
pointed out that the occlusion of such large veins could be dependent
on the coagulation of the blood in the concave spaces behind the
valves of the veins, or through the coagulation in the small
branches--_e.g._ the hypogastric veins, which is gradually carried
forward until it reaches the common iliac, and by continual increase
this vein may also be filled up. At the same time, it was demonstrated
that not infrequently, much oftener than {958} was formerly supposed,
the coagulated masses of blood are broken up and carried farther on in
the circulation, in this manner producing occlusion of the pulmonary
artery or its branches."[26]
[Footnote 26: _Archiv der Heilkunde_, Erst. Jahrg., Erst. Heft, S. 4.]
The examination of this subject finally brings Roser to this
conclusion: "Contamination of the blood is essentially the primary
cause of pyaemia; thrombosis is only a result of this morbid
contamination, and cannot, therefore, be regarded as the cause of
pyaemia, but only as an apparent part, as one of the symptoms of the
same."[27] The opinion here expressed by Roser I believe to be the one
generally entertained by the profession at this time.
[Footnote 27: _Ibid._, S. 43.]
In cases of pyaemia there are recognized two principal sources of
contamination of the blood--viz. the wound itself, and the vitiated
condition of the atmosphere surrounding the patient--contamination, in
the first place, directly from the wound through the blood-vessels;
and in the second, by the passage of disease-germs or of the poisonous
elements into the blood along the respiratory tract. E. Wagner says:
"The latest examinations in regard to the vegetable parasites have
made it very probable not only that these are the active agents, but
also--what has been clinically quite generally accepted--that
septicaemia and pyaemia owe their origin to different plants (the
first to rod bacteria, the latter to globular bacteria); and, finally,
that both may combine."[28] These germs may be generated in the wound
or be received into it from the surrounding atmosphere. The character
of the wound and the conditions surrounding the patient thus become
important subjects for the consideration of the surgeon.
[Footnote 28: _Manual of General Pathology_, p. 593.]
It has been observed, and is now generally admitted, that wounds
complicated with a fracture of the long bones of the extremities,
opening large medullary cavities and accompanied by extensive
laceration of the soft parts, always increase the danger of
blood-poisoning. This fact may be more thoroughly understood by a
brief consideration of the condition of the parts. Frequently in open
fractures large quantities of pus constantly remain in contact with
the surface of the wound, while detached fragments of bone, which
become speedily necrosed, move about with every motion of the injured
limb, lacerating more or less the surrounding tissues, and thus
exciting inflammation and suppuration. The periosteum becomes
inflamed; a widespread suppurative periostitis is the result; necrosis
of the bone from insufficient nutrition follows, while mechanical
pressure on the pus aids in its absorption. The medulla frequently
takes on suppurative inflammation, and here the surgeon fails to
receive prompt warning of danger; slowly the suppuration progresses,
without pain or other symptoms unless the disease has extended to the
other tissues; the medullary cavity at the fractured end of the bone
may be completely or partially occluded by a new osseous formation;
and in such cases the absorption of pus by the comparatively large
venous vessels of this cavity is greatly facilitated.
The soft parts may also be the seat of dangerous trouble. The same
force that produced the wound and fracture may have also contused the
soft parts, destroying in a greater or less degree their nutrition,
thus giving rise to gangrenous sloughs, or in other cases to the
formation of abscesses, etc. I will also call attention to the fact
that the laudable pus {959} in these cases is most favorably situated
for a rapid change into that commonly called ichorous. The heat of the
parts and the contact of the pus with the atmosphere will not fail to
effect its rapid decomposition.
ETIOLOGY OF SPONTANEOUS PYAEMIA.--It is unquestionable that cases of
true pyaemia have been observed in which the etiology was not
traceable to a wound; and it is equally certain that this failure to
discover such a source of contamination in the majority of cases is no
proof that it did not exist. When it is remembered that a large
portion of the alimentary canal, the respiratory and the
genito-urinary tracts, are so situated that the existence of a
contaminating wound might be absolutely undiscoverable, we are
compelled to admit the possibility of a local centre of contamination
in all these cases. But the question may be asked here with propriety,
"Is fatal pyaemia, independent of a wound, ever produced by breathing
vitiated air?" The answers to this question must generally be a
negative, although it is certainly true that poisoning of the blood
does take place to a certain degree, as is abundantly shown by the
different symptoms arising in patients thus exposed who are not
suffering with wounds. It is said that dogs exposed in this way are
found to rapidly emaciate and suffer from severe and constant
diarrhoea. The various symptoms arising in patients confined in
overcrowded and pus-infected wards, among which may be mentioned loss
of appetite, with diarrhoea and emaciation, are too well known to
require an enumeration here. Therefore it appears highly probable that
living in and breathing a vitiated atmosphere may act as a strongly
predisposing cause, only requiring a slight scratch or abrasion of the
skin, in which the infection may be said to act as an exciting cause
of pyaemia.
In reference to such complications the following questions are asked
by Roser: "Is it a specific deleterious material, a miasmatic or
contagious disease-poison, or, as it is generally expressed, a zymotic
agent? Must we regard each particular typhus-like fever, with its
remarkable changes of blood, with its various localizations in all the
organs and membranes, with its chills, furred tongue, petechiae,
delirium, etc., as we regard typhus, scarlatina, variola, etc.? or, as
Virchow teaches us, is this pyaemia, so greatly feared by all
surgeons, only an ontological idea? Is the word pyaemia only a general
name for three different conditions--viz. leucocythaemia, thrombosis,
and embolism, or ichorrhaemia and septicaemia? or are there, as many
have supposed, two ways in which pyaemia may originate? Is there one
primary miasmatic pyaemia analogous to the other epidemic, so-called
zymotic diseases? and again, a secondary pyaemia arising from
suppurative inflammation, wherein the poison is formed in the
patient's own body, which is infected by a single organ?"[29]
[Footnote 29: _Loc. cit._, S. 39.]
That this disease is caused by a specific deleterious material in the
large majority of cases is no longer a question for discussion. The
only question to consider is, whether it always arises from the same
cause. Is it possible for pyaemia to originate spontaneously? Are
there any cases of sporadic origin, or are they always due to endemic
or contagious influences? No definite answer can be given to these
questions, although, undeniably, the weight of the argument is
strongly opposed to a sporadic origin. The term miasmatic, as {960}
used by Roser, probably refers to the vitiated condition of the
atmosphere, as seen in the overcrowded surgical and obstetrical wards
of hospitals. In no other sense can the word be appropriately used in
connection with the subject of pyaemia. It is true, pyaemic diseases
are found to prevail at certain seasons and in certain localities much
more extensively than under other circumstances. The same, however, is
true of cholera, typhus fever, scarlatina, variola, and other
contagious diseases. That pyaemia is contagious has been frequently
demonstrated. I therefore conclude that the prevalence and spread of
this disease must be explained by the same rules as are applied to the
existence and propagation of these allied affections.
This inquiry into the etiology of pyaemia brings before us again the
four hypotheses which have been given in explanation of the same
number of theories. The first and second have been already abandoned
by the medical profession, after it was satisfactorily demonstrated
that they were based on false theories, and consequently there remain
for our consideration only the third and fourth.
The third hypothesis assumes that a chemical poison is developed in
the wound-secretions, which when absorbed produces pyaemia. An
examination of the subject does not justify us in asserting that this
proposition has been proved, although it is certain that the results
of experimental inquiry demand for it a more extended investigation.
In all the analyses which have thus far been made the investigators
have entirely failed to give us an adequate knowledge of this poison,
and not a word has ever been said in regard to the agency by which it
is produced, although it is universally admitted to have been only
obtained from decomposing animal substances. It is therefore pertinent
to the continuation of this inquiry to ask, By what agency is the
putrefaction of animal substances produced? It has now been fully
shown that there can be but one answer given to this question--viz.
the putrefaction of albuminoid substances can only be effected by
living organisms. We therefore conclude that the fourth hypothesis
brings us at least one step nearer the correct explanation of the
etiology of pyaemia than the third, since we justly assume that if
there is a chemical poison in decomposing albuminoid substances, it is
produced through the agency of living organisms.
ETIOLOGY OF SEPTICAEMIA.--The first question which arises in the
discussion of the etiology of this morbid condition is entirely
dependent on the scope which we give to the word septicaemia.
Sternberg says: "The view which is entertained by high authorities,
upon clinical and experimental evidence, is that there are two forms
of septicaemia--the one a septic toxaemia due to the effects of a
chemical poison or poisons evolved during the putrefactive
decomposition of certain organic substances, especially of nitrogenous
animal products; the other an infective disease produced by the rapid
multiplication in the body of the infected animal of a parasitic
organism. The best-studied and most widely known form of septicaemia,
due to the presence of a parasitic organism, is the disease known as
anthrax--charbon of the French, milzbrand of the Germans--but several
other varieties are now well established, in which similar symptoms
and pathological results are produced by organisms morphologically
different from the bacillus anthracis. Among these may {961} be
mentioned the form of septicaemia in the mouse, so well studied by
Koch, which is due to a minute bacillus, and the form of septicaemia
in the rabbit, produced by the subcutaneous injections of human
saliva, due to micrococci, which has been studied by Pasteur, Vulpian,
and myself independently."[30]
[Footnote 30: _Amer. Jour. Med. Sci._, July, 1882, p. 70.]
The terms septic toxaemia and septic intoxication are applied
indiscriminately to the same disease, and the committee appointed by
the London Pathological Society to investigate the nature and cause of
those infectious diseases known as septicaemia, etc. further report
that "ordinary wound-fever is merely septic intoxication in a very
mild form, and it is only necessary for the dose absorbed to be
sufficient in quantity for fatal consequences to ensue. Septic
intoxication is, therefore, of the commonest possible occurrence as a
complication of severe surgical injuries, but it is in so mild a form
as to bear but little resemblance to that experimentally produced on
animals."[31] The question which now arises is, Shall septic
intoxication be classified with septicaemia?
[Footnote 31: _Trans. Pathological Soc. of London_, vol. xxx. p. 14.]
We have been long accustomed to speak of this complication as a
surgical or traumatic fever; and consequently any change in this
classification must necessarily lead to confusion. Furthermore, it is
now generally supposed there is much difference in the etiology of
these morbid conditions. It is claimed that septic intoxication arises
from the absorption of a chemical poison evolved through the agency of
living organisms during the process of putrefaction in a wound, and
that the conditions are unfavorable for their development within the
blood or tissues of a living animal; but in true septicaemia the
organisms are developed in the wound during putrefaction, and then
find their way into the blood and tissues of the body, where they
rapidly multiply. Consequently, the former condition tends to a rapid
recovery--unless the quantity of poison primarily admitted to the
system has been excessive--while the latter tends to a fatal
termination.
Septic intoxication is regarded as a non-infective disease, and true
septicaemia as an infective malady. The only etiological similarity
between these morbid conditions is found in the fact that they take
their origin in putrefaction, which is effected by the action of
different organisms possessing marked morphological differences and
requiring essentially different surroundings for the maintenance of
life and reproduction. Thus, it is supposed that in cases of septic
intoxication the organism by which putrefaction is caused in the
wound-secretions can only live in the open air, and that its life is
commonly only of a few hours' duration. The brevity of bacterial
action in this instance may be due to a failure of the absorptive
power or to a changed condition in the wound-fluids, rendering them
unfit to support the organism.
It is now a well-recognized fact that all septic absorption ends so
soon as the wound-surfaces are covered with healthy granulations, but
that septic absorption, which produces septic intoxication, is most
commonly of a much shorter duration, and, consequently, that the wound
complication, which I prefer to designate traumatic fever, is
essentially an acute disease, and can only be lengthened out by
unusually favorable circumstances for the continuance of the
absorption of the poison by which it is produced. {962} The severity
and danger of the disease will necessarily depend on the amount of
poison absorbed and the resisting power of the patient; but since
there is no multiplication of the materies morbi within the body, a
rapid elimination by the natural emunctories may be reasonably
expected under favorable circumstances.
It should be observed here that the etiology of septicaemia differs
from that of traumatic fever, since the organisms in the former
condition are first formed in the wound-secretions, but quickly enter
the body, where they rapidly multiply; consequently, Chauvel has
defined surgical septicaemia as follows: "The particular intoxication
which results from the penetration and multiplication in the body of a
specific microbe designated by Pasteur under the name of septic
vibrio." The bacterial origin of this disease is now generally
accepted, and the only question in the professional mind seems to be
whether the organisms are the direct or indirect cause of the malady.
There are also some other interesting questions which have arisen in
connection with the study of this subject, and are thought to be of
sufficient importance to merit mention here. It has long been known
that dissecting wounds are most dangerous when made while examining
the body very soon after the death of the subject. Recent observations
seem to justify the conclusion that the greatest activity of the
septic agent is often, if not always, attained before the odor of
putrefaction has become fairly perceptible; and even before this odor
has reached its maximum degree of offensiveness the danger from septic
poisoning has generally disappeared. In some cases septic intoxication
is promptly followed by a slight inflammation in and about the wound,
which may entirely disappear within a few hours, but only to reappear
after a lapse of eight to fifteen days, with the first vigorous
physical exercise of the patient. Two cases of this kind have recently
come under my observation. In both instances the wounds were located
in the hands, and the exercise which developed the septicaemia
consisted in rowing a boat, and while thus engaged the local symptoms
reappeared with such severity as to cause the patients to quickly
discontinue the labor. The reappearance of the local inflammation in
both these instances was quickly followed by a rigor and the rapid
development of other constitutional symptoms, although prior to the
recurrence there was no pus, nor even marked inflammatory action, in
any part of the hands.
Professional attention was first called to the above-stated facts by
Panum in 1855, who discovered that the maximum toxic action of putrid
substances is generally developed during the first hours of bodily
activity. In this stage of incubation in cases of surgical
septicaemia, if we admit the bodily action as an etiological factor,
we observe a striking resemblance to one of the leading
characteristics of all the infectious diseases, which unquestionably
depend on some sort of septic poison. Furthermore, this analogy
becomes most striking if we contrast the effects arising from
dissecting wounds with those of the bites of poisonous serpents and
rabid animals.
Further investigation is required to settle the perplexing questions
of etiological and pathological differences in these allied morbid
conditions, for although much has been accomplished during the last
two decades, still much more remains to be done. It has only recently
been discovered {963} that the septic material in septicaemia is
absorbed by the lymphatics, while in pyaemia the poison enters the
body through the veins.
ETIOLOGY OF SEPTO-PYAEMIA.--It is now generally admitted that
remittent fever and typhoid may be associated, and this morbid
condition is commonly designated by the term typho-malarial fever. The
etiology is unquestionably dependent upon the action of the two
distinct and entirely dissimilar poisons. Scarlatina is likewise
frequently complicated by diphtheria, and here we have the combined
action of two poisons, each commonly designated as septic and supposed
by many physicians to be similar.
In a like manner, it is believed that septicaemia and pyaemia may be
associated, and take their origin in dual poisons; but since the
etiology of both these morbid conditions has been already described,
it is not deemed necessary to dwell longer on septo-pyaemia under this
division of our subject.
PATHOLOGY OF PYAEMIA.--The study of the pathology of pyaemia is
advanced by adopting the following classification, which is based on
recognized post-mortem lesions. The pathological appearances in these
forms of the disease differ widely, although the clinical symptoms are
often similar. In pyaemia simplex the pathological conditions are
essentially more negative. This variety of the disease can only
destroy life by the height and duration of the fever which is
maintained in connection with the continued existence of ichorous pus.
There is found, as an essential basis of this form of disease,
extensive suppuration in the subcutaneous tissues.
The arguments in favor of the admission of pus-corpuscles into the
blood are as follows: 1. The blood in pyaemia is known to contain more
white granular spherical bodies than are normal. The question has been
raised, Are they pus-cells or white blood-corpuscles? The answer is
difficult, and has not yet been attained. Virchow, in the mean time,
has proved that we cannot differentiate, morphologically, between the
blood- and pus-corpuscles. 2. Cohnheim has demonstrated the existence
of the wandering corpuscles in cases of inflammation. Therefore it
appears probable that in cases of pyaemia the blood may contain the
pus-corpuscles, but further investigation is needed to establish this
fact. However, the establishment of this point would still leave the
more important undetermined.
There are often important changes observed in the blood of patients
dead of pyaemia, to which I now desire to direct attention. The red
corpuscles of the blood, even in the early stage of the disease, in
many cases show signs of disintegrating into molecules, and are
observed to be accumulated in masses without showing the slightest
tendency to form rouleaux. There is a steady increase in the number of
pus- or white corpuscles in the blood of pyaemic patients during the
whole course of the disease in fatal cases. The condition of the red
corpuscles, already mentioned, becomes more and more marked toward the
fatal termination.
In all cases of pyaemia multiplex the increased coagulability of the
blood may be observed in the early stages of the disease, and steadily
increases as the disease progresses.
In pyaemia simplex this condition is less marked, although generally
present, "while we know septicaemia diminishes or destroys the {964}
coagulability of the blood. Hereby the possibility is given, at least
on the cadaver, to differentiate between pyaemia simplex and
septicaemia, although cases occur of the more fatal septic infection
in which the post-mortem condition is a complete or almost complete
negative. Therefore, in these cases the differential diagnosis on the
cadaver must be limited to this, that we are able to demonstrate the
existence of a purulent or ichorous deposit." It will be readily
observed that the difference in diagnosis mentioned above relates to
pyaemia and septicaemia, and not to the different varieties of the
former disease.
The following facts should be constantly kept in mind by the surgeon
to enable him to differentiate between the two forms of pyaemia: In
pure cases of purulent infection, without metastasis, the disease is
called pyaemia simplex, and in cases with metastasis, pyaemia
multiplex. The various conditions on which the metastasis may depend
are shown by Hueter, who says: "The metastatic abscesses of pyaemia
multiplex met with in the lungs, liver, spleen, and other internal
organs are regarded, with the greatest probability, as a result of the
embolic process. The metastatic inflammation of the serous membranes,
of the cellular tissues, and of the parotid glands, and probably also
a few metastatic inflammations of the internal organs, are at present
supposed to arise from a general inflammatory diathesis."[32] It has
already been shown by numerous experiments on animals that metastatic
abscesses in the lungs, liver, and other visceral organs only arise
after the introduction of ichorous pus, while healthy pus has
uniformly failed to produce these results.
[Footnote 33: Billroth's _Handbuch der Chirurgie_, S. 88.]
It now remains to be shown how the introduction of ichorous pus acts
in the production of pyaemia multiplex. The ichorous pus, having found
its way into the venous circulation, gives rise to the formation of
thrombi in the veins; these clots become more or less broken up, and
are carried forward by the blood to the right auricle; from this
auricle to the right ventricle; from this ventricle to the pulmonary
artery, and through its ramifications to every part of the lungs. In
the minute ramifications of this vessel are found wedge-shaped clots
of various sizes in different conditions, some softened and others
still firm. The possibility of these clots ever passing through the
lungs, and afterward being arrested in other visceral organs, has been
demonstrated on animals. It has been shown that fine particles of
foreign matter injected into the veins have passed through the lungs
and subsequently lodged in the liver. This theory enables us to
account, upon a mechanical basis, for the existence of the metastatic
abscesses in the liver which have apparently originated as the result
of primary infection.
In other cases these abscesses are supposed to arise from secondary
infection. Thus, ichorous pus, having found its way into the venous
circulation, produces primarily venous thrombi, which, as in other
instances, break up, the clots being carried in the same manner into
the terminal branches of the pulmonary artery, where they are
designated as emboli. The first action of the emboli is the mechanical
closure of these vessels, thus depriving the surrounding parts of
nutrition to a greater or less extent. It will be proper now to recall
the fact that the composition of these emboli is such as to favor
rapid suppuration; this commonly commences {965} in the clot and
surrounding tissues, having been preceded by a brief stage of
congestion and inflammation. There is also occasionally found around
these points more or less extravasation. The metastatic abscess thus
formed in the lungs is favorably situated for the production of
secondary infection. From this abscess thrombi arise in the pulmonary
veins, which become disintegrated, and are carried to the auricle,
thence to the left ventricle, and finally through the aorta, and find
lodgment in the terminal branches of the arteries of the various
organs, where they produce the characteristic lesions.
The organs which most frequently become the seat of this secondary
infection are the liver, spleen, kidneys, brain, and eyes.
Let us now briefly examine this mechanical theory. Do metastatic
abscesses arise from a single cause or from a combination of causes? I
am inclined to the opinion that the proximal cause of metastatic
abscesses in the visceral organs is the existence of emboli in the
terminal branches. The vitiated atmosphere surrounding the patient,
the existence of a wound, and the formation of ichorous pus are
conditions which should not be lost sight of. These are the elements
acting on the blood, producing in it morbid changes, and may therefore
be regarded as predisposing causes. The morbid conditions of the
blood, the increased number of white blood-corpuscles (possibly pus),
the disintegration and other changes in the red corpuscles, may be
regarded as the exciting causes of metastatic abscesses. It is thus
readily observed that emboli may form in the lungs and liver at the
same time, or the origin of those in the lungs may precede the
formation in other organs.
Is the formation of emboli in the terminal branches of arteries always
dependent on the disintegration of thrombi? The answer to this
question must, I think, be a negative, although in surgical practice
it rarely happens that the emboli take their origin from any other
cause. In the large majority of cases, unquestionably, the thrombi
primarily exist in the vicinity of the wound in which ichorous pus is
generated; but it not infrequently happens during the process of
disintegration that broken-up clots are carried forward by the current
of blood, receiving accretions on the way, until finally they fill a
large venous trunk. In confirmation of these facts relating to the
primary origin of thrombi, it is said to have been observed in
epidemics of puerperal fever, which were complicated with metastatic
abscesses of the visceral organs, that the thrombi occurred in the
pelvic veins. In case of wounds of the lower extremity the clot is
frequently found in the common iliac vein, although probably it should
always be regarded as a secondary formation. In rare cases the only
thrombi discovered at the autopsy are found situated far away from the
injury.
Observation fully establishes the fact that, after death from pyaemia,
pathological changes are much more frequently met with in the lungs
than in any of the other organs. This certainly strengthens the
embolic theory. Billroth mentions eighty-three cases of true pyaemia
multiplex, in which the metastatic abscesses occurred as follows:
seventy-five times in the lungs, seventeen times in the spleen, eight
times in the liver, and four times in the kidneys. Sedillot remarks
that in one hundred cases of pyaemia we find the lungs affected in
ninety-nine, the liver and spleen in eight, the muscles in seven, and
the heart and peripheric {966} cellular tissue in five cases. The
brain and kidneys are comparatively seldom involved.
The theory previously mentioned as the embolic relates to the
aggregation of fibrin into clots; but another theory has been recently
advanced by E. Wagner, who found in many cases the capillaries in the
lungs filled with fat, and was inclined, from the direction it
extended in these vessels, to explain a certain number of the pyaemic
cases by the fat emboli; but it has been shown that the existence of
the fat emboli in pyaemia is purely accidental and possesses no
significance. Pyaemia multiplex very frequently occurs without fat
emboli, and vice versa; either process may complicate the other, and
so the fat emboli may acquire special importance by obstructing the
respiration, and probably also in their way the embolic fat may serve
as a carrier of putrid material.
MORBID ANATOMY.--The external appearance of the body varies greatly.
The skin, in those cases in which the patient was jaundiced before
death, will be found in every part of the body to be of a dark orange
or dirty icteric tinge, but in other cases it may present a pale or
anaemic appearance. There are also sometimes found circumscribed
ecchymoses or purpuric patches, while the edges of ulcers or open
wounds are generally of a blackish or dirty yellow color. The lips and
finger-nails present a livid appearance; epithelial defects are
observed in the cornea, but these had their origin there before the
death of the patient.
The eyes in some cases are sunken deeply in their sockets, and where
the disease has been protracted there is often very great emaciation.
Rigor mortis is commonly well marked after a few hours. When death
occurs from puerperal pyaemia there are generally found some
indications of the recent parturition, although the principal
lacerations or injuries may be confined to the womb. All fluids
disappear from external wounds before the death of the patient, and
they remain dry afterward.
In some cases the cellular tissue is the seat of diffuse suppuration.
The pus formed is thin, fetid, and unhealthy. This suppuration is
limited to certain parts of the body, as an injured extremity, or, as
frequently happens, it may be found on the trunk and limbs at the same
time. The pus in this form of suppuration is exceedingly apt to
burrow, on account of the peculiarities of the tissue in which it
occurs, and also the condition of the surrounding structures,
especially the relaxed and flabby condition of the skin. These
abscesses in some instances are superficial, in others deep-seated.
There are few changes which occur in the muscles, and these are not
uniform or constant. They are occasionally the seat of abscesses,
which have been observed in the heart, tongue, and other organs. The
muscles may be of a light-brown or greenish color when they have been
covered a considerable time with pus, and are sometimes softened and
pultaceous. Suppuration may also take place beneath the fascia of the
tendons.
The brain and its membranes are frequently found in a perfectly
healthy state after death from pyaemia, although when the diseased
process has extended during the life of the patient to the lungs and
pleura, giving rise to great dyspnoea, there will generally be
observed some congestion of the membranes, an increased quantity of
fluid in the brain-substance and ventricles, and also an increased
fulness of the meningeal veins and sinuses. Occasionally there have
been observed suppurative {967} meningitis, blood extravasations on
the surface of the brain, lymph-deposits on the membranes, softening
of the cerebral tissues, and circumscribed abscesses in the substance
of the brain, which in some cases have been traceable to embolism of
its vessels. The changes in the spinal cord and its membranes are
probably similar to those found in the brain, but these parts appear
to have been rarely examined.
Virchow found emboli of the retinal and choroidal vessels. Heiberg
found these vessels occluded with colonies of micrococci. There have
also been observed opacity of the cornea, sloughing of the
conjunctival epithelium, suppurative infiltration into the periphery
of the vitreous body, and deposits of pus in Petit's canal and in the
anterior and posterior chambers. Pyaemic ophthalmia has been observed
somewhat frequently in puerperal cases, especially when preceded by
endocarditis, with deposits on the semilunar or mitral valves. In
surgical cases it is rarely seen.
Toynbee "relates several cases of purulent infection following
suppuration of the ear. Cases of disease in the mastoid cells
terminate fatally, he says, from two different causes: first, from
purulent infection, arising from the introduction of pus into the
circulation through the lateral sinus; second, from disease of the
cerebellum or its membranes. Cases of purulent infection, he further
remarks, have not been met with where the disease occurs in the
tympanic cavity."[34]
[Footnote 34: Braidwood on _Pyaemia_, pp. 168, 169.]
Numerous lesions of the osseous system have been noted in pyaemia,
probably from the fact that this disease results very frequently in
cases of bone-lesions, but these changes have very little diagnostic
importance. The following have been observed: thickening or
infiltration of the periosteum, which may be found to separate readily
from the bone after the death of the patient, or there may be pus
found between the periosteum and the bone. In the bone-structure there
were found caries and necrosis, "while in other cases the whole
thickness of the compact tissue is perforated in a honeycomb-like
manner by minute cavities filled with thickish pus or caseous matter
of a pinkish-white color."[35] "To sum up, the chief morbid
alterations met with in the bones are congestion, dilatation of the
Haversian canals and cancellated tissue, tending to abscess formation,
and the excavation of the cavities by the unhealthy pus."[36]
[Footnote 35: _Ibid._, p. 192.]
[Footnote 36: _Ibid._, p. 194.]
The pathological lesions of the joints commence with marked congestion
of the synovial membranes and increase in the synovial fluids, and
afterward the fluid is mixed with pus; these conditions are followed
by erosion of the cartilage and ligaments, the former thus becoming
separated from the bone. Both the small and large joints are
occasionally the seat of morbid changes.
The parotid gland is occasionally the seat of a secondary inflammation
during the progress of pyaemia, and this may endanger life by
interfering with respiration and deglutition. The lymphatic glands are
only secondarily affected, and even this takes place very rarely. The
changes in the glandular system, when observed, are similar to those
which happen in other tissues of the body--viz. congestion,
inflammation, and suppuration.
The arteries are usually found empty after death from this disease,
and the coats are sometimes apparently thickened. The veins, on the
contrary, are commonly found filled, or even distended, with firm
fibrinous clots. They are sometimes also found inflamed or altered,
although more {968} commonly healthy. The distended condition of the
veins gives rise to the cord-like feeling often mentioned by different
observers. In some cases of phlebitis there may be pus deposited
between the coats of these veins. The most important pathological
changes are found in the blood. These changes occur early in the
disease, become more marked toward its fatal termination, and may be
always studied after death. It is generally admitted that pus is
frequently found in the blood of these patients; but it has been shown
by numerous experiments that healthy pus never produces the
pathological changes which characterize this disease. Pyaemia is only
produced by the presence in the blood of ichorous pus or some other
decomposing animal substance, or some material having its origin in
the decomposition of the same, and no decomposition in these
substances is ever effected except through the agency of living
organisms. It therefore follows that the discovery of living organisms
in the blood of those sick and dead of this disease has given a
renewed interest to the study of its pathology. The recent
investigations made by Pasteur, Koch, Birch-Hirschfeld, and the London
Pathological Society show conclusively that in all cases of pyaemia
and septicaemia organisms are present in the blood during the entire
course of the disease, and that in the former there is found the
globular, and in the latter the rod bacteria. It has further been
observed in each morbid condition that the severity of the disease is
always increased in proportion to the increase of the organisms in the
blood, and that the bacteria found within the body are of the same
species as those in the wound from which they have gained admission.
The micrococci found in the blood of pyaemic patients are surrounded
by the decomposed products of the red and white corpuscles, which
appear in the blood-plasma in the form of pale granular bodies. There
is likewise in this disease an increased coagulability of the blood,
and it steadily increases as the disease progresses. In this condition
there may be found in the blood-vessels both thrombi and emboli. The
thrombi are occasionally observed as firm fibrinous clots, but they
may be likewise found in the rapidly fatal cases to have undergone
suppurative changes. These changes begin in the centre of the clots,
which often contain true pus or a greenish or puriform fluid.
The pericardium may contain a small amount of serum tinged with blood,
but it is seldom covered with recent lymph. Both the lung-tissue and
pleurae are commonly inflamed in this disease. The costal and visceral
layers may be agglutinated by old adhesions, but are more commonly
united together by recently formed lymph. The pleural cavities often
contain some opaque, muddy, sero-purulent fluid, mixed with blood and
having masses of lymph floating in it.
The lungs are more frequently the seat of metastatic abscesses and
other morbid changes in pyaemia multiplex than any other organs of the
body. There may be found emboli in the branches of the pulmonary
veins, and in the lung-tissue metastatic abscesses surrounded with
capillary congestion and other evidences of inflammation; "The smaller
vessels, trying to overcome this afflux of blood, may produce
ecchymosis or extravasation beneath the lining membrane of the
air-vesicles, but the minute capillary congestions are generally
observed as red points studded over the pulmonary surface, which by
and by exhibit yellowish-white or bluish-white centres. While one
part, generally the lower half of the {969} lung, is thus hepatized,
solid, and of a dark greenish color, the remainder of the lung is
emphysematous and more or less oedematous. A section of the former
presents the same appearance as is observed in the lungs of pneumonic
patients. Whether these incipient abscesses are developed from the
minute points of congestion before mentioned, by the breaking down of
the thrombic clots in their centres, or whether the pus is developed
out of the serum exuded by the walls of the engorged capillaries,
cannot be easily determined, and has as yet not been decided. These
secondary abscesses vary in size from that of a hemp-seed to that of a
hen's egg."[37] These are generally situated on the periphery of the
lungs and in the lower lobe, although in some cases they are found
imbedded deeply in the pulmonary tissue. The contents of these
abscesses are similar to those found in other parts of the body in
this disease. The bronchial mucous membrane is commonly of a bright
pink color, while its secretion is increased in quantity, and may be
clear and frothy. These changes are the result of acute bronchial
catarrh. Lobular pneumonia has been frequently observed as a
complication of pyaemia, and is supposed by some authors to be caused
by the vitiated condition of the blood; but probably it is more
frequently occasioned by infarctions and embolic abscesses, which have
been previously mentioned in this connection.
[Footnote 37: Braidwood, _op. cit._, p. 173 _et seq._]
Billroth and Sedillot observed pathological lesions involving a
solution of continuity in the spleen, liver, and kidneys, in the order
in which they are mentioned; other authors, however, assert that the
liver, next to the lungs, is the most frequent seat of purulent
deposits. Enlargement of the spleen is frequently met with in cases of
pyaemia multiplex. The metastatic abscesses found in the spleen and
kidneys are much smaller than those found in the lungs and liver, but
in other respects are of a similar character. The capillary congestion
and the accompanying infarctions require no special attention here.
The liver, like the spleen, is sometimes enlarged, and at other times
is found to have undergone fatty degeneration to a greater or less
degree; in which condition its tissues are generally soft and friable.
Abscesses in the liver are so much like those in the lungs as to need
no separate description. The same may be said of other pathological
changes found in this organ in pyaemia multiplex. The abscesses found
in the kidneys vary from the size of a hemp-seed to that of a bean,
and are surrounded by the usual zone, marking more or less definitely
the extent of the inflammation. The capsule is generally healthy.
There are also, in very rare cases of this disease, abscesses found in
the stomach and intestines, involving the thickness of the mucous
membrane; and it is further supposed that these abscesses may be found
occasionally on any portion of the mucous membrane lining the
alimentary canal. Post-mortem examinations in pyaemia multiplex have
established the fact that there is no organ in the body that may not
become the seat of pathological lesions in this disease; but there is
unquestionably a vast difference in the relative frequency of these
changes in the various organs. In some instances of this disease
peritonitis is developed, with its concomitant changes in this
membrane and the abdominal fluid, which is generally increased in
quantity and sometimes slightly tinged with blood, but more frequently
remains clear. {970} This inflammation is commonly dependent on an
extension of the inflammatory process from a metastatic abscess, which
may be situated near the periphery of some organ covered with
peritoneum, although it is claimed that pleuritis occasionally occurs
in connection with pyaemia independent of metastatic abscesses in the
lungs.
The careful study of the pathology of pyaemia multiplex renders it
exceedingly probable that the immediate agency in the production of
all these lesions is the presence in the blood of a particular species
of living organism, and that all the morbid changes which occur in the
visceral organs are secondary to those which take place in the blood,
but that the former are only dependent on the latter in a minor
degree. The pathological changes effected by these organisms seem to
be as follows, and to occur in the following order: viz.
disorganization of the blood, especially a destruction of the red and
white blood-corpuscles; the formation of granular bodies around the
organisms out of this debris; the production of an increased
coagulability of the blood; the lodgment in the blood-vessels of these
granular bodies, which are increased in size by a deposit of fibrin;
these obstructions occur most frequently in minute ramifications of
the pulmonary arteries; nutrition is effected locally by these
infarctions, and generally by the vitiated condition of the blood,
which enables the organisms under these favorable circumstances to
penetrate the adjacent tissues and produce the metastatic abscesses
and other accompanying lesions.
The pathological changes in pyaemia simplex are of the same kind as
those which have just been described as characterizing pyaemia
multiplex, with the exception of the metastatic abscesses, which are
always absent. Furthermore, the disease in both instances is believed
to have its origin from the same causes, and the dissimilarities in
the pathological lesions are equally susceptible of a rational
explanation, as are those of scarlatina simplex and scarlatina
maligna.
There were reported by the committee of the London Pathological
Society some interesting details pertaining to this form of pyaemia.
Their report shows that among the one hundred and fifty-five cases
classed as pyaemia there were twenty-four cases without visceral
abscesses; and furthermore it shows that in twenty-three of these
cases there was no suppuration, although local inflammations affected
many of the different tissues, since these patients suffered with
arthritis, cellulitis, pleuritis, meningitis, pericarditis, and
carditis. It is also added that "the post-mortem appearances, in
addition to the local secondary inflammation before noted, were in
many cases those changes common to all forms of blood poisoning. Out
of the twenty-four cases, the following are noted: Swollen spleen,
nine times; congestion of the lungs, ten times; swollen liver, six
times; cloudy swelling of the kidney, fourteen times."[38]
[Footnote 38: _Trans. London Pathological Soc._, vol. xxx. p. 26.]
In this form of pyaemia it has been supposed by some authors that the
materies morbi occasionally produces death before the metastatic
abscesses have had time to develop, but this is not always the case.
The same committee report on the above-mentioned twenty-four cases, on
this point, as follows: "The duration of the cases before the fatal
termination was very various. It is tolerably accurately recorded in
eighteen cases: of these five died in the first week, five in the
second, {971} four in the third, and the remaining four survived to
the thirtieth, forty-ninth, fifty-second, and sixty-second days."[39]
[Footnote 39: _Trans. London Pathological Soc._, p. 25 _et seq._]
The pathology of pyaemia multiplex having been already fully
described, and since the only essential difference in these morbid
conditions consists in the complete absence of the metastatic
abscesses in cases of pyaemia simplex, it is therefore thought
unnecessary to dwell here longer on this subject.
The morbid anatomy of septicaemia has been carefully studied of late,
and it is now known that the most characteristic lesions are found in
the blood and the alimentary canal.
As a manifestation of the general poisoning of the blood, it might be
expected that putrefaction would follow rapidly after the death of the
patient. In fact, Davine defines septicaemia as "putrefaction of a
living body." Observation has now thoroughly confirmed that which was
formerly an anticipation. Panum, Hemmer, and Bergmann have each called
attention to the fact that rapid decomposition follows the death of
all animals in which septicaemia has been produced for experimental
purposes. It has also been observed that putrefaction in the human
cadaver begins much sooner, and progresses much more rapidly, under
similar circumstances, when the death has been produced by this
disease than when it has occurred from any other cause. Furthermore,
this rapid decomposition is not limited to the internal organs, but
may be frequently strongly marked on the surface of the body after the
lapse of twelve hours, although it has been kept in a comparatively
dry and cool atmosphere. In those cases where the septicaemia has
originated in an external wound it has been uniformly observed that
putrefaction goes on most rapidly in the vicinity of the wound after
the death of the patient.
In every case of fatal septicaemia the post-mortem examination will
show that the coagulability of the blood has been diminished or
destroyed. In fact, it has been abundantly shown that in all cases of
true septicaemia the coagulability of the blood is more or less
diminished. The few imperfect clots of blood found after death are of
a deep-black color. The putrefaction of the soft tissues is greatly
hastened by the presence of this blood; and, consequently, this
process goes on most rapidly in the most dependent portions of the
body, especially along the course of the large veins. The septicaemic
blood possesses a peculiar putrefactive odor, and it is occasionally
found to be acid in its reaction, according to Vogel and Scherer,
making it highly probable that it will end in the formation of the
carbonate of ammonium. The chemical examinations of septicaemic blood
which have heretofore been made have completely failed to give
satisfactory results in regard either to the existence or nature of
the materies morbi in this disease, although, without doubt, there has
occasionally been found, principally in the blood of those who have
died of acute septic intoxication, a poisonous substance, which
Bergmann designated sepsin. Microscopic examinations have shown that
in the blood and also in various organs of those who have died of
septicaemia there are always present, under these circumstances, a
large number of the rod bacteria; in fact, they are more numerous than
after death from any other infectious disease. Furthermore, they are
found in the blood, lymph-glands, and cellular tissues during the
whole course of the disease.
{972} There are no pathological changes in the central nervous system
which arise directly from septicaemia, although in some cases, when
there has been some cardiac complication or very severe dyspnoea from
any cause immediately prior to the death of the patient, there may be
found hyperaemia of the membranes of the cerebro-spinal axis. The
brain and spinal cord remain unchanged.
The endo- and pericardium occasionally present a somewhat mottled
appearance resembling ecchymosis, which is evidently a deposit from
the blood, and may be washed off with water. The inner surface of the
ventricles presents a similar appearance from the same cause. In
addition to those changes which have been mentioned there are
occasionally found some slight traces of an inflammatory process in
these parts; but it never extends to the formation of pus or
ulceration, which frequently happens in cases of pyaemia. The quantity
of pericardial fluid is sometimes increased in septicaemia, and is
generally somewhat thickened, cloudy, and slightly tinged with blood.
The changes in the pleural surfaces are the same as those which have
been noted in the pericardium, but any increase of the fluid within
the pleural sacs is an exception to the general law, and is very
rarely seen. The lungs are generally found slightly congested, but
there may be some ecchymosis in exceptional cases. Pus is never found
in the lungs or within the pleural cavities in pure unmixed
septicaemia. The pathological changes in the liver resemble those in
the lungs. This organ is commonly found in a state of passive
congestion, while the color of its tissues is slightly darkened. The
congestion of the kidneys and spleen in this disease is much more
marked than that of the lungs and liver. The parenchymatous tissue of
the kidneys is commonly found in an oedematous condition, and the
tubuli uriniferi are more or less affected by a catarrhal
inflammation, which is manifested by the exfoliation of granular
epithelium. The same catarrhal condition, but in a milder form, is
found to affect the mucous membrane of the bladder. In females the
ovaries, uterus, and vagina are in a state of hyperaemia, with more or
less catarrhal inflammation of the latter organ. Septicaemia
invariably causes pregnant females to abort. There is commonly
softening of the spleen. The alimentary canal is almost constantly
affected by acute intestinal catarrh, with enlargement of the
intestinal follicles and mesenteric glands, while there are frequently
hemorrhages from the serous and mucous membranes. The various muscles
of the body and the extremities are found to be of a dark brownish-red
after the death of the patient, instead of possessing their natural
pale-red color. It may now be stated, finally, that the pathological
changes in septicaemia are less marked than those of pyaemia
multiplex.
The semiology, etiology, and pathology of septo-pyaemia consist in a
blending, in different degrees, of the essential parts of pyaemia and
septicaemia; and since the pathology of both these diseases has been
presented separately, it is deemed unnecessary to enter into a
consideration of this combination.
SYMPTOMS OF PYAEMIA.--Pyaemia very rarely, if ever, develops except in
connection with an open suppurating wound, and consequently it must
generally be regarded as a wound complication or as a secondary
diseased condition. Those open wounds are unquestionably the most
favorably situated for the development of this disease which involve
the medullary {973} cavities of the long bones, owing to the liability
of unhealthy suppuration, the difficulty of complete drainage, and the
favorable anatomical conditions for absorption.
Every form of pyaemia is frequently preceded by a distinctly marked
prodromal stage, which varies in duration from four days to two weeks.
In fact, the ordinary precursor of this disease, in all those cases in
which the bones are involved, is an attack of osteo-myelitis; but in
other cases the patient often complains of malaise, giddiness,
headache, pain in the limbs, weakness, and loss of appetite, while the
experienced surgeon will be deeply impressed with the patient's rapid
emaciation and cadaverous face. These symptoms are soon followed by
jaundiced skin, etc. The commencement of an attack of pyaemia is
commonly manifested by a chill. The importance which will naturally be
attached to this phenomenon in connection with an open wound must
depend to a certain degree on the circumstances attending its
occurrence; and therefore the following question will present itself:
Is the chill associated with suppuration? A negative answer to this
question, based on the fact that insufficient time has elapsed since
the occurrence of the injury to render suppuration possible, can never
fail to be a source of satisfaction to the surgeon, whose experience
has taught him to dread pyaemia.
Billroth has observed in 83 cases of true pyaemia multiplex that 62
commenced with a chill, and 21 without; in 81 cases of septicaemia and
simple pyaemia 24 commenced with a chill and 57 without. The number of
chills in each individual patient occurred according to the following
table:
Number of patients 19 21 14 15 9 5 2 3 4 1 1 1
Number of chills 1 2 3 4 5 6 7 8 9 10 13 14
In one patient during three weeks sixteen chills were observed, and
probably the longer the duration of the disease the greater is the
number of chills. Still, there are chronic cases with a single chill,
and acute cases with many. It rarely occurs that a patient has more
than one chill in twenty-four hours. Billroth noticed among his
patients only sixteen who had two chills, and only six who each had
three chills, in one day. The experience that fewer chills occur
during the evening and night than in the morning and afternoon has
been confirmed by statistics. Among 287 chills, 220 occurred from 8
A.M. to 8 P.M., while during the night, from 8 P.M. to 8 A.M., only 67
were observed. By this arbitrary division of the twenty-four hours
Billroth desired to take into consideration the daily exacerbation in
connection with the usual daily irritation of the wound, the
bandaging, and other manipulations. He saw, for example, a chill occur
three times from the introduction of a sound, and twenty times after
the opening of an abscess. The time which elapsed from the first
injury to the first chill is shown in the following table:
First chill began, times 14 19 15 9 4 3 2 4
Length of time after injury, in weeks 1 2 3 4 5 6 7 8
Patients who had fever before the operation were more inclined to
early chills than recently-injured healthy individuals. Billroth's
experience was to have only the first chill before the end of the
first week. It may be further stated that nervous, irritable patients
suffer much more {974} frequently from chills than those of a
phlegmatic temperament. This fact has given rise to the opinion that
the absorption of pus acts especially on the central nervous system.
The chills in pyaemia are supposed by Billroth to be associated with
inflammation, and he says: "It must be mentioned, as a matter of
observation, that chills occur almost exclusively in the commencement
of an acute inflammation, and are intermittent only in intermittent
fever and reabsorption of pus, while they do not occur in acute
septicaemia."[40] But the fever in pyaemia rarely intermits entirely;
it is generally lower, however, in the morning than in the afternoon.
This symptom is even more important than the rigors in enabling the
surgeon to make a correct diagnosis. Let it, however, be remembered
that the temperature frequently becomes very high within a few hours
after the receipt of an injury or the performance of a surgical
operation; that this high temperature may be due to septic absorption,
and that this diseased condition is what we designate as septicaemia.
Another condition, less marked, with an elevated but somewhat lower
temperature, is usually spoken of as traumatic fever. In this
condition the fever may gradually increase for a few days, and then
disappear.
[Footnote 40: _Surgical Pathology_, p. 344.]
One important peculiarity of the temperature in pyaemia are the sudden
and great changes; thus, at one hour the temperature may be slightly
raised above the normal, and at the next the thermometer may mark 105
degrees F. These sudden changes of temperature are of frequent
occurrence, are not observed to the same extent in any other disease,
and therefore supply a very important diagnostic indication. It is
impossible to know, or even to anticipate with any degree of
certainty, when the highest temperature will exist; consequently,
Billroth and other writers have suggested the desirability of having a
thermometer constantly kept in a position to indicate every change in
the heat of the body, and a careful attendant to note the same; but,
thus far, I am not aware that this has been attempted, probably on
account of the inconvenience to the patient and the additional labor
in nursing it would entail. It has been further observed that during
the existence of a chill the temperature continues to steadily
increase, and the maximum seen during the whole course of the disease
is attained during the hot stage which immediately follows the rigors.
"This condition is followed by profuse cold perspirations. The
perspirations which accompany this disease are most profuse, like
those of advanced phthisis. They never precede the rigors, but may
occur independently of them. They are either continuous in their
duration, or exhibit more or less distinct exacerbations. They are
occasionally accompanied by sudamina, and they do not abate with the
use of any known remedy.... Occasionally perspiration is scanty; but
before death a cold clammy sweat and a tawny discoloration of the skin
occur."[41]
[Footnote 41: Braidwood, _op. cit._, p. 112.]
Besides the sudamina there are frequently observed on the skin
vesicles, pustules, and boils, purpuric patches, and various
discolorations. There is frequently observed to arise in the
neighborhood of the wound a reddish erythematous blush, which soon
extends to the whole limb, and commonly begins to disappear in the
early part of the second week. This recently occurred to a patient
under my care, and was speedily followed by an abscess of the
knee-joint. The wound was situated at the hip-joint, {975} and the
first change in the color of the integument took place around its
lips. The redness extended rapidly downward until it covered the foot,
and even the toes; but the extension upward was slight, not much above
the nates, on which there was situated at the time a bed-sore. It
observed the same order in passing off as in coming on--_i.e._ where
it first made its appearance it first disappeared. The superficial
veins leading from the wound were inflamed and cord-like. This
condition of the integument and the abscess of the knee-joint were
followed by diarrhoea, on which medicines had no beneficial effect. It
continued, with occasional vomiting, until the death of the patient.
The pulse in pyaemia may be nearly normal as regards frequency, while
at other times very rapid. It has been remarked in some cases that the
pulse seldom rose above 90 per minute until near death. The pulse,
although only moderately accelerated at the commencement of the
disease, always becomes more rapid, quick, feeble, and irregular
toward the termination of the unfavorable cases, while in cases of
recovery it returns gradually to the normal standard.
In all cases in which the blood has been examined during the progress
of pyaemia the examiners have agreed in regard to its extreme
coagulability, the diminution of the number of red corpuscles, and the
increase of the granular spherical bodies. The red corpuscles, even in
the earlier stages of the disease, show evident indications of
disintegrating; and these become more and more marked as the disease
progresses, while there is a steady increase in the number of pus- or
possibly of white blood-corpuscles. Epistaxis occasionally occurs, and
also venous oozing from the wound.
The condition of the tongue in pyaemia may be regarded as an important
symptom, indicating the state of the alimentary canal--not, however,
during the prodromal stage, but after the disease has progressed a few
days. It is then observed that the tongue has become peculiarly
smooth, dry, and often excessively red. This smoothness is caused by
the collapse of the papillae, and the dryness by a diminished
secretion. The organ now frequently appears as if covered with a thin
layer of collodion which had been caused to dry on the surface, so as
to present a glazed look. Again, the tongue may be covered with brown
crusts and the teeth with sordes. These brown crusts and sordes are
usually seen in advanced cases, following the first condition
described. Much importance is attached to these brown crusts by many
experienced surgeons, and although there may be very marked
improvement in all other symptoms, still they insist on a very guarded
prognosis until the tongue has assumed a healthy appearance. Aphthae
on various parts of the mouth and pharynx are frequently present in
the more chronic cases, but are usually absent in acute cases. Herpes
of the lips sometimes occurs in the commencement of the disease.
Vomiting is comparatively rare, but there is, even in the early
stages, a complete failure of the appetite, with great thirst.
Singultus is rarely present in genuine pyaemia, but frequently so in
septicaemia, and occasionally in septo-pyaemia. Diarrhoea is not so
frequent or the stools so copious in pyaemia as in septicaemia.
Billroth observed in one hundred and eighty cases of pyaemia
thirty-two cases of diarrhoea. It is impossible to determine whether
those cases in which the diarrhoea {976} occurred were pure or mixed
pyaemia. The stools are often of a pappy consistence, and passed
involuntarily in bed. There are, however, severe cases of pyaemia with
high fever, and accompanied by obstinate constipation.
Examination of the heart may, in rare cases, show the existence of
pericarditis, although usually the only indications of disease are the
too feeble sounds. Auscultation and percussion of the lungs may yield
unsatisfactory results when the metastatic abscesses are small and
scattered, for the same reason as in miliary tuberculosis. The large
deposits in the lungs are by these means readily determined. There may
be a sensation of suffocation, the pneumonic sputa, the friction sound
of pleurisy, or the signs of pleuritic effusion; and the existence of
these symptoms or signs would naturally aid in the diagnosis of
metastatic abscesses.
Enlargement of the liver and spleen may be determined before death,
and in connection with other symptoms would aid in diagnosing deposits
in these organs.
The urine in the first stage of this disease is scanty, high-colored,
contains a large amount of salts, and is of a high specific gravity.
Epithelial, fibrinous, and blood casts, and also albumen, are
occasionally found in it during the course of the disease. Billroth
mentions a case in which there was complete suppression, with uraemia.
In many cases of pyaemia suppuration of the joints, one after another,
takes place with great rapidity and with comparatively little pain,
but occasionally some swelling, redness, etc. are present. In most
cases these suppurations are easily diagnosed. Instead of suppuration
taking place in the joints, there are cases in which it occurs in the
cellular tissue; and I have recently seen a case where abscess after
abscess formed with such rapidity that within a single week the
patient was literally covered with abscesses from the crown of his
head to the soles of his feet.
Delirium generally exists during some stage of the disease, more
frequently the last, and is then mild in its character, although
active delirium has been observed in the first stage. Patients are
low-spirited and very apprehensive of death. The face at the beginning
of the attack may be flushed or pallid, but toward the end it always
becomes careworn and haggard. The breath occasionally has a sweetish
or purulent odor.
The changes in the wound are in some cases very marked, even in the
first stage of the disease. The suppuration, which has been previously
free and healthy, may be suddenly checked, the wound becoming dry. The
discharge, if it continues, becomes scanty, thin, ichorous, or
greenish. The granulations, if previously healthy, may soon slough.
These changes may not always appear in the first stage, but should
they not then take place they may be expected later in the disease.
