Text book of veterinary medicine, Volume 3 (of 5)

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Title: Text book of veterinary medicine, Volume 3 (of 5)
Author: Law, James
Language: English
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TEXT BOOK
OF
VETERINARY MEDICINE

JAMES LAW, F.R.C.V.S.

Director of the New York State Veterinary College Cornell University,
Ithaca, N.Y.

VOL. III

DISEASES OF THE NERVOUS SYSTEM—GENITO-URINARY ORGANS—EYE—SKIN
CONSTITUTIONAL DISEASES

ITHACA
PUBLISHED BY THE AUTHOR
1901

PRESS OF
ANDRUS & CHURCH
ITHACA, N. Y.

CONTENTS

DISEASES OF THE NERVOUS SYSTEM.
GENERAL SYMPTOMATOLOGY AND DIAGNOSIS.
TROPHIC SYMPTOMS AND DISORDERS.
SENSORY SYMPTOMS AND DISORDERS.
PSYCHIC SYMPTOMS AND DISORDERS.
DIAGNOSIS, SYMPTOMS AND THEIR IMMEDIATE CAUSES. LOCALIZATION OF LESION
IN SPECIAL SYMPTOMS.
HALLUCINATIONS.
TIMIDITY. PANIC. STAMPEDE.
BALKING. RESTIVENESS.
DELIRIUM.
VICIOUSNESS. AGGRESSIVE VICE.
CATALEPSY.
INSOLATION. HEAT EXHAUSTION. SUNSTROKE. THERMIC FEVER.
EPILEPSY. FALLING SICKNESS.
ECLAMPSIA. CONVULSIONS. SPASMS.
CHOREA. ST. VITUS DANCE.
CONVULSIVE TWITCHING OF THE FACE.
VERTIGO. MEGRIMS. BLIND STAGGERS.
CONCUSSION OF THE BRAIN.
LIGHTNING STROKE. ELECTRIC SHOCK.
INTRACRANIAL HÆMORRHAGE AND THROMBOSIS. APOPLEXY. SOFTENING OF THE
BRAIN.
CEREBRAL HYPERÆMIA. MENINGO—ENCEPHALIC CONGESTION.
MENINGO—ENCEPHALITIS. STAGGERS.
CHRONIC HYDROCEPHALUS. DROPSY OF THE VENTRICLES. IMMOBILITY.
CEREBRO-SPINAL MENINGITIS.
ABSCESS OF THE BRAIN.
TUBERCULAR MENINGITIS.
TUMORS OF THE BRAIN. NEOPLASMS.
CHOLESTEATOMA.
MELANOMA OF THE ENCEPHALON.
PSAMMOMATA (GRITTY TUMORS) OF THE BRAIN.
MYXOMA OF THE BRAIN.
ACROMEGALY. HYPERTROPHY OF THE PITUITARY BODY.
CEREBELLAR DISEASE.
BULBAR PARALYSIS. DISEASE OF MEDULLA OBLONGATA.
LOCO POISONING. OXYTROPIS LAMBERTI. ASTRAGALUS MOLLISSIMUS
LEAD POISONING. PLUMBISM.
ALCOHOLIC INTOXICATION.
ANILINE POISONING.
POISONING BY NITRO-BENZOL.
POISONING BY CARBON DISULPHIDE.
TETANY.
CONGESTION OF THE SPINAL CORD IN THE HORSE AND COW.
ACUTE MYELITIS. POLIOMYELITIS. INFLAMMATION OF THE SPINAL CORD.
SPINAL MENINGITIS.
ACUTE MYELITIS IN THE DOG. MENINGO-MYELITIS.
CHRONIC MYELITIS. SCLEROSIS.
ARTERITIS (THROMBOSIS, EMBOLISM) OF THE SPINAL CORD AND MEMBRANES.
HEMORRHAGES INTO THE SPINAL MEMBRANES. Meningeal Spinal Apoplexy.
Hæmatorrachis. Hemorrhage into the Spinal Cord. Spinal Apoplexy.
Hæmatomyelia.
SPINA BIFIDA.
SPINAL CARIES. TUBERCULAR OR OTHER INFECTIVE DISEASE OF THE VERTEBRÆ.
SLOW COMPRESSION OF SPINAL CORD. PARALYSIS.
DILATATION OF THE CENTRAL CANAL OF THE SPINAL CORD. SYRINGOMYELIA.