SYMPTOMS OF SEPTICAEMIA.--These are commonly developed within
twenty-four hours after the receipt of an injury or the performance of
a surgical operation, and they may be sketched as follows: Frequent
pulse; tongue, lips, and throat dry; skin hot and the temperature of
the body high. The patient replies accurately to questions, but with
some hesitation. He is much inclined to sleep, has entirely failed to
take nourishment, drinks frequently when aroused from his lethargic
condition, and has vomited everything taken into his stomach since the
receipt of the injury or the performance of the operation. If {977}
the dressings are now removed from the wound, the foul odor of
putrefaction greets the attendants. In cases of amputation-wounds
considerable discoloration of the flaps may be observed, the edges
being blackened. Above these blackened edges the integument is
reddened and slightly oedematous. The wound having been closed with
sutures, which are now removed, there escapes a few drachms--possibly
ounces--of highly offensive fluid, the decomposed remains of blood,
etc. A further examination of the flaps on their inner surfaces show
that their capillary circulation has ceased. The tissues, instead of
presenting a life-like appearance, are now of a very dark color and
occasionally mottled with dull grayish spots, although the movements
of the ligature at the point where it embraces the femoral artery, for
example, show that the blood still rushes against the artificial
boundary.
Let us now leave our patient, without further comment, for the next
forty-eight hours, when we will resume the examination. We now find
the same dryness of the mouth that was previously noticed; the pulse
is more frequent, and has become very feeble; he complains of much
thirst, has vomited frequently, and has taken very little nourishment,
and that only at the earnest solicitations of the attendants. The
temperature is higher than at the former examination, and has been
steadily increasing; in the morning it is lower, however, than in the
evening of the same day. The patient is lethargic, and is suffering
with a profuse diarrhoea. The odor of the stools is highly offensive;
they are properly described as rice-water evacuations. The abdomen is
tympanitic; the body bathed in perspiration; the respirations rapid;
the urine scanty, high-colored, and contains albumen. The examination
of the stump shows that gangrene has extended rapidly, involving not
only the flap, but a portion of the adjacent tissues. The stench
arising from the wound is almost stifling. The decomposing fluids are
continually forming. That portion of the thigh not already gangrenous
is now very oedematous, and the integument covering it is much
discolored, being of a dark, icteric, or reddened hue.
We now allow twenty-four hours to elapse, and then make our final
examination. The patient's tongue is more moist; the body still bathed
in perspiration; the eyes dull; the conjunctivae icteric, and the same
hue extends to the body, though in a less marked degree; the pulse has
become very frequent, feeble, and not easily counted; the temperature
is below normal. Singultus is now present, and has been so during the
last twenty-four hours. Bronchial symptoms, combined with marked
oedema of the right lung, have appeared; the diarrhoea continues the
same; the gangrene is still extending.
It must be admitted that the report here offered shows only the
symptoms that are found in a single class of cases. The symptoms vary
greatly in different cases, but they are especially marked in the
acute sepsis mentioned by Massanneuve under the head of _gangrene
foudroyante_. In these cases there appears, immediately after the
receipt of an injury, enormous oedema about the wound, which extends
rapidly in every possible direction, followed by the death of the
patient within a few hours unless prompt measures are adopted. The
puncture of the cellular tissue or of the blood-vessels involved in
the oedema prior to the death of the patient gives rise to the escape
of a highly offensive gas. Roser mentions a case of this disease in
which he promptly amputated {978} the limb of the patient through the
healthy parts, without even waiting for the administration of an
anaesthetic, and his patient recovered.
The symptoms of septicaemia must necessarily depend greatly on the
condition of the patient and the amount of septic material introduced,
but it is not deemed necessary to dwell longer on this subject.
DIAGNOSIS.--It is thought that a brief presentation of the
etiological, pathological, and semiological differences may be
advantageous to busy physicians who desire to obtain, with the least
expenditure of time, an accurate knowledge of the chief points of
distinction between these morbid conditions. This effort at
differentiation is merely intended to place the most important
characteristics in marked contrast; and consequently it should be
remembered that it is not our intention to give here the complete
etiology, pathology, or semiology of either of these morbid states,
but only their essential differences. Furthermore, it is thought that
the following arrangement will facilitate the object which we desire
to accomplish:
ETIOLOGY.
PYAEMIA. | SEPTICAEMIA.
1. Pyaemia generally commences | 1. Septicaemia generally
with the putrefaction in an | commences with the
open wound of the secondary | putrefaction in an open wound
wound-fluids--pus, etc.--in | of the primary
which there are developed | wound-fluids--blood, serum,
globular bacteria, which enter| etc.--in which there are
the blood and certain tissues | developed rod bacteria, which
of the body, where they | enter the blood and certain
multiply and produce | tissues of the body, where
constitutional disturbances. | they multiply and produce
| constitutional disturbances.
2. Pyaemia is commonly preceded | 2. Septicaemia is commonly a
by some local inflammatory | primary wound-complication,
wound-complication, such as | which is generally developed
suppurative periostitis, | within forty-eight hours after
osteo-myelitis, etc., and is | the receipt of the injury.
rarely developed before the |
end of the second week after |
the receipt of the injury. |
PATHOLOGY.
1. Increased coagulability of the| 1. Diminished coagulability of
blood. | the blood.
2. There are metastatic abscesses| 2. Complete absence of purulent
in various parts of the body, | or ichorous deposits in all
especially in the lungs, | cases of unmixed septicaemia.
liver, and kidneys: serous | Post-mortem appearances may be
cavities frequently contain | completely negative, with the
sero-purulent deposits; | exception of the condition of
similar deposits are often | the blood, although there is
found in the joints; abscesses| often some oedema of the
in the cellular tissue; and | lungs.
also abundant evidence of the |
existence during the life of |
the patient of pyaemic endo- |
and pericarditis. |
SEMIOLOGY.
1. Pyaemia commonly commences | 1. Septicaemia commonly commences
with a chill. | without a chill.
2. Fever variable, but rarely | 2. Fever steadily increases, but
entirely intermits. | is lower in the morning.
3. Sudden and great changes in | 3. The temperature is high at the
temperature, followed by | beginning of the disease,
profuse perspiration. | increases until near the fatal
| termination, when it falls
| below the normal. The skin is
| moist, but without profuse
| sweatings. {979}
4. Pulse variable; toward the | 4. Pulse rapid, and gradually
fatal end rapid, feeble, and | increases in frequency toward
irregular. | the fatal end.
5. Facies at the beginning | 5. Facies expressive of a dull,
flushed or pallid, toward the | listless condition throughout
end careworn. | the whole course of the
| disease.
6. Tongue smooth, dry, and | 6. Tongue, lips, and throat dry
excessively red, later | at the commencement, toward
brown-coated, and even the | the end moist. Thirst is
teeth coated with sordes. | marked.
7. Diarrhoea with stools of a | 7. Rice-water evacuations, very
pappy consistence. | offensive; obstinate vomiting.
8. Epistaxis. | 8. Epistaxis rarely occurs.
9. Mild delirium toward the fatal| 9. A lethargic condition from the
end. | beginning, increasing toward
| the fatal end.
10. Aphthae in the mouth and |10. Icteric hue of conjunctivae;
throat, sudamina, vesicles, | singultus often present.
pustules, and purpuric |
patches. |
The differences in the local manifestations occurring in and around
the wound, during the progress of these diseases, may be summed up as
follows:
At the commencement of this | The odor of putrefaction is
disease the suppuration is | commonly very marked within
commonly checked, the wound | twenty-four hours after the
becoming dry, and if a discharge | receipt of the injury, the
continues, it becomes scanty, | integument slightly reddened
thin, ichorous, greenish, etc. | about the wound, and the
The granulations, when previously| surrounding parts somewhat
healthy, soon slough, and venous | oedematous. The wound-tissues
oozing sometimes takes place. | soon assume a dark-brown color,
There occasionally appears in the| and are occasionally mottled
later stages of this disease | with dull grayish spots, while
around the wound a reddish | the edges of the wound are at
erythematous blush, which soon | the same time blackened,
extends over the whole limb. | although the movements of the
| ligature, when arteries have
| been tied, show us that the
| blood still rushes against its
| artificial boundary.
TREATMENT.--It must be admitted that the management of either pyaemia
or septicaemia, when fully developed, is always unsatisfactory, and
generally unsuccessful; consequently, the success which has attended
the use of the prophylactic measures employed in connection with the
treatment of wounds during the last ten years has given much
satisfaction to the medical profession. The committee of the London
Pathological Society reports as follows on this subject: "The
accumulation of septic matter in the uterus after labor, in contact
with the raw surface left by the separation of the placenta, would
also present the conditions favorable to acute septic intoxication. In
the present day, when the necessity of thorough drainage of wounds is
so thoroughly understood, and the means at the surgeon's command for
carrying it out are so efficient, it can only be under peculiar
circumstances that a sufficient quantity of putrid serum or pus to
yield the fatal dose of the septic poison is allowed to accumulate in
the wound. Moreover, the antiseptic treatment of wounds, now so
largely adopted, by preventing decomposition of course renders septic
intoxication impossible. Ovariotomy would seem to furnish conditions
most favorable to septic intoxication, and a large proportion of the
deaths occurring in the first forty-eight hours {980} have always been
attributed to it. The proportion of fatal cases from this cause has,
however, of late been greatly diminished by drainage, and more
especially by the employment of the antiseptic treatment."[42]
[Footnote 42: _Trans. Path. Soc. of London_, vol. xxx. p. 15.]
We cannot repeat too frequently or too emphatically the fact that the
treatment of pyaemia and septicaemia, when fully developed, is almost
invariably unsuccessful, and that consequently he who desires to save
the greatest number of lives must make every exertion and use all
available means to prevent their development--a task which fortunately
has now been brought within the scope of possibility in the large
majority of cases. Every surgeon will readily admit that, were it
possible to secure union by first intention in all cases of wounds,
then it would be impossible for either septicaemia or pyaemia to occur
in surgical practice. Therefore, it follows that the character of the
wound, the method of operation, the surroundings of the patient, the
character of the treatment, become proper points to consider in this
division of the subject. The character of the wound and its relations
to pyaemia and septicaemia have already been briefly referred to under
the etiology of these diseases. The various methods of operating, with
their respective advantages and disadvantages, are of course not
suitable topics for discussion in this work.
The surroundings of the patient form a subject of vast importance in a
prophylactic view, and should never be lost sight of in the
construction of hospitals. I desire here to express my firm conviction
that surgical pyaemia is essentially and almost wholly a hospital
disease. The question of surroundings for the patient presents to my
mind the following demands as a sine qua non for obtaining the best
possible results in surgery: (1) Absolute cleanliness. This demand
should be strictly enforced in regard to the wound, the patient's
body, the bedding, and everything else, including nurses and
instruments. (2) Absolute purity of the atmosphere. (3) Moderate and
equable temperature, containing a proper amount of moisture. (4)
Proper quantity of nutritious and easily digestible food, with
suitable drinks, etc. (5) Cheerful and pleasant surroundings,
especially in companions, nurses, and other attendants. It may be
objected to these conditions that they can never be obtained. I must
confess that perfection in every detail cannot always be attained, but
I am thoroughly convinced that he who makes a determined effort in
this direction will succeed far better than that person who is
constantly looking about for some excuse for negligence.
The question of treatment brings up the entire subject of antiseptics.
The favorite remedies of this class are carbolic and salicylic acids,
permanganate of potassium, chloride of zinc, bichloride of mercury,
and liquor sodae chlorinatae. There is no doubt that good results may
be obtained with any of these remedies. The surgeon should never
forget that he uses medicines merely as agents to enable him to
accomplish certain objects; and, keeping this in mind, he need very
seldom fail with his antiseptic when the object is to prevent
putrefaction in an open wound. Therefore it appears certain that each
method of treatment may possess special advantages in particular
cases, and probably the same may be said of the antiseptic itself. The
importance of this subject may be more fully appreciated when it is
remembered that it is generally admitted by the best surgical
authorities {981} that more lives are lost from septic infection than
from all other causes combined during a war. The further consideration
of this subject may be arranged for convenience under the heads of
local and general treatment.
The local treatment of the wound should, if possible, be of such a
character as to prevent the absorption of either putrid substances or
pus. It therefore becomes highly important, in cases of amputation and
other operations, that all tissues injured to such a degree as to be
likely to excite either putrefaction, irritation, or inflammation
should be removed. The same care is necessary in removing all foreign
bodies from the wound in cases where no operation is to be performed.
The amputation of the injured limb may be necessary to prevent the
development of these diseases, or it may be resorted to in certain
rare cases after the origin of pyaemic symptoms; however, in the
latter instance great care should be taken to remove all the tissues
already infiltrated with serum, otherwise nothing will be gained. The
use of the surgeon's knife at the proper time may be the best
prophylactic against both pyaemia and septicaemia, but it should be
directed by an intelligent mind and the instrument guided by a
practiced hand. Again, it is found that opening a large medullary
cavity may be attended with danger to the patient. This fact teaches
us an obvious lesson.
The wound existing or the operation having been performed, the surgeon
now turns his attention to the prevention of putrefaction and
inflammation. The first source of danger requiring attention from the
surgeon is the fluid escaping from the wounded surface. Do not allow
it to undergo putrefaction in contact with the wound. It should not be
forgotten that pyaemia is an infectious disease, having its origin in
a local nidus, an open wound, in which putrefaction of pus or other
wound-fluid is taking place. The question of amputation, or of the
extirpation of the parts for the relief of this disease, should only
be entertained when the surgeon is confident that he can remove the
whole of the infiltrated tissues. In other words, the performance of
these operations after the disease has become constitutional can never
be advantageous to the patient. Even in those cases where infiltration
is limited to the lymphatics, unless all these glands so affected are
removed the operation will be unsuccessful. It has been further
recommended in the treatment of this disease, in order to prevent the
formation of metastatic abscesses, to ligate the veins in which
thrombi have formed or may be reasonably expected to form, at some
convenient point between the heart and these obstructed points. The
value of this proceeding has never been fully determined, and may be
reasonably questioned. The formation of metastatic abscesses in
various parts of the body within the reach of the surgeon's scalpel
demands his attention; and we have been taught by experience that they
should be speedily opened, which generally lowers the temperature and
diminishes the danger from septic absorption. In the performance of
this operation Lister's antiseptic system of wound-treatment should be
strictly adhered to, since it unquestionably gives the best results
which can be obtained under the circumstances. When the metastatic
inflammation which occasionally appears in the thyroid and parotid
glands during the course of this disease terminates in the formation
of pus, this should be speedily evacuated. This prompt action is often
required, particularly for the relief of the grave symptoms which are
apt {982} to arise in connection with respiration and deglutition. The
accumulation of pus within the joints in pyaemic cases should, it is
now thought, be treated in the same manner as abscesses in the
cellular tissues--_i.e._ the articulations should be opened and
thoroughly disinfected, and afterward kept in a perfectly aseptic
condition, and also rendered absolutely immovable during the
treatment.
Having directed attention to the more important local measures, we may
now briefly enter on the consideration of some of the constitutional
remedies. In the general treatment of pyaemia there have been
recommended at various times a great variety of drugs, but the general
want of success attending their use leaves comparatively few to be
mentioned here. The mineral acids are still employed, and are found to
be at least agreeable drinks, and as such can be still recommended.
The sulphites of magnesium, sodium, potassium, and lime were
recommended by Giovanni Polli for the treatment of typhus fever,
scarlet fever, small-pox, septicaemia, and pyaemia. He further
suggested that the medicine should be given until the whole quantity
taken bore to the weight of the patient's body the proportion of 1 to
1000. The experiments made on animals with these salts seem to confirm
their value in the treatment of septic diseases. It is certainly true
that animals treated with these salts are not so easily affected by
septic poison as those which have not received this treatment.
Further, it has been shown that putrid substances when mixed with
either permanganate of potassium or the sulphite of sodium, and then
injected, are harmless, although the same quantity of putrid matter
injected without either of these salts destroys life.
Brandy and other alcoholic stimulants have been strongly recommended
on account of their well-known antiseptic properties. The sulphate of
quinia is certainly, in most cases of pyaemia, a valuable agent. In
large doses it enables the surgeon to reduce the temperature of the
patient, and in smaller doses it frequently serves a valuable purpose
as a tonic. It has also considerable value as an antiseptic.
Lattin has recommended the use of large doses of ergotine in
infectious fevers, but this substance, when employed in the treatment
of pyaemia, should be given in the formative stage of the disease. The
use of drastic cathartics should be avoided, as should that of
sudorifics, on account of their prostrating effects. In some cases
hypnotics may be required to secure sleep.
Tonics are always more or less useful. The free use of stimulants and
nutritious food is also indicated. Brandy, wine, and whiskey may be
advantageously used as stimulants. Musk, ammonia, and camphor are
occasionally required. However, it should not be forgotten that in
cases where the disease has become fully developed the usual
termination is death, few recoveries being recorded. In the early
stages of this affection, by the removal of the patient from an
overcrowded hospital ward to some place where pure air and proper
hygienic arrangements can be obtained, recovery may take place, but
under other circumstances the prognosis is exceedingly grave.
The treatment of septicaemia in most particulars is the same as that
of pyaemia. The first effort should be to prevent the development of
the disease, and the second to care for the patient in cases where the
affection has already developed. It is not, of course, in our power to
limit or in any way {983} regulate the primary injury, for we are
obliged to take the patient as he is. The amount of injury to living
tissue may be great or small. The question of an operation, the
character of the same, and the subsequent management must be
determined in accordance with the circumstances of each particular
case.
The primary death of the parts is generally due chiefly to the injury
itself; the secondary, frequently to bad surgical management. Let us
now take a case in which the primary injury has been severe, greatly
diminishing, but not destroying, the circulation in the injured parts.
Here the immediate application of ice would be injurious, but a warm
application might assist nature. It is humiliating to the profession
that we are obliged even at this date to admit that the treatment of
septicaemia is largely symptomatic. The profuse choleraic diarrhoea
which generally accompanies this disease may be regarded as an effort
of nature to eliminate the septic poison; but, nevertheless, it is so
prostrating in its effects that it requires to be controlled with
properly selected astringents, and these remedies may be still further
aided by the use of stimulants and tonics.
The treatment of septicaemia may be summarized as follows: (1) A
strict adherence to the five rules given under the head of the
prophylactic treatment of pyaemia. (2) The avoidance of all
putrefaction in contact with the wound, especially prior to the
development of sufficient granulations to completely cover its
surface. This object is to be accomplished by the removal of all
necrotic tissues, the avoidance of putrescent fluids by cleanliness,
and the proper use of antiseptic agents. (3) Free use of the alkaline
sulphites and hyposulphites. These drugs should be used in all cases
where there is reason to anticipate the development of septic
diseases, as soon after the receipt of the injury as practicable, but
should not be neglected even after the disease has become fully
developed. (4) Sulphate of quinia should be used in all cases where
the temperature is above 100 degrees F., and its persistent use in
large doses may be necessary to prevent the fever from rising still
higher. It will be remembered in this connection that experience has
taught us that "a temperature of 108.5 degrees F. is the limit beyond
which life can no longer exist,"[43] and even a much lower temperature
is not without dangers. "The essential danger of fever in acute
diseases consists, then, in the deleterious influence of a high
temperature on the tissues."[44]
[Footnote 43: Liebermeister, _New Sydenham Soc. Trans._, vol. lxvi. p.
278.]
[Footnote 44: _Ibid._, p. 280.]
The treatment of puerperal septicaemia, although requiring the
application of the same principles as any other form of this disease,
may be briefly described as follows: The womb should be maintained in
a firmly-contracted state by the proper use of ergot, even as a
prophylactic measure, and also during the whole course of the disease;
the uterus and vagina should be kept in an aseptic condition by the
efficient use of antiseptics; sulphate of quinia should be given in
large doses, and repeated as often as may be necessary in order to
lower the temperature; and morphia or some form of opium should be
employed for the relief of the pain.
{984}
PUERPERAL FEVER.
BY WILLIAM T. LUSK, M.D.
DEFINITION.--Puerperal fever is an infectious disease, due, as a rule,
to the septic inoculation of the wounds which result from the
separation of the decidua and the passage of the child through the
genital canal in the act of parturition.
To maintain this definition it is, however, necessary to group by
themselves cases of childbed fever dependent upon causes which are
operative in the non-puerperal condition, though the latter imparts to
these causes oftentimes an exceptional activity and virulence. In this
category are to be placed especially scarlatina, typhus, typhoid, and
malarial fevers. It is to be borne in mind that the zymotic fevers may
provoke in the puerperal woman the same inflammatory lesions commonly
associated with puerperal fever.[1] This is in accordance with the
well-known surgical experience that a febrile paroxysm from any cause
exerts an unfavorable influence upon a wounded surface.
[Footnote 1: Hervieux, _Traite clinique et pratique des maladies
puerperales_, pp. 1073 _et seq._]
Like all brief statements, the writer is well aware that the foregoing
definition is necessarily imperfect, and stands in need of further
limitations to meet the requirements of exactness. Exceptions,
however, either apparent or real, will be noted hereafter in their
proper connections.
FREQUENCY.--In a careful search through the records preserved by the
Health Department of New York City, I found that from 1868 to 1875
inclusive the total number of deaths for nine years was 248,533. Of
these, 3342 were from diseases complicating pregnancy, from the
accidents of child-bearing, or from diseases of the puerperal state;
or, in other words, 1:75 of all the deaths occurring during that
period was the result of the performance of what we are in the habit
of regarding as a physiological function.
The deaths from miscarriage, from shock, from prolonged labor, from
instrumental delivery, from convulsions, from hemorrhage, from rupture
of the uterus, and from extra-uterine pregnancy, and deaths from
eruptive fevers, from phthisis, and from inflammatory non-puerperal
affections complicating childbirth, made a total of 1395, or about 42
per cent. of the entire number. The remaining 1947 cases, variously
reported as puerperal fever, puerperal peritonitis, metro-peritonitis,
phlebitis, phlegmasia dolens, pyaemia, and septicaemia, represent the
very serious sacrifice of life resulting from inflammatory processes
which have their starting-point in the generative apparatus. If we
apply the general term, puerperal fever, to this class of cases, it
will be seen that the malady is the cause of nearly one {985}
one-hundred-and-twenty-seventh of all the deaths occurring in the
city. The actual number of births for the nine years in question was
roughly estimated at 284,000[2]--an estimate erring upon the side of
liberality. The total number of deaths to the entire number of
confinements was, then, at least in the proportion of 1:85, or, from
puerperal fever alone, in the proportion of 1:146. Garrigues[3]
examined the records of the various city institutions during the
period in question, and from them estimated the number of births which
took place in hospitals at 10,572. The recorded deaths were 420.
Deducting these from the totals given above, the general death-rate in
civil practice from puerperal causes in New York City was in the
proportion of 1:94. Max Boehr[4] in his now-famous statistics reckons
that one-thirtieth of all married women in Prussia die in childbed.
The Puerperal Fever Commission[5] appointed by the Berlin Society of
Obstetrics and Gynaecology arrived at the conclusion that from 10-15
per cent. of the deaths occurring in women during the period of sexual
activity were due to childbed fever, and that this disease destroyed
nearly as many lives as small-pox or cholera. But puerperal fever
differs from either small-pox or cholera in that the latter presses
largely upon the aged and the very young, while the former gathers its
victims exclusively from a selected class--viz. from women in adult
life, the mothers of families, whose loss, as a rule, is a public as
well as a private calamity.
[Footnote 2: This estimate was based upon the assumption that the
natural birth-rate is 33 to the 1000--a proportion believed by the
statisticians of the Board of Health to be approximatively correct,
though probably somewhat in excess of the reality. P. Osterloh has
recently stated that my statistics were computed in so arbitrary a
manner as to render deductions from them valueless. In this, however,
he is mistaken. The most conscientious care was taken in their
preparation; wherever the possibility of error existed the fact was
distinctly indicated, and all calculations were made in such a way
that whatever corrections might be required would strengthen the
conclusions.]
[Footnote 3: "On Lying-in Institutions," _Trans. Am. Gyn. Soc._, vol.
ii., 1878.]
[Footnote 4: "Untersuchungen uber die Haufigkeit des Todes im
Wochenbett in Preussen," _Zeitschr. f. Geburtsk. und Gynaek._, vol.
iii. p. 82.]
[Footnote 5: _Zeitschr. f. Geburtsk. und Gynaek._, vol. iii. p. 1.]
For those who regard statistics with habitual distrust it may perhaps
be well to state that the foregoing frightful picture is no
exaggeration, but is less sombre than the actual truth.
Before proceeding to consider the nature of puerperal fever it is
desirable to first recall the anatomical lesions with which it is
associated. These, it will be found, are for the most part
inflammatory processes having their starting-point in injuries of the
genital passage produced by parturition, complicated in many cases by
septic changes in the blood, by secondary degeneration of
parenchymatous organs, and at times by phlegmonous and erysipelatous
affections in remote as well as in the adjacent serous and cutaneous
tissues.
MORBID ANATOMY.--The primary lesions connected with puerperal fever
are so various that the student will find it convenient to classify
them according as they are situated in the mucous membrane of the
utero-vaginal canal, the parenchyma of the uterus, the pelvic cellular
tissue, the peritoneum, the lymphatics, or the veins. Not, indeed,
that such an arrangement is strictly in accordance with clinical
experience--as a rule, the inflammatory processes are rarely limited
to a single tissue--but because the prognosis and treatment {986} are
determined in great measure by the tissue-system which is
predominantly affected. The significance of puerperal inflammations,
wherever seated, likewise depends upon whether they are local and
circumscribed or whether they present a spreading character.
Personally, I have found the following classification of
Spiegelberg[6] of great utility as a means of keeping in mind the
principal points to which inquiry should be directed in estimating the
significance of the febrile conditions of childbed:
1. Inflammation of the Genital Mucous Membrane.--Endocolpitis and
endometritis.
_a_. Superficial.
_b_. Ulcerative (diphtheritic).
2. Inflammation of the Uterine Parenchyma, and of the Subserous and
Pelvic Cellular Tissue.
_a_. Exudation circumscribed.
_b_. Phlegmonous, diffused; with lymphangitis and pyaemia (lymphatic
form of peritonitis).
3. Inflammation of the Peritoneum covering the Uterus and its
Appendages.--Pelvic peritonitis and diffused peritonitis.
4. Phlebitis Uterina and Para-uterina, with formation of thrombi,
embolism, and pyaemia.
5. Pure Septicaemia.--Putrid absorption.
[Footnote 6: "Ueber das Wesen des Puerperalfiebers," _Volkmann's
Samml. klin. Vortr._, No. 3.]
ENDOCOLPITIS AND ENDOMETRITIS.--In the superficial, catarrhal form of
inflammation the mucous membrane of the vagina is swollen and
hyperaemic, the papillae are enlarged, and the discharge is profuse;
in the vaginal portion of the cervix the labia uterina are oedematous
and covered with granulations which bleed at the slightest touch; in
the cavity of the body there are increased transudation of serum and
abundant pus-formation. The deep structures of the uterus are usually
not affected. Sometimes the inflammation extends to the
tubes--_salpingitis_--or, passing outward through the fimbriated
extremities, it may spread over the adjacent peritoneum.
The small wounds at the vaginal orifice are at times converted into
ulcers with tumefied borders. These so-called puerperal ulcers are
covered with a greenish-yellow layer. They are associated usually with
oedematous swelling of the labia. Under favorable sanitary conditions
the deposit, which consists in the main of pus-cells, clears away and
the surface heals by granulation. The ulcerative form of inflammation
is very rare outside of crowded hospitals.
Diphtheritic ulcers are situated with greatest frequency in the
neighborhood of the posterior commissure or around the vaginal
orifice. In rarer instances they are found upon the anterior wall and
in the fornix of the vagina, in the cervix, and upon the site of the
placenta. The borders are red and jagged; the base is covered with a
yellowish-gray, shreddy membrane; the secretion is purulent, alkaline,
and fetid; and the adjacent tissues are oedematous. From the vulva
they may extend to the perineum or pursue a serpiginous course down
the thighs. In the uterus and about the cervix they vary as regards
size, and are either of a rounded shape or form narrow bands. The
intervening portions of tissue which have not undergone destructive
changes swell and stand out in strong {987} relief. Where the entire
inner surface has become necrosed, it is often covered with a smeary,
chocolate-brown mass which, when washed away with a stream of water,
leaves exposed either the deepest layer of the mucous membrane or the
underlying muscular structures.
The difference between the superficial ulcerations of the genital
canal and the diphtheritic form involving destruction of the deeper
tissues is due to the presence in the latter of minute organisms
termed micrococci, the relations of which to puerperal infection will
be considered in a subsequent division.
METRITIS AND PARAMETRITIS.--In ulcerative endometritis, and even in
the extreme catarrhal form, the parenchyma of the uterus likewise
becomes involved. The changes which are designated under the term
metritis consist in the first place of oedematous infiltration of the
tissues. As a consequence, the organ contracts imperfectly and becomes
soft and flabby, so that sometimes, upon post-mortem examination, it
bears the imprint of the intestines.
In diphtheritic endometritis the gangrenous process may attack the
muscular tissue, and give rise to losses of muscular substance--a
condition known as necrotic endometritis or putrescence of the uterus.
Inflammatory changes are rarely lacking in the intermuscular
connective tissue, which exhibits in places serous or gelatinous
infiltration, with afterward pus formation, and with here and there
small abscesses. The sero-purulent infiltration of the connective
tissue is specially marked beneath the peritoneal covering of the
uterus either behind or along the sides at the attachment of the broad
ligaments. In the same situations the lymphatics, which normally are
barely perceptible to the naked eye, are sometimes enlarged to the
size of a quill, and are characterized by varicose dilatations
occurring singly or presenting a beaded arrangement. In the substance
of the uterus the dilated vessels are liable to be mistaken for small
abscesses. The pus-like substance contained in the lymphatics is
composed of pus-cells and of micrococci. From the cellular tissue
surrounding the vagina, or that beneath the peritoneal covering of the
uterus, the inflammation may spread by contiguity of tissue between
the folds of the broad ligament, and thence pass upward to the iliac
fossae. Usually the process is unilateral. After the inflammation has
crossed the linea terminalis it may take a forward direction above the
sheath of the ilio-psoas muscle to Poupart's ligament, or it may creep
upward, following the course, according to the side affected, of the
ascending or descending colon, to the region of the kidney. It is rare
for inflammation of the cellular tissue to travel around the bladder
to the front. In such cases it pursues its course between the walls of
the bladder and the uterus, and along the round ligament to the
inguinal canal. In a few cases the cellulitis mounts above Poupart's
ligament, between the peritoneum and the abdominal wall.
The course of the inflammation is not simply fortuitous, but follows
prearranged pathways in the connective tissue. Konig[7] and
Schlesinger[8] have shown that when air, water, or liquefied glue is
forced into the cellular tissue between the broad ligaments the
injected mass has a tendency to invade the iliac fossae. In
Schlesinger's experiments, if the canula of the syringe was inserted
into the anterior layer of the broad ligament, {988} the glue spread
between the folds to the abdominal end of the Fallopian tube; thence,
following the track of the vessels, it passed to the linea terminalis;
and finally mounted upward along the colon or swept forward to
Poupart's ligament until the advance was stopped at the outer border
of the round ligament. If the injection was made to the side of the
cervix through the posterior layer at the junction of the cervix and
the body, the posterior layer gradually bulged out, the peritoneum was
lifted from the side wall of the pelvis, and the glue passed beyond
the vessels to reach the iliac fossa. If the injection was made to the
side of the cervix through the anterior layer, the glue passed between
the bladder and the uterus, and forward along the round ligament to
the inguinal canal, while another portion of the fluid passed between
the layers of the broad ligament, and reached the peritoneal covering
of the side walls behind the round ligament. If the injection was made
in the median line in a peritoneal fold of Douglas's cul-de-sac, the
fluid travelled forward upon one side along the round ligament and
thence to the posterior wall of the bladder.
[Footnote 7: _Arch. der Heilkunde_, 3 Jahrg., 1862.]
[Footnote 8: _Gynaekologische Studien_, No. 1.]
The term parametritis, introduced into use by Virchow, is, properly
speaking, limited to inflammation of the connective tissue immediately
adjacent to the uterus, the older one of pelvic cellulitis furnishing
a more comprehensive designation for cases where, as a consequence of
a progressive advance from the point of departure in the genital
canal, the remoter regions have likewise been invaded.
Connective-tissue inflammation presents, as the first essential
characteristic, an acute oedema, the fluid which fills the gaps and
interspaces consisting of transuded serum rendered opaque by the
presence of pus-cells or possessing a gelatinous character. In the
mild, uncomplicated cases the oedema disappears rapidly. Where the
cell-collections are of moderate extent the entire process may vanish
without leaving a trace of its existence. If the cell-elements, on the
other hand, are present in great abundance, they, as a rule, first
undergo fatty degeneration, and, after the absorption of the fluid
portion, form a hard tumor composed of a fine granular detritus, which
under favorable circumstances likewise after a few weeks becomes
absorbed. In rare cases abscess-formation in the tumor results.
In the cellulitis resulting from septic infection, especially in cases
complicated by diphtheritis, the tissues seem as if soaked with dirty
serum, and contain scattered yellowish deposits, which soon present,
even to the naked eye, the appearance of pus-collections. This
sero-purulent oedema is always associated with lymphangitis, the
lymphatic vessels possessing varicose dilatations and beaded
arrangements similar to those already described in the uterine tissue.
The foregoing changes are most distinct in the firm connective tissue
adjacent to the uterus and at the hilum of the ovary, while they are
less clearly traced in the looser structure of the broad ligament
(Spiegelberg).
In favorable cases the inflammation is circumscribed, or at least is
limited, by the nearest lymphatic glands. In cases of intense
infection it spreads rapidly, and justifies the title bestowed upon it
by Virchow of parametritic malignant erysipelas.
PELVIC AND DIFFUSED PERITONITIS.--Inflammation of the pelvic
peritoneum may result from severe attacks of catarrhal endometritis,
the inflammatory process either traversing the uterine tissue or
passing {989} through the Fallopian tubes to the adjacent serous
membrane; or it may proceed, secondarily, from the stretching and
irritation occasioned by an associated parametritis.
As a rule, pelvic peritonitis is not attended with much exudation. The
latter is situated upon the folds of the peritoneum limiting the
cul-de-sac of Douglas, upon the ovaries, and upon the broad ligaments.
In favorable cases it consists of fibrinous flakes and fluid pus. If
the latter is abundant, it may become encysted by the formation of
adhesions between the pelvic organs.
General peritonitis may result from the extension of a pelvic
peritonitis, or from the transport of poison through the lymphatics
into the peritoneal sac. In the first case the entire peritoneum is
injected, and the contents of the abdominal cavity are loosely bound
together by pseudo-membranes, composed of pus and coagulated fibrine.
The intestines are at the same time distended and the diaphragm is
pushed upward. In the so-called peritonitis lymphatica the
inflammatory symptoms are at the outset lacking. The abdominal cavity
is found filled with a thin, stinking, greenish or brownish fluid
composed of serum and micrococci. The intestines are lax and
oedematous, and the muscular structures are paralyzed, with resulting
tympanitic distension. The peritoneal covering of the intestines is
devoid of lustre, and covered with injected patches, or is stained of
a dark-brown color. Death often ensues before the occurrence of
exudation.
Septic forms of pelvic inflammation are often associated with
oophoritis, the dilated lymphatics either extending to the substance
of the ovaries, where they may lead to the production of small
abscesses, or, as a result of blood-dissolution, the organs become
soft, pulpy, and infiltrated with discolored serum, and present
hemorrhagic spots distributed over the surface.
PHLEBITIS AND PHLEBO-THROMBOSIS.--The formation of thrombi in the
uterine and pelvic veins is sufficiently common during the puerperal
period. The coagulation may result from compression or from
enfeeblement of the circulation. A predisposition to its occurrence is
created by relaxation of the uterine tissue. A normal thrombus is in
itself harmless. In time it becomes organized, and the occluded vessel
is converted into a connective-tissue cord, or a channel may form
through it which permits the passage of the blood-stream. When,
however, pus or septic matters obtain access to a thrombus, it
undergoes rapid disintegration, and the particles get swept away into
the circulation until arrested in the ramifications of the pulmonary
artery. Wherever these poisoned emboli happen to lodge inflammation is
set up in the adjacent tissues, and abscesses result (pyaemia
multiplex). Sometimes countless collections of pus may form in the
lungs. Less commonly abscesses are found in the liver or spleen,
originating either from emboli which have already made the pulmonary
circuit or from thrombi in the pulmonary veins.
Inflammation of the veins (phlebitis) sometimes occurs when the
vessels have to traverse tissues in or near the uterus infiltrated
with purulent or septic materials. The endothelium then undergoes
proliferation, and thrombosis is produced. Phlebitic thrombi do not
necessarily break down, and may in that case act as a barrier to the
progression of septic germs into the circulation (Spiegelberg). As a
rule, however, {990} under the influence of inflammation and
infection, they become converted into puriform masses.
The thrombi grow by accretion in the direction of the heart. They may
extend from the uterus through the internal spermatic, or through the
hypogastric and common iliac veins, to the vena cava. Sometimes the
thrombus may be traced back to the placental site.
SEPTICAEMIA.--From these local conditions, sooner or later, secondary
affections develop in distant organs. The general affection is, in
great part at least, likewise of local origin. Sometimes, however,
where the poison, which enters the system through the lymphatics and
veins, is very active and abundant, death may follow from acute
septicaemia before the changes in the sexual organs have had time to
develop. The fatal result in these cases is probably due to paralysis
of the heart. After death post-mortem decomposition rapidly sets in,
the blood is sticky, and swelling is found in the various
parenchymatous organs.
The secondary affections consist in the metastatic abscesses already
noticed as produced by infected emboli, in circumscribed purulent
collections due to the conveyance of septic materials into the
blood-current through the lymphatics, in ulcerative endocarditis, in
inflammations of the pleura, the pericardium, and the meninges, and in
purulent inflammation of the joints.
A study of the nature of puerperal fever will best show how intimately
these seemingly distinct processes are linked together.
EARLIER VIEWS CONCERNING THE NATURE OF PUERPERAL FEVER.[9]--According
to the teachings of Hippocrates, Galen, and Avicenna, of Ambrose Pare,
of Sydenham, and of Smellie, the fevers of puerperal women were
attributable to the suppression of the lochia. For twenty centuries
this doctrine was accepted almost without dispute, the best clinical
observers confounding a symptom which is often lacking with the cause
of the disease itself.
[Footnote 9: For data given, and for a great variety of historical
information, vide Hervieux, _Traite clinique et pratique des maladies
puerperales_.]
In 1686, Puzos[10] taught that milk, circulating in the blood, is
attracted to the uterus during pregnancy and to the breasts after
confinement, but that milk metastases may form in other parts, and
produce the symptoms of malignant or intermittent fever. In 1746, A.
de Jussieu, Col de Villars, and Fontaine advanced in support of this
theory the fact that they had found, on opening the abdomen in women
who had died from an epidemic which raged that year in Paris, a free
lactescent fluid in the lower portion of the abdominal cavity and
clotted milk adherent to the intestines. This doctrine, which seemed
to be based upon, and to accord with, observation, found many
adherents in France. It lost ground, however, when, in 1801, Bichat
pointed out the true nature of the abdominal effusions of women who
had died in childbed, and demonstrated that they were to be found
likewise in peritoneal inflammations occurring in men and in
non-puerperal women.
[Footnote 10: _Premier Memoire sur les Depots lacteux_.]
While, during the second half of the eighteenth century, the doctrine
of milk metastasis held full sway in France, in England and Germany
the dominant leaders in medicine referred the causes of puerperal
fevers to inflammations of the womb and of the peritoneum. With the
advances made in pathological anatomy in the beginning of the present
{991} century, France taking the lead, stress was likewise laid upon
inflammations of the veins and of the lymphatics. The vitality of the
doctrine of local inflammations is well shown by the records kept by
the Health Board of this city, where a large proportion of the deaths
returned from childbed fever are entered under the head of metritis,
of peritonitis, of metro-peritonitis, and of puerperal phlebitis.
In opposition to the doctrines of the so-called localists, the theory
that puerperal fever is an essential fever, and as much a distinct
disease as typhus fever, typhoid fever, or relapsing fever, has been
strenuously advocated by some of the most distinguished clinical
teachers who have devoted their attention to obstetrical science.
Fordyce Barker, the most recent exponent of the essentiality of
puerperal fever, in his classical work upon the _Puerperal Diseases_,
states the arguments against the local origin of the diseases as
follows: 1st, that puerperal fever has no characteristic lesions; 2d,
that the lesions which do exist are often not sufficient to influence
the progress of the disease or to explain the cause of death; 3d, that
there may be inflammation, even to an intense degree, of any of the
organs in which the principal lesions of puerperal fever are found,
and yet the disease will lack some of the essential characteristics of
puerperal fever; 4th, that the lesions are essentially different from
spontaneous or idiopathic inflammations of the tissues where these
lesions are found; 5th, that puerperal fever is often communicable
from one patient to another through the medium of a third party, and
that this is not the fact in regard to simple inflammations in
puerperal women.
However, neither Barker, nor those who entertain views similar to his,
question the local origin of many febrile affections in childbed, but
claim that purely local inflammations have each their characteristic
symptoms, which differ from those of true puerperal fever, that
puerperal fever is a zymotic disease of unknown origin, and that local
lesions, where they coexist, are not the primary source of trouble,
but are secondary to changes in the blood.
In 1850, James Y. Simpson[11] published a short paper "On the Analogy
between Puerperal and Surgical Fever." This article may well be
regarded as the foundation of the modern doctrine concerning puerperal
fever, and is well worthy of perusal at the present day; for, though
in the then existing state of pathology many of the links were wanting
which have since raised the argument to nearly a mathematical
demonstration, the paper furnishes a brilliant example of the
scientific foresight which is able to discern the truth even where the
evidence lacks completeness.
[Footnote 11: _Edinburgh Medical Journal_.]
In 1847, Semmelweis, who was at that time clinical assistant to the
Lying-in Hospital at Vienna, made the startling assertion that
"puerperal patients were chiefly attacked with puerperal fever when
they had been examined by the physicians who were fresh from contact
with the poisons engendered by cadaveric decay; that fever ensued in
the practice of those who after post-mortem examination washed their
hands in the usual manner, whereas no fever or but few cases of
disease followed when the examiner had previously washed his hands in
a solution of chloride of lime." In the face of insult, ridicule, and
abuse Semmelweis {992} maintained this position for years, almost
unaided, with fanatical persistency. It was easy for his opponents,
for the most part managers of the great lying-in asylums, to show from
clinical experiences the weakness of so one-sided a theory. But the
employment of the equivocal demonstration _falsus in uno, falsus in
omnibus_, served only as a temporary defence against the laxity which
prevailed in hospital management only a quarter of a century ago.
Though Semmelweis died with no other reward than the scorn of his
contemporaries, it is impossible at the present day to so much as
contemplate the abuses he attacked without a shudder.
In 1860, Semmelweis published the result of his ripened experience in
a treatise entitled _Die Aetiologie der Begriff und die Prophylaxis
des Kindbett fiebers_, in which, abandoning his earlier exclusive
position, he maintained that puerperal fever arises from the
absorption of putrid animal substances, which produce first
alterations in the blood, and secondly exudations. He distinguished
between cases in which the infection was introduced from some external
source, and which he believed to be the most frequent variety, and
those where the poison was generated in the system. The sources from
which the infection is derived he believed to be--1st, from the dead
body, regardless of age, sex, or disease, no matter whether the latter
is of puerperal or non-puerperal origin, the virulence depending upon
the stage of decomposition; 2d, diseased persons, whose malady is
associated with decomposition of animal tissue, no matter whether the
affected person suffers from childbed fever or not, the decomposing
matter alone furnishing the product from which infection is derived;
3d, physiological animal substances in the process of decomposition.
As carriers of infection he regarded the fingers and hands of the
physician, midwife, or nurse, sponges, instruments, soiled clothing,
the atmosphere, and, in brief, anything which, after being defiled
with decomposing animal matter, was brought into contact with the
genitals of a woman during or subsequent to parturition. Absorption
takes place from the inner surface of the uterus or from traumata in
the genital canal. Infection seldom occurs in pregnancy, because of
the closure of the os internum, the absence of wounded surfaces, and
because of the rarity with which examinations are made; during
dilatation infection is common, but exceptional during the period of
expulsion, because the inner uterine surface is at that time rendered
inaccessible by the advance of the child; in the placental and
puerperal period infection occurs from utensils and instruments, but
chiefly through the access of atmospheric air when the latter is
loaded with decomposing organic matter. In rare instances
auto-infection may result from spontaneous decomposition of the
lochia, of bits of decidua, of coagula of blood, of necrosed tissue,
or in consequence of severe instrumental labors. In a word, puerperal
fever was according to Semmelweis no new specific disease, but a
variety of pyaemia.
I have been thus particular in giving prominence to the labors of
Semmelweis partly from justice to a man who was hated and despised in
his lifetime, and partly because I believe that few outside of Germany
are really cognizant of the immense service he rendered to humanity,
or that to him is really due a large part of what is now current
doctrine concerning the nature and prophylaxis of puerperal fever.
THE NATURE OF PUERPERAL FEVER AS REGARDED FROM THE {993} STANDPOINT OF
MODERN INVESTIGATION.--The older beliefs in the suppression of the
lochia and the metastases of milk have long since been relegated to
the domain of old nurses' lore, and do not call for serious
discussion. The localist theory, that puerperal fever is a metritis, a
peritonitis, a phlebitis, or an inflammation of the lymphatics, is, as
mortuary records show, still adhered to by many practitioners, and, as
we have seen, is justified by the fact that puerperal fever is, with
rare exceptions, associated at some period of its progress with
certain inflammatory processes which have their starting-point in the
generative apparatus. But the localist theory leaves out of view the
existence of blood-poisoning, and yet the coexistence of a
blood-poison with the local lesions is an essential feature of
puerperal fever. It was this defect which gave to the advocates of the
specificity of puerperal fever their real importance. The outcome of
modern investigation tends, however, to prove that the puerperal
poison is of a septic nature, and that the usual points of
introduction of the poison are the lesions of the parturient canal.
This does not, indeed, exclude other points of entry, for clinical
experience renders it probable that, under certain conditions, the
poison may be primarily introduced into the blood through the
respiratory and digestive organs. Puerperal fever is really a surgical
fever, modified, however, by the peculiar physiological conditions
which belong to the puerperal state. The argument against its septic
origin is based chiefly upon mistaken ideas concerning the nature of
septicaemia. So long as the symptoms of the latter were derived for
the most part from the effects observed as a consequence of injecting
putrid materials into the veins of dogs, a confusion arose from the
fact that the results obtained were commonly those of putrid
intoxication, and not those of true septicaemia. Under such
circumstances it was not difficult to formulate definitions of
septicaemia which could be shown to be at variance with the phenomena
which ordinarily exist in puerperal fever.
The argument that the infectious diseases of childbed are of a septic
nature can best be understood by presenting the proofs in their
orderly sequence.
1st. _It is demonstrable that septic poisons are capable of producing
the lesions ordinarily associated with puerperal fever._ Thus, it is a
matter of ordinary experience that the retention of a small bit of the
membranes within the uterus will produce fetid lochia, and, as the
result of infection, a febrile condition, which, as a rule, subsides
with the expulsion of the offending body and the use of disinfectant
washes. A virulent form of fever is not unfrequently occasioned by
retained coagula or placental debris which have undergone
decomposition. I was once sent for to see a puerperal patient
suffering from fever on the fourth day following her confinement. On
entering the room I found the stench intolerable; turning down the
sheets, I discovered that the patient was lying in a decomposing mass,
and learned that her doctor had forbidden, after the birth of her
child, the removal of the soiled linen and blankets. The patient died
in the third week from pyaemia multiplex.
Haussmann[12] reported a case of auto-infection in the rabbit which
terminated fatally. A portion of the membrane, retained in the left
cornu, {994} led to diphtheritic losses of substance in the lower
portion of the vagina, to hemorrhagic enteritis, and to peritonitis.
The same author produced death from septicaemia by injecting into the
gravid uterus of one rabbit serum from the abdomen of another which
had died from infection. The post-mortem examination showed the
muscles filled with granules and the peritoneum injected, but no
fibrino-purulent exudation. Injections into the uterus of pus from the
abdomen of a woman who had died from infectious puerperal disease
produced no effect upon rabbits two weeks gravid, while in the second
half of pregnancy premature delivery and death occurred, in one case
in one and a half, in another in two and a half, days. In the animal
which died in thirty-six hours there was commencing perimetritis and
peritonitis, while in the one that died after the lapse of sixty hours
the abdomen was found to contain fibrine and pus.[13] D'Espine
injected into the uterus of a rabbit which had just produced her young
pus from the abdomen of a woman who had died from puerperal disease
two days before. This was subsequently followed by other injections of
fetid fluids during the four days following. On the twelfth day the
animal died. The autopsy revealed peritonitis, most marked in the
pelvic cavity, inflammatory alterations in the vagina, uterus, and
tubes, small abscesses in the body of the uterus, softened clots in
the veins of the broad ligaments, and infarctions of the liver.[14]
Schuller found that subcutaneous injections of septic material in
female animals during pregnancy produced a diphtheritic ulcerative
process on the uterine surface, which determined the separation of the
placenta; diphtheritic patches, likewise, were found in the cornua of
the uterus.[15]
[Footnote 12: "Entstehung der ubertragbaren Krankheiten des
Wochenbettes," _Beitr. zur Geburtsk. und Gynaek._, Bd. iii. Heft 3, p.
345.]
[Footnote 13: _Contribution a l'etude de la septicemie puerperale_,
Paris, 1873, p. 28.]
[Footnote 14: _Ibid._, p. 394.]
[Footnote 15: "Experimentelle Beitrage zum Studium der septischen
Infection," _Deutsch. Zeitschr. fur Chir._, Bd. vi. p. 141.]
Thus we find that in the human subject and in experiments made upon
animals septic poisons introduced into the system following or near
delivery produce lesions similar to those found in puerperal fever. As
a further coincidence, we notice that, as in puerperal fever, the
lesions from direct septic poisoning have nothing characteristic about
them, producing in one case pyaemia, in another partial peritonitis,
in another general peritonitis, in another diphtheritis, while in
others the lesions are comparatively trivial, these differences being
due to variable facta, such as the qualities of the septic poisons,
the points of entry into the organism, and the resistance offered by
the invaded tissues.
2d. _Septicaemia is a disease characterized by the invariable presence
in the organism infected of minute bodies generally termed
bacteria._[16]
[Footnote 16: In 1865, Mayrhofer (_Mon. Schr. f. Geburtsk._, vol.
xxv., p. 112, 1865), at that time clinical assistant to the Lying-in
Service of Braun in Vienna, stimulated by the researches of Pasteur,
maintained that septic endometritis was the result of putrid
fermentation within the uterine cavity, and drew attention to the
vibrios--a term which he applied to the round as well as to the
rod-like bacteria--as the source, and not the product, of
putrefaction. He claimed that while in puerperal processes vibrios are
always present, in healthy women they never occur before the second,
third, or fourth day, and not always even then. The chief progress
that has been made as regards our knowledge of puerperal fever in the
last ten years has been in the direction of strengthening Mayrhofer's
argument by careful experiment, and by defining the action of
microscopic fungi in the production of septic morbid processes.]
Until very recently the whole subject of septicaemia has been in a
state of wellnigh hopeless confusion. From Gaspard and Panum, through
a long list of experimenters, hardly any two arrived at precisely
similar {995} results. Something like an approach to order has,
however, been produced since it has begun to be understood that the
effects produced by septic fluids vary with the quality of the poison
and the method of experimentation, and that to obtain identity in the
result there must be identity in all the conditions. Thus, Samuel has
shown that the same organic substance produces different effects at
different stages of decomposition; again, that the enteritis which is
commonly quoted as characteristic of septic poisoning occurs, as a
rule, in animals when the septic fluid is injected directly into the
blood, and is rare when it finds its way into the circulation through
the lymphatics, as is the case usually in clinical experiences.[17]
There is one experimental point of extreme practical importance too in
connection with puerperal septicaemia--viz. that if the injection of a
septic fluid be made directly into a vessel, toxic effects speedily
follow, but are transitory, unless the amount of the fluid be large,
or its virulence exceptional, or the animal very young;[18] whereas
very small amounts injected subcutaneously, by developing
rapidly-spreading phlegmonous inflammation, resembling malignant
erysipelas in man, are capable, after a period of incubation, of
producing fatal results; or they may, if injected into a shut cavity
or underneath a fascia, lead to the development of an inflammation of
an ichorous character. In other words, the eliminating organs suffice,
under ordinary conditions, to remove from the blood the same amount of
septic fluid which would prove fatal if injected into the tissues.[19]
To produce similar results the injections into the blood need to be
repeated at intervals. This experience leads us to the conclusion that
in the tissues septic poison possesses the capacity of
self-multiplication, and that in the local inflammation set up a
reservoir is formed from which poison is continuously poured into the
circulation.
[Footnote 17: _Loc. cit._, p. 349.]
[Footnote 18: "Traube und Gescheidlen, Versuche uber Faulniss und den
Widerstand des lebender Organismus," _Schles. Ges. f. vaterlandische
Cultur_, Feb. 13, 1874.]
[Footnote 19: In some instances in which absorption from the tissues
is very rapid the effects of subcutaneous injections may be similar to
those produced by injections made directly into the circulation, and
the local lesion be insignificant.]
This capacity of self-multiplication which septic fluids possess has
recently been found to be coincident with the presence of certain
parasitic bodies, generically termed bacteria. All carefully-made
experiments serve to show that if a septic fluid be deprived of these
organic bodies by boiling or filtration while it continues capable of
producing inflammation, the inflammation is usually of diminished
intensity and remains local in its character;[20] whereas the bacteria
retained upon the filter possess all the virulent properties of the
original fluid.[21] This does not alone necessarily prove that the
virus resides in the bacteria, for it does not exclude the possibility
that both the virus and the bacteria remain upon the filter.
[Footnote 20: In filtration through porous earthenware cylinders the
filtrate possesses no phlogogenic properties.]
[Footnote 21: Tiegel, _Correspondenzblatt fur Schweizer Aertze_, 1871,
S. 1275; Klebs, _Archiv fur exp. Pathol. und Pharmakol._, Bd. i. Heft.
1, S. 35.]
So far, attempts at isolating the microspores of septicaemia and
cultivating them separately in vehicles composed of water holding in
solution inorganic constituents, or sterilized fluids containing
organic matters, or of the semi-solid gelatinous substances
recommended by Koch, have been only partially successful in proving
them to be the sole source of {996} infection. Some earlier
experiments of Tiegel and Klebs[22] were attended with positive
results, and more recently confirmatory evidence has been furnished by
Pasteur and Doleris.[23] Hiller, rarely quoted now, arrived at
different conclusions. He found that bacteria washed in pure water
were innocuous.[24] But pure water had long before been proven by
observers to be inimical to the well-being of the organisms in
question. Schuller says that Hiller's experiments prove apparently
that while a putrid fluid may be in the highest degree poisonous, its
component parts--viz. either the fluid or the bacteria singly--are
neither deadly nor poisonous.[25] The fact is, that isolation
experiments are subject to what has hitherto been in most experiments
an unavoidable source of error. As Davaine noted early in his
observations, the physiological action of bacteria is very dependent
on the constitution of the medium in which they are developed, which
is in entire harmony with what is known of organisms much higher in
the scale. "Many plants," says Burdon-Sanderson,[26] "containing
active principles, become inert when transplanted from an appropriate
soil." Bucholtz, in a series of experiments designed to test the
influence of antiseptics upon the vitality of bacteria, found not only
a difference between those taken directly from the infusion and those
cultivated in artificial fluids, but between bacteria derived from the
same source and cultivated in modifications of the nutrient
medium.[27] Then, too, it is not always safe to transfer to the human
species the results of experiments made upon the lower animals.
Indeed, among animals, not only in different species, but in varieties
of the same species, differences in the susceptibility to septicaemic
poisons are found ranging from gradations as to the intensity of the
effect produced to absolute immunity. In anthrax, a disease analogous
to the one in question, the bacterial origin has been established
beyond dispute by the inoculation of isolated bacilli, which multiply
in the blood and permeate in enormous numbers the lungs, liver,
kidneys, spleen, and glandular structures. If the same unequivocal
testimony has as yet not been obtained from isolation experiments as
regards septicaemia, it is reasonable to suppose that this is due to
the defects in the technique, for which it is presumable the ingenuity
of investigators will in future find the remedy.
[Footnote 22: _Archiv fur exp. Pathologie und Pharmakologie_,
"Beitrage zur Kenntniss der Pathogenen Schistomyceten," Band iv. Heft
3, S. 241 und ff.; Tiegel, _loc. cit._]
[Footnote 23: In this connection may be mentioned some very
interesting experiments by Dr. George Gaffky (_Experimentellen
Erzengte Septicaemie, Mittheilungen aus den Kaiserlich, Gesundh.
Amte_), in which micrococci from the blood of septicaemic mice were
successfully cultivated in a gelatine preparation, and produced, when
inoculated in small quantities, the symptoms identical with those
obtained by inoculating the blood itself.]
[Footnote 24: "Exp. Beitrage zur Lehre von der organisirte Natur der
Contagion und von der Faulniss," _Archiv fur klinische Chirurgie_, Bd.
xvii. Heft 4, S. 669 u. ff.]
[Footnote 25: "Exp. Beitrage zum Studium der septischen Infection,"
_Deutsche Zeitschrift fur Chirurgie_, Bd. vi. S. 162.]
[Footnote 26: "Lectures on the Relations of Bacteria to Disease,"
_British Med. Journal_, March 27, 1875. See also Klebs, "Beitrage zur
Kenntniss der Pathogenen Schistomyceten," _Arch. fur Pathol. und
Pharmakol._, Bd. iii. S. 321.]
[Footnote 27: "Antiseptica und Bacterien," _Arch. f. exp. Pathol. und
Pharmakol._, Bd. iv., Heft 1 und 2.]
It is, however, from the constant presence of the bacteria in infected
wounds, and their distribution through the tissues, that the argument
in favor of connecting septic symptoms with the bacteria has been
mainly deduced. Here the ground is sufficiently solid, and, judged by
ordinary laws of scientific evidence, the pathological importance of
the microspores {997} may be regarded as established. To be sure, we
find them in tongue-scrapings of healthy individuals, but
tongue-scrapings are poisonous if injected into the tissues. That they
do not ordinarily prove so in the mouth is no more singular than that
woorari can be swallowed with impunity. Tiegel[28] has endeavored to
show that round bacteria are found normally in the internal organs of
the body; but Koch[29] states that he has on many occasions examined
normal blood and normal tissues by means which prevented the
possibility of overlooking bacteria, or of confounding them with
granular masses of equal size, and that he has never in a single
instance found organisms.
[Footnote 28: _Arch. f. Path. Anat. u. Physiol. u. f. klin. Med._,
vol. lx. p. 453.]
[Footnote 29: On _Traumatic Infective Diseases_, New Sydenham Soc.
publication p. 15.]
It is stated that bacteria are sometimes absent from the blood
withdrawn during life in septic diseases. As, however, their constant
presence has been confirmed in the vessels and glomeruli of the
kidneys, it is fair to assume that those organs, acting as filters,
must have received the colonies observed in them from the general
circulation.
The difficulty of obtaining bacteria from the blood in many cases
during life in septic diseases does not, however, as was once
supposed, invalidate the theory of their pathogenic importance.
Septicaemia is at present employed as a collective term for a number
of processes which may occur singly or in combination with one
another. When a relatively large quantity of a putrid fluid is
injected into the veins of an animal, death follows from the action of
a chemical poison (sepsin). The blood during life rarely displays the
presence of bacteria, the latter disappearing in the circulation. In
animals thus poisoned blood does not possess infectious properties.
This form is termed putrid intoxication. That the poison in these
cases is, however, produced by the bacteria is shown by experiments of
Gutmann,[30] who demonstrated that bacteria from a drop of putrid
blood cultivated in Cohn's solution developed in the fluid a poison
which, when injected into the veins of dogs, occasioned death with all
the symptoms of putrid intoxication. Still more conclusive were the
experiments of Koch. This observer injected four drops of putrid blood
beneath the skin of mice. The latter died in from four to eight hours.
There were no bacteria in the blood, and the blood was not infectious.
When, however, a single drop was injected, the mice often remained
unaffected, but in a third of the cases they became ill after
twenty-four hours, death occurring in from forty to sixty hours. The
blood during life communicated the same disease to other mice, and
bacilli were always present in large numbers. In these cases the
dissolved poison in the fluid injected was too small in amount to
destroy life, and death resulted only after a period of incubation as
a consequence of the multiplication of bacilli in the blood and in the
tissues.
[Footnote 30: Vide Semmer, "Putride Intoxication," etc., _Virchow's
Arch._, vol. lxxxi. p. 109.]
In another class of cases Koch experimented, not with putrid blood,
but with a fluid produced by macerating a piece of mouse-skin in
distilled water. Of this he injected a syringeful into the back of a
rabbit. The result was peritonitis, swelling of the spleen, gray
wedge-shaped patches in the liver, and in the lungs were found
dark-red patches the size of a pea, devoid of air--all appearances in
harmony with what is designated as pyaemia. Oval micrococci were found
in great numbers {998} everywhere throughout the body. But the point
of special interest in the present connection is the fact that
wherever these micrococci come in contact with the red
blood-corpuscles the latter stick together and become arrested in the
minute capillary network. The thrombi thus formed are further enlarged
by the deposition of micrococci, which multiply, block up individual
capillary loops, and invade contiguous tissues. In the blood-current
itself, however, the micrococci do not increase in numbers, and cannot
always be found in the circulation upon a single examination, but
Doleris[31] assures us that in puerperal fever by repeated trials,
especially after a chill, he has never failed to demonstrate their
presence.
[Footnote 31: _La Fievre Puerperale, etc._, p. 120.]
As to the exact manner in which these minute bodies exercise their
pernicious influence, whether they operate mechanically, or whether
they produce a virus in the process of nutritive activity, or whether,
as is probable, both suppositions are correct, must be decided by
future investigations. It is enough for us to note that the connection
between sepsis and bacteria is intimate and vital.
3d. _Pathogenic bacteria are invariably associated with puerperal
fever, and to them the infectious qualities of the disease are due._ I
have been explicit regarding the evidence concerning bacteria in
septic diseases, because it places the question of the infectious
group of puerperal fever cases in the following position: Experiences
occurring clinically, as well as those produced upon animals, teach us
that certain lesions and symptoms, similar to those we are accustomed
to regard as characteristic of puerperal fever, results from septic
poisoning. In a large class of cases, however, the connection between
childbed fever and sepsis has been deduced rather from analogy than
direct proof. For those who chose to regard such as due to a specific
poison peculiar to the puerperal state there was really no objection.
If, however, bacteria are characteristic of septic poisoning, the
question presents itself in a different light, and we have to inquire
whether, in the less obvious cases, bacteria are present in puerperal
fever in the proportions and groupings that we find them in other
diseases due to putrid infection. Now, it is precisely proof of this
nature that has recently been abundantly rendered.
Waldeyer,[32] Orth,[33] Heiberg,[34] and Von Recklinghausen[35] found
the tissues and lymphatics of the parametria filled with pus-like
masses, which consisted, in addition to pus-cells, chiefly of
bacteria. Bacteria swarmed in the fluid of the peritoneal cavity. In
one case examined by Waldeyer six hours after death, while the body
was still warm, the peritoneal exudation was like an emulsion, and
furnished an abundant deposit which consisted almost entirely of
bacteria. Orth injected ten minims of peritoneal fluid from a woman
dead of puerperal fever into the abdomen of a rabbit. As the animal
was dying he broke up the medulla oblongata, and found in the
peritoneal fluid enormous quantities of these {999} organisms. In
puerperal fever round bacteria have been likewise found, though in
less quantities, in the lymphatics of the diaphragm and in the fluids
of the pleura, the pericardium, and the ventricles of the brain. In
post-mortem examinations of fresh subjects the serous fluids,
withdrawn under proper precautions, do not contain round bacteria
except in cases of septic infection.[36] Orth found in the purulent
contents of the vessels of the funis, in children who died of sepsis,
precisely the same formations as existed in the exudations of the
mother.
[Footnote 32: "Ueber das Verkommen von Bacterien bei der
diphtheritischen Form des puerperal Fiebers," _Archiv fur
Gynaekologie_, vol. iii. p. 293.]
[Footnote 33: "Untersuchungen uber puerperal Fieber," _Virchow's
Archiv_, vol. lviii. p. 437.]
[Footnote 34: _Die puerperalen und pyaemischen Processe_, Leipzig,
1873.]
[Footnote 35: For the views of Von Recklinghausen I am indebted to his
pupil Steurer. Vide the writer's paper on "The Nature, Origin, and
Prevention of Puerperal Fever," _Trans. of the International Med.
Congress_, Phila., 1876.]
[Footnote 36: Klebs, "Beitrage zur Kenntniss der Pathogenen
Schistomyceten," _Archiv fur exp. Pathol. und Pharmakol._, vol. iv. p.
441 _et seq._]
Doleris, in a remarkable essay already referred to, published in
1880,[37] furnishes not only conclusive evidence of the presence of
bacteria in the various tissues and serous cavities of women dying of
puerperal fever, but has added the evidence of their pathogenic
character by cultivating them apart in sterilized fluids, and by
reproducing in animals, by means of subcutaneous injections of the
isolated bacteria, the infarctions, the blood-changes, and the
suppurative processes of the original disease.
[Footnote 37: _La Fievre Puerperale et les Organismes Inferieurs._]
So far, the generic term bacteria has been employed to indicate the
disease-germs which are the active agents of infection in puerperal
fever. It is not, however, intended to assume that the germs of septic
processes are all identical, or that they all produce precisely the
same pathological conditions. Koch, indeed, maintains that a distinct
specific bacterial form is found in such closely-allied affections as
pyaemia, septicaemia, gangrene, and erysipelas, the different forms
possessing, however, this link in common--viz. that they are alike
generated in putrefying media. Singularly enough, the bacterium termo
and the bacterium commune--to which the fetidity of matters undergoing
putrefaction is due--are in themselves harmless. They are rapidly
destroyed in the circulation, and are not inoculable. Fetid discharges
from wounds are not therefore necessarily dangerous. The putrid odor
serves a useful purpose, as it gives warning of the existence of
conditions which favor the development of life-destroying organisms;
but the latter may develop without the concurrence of the forms which
give rise to putrefaction--a fact of considerable importance in view
of the common belief that septic infection is excluded by the absence
of fetid odors.
In puerperal fever Doleris found the prevailing pathogenic organisms
consisted of bacilli or rods, and micrococci or round bacteria in the
varieties of micrococci, simple points; diplococci, double points; and
chains or wreaths. The bacilli he regarded as the source of acute,
rapid septicaemia, while pus-production was associated with the
multiplication of the round bacteria, and especially of the
diplococci.
4th. _The presence of germs in puerperal fever serves not only to fix
cases hitherto doubtful in the category of septic diseases, but
affords the most satisfactory explanation of the protean phenomena of
puerperal fever itself._
We have seen, from both Koch's and Gutmann's experiments upon animals,
that death may occur independently of bacteria by the rapid absorption
of a chemical poison developed in a putrefying fluid. Clinical
experiences, such as the speedy death sometimes observed when retained
coagula or portions of placenta undergo decomposition within the
uterine cavity, renders it probable that similar cases of putrid
intoxication are {1000} not unknown in puerperal women, though, so
far, the anatomical demonstration of the fact has not been furnished.
In cases, however, where puerperal fever has a distinct period of
incubation, and progresses step by step to the fatal ending, bacteria
are always found invading the tissues of the genital canal. In rare
cases they pass by the Fallopian tube to the peritoneal cavity and
excite salpingitis and peritonitis. More commonly from local lesions
they enter the canalicular spaces of the connective tissue forming the
framework of the genital canal, which is continuous with the
subperitoneal connective tissue of the pelvis. From the canalicular
space they enter the lymphatics. Cellulitis is excited by their
presence, and the lymphatic glands become inflamed and enlarged. In
pernicious forms they produce a sero-purulent oedema, which spreads
rapidly with a wave-like progress after the manner of erysipelas; or
in milder cases the progress of the disease-germs is arrested by the
lymphatic glands or the resistance offered by the tissues themselves,
and the ordinary circumscribed phlegmon is produced. By the lymphatics
which accompany the vessels of the Fallopian tubes they reach the
ovaries (puerperal ovaritis), and by the broad ligaments they pass to
subperitoneal tissues of the iliac and lumbar regions. Through the
same system they are conveyed to the great serous cavities of the
body. In the peritoneum they give rise, unless death occurs too
speedily, to pyaemic peritonitis, which, unlike the traumatic form, is
attended with but little pain, and for which the claim has been set up
that it is peculiar to puerperal fever. The wide stomata upon the
abdominal surface of the diaphragm allows the facile entrance of the
organisms into its lymphatics. Waldeyer found in diaphragmitis the
lymphatics of the diaphragm filled with bacteria. And thus, following
the lymphatic system, if we only admit that bacteria are the active
agents of sepsis, the frequency, in severe types of puerperal fever,
of inflammation of the serous membranes of the peritoneum, the
pleurae, the pericardium, the meninges, and the joints finds an easy
explanation. Nor is it altogether accident which determines in
different cases the precise serous membranes which are affected. The
widespread ramifications of the lymphatic system would naturally give
rise to eccentric inflammations in place of those following the
apparent continuity of tissues.
The ductus thoracicus is the principal channel through which the
bacteria enter the blood. It is possible that they may further obtain
access into the circulation through the radicles which furnish the
communications between the capillaries and the lymphatics. We have
seen that bacteria are found with difficulty in the blood during life.
A few hours after death they swarm in that fluid. That they do,
however, enter the general circulation during life is incontestable.
Steurer writes: "As the kidneys are the great filters of the human
system, I never neglected to examine them, and almost invariably found
micrococci filling the arterioles and glomeruli." This is in
correspondence with what occurs in other septic diseases, and accounts
for the albuminuria and interstitial nephritis which often supervene
in the advanced stages.
The action of the bacilli upon the blood differs materially from that
of the round bacteria. So soon as the latter come in contact with the
red corpuscles, the corpuscles stick together and form larger or
smaller clots in the blood. They then are no longer able to pass
through the minute {1001} capillary networks, but are arrested in the
larger or smaller vessels (Koch). The micrococci in the resulting
infarctions multiply, and migrate into the vessels and cellular tissue
of the neighborhood. Thus fresh foci of infection are formed. Or by
their destructive action they may, when situated near the serous
surfaces, penetrate into the serous cavities, and in this way
indirectly occasion peritonitis, pleurisy, meningitis, and purulent
inflammations of the joints. When the micrococci enter directly into
the circulation, they sometimes, in passing through the heart, adhere
to the endocardium and the valves, where they cause exudation and
ulceration, and give rise to the so-called endocarditis ulcerosa
puerperalis.[38] The red globules of the blood undergo changes of
shape, assume a stellate aspect, and rapidly disappear. The white
globules are greatly increased in numbers, and the blood itself
becomes nearly colorless. A certain amount of light is thrown upon
these blood-changes by Doleris, who added micrococci to the fresh
blood of a frog and watched the ensuing changes under the microscope.
The micrococci could be seen in the act of penetrating the red
globules, which thereupon lost their color and became shrunken, and,
following the discharge of the organisms, which meantime had
multiplied in an astonishing manner, little or nothing of the original
globules remained.
[Footnote 38: Heiberg, _Die puerperalen und pyaemischen Processe_,
Leipzig, 1873, pp. 22 and 34, with references to cases reported by
Wiege and Eberth.]
In the bacillar form of septicaemia the blood is dark and has a
semi-gelatinous appearance, compared by French writers to
partially-cooked gooseberry jelly. The red globules, though they
exhibit the various stages of deformation, are not diminished in
number. The disease is further characterized by ecchymoses and minute
apoplectic effusions, and by the absence of pus-formation. In the
artificial septicaemia produced by Koch in mice by means of bacilli
the rod-like organisms were found to enter the white corpuscles and to
compass their destruction. They did not cause the red globules to
adhere together, and there was no clogging of the capillary
circulation. All the principal structures of the animals subjected to
experiment were infiltrated with bacilli. The distribution of the
latter was apparently accomplished by the blood-vessels, and not by
the lymphatics, the bacilli probably effecting their entrance into the
vessels by virtue of their penetrative power, in place of traversing
preformed pathways. Possibly it is this action of the bacilli which
causes the weakening of the vessel-walls, as evidenced by the large
number of red corpuscles which pass out from them.
In puerperal fever it is rare to find either round bacteria or bacilli
acting singly as the agent of infection. As a rule, both forms exist
together in varying proportions, the predominant form, however,
determining in general the character of the symptoms.
Thrombosis of the veins may be a physiological phenomenon, or may be
due to an alteration of the blood, to weakness of the heart, or to
local influences. So long as the clot remains firm its influence is
limited to disturbances of the circulation. The pyaemic symptoms--viz.
suppuration of the coagulum, the separation of emboli, and the
formation of metastatic abscesses--are always dependent upon the
presence of round bacteria. In phlebitis the latter are found in the
endothelium and in the sheaths of the veins. The inflammation of the
veins is followed by {1002} thrombosis. According to Doleris,
micrococci derived from the blood are deposited upon the central
extremities of the clots; beyond these depots a fresh inflammation is
set up, followed by fibrinous coagulation. Thus the micrococci become
imprisoned between two plugs. The same process may be repeated until a
series of abscesses are formed. For a time no mischief may ensue.
Finally, however, the resistance of the outworks is overcome, an
embolus becomes detached, and an infectious abscess is opened into the
blood--an event which is announced by an intense chill and the
familiar systemic derangement.
In septic diseases death takes place from apnoea, partly from the
inability of the blood-corpuscles to carry oxygen to the tissues, and
partly from paralysis of the nerve-centres.[39]
[Footnote 39: Schuller, "Exp. Beitrage zur Studium der Septischen
Infection," _Deutsche Zeitschr. f. Chir._, vol. vi. p. 149 _et seq._]
In hospital epidemics of puerperal fever diphtheritic patches situated
upon the lesions of the vulva and in the course of the utero-vaginal
canal are sometimes observed. Steurer found these patches were always
associated with loss of substance, and were composed of disintegrated
fibrin, white and red blood-globules, and colonies of round bacteria
in great abundance. Morphologically, these so-called diphtheritic
patches are identical with those which appear in the throat.
Pallen[40] has reported an instance of the simultaneous occurrence of
puerperal diphtheritis in the mother and throat diphtheritis in the
two-weeks' old child. In lying-in hospitals it is the genital organs,
as the locus resistentiae minoris, and not the throat, which are the
usual points of attack.
[Footnote 40: _Trans. N.Y. Obst. Soc._, 1876-78, p. 78.]
The question as to the extent to which erysipelas and puerperal fever
are cognate diseases is in a fair way to be solved by recent
investigation. Orth took the contents of a vesicle from an
erysipelatous patient which contained bacteria in great abundance, and
employed the same for injections under the skin of rabbits. In this
way he succeeded in producing in these animals a species of erysipelas
malignum. In the subcutaneous oedema and affected portions of the skin
he found enormous masses of bacteria, so far exceeding in quantity the
amount introduced as to prove an abundant new production.[41] Samuel
produced similar results by the injection of ordinary putrid fluids
containing round bacteria. An affection resembling simple erysipelas
he obtained most frequently by the application of fluid to a wound
torn open after the second or third day.[42] Lukomski found that
erysipelas could be produced by fluid containing micrococci even when
putrefaction did not exist. The contents of erysipelatous vesicles
containing no micrococci excited no morbid manifestations. Where the
erysipelatous process was fresh and progressing micrococci were found
in great abundance in the lymphatics and canalicular spaces. Where the
process was retrogressive, there were no micrococci to be found, even
in cases in which inflammation existed to an intense degree.[43]
Doleris submitted to the culture-process of Pasteur fluid obtained
from vesicles which developed in the course of facial erysipelas in a
man of forty years. Micrococci in chains were found in the liquids
employed identical with those he had discovered in puerperal fever. In
many cases I have seen an erysipelatous inflammation start from a
puerperal diphtheritic ulcer {1003} upon the introitus vaginae, and
extend outward over the buttocks, the thighs, and the lower portion of
the abdomen.
[Footnote 41: "Untersuchungen uber Erysipel.," _Arch. fur exp. Pathol.
und Pharmakol._, Bd. i. S. 81.]
[Footnote 42: _Arch. fur exp. Path. und Pharmak._, Bd. i. S. 335, u.
ff.]
[Footnote 43: "Untersuchungen uber Erysipel.," _Virchow's Archiv_, Bd.
lx. S. 430.]
Virchow[44] has so far given in his adhesion to the new school as to
say: "Especially in this connection are to be mentioned the
diphtheritic process and the erysipelatous, especially erysipelas
malignum. The granular deposit in diphtheritically affected tissues,
of which I formerly spoke, has more and more proven to be of a
parasitic character. What we formerly regarded as simple, organic
granules, as infiltration or exudation, has since proven to be a dense
aggregation of micro-organisms which penetrate into the tissues and
cells to compass their destruction."
[Footnote 44: _Die Fortschritte der Krieg's Heilkunde_, Berlin, 1874.]
Thus we find in surgical fever, in puerperal fever, in diphtheria, and
in erysipelas the presence of a common element which links them
together, and which establishes the relationship which has long been
recognized as existing between these various processes.
4th. _The differences between surgical and puerperal septicaemia are
due to differences partly structural and partly physiological in the
wounded surfaces exposed to septic contamination._
A certain amount of misapprehension has arisen from the circumstance
that along with many coincidences in the symptoms of puerperal and
surgical fever there are observable differences which, from a purely
clinical point of view, would justify a separate classification of the
two affections. It will not do, however, to ignore the fact that the
conditions which prevail in the parturient canal subsequent to labor
have no strict analogue in the lesions which the surgeon is called
upon to treat, and that therefore a complete identity as to all the
clinical features of puerperal and surgical fever would hardly be
within the range of possibility.
In the puerperal state it is necessary to take into account the
blood-changes induced by pregnancy, the effects of shock and
exhaustion in protracted labors, the frequency of hemorrhage, the deep
situation of puerperal wounds, the presence of clots, decidua, and
dead tissue in a state of disintegration or decomposition, the ease
with which deleterious matters are absorbed by the wide lymphatic
interspaces, the serous infiltration of the pelvic tissues, the
exaggerated size of the lymphatics and veins, and the proximity of the
peritoneal cavity.
Samuel,[45] in speaking of the immunities and dispositions to septic
poisoning, says: "The statistical frequency of septic puerperal
disease is due to the length of the parturient canal, to the fact that
through this long passage there must pass all the pathological and
physiological excretions, and to the soiling of these parts with
fingers, instruments, and secretions which have become the bearers of
sepsis." He found, on the other hand, that it was extremely difficult
to produce a progressive ichorous condition by daily painting an open
stump with a septic fluid,[46] though the same was readily obtained
when an infinitesimal quantity of septic fluid was injected underneath
a fascia.
[Footnote 45: "Ueber die Wirkung des Faulniss Process auf den lebenden
Organismus," _Arch. f. exp. Pathologie_, vol. i. p. 343.]
[Footnote 46: _Loc. cit._, p. 339.]
5th. _In the present state of our scientific knowledge it is necessary
to admit that there is a limited number of febrile and inflammatory
disturbances occurring in puerperal women, the bacterial origin of
which may be fairly questioned._ As illustrations of this class may be
{1004} mentioned: 1. Cases of catarrhal endometritis due to errors of
diet and exposure. Indeed, I have frequently, in hospital practice,
been able to trace severe cases of cellulitis, pelvic peritonitis, and
general peritonitis occurring in the winter season to the patient
getting out of bed dripping with perspiration, and clad only in a
night-dress, and going thus barefooted over a cold, uncarpeted floor
to the water-closet. 2. Cases of puerperal disorders proceeding from
emotional causes, the nervous system furnishing the first impulse to
the disturbed action. 3. Cases of excessive vulnerability in
non-pregnant women; individuals are sometimes found so susceptible
that a parametritis follows a simple application of the tincture of
iodine to the cervix. 4. Cases of pelvic peritonitis starting from old
intra-peritoneal adhesions. 5. Cases of peritonitis and
retro-peritoneal inflammations secondary to ulcerative processes in
the caecum or the descending colon. This condition is apt to be masked
during pregnancy, but starts into activity during childbed as a
consequence of fecal accumulation or of excessive purgation.
It is by no means easy to decide as to the precise nature of local
inflammations following lacerations of the cervix and the bruising or
crushing of the soft parts in long or instrumental labors. The
marvellous absence of heat, pain, redness, and swelling in wounds
treated in strict accordance with the principles of Lister, the very
slight reaction when the atmosphere is pure, and the severity of these
symptoms in overcrowded hospitals, tend indeed to strengthen the
belief that even the simplest inflammations proceeding from wounds owe
their origin in great part to septic germs. But, on the other hand, in
hospital practice it is not uncommon to observe puerperal
inflammations and febrile conditions which possess this distinctive
peculiarity--that they in no wise visibly affect the health of
puerperal patients in their vicinity. The symptoms of blood-poisoning
too are either absent or present to a subordinate extent. Probably the
difficulty is best solved by assuming with Genzmer and Volkmann[47]
that there is such a thing as an aseptic surgical fever due to the
absorption of the products of physiological tissue-changes at the seat
of injury. In surgical cases, even where the precautions of Listerism
have been faultlessly observed, febrile movements of considerable
intensity, but of no prognostic signification, are of frequent
occurrence. While in puerperal women we can never exclude the
possibility of the septic infection of puerperal wounds, it is in
accordance with clinical experience to assume that a high fever
belonging to the aseptic class may coincide with a septic process of
insignificant proportions.
[Footnote 47: Genzmer and Volkmann, "Ueber septisches und aseptisches
Wundfieber," _Samml. klin. Vortrage_, No. 121.]
GENERAL SYMPTOMS.--As in other infectious diseases, there is, from the
time of the entry of the poison into the system up to the outbreak of
fever, a distinct period of incubation. The first febrile symptoms
usually occur within three days of the birth of the child. An attack
coming on a few hours after childbirth is indicative of infection
during or previous to labor. The third day is the one upon which
ordinarily the beginning of the fever is to be anticipated. After the
fifth day an attack is rare, and at the end of a week patients may be
regarded as having reached the point of safety. Apparent exceptions to
this rule are probably referable to cases of mild parametritis, in
which the initial {1005} fever and the pain were insufficient to
attract attention to the existence of local inflammation.
The symptoms of puerperal fever vary with the character of the local
affections and with the extent to which the general system
participates in the disturbed action. The different groups of
puerperal processes possess the following pathognomonic symptoms--viz.
increased temperature, enlargement of the spleen, disturbed
involution, and sensitiveness of the uterus upon pressure (Braun).
In most cases the fever is ushered in by chilly sensations or by a
well-defined chill. This symptom, however, does not possess much
prognostic importance. A chill is significant of a sudden change
between the temperature of the skin and that of the surrounding
medium. It may, therefore, be absent in pernicious forms of fever,
provided only that the temperature changes are inaugurated slowly,
whereas it may follow a trifling increase of the body-heat if, as
sometimes happens in sleep, the moist skin is exposed to cool currents
of air. Repeated chills indicate phlebitis and pyaemia.
In order to grasp the many symptoms of puerperal fever, it is
necessary to keep separately in mind the clinical features of each of
the local processes, although in fact the latter rarely occur singly,
but to a greater or less extent in combination with others.
The symptoms of ENDOMETRITIS AND ENDOCOLPITIS.--The uncomplicated
catarrhal inflammation of the uterus and vagina is the most frequent
and the mildest of the diseases of childbed. In endometritis the
uterus is large, flabby, and sensitive upon pressure; the after-pains
are often unusually severe, involution is retarded, and the lochia
become fetid, remain sanguinolent for a longer period than usual, and
at the outset may be temporarily suspended. Sometimes the large
intestine is distended with flatus. In endocolpitis the vaginal
discharge is thin and purulent, the patient experiences pain and
burning in the acts of defecation and urination, and, where the wounds
of the vulva and vagina assume an ulcerative character, there is often
found at the same time inflammatory oedema of the labia.
The fever in these cases is ushered in frequently, but not always, by
chilly feelings, and the temperature reaches its height usually upon
the evening of the third or fourth day, is remittent, almost
intermittent in character, and rarely exceeds 102 degrees to 103
degrees F. In mild forms the occurrence of the fever is often
overlooked or is referred to disturbance produced by the secretion of
the milk. In severer attacks the febrile symptoms may continue from
three to seven days. At the end of a week the swelling of the labia
subsides, the discharge becomes thick, and ulcers, if present, begin
to assume a healthy granulating appearance.
In diphtheritic ulcerations, and in endometritis due to decomposing
remains of the ovum, the load condition is often complicated by the
invasion of the neighboring tissues.
The symptoms of PARAMETRITIS and PERIMETRITIS (Pelvic
peritonitis[48]).--The symptoms of these two affections, as would be
naturally {1006} expected from the proximity of the peritoneum to the
pelvic connective tissue, for the most part overlap. It must be very
rare for one form to occur entirely independent of the other. For this
reason it will be found convenient to consider first the symptoms
common to both morbid processes, and subsequently to direct attention
to what are believed to be points of distinction between them.
[Footnote 48: The following clinical history, together with the
statistical details, is borrowed in great part from the description of
Olshausen ("Ueber puerperale Parametritis und Perimetritis,"
_Volkmann's Samml. klin. Vortr._, No. 28), the exactitude of which I
have had abundant opportunity to verify.]
During the period of incubation there are usually no prodromic
symptoms. Elevations of temperature in the course of the first twelve
hours following labor are equally frequent under perfectly normal
conditions. Suspicious symptoms are disturbed sleep, excessively
painful after-pains, and a pulse of 80 to 90.
The beginning of the fever occurs in 90 per cent. within the first
four days of childbed; most frequently upon the second or third day,
and taking place upon the fourth day in scarcely 12 to 15 per cent. of
the cases. If five days have elapsed without fever, the period of
danger, with very rare exceptions, may be regarded as having passed.
At the outset the fever, especially in perimetritis, is ushered in by
chilly sensations or by an intense chill. The temperature rises
rapidly, though the highest point is usually not reached before the
second, and in rare cases not before the third, day. In most cases the
heat in the axilla exceeds 103 degrees, and may even mount up to 105
degrees. The decline occurs gradually, the fever ending in 70 per
cent. in the course of a week, in 20 per cent. in two weeks, and only
in 10 per cent. extending beyond that period. Protracted cases
indicate abscess formation.
The fever does not, however, always pursue a regular course. In place
of progressively declining until the termination is reached, the high
temperature of the second day may be attained upon one or more
occasions. The morning remissions are at first slight, but become
marked as the disease approaches its close. In cases of long duration
the morning hours are often free from fever, a circumstance calculated
to mislead a physician who sees his patient but once a day. A pulse of
80 to 90 beats, a disturbed sleep, lack of appetite, and sensitiveness
to pressure upon the sides of the uterus are, however, symptoms which
should serve as a warning of some disturbing cause, and should lead
the physician to renew his visit in the latter part of the day.
If, from a mistaken notion that the morbid process has come to an end,
the patient is allowed prematurely to resume her household duties, the
pains across the abdomen and along the hip and thigh return, and an
examination reveals the existence of exudation in the pelvic cavity or
upon an iliac fossa.
Errors of this kind are most frequent in cases of parametritis
associated with slight peritoneal inflammation, as the local pain is
then insignificant, and the initial chill, happening on the third or
fourth day, is apt to be ascribed to engorgement of the breasts.
Relapses after the complete disappearance of febrile disturbance occur
in 15 to 20 per cent. They are usually shorter, but sometimes more
obstinate, than the original attack. As a rare exception may be
mentioned cases with evening remissions and morning exacerbations.
In circumscribed pelvic inflammations the pulse rarely exceeds 120
beats to the minute. A pulse of 140, of more than half a day's
duration, betokens severe septic complications, and is therefore of
evil omen. In {1007} some cases the slow pulse observed after labor
makes its influence felt in the first day or two of the fever, so that
the curious phenomenon may be witnessed of a temperature of 104
degrees coinciding for a time with a pulse ranging between 50 and 70
beats to the minute.
As regards other symptoms, headache and sleeplessness are rarely
absent. Profuse sweating follows the first febrile attack, and
frequently recurs during the course of the disease.
Pain is present at the onset in the majority of cases, and is then
usually most violent. The spontaneous pain, which is due to the
affection of the peritoneum, subsides in great part in the course of
one or two days, but the sides of the uterus remain sensitive to
pressure. In the rare cases of pure parametritis, however, this
symptom may be absent altogether. The pain, like that from the
inflammation of serous membranes, is of a lancinating character.
Sometimes it is associated only with the contractions of the uterus.
After-pains occurring under unusual circumstances, as in primiparae or
after the third day, are to be regarded with suspicion.
Vomiting occurs occasionally, but is comparatively rare unless the
peritonitis becomes diffused and spreads to the region of the stomach.
The appetite is lost, and only returns, as a rule, with the departure
of the fever. The tongue is coated and moist, and constipation is
common. In other cases there is diarrhoea with rumbling in the bowels,
but without pain or tenesmus. The urinary secretion is rarely
interfered with, and when this is the case it indicates the extension
of the inflammation to the peritoneum covering the bladder.
Most cases of perimetritis and parametritis terminate in five or ten
days, the fever and other symptoms gradually subsiding. When, as may
happen in exceptional instances, the temperature falls suddenly from a
high degree to one below the normal level, the body grows icy cold,
the pulse becomes small and irregular, and symptoms of collapse
develop. But in twelve to twenty-four hours the symptoms of collapse
subside, and the disease reaches its end with a disappearance of the
alarming manifestations.
If the fever subsides within a week exudation is somewhat rare. Its
continuance beyond that date should lead to a careful exploration of
the pelvic organs. The exudation is usually demonstrable in the course
of the second week or at the beginning of the third week. It is
recognized, according to its location, by external or by internal
examination, or, where the deposit is considerable, by both methods.
In most cases the deposit is extra-peritoneal, and is situated between
the folds of the broad ligament, above and to the sides of the vaginal
cul-de-sac. It has generally a rounded form, though with less
convexity than fibrous and ovarian tumors. Sometimes, however, the
tumor is flat below, like a board. It seldom exceeds in size that of a
large apple. In fresh exudations the sensation produced is often that
of a hard tumor surrounded by a softer layer, due to continued
succulence of the soft parts. In a few weeks they may reach or exceed
the hardness of a fibroid tumor. The older the tumor, unless
suppuration sets in, the less sensitive it becomes. Often the
exudation extends to the pelvic walls. The uterus, as a rule, is
fixed, and in cases of large tumors becomes pushed toward the opposite
side, while as a consequence of later shrinkage the fundus may be
drawn permanently toward the affected side.
{1008} The cul-de-sac of the vagina is rendered broader and flatter by
the pressure of the deposit, or, when the tumor is deep enough, the
vaginal surface may be rendered convex. Behind the uterus the
exudation is as it were flattened antero-posteriorly, and in some
cases it may be felt in the form of rigid bands between the posterior
ligaments which enclose the cul-de-sac of Douglas. The ante-uterine
tumors have a spherical shape and depress the vagina anteriorly.
Tumors situated in the iliac fossa have a more or less convex form,
and may be of such considerable size that the swelling may be
recognized by the eye through the abdominal walls. As the exudation
between the broad ligaments may in these cases have been slight from
the beginning, or may have subsequently disappeared by absorption, the
iliac tumors have often apparently a spontaneous origin.
Sometimes the uterus is surrounded by exudation, and the entire pelvis
appears as though it were a mould filled with a solid mass. The fornix
is then often pressed downward, and irregular rounded masses are to be
felt through the vaginal walls.
The recognition of parametritic tumors through the abdominal coverings
is possible when they are situated above Poupart's ligament, in the
upper portion of the broad ligaments, and in the iliac fossae.
The pain and the functional disturbances in the pelvic organs depend
upon the size and situation of these inflammatory deposits. Of the
functional troubles may be mentioned frequent and painful micturition,
obstinate constipation and difficult defecation, contractures of the
ilio-psoas muscles when the exudation is seated beneath the sheath or
between the muscle and the pelvic bones, disturbances of motility in
the abductor muscles, paresis of the lower extremities, and radiating
pains in the upper portion of the thigh and in the renal and lumbar
regions, produced by pressure upon the obturator, the crural, the
cutaneous, and the sciatic nerves.
So long as fever is present the exudation rarely diminishes. If
absorption takes place in one point, growth almost certainly follows
in some other direction. When, however, the apyretic period is
reached, the exudation, as a rule, disappears rapidly, so that often
in the course of six weeks no trace of its existence remains. In a
smaller number the solid mass may persist for months or even years.
After the fever has departed the patient usually feels well. The sleep
and appetite return, the night-sweats disappear, the pulse often falls
to 50 or 60 beats, and the temperature is in many cases for a time
subnormal in character.
Where the fever persists for from five to six weeks there is always a
suspicion of abscess formation. With the exception of afternoon fever
and night-sweats the patient may feel very comfortable. Then the
exudation becomes sensitive, the spontaneous pains recur, sleep is
lost, and locomotion, defecation, and urination occasion acute
suffering. The fever becomes violent, chills announce the presence of
pus, and finally, about the seventieth or eightieth day, perforation
of the abscess takes place. The usual seat at which the pus is
discharged is just above Poupart's ligament; next in frequency
perforation takes place into the colon, and in rare instances into the
bladder, the uterus, and vagina. Fortunately, of very rare occurrence
is the discharge of pus into the peritoneal cavity, which is {1009}
naturally followed by acute peritonitis. Another likewise unfrequent
but most dangerous accident is the septic infection of the abscess--an
occurrence referred to by Olshausen to the diffusion of intestinal
gases through the walls of the tumor.
In suppuration of parametritic exudations the pus commonly forms in
small scattered collections, and rarely gives rise to large abscesses.
Although parametritis and perimetritis are usually found associated
together, there are always cases in which the one form of inflammation
so far predominates over the other as to justify an attempt to
establish a clinical distinction between them.
In the beginning of the attack, sharp pain, high fever, and tympanitic
distension of the lower abdomen are symptomatic of inflammation in the
pelvic peritoneum. Whether the cellular tissue is simultaneously
implicated can only be determined by a digital examination after the
abdominal sensitiveness has subsided. The absence of the objective
signs of cellulitis would then contribute to prove that the case had
been one in which the peritoneum had been in the main affected. On the
other hand, moderate fever, pain elicited only on pressure, and
tympanitic distension confined to the colon, coinciding with exudation
between the folds of the broad ligament, would be indicative of a
nearly pure cellulitis.
A palpable exudation is by no means the necessary product of
peritoneal inflammation. Indeed, in many cases, the distinctive
symptoms of the latter may be present for from four to eight days, and
may then subside without leaving a trace of its existence at the
pelvic brim.
The demonstration of a fluid effusion by noting the change of level
upon shifting the position of the patient is rarely possible, either
because the quantity is too small or because it quickly becomes
confined by pseudo-membranous adhesions between the intestines.
Bandl[49] mentions as a sign of local peritonitis, sometimes
noticeable, a number of resistant points or tumors near the pelvic
brim or above one of the iliac fossae, due to a matting together of
the intestines or to their adhesion to the uterine appendages. They
are distinguished from solid tumors by their emitting a tympanitic
sound upon percussion and by their changing position in consequence of
an accumulation of urine in the bladder or of feces or gases in the
bowels. Again, all tumors may be reckoned as intra-peritoneal which
very rapidly form behind or to the side of the uterus from enclosed
exudation-products, and which at the same time rise far above the
level of the pelvic brim. If, however, they start from the cul-de-sac
of Douglas, and do not much exceed the linea terminalis, or if they
occupy an iliac fossa, it becomes very difficult to decide whether
they are of intra- or extra-peritoneal origin. The peritoneal
exudation, however, long remains soft and fluctuating. It arises, as a
rule, behind the uterus, and does not exhibit a tendency to spread to
the sides or to the anterior or posterior pelvic walls.
[Footnote 49: _Handbuch der Frauenkrankheiten_, red. Von Billroth, 5te
Abschnitt, p. --.]
Still more difficult is it to decide as to the seat of exudations met
with beneath the abdominal walls. When diffused and continuous with a
pelvic deposit the diagnosis is uncertain. It is only safe to assume
the peritoneal origin of extravasations of a rounded form, of a
fluctuating consistence, and when they are situated high up and are
disconnected from exudation at the pelvic brim. An opening of the
abscess through the {1010} navel would indicate a peritoneal source,
while the discharge through the abdominal parietes would point to a
seat in the connective tissue.
After the perforation of an abscess the fever and pain subside; the
wound, if external, either closes in the course of one or two weeks,
or fistulas form which become the source of protracted suppuration.
In psoas abscesses the exudation extends beneath the sheath of the
muscle or between the iliacus and the bone. In puerperal patients they
proceed from an inflammation originating in the broad ligament. They
are situated too deep to be easily palpated. The pains they occasion
are referred rather to the hip or knee than to the abdomen. The
contracture of the psoas muscle furnishes a diagnostic sign which
distinguishes this form from the superficial abscesses of the iliac
fossae. The pus eventually is discharged beneath Poupart's ligament,
in the lower portion of the inguinal fossa, at some point upon the
crest of the ilium, or exceptionally along the thigh. Often the
discharge is maintained for months.
The symptoms of GENERAL PERITONITIS.--This form generally begins with
the usual symptoms of pelvic inflammation, but the tenderness, which
at first was limited to the side of the uterus, gradually spreads over
the entire abdomen. The abdominal pain is of a tearing, lancinating,
sometimes colicky character. It is increased by the slightest bodily
movement, by jarring of the bed, or even by the weight of the
bed-clothes.
As a consequence of the peritoneal inflammation and of the
accompanying exudation, the muscular walls of the bowels become
paralyzed, and tympanitic distension results from the accumulation of
gases. In the dependent portions of the peritoneal cavity it is often
possible to demonstrate by percussion the presence of fluid exudation,
though distinct fluctuation is rarely to be made out. The size of the
abdomen is due much more to the tympanites than to the amount of
effusion. Sometimes the liver, with the diaphragm, is pushed by the
swollen bowels to the level of the fourth or third rib, and exercises
such a degree of compression upon the posterior portion of the lungs
as to place the patient in danger of suffocation. The respirations are
jerky and attended with a moaning sound.
The loss of muscular power in the intestines permits the contents of
the middle portion to pass unchecked toward the duodenum, and thence,
upon accidental contractions of the abdomen, they may pass to the
stomach and be ejected by vomiting. The first vomited matter has a
dark-green color, and that ejected afterward presents the color of
intestinal matter. Constipation at the outset may be subsequently
followed by colliquative diarrhoea.
The fever begins, as a rule, though not always, with an intense chill,
the temperature rises to 104 degrees, and the pulse becomes small,
hard, and resistant. Its frequency rapidly increases, varying from 120
to 160 beats to the minute. The skin is sometimes dry, sometimes
dripping with perspiration. In fatal cases, as the end approaches, the
temperature frequently falls, while the pulse becomes more rapid, the
face assumes a pinched, anxious expression, sweat gathers upon the
forehead, the extremities grow icy cold, and the patient dies in
collapse. The duration of peritonitis averages not more than from four
to six days.
In cases of recovery the pulse improves, the vomiting ceases, and the
tympanites disappears. The diffuse exudation then becomes converted
{1011} into circumscribed tumors, which on palpation are felt on the
side of the pelvis and extending upward to the level of the umbilicus.
Upon internal examination the uterus is often found depressed by the
weight of the fluid, which likewise may bulge the cul-de-sac of
Douglas into the pelvic cavity. Sometimes the exudation may become
encysted above the pelvis and leave the contents of the latter free.
In still other cases the uterus may become attached high up to the
abdominal walls, so that the vaginal portion disappears and the os is
reached with difficulty.
The peritoneal exudation may, as in pelvic inflammations, become
absorbed and disappear. When, however, it is surrounded by loops of
intestines it is apt to undergo purulent and septic changes, and the
abscesses may then become discolored and filled with stinking gases.
The patient, whose previous improvement has been watched with delight,
now loses appetite, the pulse becomes frequent, the strength fails,
and death may follow from septic fever or from rupture of abscess into
the abdominal cavity.
In the pyaemic form--a still more deadly variety of peritonitis--the
symptoms differ materially from those which have been recounted. As,
however, it constitutes only a single one of the pathological changes
connected with the poisoning of the blood through the lymphatic
system, its consideration belongs properly to the study of the septic
infection.
The symptoms of SEPTICAEMIA LYMPHATICA.--The symptoms of
blood-poisoning in the infectious diseases of childbed vary to a
considerable extent according to the channel through which the septic
germs enter the general circulation. In the murderous epidemics which
prevail in lying-in hospitals the lymphatics are, as a rule, the
vessels primarily invaded. It is to this form that the cases already
described belong, where, with diphtheritic patches upon the
utero-vaginal canal and sero-purulent oedema of the parametrium, there
are associated pyaemic peritonitis and deformation of the
blood-corpuscles; or where, following the migrations of the round
bacteria, the serous cavities become successively involved, septic
vegetations gather upon the heart, and the glomeruli of the kidneys
become choked with micrococci. The lymphatic form of septicaemia
develops soon after labor, and is always ushered in by a chill. The
temperature rises to 104 degrees or even higher, and the pulse is thin
and frequent. The abdomen swells rapidly, without being especially
painful. Indeed, painless distension of the intestines is one of the
characteristics of an acute invasion of the lymphatics. Peritoneal
effusion is absent in cases which run a rapid course, and is
distinctly recognizable only in a peritonitis of long continuance. The
effusion is not so much due to exudation as to a transudation of serum
with which micrococci are commingled. At the same time the tongue is
moist, but slightly coated, and at times quite clean. Sometimes there
is diarrhoea due to catarrh or to a diphtheritic affection of the
colon. When the bowels have been constipated the administration of a
purgative may provoke discharges which it may be found difficult to
arrest. The skin is bathed in perspiration. At the beginning and
during the course of the disease bleeding at the nose is of not
infrequent occurrence.
Toward the end the pulse runs up to 140 to 160 beats, while in many
cases the temperature falls. Immediately after death the heat of the
body may for a short time exceed the highest point reached during
life. The {1012} respirations are superficial and jerky. In many
instances the face, the neck, and the fingers are blue from defective
oxygenation of the blood. At the same time the skin becomes clammy and
the extremities cold.
The sensorium, in cases which run a rapid course, is usually affected
at an early period. The patients appear somnolent, are restless in
bed, have light delirium, and respond only when spoken to loudly. As a
rule, they make but little complaint, and, were it not for the
dyspnoea, would have nothing to disturb their sense of comfort. Very
few, even as death approaches, have any idea of the danger that
threatens them. Now and then, in place of stupor, great restlessness,
and even a maniacal condition, is developed. Albumen is usually found
in the urine.
Pleurisy, so frequently associated with lymphatic septicaemia, is
frequently double, more rarely single, and begins, as a rule, with
sharp pain in the side and an aggravation of the previous dyspnoea.
Pericarditis is less frequent, and occurs usually without symptoms
toward the close of life. The joint affections are characterized by
redness and swelling, and by pain, which is sometimes so great that
touching the inflamed part suffices to arouse the patient from sopor.
Sometimes fluctuation is felt, but death occurs before perforation and
discharge of the pus.
The most frequent ending is death, which follows in from two to
twenty-one days, and, as a rule, between four and seven days. Recovery
is, however, possible.
The symptoms of SEPTICAEMIA VENOSA (phlebitis uterina, pyaemia
metastatica).--The putrid infection of a thrombus at the placental
site may take place within twenty-four to forty-eight hours after
labor. Usually, however, the approach is insidious, and the disease
develops from an apparently insignificant endometritis or
parametritis; or the patient, with the exception perhaps of a tired
feeling, of slight chilly sensations, and of profuse perspiration, may
not have been conscious of any indisposition for days preceding the
attack, or even until the first getting up from childbed. The initial
chill in typical cases is characterized by its violence and duration.
In some cases it may last for hours. It is accompanied and followed by
high temperature, the febrile attack ending with profuse perspiration
as in intermittent fever, with which it is apt to be confounded. The
fall in temperature often assumes the form of a prolonged remission.
In many cases the pulse rises and falls with the variations in the
body heat, while in others it remains permanently above the average. A
frequent pulse is always a suspicious symptom in childbed, even where
the other symptoms are apparently normal.
Erratic chills announce the lodgment of emboli in distant organs. With
the formation of metastatic abscesses in the lungs and other
parenchymatous organs the typical character of the disease changes. In
place of chills occurring at irregular intervals, followed by
remissions and periods of apparent improvement, the fever is
continuous, the pulse becomes small and rapid, while sopor, slight
delirium, a dry skin, a dry, brown, cracked tongue, and a moderately
tympanitic abdomen, give the case the appearance of one of typhus
fever.