NEURASTHENIA IN PREGNANT EWES.
NEURITIS. PERINEURITIS.
NEURALGIA.
ATROPHY OF NERVES.
DISEASES OF THE URINARY ORGANS.
PHYSICAL PROPERTIES OF THE URINE.
GENERAL SYMPTOMS OF URINARY DISEASE.
HEMATURIA.
ACUTE CONGESTION OF THE KIDNEYS IN SOLIPEDS.
ACUTE CONGESTION OF THE KIDNEYS IN CATTLE.
ACUTE CONGESTION OF THE KIDNEYS IN SHEEP AND GOAT.
ACUTE CONGESTION OF THE KIDNEYS IN SWINE.
CONGESTION OF THE KIDNEYS IN CARNIVORA.
NEPHRITIS.
ACUTE NEPHRITIS. ACUTE BRIGHT’S DISEASE.
PURULENT NEPHRITIS.
PERINEPHRITIS.
PYELITIS. PYELONEPHRITIS. INFLAMMATION OF THE RENAL PELVIS.
CHRONIC NEPHRITIS.
HYPERTROPHY OF THE KIDNEY.
ATROPHY OF THE KIDNEY.
FATTY DEGENERATION OF THE KIDNEY
AMYLOID KIDNEY. LARDACEOUS OR WAXY KIDNEY.
RENAL CALCULUS.
INJURIES OF THE URETERS.
URETERITIS.
ACUTE CATARRHAL CYSTITIS.
ACUTE CROUPOUS CYSTITIS.
CHRONIC CATARRHAL CYSTITIS.
CYSTITIS IN THE OX.
CYSTITIS IN DOGS.
ATONY AND PARALYSIS OF THE BLADDER.
TUMORS OF THE BLADDER.
VESICAL PARASITES.
SPASM OF NECK OF BLADDER.
RUPTURE AND LACERATION OF THE BLADDER.
EVERSION OF THE BLADDER.
HERNIA OF THE BLADDER.
ANOMALIES OF THE BLADDER.
URETHRAL ANOMALIES.
ACUTE URETHRITIS. CATARRH OF THE URETHRA.
WOUNDS OF THE URETHRA.
FOREIGN BODIES IN THE URETHRA.
STRICTURE OF THE URETHRA.
ACUTE PROSTATITIS AND HYPERÆMIA OF THE PROSTATE.
CHRONIC PROSTATITIS.
HYPERTROPHY OF THE PROSTATE.
TUBERCULOSIS OF THE PROSTATE.
CANCER OF THE PROSTATE.
PROSTATIC CYSTS.
CALCULUS OF THE PROSTATE.
DISEASES OF THE FEMALE GENERATIVE ORGANS. Malposition of ovary and
womb. Hernia of the ovaries.
UNDEVELOPED OVARIES. ABSENCE OF OVARIES.
ATROPHY OF OVARIES.
SUPERNUMERARY OVARIES.
IRRITABLE OVARY. NEURALGIA OF THE OVARY.
HÆMORRHAGE ON THE OVARY.
INFLAMMATION OF THE OVARIES. OÖPHORITIS. PERIOÖPHORITIS.
OVARIAN CYSTS.
DERMOID CYSTS OF THE OVARY. PILOUS CYSTS.
SOLID OVARIAN TUMORS.
INFLAMMATION OF THE FALLOPIAN TUBES. SALPINGITIS.
DISEASES OF THE OVIDUCT IN BIRDS.
HYDROMETRA AND PYOMETRA.
UTERINE TUMORS.
UTERINE TUBERCLE.
IMPERFORATE HYMEN.
VAGINITIS. LEUCORRHŒA.
TUMORS OF THE VAGINA.
PARTURITION FEVER (COLLAPSE). MILK FEVER. PARTURIENT APOPLEXY. CALVING
FEVER. PARTURITION PARESIS.
DISEASES OF THE EYE. DESIRABLE FEATURES IN THE EYE.
DEFECTS, BLEMISHES AND ABNORMALITIES OF THE HORSE’S EYE.
SYSTEMATIC INSPECTION OF THE EYE.
OPHTHALMOSCOPE.
WOUNDS OF THE EYELIDS.
DEFICIENCY OF THE EYELIDS. COLOBOMA PALPEBRARUM.
ORGANIC UNION OF THE EYELIDS. ANKYLOBLEPHARON. NARROWED FISSURE
BETWEEN THE LIDS. BLEPHAROPHYMOSIS.
WIDENED PALPEBRAL FISSURE.
LAGOPHTHALMOS. INABILITY TO CLOSE EYELIDS.
ADHESION OF THE EYELID TO THE BULB. SYMBLEPHARON.