Peritonitis is present in hardly one-third of the cases. The abdomen
is therefore flat and soft, and often is not sensitive upon pressure.
Icterus, due to disintegration of the blood-corpuscles, is an ominous
symptom.
Death usually occurs in the second or third week. In the {1013}
typhus-like cases, however, it may follow the first attack speedily.
Recovery is possible where the organs secondarily affected are not of
too great importance.
A combination of the lymphatic and venous forms of septicaemia is not
uncommon in cases running a protracted course.
The symptoms of PURE SEPTICAEMIA.--Under the title of pure septicaemia
should be placed cases in which the absorption of putrid materials
into the blood gives rise to symptoms of intense blood-poisoning
without the development of local lesions. A common example of this
form is met with in the fever which results from the presence in the
uterus of decomposing coagula or portions of retained ovum, the fever
subsiding with the removal of the disturbing cause. In like manner we
sometimes meet with cases of intense septic poisoning followed by
speedy death, in which the post-mortem examination reveals only
changes in the blood and softening of the parenchymatous organs. The
symptoms are often similar to those produced by the injection of
putrid materials containing rod-like bacteria into the vessels of
animals. As the long bacteria do not possess the capacity of
self-reproduction in the blood, to produce fatal results the quantity
of putrid fluid injected must be large or be frequently repeated. This
form is said not to be inoculable.
CAUSES.--The effects of a poisoned state of the atmosphere as a cause
of puerperal fever is best observed in the so-called nosocomial
malaria of hospitals. In days gone by, before I had learned by
experience that the safe conduct of a lying-in service depends upon
the fastidious exclusion of every source of contamination, I had
frequent occasion to witness febrile outbreaks among puerperal women
in the Bellevue Hospital, which were instantly arrested by the simple
transfer of the inmates of the affected ward to a wholesome locality,
though no changes were simultaneously made in either the personnel or
the utensils of the service. In these instances it seems fair to
assume that the previous unhealthy condition was not due to the direct
transfer of an inoculable matter from patient to patient by the
attendants, but by something residing in the air of the vacated
apartment. In the inquiry as to the production of this condition it
can be assumed that it is not caused by aggregation alone. The medical
wards of Bellevue, always crowded, have often furnished in times of
need safe receptacles for puerperal patients. It is certainly not due
to the presence of the ordinary constituents of the atmosphere. We
must therefore look for some additional element capable of unfavorably
affecting the economy. What this element really is, is demonstrated by
a familiar clinical experience. When the disturbance produced by
nosocomial malaria is not at an early stage arrested by change of
locality, the secretions of patients affected become inoculable. Then
the epidemic spreads rapidly, and assumes continuously a more and more
severe type. If during an epidemic the external genitals be carefully
watched, now and then diphtheritic patches will be noticed to form
upon them. At first these patches may disappear or yield readily to
treatment. When an epidemic has assumed a pestilential form the
patches, which may in isolated cases make their appearance at any time
in a hospital, are rarely absent in fatal cases. The composition of
the patches tells the tale of what it is in the atmosphere which
accomplishes the charnel-house work. Favoring conditions have led to
the multiplication of disease-germs {1014} in the air, and have fitted
them to become the active producers of disease.
In a patient dying in the early stages of an epidemic there may be no
diphtheritic manifestations, though the tissues and secretions are
filled with bacteria. As, however, the epidemic gains headway, the
lesions of the generative apparatus, and especially of the external
organs, which are most exposed to air, become covered with patches
which swarm with micrococci. Under the conditions named it is
certainly more in accord with ordinary scientific reasoning to
conclude that the micrococci play an important part in the production
of puerperal fever than that the puerperal fever produces the
micrococci.
To be sure, bacteria or their spores are always present in the air,
and it may be fairly asked how patients are ever spared from their
perverse industry. The answer is, that the effect produced by the
atmosphere of a hospital is dependent partly upon the quantity, and
partly upon the quality, of the suspended germs. Floating spores, when
sparsely distributed, rarely possess the power of invading a healthy
organism. In the inauguration of an epidemic the first patient
severely attacked is usually one whose powers of resistance are broken
down by prolonged labor, by hemorrhage, by poverty, or some other
condition leading to impaired vitality.
Puerperal-fever epidemics due to contamination of the atmosphere, and
not to direct contagion, do not at once reach the maximum of
intensity. At first the temperature tables indicate the prevalence of
milk fever; next follow cases closely resembling those of mild paludal
poisoning; and, finally, if these warnings are unheeded and reliance
is placed upon antiperiodic remedies rather than upon prompt closure
of the threatened ward, the pestilence develops. In the conduct of
lying-in hospitals it should never be forgotten that with the
multiplication of the septic germs the danger increases.
At the same time, the quality of the agents which pervade the air
where hospital patients are confined is an important element in the
genesis of febrile outbreaks. The bacterium termo, which causes
putrefaction, is not in itself, as we have already mentioned, a source
of danger. A stinking odor is not necessarily incompatible with a low
mortality-rate. The importance of the common forms of bacteria,
according to Pasteur, results from the fact that by their power to
consume oxygen they pave the way for the active development of the
pernicious germs, nearly all of which thrive only in media in which
that element has been materially diminished. Again, there is reason to
believe that the same germs are not[50] always equally active for
evil. Gravitz claims that the ordinary varieties of aspergillus and
penicillium found everywhere on the surface of the ground, on
moistened walls, on food of every variety, on decaying leaves and
fruit, and whose spores are universally present in the purest air, can
by a succession of cultures be gradually brought to flourish in a warm
alkaline fluid, and that they then acquire the capacity to penetrate
living tissues, to proliferate in them, to excite local necroses, and
to cause death in the course of three days. The resistance of
micrococci to carbolic and salicylic acids is found experimentally to
depend in a measure upon the {1015} nature of the vehicle in which
they are cultivated (Buchholz). The action of septic fluids varies too
with the age of the infusions, with the materials employed, and with
the conditions under which the poison-germs are generated.
[Footnote 50: Gravitz, "Ueber Schimmel vegetationen im thierischen
organismus," _Virch. Arch._, vol. lxxxi, p. 355.]
Micrococci multiply in hospitals when organic materials favorable to
their growth are present in sufficient quantities. Perrin, Quenquand
and others have shown that the hospital wards in Paris, especially
those upon the surgical and maternity divisions, contain an infinite
number of vibrios, bacteria, and all the coccus forms (Charpentier).
Robin[51] has demonstrated the existence of albuminoid matters in
water condensed upon vessels containing freezing mixtures and placed
in overcrowded wards of hospitals. When the results of crowding become
manifest, these albuminoid matters not only impart a fetid odor and
putrefy with great rapidity, but rapidly impart putrefaction to
healthy muscle and normal blood with which they are brought into
contact. Pasteur was able by the microscopic examination of the lochia
from patients in the services of Hervieux and Lucas-Champonniere to
predict, from the character of the contained organisms, an impending
attack of fever in advance of the slightest symptom betokening danger.
[Footnote 51: _Lecons sur les Humeurs_, Paris, 1867, p. 195.]
It is unquestionably the lochial discharge which makes it such a
difficult task to keep a maternity ward in a healthful condition.
Putrid blood has been found to be the most favorable material for
septic experiments. It was noticeable in Bellevue Hospital that
febrile outbreaks always arose in, and were usually confined to, the
ward in the hospital which, by a bad arrangement, was assigned to
patients for the first four or five days following confinement--_i.e._
during the period of the lochia cruenta. As puerperal fever is rare
after the fifth day, this at first sight would seem natural. But if a
patient was transferred directly after confinement, during one of
these unhealthy periods, to the ward containing the patients who had
passed the first five days, but had not completed the ten days, she
would escape the fever. It was always the same ward that required to
be disinfected. In a communicating apartment all the confinements took
place, and at all times, therefore, the conditions were present for
loading the atmosphere with the products of decomposing blood. In the
summer months, so long as the windows were open and the air was
diluted by the continuous passage of fresh currents, the patients
enjoyed immunity from nosocomial malaria. In the autumn, so soon as it
became necessary to close the windows partially on account of the cool
nights, it was not uncommon for the more trivial disturbances, such as
so-called milk fever, the hospital pulse, and catarrhal affections of
the genitalia, to manifest themselves. Through the months of February,
March, and April the mortality was usually greatest. During the winter
months there was, as a rule, crowding of patients, insufficient
ventilation, stagnation of the air, and the rapid accumulation of
disease-germs. That the later winter months should prove the most
perilous is in accordance not only with the theory of continuous
accumulation, but with the experimental fact that weeks sometimes
elapse before a decomposing substance acquires the highest degree of
virulence.
Apart from the nosocomial malaria of hospitals, there is reason to
believe in the influence at times of certain general widespread
atmospheric {1016} states which affect the entire community. In the
year 1871 the mortality from childbed in New York was 399; in 1872,
503; in 1873, 431; in 1874, 439; and in 1875, 420. Now, the excess in
the deaths for 1872 was due wholly to an increase in the cases of
metria, those from ordinary accidents remaining nearly the same as in
the preceding years. The disease certainly did not extend into the
city from the hospitals serving as foci, for the mortality at Bellevue
Hospital was hardly more than half the usual average. There was no
especial mortality that year from either diphtheria, erysipelas, or
scarlatina, but the aggregate mortality was the largest known in the
history of the city. There are no positive data connecting the civil
deaths from puerperal fever in 1872 with parasiticism, but the
prevalence of epizootics, of epidemic catarrhal affections, of
peculiarly fatal forms of pneumonia and other diseases which are now
attributed to the presence of minute organisms in the atmosphere,
renders such a source highly probable.
It is proper to say here that, though the argument is very strong in
favor of regarding the genitalia of puerperal women as the exclusive
point of entry of infectious materials into the system, it seems
impossible at the present time to make all the facts coincide with
such a theory. I have the records of a number of cases occurring
during an epidemic of puerperal fever in which patients were either
attacked with fever previous to parturition, or in whose cases the
unusual length of labor, the frequency of post-partum hemorrhage, and
the imperfect contraction of the uterus immediately after confinement
were signs of some abnormal influence exercised upon the economy at an
early period of labor previous to the existence of traumatism. That
deleterious materials may find other channels for entering the system
than a wounded surface is evidenced by the cachectic condition not
unfrequently produced in physicians by too assiduous attendance in
dissecting-rooms and places in which _post-mortem_ examinations are
conducted. One severe and rapidly fatal case of puerperal fever which
occurred in Bellevue Hospital I find it impossible to attribute to any
other cause than that the woman for five months previous to her
confinement served as a helper in a lying-in ward. The post-mortem
examination disclosed no special local lesions, but her symptoms were
those of intense septicaemia. French writers report instances of
toxaemic conditions developing in young midwives during
puerperal-fever epidemics. While we are not prepared to go as far as
Tarnier, who says, "It is probable that the lungs, by their extent and
activity, offer conditions most favorable to absorption, and that
often, if not always, it is by them that poisoning occurs," it does
not yet seem time to give up the idea that under exceptional
circumstances the respiratory and the digestive tracts may allow the
passage of materials of a septic character.
Another and frequent source of puerperal fever is by direct
inoculation. Any material of a septic character, introduced into the
genital passages of a woman during or after confinement, may produce a
general infection of the system. But the point upon which I wish
especially to dwell is that it is possible to trace epidemics of
puerperal fever directly to the carrying of puerperal poison from
patient to patient through the medium of attendants. In such cases
changes in wards and the most rigid sanitary precautions avail but
little, so long as the affected personnel is continued {1017} in
charge. Unless this fact is fully recognized, all the cleverest
devices in hospital construction will fail to prevent the occurrence
of disasters. In theory, the doctrine of the contagiousness of
puerperal fever has ceased to be the subject of dispute; and yet no
longer than thirty years ago it was combated as a pernicious heresy by
both Meigs and Hodge of Philadelphia, at that time regarded as the
best authorities upon obstetrical questions in this country. Hodge,
addressing his students, said: "The result of the whole discussion
will, I trust, serve not only to exalt your views of the value and
dignity of our profession, but to divest your minds of the
overpowering dread that you can ever become, especially in women under
the extremely interesting circumstances of gestation and parturition,
the ministers of evil--that you can ever convey, in any possible
manner, a horrible virus so destructive in its effects and so
mysterious in its operations as that attributed to puerperal fever;"
and Meigs, in his letters to students, writes: "I prefer to attribute
them to accident or to Providence, of which I can form a conception,
rather than to a contagion of which I cannot form any clear idea, at
least as to this particular malady." Contrasted with these rhetorical
utterances, in an essay published in 1843 by Prof. Oliver Wendell
Holmes, entitled _Puerperal Fever as a Private Pestilence_, the
opposing testimony in favor of contagion was presented with equal
literary and scientific skill. The evidence was complete and
conclusive, and has exercised a most beneficial influence upon the
practice of midwifery in America. With his many claims to our
admiration and esteem there is probably no title which Prof. Holmes
wears with greater pride than that of pioneer in a movement that has
done so much to prevent the slaughter of innocent women and the
wrecking of happy homes.
Thanks to changed theoretical views, physicians seem now rarely to be
the carriers of contagion. At least, in studying the records of New
York City for nine years, I find that the occurrence of two deaths
from puerperal disease, following one another so closely as to lead to
the suspicion of inoculation, occurred to thirty physicians; a
sequence of three cases occurred in the practice of three physicians:
one physician lost three cases, and afterward two, in succession; one
physician had once two deaths, once three deaths, and twice four
deaths, following one another; finally, a physician reported once a
loss of two cases near together, then of six patients in six months
and then of six patients in six weeks. Thus in the practice of more
than twelve hundred physicians in nine years I find, excluding cases
occurring in hospitals, that the experience of thirty-six only lends
color to the idea that puerperal fever is due to criminal neglect on
the part of the medical profession. Undoubtedly in many of these
cases, too, the responsibility is only apparent, as when a
practitioner has, for example, had the misfortune to lose in one week
a woman from puerperal convulsions, and another in the following week
from placental hemorrhage. Singularly enough, not one of the sequences
mentioned occurred in the practice of a physician connected with a
lying-in hospital. In face of the charge that the physicians holding
obstetrical appointments in public institutions are active
disseminators of puerperal fever through populous communities, I find
that the total loss from all puerperal causes, occurring in the
private practice of ten physicians intimately associated with such
institutions, numbered during the nine years but twenty-one cases. Of
these, thirteen were the result of ordinary {1018} accidents, and only
eight cases of metria proper, of which one was developed before the
physician was called in attendance; whereas a single physician,
holding no hospital appointment, lost during the same time
twenty-seven cases, of which twenty-one were cases of metria.
There is, however, a survival of the older ideas, chiefly to be seen
among the laity, in propositions to secure absolute immunity from
puerperal fever in hospital patients by confining them in wooden
structures or by conducting births under carbolic acid spray.
I have been interested in endeavoring to ascertain how far experience
corresponds with Semmelweis's original theory that puerperal fever
owes its origin to poisonous materials obtained from dissecting-rooms
and introduced into the genital canal by the hands of physicians
attending cases of labor. With this view I have made personal
application to a number of gentlemen who have engaged in midwifery
practice while performing the functions of demonstrators of anatomy in
our medical schools. H. B. Sands, of the College of Physicians and
Surgeons, reports that in the five years during which he held the
office of demonstrator he attended about sixty cases of labor. All did
well. He lost his first patient, from childbed, a short time after he
had resigned his position in the dissecting-room. J. W. Wright, the
present professor of surgery in the Medical Department of the New York
University, who held for one year the position of demonstrator in the
Woman's College, writes me that "during the year I attended one
hundred and four cases, including twenty-two forceps cases, two of
craniotomy, two of podalic version, and four of breech presentation.
Of this number I lost two cases, one from phlegmasia dolens
complicating uraemia, from both of which troubles the patient had
suffered during her previous labor, and one from double pneumonia, the
result of unusual exposure following confinement. Out of these one
hundred and four cases I can recall but three or four cases of
metritis, and those of a mild character; I have never thought they had
any special connection with my duties in the dissecting-room. I may
add that for ten years I have attended a pretty large number of
confinements each year, and that during the whole of this time I have
been in the habit of making autopsies as occasion has offered, and of
handling and examining pathological specimens both in and out of the
dissecting-room, notwithstanding which my death-record among this
class of cases has been unusually low." Samuel B. Ward, formerly
demonstrator at the Woman's College, at present professor of surgery
in the Medical School at Albany, writes: "While I was daily in the
dissecting-room during the winter sessions of the school from 1868 to
1872, I attended thirty-two confinements, of which I have notes. All
of the patients recovered, nor did any of them suffer from any
complication that could be traced to infection." It is familiarly
known that after Semmelweis had introduced the practice, among the
physicians attending patients at the large lying-in hospital in
Vienna, of washing the hands in a solution of chloride of lime, there
was a great diminution in the mortality which prevailed,
notwithstanding which G. Braun reports, however, that in 1857, in the
month of July, in two hundred and forty-five deliveries there were
seventeen deaths. The following month Klein gave orders to suspend the
use of disinfectants. By chance, in August there were only six deaths
out of two {1019} hundred and fifty confinements, and in September, of
two hundred and seventy-five patients, none died. From 1857 to 1860
the mortality was slight, though disinfectants were not used, while
during the three following years, in spite of the systematic and
persistent employment of these agents, the death-rate once more
assumed formidable proportions.[52]
[Footnote 52: Braun, _Ruckblicke auf die Gesundheits Verhaltnisse
unter den Wochnerinnen_, u. s. w., S. 32, 33.]
Of course I do not wish to underrate the importance of Semmelweis's
labors. There is no question but that it is a perilous experiment to
pass from the dissecting-room to a patient in labor without employing
rigorous measures to disinfect the hands and all parts of the person
brought into contact with the dead body. But it is well to call
attention to the fact that puerperal fever is not due to any single,
simple cause, nor can be effectually guarded against by a single
precaution; and, again, that an infectious poison does not of
necessity exist in every cadaver examined. Hausmann found that
injections into the vagina of gravid rabbits, in the latter half of
pregnancy, of serum from the corpse of a person who had not died of
septicaemia produced no fatal results, while rapid death resulted from
injections, under the same conditions, of pus from the abdomen of a
woman who had died from puerperal infectious disease.[53]
[Footnote 53: "Untersuchungen und Versuche uber die Entstehung der
ubertragbaren Krankheiten des Wochenbettes," _Beitr. zur Geb. und
Gynaek._, Bd. iii, Heft 3, S. 374.]
Barnes and other English writers lay considerable stress upon cases of
puerperal fever due neither to contagion nor to atmospheric
conditions, but to the poisoning of the patient by her own secretions.
There is justification for this view in the fact that even normal
lochia contain bacteria, and when inoculated into animals produce in
them affections of an ichorrhaemic and septicaemic nature. When death
takes place the tissues of animals thus treated are found to be filled
with round bacteria. Furthermore, the disease artificially produced is
in itself infectious, and can be continuously propagated in other
animals. But it may be asked, "Does not this admission cut both ways?
How is it possible, if even normal lochia possess virulent qualities,
that childbed is ever unattended by accessions of fever?" To this we
can only answer that the reasons for immunity in ordinary cases are
only known in part. Karewski[54] and other experimental investigators
have shown that the virulence of the lochia increases proportionately
to the number of days that have transpired since the birth of the
child, and that during the first three days the lochia are
comparatively harmless. Meantime, the retraction of the uterus, the
closure of the sinuses, and the formation upon the wounded surfaces of
protecting granulations, all act as natural barriers to the
penetration of poison-germs. But, aside from these reasons, there is
undoubtedly an unknown quantity calling for further investigation,
which, in the absence of positive knowledge, we are content to term
the predisposition of the individual patient. The vagina after
childbirth possesses all the conditions most favorable for the
production of putrefaction--viz. the access of air, fostering warmth,
and stagnating fluids charged with dead tissue. It is probable that
the first of these needful conditions is, in normal labors, happily
wanting in the uterine cavity. In these days of intra-uterine
medication it is well to {1020} bear in mind the relatively greater
frequency of infection through vaginal and cervical wounds, as
compared with that which takes place through the denuded intra-uterine
surface. The term auto-infection may, with propriety, be employed as a
distinctive appellation to designate those attacks of fever which, in
the absence of any demonstrable cause, occur in the early days of
childbed, and which there, quoad vitam, pursue a favorable course, and
to cases of so-called late infection--_i.e._ where, after the fifth
day, the accidental opening of a healing wound permits the tardy
absorption of poisonous secretions; but with the reserve that the
primary cause is, in point of fact, atmospheric, and the predisposing
condition the susceptibility of the individual. Cases of
auto-infection are in this country extremely rare, if not unknown
altogether, in salubrious or rural districts.
[Footnote 54: "Experimentelle Untersuchungen ueber die Einwirkungen
puerperaler secrete auf den thierischen organismus," _Zeitschr. f.
Geb. und Gynaek._, Bd. vii, 2te Th., S. 331.]
On another occasion I have shown that in New York City the death-rate
from puerperal fever is nearly twice as great during the six months
from December to May, inclusive, as from June to November. The
greatest mortality occurred in February and March, comprising rather
more than one-fourth the entire amount. The smallest number of deaths
occurred in September and October, in which months but one-thirteenth
of the entire number took place.
That puerperal fever, in its harvest of death, does not spare the
wealthy and well-to-do classes is too familiar a truth to be worthy of
discussion. That, however, the wealthy do enjoy special immunities as
compared with the less-favored members of society, I have shown by
comparisons made between sections of the city which, though lying side
by side, exhibit in a marked degree the two extremes of wealth and
poverty. Thus, the mortality among the representatives of the lower
social strata, in proportion to population, was from three to six
times as great as that among the more fortunate classes.
RELATIONS TO ZYMOTIC DISEASES.--In investigating, some years ago, the
nature, causes, and prevention of puerperal fever,[55] I prepared,
from the statistics of the Health Board of New York City, tables
extending over a period of nine years to answer the inquiry as to
whether there was any relation between the frequency of deaths from
scarlatina, diphtheria, and erysipelas and those from metria. Previous
to their publication I was anticipated in my deductions by a paper
upon the same subject by Matthews Duncan.[56] Neither Duncan nor
myself found any such relation existing between the statistical
frequency of puerperal fever and the zymotic diseases mentioned. There
was, however, nothing in our investigations to invalidate any direct
testimony which tends to show that, in individual cases, a real
connection between puerperal fever and the zymotic diseases may exist.
Indeed, it seems to me to be fairly established that a poison may be
conveyed from patients suffering from either of the foregoing morbid
processes which may be absorbed by the puerperal woman, and may in her
give rise to an infectious fever possessing an intense degree of
virulence. My friend Prof. Barker has recently drawn attention to the
important relations of intermittent fever to the puerperal state. I
have not, however, thought it advisable to complicate {1021} the
present discussion with any extended notice of his very valuable
observations. So far as malarial fever occurs unequivocally as such in
puerperal women, there is no more reason for establishing a special
category for puerperal malaria than for puerperal typhoid or puerperal
small-pox. In the class of cases characterized by sharp chills,
intense fever, irregular remissions, and profuse perspiration, which
pursue a pernicious course unaffected by antiperiodic remedies, the
nature is extremely dubious. The same symptoms are likewise
characteristic of certain forms of pyaemia, and I cannot learn that
such cases are familiar in the practice of those of our physicians who
practise outside of cities in districts where malarial affections are
most prevalent.
[Footnote 55: _Trans. of the International Med. Congress_,
Philadelphia, 1876.]
[Footnote 56: "On the Alleged Occasional Epidemic Prevalence of
Puerperal Pyaemia, or Puerperal Fever and Erysipelas," _Edinburgh Med.
Journal_, March, 1876, p. 774.]
PREVENTION.--Of the 3342 deaths from puerperal causes in New York City
from 1868 to 1875, inclusive, 420 occurred in hospital, or one-eighth
of the entire number. Of the 1947 cases of metria, about 300, or not
quite one-sixth, were contributed by the hospitals. After such a
showing the first impulse would be to cry out loudly for the
suppression of the maternities. But a wiser policy suggests an inquiry
as to whether the large mortality mentioned is an evil necessity. The
following reports will show how much may be done in the present state
of our scientific knowledge to so control the conditions which favor
the generation of puerperal diseases in large hospitals as to make
them safe asylums for the needy.
Goodell[57] has stated that at the Preston Retreat in 756 cases of
labor there have been but 2 deaths from septic disease. Winckel[58] of
the Lying-in Institution in Dresden reported, in 1873, 18 deaths from
metria, or 1.8 per cent., but from the 10th of January to the 7th of
July in 570 births there was but 1 case of septic disease; in the year
1872 the death-rate exceeded 5 per cent. The reduction in mortality
was no fortuitous circumstance, but was due to rigid measures for the
prevention of disease. Stadfeldt[59] reduced the mortality from
puerperal fever in the Maternity Hospital of Copenhagen from 1 to 37,
the proportion between the years 1865 and 1869, to 1 in 87 between the
years 1870-74. Johnston[60] reports, in the Rotunda Hospital of
Dublin, during the seven years of his mastership, 7860 births with 169
deaths, of which 85, or 1 in 91, were from metria. Braun von
Fernwald[61] in sixteen years reports 61,949 confinements in the vast
Maternity Hospital of Vienna, with 825 deaths from puerperal fever, or
1.3 per cent. In a visit made by me to the Vienna Maternity in 1883, I
was informed that the recent mortality, including difficult
operations, had been reduced to one-half of 1 per cent.
Spiegelberg[62] lost, in 901 confinements at Breslau, only 5 cases of
puerperal fever. Beurmann[63] reports that in the Hopital
Lariboisiere, under the administration of M. Siredey, the death-rate
in 1877 was 1 in 145, and in 1878, 1 in 199, confinements; in the
Hopital Cochin, under the charge of M. Polaillon, the total mortality
from 1873 to 1877 was 1 to 108.7. In 1877 there was but 1 death from
puerperal causes in 807 confinements. Upon Prof. Streng's division of
the magnificent {1022} maternity in Prague, I was told that, in
1882-83, in over 1100 confinements there had been no death from septic
causes.
[Footnote 57: _On the Means employed at the Preston Retreat for the
Prevention and Treatment of Puerperal Diseases_, p. 13.]
[Footnote 58: _Berichte und Studien_, Leipsic, 1874, S. 183.]
[Footnote 59: _Les maternites, leur organsation et administration_,
Copenhagen, 1876.]
[Footnote 60: _Clinical Reports_, from 1870 to 1876, inclusive.]
[Footnote 61: _Lehrbuch der gesammten Gynaekologie_, S. 885.]
[Footnote 62: _Ibid._, S. 748.]
[Footnote 63: _Recherches sur la mortalite des femmes en couches dans
les hopitaux_, Paris, 1879.]
When the maternity service was transferred in 1872 from Bellevue
Hospital to Blackwell's Island, it became necessary to make some
provision for so-called street-cases--_i.e._ women taken suddenly in
labor without homes, and representing the extremes of penury and want.
At first they were received, in part, by the various private
institutions of charity in New York City, but these in 1877 decided to
exclude them thenceforth, on the ground that their condition at the
time of their reception was such as to endanger the lives of the
inmates for whom the charities were specially provided. An old
engine-house was then put in readiness by the city, and under the name
of the Emergency Hospital was placed under the charge of Henry F.
Walker[64] and myself. The number of confinements in the Emergency has
averaged 220 annually. The death-rate from all causes has been 2 per
cent., which, though large, is not an unfavorable showing when we
remember that the patients all belong to the homeless class, that all
were taken in labor before their entrance, and that many of them were
in a deplorable condition at the time of their admission. The
hospital, too, receives a considerable number of patients annually who
are sent there only after protracted, and often severe, operative
measures have been fruitlessly attempted outside its walls.[65] The
building possesses, for maternity purposes, two fairly ventilated
rooms. Excellent nurses are furnished by the New York Training School
for Nurses. Mr. Osborn, a liberal private citizen, has had constructed
in the rear, but detached from the main house, a small pavilion,
modelled after that of Tarnier, for the reception of infectious cases.
The Commissioners of Charities have promptly responded to every call
made upon them to extend the facilities for the care of patients.
[Footnote 64: Dr. Walker has since resigned, and my present colleague
is Prof. Wm. M. Polk.]
[Footnote 65: From Oct., 1883, to Aug., 1884, there have been confined
168 women in the hospital. Twenty were brought in from the street just
after the birth of the child. Of these 188, not one suffered from any
puerperal affection. There were 2 deaths--1 from intestinal
ulcerations, possibly the result of the corrosive sublimate
irrigations, and 1 from exhaustion. This latter patient had been
thirty-six hours in labor before she was brought to the hospital, and
died four hours after admission. Under the admirable management of
Miss Hart, the matron, in addition to the slight mortality, there has
likewise been almost complete absence of even trivial temperature
elevations.]
Surely these results do not support the idea that it is better for a
woman to be confined in a street-gutter than to enter the portals of a
lying-in asylum. Goodell's experience shows that a hospital for
respectable married women may be so conducted that its inmates may
enjoy absolutely a greater degree of safety than do women in their
homes surrounded by all the aids that wealth can command. Equally good
results are not to be obtained in hospitals which are open to
unfortunates of every class. But there is much misapprehension and
confusion of ideas respecting the fate of these women when no
charitable provision is made for them. In Copenhagen the Maternity
Hospital is closed for from six to eight weeks in the summer-time.
During this period unmarried parturient women receive pecuniary
assistance from the hospital to enable them to obtain a place in which
to be confined. Now, Stadfeldt reports a larger mortality among this
class than among those delivered in the hospital. Yet they are
confined at a favorable season of the year, without any communication
with the furniture, the sage-femmes, or the {1023} physicians of the
hospital. As they fortunately receive nothing but money, that can
hardly be suspected of communicating contagion. What their fate would
be in New York City perhaps may be judged from the following facts:
Excluding cases confined in hospitals, nearly one-thirtieth of all the
deaths and one-twenty-fourth of the cases of metria between 1867 and
1875 are reported by four practitioners. Ten practitioners out of
twelve hundred signed the death-certificates of one-fifteenth of the
women dying from puerperal causes, and one-tenth of the cases of
metria. But it is not to be supposed that these deaths were all the
result of malpractice and incompetence. The true history of most of
them probably was that the doctor was engaged to attend the case of
confinement for a small fee, with the understanding that he should
make no calls subsequently, unless specially summoned by the friends
of the patient. The latter, left to ignorant care or perhaps without
any assistance whatever, and exposed to all the pernicious influences
bred by poverty, when illness supervened probably did not call the
physician to her aid until the time for help had passed, so that in
the end his professional functions were confined to procuring the
requisite permit for burial.
Humanity demands that charity should furnish places of refuge in which
poor outcasts can receive assistance during the perils of
child-bearing. If we must, then, have maternities, we should make them
safe, and this can be in great measure accomplished by remembering the
twofold source of danger arising from a poisoned atmosphere and direct
inoculation. A hospital must be clean, spacious, and well-ventilated,
or its atmosphere will become charged with the spores of septic fungi
and produce nosocomial malaria. The most rigid sanitary precautions
observed by the attendants will not prevent a badly-ventilated ward
from becoming unwholesome, unless unoccupied wards are kept to which
patients can be transferred upon the first admonition of danger.
Goodell states that at the Preston Retreat the wards are used
invariably in rotation. In connection with the Maternity at Copenhagen
there are a number of small supplementary hospitals scattered through
the city, which serve as safety-valves for the central institution.
Artificial methods of ventilation render the task of keeping the wards
wholesome comparatively easy. They do not need, however, to be
complicated and expensive. The good repute of the Rotunda Hospital, it
seems to me, is in large measure due to the natural ventilation
afforded by open fireplaces.
In the Vienna Clinic, according to C. Braun, the mortality between
1834 and 1862 averaged 6 per cent., and in 1842 the enormous total of
521 deaths to 3067 confinements was reached. With the introduction in
1862 of what is known as Bohm's heating and ventilation system an
immediate improvement was experienced. In the sixteen years from 1863
to 1878, inclusive, the total mortality has been 1.6 per cent., though
in that time 5464 practitioners have received an obstetrical training
in its wards. In commenting upon this change, Braun says: "I have now
from practical experience arrived at the knowledge of the fact that
the rapid and thorough prevention of putridity by adequate ventilation
is to be regarded as a good preventive measure against puerperal
fever; that it is not the number of patients in a lying-in hospital,
nor yet the number of patients in a single room, but the deficient
circulation of air--a fault {1024} which may inhere to separate
compartments in the smallest maternities--which is the important
feature in the spread of puerperal fever; that puerperal women are to
be protected from childbed diseases not by isolated buildings and
gardens, nor by walls, but by the permanent introduction of great
quantities of pure, warm air." He then adds, what is in thorough
accord with my own experience, "Before new institutions are built
greater attention than heretofore should be paid to the ventilation of
the old structures, and, where this is found defective, a system
should be substituted corresponding to the scientific requirements."
In the year 1872 puerperal fever destroyed 28 women of 156 who were
confined in the Bellevue Hospital. The service was then broken up, and
a great outcry arose against "tainted hospitals." Wooden pavilions
were accordingly erected on Blackwell's Island for the reception of
lying-in women. These buildings were constructed upon what is known as
the cottage plan. They were favorably situated in an airy location
remote from the general hospital. They were, however, heated by large
iron stoves, and no means of ventilating the wards was provided,
except by lowering the windows. In less than three months from their
occupancy an epidemic of puerperal fever made it necessary to remove
the service for a time to the Charity Hospital. The same result
followed every subsequent attempt to utilize them for maternity
purposes, until, after three years' trial, it was found necessary to
abandon them altogether.
In private practice it is likewise important that the lying-in room
should be provided with plenty of light and air. The physician should
insist upon the value of ventilation as a means of contributing to the
speedy recovery of childbed women. By hermetically sealing the
windows, through false fears of his patient's taking cold, he exposes
her to the risk of becoming poisoned with her own exhalations.
But the early experiences of the Hopital Cochin and the Hopital
Lariboisiere, costly, palace-like structures, with every appliance of
art, prove that fresh air alone does not protect patients from the
consequences of inoculation.
The great improvement in the condition of maternity patients in recent
years has been due to the application of Lister's principles to
obstetric practice. Complete antisepsis in the surgical sense is, of
course, impracticable. Adequate antisepsis has, however, been proved
to result from the observance of a variety of precautions which have
been the slow outcome of experience. These, in brief, in hospitals,
consist in protecting the patient from every known form of
contamination, and in the prompt removal and isolation of every
puerperal woman who manifests febrile symptoms.
In citing the examples of the Hopital Cochin and the Hopital
Lariboisiere, I was led to the selection because these hospitals most
strikingly illustrate the extent of the triumph of the new doctrines.
Whereas at the Lariboisiere the mortality in 1854, the year of its
opening, exceeded 10 per cent., as a result of the prophylactic
measures adopted by M. Siredey the mortality was 1 to 145 in 1877, and
1 to 199 in 1878. And at the Hopital Cochin, in 1878,
Lucas-Champonniere, with 770 confinements, was able to report but 2
deaths from puerperal causes.
{1025} As regards details, the bedsteads should be of iron and should
be frequently scrubbed with a carbolic solution; after each
confinement the palliasse upon which the woman lay should be washed in
boiling water and the straw should be burned; in place of the usual
rubber covering to the bed, Tarnier recommends tarred paper, which is
antiseptic, and costs so little that it need be used in but a single
case; all soiled linen should be instantly removed from the ward,
either to be burned or disinfected by prolonged boiling; sponges
should be banished, as, when they have once been soaked with blood,
not even carbolic acid can make them safe; nurses employed in the
puerperal wards ought not to have access to cases of labor, as
D'Espine and Karewski[66] have shown that the lochia of even a healthy
person on the third day will poison a rabbit; a patient attacked with
fever should be immediately removed, and the nurse in attendance
should go with her. At the Emergency Hospital, with the first
appearance of catarrhal affection of the genital organs or of
so-called milk fever, the wards are immediately emptied and fumigated
with sulphurous acid. In spite of recent scepticism regarding the
value of the fumes of sulphurous acid as a germicide and disinfectant,
I do not hesitate to express, after long experience, my firm
conviction as to their efficacy.
[Footnote 66: D'Espine, _"Contributions a l'etude de la septicemie
puerperale,"_ p. 18; Karewski, _loc. cit._]
Doleris[67] formulates the indications for effective prophylaxis as
follows: 1, prevent the introduction of germs (antisepsis before
confinement); 2, paralyze their action (antisepsis after confinement);
3, shut up the doors--veins, lymphatics, and Fallopian tubes
(employment of means which promote uterine contraction).
[Footnote 67: _La fievre puerperale_, 1880, p. 303.]
The first duty of the physician is to refrain from attending a case of
labor when fresh from the presence of contagious diseases or from
contact with septic materials, whether derived from the
dissecting-room or the clinic. Scepticism regarding these sources of
danger is sure in the long run to be severely punished. In a doubtful
case the least concession should consist in a full bath and a complete
change of clothing. A special coat for confinement purposes, stained
with blood and amniotic fluid, is liable to convey infection. In every
case of labor, whether in hospital or private practice, the hands and
forearms should be freely bathed in a carbolic solution before making
a vaginal examination. A nail-brush should form a part of the ordinary
obstetric equipment. Frequent examinations during labor should be
avoided. All instruments employed during or subsequent to confinement
should be carefully disinfected. In prolonged labors, after operation,
in cases of dystocia, or where the membranes have ruptured prematurely
and the foetus is dead, it is a useful precaution after delivery to
wash both uterus and vagina with warm carbolized water or solution of
corrosive sublimate (1:2000). In Vienna both Spaeth and Braun after
difficult labors introduce a suppository of iodoform, 2 to 2-1/2
inches in length, into the uterine cavity. The formula recommended
consists of--
Rx. Iodoformi, 20 grammes;
Gummi Arabici,
Glycerinae,
Amyli puri, _aa._ 2 grammes;
Ft. Bacilli, No. iij.
{1026} In their introduction the half-hand (left) should be passed to
the cervix; the iodoform bacillus should be seized by a pair of
polypus forceps and pushed into the cervical canal. The hand in the
vagina should then be used to shove the suppository upward past the
internal os. No symptoms of poisoning from the iodoform have been
observed. The disinfection is complete and prolonged. In hospitals the
woman should be bathed before entering the lying-in ward, and the
vagina should in all cases be disinfected with carbolic acid or
corrosive sublimate both before and immediately after labor. The
conduct of labor under carbolic acid spray is commended by Fancourt
Barnes. Doleris advises the application of a compress soaked in
carbolic fluid to the external genitals during the progress of labor.
Tarnier advises dressing the vulva, so soon as the head begins to
emerge, with a pledget soaked in carbolized oil (1:10). With the
recession of the head during the interval between pains a portion of
the oil is carried upward into the vagina.
In the puerperal period the warm carbolized douche stimulates uterine
retraction and promotes the rapid healing of wounds in the vaginal
canal; in hospital practice it possesses the additional advantage of
preventing the accumulation of putrid albuminoid matters in the air.
In private practice the patient should employ a new syringe; in
hospitals every woman should be supplied with a glass tube to be
attached to the irrigator. When not in use these tubes should be
immersed in carbolic acid. The stream injected into the vagina should
be continuous, like that furnished by the fountain syringe. With my
hospital patients, in place of cloths to the vulva I have been in the
habit of using oakum. By soaking the latter in a solution of carbolic
acid the vulva is surrounded by an antiseptic atmosphere.[68]
[Footnote 68: I know that of late there has been a strong reaction
against the use of vaginal injections in normal childbed, but
personally I have experienced none of the disagreeable effects
ascribed to them. Indeed, both my hospital and private patients alike
speak of them as soothing and grateful. I therefore have had no ground
to discontinue them. That they are indispensable I do not claim. They
are no longer used in Vienna, in Prague, nor in the New York
Maternity, and yet, none the less, their results have since been in
the highest degree satisfactory. At these institutions, however,
vaginal disinfection is vigorously resorted to during and immediately
subsequent to labor, and during childbed some form of antiseptic pad
over the vulva is employed.]
Pedantic as these directions may seem, they are justified by
experience, and the carrying out of the details given easily becomes a
matter of habit. That by such precautions puerperal fever is destined
to be erased from the list of dangerous diseases attacking the woman
in childbed is saying more than is warranted. Nevertheless, it is true
that a physician ought never to lose the sense of personal
responsibility for its occurrence. Indeed, puerperal fever ought to be
regarded as a preventable disease, and an attack as the evidence that
some source of danger has been overlooked, though, owing to the
imperfection of our knowledge, it may easily happen that even with the
keenest scrutiny the precise cause in an individual case may escape
detection.[69]
[Footnote 69: Since the above was written Dr. Garrigues has furnished
a most extraordinary example of the efficacy of the antiseptic
treatment at the New York Maternity Hospital. From the years 1875 to
1882, inclusive, the number of confinements was 2827; the deaths 116,
or a little over 4 per cent. The highest percentage was reached in
1877--viz. 6.67; the lowest in 1881, when it fell to 2.36. In 1883, of
345 women confined, 30 died. In September of that year there were 9
deaths, and of 5 puerperae who were seriously ill, 1 died later. At
this time he introduced a series of reforms of which the following,
omitting details, gives the essentials: Wards fumigated with
sulphurous acid fumes, and the floors and furniture washed with a
solution of corrosive sublimate (1:1000). Every patient, on entering
the lying-in ward after the bath, had her abdomen, buttocks, genitals,
and thighs washed with sublimate solution (1:2000). During labor
vagina irrigated with latter solution. In prolonged labors irrigation
repeated every three hours. Great care of hands on part of doctor and
nurses. Glycerine and corrosive sublimate (1:1000) used for
lubricating fingers before making internal examinations. Antiseptic
pad applied to the head during its egress, and to the vulva until the
secondines had been expelled. Absorbent cotton covered with netting
soaked in corrosive sublimate solution applied to external genitals
during childbed period. This latter applied and removed with the same
care as in dressing a wound after a capital operation. Irrigation,
first of the vagina and afterward of the uterus, immediately after
labor in cases where the hand or instruments had been passed into the
uterine cavity.
When the details of this treatment were first published by Garrigues,
many took a humorous view of it, but mark the result: In the following
162 confinements there were no deaths, and from October to July,
inclusive, of the present year, of 409 patients confined, though many
operations were performed, 5 died; but of these, 3 only were from
septic causes, and they, Garrigues believes, were the result of the
neglect of certain of the prescribed details.]
{1027} Before terminating this section upon the prophylaxis of
puerperal fever, I take great satisfaction in furnishing from
Tarnier's recent treatise the following description, by Pinard, of the
ingenious pavilion designed by Tarnier to make it possible to secure
for hospital patients, at the minimum expense, the benefits of
isolation, and to provide for each room in the pavilion all the
conditions favorable to rapid and complete disinfection.
The pavilions are two-storied and of a rectangular shape, twenty-four
feet in width by forty-six feet in length. The front and rear face to
the north and south, the ends to the east and west. Two main
partitions divide the interior into three divisions. Each end division
is subdivided by a central partition into two chambers, so that each
story has five compartments--a central one for the attendants, and
four at the four corners destined for the reception of patients. On
the ground floor the central compartment consists of a vestibule
facing to the north, and an office facing to the south. On the former
are placed the staircase, the water-closet, and a reception-closet. In
addition to the main entrance there are three interior doors--one
leading to the water-closet, one to the closet, and one to the office.
The latter, for the occupation of the person on duty, contains a
heater, a portable bath, a table, chairs, and wardrobe. Two windows
face the south. The office has two doors, one opening into the
vestibule, and the other, in the opposite side, opens directly
outward. The four corner rooms for patients have each a door and a
window, the latter looking from the end of the partition and reaching
to the floor, and the former opening out from the facade. These four
rooms are therefore not only independent of one another, but have no
communication with the vestibule or the central office. On the second
floor the arrangement is similar, except that the rooms open upon a
balcony, by means of which communication from the outside is rendered
possible. Upon each facade a glazed screen furnishes shelter in rainy
weather. The screen extends to the roof, but is not in direct contact
with the walls, a space being left for a current of air. The eight
rooms for patients, four on each story, are severally fourteen feet
long, eleven and a half feet wide, and ten feet high. Below, the
floors are of asphaltum; above, of flags or slates. The walls and
ceilings are stuccoed and covered with oil paint. The corners are
rounded to prevent the accumulation of dust. To facilitate {1028}
washing, the floors slant toward a gutter communicating by means of a
pipe with the sewer. In each room panes of glass enable patients and
the office attendant to see one another, so that surveillance is
secured without sacrificing the principle of isolation. The furniture
of the rooms consists of an iron bedstead with metallic springs. The
pillow, bolster, and palliasse are stuffed with straw. In addition,
each room is provided with a night table, a round table, a chair, a
stool, and a crib--all of iron. A bell-rope at the bedside, the wire
of which passes to the office by the outside of the building, enables
the patient to summon assistance. Each room likewise contains a
washstand, with faucets for hot and cold water, the latter supplied
from a cistern on the roof, the former from the office heater. The
patients remain in the rooms where they are confined until they are
discharged. When this takes place the chamber is aired, the furniture
is removed and washed with care, the straw is burned, and the walls
are washed with an abundant supply of water. If a patient is taken
ill, she is carefully isolated, and has assigned to her her own
especial attendant and physician, who do not come into contact with
other puerperal patients.
That the plans of construction in the Tarnier pavilions would require
some modification to adapt them to the rigor of our winters seems
probable, but the principles which they illustrate are sufficiently
vindicated by the results so far reported--viz. 6 deaths in 1062
confinements, whereas in the old Maternity the death-rate, formerly
amounting to 5 per cent., still aggregates 2 to the 100.
TREATMENT.--When the septic germs characteristic of putrid infection
have once entered the blood, they are beyond the reach of the
physician. Except, however, in cases of acute septicaemia, where the
quantity of poison introduced at the outset is excessive, the patient
rallies from the immediate shock, and, provided no fresh pyrogenic
material finds its way into the system, recovery is to be anticipated.
The indications for treatment are, therefore, to neutralize the
puerperal poison at the point of production, in order to prevent its
causing further mischief, and to adopt measures calculated to enable
the patient to tolerate its presence, when once absorbed, until it is
either eliminated or loses its harmful properties.
Toward the fulfilment of the first indication it is to be recommended
that in every case of fever of puerperal origin the vagina be cleansed
with a 2 to 3 per cent. solution of carbolic acid or corrosive
sublimate (1:3000) every four to six hours. The douche in itself is
absolutely harmless. In most cases the infection starts from the
wounds of the vagina and of the cervix. Then, too, the tendency of the
secretions to stagnate in the vaginal cul-de-sac, bathing as they do
the cervical portion, is a prolific source of septic trouble. In all
but the mildest cases the vaginal orifice should be examined with
reference to the existence of puerperal ulcers. All necrotic patches
should be touched with hydrochloric acid, with a 10 per cent. solution
of carbolic acid, with iodoform, or, what I personally prefer, a
mixture composed of equal parts of the solution of the persulphate of
iron and the compound tincture of iodine. The latter acts as a
powerful antiseptic, while the former, by corrugating the tissues,
closes the lymphatics and shuts up the portals through which the
septic germs penetrate into the system.
{1029} Intra-uterine injections should be resorted to with extreme
circumspection. They are not indicated by a simple rise of
temperature. A very large proportion of the febrile attacks which
occur in childbed run an absolutely favorable course. Unless the
infection--and this is not the rule, but the exception--proceeds from
the uterine cavity, they are unnecessary. In circumscribed
inflammations, where the morbific poison loses its virulence at a
short distance from the puerperal lesion, they are often injurious. It
is difficult, if not impossible, to so conduct them as to avoid
opening up afresh recent granulating wounds. Yet the practice of local
disinfection is warmly advocated by Fritsch, Schuller, Langenbuch, and
Schroeder as a prophylactic against puerperal affections. On the other
hand, Braun von Fernwald, with his vast opportunities for judging
obstetrical questions, writes with reference to this: "We must protest
against injections made by physicians into the uterine cavity. Such
meddlesomeness is more likely to do harm than good." This corresponds
with my own experience. In theory, the proposition to treat the uterus
as one would any other pus-secreting cavity seems rational, but I have
found that every attempt to carry the theory to its logical conclusion
in hospital practice has been followed by a rise in the puerperal
death-rate. Runge reports an epidemic of puerperal fever in
Gusserrow's clinic brought about by the employment of intra-uterine
irrigations, during which the mortality rose to 3.8 per cent. With the
abolition of the irrigations the mortality sank to .39 per cent. In
1880, Fischel[70] introduced the so-called permanent irrigations into
the Prague maternity. Of 880 patients, 9 died of sepsis. The
irrigations were then prohibited. The following year, of 933 patients,
only 2 died from the same cause, and in 1882, of 521 patients, there
were no deaths from sepsis. Fehling, who limited the use of
intra-uterine injections to special momentary indications, reported,
in 1880, 415 confinements without a single death.
[Footnote 70: "Zur Therapie der Puerperalen Sepsis," _Arch. f.
Gynaek._, vol. xx. p. 41.]
Among the accidents which have been referred to the use of injections
are convulsions, shock, and carbolic-acid or corrosive-sublimate
poisoning; but the chief danger lies in the possibility of conveying
the infectious materials from the vagina to the previously normal
uterus. There seems to be no question as to the superior effectiveness
of corrosive sublimate as a germicide. It not only acts more rapidly
than carbolic acid, but its action is more permanent. In the usual
proportion of 1:2000 it is apt, when repeated frequently as a vaginal
douche, to corrugate the vagina and cervix. When used for
intra-uterine irrigation great pains should be taken that no portion
of the fluid remain behind in the uterine cavity. Since its
introduction into the Emergency Hospital there has been one death from
ulceration in the colon, which possibly was attributable to its use.
It is to be hoped the claim that corrosive sublimate is an efficient
antiseptic in the proportion of 1:10,000 may prove well founded.
In pressing the necessity of caution and discrimination, I have not,
however, intended to discourage the employment of intra-uterine
antisepsis in cases where it is strictly indicated. Thus, it would be
folly, in a fever due to the decomposition of placental debris, of
shreds of decidua, of strips of membrane, or of retained coagula, or
in diphtheritis of the mucous membrane, to treat the general symptoms
and neglect {1030} the local cause of difficulty. In a specific case
it may prove difficult to decide as to the correct course to pursue.
In general it may be stated that it is proper to wash out the entire
length of the genital canal when fever follows prolonged operations
conducted within the uterine cavity or the birth of a dead foetus, and
in cases of fever associated with a fetid discharge which persists in
spite of the vaginal douche, with the presence of recognizable
portions of the ovum or its dependencies in the lochia, with the
repeated discharge of decomposed coagula, or with a large, flabby
uterus. It will, however, be seen that with proper disinfection during
and immediately after labor, the occasions for late intra-uterine
injections are extremely rare.
The operation of cleansing the uterus should be conducted with the
most scrupulous care. The syringe employed should produce a continuous
and not an interrupted stream, and all air should be expelled from the
pipe. The tube to be passed through the cervix should be of glass, of
the size of the little finger, and bent somewhat to conform to the
pelvic curve. The vagina should first be subjected to a thorough
disinfection, by way of precaution against conveying septic materials
into the uterus. The introduction of the tube should be made with the
guidance of two fingers passed through the external os. But slight
force is requisite to reach the internal os. It is neither necessary
nor desirable to push the tube to the fundus. The fluid injected
should be tepid, and, if carbolic acid is used, of the strength of two
or three drachms to the pint; if corrosive sublimate is employed, the
strength should not exceed 1:3000. It should be introduced very
slowly, and pains should be taken to ensure its unimpeded escape,
which can usually be accomplished by pressing the anterior wall of the
cervix forward by means of the glass tube. Langenbuch recommends
securing permanent drainage by leaving a bit of rubber tubing in the
cervical canal--a plan concerning the merits of which I am not able to
speak from experience. The tube is said to be well tolerated, and to
possess the advantage of enabling subsequent injections to be
performed without disturbing the patient.
In many cases the results of intra-uterine treatment are very
striking. Often the temperature falls notably within an hour or two of
the operation. This result is, however, rarely permanent. Usually the
fever recurs, and the operation has to be repeated. The patient should
be carefully watched, and with the first sign of returning danger the
injection should be repeated. Two or three injections may thus be
called for in twenty-four hours, and they may require to be continued
for a week. Still, by the means indicated a certain pretty large
proportion of women seemingly destined to destruction in the end make
favorable recoveries.[71]
[Footnote 71: The admirable monograph of Dr. T. G. Thomas, entitled
_The Prevention and Treatment of Puerperal Fever_, has already done
much good in calling the attention of the profession at large to the
practice of local disinfection. His experience, however, based upon a
very large consulting practice, has perhaps been of a kind to furnish
him with an undue proportion of puerperal cases calling for
intra-uterine treatment. With increasing care in the management of
labor and of the birth of the child there seems reason to hope that
the necessity for the treatment he so eloquently advocates may, in the
near future, disappear entirely.]
Ehrendorfer[72] relates a case of septic endometritis and erysipelas
{1031} starting from the genital organs, in Spaeth's Clinic, where,
after seven days of ineffective uterine irrigations, two bacilli,
containing together ten grains of iodoform, were introduced into the
uterus. The washings with carbolic acid were then stopped. On the next
day the discharge was diminished and the odor was less marked. On the
fourth day two new iodoform bacilli were introduced. The patient, in
spite of the fact that the erysipelas spread over nearly the entire
body, eventually recovered.
[Footnote 72: "Ueber die Verwendung der Jodoform staebchen bei der
intrauterinen nach behandlung im Wochenbette," _Arch. f. Gynaek._,
vol. xxii. S. 88.]
Of the symptoms, the first in order which calls for treatment is
usually the peritoneal pain. It is, as we have seen, commonly of a
lancinating character, and is associated with hurried breathing and
extreme frequency of the pulse. So soon as the pain is once fairly
under control the violence of the onset begins to abate. It should be
met, therefore, by the hypodermic injection of from one-sixth to
one-third grain of morphia in solution. The anodyne action should be
maintained by doses administered by the mouth in quantities and at
intervals suited to the severity of the case. The most important
object to be secured is freedom from spontaneous pain. It is,
moreover, good practice to push the opiate until pain elicited by
pressure is likewise controlled, provided it can be accomplished
without producing narcosis. In susceptible patients and in localized
inflammations the quantity required may not be very great, while in
acute general peritonitis the tolerance of the drug exhibited by
puerperal women is sometimes extraordinary. Thus, a patient of Alonzo
Clark took the equivalent of 934 grains of opium in four days; a
patient of Fordyce Barker 13,969 drops of Magendie's solution in
eleven days; and one of my own, at the Maternity, the equivalent of
over 1700 grains of opium in seven days.[73] In this latter instance
the patient was to all appearance moribund when the treatment was
begun. Thus, the features were pinched, the face was drawn, the pupils
were dilated, the finger-tips were blue and cold, the respirations
were rapid, and the pulse was scarcely perceptible. In this condition
the large doses of opium did not produce narcosis, but were followed
by restoration of the circulation, by normal breathing, and by the
disappearance of the symptoms of shock. Any attempt to relax the
treatment was at once succeeded by a recurrence of the alarming
symptoms. At the expiration of the disease the opium was discontinued
abruptly without detriment to the patient.
[Footnote 73: The details of this case have been reported in the _Am.
Jour. of Obst._, Oct., 1880, p. 864, by Dr. F. M. Welles, who
conducted the administration of the opium.]
In contrast to cases of acute peritonitis an extreme susceptibility to
opium is often observed in the pyaemic variety. Here opiates seem to
me rarely to do good. They do not hinder the migrations of the round
bacteria, there is rarely pain to relieve, and I have sometimes
thought that their administration was simply the addition of a second
poison to the one which already was overwhelming the nervous system.
In pelvic peritonitis, in the course of forty-eight hours plastic
exudation is thrown out and the pain to a great extent subsides. From
this time very moderate doses of opium, as a rule, are needed to make
the patient comfortable.
In France leeches applied to the abdomen are much used as a means of
relieving peritoneal sensitiveness. That they do this is beyond
question. {1032} Their disuse in this country is due probably more to
popular prejudice than to their inefficacy.
In the beginning of an attack a turpentine stupe to the abdomen is a
source of comfort to many women, while the sharp counter-irritation
exercises possibly a favorable influence upon the course of the
disease. At a later period I commonly employ flannels wrung out in
water and covered with oil-silk to prevent speedy evaporation. It is
an old experience that in the beginning of a puerperal fever the
provocation of loose stools by purgatives is frequently followed by a
fall in the temperature and a great improvement in the patient's
condition. The result, however, is far from uniform, as in other cases
these artificial diarrhoeas have a tendency to aggravate the
peritoneal symptoms. Owing to this uncertainty in their action,
purgative remedies should be administered with caution, not from any
theory as to their eliminative powers, but because of the ascertained
existence of fecal accumulation. In pelvic inflammations castor oil in
two- or three-tablespoonful doses, or five to ten grains of calomel
rubbed up with twenty grains of bicarbonate of sodium, as recommended
by Barker, may be given when thus indicated. After the bowels have
once been freed, however, the purgative should not be repeated. In
cases of intense local inflammation and in general peritonitis enemata
should alone be employed for the removal of constipation.
Every increase of body-heat is associated with rapid tissue-waste,
with enfeebled heart-action and with exhaustion of the nerve-centres.
Since the modern recognition of the deleterious effects of high
temperatures per se, antipyretic remedies in place of the old-time
cardiac sedatives have come to play the leading role in the treatment
of fevers.
Of internal antipyretic agents quinia enjoys a deservedly high repute.
In the remitting forms of fever it may be administered in five-grain
doses at intervals of four to six hours. Given thus in medium doses,
it moderates the fever, diminishes the sweating, and in most patients
lessens gastric and intestinal disturbances. In continued fevers it
should, on the contrary, be given in a single dose large enough to
procure a distinct remission. By making a break in the febrile
symptoms, if only of a few hours' duration, a retardation of the
destructive processes is accomplished. At the first administration
twenty to thirty grains may be given. In favorable cases the
temperature falls in the course of a few hours below 101 degrees. When
the high temperature is only temporarily held in check, at the end of
twenty-four hours, if all symptoms of cinchonism have disappeared, the
same dose should be repeated. If the doses mentioned, given in the
manner prescribed, produce no perceptible effect upon the fever, their
continuance may be regarded as unnecessary.
C. Braun and Richter speak favorably of the action of salicylate of
sodium.[74] It possesses antipyretic properties, though in a less
degree than quinia. It is, however, rapidly absorbed, circulates
through all the parenchymatous organs, and finally is discharged
unchanged in the urine. It is said by Binz, in small doses, to hinder
the action of the disease-producing ferments, while it leaves
untouched the normal ferments of the organism. It is of special
service where quinia is not well tolerated, or when given fifteen to
twenty grains at a time every four to six hours as {1033} an adjuvant
to large single doses of quinia. The remedy should be continued until
all traces of febrile disturbance have disappeared.
[Footnote 74: Richter, "Ueber intrauterine Injectionen," etc.,
_Zeitschr. fur Geburtsk. und Gynaek._, Bd. ii. Heft 1, p. 146.]
A more powerful remedy than salicylic acid, where quinia has failed,
is the Warburg's tincture. Some patients find, however, that it is
somewhat difficult to retain upon the stomach.
Not many years ago, owing to the encomiums of Fordyce Barker,[75] the
tincture of veratrum viride was in great favor in puerperal fever as a
means of reducing the excited pulse of inflammation. The plan
recommended was to administer five drops hourly, in conjunction
usually with morphia, until the pulse was brought down to 70 or 80
beats to the minute. If the pulse had once been reduced, then three,
two, or one drop hourly would be found sufficient to control it.
Vomiting and collapse from its use were no cause for alarm, as they
were temporary symptoms, and were followed by a fall of the pulse to
30 or 40 a minute, which was rather of favorable prognostic
significance. In the rapid pulse of exhaustion, however, veratrum
should not be given. Since the introduction of the thermometer into
practice the reduction of the pulse by veratrum has been found to be
associated with a fall in the temperature of the body. Of late,
however, veratrum has gone rather out of vogue, not because it is not
a very effective agent, but because its administration is an art to be
acquired, and cannot safely be entrusted to an unskilled assistant.
Then, too, in the last ten years there has grown up a better
acquaintance with less dangerous remedies.
[Footnote 75: _The Puerperal Diseases_, p. 347.]
Braun recommends in severe cases, where quinia alone is without
effect, to give in addition from twelve to twenty-four grains of
digitalis in infusion per diem until its specific action is produced.
Unlike veratrum, digitalis effects a permanent slowing of the heart.
By prolonging the cardiac diastole and contracting the arterioles it
allows the left ventricle to fill, restores the arterial tension,
diminishes correspondingly the intravenous pressure, and promotes
absorption. Its tendency to produce gastric disturbances and the
distrust felt as to its safety have prevented its becoming popular in
practice.
Alcohol as an adjuvant to treatment is indicated in all cases, whether
quinia or salicylic acid or veratrum be simultaneously employed. It
stimulates and sustains the heart, it retards tissue-waste, and is in
itself an antipyretic of no mean value. Usually I give it in
conjunction with quinia, one or two teaspoonfuls hourly of either
whiskey, rum, or brandy, in accordance with the recommendation of
Breisky.[76] But many years before I had learned from my friend Prof.
Barker that the specific influence of veratrum was in many cases not
obtained until the use of alcohol was combined with it.
[Footnote 76: _Ueber Alcohol und Chinin-behandlung_, Bern, 1875.]
The antipyretic action of drugs is probably due for the most part to
some direct influence they exert upon the oxygenation of the tissues.
Of course the less the fire the less the heat. It is well, however, to
support their internal administration by the external employment of
cold. Cold owes its effect in fevers partly to the abstraction of heat
from the body-surface, and in a still more important degree to the
impression which it produces upon the nervous system. In healthy
persons the action of cold is to increase the consumption of oxygen
and the production of carbonic {1034} acid. The additional heat thus
generated renders it possible to sustain the vicissitudes of climate.
In fevers the primary effect of cold is similar in character. Its main
therapeutical action is derived from its secondary influence upon the
nerve-centre which regulates the body-heat. If the cold employed be
sufficiently intense or sufficiently prolonged, there follows, not
always immediately, but in the course of an hour or two, a marked
lowering of the temperature, which can only be accounted for by
assuming an indirect influence exerted through the sympathetic nerve
and the medulla oblongata. This peculiarity renders the external
application of cold a most valuable addition to the therapeutical
resources available in fevers.
In cases of moderate severity frequently sponging the patient with
cold water will be found to be a grateful practice. An ice-cap to the
head, where the blood lies near the surface, will often affect the
entire temperature of the body. From immemorial times it has been
employed to control delirium and promote sleep. An ice-bag placed over
the inguinal region is locally beneficial to deep-seated pelvic
inflammations, and, according to Braun, is capable of effecting a
rapid fall of temperature. Ice-cold drinks should be freely allowed.
Schroeder recommends a permanent stream of cold water in the uterine
cavity by means of a large irrigator and a drainage-tube; others
advise cold rectal injections maintained for long periods by the aid
of a tube with a double current.
In fevers of great violence the systematic application of cold by
means of baths or the wet pack is capable in some cases of rendering
important service. The temperature of the bath should range from 70
degrees to 80 degrees. Its duration should not exceed ten minutes. The
patient should, when removed to the bed, be wrapped in a sheet without
drying, and should be comfortably covered. In employing the wet pack
two beds should be placed side by side. The body and thighs of the
patient should be wrapped in a sheet wrung out in cold water, and be
allowed to remain in the pack from ten to twenty minutes. As the sheet
becomes heated the patient should be placed in a fresh one upon the
second bed, and the transfers should be continued until the desired
fall of temperature is effected. Braun claims that four packs are
equivalent in action to one full bath.
Both these methods are, however, open to the objection that they
cannot be carried out without considerable disturbance of the
patient--a point of no small importance in cases of peritonitis. G. B.
Kibbie has invented a fever-cot which obviates the ordinary
difficulties of this mode of treatment. The cot is covered with "a
strong, elastic cotton netting, manufactured for the purpose, through
which water readily passes to the bottom below, which is of rubber
cloth so adjusted as to convey it to a vessel at the foot." T. G.
Thomas,[77] who has employed this apparatus extensively to reduce high
temperatures after ovariotomies, explains as follows the modus
operandi: "Upon this cot a folded blanket is laid, so as to protect
the patient's body from cutting by the cords of the netting, and at
one end is placed a pillow covered with india-rubber cloth, and a
folded sheet is laid across the middle of the cot about two-thirds of
its extent. Upon this the patient is now laid; her {1035} clothing is
lifted up to the armpits, and the body enveloped by the folded sheet,
which extends from the axillae to a little below the trochanters. The
legs are covered by flannel drawers and the feet by warm woollen
stockings, and against the soles of the latter bottles of warm water
are placed. Two blankets are then placed over her, and the application
of water is made. Turning the blankets down below the pelvis, the
physician now takes a large pitcher of water, at from 75 degrees to 80
degrees, and pours it gently over the sheet. This it saturates, and
then, percolating the network, it is caught by the india-rubber apron
beneath, and, running down the gutter formed by this, is received in a
tub placed at its extremity for that purpose. Water at higher or lower
degrees of heat than this may be used. As a rule, it is better to
begin with a high temperature, 85 degrees, or even 90 degrees, and
gradually diminish it. The patient now lies in a thoroughly soaked
sheet, with warm bottles to her feet, and is covered up carefully with
dry blankets. Neither the portion of the thorax above the shoulders
nor the inferior extremities are wet at all. The water is applied only
to the trunk. The first effect of the affusion is often to elevate the
temperature--a fact noticed by Currie himself--but the next affusion,
practised at the end of an hour, pretty surely brings it down. It is
better to pour water at a moderate degree of coldness over the surface
for ten or fifteen minutes than to pour a colder fluid for a shorter
time. The water slowly poured robs the body of heat more surely than
when used in the other way. The water collected in the tub at the foot
of the bed, having passed over the body, is usually 8 degrees or 10
degrees warmer than it was when poured from the pitcher. On one
occasion Dr. Van Vorst, my assistant, tells me that it had gained 12
degrees. At the end of every hour the result of the affusion is tested
by the thermometer, and if the temperature has not fallen another
affusion is practised, and this is kept up until the temperature comes
down to 100 degrees, or even less. It must be appreciated that the
patient lies constantly in a cold wet sheet, but this never becomes a
fomentation, for the reason that as soon as it abstracts from the body
sufficient heat to do so it is again wet with cold water and goes on
still with its work of heat-abstraction. I have kept patients upon
this cot enveloped in the wet sheet for two and three weeks, without
discomfort to them and with the most marked control over the degree of
animal heat. Ordinarily, after the temperature has come down to 99
degrees or 100 degrees, four or five hours will pass before affusion
again becomes necessary."
[Footnote 77: "The Most Effectual Method of Controlling the High
Temperature occurring after Ovariotomy," _N.Y. Med. Jour._, August,
1878.]
Since reading this account, I have made a good many trials of the
method upon puerperal women, and have not found that it agrees with
all in an equal degree. In some instances the affusions have been
followed, in spite of hot bottles to the feet and the administration
of stimulants, by such a degree of depression and impairment of
cardiac force, as shown by the persistent coldness of the extremities,
that it has been necessary to discontinue them. On the other hand, I
can look back upon cases, apparently so desperate that the condition
of the patients was looked upon as hopeless, where they proved the
means of saving life as by a miracle. Of course, the difference
depends upon whether the high temperature is the sole cause of the
alarming symptoms, or whether the latter are in part due to
blood-dissolution and secondary changes in the parenchymatous organs.
{1036} The use of the coil in fever, whether of rubber or of metal
tubing, I can highly recommend. Either the night-dress or a towel
should be placed between the coil and the skin. A current of cold
water passing through the tube rapidly abstracts the surface heat, and
is usually grateful to the patient. The lowering of the temperature by
this means is much slower than by cold affusions. Disturbance of the
patient is, however, avoided, and the method, so far as I have tried
it, has been free from the objections incident to the direct
application of water to the skin.
It is hardly necessary to state that in puerperal, as in other fevers,
the patient's strength requires to be sustained and the waste of
tissue to be repaired, as far as possible, by the regulated
administration of liquid food, as milk and beef-tea, in such
quantities as can be borne by the stomach, and at one to two hours'
intervals.
In the treatment of encysted peritoneal effusions, and in inflammatory
exudations into the pelvic and adjacent cellular tissue, after the
acute symptoms have subsided the attention should be directed to the
afternoon fever and to promoting the assimilation of food. So soon as
the sweating and fever are checked the absorption of the plastic
materials begins. The most important agents for accomplishing this
object are quinia, in moderate doses, combined with some form of
alcohol and with tepid sponging. Deep-seated pain in the iliac region
is best relieved by a large blister upon the side over the point where
the tenderness is felt. Prolonged rest in bed should be enjoined. Even
after convalescence is well advanced, so long as the exudation remains
unabsorbed the resumption of household duties is pretty certain to be
followed by a relapse or by the development of a chronic condition of
a most intractable description. The sooner the patient's stomach can
be got to digest and absorb beefsteak and iron the more speedy will be
her recovery.
In pelvic exudations the hot vaginal douche, warm baths, and the
application of flannels wrung out in water to the abdomen aid in
diminishing the local pain, and, perhaps, in causing a disappearance
of the tumor. The action of mercurials or of iodide of potassium in
melting away plastic inflammatory materials is sometimes very
striking, but more frequently they either do no good or else do harm
by disturbing the digestion.
If fever, chills, and sweating announce the presence of pus, the most
careful exploration should be made to determine, if possible, the seat
of suppuration. It is of great advantage to treat pelvic abscesses as
abscesses are treated elsewhere in the body. If the redness of the
skin above Poupart's ligament indicates a tendency to point in that
direction, an aspirator-needle should be introduced to make sure of
the diagnosis. If the sac is near the surface, a free incision should
be made and the pus should be allowed to escape. In many cases I make
these incisions three to four inches in length. The redness of the
external skin makes it certain that the abscess has become adherent to
the abdominal wall, and that the incision consequently will not
communicate with the peritoneum. After the abscess has been opened it
should be cleansed twice daily, and the cavity should be filled with
oakum. If, after a time, the granulations become flabby, Peruvian
balsam or iodoform should be introduced into the sac at each change of
the dressing. I can recommend this plan as essentially a mild
procedure. With a large opening for the discharge of {1037} pus the
fever and sweating disappear, the appetite returns, and the abscess
fills rapidly by granulation. With a small incision hectic is apt to
persist, and the abscess to end in the formation of interminable
fistulae.
If softening and bagginess or distinct fluctuation indicate that the
pus can be reached through the vaginal cul-de-sac, the
aspirator-needle should be inserted deeply at the suspected point, and
if a large amount of pus is detected, an incision should be made with
a long-handled bistoury, using the needle as a director, and making
the opening large enough to permit the introduction of a
drainage-tube. I prefer for this purpose a self-retaining Nelaton
catheter, which is easily passed by means of a uterine sound inserted
into the eye at the extremity. Through the tube--without disturbing
the patient--the pus-cavity can be washed as frequently as required,
and with drainage and cleanliness cases of the longest standing may be
expected to recover.
P. F. Munde[78] has reported a number of cases of chronic character
where the aspiration of pus has been followed by rapid absorption of
the intra-pelvic exudation. The presence of pus was suspected because
of a boggy, doughy feeling in the exudation tumor.
[Footnote 78: "Diagnosis and Treatment of Obscure Pelvic Abscess,"
etc., _Arch. of Med._, December, 1880.]
{1038}
BERIBERI.
BY DUANE B. SIMMONS, M.D.
DEFINITION.--Beriberi is a disease of inanition, most common in
tropical countries, though found in high latitudes (41 degrees N.),
especially in low-lying seaboard towns, during the summer months, and
is both endemic and epidemic. It is usually chronic in form, but is
subject to exacerbations of varying degrees, and has for its
characteristic symptoms anaesthesia of the skin, hyperaesthesia and
paralysis of the muscles, anasarca, palpitation, cardiac and arterial
murmurs (in the wet form), praecordial oppression, and abdominal
pulsation.
HISTORY AND GEOGRAPHICAL DISTRIBUTION.--It was for a long time
confounded with a great variety of other diseases. The Anglo-Indian
physicians of Ceylon and the Malabar coast were no doubt the first to
recognize the specific nature of the disease, though it is claimed
that Chinese medical works of the thirteenth century contain a fairly
accurate description of it.
The literature of beriberi, at the first glance, appears to be very
meagre, as some of the most popular medical works make no mention of
the disease at all, while others only give it a passing notice. Its
bibliography, however, is very considerable, as may be seen in the
exhaustive list in Billings' _Index Catalogue_, but for want of space
we refer only to the most recent contributions to the subject. These
are--an article by A. LeRoy de Mericourt;[1] an essay by Tarissan,
entitled _Beriberi in Brazil_; an article by Anderson,[2] and an essay
by myself.[3]
[Footnote 1: _Dictionnaire Encyclopedique des Sciences Medicales_,
Paris, 1876.]
[Footnote 2: _Guy's Hospital Reports_.]
[Footnote 3: _Chinese Maritime Customs Medical Report_ (1880).]
For a long time beriberi was supposed to have a peculiar territorial
limitation. It is now known to be more or less prevalent on all the
islands and shores of Eastern Asia and Africa from Japan to the Cape
of Good Hope, and in Brazil.
ETIOLOGY.--I know of no disease in regard to which a greater diversity
of opinion exists as to its cause. Indeed, as one has observed,
"autant d'auteurs, autant d'opinions diverses." Ten years' study and
observation of the malady under a great variety of circumstances and
conditions have led me to the definite conclusion that its exciting
cause is a specific poison or germ, having many striking resemblances
in its mode of production to paludal or marsh miasm, though entirely
distinct and separate from it. A great variety of predisposing causes,
however, exert a powerful influence in rendering individuals or
classes susceptible to the {1039} disease, such as age, sex,[4]
occupation, race, mode of life, diet, and climate.
[Footnote 4: Women suffer from the disease much less frequently than
men.]
CLINICAL HISTORY AND SYMPTOMS.--There are three forms of the disease:
1st. Beriberi hydrops (wet beriberi), in which there is a hydraemic
condition of the blood, distension of the general areolar tissue, with
serum, and effusion into the serous cavities. 2d. Beriberi atrophia
(dry or atrophic beriberi), in which there is a notable deficiency of
fluids in the vessels and areolar tissue, and atrophy of the muscles.
3d. Mixed beriberi, in which the above forms lose the sharp lines of
distinction and merge into each other. Cases complicated with
dysentery, diarrhoea, and especially with continued fevers of the
typhoid type, are not uncommon.[5] These last, besides being of grave
prognosis, are frequently very embarrassing and difficult of
diagnosis.
[Footnote 5: Some authors have designated fatty or convulsive forms of
the disease, which I think unnecessary.]
In general terms, wet beriberi may be divided into two stages--the
prodromic stage and the stage of attack; and into several types--the
acute or pernicious, and the chronic. From the very insidious nature
of the approach of the disease, sometimes extending over a period of
several weeks, it is often very difficult, or even impossible, to
determine the exact time of its invasion. It is generally admitted
that a residence of some weeks in an infected locality is necessary
before any decided symptoms make their appearance. As in many other
diseases of slow development, the symptoms of the prodromic stage are
certain not easily defined feelings of indisposition, such as an
occasional sense of chilliness, inaptitude for mental exertion, and
especially a tired feeling in the lower extremities. A period of
uncertain length now intervenes, during which the characteristic
symptoms appear and constitute the stage of attack. The first of these
symptoms is, generally, anaesthesia of the skin over the anterior
tibial muscles, in the tips of the fingers, and around the mouth, in
the order given. Paralysis in varying degrees next declares itself in
certain groups of muscles, usually those immediately underlying the
regions of anaesthesia. One of the consequences of this is a drooping
of the toes, causing the patient while walking to lift the feet high
so as to clear the ground, thus occasioning the peculiar gait noticed
by many observers as characteristic of the disease. A sense of
constriction in the muscles of the calves is experienced at the same
time, arising from a veritable contraction, which causes their
apparent enlargement and hardening, with tension of the tendo
achillis. A feeling of tightness in the chest usually accompanies this
condition, due, no doubt, to partial paralysis of the muscles of
respiration. If firm pressure be now made upon the muscles in various
parts of the body, a greater or less degree of tenderness will be
found to exist in many of them, and especially those occupying the
posterior part of the leg, back of the forearm, inside of the arm, and
upper part of the chest. Tenderness of the periosteum of the long
bones and a peculiar roughness of their surfaces often exist also.
Palpitation of the heart, especially on making any considerable
exertion, is a frequent and often troublesome symptom, even at this
stage of the disease.
Up to this point the above symptoms are common to both the wet and
{1040} dry forms of the malady, and to them the characteristic
features either of beriberi hydrops or atrophia are now added. The
first manifestation of anasarca, the pathognomonic symptom of wet
beriberi, is in an oedematous condition of the areolar tissue of the
anterior part of the legs. This, in reality, is more or less general
even at an early stage of the disease, as is evident from the plump
appearance of the patient and a certain sallow-white color of the
skin, especially of that of the face. In uncomplicated cases the
temperature is normal, or it may be at times a little below the normal
point. There is also little or no increase in the frequency of the
pulse. Its quality, however, is changed, and somewhat characteristic
for both forms of the disease. Thus in the wet form it is full, large,
and easily compressible, indicating a great diminution of arterial
tone, while in the dry form there is nearly an opposite condition. If
the heart be now examined, a decided systolic murmur will be heard,
most distinctly over the pulmonary valves; and in most cases of wet
beriberi it exists in all the large arterial trunks. The heart
furnishes the usual signs of dilatation and want of tone. In the dry
form the cardiac murmurs are either slight or wanting altogether, and
the area of cardiac dulness is variable, and frequently diminishes as
the disease advances.
In both wet and dry beriberi the appetite is little impaired in the
earlier stages, but if in the former the stomach is over-distended,
there is increased praecordial oppression, and sometimes sudden death.
The bowels in the wet form are sluggish, and urine scanty; in the
other there is but little deviation from the normal in these respects.
The cases of the subacute type are by far the most numerous. From this
it is evident that the acute or pernicious type of the malady is, in
most cases, only an exaggeration of the subacute, as observed in some
other diseases, notably rheumatism and those of marsh malarial origin.
The term pernicious is, strictly speaking, applicable to the wet form
of the disease only, as the dry form is rarely, if ever, rapidly
fatal. A marked case of wet beriberi is always to be regarded as
dangerous, from the suddenness with which pernicious symptoms often
declare themselves. In these the anasarca (which, as has been stated,
constitutes the leading clinical difference between the two forms of
the malady) plays an important role. It often happens that in the
course of a few hours the local oedema in the extremities and the
slight puffiness of the face become general and extreme, and the neck
is enormously swollen by the distension of the veins, both deep and
superficial. The pleural and pericardial sacs are more or less
distended with serum, thus mechanically embarrassing the action of the
organs they contain. The action of the heart now becomes laborious,
the lungs oedematous and filled with coarse rales, and a terrible
sense of suffocation comes over the patient, causing him to seek
relief by constant change of position. The stomach is irritable, a
greenish-yellow fluid is vomited, and death closes the scene. The
acute stage of dry beriberi, on the contrary, is characterized by a
rapid diminution of the fluids of the body and muscular atrophy.
The annual appearance in the same individual of either wet or dry
beriberi, and its long continuance, constitute the chronic type of the
disease.
MORBID ANATOMY.--The morbid anatomical changes in beriberi vary
considerably with its form. Few, if any, observers claim seriously to
{1041} have found in either the wet or dry form of the disease
evidences of acute inflammatory action in any of the tissues or
organs. The blood undoubtedly undergoes important morbid changes,
whereby its nutritive and oxygenating power is impaired, indicating
that this is a disease of inanition. This shows itself most markedly
in necrobiotic and degenerative changes, especially in the muscular
tissues, which are the seat of the leading morbid phenomena in all
stages of both forms of this disease. The respiratory, digestive, and
glandular systems rarely undergo morbid changes other than those of a
secondary or passive kind, such as engorgement with serum and venous
blood.
The condition of the organs contained in the cranial and spinal
cavities is variable and inconstant. According to some observers, the
substance of the brain and spinal cord is hardened. The greater number
by far, however, have found it more or less softened.[6] The heart in
wet beriberi is habitually large and flabby, its muscular tissue
softened and of a pale-yellow and macerated appearance. Its cavities
are engorged with dark blood, sometimes fluid, but more often clotted.
These clots are often voluminous in the right heart, semi-fibrinous,
and extend into the pulmonary artery and great venous trunks, which
are enormously enlarged. The cardiac muscular tissue I always found to
have undergone metamorphic changes, varying from granular clouding to
advanced fatty degeneration.[7] The tissue of the paralyzed voluntary
muscles undergoes degenerative changes in both forms of the disease.
In the extreme atrophy of dry beriberi I have not unfrequently found
many of the sarcolemma sheaths completely emptied of their contents.
The power of regeneration in these cases is often wonderfully
displayed by an almost complete restoration of the lost elements, and,
in a corresponding degree, of the function of the part.
[Footnote 6: The former condition was undoubtedly observed in
autopsies made of the dry or atrophic form of the disease, though this
fact is not mentioned. The latter, or softened, condition of the
cerebro-spinal contents belongs to the wet form of the disease (my own
cases being of this kind). I regard this softening as not ante-mortem,
but as consecutive to serous imbibition (as observed by Eismann and
Sanders in chlorosis), and as taking place during the last moments of
life or after death, when the vital forces no longer oppose themselves
to the mechanical disintegrating power of the fluid with which the
nervous as well as all the other tissues of the body are engorged.]
[Footnote 7: I believe this to be the condition of the heart-muscle in
all cases of death from the wet form of beriberi. In this opinion I am
supported by Oudenhoven and many of the Dutch observers.]
It would appear that in wet beriberi the heart is first weakened by
paresis of the cardiac ganglia, with consequent incomplete emptying of
its cavities. This, in connection with rapid degenerative changes in
its muscular tissue, causes the walls to yield to the blood-pressure,
producing dilatation and tricuspid insufficiency, with regurgitation
and consequent capillary stasis and dropsy. Vaso-motor
nerve-paralysis, acting at the same time on the pulmonary artery and
arterioles, and on other large arterial trunks, probably gives rise to
the murmurs heard in them. In the dry form of the disease the
vaso-motor nerve-paralysis is less pronounced, and the degenerative
changes in the muscular tissue of the heart slower, while the marked
decrease in the fluids of the system and the great failure of
nutrition tend toward atrophic changes. From this it follows that we
usually have, instead of a large dilated heart, a small weak one, with
a narrow tricuspid orifice instead of a dilated one; little or no
{1042} intercostal pulsation, and hence less cardiac dulness; no
venous distension or capillary stasis, and hence no dropsy.
PROGNOSIS.--In temperate climates the prognosis of uncomplicated
beriberi is favorable in a majority of cases. In seasons of its
epidemic prevalence, however, all cases of the wet form of the disease
must be carefully watched, as it not unfrequently happens that grave
symptoms suddenly appear at a time when no danger has been
anticipated. An unfavorable prognosis may be ventured when, in a case
of wet beriberi, relief is not obtained by free purging or when
vomiting sets in. In dry beriberi the termination in death is
exceedingly rare as a direct result of the action of the poison
producing the disease, so that when death does occur it is chiefly
from exhaustion. The time of recovery depends on the amount of
muscular degeneration, and also upon the season of the year when the
attack occurred, as all cases of both forms of beriberi usually get
well without treatment during the winter months.
TREATMENT.--The well-established fact of the influence of certain
localities in the production of beriberi makes the removal of the
patient from them a hygienic measure of great importance, and this is
frequently the only treatment necessary if it can be done early. The
effect of the change is often almost magical, especially if it be made
to an elevated locality and among the mountains.
Diet is an important element in the treatment of beriberi. At the head
of the list of foods to be avoided is rice. Coarsely prepared grains,
such as wheat, barley, certain kinds of beans,[8] apparently because
of more or less laxative properties, are preferable as articles of
food.
[Footnote 8: A small red bean called adzuke, possessing both laxative
and diuretic properties, is a favorite remedy with the Japanese for
beriberi. It is used alone or mixed with rice, and is not unfrequently
the only means resorted to for the successful cure of mild cases.]
No drug has been discovered possessing specific properties in this
disease. In the wet form, medication consists in the administration of
drugs calculated to draw off the excess of serum in the areolar
tissues and in the serous sacs. First in point of efficacy for this
purpose are the hydragogue cathartics. In my own practice the sulphate
of magnesia, in large and repeated doses, has given the best results;
elaterium, a powder of jalap, squill, and digitalis, and, in fact, any
medicine which will give frequent and copious stools, are sure to
afford marked relief to the more urgent symptoms, and in many cases
will alone effect a cure. Care must be taken, however, not to exhaust
the patient, though I have never seen the judicious use of this method
of treatment do harm.
Copious bleeding is recommended by Anderson, especially in the stage
of greatest danger, but I have never been able to convince myself of
its safety.
The almost specific virtue claimed by the old Indian physicians for
treeak farook is no doubt due to its cathartic properties.
Diuretics are indicated for the same reason as cathartics, and any of
the more active are productive of good results. They are too slow in
their action, however, to be relied on otherwise than as adjuvants to
cathartics. I have found juniper gin to answer an excellent purpose,
both as a stimulant and diuretic, where there was danger of exhaustion
from the free use of cathartics.
The medical treatment of dry beriberi differs materially from that of
{1043} the wet disease. Cathartics and diuretics are alike useless,
and the former injurious. The ordinary means, such as electricity,
strychnia, frictions, etc., employed in cases of muscular atrophy and
paralysis from other causes, are indicated when the active stage has
passed, but they are useless, and even injurious, before this time.
The muscular hyperaesthesia common to both forms of the disease may be
generally greatly relieved by anodyne liniments containing aconite.
The internal use of the latter is highly recommended by some.
Hypodermic injections of morphia afford relief to the painful sense of
constriction in the calves of the legs so often complained of.
{1045}
INDEX TO VOLUME I.
A.
Abdomen, state of, in cholera, 741
in general peritonitis of puerperal fever, 1010
in relapsing fever, 390
in septicaemia, 977
in septicaemia lymphatica, 1011
in septicaemia venosa, 1012
Abdominal cavity, lesions of, in general peritonitis of puerperal
fever, 989
glands, lesions of, in typhoid fever, 264
organs, alterations of, in scarlet fever, 531
Abortion from septicaemia, 972
Abortive form of the plague, 777
of relapsing fever, 395
of typhoid fever, 298
of typhus fever, 354
Abortive treatment of erysipelas, value, 638
Abscess in symptomatic parotitis, date of pointing, 627
metastatic, of lungs, complicating relapsing fever, 404
Abscesses complicating cholera, 735
variola, 445
following the plague, 781
frequency of, in pyaemia, 976
in erysipelas, treatment, 638
in para- and perimetritis, 1008
in puerperal fever, 989
metastatic, of pyaemia, modes of production, 963
of pyaemia, treatment, 981
pelvic, of puerperal fever, treatment, 1036
pulmonary, in puerperal fever, 989
Acids, mineral, use of, in cholera, 768
Aconite, use of, in rubeola, 580
in scarlet fever, 543
in yellow fever, 651
Acute diseases, relation of, to rubeola, 561
form of glanders in man, 920
in horse, 914
Adenitis complicating scarlet fever, 511
vaccination, 468
Adenopathy complicating erysipelas, 634
Adhesions from infiltration, 55
Adulteration of food, 197
Adynamic form of typhus fever, 354
Age, influence of, on causation of anthrax in man, 940
of cerebro-spinal meningitis, 802
of diphtheria, 680
of erysipelas, 630
of influenza, 860
of idiopathic parotitis, 620
of the plague, 775
of pertussis, 839
of relapsing fever, 371
of rotheln, 583
of rubeola, 561
of typhoid fever, 242
of typhus fever, 342
proper for vaccination, 477
Aged, typhoid fever in the, 301
Agminated glands, lesions of, in cholera, 745
Air, amount supplied in ventilation, 179
carbonic acid as a cause of impurity, 177
-currents, direction of, test, 178
distribution of, in ventilation, 180
estimation of carbonic acid, 178
fresh, value of, in convalescence, 206
humidity of, as a cause of disease, 133
impure, as a cause of disease, 177
influence of, on causation of glanders, 912
impurities of, due to offensive effluvia, 181
sources of impurity, 177
standards of impurity, 178
transmission of the plague by, 776
velocity of, in ventilation, 180
vitiated, as a cause of pyaemia, 959
supply, method of calculating amount of, in ventilation, 179
Albuminoid infiltration, 72
Albuminuria complicating diphtheria, 674
relapsing fever, 407
scarlet fever, 525
typhus fever, 355
following rubeola, 574
in typhoid fever, treatment, 334
Alcohol, use of, in algid form of pernicious malarial fever, 608
in anthrax, 938, 944
in cerebro-spinal meningitis, 831
in cholera, 767
in influenza, 876
in puerperal fever, 1033
in pyaemia, 982
in scarlet fever, 544
in typhoid fever, 324
in typhus fever, 366
Algid form of pernicious malarial fever, 606
causes of death, 607
frequency, 607
mortality-rate, 607
symptoms, 606
treatment, 607
Alum, use of, in pertussis, 845
Ammonium bromide, use of, in pertussis, 846
carbonate, use of, in scarlet fever, 544
chloride, use of, in diphtheria, 704, 705
Amyloid bodies, 86
degeneration, 84
Anaesthesia of skin in beriberi, 1039
significance of, in general diagnosis, 165
Anaesthetic form of leprosy, 790
Analysis of urine, importance of, in general diagnosis, 165
Anasarca, 69
complicating scarlet fever, 529
date of appearance in scarlet fever, 529
in beriberi, 1040
Anginose form of anthrax, 941
of scarlet fever, 510
Animals, cerebro-spinal meningitis in, 804
diphtheria in, 683
transmission of diphtheria from, 683
Animal vaccine, advantages, 475
Anodyne liniments, use of, in beriberi, 1043
Anorexia in relapsing fever, 389
in typhoid fever, 285
in typhus fever, 350
significance of, in general diagnosis, 162
ANTHRAX, OR MALIGNANT PUSTULE, 926
Synonyms, 926
Definition, 926
History, 926
Geographical distribution, 926
Etiology--specific origin, 928
Modes of transmission, 928
Transmission from eating flesh of anthrax animals, 928
by milk, 929
by insects, 929
by alkaline soils, 929
Season, relation of, to causation, 931
Plethora, relation of, to causation, 931
Sex, relation of, to causation, 931
Age, relation of, to causation, 931
Bacillus, 931
relation to causation, 931
physical characters, 932
effect of heat and cold on activity, 933
effect of oxygen on activity, 933
mode of entering body, 933
effect on blood-vessels, 934
Forms, 934
Symptoms--Incubation period, 934
duration of, 934
Apoplectiform form, 934
Anthrax fever, 934
Localized external anthrax, 935
Character and seat of lesions, 935
Morbid anatomy--changes in blood, 935
Spleen, 935
Lymphatic glands, 935
Connective tissue and muscles, 935
Gastro-intestinal tract, 936
Vagina and uterus, 936
Liver and kidneys, 936
Diagnosis--from other bacteridian diseases, 936
Swine plague, 936
Prognosis, 936
Mortality, 936
Treatment, 937
Preventive, 936
Drainage of anthrax soil, 937
Disinfection of stables, etc., 937
Disposal of carcases of sick animals, 937
Isolation, 937
By inoculation, 937
Methods of, 937
Pasteur's method, 937
Dangers in, 938
General, alcohol, 938
Use of carbolic acid, 938
nitro-muriatic acid, 938
potassium iodide, hypodermically, 938
quinia sulphate, hypodermically, 938
Local, 938
Cauterization, 938
Incision of nodule, 938
_Anthrax or Malignant Pustule in Man_, 939
Synonyms, 939
History, 939
Etiology, 939
Origin from lower animals, 939
Modes of infection, 939
direct, 939
by handling sick animals, 939
by insect-bites, etc., 939
by food, 939
by blood, 939
by air, 939
Occupation, relation of, to causation, 939
Age and sex, relation of, to causation, 940
Relative susceptibility of man and animals, 940
Forms, 940
Symptoms--of incubation period, 940
Local lesions, 940
Temperature, 940
Relation of, to local lesions, 940
Malignant anthrax, 940
Symptoms, 940
local, 940, 941
general, 941
Anthrax intestinalis, 941
Symptoms, 941
general, 941
eruptions, 941
gastro-intestinal tract, 941
nervous system, 941
Duration, 941
Anthrax angina, 941
Symptoms, 941
general, 941
local, 941
Duration, 941
Morbid anatomy, 941
Changes in blood, 942
Spleen, 942
Lymphatic glands, 942
Liver and kidneys, 942
Skin and mucous membranes, 942
Appearance of pustule, 942
Position of bacillus, 942
Diagnosis--signs, pathognomonic of, 942
From bites of insects, 942
Boils and carbuncles, 942
Plague-boil, 942
Glanderous nodule, 942
Importance of detection of bacillus, 942
Of malignant anthrax oedema, 942
Internal anthrax, 943
Prognosis, 943
Mortality, 943
Treatment--Preventive, 943
Disinfection, 943
Local, 943
Cauterization of preliminary papule in external form, 943
Method of cauterization, 943
Excision of parent nucleus, 943
Caustics used in, 943
Hypodermic injections into swelling, 943
Constitutional, 944
Carbolic acid, use of, 944
Alcohol, use of, 944
Diet, 944
Of anthrax oedema, 944
Antipyretics, use of, in relapsing fever, 428
in cerebro-spinal meningitis, 833
Antisepsis in septicaemia, 983
value of, in prevention of puerperal fever, 1024
Antiseptic treatment of scarlet fever, 545
Antiseptics, use of, in cholera, 770
in glanders in man, 924
in pyaemia, 980
Aphasia in cerebro-spinal meningitis, 810
Apoplectic form of anthrax in animals, 934
Appetite in cerebro-spinal meningitis, 814
as a guide to necessary amount of food, 195
loss of, significance, in general diagnosis, 162
Arcus senilis, significance, in general diagnosis, 151
Argyria, 93
Arsenic, use of, in relapsing fever, 427
Arsenical poison as cause of obscure diseases, 193
Arterial emboli, 63
murmur in beriberi, 1040
thrombosis following typhoid fever, 293
Arteritis from thrombosis, 61
in pyaemia, 967
Articular enlargement, significance of, in general diagnosis, 160
Artificial alimentation in diphtheria, 713
Asthenic form of simple continued fever, 233
of inflammation, 46
Ataxic form of typhus fever, 354
Ataxo-adynamic form of typhus fever, 354
Atmosphere, impure, influence of, on causation of puerperal fever,
1013, 1014
necessity of, for prevention of pyaemia and septicaemia, 980
Atmospheric variations as a cause of diphtheria, 682
Atrophy following diphtheritic paralysis, 676
Atropia, use of, in relapsing fever, 429
Auditory nerve, lesion of, in cerebro-spinal meningitis, 824
B.
Bacillus of anthrax, characters of, 931, 932
mode of entering body, 933
of glanders, 914
of pearly distemper, innocuousness of, from cooking, 105
species of, 142
tuberculosis, 99 _et seq._
description, 100
duration of effects, 104
cultivation, 100
local and general effects of invasion, 103
methods of detection, 102
milk as a means of dissemination, 105
mode of entrance into intestinal canal, 104
into respiratory organs, 104
typhosus, 258
Bacteria in healthy bodies, 144
influence of, on causation of pyaemia, 958
liability to error, from minuteness, 143
of cholera, 748
of leprosy, 791
of puerperal fever, 995
Bacterium termo as a cause of putrefaction, 142
Barometric variations, influence of, on course and causation of
disease, 134
Bartholini's glands, suppuration of, complicating typhoid fever, 296
Baths, cold, use of, in puerperal fever, 1034
in relapsing fever, 428
warm, use of, in hydrophobia, 907
in variola, 453
Bed-linen, as a means of disseminating typhoid fever, 253
Bed-sores, complicating relapsing fever, 400
typhoid fever, 297
typhus fever, 355
in typhoid fever, treatment of, 335
Belladonna as a prophylactic in scarlet fever, 536
use of, in cerebro-spinal meningitis, 833
in pertussis, 846
Benignant tumors, 114
Benzoic acid as a prophylactic in scarlet fever, 537
BERIBERI, 1038
Definition, 1038
Geographical distribution, 1038
History, 1038
Etiology--Specific poison, 1038
resemblance of, to marsh-miasm, 1038
Predisposing causes, 1039
Varieties, 1039
Symptoms--Anaesthesia of skin, 1039
Muscular paralysis, 1039
Peculiarity of gait, 1039
Cramps, 1039
Muscular tenderness, 1039
Periosteal tenderness, 1039
Palpitation of heart, 1039
Symptoms, special--Of wet form, 1040
Anasarca, 1040
Quality of pulse, 1040
Cardiac murmur, 1040
Arterial murmur, 1040
Of dry form, 1040
Quality of pulse, 1040
Condition of heart, 1040
Morbid anatomy, 1040
Alterations in blood, 1041
Heart, 1041
Muscles, 1041
Prognosis, 1042
Treatment--By change of residence, 1042
By diet, 1042
Of wet form by hydragogue cathartics, 1042
Sulphate of magnesium, 1042
Elaterium, 1042
Treeak farook, 1042
Diuretics, 1042
Juniper gin, 1042
Of the dry form by electricity, 1043
Strychnia, 1043
Frictions, 1043
Use of anodyne liniments, 1043
Use of hypodermics of morphia, 1043
Bites of rabid dogs, treatment, 905
Bladder, diphtheria of, general sepsis from, 674
lesions of, in rabies, 903
in relapsing fever, 414
symptoms of diphtheria of, 674
Blindness in cerebro-spinal meningitis, 811
Blisters, use of, in cerebro-spinal meningitis, 830
Blood, alterations of, in anthrax, 935-942
in beriberi, 1041
in cerebro-spinal meningitis, 824
in cholera, 747
in pyaemia, 968
in relapsing fever, 411
in scarlet fever, 530
in septicaemia, 971
in typhoid fever, 268
in typhus fever, 356
altered, as a cause of symptomatic parotitis, 626
condition of, in pyaemia, 963
contamination of, sources, in pyaemia, 958
degeneration of, complicating diphtheria, 675
Blood-vessels, calcification of, 88, 90
changes in inflammation, 43
lesions of, in typhoid fever, 267
new formation of, 55
Body, portion of, most suitable for vaccinating, 477
Bones, chronic diseases of, following rubeola, 574
cranial, lesions of, in symptomatic parotitis, 626
in glanders, 922
in pyaemia, 967
Bone-marrow, lesions of, in relapsing fever, 417
Boric acid, use of, in diphtheria, 709
Bovine vaccine, 473
Bowels, state of, in relapsing fever, 390
in remittent fever, 602
condition of, in typhus fever, 350
Brain, lesions of, in cerebro-spinal meningitis, 823
in cholera, 746
in glanders, 923
in relapsing fever, 413
in typhoid fever, 266
in typhus fever, 358
and membranes, lesions of, in cerebro-spinal meningitis, 822
in pyaemia, 966
and spinal cord, lesions of, in rabies and hydrophobia, 903
softening of, following cerebro-spinal meningitis, 820
Breath, odor of, in typhus fever, 353
Bright's disease, aggravation of, by influenza, 870
Bromine, use of, in diphtheria, 708
Bromide of potassium, use of, in relapsing fever, 430
Bronchi, lesions of, in rabies and hydrophobia, 902
symptoms of formation of diphtheritic membrane, 671
Bronchial glands, lesions of, in influenza, 872
Bronchitis, complicating influenza, 868
rubeola, 571
typhoid fever, 294
typhus fever, 355
frequency of, in typhoid fever, 277
in rubeola, treatment, 581
in septicaemia, 977
in typhus fever, 353, 354
Broncho-pneumonia, complicating diphtheria, 672
Bryce's test of vaccinal infection, 461
Buboes, characters of, in grave form of the plague, 778
date of appearance of, in grave form of the plague, 778
of the plague, treatment, 784
pathology of, in the plague, 781
seat of, in grave form of the plague, 778
C.