INFLAMMATION OF THE EYELIDS. BLEPHARITIS.
ŒDEMA OF EYELIDS.
EMPHYSEMA OF THE EYELIDS.
DISEASE OF THE MEIBOMIAN GLANDS. BLEPHARADENITIS. SEBORRHŒA.
HORDEOLUM. STYE. ACNE.
CHALAZION.
TUBERCULOSIS OF THE EYELID.
TURNED IN EYELASH. TRICHIASIS.
ENTROPION. TURNING IN OF THE EYELID.
TURNING OUT OF THE EYELID. ECTROPION.
TUMORS OF THE EYELIDS.
FRACTURE OF THE ORBIT.
BRUISES AND WOUNDS OF THE ORBIT.
RETRO-BULBAR ABSCESS.
PERIOSTITIS OF THE ORBIT.
TUMORS OF THE ORBIT.
DISEASE OF THE LACHRYMAL GLAND AND DUCTS. DACRYO-ADENITIS.
OBSTRUCTION OF THE LACHRYMAL PUNCTA. ATRESIA. INFLAMMATION.
WOUND AND FISTULA OF THE LACHRYMAL SAC.
CATARRH OF THE LACHRYMAL SAC. DACRYOCYSTITIS.
STENOSIS OF THE LACHRYMO-NASAL DUCT.
DISEASE OF THE LACHRYMAL CARUNCLE.
WOUNDS AND INFLAMMATION OF THE MEMBRANA NICTITANS.
TUMORS AND HYPERTROPHY OF THE MEMBRANA NICTITANS.
ADENOMA OF THE GLAND OF HARDER.
FOREIGN BODIES IN THE CONJUNCTIVAL SAC.
WOUNDS OF THE CONJUNCTIVA.
BURNS OF THE CONJUNCTIVA.
SIMPLE ACUTE CATARRHAL CONJUNCTIVITIS.
CHRONIC CONJUNCTIVITIS.
PURULENT CONJUNCTIVITIS. BLENNORRHŒA.
INFECTIOUS CONJUNCTIVITIS IN HERBIVORA. ENZOOTIC OPHTHALMIA.
VARIOLOUS CONJUNCTIVITIS.
APHTHOUS CONJUNCTIVITIS. PHLYCTENULAR CONJUNCTIVITIS.
DIPHTHERITIC CONJUNCTIVITIS IN BIRDS.
FOLLICULAR CONJUNCTIVITIS.
NEOPLASMS OF THE CONJUNCTIVA.
PTERYGIUM.
XEROSIS CORNEÆ (EPITHELIALIS). DRY KERATITIS.
WOUNDS OF THE CORNEA.
FOREIGN BODIES IN THE CORNEA.
ACUTE KERATITIS. INFLAMMATION OF THE CORNEA.
POISONING WITH COTTON SEED OR COTTON SEED MEAL.
CHRONIC KERATITIS.
OPACITY OF THE CORNEA. NEBULA. MACULA. LEUCOMA.
ULCER OF THE CORNEA.
CORNEAL STAPHYLOMA.
ECTASIA CORNEÆ. KERATOCONUS. CONICAL CORNEA.
KERATOGLOBUS.
TUMORS OF THE CORNEA.
WOUNDS OF THE SCLERA.
EPISCLERITIS. INFLAMMATION OF THE SCLERA.
ECTASIA (BULGING) OF THE SCLERA.
PROLAPSE OF THE IRIS.
INTERNAL OPHTHALMIA.
SIMPLE IRITIS.
SYMPTOMATIC OR METASTATIC IRITIS.
FOREIGN BODIES IN THE IRIS.
COLOBOMA IRIDIS. CONGENITAL APERTURE IN IRIS.
DOUBLE PUPIL.
ALBINISM. WATCH EYE.
PERSISTENT PUPILLARY MEMBRANE.
OCCLUDED PUPIL.
CYCLITIS.
CYSTS OF THE IRIS AND CORPORA NIGRA.
TUBERCULOSIS OF THE IRIS.
CHOROIDITIS.
DETACHMENT OF THE CHOROID.
RECURRENT OPHTHALMIA OF SOLIPEDS. PERIODIC OPHTHALMIA. MOONBLINDNESS.
PANOPHTHALMITIS.
GLAUCOMA.
EXOPHTHALMOS.
HYDROPHTHALMOS OR BUPHTHALMUS CONGENITUS.
CATARACT. OPACITY OF THE LENS OR ITS CAPSULE.
DISLOCATION OF THE LENS.
PERSISTENT ARTERIA HYALOIDEA.
OPACITY OF THE VITREOUS.
RETINITIS.
DETACHMENT OF THE RETINA.
RETINAL HEMORRHAGE.
TUMORS OF THE RETINA.
INFLAMMATION OF THE OPTIC NERVE. PAPILLITIS.
RETRO-BULBAR OPTIC NEURITIS.