Cadaveric rigidity after cholera, 741
Caecum and colon, lesions of, in typhoid fever, 263
Calcification, 87
causes, 87
of blood-vessels, 88, 90
of thrombi, 60, 89
Calabar bean, use of, in cerebro-spinal meningitis, 834
Calm stage of yellow fever, 645
Calomel as a specific in typhoid fever, 336
use of, in cholera, 766
in hemorrhagic form of pernicious malarial fever, 613
Camphor, use of, in cholera, 768
Cancer, 117, 123
hereditary nature, 129
relation of, to epithelial tumors, 118
Capillary bronchitis, complicating influenza, 868
Capillaries, intestinal, lesions of, in cholera, 745
Carbolic acid, use of, in anthrax, 938
in diphtheria, 707
in glanders, 924
in scarlet fever, 545
Carbonic acid, as a cause of impure air, 177
amount of, in pure and impure air, 178
Carbuncles, character of, in grave form of the plague, 778
seat of, in grave form of plague, 778
Cardiac degeneration, complicating diphtheria, 675
following typhoid fever, 293
complicating typhus fever, 355
dilatation, complicating scarlet fever, 523
inflammation, complicating scarlet fever, 522
murmur in beriberi, 1040
sounds in typhoid fever, 276
thrombi in diphtheria, 687
Caseation, 79
Cataract, hereditary, nature, 129
Catarrh, absence of, in rubeola, 568
of influenza, treatment, 874
Catarrhal affections as predisposing causes of pertussis, 839
inflammation, 52
pneumonia, complicating influenza, 869
pock in vaccinia, 463
symptoms in influenza, 866
in prodromal stage of rubeola, 564
Causes of otitis in scarlet fever, 520
Caustics, use of, in hydrophobia, 905
Cauterization, use of, in external anthrax, 938, 943
Cathartics, use of, in wet beriberi, 1042
in scarlet fever, 554
Cellular tissue, lesions of, in pyaemia, 966
Cellulitis, pelvic, in puerperal fever, 988
Cerebral softening from embolism, 65
symptoms in yellow fever, 644
Cerebro-spinal meningitis, 795
Certificates of death, duty of a physician in regard to, 210
Cesspools beneath dwellings, dangers of, 192
contamination of water by, 192
evils of, 126
Change of residence as cause of typhoid fever, 244
Cheesy degeneration, 79
metamorphosis, 79
Chicken-pox, 481
Child-bed fever, relation to erysipelas, 630
Childhood, influence of, on occurrence of pertussis, 839
Children, causes of frequency of diphtheria in, 682
typhoid fever in, 301
Chills in pyaemia, 973
Chinolin, use of, in diphtheria, 703
Chloral hydrate, use of, in cerebro-spinal meningitis, 834
in hydrophobia, 907
in pertussis, 846
in relapsing fever, 430
Chloride test for detecting pollution of water-supply, 192
Chloroform, use of, in cholera, 768
in hydrophobia, 907
in relapsing fever, 431
CHOLERA, 715
Definition, 715
Synonyms, 715
History, 715 _et seq._
Etiology--predisposing causes, 720
Influence of high temperature in origin and spread, 720
Season, influence of, on causation, 720
Over-crowding and filth as causes, 720
Intemperance as a cause, 721
Contagiousness, 721
Modes of transmission, 721
Channels of entrance into system, 721
Propagation of, by fomites, 721
by drinking-water, 723
Cases illustrating spread of, by drinking-water, 724
Influence of height of subsoil-water on prevalence, 722
Humidity of soil as a cause, 722
Special fomites of, 723
Cases illustrating spread of, by fomites, 727
Cases illustrating contagiousness, 728
Objections to contagious nature, 729
Individual immunity, 730
Different grades of, from intensity of poison, 731
Specific origin, 747
Nature of poison, 748
Influence of bacteria in production, 748
Koch's investigations in regard to bacilli, 745, 749
Symptoms, 731
Mild forms, 732
"Cholerine" stage, 732
Number of stools in mild forms, 732
Character of stools in mild forms, 732
Grave forms, 733
Physiognomy in grave forms, 733
Stools in grave forms, 733
Typhoid state, 734
Stage of collapse, 734
Reaction, 734
Convalescence, 735
Temperature, 736
Difference between axillary, vaginal, and rectal temperature, 736
Special symptoms--Low temperature of mouth, 736
Condition of skin, 736
Color of skin, 737
Condition of heart and pulse, 737
Veins, 737
Vomiting, 738
Character of vomit, 738
Diarrhoea, 738
Results of diarrhoea, 738
Characters of stools, 739
Condition of urine, 739
Cramps, 740
Causes of cramps, 740
State of abdomen, 741
of nervous system, 741
Complications and sequelae, 735
Complicated by diphtheritic exudations, 735
Inflammation of parotid and submaxillary glands, 735
Abscesses and ulcers, 735
Cutaneous eruptions, 735
Morbid anatomy--general appearance after death, 741
Cadaveric rigidity, 741
Muscular contractions after death, 741
Appearance, post-mortem, of abdominal cavity, 743
Changes in stomach, 743
Intestinal canal, 743
Intestinal mucous membrane, 743
Nature of exfoliation from intestinal canal, 744
Changes in isolated and agminated glands, 745
Capillaries and veins of intestinal canal, 745
Liver, 745
Gall-bladder, 746
Spleen, 746
Heart, 746
Pericardium, 747
Lungs, 746
Brain and spinal marrow, 746
Kidneys, 746
Blood, 747
Diagnosis--from cholera morbus, 750
from irritant poisoning, 752
Order of symptoms as a ground for, 753
Prognosis, 753
Symptoms indicating favorable and unfavorable, 754
Mortality--in different epidemics, 754
Influence of age, 754
Sex, 754
Social condition, 754
Treatment, 759
Preventive, 755
Disinfection, 758
Modes of applying disinfectants, 758
Importance of maintaining high degree of health during
epidemics, 758
Quarantine and sanitary cordons for prevention, 755 _et seq._
Mode of carrying out quarantine, 757
Cases illustrating value of quarantine, 757
Use of drinking-water during epidemics, 759
General management, 760
Importance of early recognition, 732
Necessity of rest, 760
of prompt, 760
Diarrhoea, 760
Vomiting, 761
Hiccough, 762
Injection of sodium chloride into veins, 762
Stage of collapse, 763
Diet of stage of reaction, 763
For restoration of circulation in stage of collapse, 763
Stage of reaction, 763
Undue reaction, 764
Urinary suppression in stage of reaction, 764
Convalescence, 764
Use of venesection in, 764
Emetics, 765
Calomel, 766
Alcohol, 767
Opiates, 767
Mineral acids, 768
Camphor, 768
Chloroform, 768
Intravenous injections, 768
Hot applications, 769
Cold affusions, 769
Of cramps, 769
Necessity of cold water to allay thirst, 770
Use of antiseptic remedies, 770
Cholerine, 732
Chorea, following typhoid fever, 293
Chronic diseases, relation of, to rubeola, 561
forms of erysipelas, 634
of glanders, 915, 923
Cicatrix, condition during incubation of hydrophobia, 895
in hydrophobia, excision, 906-908
in vaccinia, description, 460
Classification of puerperal inflammations, 986
Cleanliness, importance of, in prevention of pyaemia, 980
in variola, 454
Climate, as a cause of disease, 185
definition of term, 185
influence of, on causation of influenza, 860
on causation of rabies and hydrophobia, 887
of rubeola, 560
Clinical history of influenza, 864
Clothing as a cause of disease, 198
Cloudy swelling, 72
Coagulation of exudations, 43
Cohnheim's theory of production of morbid growths, 106
Colchicum, use of, in dengue, 885
Cold as a cause of disease, 133
and damp, influence of, on causation of glanders, 912
bath, use of, in diphtheria, 702
in puerperal fever, 1034
in typhoid fever, 327
Contra-indications to use of, in diphtheria, 703
Use of, in algid form of pernicious malarial fever, 608
in cerebro-spinal meningitis, 830
in cholera, 769
in diphtheria, 702
in puerperal fever, 1033
in the hyperpyrexia of scarlet fever, 541
in scarlet fever, 542
in yellow fever, 651
water, intra-uterine injections of, in puerperal fever, 1034
mode of applying, in scarlet fever, 542
Cold stage of intermittent fever, 592
of intermittent fever, theory of cause, 593
treatment, 594
of yellow fever, treatment, 653
Cold water, use of, in typhus fever, 364
Collapse in cerebro-spinal meningitis, treatment, 831
in cholera, 734
treatment, 763
of lungs, complicating influenza, 869
Collections of water, influence on health of a community, 187
Colloid degeneration, 83
metamorphosis, 83
Color of skin, significance of, in general diagnosis, 159
Coma, in cerebro-spinal meningitis, 812
significance of, in general diagnosis, 166
Comatose form of pernicious malarial fever, 608
Diagnosis, 609
Symptoms, 609
Treatment, 609
Coma-vigil in typhus fever, 349
Compresses, hot water, use of, in variola, 453
Complications of cholera, 735
of erysipelas, 633
of idiopathic parotitis, 623
of influenza, 868
of pertussis, 843
of plague, 780
of relapsing fever, 396-410
of rotheln, 587
of rubeola, 570
causes, 570
of scarlet fever, 510
of typhoid fever, 292
treatment, 335
of vaccination, 468
of vaccinia, 464
of varicella, 483
of variola, 445
Confluent small-pox, 440
Conjunctiva, condition of, in human glanders, 921
symptoms of diphtheria of, 670
Conjunctival diphtheria, local treatment, 712
Conjunctivitis, diphtheritic, symptoms, 670
Consanguineous marriages, effects, 131
Constipation in cerebro-spinal meningitis, 814
in grave form of the plague, 779
in rubeola, treatment, 581
in typhoid fever, treatment, 333
in typhus fever, treatment, 367
significance of, in general diagnosis, 163
Constitutional infection, absence of, in vaccinia, 460
of syphilis, hereditary nature, 127
taints, conveyance of, by vaccination, 471
treatment of anthrax, 944
of pyaemia, 982
Contagion as a cause of disease, 135, 200
definition of, 200
of dengue, 884
of erysipelas, manner of propagation, 630
nature, 630
of influenza, 862
of relapsing fever, transmission, 373
of rabies and hydrophobia, 891
dissemination, 891
of rotheln, nature, 583
of rubeola, modes of dissemination, 558
mode of entering the body, 558
nature, 557
in typhus fever, nature, 343
modes of transmission, 344
Contagium of variola, duration of activity, 435
mode of entering body, 435
nature, 435
period of greatest activity, 435
Contagious diseases, characteristics, 137
Contagious nature of cholera, objections to, 729
Contagiousness of anthrax, 928
of cerebro-spinal meningitis, 803
of cholera, 721
of dengue, 884
of diphtheria, 678
of erysipelas, 630
of glanders, 911
of influenza, 862, 863
of leprosy, 788
of the plague, 776
of puerperal fever, 1017
of pyaemia, 960
of rabies and hydrophobia, 891
of scarlet fever, 494
of typhoid fever, 248
of typhus fever, 343
period of greatest, 345
of varicella, 481
of variola, 435
Convalescence, choice of diet, 206
in cerebro-spinal meningitis, 819
management, 835
in cholera, 735
management, 764
in chronic glanders in man, 922
in dengue, 882
in grave form of the plague, 779
in erysipelas, management, 639
in influenza, treatment, 875
in relapsing fever, 393
in scarlet fever, management, 544
in typhoid fever, management, 335
in typhus fever, management, 368
Convulsions during hot stage of intermittent fever, treatment, 597
in cerebro-spinal meningitis, 810
in relapsing fever, 384
complicating rubeola, 572
in prodromal stage of rubeola, 565
in rubeola, treatment, 581
in yellow fever, treatment, 653
Cooking, necessity of a physician's knowledge of, 196
Corpuscles, pus-, 43
Corrosive sublimate, use of, as antiseptic in puerperal fever, 1025,
1029
Coryza, chronic, following rubeola, 574
complicating scarlet fever, 520
of scarlet fever, treatment, 546
Cough, in rubeola, treatment, 581
significance of, in general diagnosis, 158
Counterirritants, use of, in pertussis, 848
Course of vaccinia, 458
irregularities, 460
Cow-pox, 456
spontaneous, 456
Cramps in beriberi, 1039
in cholera, 740
treatment, 769
causes, 740
Cretinism and goitre, hereditary nature, 128
Croup, respiration, 157
Croupous inflammation distinguished from croup, 49
of fauces, complicating scarlet fever, 516
membrane, 685
characters, 685
mode of formation, 685
metamorphosis, 80
Crust in vaccinia, composition, 464
Crusts, objections to use of, in vaccination, 476
Cubebs, use of, in diphtheria, 709
Cultivation of bacillus tuberculosis, 100
Curare, use of, in treatment of hydrophobia, 907
Cutaneous deposits in glanders, microscopic characters, 917
diphtheria, treatment, 713
lesions of glanders in man, 922
symptoms of glanders in man, 921
Cysts, definition, 115, 121
D.
Deaf-mutism following cerebro-spinal meningitis, 819
Deafness in cerebro-spinal meningitis, 811
Death, causes of, in cerebro-spinal meningitis, 818
in glanders, 915
Debility in cerebro-spinal meningitis, 813
in influenza, treatment, 876
influence of, in causation of glanders, 912
in relapsing fever, 386
Decline, stage of, in pertussis, 841
Decubitus, significance of, in general diagnosis, 150
Definition of anthrax, 926
of beriberi, 1038
of cerebro-spinal meningitis, 795
of cholera, 715
of contagion, 200
of cysts, 115, 121
of dengue, 880
of diphtheria, 656
of erysipelas, 629
of glanders, 909
of idiopathic parotitis, 620
of influenza, 851
of leprosy, 785
of pernicious malarial fever, 605
of pertussis, 836
of the plague, 771
of puerperal fever, 984
of pyaemia, 953
of rabies and hydrophobia, 886
of relapsing fever, 369
of remittent fever, 598
of rotheln, 582
of rubeola, 557
of septicaemia, 953
of simple continued fever, 231
of symptomatic parotitis, 625
of term "climate," 185
of typhoid fever, 237
of typho-malarial fever, 614
of vaccinia, 455
of varicella, 481
of variola, 434
of yellow fever, 640
Degeneration, 72
amyloid, 84
cheesy, 79
colloid, 83
fibrinous, 80
fatty, 74
granular, 72
hyaline, 80
lardaceous, 84
mucous, 82
of tubercle, 96
parenchymatous, 73
waxy, 84
Deglutition, difficult, in idiopathic parotitis, treatment, 624
Delirium in cerebro-spinal meningitis, 812
in erysipelas, treatment, 637
in idiopathic parotitis, treatment, 624
in pyaemia, 971
in relapsing fever, 384
in typhoid fever, 278
treatment, 334
in typhus fever, 348
treatment, 366
in yellow fever, treatment, 653
significance of, in general diagnosis, 166
Demonstration of bacillus of glanders, 914
DENGUE, 879
Synonyms, 879
History, 879
Definition, 880
Etiology, 883
Specific origin, 884
Contagiousness, 884
Symptoms--prodromal stage, 880
Mode of onset, 880
Temperature, 881
Pulse, 881
Delirium, 881
Facies, 881
State of gastro-intestinal tract, 881
State of tongue, 881
Stomach and bowels, 881
State of urine, 881
Eruptions, 881
Hemorrhages, 882
Prostration, 882
Convalescence, 882
Duration of, 882
Morbid anatomy, 882
Specific nature of, 882
Relation to acute articular rheumatism, 883
Changes in abdominal organs, 883
Diagnosis, 884
From acute articular rheumatism, 884
From yellow fever, 884
Prognosis, 885
Treatment, 885
Use of colchicum, 885
quinia, 885
opium, 885
Depletion, local, use of, in cerebro-spinal meningitis, 830
Depressing emotions, as a cause of typhoid fever, 245
Dermatitis, complicating vaccination, 468
vaccination, treatment, 469
Desquamation, date of, in mild scarlet fever, 506
in erysipelas, 633
in relapsing fever, 377
Desiccation in varicella, 482
in variola, 440
Diagnosis, general, 148
divisions of, 148
main direction of inquiries, 148
proper method of procedure, 150
significance of alteration of voice in, 158
of anthrax in animals, 936
in man, 942
of cerebro-spinal meningitis, 826
of cholera, 750
of comatose form of pernicious malarial fever, 609
of dengue, 884
of diphtheria, 689
of erysipelas, 635
of idiopathic parotitis, 624
of glanders in horse, 918
of glanders in man, 923
of influenza, 872
of intermittent fever, 594
of leprosy, 792
of the plague, 782
of pyaemia from septicaemia, 978, 979
of remittent fever, 600
of rabies and hydrophobia, 900
of relapsing fever, 418-422
of rotheln, 587
of rubeola, 575
of scarlet fever, 532
of simple continued fever, 234
of symptomatic parotitis, 627
of typhoid fever, 311-314
of typho-malarial fever, 616
of typhus fever, 358, 359
of vaccinia, 464
of varicella, 483
of variola, 447
of varioloid, 444
of yellow fever, 648
Diaphoretics, use of, in yellow fever, 649
Diarrhoea in cerebro-spinal meningitis, 814
in cholera, 738
results, 738
treatment, 760
in mild scarlet fever, 503
in pyaemia, 975
in relapsing fever, 405
in rubeola, treatment, 581
in septicaemia, 977
treatment, 983
in typhoid fever, 287
treatment, 331
Diarrhoeal diseases from impure water, 182
Diathesis, 127
hereditary, transmission, 130
Diet in anthrax, 944
in beriberi, 1042
in cerebro-spinal meningitis, 834
in cholera, 763
in convalescence, 206
in erysipelas, 639
in glanders, 924
in influenza, 874
in relapsing fever, 430
in pertussis, 848
in puerperal fever, 1036
in pyaemia, 982
in rubeola, 579
in typhoid fever, 323
in typho-malarial fever, 619
in typhus fever, 362
in yellow fever, 654
of convalescence, 206
Digestion, condition of, in cerebro-spinal meningitis, 814
Digestive tract, condition of, in glanders, 921
in idiopathic parotitis, 623
Digitalis, use of, in puerperal fever, 1033
in relapsing fever, 428
in scarlet fever, 543
in typhoid fever, 330
in yellow fever, 651
DIPHTHERIA, 656
Synonyms, 656
Definition, 656
History, 656 _et seq._
Panum's view regarding relation of bacteria to, 667
Etiology--Age, influence of, on causation, 680
Sex, influence of, on causation, 680
Causes of frequency of, in childhood, 680
Pharyngeal, buccal, and nasal catarrh a cause of, in children, 680
Physiological causes of, greater frequency in childhood, 681
Family predisposition, 681
Thermometric and barometric changes a cause, 682
Season as a cause, 682
Filth as a cause, 682
Polluted air as a cause, 682
water as a cause, 683
milk as a cause, 683
Contagiousness, 678
Modes of transmission of poison, 678
In the lower animals, 683
Transmission of, from lower animals to man, 683
Artificial production of membrane, 684
Invasion, 676
duration of incubation period, 679
Symptoms--Prodromal stage, 667
duration, 667
localized redness of mucous membranes, 667
Different manifestations of diphtheritic process, 668
Severe form, 668
appearance of membrane in severe form, 668
Gangrenous condition of membrane, 669
Swellings of glands at angle of jaw as sign of invasion of nasal
cavities, 669, 670
Mode of invasion of nasal cavities, 669
Mode of spread to nasal cavities, 669
Nasal form, 669
Conjunctival form, 670
Aural form, 670
Laryngeal form, 671
Formation of membrane in larynx, 671
Tracheal and bronchial forms, 671
primary form, 672
Oral form, 672, 673
Intestinal form, 673
Of wounds, 673
Eruption of, 674
Vulvar and vaginal forms, 674
In puerperal women, 674
Vesical form, 674
Placental, 674
Liability of open wounds, 672, 679
Tendency to second attacks from chronic nasal and pharyngeal catarrh
following, 670
Complications and sequelae, 672
complicated by fibrinous pneumonia, 672
by broncho-pneumonia, 672
by erysipelas, 673
by urticaria and purpura, 674
by kidney affections, 674
by albuminuria, 674
by granular degeneration of blood, 675
by cardiac degeneration, 675
by symptoms of cardiac degeneration, 675
by embolism, 675
by acute endocarditis, 675
by leucocythaemia and Hodgkin's disease, 675
by nervous diseases, 675
by paralysis, 676
seat of, 676
date of appearance, 676
fatty degeneration and atrophy following, 676
sensory, 676
Secondary form, 671
Morbid anatomy--characters of the membrane, 685
Mode of formation of membrane, 685
Varieties of membrane in, 686
Rindfleisch's definition of diphtheritic inflammation, 686
Changes in the heart, 686
fatty and granular degeneration, 686
endocarditis, 687
cardiac thrombi, 687
Changes in lungs, 687
Spleen, 687
Liver, 687
Kidneys, 687
Muscles, 687
Lymphatic glands, 687
Mucous membranes, 688
Influence of different mucous membranes upon characters of false
membrane, 688
epithelia upon growth and spread of false membrane, 688
Changes in intestines, 689
nervous system, 689
Diagnosis--significance of localized pharyngeal injection, 689
From muguet or thrush, 690
Follicular stomatitis, 690
Significance of glandular swelling, 690
lymphadenitis in nasal form, 690
Of laryngeal form, 691
Significance of absence of fever, 691
Of paralysis, 691
Prognosis--symptoms indicating favorable, 692
unfavorable, 692
Significance of glandular swelling, 692
In nasal, 692
Of fetid and putrid discharges, 693
Of epistaxis, 693
In laryngeal, 692
In tracheal, 692
Of tracheotomy, 692
significance of state of pulse after, 692
of dry respiration after, 692
of temperature-range after, 692
of character of membrane, 692
Influence of temperature, 693
state of pulse, 693
complications, 693
bronchitis and pneumonia, 693
endocarditis, 693
albuminuria, 693
affections of sensorium, 693
purpura, 693
icteric discoloration of skin, 693
Of relapses, 694
Treatment--hyperpyrexia, 694
Reflex symptoms, 694
Vomiting, 694
Futility of expectant, 694
Use of stimulants, 694
Amount of stimulants necessary, 695
Importance of general treatment, 695
Futility of venesection, 695
Prophylactic, 696
Danger of self-infection, 696
Prevention of self-infection, 696
Isolation, 696
Closure of schools and public places during epidemics, 697
Disinfection, 698
Special, 701
Local, 701, 709
by steam, 701
Use of water, 702
Ice and cold, 702
Cold baths, 702
Mode of applying cold, 702
Contra-indications to use of cold, 703
Solvents of pseudo-membrane, 703
Use of lime-water, 703
Slaking lime, 703
Lactic acid, 703
Pepsin, neurin, and chinolin, 703
Papayotin, 703
Pilocarpine, 704
objections to, 704
Turpentine inhalations, 704
Ammonium chloride, 704
Mercury, 705
Tincture of chloride of iron, 706
Carbolic acid, 707
Salicylic acid, 707
Quinia, 708
Bromine, 708
Boric acid, 709
Sodium salicylate, 709
Ozone, 709
Sulphur and cubebs, 709
Chlorate of potassium, 699
Dose of chlorate of potassium, 700
Danger in large doses of chlorate of potassium, 701
Mechanical removal of membrane, 709
Cauterization of membrane, 709
Glandular swellings, 710
Abscess of glands, 710
Of nasal form, 710
danger of permitting sleep in, 712
local applications, 710
Of conjunctival form, 712
Of laryngeal form, 712
use of emetics, 712
Of paralysis, 713
by strychnia, 713
by electricity, 713
artificial alimentation, 713
Of cutaneous form, 713
Diphtheria, complicating rubeola, 573
scarlet fever, 514
of genitalia in puerperal fever, 1002
Diphtheritic endometritis, 987
exudations, complicating rubeola, 735
membrane, cauterization, 709
mechanical removal, 709
conjunctivitis, 670
treatment, 712
inflammation, causes, 51
distinguished from diphtheria, 50
paralysis, treatment, 713
pock in vaccinia, 463
Disease, 35
Causes, 125, 175
arsenical poisoning, 193
climate, 185
cold, 133
contagion, 135, 200
epidemic influences, 135
errors of diet, 135
exciting, 125
exercise, abnormal, 134, 198
deficient, 135
functional, 134
habitation, 186
heat, 133
hereditary, 132
humidity of atmosphere, 133
improper clothing, 198
impure air, 177
ice, 185
water, 182
ingestive, 135
intemperance, 197
mental, 204
minute organisms, 141
predisposing, 125
pre-natal, 126, 175
poisons and misuse of medicines, 135
soil, condition of, 187
Definition of, 135
Elevation of site, influence of, 134
Means of discovery, 175
Abdominal, hot climate as a cause, 133
Respiratory, cold as a cause, 133
Prevention, 175
Respiration in, 156
Theory of--bioplastic, 140
chemical, 138, 140
fermentation, 138
germ, 138
points of objection, 142
undecided state, 147
Zymotic, table of, 136
Disinfectants, varieties, 202
Disinfection in anthrax, 937, 943
in cholera, 758
in diphtheria, 698
of glanders, 925
in the plague, 784
in puerperal fever, 1025, 1028
in pyaemia and septicaemia, 980
in scarlet fever, 201, 538
in typhus fever, 362
methods, 201
practical difficulties, 201
principles, 201
Dissecting poison, relation of, to causation of puerperal fever, 1018
wounds, relation of, to causation of septicaemia, 962
Dissemination of influenza, 863
in typhoid fever, 249
of puerperal fever by physicians, 1018
Diuretics, use of, in scarlet fever, 555
in wet beriberi, 1042
DRAINAGE AND SEWERAGE, 213
Back, ventilation of traps, 221
Disposal of liquid wastes by irrigation, 225
Frequency of leakage in waste-pipes, 222
Necessity of, in prevention of typhoid fever, 321
Of houses, 188
Necessity of abundant water-supply in, 220
Of soil, 226
Perfect, fundamental requirements, 213
Removal of human excrement, 215
of liquid household wastes, 220
Varieties of grease-traps, 221
Ventilation of waste-pipes, 223
Drainage-pipes, effects of large traps, 220
of too large bore, 220
of vertical position, 220
Drinking-water as a medium of disseminating typhoid fever, 248
propagation of cholera by, 723
Dropsies, 67-71
Drugs, use of, in the plague, 784
Dry form of beriberi, symptoms, 1040
treatment, 1043
Duration of cerebro-spinal meningitis, 818
of dengue, 882
of anthrax, 940, 941
of acute form of glanders in horses, 915
of chronic form of glanders in horses, 915
of acute form of glanders in man, 921
of chronic form of glanders in man, 922
of influenza, 865
of malignant scarlet fever, 508
of mild scarlet fever, 506
of prodromal stage of rubeola, 565
of remittent fever, 602
of rabies and hydrophobia, 900
of septicaemia lymphatica, 1012
Dysentery complicating relapsing fever, 406
typhus fever, 355
Dysphagia, significance of, in general diagnosis, 162
Dyspnoea, causes, 157
E.
Ear, affections of, in rubeola, treatment, 581
diseases of, complicating rubeola, 570
displacement of lobe in idiopathic parotitis, 624
internal, lesions of, in cerebro-spinal meningitis, 824
lesions of, in pyaemia, 967
in symptomatic parotitis, 626
middle, suppuration of, in cerebro-spinal meningitis, 811
symptoms of diphtheria, 670
Ears, significance of appearance of, in general diagnosis, 151
Early stages of yellow fever, treatment, 649
Earth-closets, 218
Effluvia, offensive, symptoms due to, 181
Effusions, 67
causes, 68-71
distinguished from exudations, 67
Elaterium, use of, in wet beriberi, 1042
in dry beriberi, 1043
Electricity, use of, in diphtheritic paralysis, 713
Elevated temperature as a cause of typhoid fever, 246
Emaciation, causes, 160
significance of, in diagnosis, 159
Emboli, action of, in production of metastatic abscesses in pyaemia,
967
Embolism, 62
complicating diphtheria, 675
from septic thrombus, 66
hemorrhagic results, 64, 65
in typhoid fever, treatment, 335
mechanical effects, 63
necrosis from, 64, 65
results, 64
softening, cerebral, from, 65
symptoms, 66
Embolus, 62
arterial, 63
venous, 63
terminations, 65
Emetics, use of, in cerebro-spinal meningitis, 830
in cholera, 765
during cold stage of intermittent fever, 595
in influenza, 876
in laryngeal diphtheria, 712
in pertussis, 845
Emphysema, aggravation of, by influenza, 870
significance of, in general diagnosis, 159
Endocarditis, acute, complicating diphtheria, 675
in diphtheria, 687
in puerperal fever, 990
Endo- and pericardium, lesions of, in septicaemia, 972
Endocolpitis in puerperal fever, 986, 1005
Endometritis in puerperal fever, 986
Enthetic febrile diseases, hereditary nature, 130
Epidemic causation of disease, 135
Epidemics of rubeola, frequency, 560
frequency in the new-born, 563
Epiglottis, symptoms of diphtheria, 671
Epistaxis in relapsing fever, 393
complicating rubeola, 570
in remittent fever, 602
in rubeola, treatment, 580
in typhoid fever, 273
treatment, 335
Epithelia, influence of different, in spread of diphtheritic membrane,
688
Ergot, use of, in cerebro-spinal meningitis, 833
Ergotine, use of, in pyaemia, 982
Eruption, absence of, in rubeola, 568
causes of absence of, in mild scarlet fever, 505
in cerebro-spinal meningitis, 816, 817
in dengue, 881
in diphtheria, 674
in influenza, 866
in malignant scarlet fever, 507
in mild scarlet fever, 504
in pyaemia, 974
in relapsing fever, 376
in rotheln, 585, 586
in rubeola, 566
peculiarities in character, 569
in seat, 509
relapses, 570
retrocession of, in rubeola, treatment, 580
in tubercular form of leprosy, 789
in typhoid fever, 273
in typhus fever, 351
in varicella, 487
in variola, 437
characters, 438
position, 438
in varioloid, 444
Eruptive stage of rubeola, duration of, 567
symptoms of, 565
of variola, treatment, 452
ERYSIPELAS, 629
Definition, 629
Synonyms, 629
Classification, 629
History, 629
Etiology, 629
Unity of the origin, 629
Age and sex as a cause, 630
Season as a cause, 630
Contagiousness, 630
Nature of contagion, 630
Manner of propagation, 630
Relation to childbed fever, 630
Symptoms--initial, 631
Characters of cutaneous lesions, 631
Course of cutaneous lesions, 631
Severe varieties of cutaneous lesions, 632
Migration of cutaneous lesions, 632
Swelling of integument, 632
Starting-point of cutaneous lesions, 632
Physiognomy, 632
Condition of tongue, 633
of fauces and buccal membrane, 633
General symptoms of grave form, 633
pulse, 633
temperature, 633
Occurrence of gangrene, 633
Resolution, 633
Desquamation, 633
Complications and sequelae, 633
Complicated by lymphangitis and adenopathy, 634
By pneumonia, 634
By pleuritis, 634
By inflammation of joints, 634
By inflammations of serous membranes, 634
By pyaemia and septicaemia, 634
By eye diseases, 634
Followed by seborrhoea of scalp, 633
By loss of hair, 633
Modification of previous skin disorders, 634
Chronic forms, 634
Variety and nature of chronic forms, 634
Morbid anatomy, 635
Changes in skin, 635
Viscera, 635
Mucous surfaces, 635
Diagnosis, 635
From dermatitis, 636
From eczema, 636
From erythema, 636
From pemphigus, 636
From scarlet fever, 636
From urticaria, 636
Prognosis--symptoms indicating unfavorable, 636
Treatment--preventive, 636
Hygienic, 637
General, 637
Hyperpyrexia, 637
Delirium, 637
Local, 637
Value of abortive, 638
Surgical, 638
Mouth complications, 638
Nasal complications, 638
Abscesses, 638
Value of expectant, 639
Convalescence, 639
Diet, 639
Use of quinia, 637
tincture of the chloride of iron, 637
Erysipelas, complicating diphtheria, 673
typhus fever, 355
vaccination, 469
variola, 445
relation of, to puerperal fever, 1002
Etiology, general, 125
of anthrax in animals, 928
in man, 939
of beriberi, 1038
of cerebro-spinal meningitis, 801
of cholera, 720
of dengue, 883
of diphtheria, 680
of erysipelas, 629
of glanders in horse, 911
in man, 919
of idiopathic parotitis, 620
of influenza, 859
of leprosy, 787
of pertussis, 838
of the plague, 774
of puerperal fever, 1013
of pyaemia, 955
of rabies and hydrophobia, 887
of relapsing fever, 370
of remittent fever, 598
of rotheln, 583
of rubeola, 557
of scarlet fever, 487
of septicaemia, 960
of septo-pyaemia, 963
of simple continued fever, 232
of symptomatic parotitis, 625
of typhoid fever, 242
of typhus fever, 341
of varicella, 481
of variola, 435
of yellow fever, 640
Eucalyptus, use of, in typhoid fever, 331
Excision of cicatrix for prevention of hydrophobia, 908
of primary nucleus in anthrax, 943
Exciting cause, mechanical nature of, in symptomatic parotitis, 626
of the plague, 775
of typhoid fever, 248
of typhus fever, 343
Excrement, human, disposal of, by privy-vaults, 219
dry conservancy, 218 _et seq._
removal of, by water-carriage, 215
Exercise, abnormal, as a cause of disease, 134
amount necessary for health, 198
as a part of a systematic education, 199
deficiency of, a cause of disease, 135
Du Bois Reymond's definition, 198
importance of, in preservation of health, 198
relation of, to mental work, 199
Expectant treatment of erysipelas, value, 639
Expectoration, significance of, in diagnosis, 158
External anthrax, localized, 935
Exudation, distinction from transudation, 42
in inflammation, 42
in peri- and parametritis of puerperal fever, 1007
in pelvic peritonitis, 989
Eye, affections of, following cerebro-spinal meningitis, 819
in rubeola, treatment, 581
condition of, in cerebro-spinal meningitis, 810
diseases of, complicating erysipelas, 634
rubeola, 571
variola, 445
lesions of, in cerebro-spinal meningitis, 824
in pyaemia, 967
Eyes, appearance of, significance in general diagnosis, 151
F.
Face, appearance of, in typhus fever, 348
Family predisposition to diphtheria, 681
Faradization, use of, in rabies and hydrophobia, 907
Farcy, 909
Fatigue as a cause of typhus fever, 342
Fat, sources of, in the body, 74
Fatty degeneration, 74
causes, 78
following diphtheritic paralysis, 676
infiltration, 76
metamorphosis, 74, 79
Fauces, condition of, in cerebro-spinal meningitis, 814
in erysipelas, 633
in malignant scarlet fever, 508
in typhoid fever, 286
inflammation of, complicating rubeola, 571
significance of appearance of, in general diagnosis, 152
Faucial and nasal mucous membrane, condition of, in mild scarlet
fever, 504
Febrifuge, use of, in relapsing fever, 428
Febrile stage of grave form of the plague, 778
Fermentation theory of disease, 138
Fever, agents producing heat in, 40, 41
definition, 38
inflammatory, 37
distinguished from idiopathic, 37
influence of vaso-motor system on production of heat in, 39
intermittent, 592
malarial, 589
pernicious malarial, 605
puerperal, 984
relapsing, 369
remittent, 598
sanitary effects, 41
scarlet, 486
secondary, in variola, 439
simple continued, 231
symptoms, 38
temperature, 38-40
traumatic, 37
typho-malarial, 614
typhoid, 237
typhus, 338
yellow, 640
Fibrinous degeneration, 80
inflammation, 49
Filtering power of soil, 187
Filth as a cause of cholera, 721
diphtheria, 682
the plague, 774
relapsing fever, 370
Foetus, effects of maternal impression upon, 131
Fomites, propagation of cholera by, 721
special, of cholera, 723
Food, adulterations, 197
appetite as a guide to necessary amount, 195
as a cause of disease, 195
infants, 196
patient's sensations as a guide to choice of, in disease, 205
popular errors in regard to, 195
to overeating, 195
preparation of, necessity of a physician's knowledge of, 196
proper, necessity of, in prevention of pyaemia and septicaemia, 980
transmission of anthrax by, 929
Formad on peculiarities of scrofulous habit, 101
Forms of anthrax in animals and man, 934, 940
of leprosy, 789
of the plague, 777
of rabies, 895
of relapsing fever, 395
of vaccine, 476
Fourth ventricle, lesions of, in cerebro-spinal meningitis, 824
Fraenum linguae, ulceration of, in pertussis, 841
Frequency of puerperal fever, 984
of typho-malarial fever, 616
Frictions, use of, in dry beriberi, 1043
Frontal pains in influenza, 867
Fruit, propagation of malaria by, 591
Fulminant form of the plague, 779
Furious form of rabies, 896
Furuncles, complicating variola, 445
G.
Gait, peculiarity of, in beriberi, 1039
Gall-bladder, lesions of, in cholera, 746
in typhoid fever, 266
Gangrene, 56
complicating vaccination, 468
following typhoid fever, 293
typhus fever, 355
in erysipelas, 633
in symptomatic parotitis, treatment of, 628
of neck, complicating scarlet fever, 512
pulmonary, complicating relapsing fever, 404
Gangrenous affections following rubeola, 574
Gastro-intestinal canal, condition of, in dengue, 881
condition of, in yellow fever, 644
lesions of, in anthrax, 936
in influenza, 872
in rabies and hydrophobia, 902
in relapsing fever, 413
symptoms in influenza, 866
in mild scarlet fever, 505
in malignant scarlet fever, 507
of septicaemia lymphatica, 1011
Gelsemium, use of, in yellow fever, 651
GENERAL ETIOLOGY, 125
General dropsies, 71
treatment of erysipelas, 639
of glanders in horse and man, 919, 920
Genitalia, gangrene of, complicating variola, 446
Geographical distribution of anthrax, 926
of beriberi, 1038
of glanders, 909
of rabies and hydrophobia, 886
of relapsing fever, 369
of typhoid fever, 241
Germ, specific, of glanders, nature of, 914
of rabies and hydrophobia, 892
point of election of, 892
Germ-theory of disease, 138
of scarlet fever, 488
Giddiness, significance of, in general diagnosis, 166
GLANDERS (FARCY), 909
Synonyms, 909
Definition, 909
History, 909
Geographical distribution, 909
Etiology--Contagiousness, 911
Specific nature, 911
Predisposing causes, 912
Ill-health, relation of, to causation, 912
Cold and damp stables, relation of, to causation, 912
Debility from chronic diseases, relation of, to causation, 912
Infection, channels of, 913
Particular nature of the germ, 914
Virulence of the germ, 914
Modes of culture of germ, 914
Demonstration of bacillus of, 914
Symptoms--in horses, 914
Acute form, 914
Incubation period, 914
Mode of onset, 914
Local lesions, 915
Appearance of nostrils, 915
of lymphatics, 915
Enlargement of joints, 915
Appearance of ulcers, 915
Mode of death in, 915
Chronic form, 915
Premonitory symptoms, 915
Condition of general health, 915
Local lesions, 915
Lymphatics, 915
Bronchial and pulmonary form, 916
Acute cutaneous form (farcy), 916
Local lesions, 916
Chronic cutaneous form (chronic farcy), 916
Local lesions, 916
Duration, 915
Morbid anatomy, 916
Nasal lesions, characters of, 917
Pulmonary lesions, characters of, 917
Cutaneous lesions, characters of, 917
Diffuse glanderous swellings, 917
of nose, 918
of lungs, 918
of muscles, 918
Diagnosis, 918
Value of inoculation in, 918
Prognosis, 918
Unfavorable nature of, 918
Treatment--in animals, 918
Not commendable, 918
Local, 918
General, 919
Diet in, 919
Preventive, 919
Extermination of disease in animals, 919
_Glanders in Man_, 919
History of, 919
Etiology, 919
Modes of infection, 919
immediate, 919
mediate, 920
Influence of occupation, 920
Influence of ill-health, 920
Symptoms--incubation period, 920
Appearance of wound, 920
General, 920
Mode of onset, 920
Character and seat of local lesions, 921
Appearance of sores, 921
Condition of nasal mucous membrane, 921
of submaxillary glands, 921
of conjunctiva, 921
Digestive tract, 921
Nervous system, 921
Temperature in, 921
Pulse in, 921
Chronic form, 921
General, 921
Local, 921
Cutaneous lesion, 922
Respiratory lesions, 922
Lymphatic glands, 922
Digestive tract, 922
Convalescence, 922
Duration of acute forms, 921
of chronic forms, 922
Morbid anatomy--changes in mucous membranes, 922
Lungs and pleurae, 922
Gastro-intestinal tract, 922
Spleen and liver, 922
Joints, 922
Bones, 922
Brain and membranes, 923
Microscopy of lesions, 923
Diagnosis, 923
Pathognomonic signs in, 923
From rheumatic fever, 923
Chronic form, from pyaemia and septicaemia, 923
From syphilis, 924
From miliary tuberculosis, 924
Presence of bacillus not conclusive, 924
Value of inoculation in, 924
Prognosis--unfavorable nature of, 924
Treatment--External cases, 924
Erysipelatoid swellings, 924
Abscesses and tumors, 924
Nasal ulcers, 924
Importance of general treatment, 924
Use of antiseptics, 924
Diet, 924
Preventive, 925
Extinction of affection in animals, 925
Necessity of disinfection, 925
Glanderous swelling, diffuse, 917
Glands at angle of jaw, swelling of, symptomatic of nasal invasion, in
diphtheria, 669, 670
Glandular abscesses in diphtheria, treatment, 710
degenerations, 72
swellings in diphtheria, treatment, 709
Glycosuria, complicating relapsing fever, 410
Gout, hereditary nature, 127
Granuloma, 120, 124
Grave forms of cholera, physiognomy, 734
stools, 733
symptoms, 732
of the plague, 777
of relapsing fever, 395
Grease-traps, varieties, 221
GROWTHS, MORBID, 105
Gums, significance of state of, in general diagnosis, 151
H.
Habits, depressing, as a cause of cerebro-spinal meningitis, 802
Haematemesis, significance of, in general diagnosis, 163
in relapsing fever, 390
Haematoidin, 91
Haematoma, 115, 122
Haematuria in relapsing fever, 390
Haemoglobin, 90
Haemophilia, hereditary nature, 129
Haemoptysis, significance of, in general diagnosis, 163
Haemostatics, use of, in yellow fever, 652
Hair, appearance of, in typhoid fever, 275
loss of, following erysipelas, 633
Headache in cerebro-spinal meningitis, 808
in idiopathic parotitis, 624
in influenza, 867
treatment, 874
in relapsing fever, 383
in typhoid fever, 277
treatment, 334
in typhus fever, 348
treatment, 366
Health, importance of exercise in preservation, 198
Health-resorts, disease from, 185
Hearing, impairment of, following cerebro-spinal meningitis, 819
disorders of, in relapsing fever, 400
modifications of, in typhoid fever, 279
significance of, in general diagnosis, 166
Heart, alterations of, in beriberi, 1041
condition of, in beriberi, 1040
in cholera, 737
in pyaemia, 976
in typhus fever, 351
disease, complicating influenza, 870
lesions of, in cholera, 746
in diphtheria, 686
in relapsing fever, 411
in septicaemia, 972
in typhoid fever, 267
in typhus fever, 357
and blood-vessels, lesions of, in rabies and hydrophobia, 902
palpitation of, in beriberi, 1039
Heart-clot, complicating relapsing fever, 402
rubeola, 672
scarlet fever, 523
Heat as a cause of disease, 133
use of, in cholera, 769
Hemorrhages in dengue, 882
in hemorrhagic form of pernicious malarial fever, treatment, 612
in remittent fever, treatment, 605
in yellow fever, 646
treatment, 651
intestinal, in typhoid fever, 287, 288
treatment, 332
Hemorrhagic form of pernicious malarial fever, 609
causes, 610
seat of hemorrhages, 610
symptoms, 611
treatment, 612
of scarlet fever, 509
of variola, treatment, 454
infarction, 64
rubeola, 569
small-pox, 442
variola, morbid anatomy of pock in, 447
Hepatic abscess following typhoid fever, 295
Heredity as a cause of disease, 175
influence of, on marriage, 176
relation of, to life insurance, 175
as a cause of leprosy, 787
Hereditary diathesis, transmutation, 130
nature of syphilis, 127
of non-malignant morbid growths, 129
of nervous diseases, 129
of organic disease, 129
of rickets, 128
predisposition to disease, 126
Herpes labialis, complicating influenza, 874
Hiccough in cholera, 762
in relapsing fever, 405
significance of, in general diagnosis, 158
Histoid tumors, 116
History of anthrax in animals and man, 926, 939
of beriberi, 1038
of cerebro-spinal meningitis, 796
of cholera, 715
of dengue, 879
of diphtheria, 656
of erysipelas, 629
of glanders in horses, 909
in man, 919
of influenza, 852 _et seq._
of pertussis, 836
of rabies and hydrophobia, 886
of relapsing fever, 369
of rotheln, 582
of rubeola, 557
of pyaemia and septicaemia, 945-952
of scarlet fever, 486
of simple continued fever, 231
of typhoid fever, 238
of typhus fever, 338
of vaccination, 465
of vaccinia, 456
of varicella, 481
of variola, 434
Hodgkin's disease, complicating diphtheria, 675
Horse-pock vaccine, 473
Hospitals for infectious diseases, necessity, 203
Hospital, maternity, advantages, 1021
Hot stage of intermittent fever, treatment, 595
House-drainage, 188
disconnection of, from sewer, 190
testing, 190
House-plumbing, 190
Houses, sanitary inspection, 187, 193
House-sewerage, 188
dangers to health from, 189, 191
examination of a system, 188
main points in a good system, 191
peppermint-test for defects, 190
Human excrement, removal of, by drainage, 215
Humanized and animal vaccine, relative merits, 473
vaccine, points of superiority, 473
Humidity of air as a cause of disease, 133
Hunger, influence of, on causation of rabies and hydrophobia, 888
Hyaline degeneration, 80
Hydro-bilirubin, 91
Hydrocephalus, following cerebro-spinal meningitis, 819
Hydrochloric acid, local use of, in puerperal fever, 1028
Hydrophobia, 886
Hygiene, 173
importance of perfect, in cholera epidemics, 758
in pertussis, 848
public, relation of physicians to, 207
Hygienic treatment of erysipelas, 637
of hydrophobia, 906
of scarlet fever, 539
of typhoid fever, 322
of yellow fever, 654
Hygroma, 116, 122
Hyperpyrexia in diphtheria, treatment, 694
in erysipelas, treatment, 637
in puerperal fever, treatment, 1032
in relapsing fever, treatment, 426
in rubeola, treatment, 579
in scarlet fever, treatment, 541
in typhoid fever, treatment, 327
in typhus fever, treatment, 364
in yellow fever, treatment, 651
Hypodermatic injection of anthrax swellings, 938, 943
I.
Ice, impure, as a cause of disease, 185
use of, in diphtheria, 702
in scarlet fever, 542
Idiopathic parotitis, 620
Idiosyncrasy as a cause of typhoid fever, 245
influence of, in causation of variola, 436
Ill-health, influence of, in causation of glanders, 912, 920
Impure air as a cause of disease, 177
evil effects of, 181
water, as a cause of disease, 182
Impurities of water, from living organisms, 184
nature, 184
Incubation of relapsing fever, 376
of scarlet fever, 492
of typhus fever, 346
of varicella, 481
of variola, 436
period of anthrax in animals, 934
in man, 940
of diphtheria, duration of, 679
of glanders in horse, 914
in man, 920
of influenza, 863
of intermittent fever, 592
of the plague, 777
of rabies and hydrophobia, 894
of rotheln, 585
of typhoid fever, 259
of yellow fever, 643
stage of idiopathic parotitis, duration, 621
of idiopathic parotitis, 621
of puerperal fever, 1004
of pyaemia, 973
of rubeola, 563
Indications for treatment of puerperal fever, 1028
of septicaemia, 982
of yellow fever, 649
Infants' food, 196
Infarction, hemorrhagic, 164
Infection, 200
channels of, in glanders, 913
modes of, in human anthrax, 939
Infiltration, albuminoid, 72
amyloid, 84
fatty, 76
INFLAMMATION, 37
Characteristics, 37
Heat, 37
Redness, 37
causes, 37
Pain, 41
causes, 41
Swelling, 41
causes, 41
Exudation, 42
Reuss on distinction of exudation from transudation, 42
Migration of white corpuscles, 42
Coagulation of exudation, 43
Changes in the blood-vessels, 43
Disturbance of functions, 44
Varieties of--hemorrhagic, 48
Diphtheritic, 50
Productive, 51
Catarrhal, 52
Phlegmonous, 52
Acute, 53
Chronic, 53
Interstitial, 53
Parenchymatous, 53
Termination, 54, 55, 56
Resolution, 54
New formations, 54
Cicatrization, 55
Abscesses, 56
Destruction of tissue, 56
Causes, toxic, 43
traumatic, 44
parasitic, 45
infectious, 45
constitutional, 46
trophic, 46
Course, 46
Sthenic and asthenic, 46
Serous, 47
Typhoidal, 47
symptoms, 47
Purulent, 48
Suppurative, relation of microbia, 48
Fibrinous, 49
of fauces, catarrhal and diphtheritic, complicating typhoid fever,
295
of neck, complicating parotitis, 511
simple, complicating vaccination, 468
Inflammations, serous, complicating typhus fever, 355
Inflammatory fevers, 37
form of typhus fever, 354
rubeola, 568
INFLUENZA--Definition, 851
Synonyms, 851
History, 852 _et seq._
Etiology, 859
Predisposing causes, 859
Age, relation of, to causation, 860
Social condition, relation of, to causation, 860
Sex, relation of, to causation, 860
Occupation, relation of, to causation, 860
Race, relation of, to causation, 860
Over-crowding and filth, relation of, to causation, 860
Season, relation of, to causation, 860
Climate, relation of, to causation, 860
Air, condition of, to causation, 860
Winds, relation of, to spread, 860
Mode of onset of epidemics, 860, 861
Duration of epidemics, 861
Exciting causes, 862
Specific poison, 863
Contagiousness, 862
Dissemination, 863
Relation of, to other epidemic diseases, 863
Incubation period, 863
Clinical history, 864
Variations in intensity of symptoms, 864
Symptoms of mild cases, 864
of severe cases, 864
Symptomatology, 865
Analysis of symptoms, 865
Fever, 865
Temperature, 865
Pulse, 866
Urine, 866
Skin, 866
Eruptions, 866
Gastro-intestinal system, 866
Nausea and vomiting, 866
Physiognomy, 866
Catarrhal symptoms, 866
Condition of mucous membrane, 866
Hoarseness, 867
Cough and dyspnoea, 867
Nervous system, 867
Headache, 867
Frontal pain, 867
Pains in limbs, 868
Pleurodynia, 868
Delirium, 868
Dizziness, 868
Sleeplessness, 868
Hebetude and torpor, 868
Muscular twitchings, 868
Mental condition, 868
Duration, 865
Complications and sequelae, 868
Inflammations of lungs, 868
Bronchitis and capillary bronchitis, 868, 869
Catarrhal pneumonia, 869
Lobar pneumonia, 869
Localized pulmonary collapse, 869
Gangrene of lungs, 870
Pleurisy, 870
Pericarditis, 870
Laryngitis and chronic bronchitis, 870
Inflammation of middle ear, 870
Parotitis, 870
Herpes labialis, 870
Phthisis, 870
Emphysema, aggravation, 870
Old neuralgias, aggravation, 870
Heart disease, aggravation, 870
Bright's disease, aggravation, 870
Pregnancy, 870
Intermittent fever, 870
Morbid anatomy, 871
Essential lesions, 871
Appearance of respiratory tract, 871
Changes in gastro-intestinal tract, 872
Bronchial glands, 872
Lung tissue, 872
Pathology--Not a simple acute inflammation, 871
Specific character, 871
Diagnosis--From non-specific catarrhal affections, 872
From typhoid fever, 872
Prognosis--Influence of age, 872
pre-existing organic disease, 872
of character of epidemic, 872
Mortality, 872, 873
Variability in different epidemics, 873
Rate of, 873
Cause of death, 873
Treatment--preventive, 873
Mild forms, 874
Catarrh, 874
Headache, 874
Cough, 875
Use of quinine, 874
Opium, 874
Fat inunctions, 874
Diet, 874
Severe forms, 875
Indications for treatment, 875
High temperature, 875
Cough, 876
Sub-sternal and chest pains, 876
Use of diaphoretics, 875
Bloodletting, 875
Emetics, 876
Purgatives, 876
Quinine, 876
Mineral acids, 876
Expectorants, 877
Opium, 876
Alcohol, 877
Chloral, 877
Diarrhoea, 877
Debility, 877
Lung complications, 877
Diet in, 875
Convalescence, 878
Danger of depressing measures, 878
Inhalations, use of, in pertussis, 844
Initial stage of pertussis, 840
symptoms of yellow fever, 644
Injections, intravenous, use of, in cholera, 768
in hydrophobia, 908
in puerperal fever, 1029
vaginal, use of, in prevention of puerperal fever, 1026
Inoculation as a means of diagnosis in glanders, 918
in hydrophobia, 902
as a prophylactic in anthrax, 937
in rabies and hydrophobia, 905
in scarlet fever, 536
of leprosy, 788
of rubeola, 559
of small-pox, 465
Insects, propagation of anthrax by, 929
Insomnia in typhoid fever, treatment, 334
in typho-malarial fever, treatment, 619
in typhus fever, treatment, 366
Inspection of houses, sanitary, 187
Insusceptibility to rabies and hydrophobia, 894
Intellect, impairment of, following cerebro-spinal meningitis, 819
following typhoid fever, 292
Intellectual condition in typhus fever, 348
Intemperance as a cause of cholera, 721
of disease, 197
of relapsing fever, 370
of typhoid fever, 245
of typhus fever, 342
Intermission in intermittent fever, 594
in relapsing fever, 381
INTERMITTENT FEVER, 592
Incubation period, 592
Symptoms--prodromal stage, 592
Paroxysm, 592
Cold stage, 592
theory of cause of cold stage, 593
Hot stage, 593
duration of hot stage, 593
relation of type to duration of hot stage, 593
Sweating stage, 593
Nausea and vomiting during paroxysm, 593
Intermission, 594
Duration of intermission, 594
Relative frequency of different types, 594
Convertibility of different types, 594
Morbid anatomy, 594
Treatment--cold stage, 594
Use of quinia, 595
Opium, 595
Emetics, 595
Hot stage, 595
Use of opium, 595
Quinia, 596
Purgatives, 596
Of convulsions, 597
Sweating stage, 597
Use of quinia, 597
Causes of failure of quinia, 597
Adjuvants to quinia in preventing return of paroxysms, 598
Use of nitric acid to prevent return of paroxysms, 598
Internal anthrax in animals, 934
Interstitial inflammation, 53
Intestinal anthrax in man, 941
canal, lesions of, in cholera, 743
catarrh, chronic, following rubeola, 574
complicating rubeola, 572
tract, lesion of, in typhus fever, 357
Intestines, lesions of, in diphtheria, 689
symptoms of diphtheria of, 673
Intravenous injection of warm water in hydrophobia, 908
Inunction in scarlet fever, 541
Inunctions, use of, in rubeola, 580
Invasion of cerebro-spinal meningitis, 806
of diphtheria, 676
of variola, 438
stage of grave form of the plague, 777
of idiopathic parotitis, duration, 621
treatment, 624
of variola, treatment, 452
of varioloid, 443
Iodine as a specific in typhoid fever, 336, 337
Iodoform, intra-uterine use of, in puerperal fever, 1025
Iron, persulphate, local use of, in puerperal fever, 1028
tincture of the chloride, use of, in diphtheria, 706
in erysipelas, 637
in yellow fever, 652
Irregular forms of scarlet fever, 508
Irrigation, disposal of liquid wastes by, 225
Irritability of nervous system in hydrophobia, 899
Irritants, influence of, in production of morbid growths, 108
Isolated glands, lesions of, in cholera, 745
Isolation in anthrax, 937
in diphtheria, 696
in the plague, 783
in rubeola, 578
in scarlet fever, 536
necessity of, in typhus fever, 361
principles of, in disease, 203
J.
Jaborandi, use of, in scarlet fever, 552
in yellow fever, 650
Jaundice in relapsing fever, 391
in septicaemia venosa, 1012
complicating typhoid fever, 295
typhus fever, 356
in remittent fever, 601
in yellow fever, 646
Joints, chronic diseases of, following rubeola, 574
condition of, in glanders in man, 920
inflammation of, complicating erysipelas, 634
lesions of, in pyaemia, 967
purulent inflammation of, in puerperal fever, 990
suppuration of, in pyaemia, 976
swelling of, in cerebro-spinal meningitis, 814
in relapsing fever, 400
Jugular veins, pulsation of, significance in general diagnosis, 156
Juniper gin, use of, in wet beriberi, 1042
K.
Kibbie's fever-cot, use of, in puerperal fever, 1034, 1035
Kidney affections, complicating diphtheria, 676
complications in hemorrhagic form of pernicious malarial fever,
treatment, 612
Kidneys, lesions of, in anthrax in animals, 937
in man, 942
in cholera, 746
in diphtheria, 687
in pyaemia, 969
in rabies and hydrophobia, 903
in relapsing fever, 414
in scarlet fever, 526
in septicaemia, 972
in typhoid fever, 268
in typhus fever, 357
Koch's investigation of bacillus tuberculosis, 99
of cholera bacilli, 745-749
of bacteria of puerperal fever, 997
L.