ATROPHY. PARALYSIS OF THE OPTIC NERVE. AMBLYOPIA. AMAUROSIS.
ANOPHTHALMOS. ATROPHY OF THE EYEBALL. PHTHISIS BULBI. MICROPHTHALMOS.
LUXATIO BULBI. DISLOCATION OF THE GLOBE OF THE EYE.
ARTIFICIAL EYE.
STRABISMUS. SQUINTING. LACK OF MUSCULAR BALANCE.
NYSTAGMUS. OSCILLATORY MOVEMENT OF THE EYE.
DISEASES OF THE SKIN.
GENERAL CAUSES OF SKIN DISEASES.
DIAGNOSIS OF SKIN DISEASES.
GENERAL PRINCIPLES OF TREATMENT OF SKIN DISEASES.
ERYTHEMA. ERYTHEMATOUS DERMATITIS.
INTERTRIGO. INTERTRIGO OF CHAFING.
ERYTHEMA CALORICUM
BUCKWHEAT ERYTHEMA
ERYTHEMA FROM IRRITANTS.
DERMATITIS.
ECZEMA. A BOILING OUT. A PUSTULE.
ACUTE ECZEMA IN SOLIPEDS. DORSAL ASPECT.
CHRONIC ECZEMA OF THE HEAD IN SOLIPEDS.
CHRONIC MOIST ECZEMA (IMPETIGO) AT THE MANE AND TAIL.
CHRONIC ECZEMA OF THE CARPUS AND TARSUS; MALANDERS
ECZEMA OF ALIMENTARY ORIGIN IN CATTLE. STARVATION MANGE. STALK
DISEASE. MALT ECZEMA. POTATO ECZEMA.
MOIST ECZEMA OF THE PASTERNS IN THE OX.
MOIST ECZEMA OF THE TAIL, NECK, CHINE AND DEWLAP OF CATTLE.
CHRONIC ECZEMA IN CATTLE.
ECZEMA IN SHEEP.
ECZEMA IN SWINE.
VESICULAR IRRUPTION IN PIGS. PITCHY AFFECTION. SEBORRHŒA.
GRANULAR ERUPTION IN SWINE.
ACUTE ECZEMA OF THE DOG.
OTHER ACUTE ECZEMAS IN DOGS.
CHRONIC ECZEMA IN THE DOG.
LICHEN. HEAT PAPULES. PRICKLY HEAT.
PITYRIASIS
PITYRIASIS IN CATTLE.
PITYRIASIS IN THE DOG AND CAT.
CONTAGIOUS PUSTULAR DERMATITIS IN THE HORSE. ACNE.
PEMPHIGUS IN HORSE, OX, PIG AND DOG.
CRACKED HEELS IN HORSES. SCRATCHES.
SEBORRHŒA OF THE DIGITAL REGION
CUTANEOUS HEMORRHAGE
ULCERATION. GANGRENE. BED SORES.
CUTANEOUS HYPERTROPHY. ELEPHANTIASIS. PACHYDERMIA.
ICHTHYOSIS. FISH-SKIN DISEASE.
FURUNCULUS. BOIL.
HYPERPLASIA OF THE SKIN.
ALOPECIA CONGENITA. CONGENITAL BALDNESS.
ALOPECIA. POST PARTEM. ALOPECIA AREATA.
TRICHORRHEXIS NODOSA. NODULAR SWELLING AND SPLITTING OF HAIR.
CONSTITUTIONAL DISEASES. RHEUMATISM.
SYMPTOMS OF ACUTE ARTICULAR RHEUMATISM IN THE HORSE.
SYMPTOMS OF CHRONIC ARTICULAR RHEUMATISM IN THE HORSE.
SYMPTOMS OF MUSCULAR RHEUMATISM IN HORSES.
SYMPTOMS OF ACUTE ARTICULAR RHEUMATISM IN CATTLE.
SYMPTOMS OF MUSCULAR RHEUMATISM IN CATTLE.
SYMPTOMS OF RHEUMATISM IN SHEEP.
SYMPTOMS OF ARTICULAR RHEUMATISM IN SWINE.
SYMPTOMS OF ARTICULAR RHEUMATISM IN THE DOG.
SYMPTOMS OF MUSCULAR RHEUMATISM IN THE DOG.
PREVENTION AND TREATMENT OF RHEUMATISM.
GOUT. PODAGRA. ARTHRITIS URICA.
SCURVY
GOITRE. BRONCHOCELE. ENLARGEMENT OF THE THYROID.
EXOPHTHALMIC GOITRE.
RACHITIS. RICKETS.
BRAN DISEASE
OSTEO-MALACIA (MALAXOS SOFT)
RAREFYING OSTEITIS. OSTEOPOROSIS. OSTEO-MALACIA OF THE HORSE. BIG
HEAD.
OSTEO-MALACIA IN OTHER ANIMALS.
INDEX.

VETERINARY MEDICINE.

DISEASES OF THE NERVOUS SYSTEM.

Nervous control of bodily functions: affected through disease of nerve
centres or nerve trunks, sensory, motor, vaso-motor, etc. Modes of
impaired nervous function: objective; subjective. Nervous
characteristics in different breeds, individuals, sexes, castrated
animals. Nervous disorder from microbian toxins, narcotics, nervous
stimulants, etc.

All bodily functions are more or less directly controlled by the nervous
system, hence nervous troubles are interwoven with the diseases of all
other organs. Disorder of the nerve centres or nerve trunks affects the
most distant parts over which these preside, or to and from which they
convey nervous impulse. In different cases we see this operating through
the sensory or motor functions, through lack of coördination or of
balance, through modification of the circulation, respiration,
secretion, absorption, nutrition, metabolism, special sensation,
intellection, emotion, etc. These manifestations are less evident or
less diagnostic in the lower animal, because we cannot fully avail of
the subjective symptoms. While the human patient can tell us his
feelings and experience in their regular order and succession, we can
only infer most of these in the animal, through dependent objective
symptoms. In many cases we cannot even infer for lack of these dependent
symptoms.

The practitioner must carefully watch for and accurately observe all
objective symptoms, and seek to rightly interpret them. Among other
things he must note the nervous conformation, organization and
susceptibility; the hereditary nervous characteristics as seen in
breeds, temperament, habit, aptitude to learn, docility, instinct,
intelligence, emotions and affections, and judge the case in the light
of these. Similarly he must take into account the hereditary, racial and
individual irritability, obstinacy, restiveness, vice, alertness,
sluggishness, stupidity, moroseness, and diagnose accordingly.
Congestion, anæmia, coma, paresis, paralysis, may result from the
nervous disorder and offer valuable concurrent testimony to the same.
Allowance must always be made for the _use_ to which the animal has been
put, thus _sexuality_ tells strongly in the horse, bull, boar, or ram
which has been used for breeding and has become relatively indocile and
even dangerous; _food_ tells in the horse that “shows his corn”, and in
the dog fed on flesh; the comparatively untrained English race horse is
far less docile than the one inured to saddle or harness and the horse
fresh from the range, though previously trained, is far less tractable
than the one in steady work. The _sexual products_ are especially liable
to modify the temper, hence the docility of the gelding, and castrated
mare, and the undisturbed life and steady growth and fattening of
castrated animals from cattle to capons.

_The products of certain diseases_ and many _drugs_ derange the
innervation and intellection. Of this we have examples in the hebetude
of the victims of milk sickness and dourine, in the wild delirium of
rabies, in the varied nervous disorders that attend on the use of
narcotics, essential oils, alcohol, chloral, sulphonal, trional,
strychnia, lead, phosphorus, arsenic, etc.

GENERAL SYMPTOMATOLOGY AND DIAGNOSIS.

Motor disorders: paralysis, paresis, hemiplegia, crossed hemiplegia,
spinal hemiplegia, paraplegia, monoplegia, local palsy,
pseudo-paralysis, spasm,—tonic,—clonic, tremor, hemispasm, monospasm,
spasm of eyeball, spasm of head, paraplegic spasm, general
spasms—convulsions, local spasms. Incoördination. Staggering. Reflex
action. Morbid reflex: increased reflex, reflex tonic spasm.

It seems desirable to note specially some of the more prominent morbid
nervous phenomena and conditions, with lesions or other conditions which
cause them, before considering what are usually recognized as special
diseases.

MOTOR DISORDERS.

=Paralysis= (_Akinesis_) is loss of voluntary or involuntary muscular
movement through defective innervation.

=Paresis= is a paralysis which is partial in degree; power of motion is
impaired but not completely lost.

=Hemiplegia= is the loss of voluntary motion in many muscles on one side
of the face or body. In general hemiplegia, the following muscles are
usually excepted: muscles of the tongue, of mastication, of the eye, of
respiration, of the neck and trunk, generally and of the proximal part
of the limbs. The hind limbs are usually most affected, and muscles that
are most exclusively under the control of the will those dominated by
the cortical centres of the brain. When due to a clot on the brain or
degeneration it occurs on the side opposite to that occupied by the
clot, on account of the motor fibres crossing at the anterior pyramids
of the medulla. Hemianæsthesia is a rare attendant and when present is
often on the side opposite to the hemiplegia. Sensory fibres cross in
the spinal cord, and the lesion is probably spinal.

=Crossed Hemiplegia= is motor paralysis of certain cephalic nerves (3d,
7th, 5th, 6th, and 8th,) on the same side with the clot or lesion, and
of the muscles of the trunk on the other side. The cranial nerves
proceed to muscles on the same side as their origin, while filaments
going to the trunk through the spinal cord, cross in the pyramids
(motor), or spinal cord (sensory). In crossed hemiplegia, hemianæsthesia
is common with both forms of paralysis on one side.