Lactic acid, use of, in diphtheria, 703
Lardaceous degeneration, 84
Laryngeal diphtheria, local treatment, 712
prognosis, 692
Laryngitis, complicating rubeola, 571
typhoid fever, 294
Larynx, inflammation of, complicating variola, 446
lesions of, in hydrophobia, 902
in relapsing fever, 413
in typhoid fever, 266
symptoms of diphtheria, 671
Latent form of typhoid fever, 300
Leeches, use of, in puerperal fever, 1031
LEPROSY, 785
Definition, 785
Synonyms, 785
History, 785
Etiology, 787
Heredity as a cause, 787, 788
Contagiousness, 788
Transmission, by inoculation, 788, 789
Sex as a cause, 789
Forms, 789
Symptoms--prodromal stage, 789
Duration of prodromal stage, 789
Tubercular form, 789
Local, 789
Eruptions, 789
Earlier eruptions, 790
Characteristic eruptions, 790
General, 790
Duration, 790
Anaesthetic form, 790
Local, 790
General, 791
Duration, 791
Morbid anatomy, 791
Changes in nerves, 791
Skin, 791
Bacteria, 792
Seat of bacteria, 792
Diagnosis, 792
Prognosis, 793
Treatment, 793
Futility of specific, in, 793
Indications, 793
Prophylaxis, 794
Segregation of afflicted, 794
Quarantine in, 794
Local, 794
Lesions characteristic of anthrax, 935
Lethargic form of rabies in dogs, 897
Leucocytes, death of, as a cause of thrombosis, 57
migration, 42
Leucocythaemia, complicating diphtheria, 675
Lime-water, use of, in diphtheria, 703
Limbs, significance of appearance in general diagnosis, 160
Listerine as a prophylactic in scarlet fever, 537
Liver, abscess of, following typhoid fever, 295
enlargement of, in pyaemia, 976
lesions of, in cholera, 745
in diphtheria, 687
in glanders, 918, 922
in pyaemia, 969
in remittent fever, 602
in relapsing fever, 414
in scarlet fever, 531
in typhoid fever, 265
in typhus fever, 357
in yellow fever, 649
Local dropsies, 71
lesions of glanders, 915, 921
symptoms of glanders in animals, 914
of glanders in man, 921
treatment of anthrax in animals, 938
of anthrax in man, 943
of diphtheria, 701, 709
of erysipelas, 637
of glanders in horse, 918
in man, 924
of pyaemia, 981
of septicaemia, 983
Lochial discharge, influence of, on causation of puerperal fever, 1015
Lung diseases, complicating influenza, 868
complicating influenza, treatment, 877
Lungs, gangrene of, in influenza, 870
hypostatic congestion of, in typhus fever, 353
lesions of, in cholera, 746
in diphtheria, 687
in glanders, 917, 922
in influenza, 872
in pyaemia, 968
in relapsing fever, 413
in septicaemia, 972
in typhoid fever, 266
Lymph, dried, use of, in vaccination, 477
of vaccinia, microscopical characters, 463
vaccine, proper time for collecting, 479
Lymphangitis, complicating erysipelas, 634
vaccination, 468
Lymphatic glands, condition of, in anthrax, 940
in glanders in horses, 915
in man, 921
in malignant scarlet fever, 508
in rotheln, 586
lesions of, in human anthrax, 942
in anthrax of lower animals, 935
in diphtheria, 687
in relapsing fever, 417
pigmentation of, 92
Lymphatics, as channel of entrance of poison of septicaemia, 963
lesions of, in symptomatic parotitis, 626
Lymphatic swellings, seat of, in grave form of the plague, 778
system, lesions of, in the plague, 781
Lymphoma, 120, 124
M.
Magnesium sulphate, use of, in wet beriberi, 1042
Malaria, 89
action of poison on system, 591
entrance into system, modes of, 591
communicability by drinking-water, 590
by fruit, 591
by milk, 590
conditions necessary to mature the poison, 589
duration of incubation of poison, 591
from impure water, 182
influence of moisture in production, 187
means of access of the poison, 590
nature of the poison, 589
non-interchangeableness of the poison, 591
ponderability of the poison, 590
production, 187
specific nature of poison, 591
MALARIAL FEVER, PERNICIOUS, 605
Definition, 605
Varieties, 606
Algid or congestive form, 606
Causes, 606
Frequency, 607
Cases illustrating clinical history, 606
Causes of death, 607
Mortality-rate, 607
Treatment, 607
General indications for treatment, 608
Use of ice and cold in treatment, 608
Opium, 608
Alcohol, 608
Comatose form, 608
Symptoms, 608
Previous condition of persons attacked, 609
Diagnosis from congestive form, 609
Treatment, 609
Hemorrhagic form of, 609
Causes, 610
Seat of hemorrhages, 610
Cases illustrating clinical history, 611
Treatment, 612
Indications for treatment, 612
Use of quinia, 612
Hemorrhages, 612
Renal complications, 613
Depurative, 613
Use of calomel and purgatives, 613
Malarial fevers, 589
definition, 589
nature of remittent fever, 598
Malignant anthrax oedema, 940
pustule, 926
tumors, 114
Mania following cerebro-spinal meningitis, 819
Maternity hospitals, advantages of, 1021
Marriages, influence of, hereditary, 176
of diseased persons, 176
transmission of hereditary proclivities by, 131
Marriages, consanguineous, 131
Marson's theory of multiple vaccination, 467
Masked forms of yellow fever, symptoms, 654
Maturation in variola, 439
Measles, 557
relations of, to idiopathic parotitis, 620
Mechanism of transudation, 68
Medical diagnosis, general, 148
Melanaemia, 92
Melanin, 92
Membrane, appearance of, in severe form of diphtheria, 668
diphtheritic, artificial production, 684
characters, 685
mode of formation, 685
varieties, 686
gangrenous condition of, in diphtheria, 669
MENINGITIS, EPIDEMIC CEREBRO-SPINAL, 795
Definition, 795
Synonyms, 795
History, 796
Etiology, 801
Seasons as a cause, 802
Meteorological agencies, 802
Localities, 802
Age, influence, 802
Sex, influence, 802
Depressing and debilitating habits, 803
Contagiousness, 803
Morbific principle, 803
Pandemic nature, 804
In the lower animals, 804
Types, 804
Forms, 805, 806
Symptoms--summary of, 806
Modes of onset, 806, 807
Individual, 808
Pain in the head, 808
spine, 808
Hyperaesthesia and anaesthesia of skin, 808
Spinal rigidity or opisthotonos, 809
duration of, 809
Convulsions, 809
Paralysis, 810
Aphasia, 810
Condition of eyes, 810
pupils, in, 810
strabismus, 810
blindness, 811
Deafness, 811
Suppurative inflammation of middle ear, 811
Physiognomy, 812
Delirium, 812
Coma, 812
Vertigo, 812
Debility, 813
Condition of tongue, 813
Nausea and vomiting, 813
Characters of matter vomited, 813
Appetite and digestion, 814
Thirst, 814
Constipation and diarrhoea, 814
Condition of fauces, 814
Urine, 814
Swelling of joints and limbs, 814
Respiration, 814
Pulse, 815
Temperature, 815
fluctuations of, 816
Eruptions, 816
irregularity of, 816, 817
petechiae and ecchymoses, 816, 817
bullae and pemphigus, 817
Cause of death, 818
Duration, 818
Convalescence, 819
characters, 819
cause of tardy, 819
Relapses, 820
frequency, 820
Sequelae, 819
Followed by eye affections, 819
Impairment of hearing, 819
Deaf-mutism, 819
Impaired intellect and mania, 819
Hydrocephalus, 819
Paresis and paralysis, 819
Softening of brain, 820
Difficulty of speech, 820
Severe neuralgic pains, 820
Mortality of, 820, 828
variability of death-rate, 820, 828
influence of age upon, 828
Morbid anatomy, 820
General appearance of body after death, 820
Changes in the muscles, 821
in brain and membranes, 821
Changes due to congestion of brain and membranes, 821
to inflammation of meninges, 822
to softening of the brain, 823
Changes in pia mater, 821
in brain-tissue, 823
in spinal cord and membranes, 823
position of, 823
in internal and auditory apparatus, 824
Softening of fourth ventricle and auditory nerve, 824
Changes in eye and optic nerve, 824
in the viscera, 824
Absence of enlargement of spleen, 824
Changes in blood, 824
Amount of fibrine in blood before death, 825
after death, 825
Changes in blood-corpuscles, 825
Summary of pathology, 826
Diagnosis of, 826
From sporadic meningitis, 827
Functional and hysterical nervous affections, 827
Typhoid fever, 827
Typhus fever, 827
Prognosis of, 828
Symptoms indicating unfavorable, 829
favorable, 829
Imprudence of absolute, in, 829
Treatment, 829
Emetics, 830
Purgatives, 830
Futility of venesection, 830
Local depletion, 830
Cold applications, 830
Blisters, 830
Mode of using blisters, 831
Of coldness of skin, 831
Of collapse, 831
Use of alcohol, 831
Opium, 832
Value of opium, 833
Use of quinia, 833
Antipyretics, 833
Mercury, 833
Calabar bean, 834
Belladonna, 833
Ergot, 833
Potassium bromide, 834
Hydrate of chloral, 834
Potassium iodide, 834
Management of convalescence, 835
Diet in, 834
Meningitis, granular, following rubeola, 574
Menstrual disorders, complicating relapsing fever, 410
typhoid fever, 296
Menstruation, complicating typhus fever, 356
significance of abnormal, in general diagnosis, 165
Mental condition in hydrophobia, 899
in influenza, 868
in septicaemia lymphatica of puerperal fever, 1012
in typhoid fever, 277
disorders following the plague, 781
impressions, influence of, in causation of yellow fever, 643
overwork as a cause of typhus fever, 342
strain, symptoms due to, 205
work, relation of, to exercise, 199
Mercury, use of, in cerebro-spinal meningitis, 833
in diphtheria, 705
Metamorphosis, cheesy, 79
colloid, 83
croupous, 80
fatty, 74, 79
mucous, 82
Metastasis in idiopathic parotitis, 623, 624
treatment, 625
in pyaemia, pathology, 964
of tumors, 110
Methods of disinfection, 201
of vaccinating, 478
Metritis in puerperal fever, lesions, 987
Meteorism in typhoid fever, 286
Micro-organisms of puerperal fever, 1015
in pyaemia, blood-changes effected, 970
Microbes, as poison producers and carriers, 141
difficulty of separation of, from surrounding material, 146
liability to error from minuteness, 143
Microbia in inflammation, 45, 48
Micrococci, 141
in healthy bodies, 144
Microscopic organisms, classification, 141
Microscopy of glanderous lesions in man, 923
Migration of leucocytes, 42
Mild forms of cholera, 731
character of stools, 732
number of stools, 732
of influenza, treatment, 874
form of typhus fever, 354
of yellow fever, symptoms, 644
Milk, adulteration, 197
as a cause of disease, 197
as a medium of dissemination of anthrax, 929
of malaria, 590
of rabies and hydrophobia, 891
of scarlet fever, 491
of typhoid fever, 252
as a vehicle of bacillus tuberculosis, 105
polluted, as a cause of diphtheria, 683
Mind, state of, in relapsing fever, 384
Miscarriage, complicating typhus fever, 356
Modern conveniences questionable benefits, 215
Moral sense, perversion of, following typhoid fever, 292
Morbid anatomy, of anthrax in animals, 935
in man, 941
of beriberi, 1040
of cerebro-spinal meningitis, 820
of cholera, 741
of dengue, 882
of diphtheria, 685
of erysipelas, 635
of glanders in horses, 916
in man, 922
of idiopathic parotitis, 621
of influenza, 871
of intermittent fever, 594
of leprosy, 791
of pertussis, 843
of the plague, 781
of puerperal fever, 985
of pyaemia, 966
of pyaemia simplex, 970
of rabies and hydrophobia, 902
of relapsing fever, 413-417
of remittent fever, 602
of rubeola, 575
of scarlet fever, 530
of septicaemia, 971
of septo-pyaemia, 972
of simple continued fever, 235
of symptomatic parotitis, 626
of typhoid fever, 260
of typhus fever, 356
of vaccinal pock, 463
of varicella, 483
of variola, 446
of yellow fever, 649
growths, 105
classifications, 114, 122
Cohnheim's theory of origin, 106
influence of an irritant in production, 108
method of origin, 106
non-malignant, hereditary nature, 129
processes, 35
Morbific principle of cerebro-spinal meningitis, 803
Morphia, hypodermic use of, in beriberi, 1043
use of, in rabies and hydrophobia, 907
Mortality of anthrax in animals, 936
in man, 943
of cerebro-spinal meningitis, 820, 828
in cholera, 754
of glanders in man, 924
of influenza, 872
of pertussis, 841
of the plague, 780
of puerperal fever, 1020
of rabies and hydrophobia, 894
in relapsing fever, 422
of remittent fever, 599
of rubeola, 577
of scarlet fever, 534
of typhoid fever, 316-320
of typho-malarial fever, 616
of typhus fever, 360, 361
of yellow fever, 647, 648
Mouth, condition of, in idiopathic parotitis, 622
of mucous membrane of, in erysipelas, 633
complications in erysipelas, treatment, 638
symptoms of diphtheria, 672, 673
Mucous degeneration, 82
membranes of palate and fauces, appearance of, in prodromal stage of
rubeola, 564
condition of, in confluent small-pox, 441
in rotheln, 586
eruptions of varicella on, 483
influence of different, upon the character of diphtheritic
membrane, 688
lesions of, in diphtheria, 688
in glanders in man, 922
in rabies and hydrophobia, 902
in erysipelas, 635
localized redness of, symptomatic of prodromal stage of
diphtheria, 667
variolous pustules upon, 439
metamorphosis, 82
softening, 82
Multiple tumors, 110
Mumps, 620
Murmurs, arterial, in beriberi, 1040
cardiac, in beriberi, 1040
Muscles, alteration of, in beriberi, 1041
lesions of, in cerebro-spinal meningitis, 821
in diphtheria, 687
in pyaemia, 966
in typhoid fever, 267
of neck, suppuration of, in symptomatic parotitis, 626
voluntary, lesions of, in relapsing fever, 410
Muscular pains in yellow fever, 644
paralysis in beriberi, 1039
rigidity after cholera, 741
spasm, in typhoid fever, 279
tenderness in beriberi, 1039
tremor in typhoid fever, 279
in typhus fever, 349
N.
Naevi, vaccination as a means of destroying, 468
Nails, appearance of, in typhoid fever, 275
Nasal cavities, condition of, in malignant scarlet fever, 508, 520
mode of invasion of, in diphtheria, 669
complications in erysipelas, treatment, 638
diphtheria, local treatment, 710
prognosis, 692
form of diphtheria, symptoms, 669
lesions in glanders, 917
mucous membrane, condition of, in influenza, 866
Nationality in relation to relapsing fever, 371
Nature of puerperal fever, views concerning, 990-1004
of vaccinia, 455
Nausea, during intermittent fever paroxysm, 593
in cerebro-spinal meningitis, 813
in influenza, 866
in relapsing fever, 390
in rubeola, treatment, 581
in typhoid fever, 285
in typhus fever, 350
in yellow fever, treatment, 652
significance of, in general treatment, 162
Negroes, insusceptibility of, to yellow fever, 644
Neck, significance of appearance of, in diagnosis, 152
Necrosis from embolism, 64, 65
Neoplasms, 105
Nephritis, complicating scarlet fever, 525
in scarlet fever, treatment, 550-555
Nerves, lesions of, in leprosy, 791
in symptomatic parotitis, 626
Nervous diseases, complicating diphtheria, 675, 676
hereditary nature of, 129
influence of, upon susceptibility to rubeola, 561
symptoms in relapsing fever, 383-385
complicating scarlet fever, 510
of dengue, 882
of influenza, 867
of malignant scarlet fever, 507
Nervous system, chronic diseases of, following rubeola, 574
condition of, in cholera, 741
in remittent fever, 602
lesion of, in diphtheria, 689
in septicaemia, 972
Neuralgia, following cerebro-spinal meningitis, 820
in yellow fever, 644
Neuralgias, old, aggravation of, in influenza, 870
Neurine, use of, in diphtheria, 703
Nitric acid, use of, to prevent the return of intermittent fever
paroxysm, 598
Nitro-muriatic acid, use of, in anthrax, 938
Nodule, nasal, in glanders, 917
Nomenclature of pyaemia, 953
of septicaemia, 953
Nose, inflammation of, complicating variola, 445
Nostrils, condition of, in glanders in man, 921
Nourishment, necessity of, in typhus fever, 363
Nuisance, legal views as to what constitutes, 182
O.
Obesity, tendency to, following typhoid fever, 298
Obstetrical scarlatina, 498
Occupation, influence of, in causation of anthrax, 939
of glanders, 920
of influenza, 860
of typhoid fever, 244
of typhus fever, 343
relation of, to relapsing fever, 372
Odor of body, significance of, in general diagnosis, 159
of relapsing fever, 378
Oedema, 69
complicating relapsing fever, 400
scarlet fever, 529
typhoid fever, 297
from nervous influence, 71
of glottis, complicating scarlet fever, 512, 529
of lungs, Welch on cause of, 72
significance of, in general diagnosis, 159
Oesophagus, lesions of, in typhoid fever, 265
Offensive effluvia, symptoms due to, 181
Oil, inunctions of, in the plague, 784
Open wounds, liability of, to diphtheria, 679
Opisthotonos in cerebro-spinal meningitis, 809
Opium, use of, during cold stage of intermittent fever, 595
during hot stage of intermittent fever, 595
in algid form of pernicious malarial fever, 608
in cerebro-spinal meningitis, 832
in cholera, 767
in dengue, 885
in influenza, 874, 877
in puerperal fever, 1031
in relapsing fever, 429
in remittent fever, 604
in typhus fever, 366
Ophthalmia, chronic, following rubeola, 574
Optic nerve, lesions of, in cerebro-spinal meningitis, 824
Organic disease, hereditary nature of, 129
Organisms, microscopic, classification, 141
minute, convertibility, 145
Organoid tumors, 116
Origin of vaccinia, 457
Origins, specific, of the plague, 776
Ossification, 87
Otitis, chronic, following rubeola, 574
complicating scarlet fever, 520
in scarlet fever, results, 521
treatment, 547
Ovaries, lesions of, in septicaemia, 972
in pelvic peritonitis in puerperal fever, 989
Overcrowding as a cause of cholera, 721
of typhus fever, 341
Overwork as a cause of disease, 204
of the plague, 775
Ozone, use of, in diphtheria, 709
P.
Pain, in idiopathic parotitis, 623
in inflammation, 41
significance of, in general diagnosis, 165
Pains, muscular and joint, in relapsing fever, 385
of general peritonitis in puerperal fever, 1010
peritoneal, in para- and perimetritis of puerperal fever, 1007
rheumatic, in relapsing fever, 399
Palpitation of heart in beriberi, 1039
Pancreas, lesions of, in relapsing fever, 417
Pandemic nature of cerebro-spinal meningitis, 804
Panum's view of bacteria of diphtheria, 667
Papayotin, use of, in diphtheria, 703
Papule in variola, morbid anatomy, 446
Paralysis, complicating diphtheria, 676
variola, 445
diphtheritic, date of appearance, 676
seat, 676
treatment, 713
following cerebro-spinal meningitis, 819
typhoid fever, 293
in cerebro-spinal meningitis, 810
local, in relapsing fever, 398
motor, in relapsing fever, 385
muscular, in beriberi, 1039
sensory, in diphtheria, 676
Paralytic form of rabies in dogs, 896
stage of hydrophobia in man, 900
Parenchymatous inflammation, 53
Para- and perimetritis in puerperal fever, symptoms, 1005
Parametritis in puerperal fever, lesions, 987
Paresis following cerebro-spinal meningitis, 819
Parotid glands, lesions of, in idiopathic parotitis, 621
gland, lesions of, in symptomatic parotitis, 626
in pyaemia, 967
swelling, character of, in symptomatic parotitis, 627
complicating typhoid fever, 296
PAROTITIS, IDIOPATHIC, 620
Definition, 620
Nature, 620
Etiology--predisposing causes, 620
Age, influence, 620
Sex, influence, 620
Season, influence, 620
Relation to measles, diphtheria, and scarlet fever, 620
Peculiarities in mode of occurrence, 621
Anatomical appearance, 621
Changes in parotid gland, 621
Symptoms, 621
Duration of incubation stage, 621
Of invasion stage, 621
Actual attack, 621
Local, 621
Physiognomy, 622
Mouth and tongue, 622
Digestive tract, 622
Temperature and pulse, 623
Respiration, 623
Pain, 623
General, 623
Complications, 623
Metastasis, 623
Frequency, 623
Date of appearance, 623
Orchitis, 623
Symptoms, 624
Diagnosis, 624
Significance of outward displacement of lobe of ear, 624
Prognosis, 624
Result of metastatic orchitis, 624
Treatment, 624
Delirium and headache, 624
Difficult deglutition, 624
Sleeplessness, 625
Local, 625
Suppuration of gland, 625
Incomplete resolution, 625
Metastasis, 625
in females, 625
with depression, 625
PAROTITIS, SYMPTOMATIC or METASTATIC, 625
Definition, 625
Etiology, 625
Mechanical nature of exciting cause, 626
Altered blood as a cause, 626
Morbid anatomy, 626
Changes in parotid gland, 626
Suppuration of muscles of neck, 626
Changes in periosteum and cranial bones, 626
lymphatics, veins, and nerves, 626
in middle ear, 626
Thrombi of jugular veins, 626
Symptoms, 626
Characters of swelling, 627
Date of pointing of abscess, 627
Physiognomy, 627
Prognosis, 627
Of bilateral form, 627
Diagnosis--from idiopathic parotitis, 627
Treatment of, 627
Local, 628
Of incomplete resolution, 628
Of gangrene, 628
Parotitis, complicating cholera, 735
influenza, 870
relapsing fever, 404
typhus fever, 356
treatment, 367
Paroxysm of intermittent fever, 592
primary, of relapsing fever, 375, 378
of remittent fever, 599
Paroxysms of hydrophobia in man, 899
of pertussis, characters, 837
duration, 840
frequency, 840
of rabies in dogs, 896
Pasteur's experiments as to infectiveness of rabies, 892, 893
method of inoculation in anthrax, 937
for prevention of rabies and hydrophobia, 905
Pathognomonic lesions of rabies in dogs, 903
Pathology of glanders in man, 916, 918
of influenza, 871
of pyaemia, 963
Pearly distemper, relation of, to tuberculosis, 99
Pelvic abscesses in puerperal fever, treatment, 1036
cellulitis in puerperal fever, lesions, 988
exudations, treatment of, in puerperal fever, 1036
peritonitis, in puerperal fever, lesions, 988
Peppermint-test for defects in plumbing, 190
Pepsin, use of, in diphtheria, 703
Perforation, intestinal, in typhoid fever, 289, 290
in typhoid fever, treatment, 333
Pericarditis in relapsing fever, 402
complicating influenza, 870
Pericardium, lesions of, in cholera, 747
in pyaemia, 968
Peri-glandular lesions in the plague, 782
Periostitis, complicating typhoid fever, 297
Peritoneal effusions, encysted, in puerperal fever, treatment, 1036
Peritoneum, lesions of, in relapsing fever, 417
Peritonitis, complicating relapsing fever, 406
typhoid fever, 295
general, in puerperal fever lesions, 989
in puerperal fever, symptoms, 1010
pelvic and diffused, of puerperal fever, 988
Pernicious malarial fever, 605
Perspiration in pyaemia, 974
in yellow fever, 645
PERTUSSIS, 836
History, 836
Definition, 836
Etiology, 838
Specific poison, 838
seat, 838
period of greatest virulence, 838
inoculation of animals with, 839
Childhood, influence of, in occurrence, 839
Age at which most prevalent, 839
Sex, influence of, in causation, 839
Catarrhal affections as predisposing causes, 839
Symptoms, 840, 841
Initial stage, 840
Second stage, 840
Stage of decline, 841
Paroxysm, characters of, 837
duration, 840
frequency, 840
Fraenum linguae, ulceration, 841
Urine, condition, 841
Mortality, 841
Morbid anatomy, 843
Complications, 843
Prophylaxis, 843
Treatment, 844
Inhalations, 844
Emetics, 845
Potassium carbonate, 845
Alum, 845
Belladonna, 846
Ammonium bromide, 846
Chloral hydrate, 846
Quinia, 847
Pilocarpine muriate, 847
Sodium benzoate, 847
Caustic irritation, 848
Diet, 848
Hygiene, 848
Pertussis, following the plague, 781
Petechiae, characters of, in grave form of the plague, 779
Petrifaction, 87
Peyer's patches, lesions of, in typhoid fever, 261
Pharyngeal spasm in rabies and hydrophobia, 899
Pharyngitis in scarlet fever, treatment, 545
and tonsillitis, complicating relapsing fever, 405
Pharynx, lesions of, in rabies and hydrophobia, 902
in relapsing fever, 413
in typhoid fever, 265
Phlebitis and phlebo-thrombosis, lesions of, in puerperal fever, 989
Phlegmonous inflammation, 52
Phthisis, complicating influenza, 870
following typhus fever, 355
from damp soil, 187
pulmonary, hereditary nature of, 128
Physicians as carriers of contagion in puerperal fever, 1017
mortality in, 207
relation of, to public hygiene, 207
Physiognomy of cerebro-spinal meningitis, 812
of dengue, 881
of erysipelas, 632
of hydrophobia, 899
of idiopathic parotitis, 622
of influenza, 866
of symptomatic parotitis, 627
of relapsing fever, 376
of typhoid fever, 272
of yellow fever, 644
significance of, in general diagnosis, 150, 151
Pigmentation, 90
Pilocarpine, use of, in diphtheria, 704
in rabies and hydrophobia, 907
muriate, use of, in pertussis, 847
Pitting, frequency of, in varicella, 482
prevention of, in variola, 452
Placenta, symptoms of diphtheria, 674
PLAGUE, THE, 771
Definition, 771
Synonyms, 771
Classification, 771
History, 772
Etiology--Predisposing causes of, 774
Poverty and filth, 774
Bodily and mental overwork, 775
Sex and age, influence, 775
Season, 775
Exciting causes, 775
Dissemination by bodies dead from, 775
Specific origin, 776
Contagiousness, 776
Nature of the poison, 776
Air as a medium of transmission, 776
Period of incubation, 777
Forms of, 777
Grave or ordinary form, 777
Fulminant form, 779
Abortive form, 780
Symptoms, 777
Grave form, different modes of onset, 779
Invasion stage, 777
Second stage, or stage of fever, 778
Stage of fully-developed local manifestations, 778
Seat of enlarged lymphatics, 778
of buboes, 778
Characters of bubonic swellings, 778
Date of appearance of buboes, 778
Seat and character of carbuncles, 778
of petechiae, 779
Character of vomited matter, 779
Constipation, 779
Condition of urine, 779
Stage of convalescence, 779
Fulminant form, 779
duration, 779
Abortive form, 780
General duration of, 780
Complications and sequelae, 780
Followed by catarrhal pneumonia, 781
Pertussis, 781
Mental troubles, 781
Ulcers and abscesses, 781
Morbid anatomy, 781
Changes in lymphatic system, 781
Appearance of buboes, 781
Peri-glandular tissue, 782
Abdominal viscera, 781
Diagnosis, 782
Prognosis, 780
Mortality, 780
Treatment, 782
Preventive, 782
Isolation, 783
Quarantine, 783
Disinfection, 784
Clinical, 784
Inunction of oil, 784
Buboes, 784
Drugs used, 784
Pleura, lesions of, in pyaemia, 968
in relapsing fever, 413
in septicaemia, 972
Pleurisy, complicating typhoid fever, 294
typhus fever, 355
in septicaemia lymphatica of puerperal fever, 1012
Pleuritis, complicating erysipelas, 634
influenza, 870
relapsing fever, 404
scarlet fever, 523
in scarlet fever, treatment, 556
Plumbing, examination of defects, 190
of houses, 188
Pneumonia, catarrhal, complicating influenza, 869
following the plague, 781
complicating erysipelas, 634
relapsing fever, 404
rubeola, 571
typhoid fever, 294
typhus fever, 355
fibrinous, complicating diphtheria, 672
in rubeola, treatment, 581
in typhoid fever, treatment, 335
lobar, complicating influenza, 869
Pneumonias, nature of, complicating influenza, 870
Pock of vaccinia, date of appearance, 459
depression, 459
desquamation, 460
development, 459
incrustation, 460
in variola, characters of mature, 439
Poison, diphtheritic, fixity, 678
transmission, 678
influence of intensity of, on severity of cholera, 730, 731
of anthrax, modes of transmission, 929
of cholera, nature, 749
of malaria, nature, 589, 591
of the plague, nature, 776
of yellow fever, birthplace, 641
characteristics, 641
influence of heat and cold on development, 641
transportability, 641
specific, of beriberi, 1038
of pertussis, 838
Polluted soil as a means of disseminating typhoid fever, 253
Potassium bromide, use of, in cerebro-spinal meningitis, 834
carbonate, use of, in pertussis, 845
chlorate, danger of large doses, 701
use of, in diphtheria, 699, 700
iodide, use of, in cerebro-spinal meningitis, 834
Poverty as a cause of typhus fever, 342
Predisposing causes of beriberi, 1042
of cholera, 720
of glanders in horse, 912
of idiopathic parotitis, 620
of the plague, 774
of typhoid fever, 242
of typhus fever, 341
Predisposition to disease, hereditary nature, 126
Predispositions, inherited, evidence, 132
Pregnancy, complicating influenza, 871
typhoid fever, 296
Preliminary papule of anthrax, treatment, 943
Premonitory symptoms of rabies and hydrophobia, 895
of scarlet fever, 502
Prevention of anthrax by inoculation, 937
Preventive treatment of anthrax in animals, 936
in man, 943
of cholera, 755
of erysipelas, 636
of glanders in horses, 919
in man, 925
of influenza, 873
of the plague, 782
of puerperal fever, 1021
of pyaemia and septicaemia, 979, 980, 983
of rabies and hydrophobia, 903
of scarlet fever, 536
of typhoid fever, 321
of typhus fever, 361
Previous attacks of variola, protection from, 436
Primary vaccine, 473
Privy vaults, contamination of water-supply by, 192
dangers from, 192
PROCESSES, GENERAL MORBID, 35
Prodromal stage of diphtheria, 667
of intermittent fever, 592
of leprosy, 789
of remittent fever, 599
of rotheln, 585
of rubeola, 564
of varicella, 482
Prognosis, general, 167
of anthrax in animals, 936
in man, 943
of beriberi, 1042
of cerebro-spinal meningitis, 828
of cholera, 753
of dengue, 885
of diphtheria, 692-694
of erysipelas, 636
of idiopathic parotitis, 624
of influenza, 872
of intermittent fever, 594
of glanders in horse, 918
in man, 924
of leprosy, 793
of the plague, 782
of relapsing fever, 422-425
of remittent fever, 602
of rotheln, 588
of scarlet fever, 533
of simple continued fever, 235
of symptomatic parotitis, 627
of typho-malarial fever, 616
of typhoid fever, 314-316
of typhus fever, 359, 360
of vaccinia, 464
of varicella, 484
of variola, 450
of varioloid, 444
in yellow fever, 646, 647
effect of constitution, 168
of nature of malady, 169
of present state of patient, 169
influence of nursing, 169
modifying effects of medicinal agents, 169
Prophylactic treatment of diphtheria, 696
Prophylaxis, individual, in contagious diseases, 206
of leprosy, 794
of pertussis, 843
of puerperal fever, 1021
Prostration in dengue, 882
in typhus fever, 348
treatment, 365
Protective power of vaccination, 466
duration of, 468
against pertussis, 468
Pseudo-membrane, solvents of, 703
Psoas abscess in puerperal fever, 1010
Psychical treatment of hydrophobia, 906
Public sewers, 224
PUERPERAL FEVER, 984
Definition, 984
Frequency, 984
Etiology, 1013
Atmosphere, impure, influence on causation, 1013, 1014
Malaria, nosocomial, influence on causation, 1013
Micro-organisms, influence on causation, 1013-1015
Lochial discharge, influence on causation, 1015
Atmosphere, peculiar states of, on causation, 1016
Direct inoculation, 1016
Contagiousness of, 1017
Contagion, physicians as carriers of, 1017
Dissecting poison, 1018
Self-inoculation, 1019
Morbid anatomy, 985
Spiegelberg's classification of puerperal inflammations, 986
Endocolpitis and endometritis, 986
Diphtheritic ulceration, 986
Metritis and parametritis, 987
Diphtheritic endometritis, 987
Pelvic cellulitis, 988
Cellulitis from specific infection, 988
Peritonitis, pelvic and diffused, 988
exudation in, 989
general, 989
appearance of abdominal cavity, 989
ovaries, 989
Phlebitis and phlebo-thrombosis, 989
Thrombi in uterine and pelvic veins, 989
Abscesses, 989
pulmonary, 989
Veins, inflammation, 989
Thrombi, growth, 990
Septicaemia, 990
Abscesses, metastatic, 990
Endocarditis, ulcerative, 990
Pleuritis, 990
Joints, purulent inflammation, 990
Earlier views concerning nature, 990
Modern view concerning nature, 992
Septic origin, 993-1003
Bacteria, relation to causation, 994
Koch's investigations of, 997
physical characters, 999
modes of entering the circulation, 1000
action of, upon the blood, 1000
Diphtheria of genitalia, characters, 1002
Relation of, to erysipelas, 1002
Inflammatory affections of non-specific origin, 1003
Symptoms, general, 1004
Incubation period, 1004
Chill, significance of, 1005
Of endometritis and endocolpitis, 1005
temperature, 1005
Parametritis and perimetritis, 1005
Incubation, 1006
Temperature, 1006
Pulse, 1006
Relapse, 1006
Headache, 1007
Pains, 1007
Vomiting, 1007
Duration, 1007
Exudation, 1007
Uterus fixity of, 1007
Tumors in iliac fossa, 1008
Abscesses, 1008
location, 1008
pointing of, 1008
Local peritonitis, 1009
Of psoas abscess, 1010
Of peritonitis, general, 1010
Pains, 1010
Abdomen, state, 1010
Respiration, 1010
Vomiting, 1010
Vomit, characters, 1010
Fever, 1010
Skin, 1010
Pulse, 1010
Pyaemic form, 1011
Of septicaemia lymphatica, 1011
Mode of onset, 1011
Temperature in, 1011
Abdomen, state, 1011
Skin, state, 1011
Vomiting, 1011
Tongue, condition, 1011
Pulse, condition, 1011
Respiration, 1012
Pleurisy in, 1012
Endocarditis, 1012
Mental condition, 1012
Joint affections in, 1012
Duration, 1012
Of septicaemia venosa, 1012
Chills in, 1012
Fever in, 1012
Temperature in, 1012
Pulse in, 1012
Abdomen, state of, 1012
Uterus in, 1012
Of pure septicaemia, 1013
Mortality, 1020
Relation of, to zymotic diseases, 1020
Prophylaxis, 1021
Maternity hospitals, advantages, 1021
Necessity of light and air, 1024
Antisepsis, value, 1024
methods, 1025
Sulphurous acid, use, 1025
Corrosive sublimate, use, 1025
Iodoform, use of, intra-uterine, 1025
Vaginal injections, carbolized, use, 1025
Tarnier's maternity pavilions for prevention, 1027
Treatment--indications, 1028
Disinfection, 1028
Local, 1028
Use of hydrochloric acid, 1028
Persulphate of iron, 1028
Intra-uterine injections, use, 1029
dangers of, 1029
methods, 1029
Corrosive sublimate, use, 1025, 1029
Pain, peritoneal, 1031
Use of opium, 1031
in pyaemic variety, 1031
Leeches, 1031
Turpentine stupes, 1032
Hyperpyrexia, 1032
Use of purgatives, 1032
Quinia, 1032
Sodium salicylate, 1032
Veratrum viride, 1033
Digitalis, 1033
Alcohol, 1033
Cold in, 1033
Cold, method of applying, 1034
Cold water, intra-uterine injections, 1034
Baths, cold, use, 1034
Kibbie's fever-cot, use, 1034, 1035
Coil, 1036
Diet, 1036
Encysted peritoneal effusions, 1036
Quinia, use, 1036
Pelvic exudations, 1036
Pelvic abscesses, 1036
Puerperal septicaemia, relations of, to obstetrical scarlatina, 499
women, general sepsis from diphtheria in, 674
symptoms of diphtheria in, 674
Pulmonary abscess in puerperal fever, 989
collapse, complicating influenza, 869
complications of typhus fever, treatment, 367
oedema, complicating rubeola, 572
Pulsation of jugular veins, significance of, in general diagnosis, 156
Pulse and temperature, relation of, in yellow fever, 644
average frequency in health and disease, 154
characters of, in erysipelas, 633
in idiopathic parotitis, 623
in general peritonitis of puerperal fever, 1010
in septicaemia, 977
Pulse, characters of, in septicaemia lymphatica of puerperal fever,
1011
venosa of puerperal fever, 1012
condition of, in acute glanders in man, 921
in beriberi, 1040
in cerebro-spinal meningitis, 815
in cholera, 737
in dengue, 881
in influenza, 866
in pyaemia, 975
in relapsing fever, 382
in typhus fever, 351
significance of, in general diagnosis, 152
in malignant scarlet fever, 507
in typhoid fever, 275
kinds of, 154
methods of examining, 153
relation to respiration, 154
temperature, relation of, in relapsing fever, 382
Pupil, significance of state of, in general diagnosis, 151
Pupils, condition of, in cerebro-spinal meningitis, 810
Pure septicaemia of puerperal fever, 1013
Purgatives, use of, during hot stage of intermittent fever, 596
in cerebro-spinal meningitis, 830
in hemorrhagic form of pernicious malarial fever, 613
in puerperal fever, 1032
in remittent fever, 604
Purity of water, standards of, 184
Purpura, complicating diphtheria, 674
Pus, 48
influence of, in production of pyaemia, 955
in stools, significance in diagnosis, 164
Pustule, malignant, 926
Putrefaction of cadaver, rapidity of, in puerperal fever, 971
Putrified flesh as a means of disseminating typhoid fever, 257
PYAEMIA AND SEPTICAEMIA, 945-955
History, 945-952
Nomenclature, 952
Pyaemia, 953
Definition, 953
Septicaemia, 953
Definition, 954
Etiology of pyaemia, 955
Theories concerning, 955
Pus, influence of, in production, 955
Character of production, 956
Thrombosis, relation of, to causation, 957, 958
Contamination of blood, influence of, in causation, 958
sources, 958
Germs, disease-, influence of, in causation, 958
Wounds, characters of, influence on causation, 958
Etiology of spontaneous pyaemia, 959
Wounds of alimentary canal and genito-urinary apparatus as cause,
959
Air, vitiated, influence of, on causation, 959
Spontaneous origin, 959
Contagiousness, 960
Chemical origin, 960
Living organisms, influence of, on causation, 958-960
Etiology of septicaemia, 960
Septic intoxication, relation of, to, 961
Traumatic fever, relation of, to, 962
Dissecting wounds, relation of, to causation, 962
Putrid substances, maximum toxic action of, on the body, 962
Lymphatics as channel of entrance of poison, 963
Etiology of septo-pyaemia, 963
Pathology, 963
Condition of blood, 963
in pyaemia simplex, 963
multiplex, 963
Metastasis, conditions, 964
Pus, mode of entering the circulation, 964
Metastatic abscesses, production, 964
from primary infection, 964
from secondary infection, 964
Emboli, action of, in production of metastatic abscesses, 964
Thrombi, action of, in production of metastatic abscesses, 965
Seat of pathological changes, 965
Fat emboli, influence of, in production, 966
Morbid anatomy, 966
Of pyaemia, 966
Appearance of body, 966
Rigor mortis, 966
Lesions of cellular tissue, 966
Muscles, 966
Brain and membrane, 966
Retina and choroid, 967
Cornea, 967
Ear, 967
Bones, 967
Joints, 967
Parotid gland, 967
Arteries and veins, 967
Blood, 968
Pericardium, 968
Pleurae, 968
Lungs, 968
Liver, 969
Spleen, 969
Kidneys, 969
Micro-organism in blood, changes effected by, 970
Pyaemia simplex, 970
Absence of abscesses in, 970
Septicaemia, 971
Putrefaction of bodies, rapidity of, 971
Blood, lesions of, 971
Sepsin, nature, 971
Lesions, nervous system, 972
Endo- and pericardium, 972
Lungs, 972
Pleurae, 972
Kidneys, 972
Spleen, 972
Uterus, 972
Ovaries, 972
Bladder, 972
Of septo-pyaemia, 972
Symptoms, 972
Of pyaemia, 972
Prodromal stage, 973
Chills, date of appearance, 973
frequency, 973
Temperature, 974
Perspiration, 974
Eruptions, 974
Pulse, 975
Tongue, condition of, 975
Vomiting, 975
Singultus, 975
Diarrhoea, 975
Stools, character of, 976
Heart, condition of, 976
Lungs, condition of, 976
Liver and spleen, enlargement, 976
Urine, 976
Joints, suppuration, 976
Abscesses, frequency, 976
Delirium, 976
Breath, odor of, 976
Wound, changes, 976
Of septicaemia, 976
General, 976
Wound, condition of, 977
Temperature, 977
Abdomen, state of, 977
Pulse, 977
Diarrhoea, 977
Vomiting, 977
Tongue, 977
Singultus, 977
Bronchitis in, 977
Of gangrene foudroyante, 977
Skin, condition, 977
Diagnosis, 978
Of pyaemia from septicaemia, table showing, 978, 979
Treatment, 979
In fully-developed cases unsuccessful, 980
Preventive, 979, 980
Cleanliness, necessity of, in prevention, 980
Atmosphere, pure, necessity of, in prevention, 980
Food and drink, proper, necessity of, in prevention, 980
Cheerful and pleasant surroundings, in prevention, 980
Antiseptics, use of, 980
Local, 981
Of wound, 981
Metastatic abscesses, 981
Constitutional, 982
Sulphites of magnesium, sodium, potassium, and lime, use of, 982
Use of alcohol, 982
Quinia, 982
Ergotine, 982
Diet, 982
Stimulants, 982
Of septicaemia, 982
Indications for, 982
Local, 983
Preventive, 983
Of wound, 983
Diarrhoea, 983
Antisepsis, 983
Sulphites and hyposulphites, use of, 983
Quinia, use of, 983
Of puerperal septicaemia, 983
complicating erysipelas, 634
typhoid fever, 295
typhus fever, 356
Pyaemic form of general peritonitis of puerperal fever, 1010
Q.
Quarantine in cholera, 204, 755
in leprosy, 794
in the plague, 783
Quinia, use of, in cerebro-spinal meningitis, 833
in dengue, 885
in diphtheria, 708, 712
in erysipelas, 637
in influenza, 874-876
during cold stage of intermittent fever, 595
hot stage of intermittent fever, 596
sweating stage of intermittent fever, 597
to prevent the return of intermittent fever, paroxysm, 598
in hemorrhagic form of pernicious malarial fever, 612
in pertussis, 847
in puerperal fever, 1032, 1036
in pyaemia, 982
in relapsing fever, 426
in remittent fever, 603
in rubeola, 580
in scarlet fever, 543
in septicaemia, 983
in typhoid fever, 330
in typho-malarial fever, 618
in typhus fever, 365
in yellow fever, 651
and opium, use of, in yellow fever, 651
R.
RABIES AND HYDROPHOBIA, 886
Synonyms, 886
Definition, 886
History, 886
Geographical distribution, 886
Etiology, 887
Climate, relation of, to causation, 887
Season, relation of, to causation, 887
Summer heats, relation of, to causation, 887
Hunger and thirst, relation of, to causation, 888
Improper food, relation of, to causation 888
Sex, relation of, to causation, 888
Liability of special breeds, 889
From skunk-bite, 889
Spontaneous origin, 890
Contagion, 891
Modes of dissemination, 891
Milk, propagation by, 891
Saliva, propagation by, 891
Specific germ, 892
Pasteur's experiments as to infectiousness, 892
Point of election of germ, 892
Antagonism between blood and germ, 892, 893
Localization of the virus in the wound, 893
Relation of successful inoculation to bites, 893
Insusceptibility to, 894
Incubation, 894
Duration of, in lower animals, 894
in man, 894
Condition of cicatrix during, 895
Symptoms, 895
In dogs, 895
Importance of recognizing premonitory, 895
Of prodromal stage, 895
Of furious form, 896
During paroxysms, 896
Between paroxysms, 896
Of paralytic form, 896, 897
Of lethargic form, 897
Popular fallacies regarding, 897
In horse and other animals, 897
In man, 898
Symptoms, 898
Prodromal stage, 898
Appearance of wound, 898, 899
Of paroxysms, 899
Duration, 899
Reflex irritability during, 899
Facies during, 899
Mental condition, 900
Delirium during, 900
Relative severity in men and women, 900
Paralytic stage, 900
duration, 900
Without paroxysms, 900
Diagnosis, 900
Pathognomonic features in, 900
From tetanus, 900
From diphtheria, 900
From pharyngeal anthrax, 900
From acute mania, 900
From epilepsy, 901
From hysteria, 901
From pseudo-hydrophobia, 901
Inoculation in doubtful cases, 902
Morbid anatomy, 902
Post-mortem appearance of body, 902
Changes in mucous membranes, 902
Bronchi and pharynx, 902
Lungs, 902
Heart and blood-vessels, 902
Gastro-intestinal tract, 902
Liver and spleen, 902
Kidneys, 902
Bladder, 902
Brain and spinal cord, 902
Pathognomonic changes in dogs, 903
Treatment, 903
Preventive, 903
Registration of dogs, 904
Modes of preventing diffusion, 904
Inoculation, 904
Pasteur's method, 905
Of bites, 905
Use of caustics, 905
Excision of cicatrix, 906, 908
Futility of eliminating measures, 906
Hygienic, 906
Psychical, importance of, 906
Therapeutic, 907
Use of chloroform, 907
Chloral, 907
Pilocarpine, 907
Curare, 907
Morphia, 907
Atropia and daturia, 907
Vaccine virus, 907
Warm baths, 907
Faradization, 907
Inhalation of oxygen, 907
Importance of rest and quiet, 907
Intravenous injections, 908
Venesection, 908
Race, influence of, in causation of variola, 436
protection as a preventive of small-pox, 130
relation of, as causation of rubeola, 561
Rachialgia in cerebro-spinal meningitis, 808
Rash of variola, date of appearance of, 437
significance of, 437
variolous, 437
Raspberry excrescence in vaccinia, 461
Reaction in cholera, 734
treatment, 763
Reflex irritability in hydrophobia, 899
symptoms in diphtheria, treatment, 694
Registration of dogs for prevention of rabies, 904
Relapse, in relapsing fever, 381
Relapses, cause of, in typhoid fever, 309
duration of, in typhoid fever, 304
frequency of, in typhoid fever, 302
in cerebro-spinal meningitis, 820
of diphtheria, prognosis of, 694
in rubeola, 563
RELAPSING FEVER, 369
Definition, 369
Synonyms, 369
History and geographical distribution, 369
Etiology, 370
Destitution and filth as causes, 370
Intemperance as a cause, 370
Starvation and over-crowding as a cause, 371
Age, relation of, to causation, 371
Sex, relation of, to causation, 371
Nationality, relation of, to causation, 371
Season, relation of, to causation, 371
Occupation, relation of, to causation, 372
Specific origin, 370, 372
Contagious nature, 372
Transmission of contagion, 373
Area of contagious atmosphere, 373
Spirillum, 373
Mode of detecting, 373
Inoculation, 374
Incubation period, 376
General clinical description, 374
Invasion, 376
Special symptoms, 376
Odor, 378
Physiognomy, 376
Bronzing of face, 376
Eruptions, 377
Hepatic eruptions, 377
Sudamina, 377
Desquamation, 377
Primary paroxysms, duration, 378
Temperature, 378
at crisis, 378
peculiarities, 382
Relapse, 381
Duration, 381
Absence, 380
Frequency, 382
Later relapses, 381
Cases illustrating frequency of relapses, 394
Average duration of paroxysms, 381
Intermission, duration, 381
Pulse, 382
Relation of pulse to temperature, 382
Character of pulse during paroxysm, 383
Pulse at crisis, 382
During intermission, 383
Character of heart-sounds, 383
Convulsions, 384
Mental condition, 384
Headache, 383
Wakefulness, 384
Vertigo, 384
Delirium, 384
General tremor, 384
Muscular rigidity, 384
Muscular and joint pains, 385
Cause of muscular and joint pains, 385
Seat of muscular and joint pains, 385
Motor paralysis, 385
Debility, 386
Perversion of special senses, 386
Respiration, 386
Relation of respiration, temperature, and pulse, 386
Bronchitis and pneumonia, 387
Condition of urine, 387
Urine of paroxysm, 388
of intermission, 388
Thirst, 389
Anorexia, 389
Condition of tongue, 389
Nausea and vomiting, 390
Haematemesis, 390
Condition of bowels, 390
of abdomen, 390
Spleen, enlargement, 391
Liver, enlargement, 391
Jaundice, significance of, 391
Epistaxis, 393
Hemorrhages, 393
Convalescence, 393
Varieties, 395
Grave form, 395
Multiple or protracted form, 395
Abortive form, 395
Case illustrating subintrant form, 396
Complications, 396
Peculiarities of temperature, 397
Mental hebetude, 398
Local palsies, 398
Severe rheumatic pains, 399
Disorders of vision, 399
Ophthalmia, 399
Disorders of hearing, 400
Otorrhoea, 400
Swellings and effusions of joints, 400
Bed-sores, 400
Gangrene, 400
Abscesses, 400
Anaemia, 400
Oedema, 400
Sudden collapse and syncope, 401
Hemorrhages from mucous surfaces, 401
Pericarditis, 402
Heart-clot, 402
Thrombosis and embolism, 402
Laryngitis, 403
Bronchitis, 403
Splenic enlargement, 403
Rupture of spleen, 403
Parotitis, 404
Pleurisy, 404
Pneumonia, 404
Pulmonary gangrene, 404
Metastatic abscesses of lungs, 404
Pharyngitis and tonsillitis, 405
Hiccough, 405
Diarrhoea, 405
Dysentery, 406
stools, 406
Suppuration of mesenteric glands, 406
General and local peritonitis, 406
Emaciation, 407
Renal disorders, 408
Albuminuria, 407
Suppression of urine, 407
Incontinence of urine, 407
Haematuria, 409
Glycosuria, 410
Metastatic inflammation of kidneys, 410
Disorders of menstruation, 410
Pregnancy, 410
Sequelae, 398
Local palsies, 398
Acute miliary tuberculosis, 404
Dyspepsia, 406
Anaemia, 400
Morbid anatomy, 410
Post-mortem appearance of body, 410
Changes in voluntary muscles, 410
Blood, 411
Granule-cells of blood, 412
Changes in pericardium, 411
Heat, 411
Gastro-intestinal canal, 412
Solitary and agminated glands, 413
Mesenteric glands, 413
Larynx and pharynx, 413
Pleura, 413
Lungs, 413
Brain and membranes, 413
Liver, 414
Bile-ducts and gall-bladder, 415
Spleen and capsule, 416
Pancreas, 417
Peritoneum, 417
Kidneys, 414
Bladder, 414
Lymphatic glands, 417
Marrow of bones, 417
Diagnosis, 418
Presence of spirillum as a means, 418
From typhus fever, 418
From typhoid fever, 419
Grave form of, from typhoid fever, 420
From bilious remittent fever, 420
Yellow fever, 420
Small-pox, 421
Acute gastro-hepatic catarrh, 421
Simple febricula, 421
Rheumatic fever, 421
Acute yellow atrophy of liver, 422
Parotitis, 422
Cerebral diseases, 422
Prognosis, 422
Symptoms indicating unfavorable, 424
Influence of variations of temperature, 424
Cerebral symptoms, 424
Character of eruption, 425
Hiccough upon, 425
Epistaxis, 425
Cough upon, 425
Heart complications on, 425
Hepatic enlargement upon, 425
Splenic enlargement upon, 425
Jaundice upon, 425
Albuminuria, 425
Mortality--bilious typhoid form, 422
Influence of type of disease, 423
Stage of disease, 423
Season, 423
Habits and previous health, 424
Sex, 424
Age, 424
Race, 424
Cause of death in, 426
Treatment--indications for treatment in regular cases, 426
Hyperpyrexia, 426
Cause of failure of antipyretics, 429
Insomnia, 429
Headache, 429
Nausea and vomiting, 430
Constipation, 430
Jaundice, 431
Muscular tremor, 432
soreness and pains, 432
At critical fall of temperature, 432
Renal complications, 432
Epistaxis, 432
Collapse, 433
Necessity of absolute rest in, 432
Resume of treatment, 432
Diet, 430
Special remedies, 431
Use of antiperiodics, 428
Arsenic, 427
Atropia, 429
Bromide and chloral, 430
Blisters, 431
Chloroform, 431
Cold baths, 428
Digitalis and other antipyretics, 428
Hyposulphite of sodium, 428
Opium, 429
Quinia, 426
Salicylic acid and salicylates, 428
Simple febrifuges, 428
Stimulants, 430
Venesection, 431
REMITTENT FEVER, 598
Definition, 598
Malarial nature, 598
Etiology, 598, 599
Relation of, to intermittent fever, 599
Symptoms, 599
Prodromal stage, 599
Paroxysm, 599
Temperature, 599
Epistaxis, 602
State of tongue, 600
Stomach, 602
Bowels, 602
Urine, 602
Jaundice, 600
cause, 600
Nervous symptoms, 602
Physiognomy, 600
Pulse in, 602
Duration of, 602
Diagnosis, 600
From intermittent fever, 600
From typhoid fever, 600
From yellow fever, 600
Prognosis, 602
Mortality, 599
Morbid anatomy, 602
Changes in skin, 603
Liver, 602
Spleen, 602
Treatment, 603
Main indications, 603
Use of quinia, 603
Amount of quinia, 603
Causes of failure of quinia, 604
Adjuvants to quinia, 604
Use of depuratives, 604
Purgatives, 604
Opium, 604
Of hemorrhage, 605
Of tympanites, 605
Of vomiting, 605
Renal disease, complicating relapsing fever, 408
scarlet fever, 525
Residence, change of, in treatment of beriberi, 1042
Resolution, incomplete, in idiopathic parotitis, treatment, 625
of symptomatic parotitis, treatment, 628
of erysipelas, 633
of inflammation, 54
Respiration in cerebro-spinal meningitis, 814
characters of, in idiopathic parotitis, 623
in general peritonitis of puerperal fever, 1010
in mild scarlet fever, 504
in relapsing fever, 386
in septicaemia lymphatica, 1012
in typhoid fever, 276
in typhus fever, 352
in croup, 157
in disease, 156
kinds of, 156
significance of, in general diagnosis, 156
Respiratory diseases, relation of, to rubeola, 561
organs, lesions of, in typhus fever, 356
spread of diphtheria into, 671
tract, alterations of, in scarlet fever, 531
Rest, necessity of, in cholera, 760
in rabies and hydrophobia, 907
in relapsing fever, 432
in yellow fever, 654
Retention-cysts, 116, 122
Retro-vaccine, 473
Re-vaccination, time of, 467
Rheumatic and cardiac inflammation in scarlet fever, treatment, 556
Rheumatism, complicating scarlet fever, 521
Rickets, hereditary nature, 128
Rigidity, muscular, in relapsing fever, 384
Rindfleisch's definition of diphtheritic inflammation, 686
ROTHELN, 582
Definition, 582
Synonyms, 582
History, 582
Etiology, 583
Age as a cause, 583
Sex as a cause, 583
Specific origin, 583
Nature of contagion, 583
Modes of transmission, 583
Period of greatest contagiousness, 583
Distinct nature, 584
Frequency of second attacks, 584
Relapses, 584
Symptoms, 585
Incubation period, 583, 585
Duration of incubation period, 583
Prodromal stage, 585
Eruption, 585
Duration of eruption, 585
Characters of eruption, 586
Types of eruption, 586
Condition of mucous membranes, 586
Swelling of lymphatic glands, 586
Temperature, 587
Complications and sequelae, 587
Diagnosis, 587
From measles, 587
From scarlet fever, 587
From symptomatic skin eruptions, 588
Prognosis of, 588
Treatment of, 588
RUBEOLA, 557
Definition, 557
Synonyms, 557
History, 557
Etiology, 557
Nature of contagion, 558
Relation of straw fungus, 558
Mode of entrance into body, 558
Modes of dissemination of contagion, 559
Inoculation, 559
Stage when most easily propagated, 560
Race, influence of, 561
Age, influence of, 561
Sex, influence of, 562
Climate as a cause, 560
Pregnancy and parturition as a cause, 561
Scrofula as a cause, 561
Diseases of respiratory organs as a cause, 561
Relation of, to acute diseases, 561
to chronic diseases, 561
to whooping cough, 561
Influence of nervous diseases upon susceptibility, 561
Frequency of epidemics, 560
in new-born, 562
second attacks, 563
Relapses in, 563
Symptoms, 563
Incubation stage, 563
Duration of incubation stage, 560
Prodromal stage, 564
Temperature, 564
Catarrhal symptoms, 564
Punctated appearance of palatal and faucial mucous membrane, 564
Convulsions, 565
Duration of, 565
Eruptive stage, 565
Temperature of, 566
Character and seat of eruption, 566
General symptoms, 567
Symptoms at decline, 567
Temperature at decline, 567
Duration of eruptive stage, 567
Varieties of, 568
Inflammatory or synochal, 568
Hemorrhagic (rubeola nigra), 569
Without eruption, 568
catarrh, 568
Deviations from ordinary course, 569
Peculiarities in seat of eruption, 569
in character of eruption, 569
Relapses of eruption, 570
Complications, 570
Causes, 570
Complicated with epistaxis, 570
Skin disorders, 570
Pemphigoid eruptions, 571
Ear diseases, 570
Eye diseases, 571
Faucial inflammation, 571
Laryngitis, 571
Bronchitis and capillary bronchitis, 571
Pneumonia, 571
Pulmonary oedema, 572
Acute miliary tuberculosis, 572
Heart-clot, 572
Intestinal catarrh, 572
Convulsions, 572
Diphtheria, 573
Sequelae, 573
Followed by general miliary tuberculosis, 574
Chronic pulmonary tuberculosis, 573
Coryza, 574
Ophthalmia, 574
Otitis, 574
Intestinal catarrh, 574
Cutaneous diseases, 574
Bone and joint disease, 574
Nervous affections, 574
Granular meningitis, 574
Albuminuria, 574
Gangrenous affections, 574
Morbid anatomy, 575
Changes in skin, 575
Diagnosis, 575
Value of punctated appearance of palatal and faucial mucous
membranes, 575
Salient points in diagnosis, 575
From rotheln, 576
Scarlet fever, 576
Variola, 576
Roseola and erythema, 577
Typhus, 577
Roseola syphilitica, 577
Prognosis, 577
Factors to be considered in making, 577
Influence of hygienic surroundings, 577
previous health, 578
complications, 578
Mortality, 578
Influence of stage of disease, 578
of age, 578
Treatment, 578
Preventive, 578
Isolation, 578
Hygienic, 579
Diet, 579
Uncomplicated cases, 579
Results, 579
Hyperpyrexia, 580
Retrocession of eruption, 580
Epistaxis, 580
Diarrhoea, 581
Nausea and vomiting, 581
Constipation, 581
Cough, 581
Eye complications, 581
Aural complications, 581
Bronchitis and pneumonia, 581
Convulsions, 581
Use of aconite, 580
Inunctions, 580
Quinia, 580
Stimulants, 580
S.