=Spinal Hemiplegia= has the face and head sound (except sometimes the
iris), and half the body paralyzed on the side opposite to that on which
the spinal lesion (clot) exists. If anæsthesia exists it is on the side
opposite to the lesion and posterior to it—the sensory filaments
crossing just before leaving the cord.

=Paraplegia= is loss of voluntary power of one transverse half of the
body; usually the posterior, and affects the tail, and has coincident
anæsthesia, being due to a spinal lesion. Anal and vesical sphincters
may or may not be paralyzed according as the lesions implicate their
respective spinal centres or not. If there is neither anæsthesia nor
vesical paralysis the lesion may be cerebral, in the paracentral lobes
of both hemispheres (meso-vertix at the fissure of Rolando).

=Monoplegia= is a circumscribed paralysis, as of one limb, or on one
side of the face, one group of muscles or a single muscle. It may be due
to cerebral, spinal or nervous lesion. _Cerebral monoplegias_ are
distinguished by: 1st, initial spasm; 2nd, absence of anæsthesia; 3d,
persistence of nutrition; 4th, paralysis greatest in the distal portion
of the member.

=Localized Paralysis= is usually due to lesion of a nerve, and is both
motor and sensory. If due to a spinal lesion it usually affects one or
more groups of muscles. In case the lesion is in the nerve, be guided,
in investigating it, by Van der Kolk’s law, that the sensory fibres are
usually distributed in the skin corresponding to the muscles which
receive the motor fibres.

=Pseudo-paralysis= occurs from muscular disease, injury, inflammation or
degeneration and has no appreciable central nor nervous lesion nor
anæsthesia.

=Spasm= (_Hyperkinesis_); abnormal violent muscular contractions with or
without loss of consciousness.

=Tonic= (_tetanic_) =Spasm= is violent and continuous.

=Clonic Spasm= is rapidly intermittent:—Contractions and relaxations.

=Tremor= (_trembling_) consists in small, intermittent, involuntary
contractions.

=Hemispasm= affects the face, or limbs, or both, on one side of the body
and may precede hemiplegia.

=Monospasm= affects one limb, one group of muscles or a single muscle.
It may be due to lesion of the brain, of the spinal cord or of the
nerves. Thus it may imply commencing disease of the motor centres or
tracts.

=Spasms of the Eyeballs= (rolling of globe to one side), and =Spasms of
the Eyeballs and Head=, are important indications of apoplexy. They
imply disorder (commencing irritation) of the cerebral motor areas.
Advanced disease would probably determine hebetude, coma, drowsiness, or
palsy. If epileptiform it turns away from the lesion. If hemiplegic it
turns toward the lesion and away from the paralysis. If lesion of the
pons it turns away from the lesion.

=Paraplegic Spasm= is a tonic spasm, partial in degree, causing stiff,
tetanoid (spastic) walk. In all four extremities there may be mixed
paresis and contraction. This often attends on hemorrhage into the
meninges.

=General Spasms=, convulsions as in Eclampsia, Epilepsy, Chorea,
Tetanus.

=Local Spasms= may be rhythmic or not, in slight cases to be seen only
in the eyelids or superficial muscles as twitching, and occur in
neurasthenia, or in poisoning by strychnia, brucia and other motor nerve
poisons.

=Incoördination= (_Dyskinesis_) is the lack of the harmonious balanced
movement of the various groups of muscles. Coördination of movement is
due to a special mechanism in the spinal cord, and extending forward
through the medulla oblongata, pons, and crura cerebri to the floor of
the third ventricle. In the form of _ataxia_ (lack of power of muscular
control) it is usually the result of degeneration (sclerosis) of the
superior columns of the cord, of the medulla, pons or crura. It may
occur from degeneration or destructive change in the cerebellum, or from
disease or section of the posterior roots of spinal nerves, or finally
from the action of certain narcotic poisons (ptomaines, toxins).

=Staggering= (_titubation_) occurs from lesions of the cerebellum,
medulla or pons; also from alcohol, opium, and other narcotics.

=Reflex Action.= The normal stimulation of different functions, motor,
secretory, circulatory, etc., depends on the nerve centres in the spinal
cord, which are roused into action by a centripetal impulse derived from
a distant part. Thus the balanced contraction of the different muscles
which preserves the equilibrium of the body, depends on the apprehension
by the nerve centres, consciously or subconsciously, of such
contractions (muscular sense), and it is largely under the control of
the will. Here three impulses act coördinately: 1st, the afferent
impulse from the muscle to the nerve centre; 2d, the efferent impulse
from the nerve centre to the muscle; and 3d, the inhibitory or
controlling, voluntary impulse from the sensorium to the nerve centre
involved. In another case, savory odors, sapid flavors and masticatory
movements cause a free secretion from the salivary glands. Again, the
scratching of a dog’s breast causes him to move his hind limb as if he
were himself doing the scratching. Again, the pricking of a limb causes
the prompt, even if involuntary, contraction of its muscles to withdraw
it from the source of irritation.

=Morbid Reflex.= Reflex action may be modified in various ways as the
result of disease or injury. It may become excessive from irritability
of the organ from which the centripetal impulse starts, or of the reflex
centre in the spinal cord, or of the muscle or other organ to which the
centrifugal impulse is directed, or, finally, from impairment of, or
separation from the inhibitory centre in the cerebrum. It may be
impaired or abolished from degeneration or destruction of any of the
tissues just named, or of the conducting nerves which connect them to
each other.

The contraction and closure of the pupil under light is a reflex act
from the retina on the optic lobes, etc., and from these through the
motor oculi to the iris. This reflex is lost and the iris fails to
contract in: anæsthesia of the retina; atrophy of the optic nerve;
disease of the optic lobe; superior (posterior) spinal sclerosis;
disease of the motor oculi; or disease of the iris.

The lumbar reflex is lost in many febrile states in the horse, so that
pinching of the loins fails to produce wincing, and this becomes a test
of the active persistence of the disorder.

=Encreased Reflex= is often noticed when the parts, including the spinal
reflex centre, are disconnected from the brain: as in lesions or disease
of the cord in front (cephalad) of its reflex centre. Here the cerebral
or voluntary inhibition is lost.

=Reflex Tonic Spasm= of muscles around a diseased or dislocated joint,
or of those controlling its action, often affords a valuable means of
diagnosis, the possibility of nervous, muscular and tendinous disease
being excluded.

TROPHIC SYMPTOMS AND DISORDERS.

Degenerative atrophy, in hæmoglobinuria, laryngeal hemiplegia,
neurectomy, nerve lesion, brain or cord lesion, lead poisoning,
disuse. Dermatitis, ulceration, morbid secretion, polyuria,
mellituria, albuminuria, poisonous milk.

=Degenerative Atrophy=. From section, disease, atrophy or degeneration
of nerves or nerve centres, the muscles, which they normally innervate,
waste, often to an extreme degree. As examples of this we see the
atrophy of the triceps extensor cruris and other groups in
hæmoglobinuria, of the intrinsic laryngeal muscles in _roaring_, of the
muscles supplied in neurectomy, and of groups of muscles in myelitis,
broken back, lead paralysis, and scapular muscular atrophy. True to the
law of wasting of physiologically inert organs, the nerves are atrophied
and degenerated, and often also the bones, joints and skin.

The degeneration of an active organ applies to the nervous tissues
themselves. According to the law of Waller, the nerve fibre (axis
cylinder), when cut off from its nutritive centre (cell body with
nucleus) degenerates and ultimately perishes. The axis cylinder is a
component part of the neuron, which includes also its continuation in
the cell and nucleus, and when the latter, which is the source and
origin of both nerve impulse and trophic control, is lost, the inactive
axis of the nerve fibre degenerates. This law is now availed of in
tracing the distribution of nerve filaments, the degeneration being
found in those that have been cut off from their nerve cells while those
that come into the nerve trunk from other sources, distal of the injury,
maintain their integrity.

In addition to this peripheral atrophy, a degeneration central of the
injury to the nerve is seen under certain conditions, but especially in
intrauterine life. In such cases the atrophy may extend up to and
include the central nerve cells, causing a secondary central nervous
lesion from an initial peripheral one.

By bearing these laws of nerve atrophy in mind, lesions that would
otherwise be obscure, may be satisfactorily accounted for.

=Eruptions and Ulcerations of Nervous Origin.= Herpes or shingles in man
is now recognized as a nervous disease, circumscribed to the
distribution of given nerves and occurring unilaterally or bilaterally.
Deep-seated dermatitis, vesicles, neuralgia, pain, itching and
formication are common accompaniments. The whole is traced to disease of
the ganglion on the posterior (superior) root of the spinal nerve
distributed to the part. This establishes a principle, and in
inscrutable and obstinate, circumscribed skin disease the veterinarian
should see if it coincides with the distribution of one or more sensory
spinal nerves.

_Ulcerations_ are often caused by the lack of protection of a part after
paralysis, thus perforation of the cornea will follow section or disease
of the trigeminus. These may be prevented by carefully covering the
part, and even cured by a fine protective covering like collodion.

=Alteration of the Secretions= often follow on section of the
sympathetic trunks, that of the cervical sympathetic in rabbits causing
excessive congestion of the facial skin, with exudation and scabby
product, also profuse secretion of sweat, tears, and ear cerumen and
dry, scaly skin.