Salicylic acid, use of, in diphtheria, 707
in relapsing fever, 428
Saliva, propagation of rabies and hydrophobia by, 891
Salivary glands, lesions of, in typhoid fever, 268
Sanitary inspection of houses, 187
Sarcoma, 118
SCARLET FEVER, 486
History, 486
Etiology--Specific origin, 487
Germ theory, 488
Microbes, 488
Modes of cultivation of microbes, 488
Modes of entering the system, 490
Modes of communication, 490
Dissemination of, by milk, 491
Fixity of the poison, 491
Solid nature of the poison, 492
Duration of incubation, 492, 493
Contagiousness, 494
Area of contagiousness, 494
Age, influence of, in causation, 500
Variations in type, 494
Surgical, 495
distinguished from septicaemic efflorescence, 497
effect of poison upon inflammation of wounds, 498
Obstetrical, 498
liability of parturient women to, 498
relation of, to puerperal septicaemia, 499
Immunity of infants, 500
Clinical facts regarding, 501
Relapses in, 501
Frequency of second attacks, 501
Sympathetic sore throat in, 502
albuminuria in, 502
Symptoms, 502
Ordinary form, 502
Premonitory, 502
Nervous system, 503
Vomiting in, significance, 503
Diarrhoea, 503
Condition of tongue, 504
of faucial and nasal membranes, 504
Respiratory, 504
Efflorescence, 504
Seat of greatest intensity of eruption, 504
Cause of absence of eruption, 505
Date of desquamation, 506
Temperature, 505
Digestive system, 505
Urine, characters, 505
Duration, 506
Malignant or grave form, 507
Digestive system, 507
Pulse, 507
Eruption, 507
Temperature, 507
Nervous symptoms, 507
Condition of fauces, 508
Of throat, 508
Nasal cavities, 508
Lymphatic glands, 508
Duration, 508
Irregular form, 508
Causes, 508
Absence of eruption, 508
Hemorrhagic form, 509
Anginose form, 510
Complications and sequelae, 510
Complicated by severe nervous symptoms 510
Throat symptoms, 511
Adenitis, 511
Inflammation of neck, 511
Gangrene of neck, 512
Oedema of glottis, 512
Diphtheria, 514
course of diphtheria, complicating, 516
Croupous inflammation of fauces, 516
Coryza, 520
Otitis, 520
course of otitis, complicating, 520
results of otitis, complicating, 521
By rheumatism, 521
By cardiac inflammations, 522
By dilatation of heart, 523
By heart-clot, 523
By pleuritis, 523
By nephritis, 525
By glomerulo-nephritis, 527
By albuminuria, 525
By anasarca and oedema, 529
Order and date of appearance of anasarca, 529
By head symptoms due to uraemia, 530
Morbid anatomy, 530
Changes in the blood, 530
Respiratory tract, 531
Abdominal organs, 531
Post-mortem appearance of eruption, 532
Changes in the kidneys, 526
hyaline degeneration of kidneys, 527
intestinal nephritis, 528
parenchymatous nephritis, 526
Changes in the liver, 531
Diagnosis, 532
From measles, 532
From erythema, 533
From rotheln, 533
From diphtheria, 533
Prognosis, 533
Influence of complications upon, 533, 535
type upon, 534
age upon, 534
Of grave cases, 535
Mortality, 534
Treatment, 536
Preventive, 536
Isolation in, 537
Inoculation as a prophylactic, 536
Belladonna as a prophylactic, 536
Sodium sulpho-carbolate as a prophylactic, 537
Listerine as a prophylactic, 537
Boric acid as a prophylactic, 537
Disinfection in, 201, 538
Hygienic, 539
Therapeutic, 539
Mild cases, 540
Inunction in, 541
Hyperpyrexia, 541
by cold, 541
Mode of applying cold, 542
Antiseptic, 545
Complications and sequelae, 545
Pharyngitis, 545
local, 546
Coryza, 546
local, 547
Otitis, 547
local, 549
paracentesis of tympanum, 548
Nephritis and albuminuria, 550
modes of producing diaphoresis, 551
local, 555
Convulsions, 556
Rheumatic and cardiac inflammation, 556
Pleuritis, 556
Convalescence, 544
Use of aconite and veratrum viride, 543
Alcohol, 544
Ammonium carbonate, 544
Carbolic acid, 545
Cathartics, 554
Diuretics, 555
Digitalis, 543, 555
Ice, 542
Jaborandi and pilocarpine, 552
Sodium salicylate, 543
Quinia, 543
Scarlet fever, relation of, to idiopathic parotitis, 620
Scarlatina, disinfection in, 201, 538
Schools, closure of, for prevention of disease, 203
Scrofula, relation of, to causation of rubeola, 561
relation to tuberculosis, 96, 101
Scrofulosis, hereditary disposition to, 127
Scrofulous habit, peculiarities of tissue, 101
Scurvy, complicating typhus fever, 355
Season, influence of, on causation of anthrax, 931, 940
of cerebro-spinal meningitis, 802
of diphtheria, 682
of typhoid fever, 245
of erysipelas, 630
of idiopathic parotitis, 620
of influenza, 860
of the plague, 775
of rabies and hydrophobia, 887
of relapsing fever, 371
of typhus fever, 343
of variola, 435
on cholera, 720
proper, for vaccination, 477
Seborrhoea, following erysipelas, 633
Second attack of rubeola, frequency of, 563
stage of pertussis, 840
Secondary form of diphtheria, 671
Segregation of lepers, 794
Self-infection, danger of, in treating diphtheria, 696
prevention of, in treating diphtheria, 696
Sensibility, altered, significance of, in general diagnosis, 161
modifications of, in typhoid fever, 279
Sepsin, 971
Septicaemia, 945
complicating erysipelas, 634
distinguished from pyaemia, 978, 979
lymphatica of puerperal fever, 1011
venosa, 1012
Sequelae of cerebro-spinal meningitis, 819
of cholera, 735
of erysipelas, 633
of grave form of the plague, 780, 781
of influenza, 868
of relapsing fever, 396
of rotheln, 587
of rubeola, 573
treatment, 580
of scarlet fever, 510
of vaccinia, 464
of variola, 445
Serous inflammation, 47
inflammations complicating erysipelas, 634
Severe form of diphtheria, symptoms, 668
of influenza, treatment, 875
of typhus fever, 354
Sewerage, 213
Sewer- and soil-pipes, importance of position, 188
Sewer-gas, 189
diseases produced by, 190
symptoms due to, 189
Sewers, characters of efficient, 224
public, 224
ventilation of, 224
Sewer-traps, test as to their efficiency, 190
varieties, 191
Sex, influence of, on causation of cerebro-spinal meningitis, 802
of diphtheria, 680
of erysipelas, 630
of idiopathic parotitis, 620
of influenza, 860
of leprosy, 789
of pertussis, 839
of the plague, 775
of rabies and hydrophobia, 880
of relapsing fever, 371
of rotheln, 583
of variola, 436
typhoid fever, 243
relation of, to causation of rubeola, 563
Silver nitrate, use of, in typhoid fever, 332
Simon's triangles, 437
SIMPLE CONTINUED FEVER, 231
Definition, 231
Synonyms, 231
History, 231
Etiology, 232
Symptoms, 233
Asthenic form, 233
Morbid anatomy, 235
Diagnosis, 234
From typhoid fever, 234
From typhus fever, 234
From relapsing fever, 235
From tubercular meningitis, 235
Prognosis, 235
Treatment, 236
Simple form of yellow fever, treatment, 649
Singultus in pyaemia, 975
in septicaemia, 977
significance of, in general diagnosis, 158
Skin, alterations in sensibility of, in cerebro-spinal meningitis, 808
anaesthesia of, in beriberi, 1039
appearance of, in typhoid fever, 273
character of lesions in erysipelas, 631
chronic diseases of, following rubeola, 574
color of, in cholera, 737
condition of, in cholera, 736
in influenza, 866
in septicaemia, 977
coolness of, in cerebro-spinal meningitis, treatment, 831
diseases of, complicating vaccination, 471
effects on course of erysipelas, 634
following vaccination, 471
disorders of, complicating rubeola, 570
eruptions of, complicating cholera, 735
in pyaemia, 974
erysipelas of, migration, 632
hyperaesthesia of, in typhus fever, 352
lesions of, in erysipelas, 635
course of, 631
in leprosy, 791
in remittent fever, 603
in rubeola, 575
morbid anatomy of lesions of, in variola, 446
odor of, in typhoid fever, 273
in typhus fever, 352
significance of color of, in general diagnosis, 159
swelling of, in erysipelas, 632
Skunk-bites as cause of rabies and hydrophobia, 889
Slaking lime, use of, in diphtheria, 703
Sleep, danger of prolonged, in nasal diphtheria, 712
Sleeplessness in idiopathic parotitis, treatment, 625
Small-pox, 434
black, 442
freedom of liability to, from race-protection, 130
Sodium benzoate, use of, in pertussis, 847
chloride, venous injection of, in cholera, 762, 768
hyposulphite, use of, in relapsing fever, 428
salicylate, use of, in diphtheria, 707
in puerperal fever, 1032
in scarlet fever, 543
in typhoid fever, 330
sulpho-carbolate as a prophylactic in scarlet fever, 537
Softening, cerebral, from embolism, 65
mucous, 82
Soil, character of, as cause of disease, 187
composition of, 187
diminished dryness of, a cause of phthisis, 187
drainage of, for prevention of anthrax, 937
of disease, 226
examination, 188
filtering power, 187
humidity of, as a cause of cholera, 722
Soils, alkaline, relation of, to causation of anthrax, 930
Soil-pipes, importance of position of, 188
tests as to their efficiency, 190
ventilation of, 189
Solitary glands, lesions of, in typhoid fever, 261
Spasm of pharyngeal and respiratory muscles in hydrophobia, 899
Special senses, perversion of, in relapsing fever, 386
in typhus fever, 349
Specific origin of anthrax, 720, 726
of cholera, 727
of glanders, 911
of rotheln, 583
of yellow fever, 640
Speech, impairment of, following cerebro-spinal meningitis, 820
Spinal cord, lesions of, in cerebro-spinal meningitis, 823
marrow, lesions of, in cholera, 746
rigidity in cerebro-spinal meningitis, 809
Spirillum, 142
of relapsing fever, 373
Spleen, condition of, in relapsing fever, 391
enlargement of, in pyaemia, 976
lesions of, in anthrax in animals, 935
in man, 942
in cholera, 746
in diphtheria, 687
in glanders, 922
in hydrophobia, 903
in pyaemia, 969
in relapsing fever, 416
in remittent fever, 602
in septicaemia, 972
in typhoid fever, 264
in typhus fever, 357
rupture of, in relapsing fever, 403
Spontaneous cow-pox, 456
origin of pyaemia, 959
of typhoid fever, 254
Stages of yellow fever, 645
Standards of purity of water, 184
Starvation and over-crowding as causes of relapsing fever, 370
Steam, use of, in diphtheria, 701
Sthenic inflammation, 46
Stimulants, use of, in diphtheria, 695
in relapsing fever, 431
in rubeola, 580
in variola, 453
Stomach, lesions of, in cholera, 743
state of, in remittent fever, 602
Stools, as a medium of disseminating typhoid fever, 249
character of, in cholera, 739
in pyaemia, 976
in typhoid fever, 287
in typho-malarial fever, necessity of disinfecting, 619
necessity of disinfection in prevention of typhoid fever, 321
significance of, in general diagnosis, 163
Strabismus in cerebro-spinal meningitis, 810
Straw-fungus, relation of, to rubeola, 558
Strychnia, use of, in diphtheritic paralysis, 713
in dry beriberi, 1043
Stupor in typhoid fever, treatment, 334
in typhus fever, treatment, 366
Subsoil-water, level of, 188
Sudamina in typhoid fever, 274
in typhus fever, 352
Sulphites and hyposulphites, use of, in pyaemia, 982
in septicaemia, 983
Sulphur, use of, in diphtheria, 709
Summer heats, relation of, to causation of rabies and hydrophobia, 887
Suppuration in idiopathic parotitis, treatment, 625
influence of minute organisms in production of, 144
Suppurative stage of variola, 439
Surgical scarlatina, 495
treatment of erysipelas, 638
Swelling of parotid glands in cerebro-spinal meningitis, 814
Swellings, significance of, in diagnosis, 159
Sweating stage of intermittent fever, 593
of intermittent fever, treatment, 597
Symptomatic parotitis, 625
Symptomatology, general, 148
Symptoms at decline of eruptive stage of rubeola, 567
constitutional, of vaccinia, 459
due to sewer-gas, 189
general, of idiopathic parotitis, 623
of anaesthetic form of leprosy, 791
of tubercular form of leprosy, 790
of confluent small-pox, 441
local, of anthrax, 935, 940
of idiopathic parotitis, 621
anaesthetic form of leprosy, 790
of glanders, 914, 915, 921
of tubercular form of leprosy, 789
nervous, in mild scarlet fever, 503
in typhus fever, 348
special, in typhus fever, 347
of anthrax in animals, 934
in man, 940
angina, 941
intestinalis, 941
of malignant anthrax, 940
of beriberi, 1039
of cerebro-spinal meningitis, 806
of cholera, 731
of comatose form of pernicious malarial fever, 608
of dengue, 884
of diphtheria, 667
of endometritis and endocolpitis of puerperal fever, 1005
of erysipelas, 631
of glanders in horses, 914
in man, 920
of hydrophobia, in man, 898
of influenza, 865
of idiopathic parotitis, 621
of intermittent fever, 592
of gangrene foudroyante, 977
of general peritonitis of puerperal fever, 1010
of leprosy, 789
of malignant scarlet fever, 507
of para- and perimetritis in puerperal fever, 1005
of pertussis, 840
of the plague, 777
of puerperal fever, 1004
of pyaemia, 972
of rabies and hydrophobia in dogs, 895
of relapsing fever, 374
of remittent fever, 599
of rotheln, 585
of rubeola, 563
of scarlet fever, 502
of septicaemia, 976
lymphatica of puerperal fever, 1011
venosa of puerperal fever, 1012
of simple continued fever, 233
of symptomatic parotitis, 626
of typho-malarial fever, 615
of typhoid fever, 268
of typhus fever, 346
of vaccinia, 458
of varicella, 481
of variola, 436
of varioloid, 443
of yellow fever, 644
Synonyms of anthrax, 926
of cerebro-spinal meningitis, 795
of cholera, 715
of dengue, 879
of diphtheria, 656
of erysipelas, 629
of glanders, 909
of influenza, 851
of leprosy, 785
of the plague, 771
of rabies and hydrophobia, 886
of relapsing fever, 369
of rotheln, 582
of rubeola, 557
of simple continued fever, 231
of typhoid fever, 237
of typhus fever, 338
of vaccinia, 455
of vaccination, 465
of varicella, 481
of variola, 434
of yellow fever, 640
Syphilis, complicating vaccination, 469
modes of preventing, 470
treatment of, 471
constitutional, hereditary nature of, 127
T.
Taches bleuatres in typhoid fever, 275
in typhus fever, 352
Tarnier's maternity pavilions for prevention of puerperal fever, 1028
Taste, modifications of, in typhoid fever, 280
significance of modification, in general diagnosis, 162
Technics of vaccination, 472
Teeth, significance of condition, in diagnosis, 152
Temperature in anthrax in man, 940
at decline of eruptive stage of rubeola, 567
elevated, influence of, in origin and spread of cholera, 720
in cerebro-spinal meningitis, 815
in cholera, 736
in dengue, 881
in eruptive stage of rubeola, 565
in erysipelas, 633
in fevers, 38-40
in general peritonitis of puerperal fever, 1010
in idiopathic parotitis, 623
in influenza, 864
in malignant scarlet fever, 507
in mild scarlet fever, 505
in para- and perimetritis in puerperal fever, 1006
in prodromal stage of rubeola, 564
in pyaemia, 974
in relapsing fever, 378, 382
in remittent fever, 599
in rotheln, 587
in septicaemia, 977
venosa of puerperal fever, 1012
in typhoid fever, 280
in typhus fever, 349
significance of, in general diagnosis, 158
respiration and pulse, relations of, in relapsing fever, 386
Tenderness, muscular, in beriberi, 1039
Teratoid tumors, 124
Test, peppermint, for defects in plumbing, 198
Tests as to efficiency of soil-pipes, 190
The plague, 771
Thermometer, use of, in typhoid fever, 284
Thirst in cerebro-spinal meningitis, 814
in rabies and hydrophobia, 899
in relapsing fever, 389
in typhoid fever, 285
in typhus fever, 350
treatment, 367
significance of, in general diagnosis, 162
treatment of, in cholera, 770
Throat symptoms, complicating scarlet fever, 511
Thoracic duct, obstruction of, as cause of dropsy, 69
Thrombi, action of, in production of metastatic abscesses in pyaemia,
965
calcification of, 60, 89
in uterine pelvic veins, 989
growth of, in puerperal fever, 989
Thrombosis, 56
relation of, to causation of pyaemia, 957
and embolism, 56
causes, 57
symptoms, 66
in relapsing fever, 402
in typhoid fever, treatment, 335
THROMBUS, 56
Calcification, 60, 88
Characteristics, 59
Changes, 60
Composition, 56
Distinguished from thrombosis, 56
From compression, 58
From death of leucocytes, 57
From dilatation, 58
From marasmus, 59
From traumatism, 58
Mechanical effects, 62
Organization, 60
Softening, 61
Varieties, 57, 58
Tongue, condition of, in cerebro-spinal meningitis, 813
in dengue, 881
in erysipelas, 633
in idiopathic parotitis, 622
in mild scarlet fever, 504
in typhus fever, 350
in yellow fever, 644
state of, in pyaemia, 975
in relapsing fever, 389
in remittent fever, 600
in septicaemia, 977
in typhoid fever, 285
signification of state of, in diagnosis, 152
Tracheal diphtheria, prognosis of, 692
Trachea, formation of diphtheritic membrane in, 671
Tracheotomy in diphtheria, prognosis of, 692
Transmission of cholera, 721, 723
of variola, 435
Transudation, 68
causes, 69
mechanism, 68
Traps, ventilation, 221
Traumatic fever, relation of, to septicaemia, 961
fevers, 37
Treatment of anthrax in animals, 938
in man, 943
preventive, of anthrax, 936, 943
of beriberi, 1042
of cerebro-spinal meningitis, 829
of cholera, 759
of dengue, 885
of diphtheria, 694
general, importance of, in diphtheria, 695
of erysipelas, 636
of idiopathic parotitis, 624
local, of idiopathic parotitis, 625
of intermittent fever, 594
of leprosy, 793
local, of leprosy, 794
of comatose form of pernicious malarial fever, 609
of glanders in horse, 918
in man, 924
preventive, in horse, 919
in man, 925
of influenza, 873
of pertussis, 844
of the plague, 782
of puerperal fever, 1028
of septicaemia, 983
of pyaemia, 979
of rabies and hydrophobia, 903
preventive, 903
of relapsing fever, 426-433
of remittent fever, 603
of rotheln, 587
of rubeola, 578
hygienic, of rubeola, 579
preventive, of rubeola, 578
of scarlet fever, 536
of septicaemia, 982
of simple continued fever, 236
of symptomatic parotitis, 627
local, of symptomatic parotitis, 628
of typhoid fever, 320
of typho-malarial fever, 618
of typhus fever, 361
of variola, 451
hygienic, of variola, 451
of variola, preventive, 451
of varioloid, 451
of yellow fever, 649
Treeak farook, use of, in wet beriberi, 1042
TUBERCLE, 94
Calcification, 96
Cheesy degeneration, 96
Fibrous transformation, 96
Histology, 95
Horn-like change, 96
Infectious origin, 97
Inoculability, 97
Miliary and gray, cause of infectious qualities, 99
Origin of, from absorption of cheesy products, 97
Tubercular form of leprosy, 789
TUBERCULOSIS, 94
Bacilli of, 99, 100 _et seq._
Dissemination, 103
Hereditary nature, 101
Primary seat, 104
Relation of, to pearly distemper, 99
to scrofula, 101
Tuberculosis, acute miliary, complicating rubeola, 572
chronic pulmonary, following rubeola, 573
general miliary, following relapsing fever, 404
following rubeola, 574
relation of, to pearly distemper, 99
to scrofula, 96, 101
TUMORS, 105
Method of origin, 106
Cohnheim's theory of origin, 106
Influence of irritants in producing, 108
Growth, 109
concentric, 109
continuous, 109
eccentric, 109
influence of seat, 109
rapidity, 109
Primary, 110, 111
Secondary, 110, 112
Metastasis, 110
Multiple, 110
Recurrence, 110
Transplantation, 110
Embolic nature, 112
Changes occurring, 113
inflammatory, 113
Analogy of structure in primary and secondary, 113
Benignant, 114
Cachexia, 114
Malignant, 114
Resemblance of, to normal tissue of body, 115
Histoid, 116
Organoid, 116
Relation of, to each other, 117
Connective tissue, 118, 122
Cystic, 115, 116, 121
Influence of age upon development, 119
Classification, 114, 121
Infective group, 120, 124
Epithelial group, 123
Congenital, 124
Turpentine inhalations in diphtheria, 704
stupes, use of, in puerperal fever, 1032
use of, in typhoid fever, 326
Tympanites in remittent fever, treatment, 605
in typhoid fever, 286
treatment of, 332
in typho-malarial fever, treatment, 619
in typhus fever, 350
Tympanum, paracentesis of, in scarlet fever, 548
Types of cerebro-spinal meningitis, 804
of intermittent fever, 594
of scarlet fever, 494
of varioloid, 444
TYPHOID FEVER, 237
Synonyms, 237
Definitions, 237
History, 238
Geographical distribution, 241
Etiology, 242
Predisposing causes, 242
Age, influence of, 242
Sex, influence of, 243
Occupation, influence of, 244
Change of residence, influence of, 244
Idiosyncrasy, influence of, 245
Depressing emotions, influence of, 245
Intemperance, influence of, 245
Previous ill-health, influence of, 245
Season, influence of, 245
Elevated temperature, influence of, 246
Rise and fall of subsoil-water, influence of, 247
Exciting causes, 248
Contagiousness, 248
Dissemination, 249
Cases illustrating modes of dissemination, 250
Dissemination of, by drinking-water, 248
By stools, 249
By milk, 252
By atmosphere, 252
By bed-linen, etc., 253
By polluted soil, 253
By putrefied flesh, 257
Spontaneous origin, 254
Duration of virulence of germs, 256
Bacillus typhosus, 258
Incubation period, 259
Morbid anatomy, 260
Lesions peculiar to, 261
Changes in Peyer's patches, 261
Solitary glands, 261
Softening of Peyer's patches and solitary glands, 263
Cicatrization of Peyer's patches and solitary glands, 263
Changes in caecum and colon, 263
Spleen, 264
Abdominal glands, 264
Lesions not peculiar to, 265
Changes in liver and gall-bladder, 265
Pharynx and oesophagus, 265
Larynx and lungs, 266
Brain and membranes, 266
Muscles, 267
Heart and blood-vessels, 267
Blood, 268
Salivary glands, 268
Kidneys, 268
Symptoms, 268
Clinical description, 268
Physiognomy, 272
Epistaxis, 273
Condition of skin, 273
Odor, 273
Eruption, 273
Sudamina, 274
Taches bleuatres, 275
Condition of hair and nails, 275
Pulse, 275
Heart-sounds, 276
Respiration, 276
Frequency of bronchitis, 277
Mental condition, 277
Headache, 277
Delirium, 278
Muscular spasm, 279
tremor, 279
Modifications of sensibility, 279
Hearing, 280
Vision, 280
Taste, 280
Temperature, 280
State of tongue, 285
Fauces, 286
Nausea and vomiting, 285
Anorexia, 285
Thirst, 285
Gurgling, 286
Meteorism or tympanites, 286
Diarrhoea, 287
Character of stools, 287
Intestinal hemorrhage, 287
frequency, 288
causes, 288
importance, 288
Intestinal perforation, 289
frequency, 290
causes, 290
date of appearance, 290
importance, 289
Condition of urine, 291
amount of solids, 291
presence of albumen, 292
Complications and sequelae, 292
Complicated by pyaemia, 294
Laryngitis, 294
Bronchitis and pneumonia, 294
Pleurisy, 294
Jaundice, 295
Peritonitis, 295
Catarrhal and diphtheritic inflammation of fauces, 295
Parotid swelling, 296
Menstrual disorders, 296
Pregnancy, 296
Suppuration of Bartholini's glands, 296
Periostitis, 297
Oedema, 297
Bed-sores, 297
Followed by impaired intellect, 292
Perversion of the moral sense, 292
Paralysis and chorea, 293
Cardiac degeneration, 293
Arterial thrombosis, 293
Venous thrombosis, 294
Gangrene of vulva and vagina, 293
Hepatic abscess, 295
Tendency to stoutness, 298
Varieties of, 298
Abortive form, 298
Latent form, 300
In children, 301
In aged persons, 302
Relapses in, 302
frequency, 302
course, 303
cases illustrating, 304
causes, 308
Duration, 310
Diagnosis, 311
From typhus, 311
From influenza, 312
From relapsing fever, 312
From epidemic cerebro-spinal meningitis, 313
From simple continued fever, 313
From remittent fever, 312
From the eruptive fevers, 313
From acute tuberculosis, 313
From trichinosis, 314
From the specific inflammations, 314
From acute tubercular meningitis, 314
Prognosis, 314
Symptoms indicating unfavorable, 314
favorable, 316
Influence of hyperpyrexia upon, 314
Nervous symptoms, 315
Heart symptoms, 316
Condition of pulse, 316
Abdominal symptoms upon, 316
Mortality, 316
Tables showing, 317, 318
Influence of season, 318
Sex, 319
Age, 319
Treatment, 319
Habits, 320
Social condition, 320
Recent residence, 320
Corpulence, 320
Organic disease, 320
Childhood, 320
Treatment, 320
Preventive, 321
Necessity of proper drainage in prevention, 321
Disinfection of stools, 321
Hygienic, 322
Importance of ventilation, 323
administering water, 325
Diet, 323
Mild cases, 326
Hyperpyrexia, 327
by cold baths, 327-329
Typho-malarial form, 331
Vomiting, 331
Diarrhoea, 331
Tympanites, 332
Intestinal hemorrhage, 332
perforation, 333
Constipation, 333
Headache, 334
Insomnia, 334
Stupor, 334
Delirium, 334
Albuminuria, 334
Complications, 335
Epistaxis, 335
Pneumonia, 335
Hypostatic congestion of lungs, 335
Thrombosis and embolism, 335
Bed-sores, 335
Convalescence, 335
Use of alcohol, 324
Digitalis, 330
Eucalyptus, 331
Quinia, 330
Silver nitrate, 332
Sodium salicylate, 330
Turpentine, 326
Specific, 336
By calomel, 336
By iodine, 336, 337
Use of thermometer, 284
Typhoidal inflammation, 47
Typhoid state of cholera, 734
following variola, 445
TYPHO-MALARIAL FEVERS, 614
Definition, 614
Frequency, 616
Symptoms, 615
Diagnosis, 616
Prognosis, 616
Mortality, 616
relative mortality of white and black races, 616
Treatment, 618
Of typhoidal element, 618
Of malarial element, 618
Use of quinia, 618
Depurative treatment, 618
Necessity of disinfection of stools, 619
Of tympanites, 619
Of insomnia, 619
Diet, 619
Typho-malarial form of typhoid fever, treatment, 331
TYPHUS FEVER, 338
Synonyms, 338
History, 338
Etiology--Predisposing causes, 341
Over-crowding as a cause, 341
Age, influence of, 342
Debility and fatigue, influence of, 342
Mental and physical overwork, 342
Intemperance, 342
Poverty, 342
Barometric and thermometric variations, 343
Season, 343
Occupation, 343
Individual susceptibility to, 343
Exciting causes, 343
Contagiousness, 343
Nature of contagion, 343
Modes of transmission of contagion, 344
Communication of, by fomites, 345
Period of contagiousness, 345
Spontaneous origin, 345
Period of incubation, 346
Symptoms--Clinical description, 346
Special symptoms, 347
Prostration, 348
Nervous symptoms, 348
Appearance of face, 348
Intellectual condition, 348
Headache, 348
Delirium, 348
Wakefulness, 349
Coma vigil, 349
Perversion of special senses, 349
Muscular tremor, 349
Temperature, 349
Condition of tongue, 350
Anorexia, 350
Thirst, 350
Nausea and vomiting, 350
Condition of bowels, 350
Tympanites, 350
Gurgling, 350
Eruption, 351
Duration of eruption, 351
Taches bleuatres, 352
Sudamina, 352
Hyperaesthesia of skin, 352
Odor, 352
Condition of pulse, 351
of heart, 351
Respiration, 352
Pneumonia, 353, 355
Bronchitis, 353, 355
Odor of breath, 353
Hypostatic congestion of lungs, 353
Changes in urine, 353
Varieties of, 353
Mild form, 354
Severe form, 354
Ataxic form, 354
Adynamic form, 354
Ataxo-adynamic form, 354
Inflammatory form, 354
Walking form, 354
Abortive form, 354
Complications and sequelae, 354
Complicated by erysipelas, 355
Cardiac degeneration, 355
Bronchitis and pneumonia, 353, 355
Pleurisy, 355
Albuminuria, 355
Bed-sores, 355
Scurvy, 355
Dysentery, 355
Jaundice, 356
Parotitis, 356
Serous inflammations, 356
Pyaemia, 356
Disorders of menstruation, 356
Miscarriage, 356
Followed by pulmonary gangrene and phthisis, 355
Morbid anatomy, 356
Alteration of blood, 356
Changes in respiratory organs, 356
Heart and membranes, 357
Liver and kidneys, 357
Spleen, 357
Intestinal tract, 357
Brain and membranes, 358
Diagnosis, 358
From typhoid fever, 358
From meningitis, 358
From measles, 358
From typhoid pneumonia, 359
From delirium tremens, 359
From purpura, 359
Prognosis of, 359
Symptoms indicating favorable, 360
unfavorable, 360
Influence of age, 359
Sex, 359
Former habits, 359
Convalescence from previous illness, 359
Obesity, 359
Mental and physical overwork, 360
Social condition, 360
Race, 360
Mortality, 360
Difference of, in hospital and private cases, 361
Treatment, 361
Preventive, 361
Necessity of isolation, 361
Disinfection, 362
Diet, 362
Quantity of nourishment necessary, 363
Futility of abortive treatment, 363
General treatment, 364
Mild cases, 364
Hyperpyrexia, 364
By cold water, 364
By cold baths, 364
Mode of using cold bath, 364
Prostration, 365
Headache, 366
Delirium, 366
Insomnia, 366
Stupor, 366
Urinary complications, 366
Thirst, 367
Vomiting, 367
Constipation, 367
Parotitis, 367
Pulmonary complications, 367
Use of alcohol in, 366
Opium in, 366
Quinia in, 365
Of convalescence, 368
Necessity of continuing stimulants during convalescence, 368
Tyrosis, 79
U.
Ulceration, complicating vaccination, 468
Ulcers, complicating cholera, 735
following the plague, 781
Umbilication in vaccinia, mechanism of, 464
in varicella, 482
in variola, 438
cause of, 447
Uraemia in scarlet fever, 530
Urinary complications in typhus fever, treatment, 366
Urine, analysis of, importance in general diagnosis, 165
condition of, in cerebro-spinal meningitis, 814
in cholera, 739
in dengue, 881
in influenza, 866
in mild scarlet fever, 506
in grave form of the plague, 779
in pertussis, 841
in pyaemia, 976
in relapsing fever, 387
in remittent fever, 602
in typhoid fever, 291, 292
in yellow fever, 644
suppression of, complicating relapsing fever, 407
in cholera, treatment, 764
in yellow fever, treatment, 653
Urination, difficult, significance of, in diagnosis, 164
Urobilin, 91
Urticaria, complicating diphtheria, 674
Uterus, fixity of, in para- and perimetritis of puerperal fever, 1007
lesions of, in septicaemia, 972
V.
VACCINIA, 455
Definition, 455
Synonyms, 455
History, 458
Etiology, 458
Nature, 455
Variolous origin, 457
Meteorological conditions as a cause, 458
Symptoms, 458
General course, 458
Constitutional, 459
Development of pock, 459
Date of appearance of pock, 459
incrustation of pock, 460
falling off of crust, 460
Description of cicatrix, 460
Irregularities in course, 460
Raspberry excrescence of pock, 461
Lack of elevation in pock, 461
Absence of a constitutional infection, 460
Bryce's test for determining constitutional infection, 461
Diphtheritic pock, 463
Catarrhal pock, 463
Morbid anatomy, 462
Pock, 463
Microspheres and vaccinals of lymph, 463
Microscopical characters of the lymph, 463
Mechanism of umbilication, 464
Composition of crust, 464
Complications and sequelae, 464
VACCINATION, 465
Synonyms, 465
History of, 465
Protective power of, 461
theories regarding, 461
duration of, 468
against pertussis, 468
Marson's theory of multiple insertions, 467
Time of revaccination, 467
As a means of destroying naevi, 468
Complications, 468
Simple inflammatory, 468
Complicated by dermatitis, 468
Treatment of dermatitis, 469
Complicated by lymphangitis and adenitis, 468
By ulceration and gangrene, 468
Erysipelas, 469
treatment, 469
Complicated by syphilis, 469
treatment, 471
Modes of preventing transmission of syphilis, 470
Complicated by skin diseases, 471
by eczema, 472
Impetigo contagiosa, its relations to, 472
Followed by cutaneous affections, 471
by eczema, 472
Conveyance of constitutional taints in, 471
Technics of, 472
Varieties of virus, 472
Primary vaccine, 473
Horse-pox vaccine, 473
Retro-vaccine, 473
Bovine vaccine, 473
Variola vaccine, 473
So-called points of superiority of humanized vaccine, 473
Relative merits of animal and humanized vaccine, 473
Advantages of animal over humanized virus, 475
Forms of vaccine, 476
Objections to use of crust, 476
Use of dried lymph, 477
liquid or tube lymph, 476
Proper season, 477
Age, 477
Part of body most suitable for, 477
Modes of operating, 478
applying the virus, 478
Storage and preservation of virus, 479
Proper time of collecting lymph for storage, 479
Proper manner of transporting, 480
Vaccination, neglect of, as a cause of variola, 436
Vaccine virus, varieties of, 472
use of, in treatment of rabies and hydrophobia, 907
Vagina, symptoms of diphtheria of, 674
Vaginal injections, use of, for prevention of puerperal fever, 1025
Variations, barometric, influence of, upon course of diseases, 134
VARICELLA, 481
Definition, 481
Synonyms, 481
History, 481
Etiology, 481
Contagiousness, 481
Symptoms, 481
Period of incubation, 482
General, 482
Prodromal stage, 482
Eruption, 482
Umbilication of eruption, 482
Date of appearance of desiccation, 482
Frequency of scarring, 482
Appearance of vesicles on mucous membrane, 483
Morbid anatomy, 483
Complications, 483
Diagnosis, 483
From variola and varioloid, 484
From vaccinia, 484
From impetigo, 483
contagiosum, 483
From eczema pustulosum, 483
Prognosis, 484
Treatment, 485
_Varicella Prurigo_, nature, 484
Varieties of beriberi, 1039
of grease-traps, 221
of pernicious malarial fever, 606
of rubeola, 568
of sewer-traps, 191
of typhoid fever, 298
VARIOLA, 434
Definition, 434
Synonyms, 434
History, 434
Etiology, 435
Contagiousness, 435
Nature of contagium, 435
Mode of entrance of contagium, 435
Duration of activity of contagium, 435
Period of greatest activity of contagium, 435
Modes of transmission, 435
Race, influence of, 436
Season, influence of, 436
Sex, influence of, 436
Neglect of vaccination as a cause, 436
Individual idiosyncrasy, 436
Protection from, by previous attacks, 436
Effect of pre-existing skin disorders, 436
Symptoms, 436
Stage of incubation, 436
Invasion, 436
Variolous rash, 437
date of appearance, 437
significance, 437
Simon's triangle, 437
Stage of invasion, 438
Eruptive stage, 438
Characters of eruption, 438
Position of eruption, 438
Stage of vesication, 438
Umbilication, 438
Maturation, 439
Characters of mature pock, 439
Condition of patient in suppuration stage, 439
Pustules on mucous surfaces, 439
Stage of desiccation, 439
General, during desiccation, 440
Secondary fever, 439
Date of appearance of secondary fever, 439
Confluent variety, 440
Seat of lesion, 441
Condition of mucous surfaces in confluent, 441
General condition in confluent, 441
Hemorrhagic variety, 442
First form, 442
Second form, 443
Lesions of, 443
Variolic purpura, 442
Complications and sequelae, 445
Complicated by eye diseases, 445
Erysipelas, 445
Nasal inflammation, 445
Furuncles and abscesses, 445
Muscular paralysis and hemiplegic attacks, 445
Laryngitis, 446
Gangrene of genitalia, 446
Followed by a typhoid state, 445
Pathology and morbid anatomy, 446
Cutaneous lesions, 446
Formation of papule, 446
Vesicle, 446
Cause of umbilication, 447
Repair of pock, 447
Hemorrhagic variety, 447
Changes of viscera, 447
Diagnosis, 447
From measles, 448
From scarlatina, 449
From pustular skin diseases, 449
From dermatitis medicamentosa, 449
From syphiloderm, 449
From acneform disease, 449
From typhoid fever, 450
From typhus fever, 450
Prognosis, 450
Symptoms indicating unfavorable, 450
Influence of sudden defervescence of eruption, 450
Pregnancy and childbed, 450
Fatality of, in the unvaccinated, 450
Influence of vaccination after development, 451
Treatment, 451
Preventive, 451
Hygienic, 451
Necessity of cleanliness, 454
Invasion stage, 452
Eruption, 452
Exclusion of sunlight for prevention of pitting, 452
Use of warm baths, 453
Hot water compresses, 453
Stimulants, 454
Hemorrhagic form, 454
Disposition of clothes and body after death, 454
Variola of vaccine, 473
Variolic purpura, 442
VARIOLOID, 443
Symptoms, 443
Invasion stage, 443
Eruption, 444
Types of, 444
Identity with variola, 444
Treatment, 451
Veins, condition of, in cholera, 737
intestinal, lesions of, in cholera, 745
jugular, thrombi of, in symptomatic parotitis, 626
lesions of, in pyaemia, 967
in symptomatic parotitis, 626
Venesection in cholera, 764
in rabies and hydrophobia, 908
in relapsing fever, 431
futility of, in cerebro-spinal meningitis, 830
VENTILATION, 177 _et seq._
Defects, 179
Distribution of air, 180
Estimation of carbonic acid in air, 178
Insufficient, evil effects, 181
Importance of, in treatment of typhoid fever, 323
Methods of calculating amount of air-supply, 179
Modes of investigating merits of a plan, 179
Of waste-pipes in drainage, 223
Of soil-pipes, 189
Proper size of flues and registers, 179
Relation of, to heating apparatus, 180
Varieties of ventilators, 180
Velocity of air, 180
Ventilators, varieties, 180
Venous emboli, 63
thrombosis, following typhoid fever, 294
Veratrum viride, use of, in puerperal fever, 1033
in scarlet fever, 543
in yellow fever, 651
Vertigo in cerebro-spinal meningitis, 812
in relapsing fever, 384
significance of, in general diagnosis, 158
Vesication in variola, 438
Vesicle in variola, morbid anatomy of, 446
Views, earlier, concerning nature of puerperal fever, 990
modern, concerning nature of puerperal fever, 992
Virus of anthrax, period of greatest virulence, 928
of rabies, localization of, in wound, 893
of vaccination, varieties of, 472
vaccine, manner of transporting, 480
storage, 479
Viscera, lesions of abdominal, in the plague, 781
in cerebro-spinal meningitis, 824
in erysipelas, 635
in variola, 447
Vision, modifications of, in relapsing fever, 399
in typhoid fever, 280
Vital statistics, registration, 208
Voice, alteration of, in diagnosis, 158
Vomit, character of, in cerebro-spinal meningitis, 813
in cholera, 738
in grave form of the plague, 779
Vomiting during intermittent fever paroxysm, 593
in cerebro-spinal meningitis, 813
in cholera, 738
treatment, 761
in diphtheria, treatment, 694
in general peritonitis of puerperal fever, 1010
in mild scarlet fever, 503
in para- and perimetritis of puerperal fever, 1007
in pyaemia, 975
in remittent fever, treatment, 605
in rubeola, treatment, 581
in septicaemia, 977
in typhoid fever, 285
treatment, 331
in typhus fever, 350
treatment, 367
in yellow fever, 644
treatment, 652
significance of, in general diagnosis, 162
Vulva, symptoms of diphtheria, 674
W.
Wakefulness in relapsing fever, 384
in typhus fever, 349
Walk, significance of, in diagnosis, 161
Walking form of typhus fever, 354
of yellow fever, symptoms, 654
Washstands, stationary, dangers from, 216
Waste-pipes, effects of large bore in, 220
leakage in, 222
tests for, 222
ventilation, 223
Water, collections of, effect upon public health, 187
fear of, in rabies and hydrophobia, 899
height of subsoil, influence of, on prevalence of cholera, 722
importance of, in treatment of typhoid fever, 325
impure, microscopic characters of, 184
diarrhoeal affections from, 182
disease from, 182
chemical examination of, 183, 184
value of chemical examination of, 183, 184
impurity of, from metallic salts, 182
from organisms, 184
nature of impurities, 182
polluted, as a cause of diphtheria, 683
stagnant, production of malaria by, 187
standards of purity, 184
subsoil, level of, 188
supply, contamination of, from privy-vaults, 192
cess-pools, 192
chloride test for detecting impurities in, 192
tables of analyses, 184
use of, in diphtheria, 702
Water-closets, defects of, 217
location, 218
varieties, 191
ventilation, 192, 217
Waxy degeneration, 84
Welch on cause of oedema of lungs, 72
Wet form of beriberi, symptoms, 1040
treatment, 1042
Whooping cough, 836
relation of, to rubeola, 561
Winds, influence of, on spread of influenza, 860
Wound, appearance of, in rabies and hydrophobia, 895, 899
changes in, in pyaemia, 976
condition of, in septicaemia, 977
influence of characters of, in causation of pyaemia, 958
treatment of, in pyaemia, 981
in septicaemia, 983
Wounds, diphtheria of, 673
Y.
YELLOW FEVER, 640
Synonyms, 640
Definition, 640
Etiology, 640
Specific origin, 640
Poison of, inconvertibility, 840
Birthplace, 641
Characteristics, 641
Ponderability, 641
Vitality, 641
Influence of heat and cold on development, 641
Impossibility of transportation of, by air, 641
Transportability of, by fomites, etc., 641
Nature of fomites, 641, 642
Fixity of, 643
Slowness of extension, 643
Medium of admission to system, 642
Localization of epidemics by atmospheric impregnation, 642
Anxiety, grief, and fatigue as causes, 643
Insusceptibility, in negroes, 644
from idiosyncrasy, 643
Protective power of previous attacks, 643
Duration of incubation period, 643
Symptoms, 644
Mild cases, 644
Initial, 644
Physiognomy, 644
Neuralgia and muscular pains, 644
Cerebral, 644
Condition of tongue, 644
Gastro-intestinal canal, 644
Vomiting, 644
Character of matters vomited, 644
Condition of urine, 644
Pulse, 644
Relation of pulse to temperature, 645
Perspiration, 645
Stages, 645
Masked forms, 653
Walking forms, 654
Paroxysmal stage, 645
Calm stage, 645
Hemorrhages and jaundice, 646
Prognosis, 646
Symptoms indicating unfavorable, 646
Influence of crowding the sick, 646
Pregnancy and parturition, 647
Condition of patient at time of attack, 647
Temperature, 647
In hospital cases, 647
Mortality, 647
Variableness, 647
Difference in hospital and private cases, 648
Diagnosis, 648
Significance of physiognomy, 648
State of pulse, 648
Albuminous urine, 648
Hemorrhagic tendency, 648
Yellow discoloration of skin, 648
Morbid anatomy, 649
Changes in liver, 649
Treatment, 649
Futility of abortive, 649
Importance of early, 649
Indications for, 649
Simple form, 649
Early stages, 649
Diaphoresis, 650
Jaborandi, 650
Neuralgias and muscular pains, 651
Hyperpyrexia, 651
by cold, 651
Hemorrhages, 651
by tincture of iron, 652
Nausea and vomiting, 652
Urinary suppression, 652
Failure of reaction from cold stage, 653
Convulsions and delirium, 653
Use of digitalis, 651
Aconite, 651
Veratrum viride, 651
Gelsemium, 651
Haemostatics, 652
Quinia, 650, 651
Quinia and opium in combination, 651
Hygienic, 654
Necessity of absolute rest, 654
Diet, 654
Children, 655
Typhoid cases, 655
Time of return to solid food, 655
Z.
Zymosis, meaning of term, 137
Zymotic diseases, relation of, to puerperal fever, 1020
table, 136
END OF VOL. I.
*** End of this LibraryBlog Digital Book "A System of Practical Medicine by American Authors, Vol. I - Volume 1: Pathology and General Diseases" ***
Copyright 2023 LibraryBlog. All rights reserved.