=Polyuria= is determined by section of one point of the medulla behind
the root of the vagus, _mellituria_ by puncture between the vagus and
auditory nerves (the hepatic vaso-motor centre), and _albuminuria_ by a
puncture in front of the latter. Impairment of the hepatic vaso-motor
tracts in the spinal cord, or of the anterior or posterior cervical
sympathetic ganglia, or of the first thoracic ganglion equally
determines nervous mellituria.

=Poisonous milk= produced in hard worked mares, or over-excited dams of
other species, causing dyspepsia, diarrhœa, arthritis or other trouble
in the suckling, must be in part attributed to nervous disorder.

Practically all secretions and nutrition are largely under nervous
control, so that modifications in quantity or quality can often be
attributed to nervous influence.

SENSORY SYMPTOMS AND DISORDERS.

Hyperæsthesia, cutaneous, thermic, muscular, visceral. Paræsthesia,
pressure on nerve. Anæsthesia, partial, drug. Analgesia. Hyperalgesia.

These are necessarily much less obvious to the veterinarian than to the
physician of man. Yet in certain cases they may be observed directly,
and in others deduced from dependent symptoms.

=Hyperæsthesia= is a state of exalted excitability of any part of the
sensory nervous apparatus.

=Cutaneous hyperæsthesia= is that condition in which the slightest touch
gives rise to an instant and extreme response. Some nervously organized
mares which are dangerously ticklish and irritable, afford physiological
examples. The surface soreness and sensitiveness which exist in the
febrile chill, in wounds, dermatitis and neuralgia give pathological
examples. It is further seen in certain cases of meningitis (cerebral
and spinal), spinal irritations, rabies, tetanus and neuritis.

=Hyperæsthesia to cold= is seen in neuralgia, rheumatism, the early
stages of many fevers (chill), in myelitis, neuritis, nerve injuries,
and in posterior (superior) spinal sclerosis.

=Hyperæsthesia of the muscles= may be noted in tetanus, muscular
rheumatism and neuralgia.

_Visceral hyperæsthesia_ is shown in many cases of spasms of involuntary
muscles (colic, arrest of intestinal calculi, gall stones or urinary
concretions), and in inflammation of serous membranes (pleurisy,
peritonitis).

=Paræsthesia.= This is a painful or morbid sensation caused by a lesion
in the central nervous structures or in the nerves, but referred by the
sufferer to some peripheral organ over which such centre presides. It
may even be referred to an organ or part that has been amputated or
otherwise removed. This may cause lameness of a kind to indicate
suffering in a given muscle, tendon or joint, when the cause is purely
central. In dourine, sexual acts are excited which have their real
source in the nerve centres. The rabid dog snaps at imaginary flies in
mid-winter, when such insects are only phantoms of his brain.

=Pressure on a nerve trunk= induces sensations of tingling, vibration,
formication, heat, cold, and paresis, referred by the mind to the part
to which that nerve is distributed, and when the pressure is removed
these sensations recede in the order in which they came. This may
explain some occult cases of lameness.

=Itching= may be a pure, persistent neurosis without any skin lesion.
Treatment should then be addressed to the nervous system.

=Anæsthesia=, or absence of sensation, is in its degree partial or
complete. The latter is familiar as occurring in parts the sensory
nerves of which have been cut across, also in parts the sensory nerve or
nerve centres of which have become completely degenerated. There is no
response to the prick of a needle, the touch of a hot wire, to pinching
or cutting. If the nerve remains intact as far as the spinal centres,
reflex action may still occur, but the patient himself has no
consciousness of this nor of the injury causing it. Accordingly, he
makes no movement of head, ears, eyes, or other parts still dominated by
the brain.

In =partial or imperfect anæsthesia= the response to irritation is less
marked and may be even delayed. In some forms of central lesions the
response to a prick may be delayed two, five, or ten seconds, or even
more.

_Anæsthesia_ causes awkwardness or uncertainty of movement, especially
if the subject is blindfolded.

_Anæsthesia_ may be =induced by medicine=, as in the general anæsthesia
of etherisation, or the local anæsthesia caused by the topical
application of cocaine or carbolic acid.

=Analgesia=, or insensibility to pain, may be present in cases in which
ordinary sensations are still felt. It may be caused by cocaine,
alcohol, and to some extent by carbolic acid.

=Hyperalgesia= is the opposite of this condition, and may be seen in
certain irritable conditions of the nerve centres.

PSYCHIC SYMPTOMS AND DISORDERS.

Limitation in lower animals. Effects of age training, race heredity,
individual and racial peculiarities, exhaustion, prostration,
dementia, cerebral congestion, compression, degeneration, narcotics,
ptomaines, toxins. Controlling absorption in another trouble.
Delusions, hallucinations, vice, violence, œstrum, fatigue. Cerebral
source of motions.

These have a much more restricted field in the lower animals than in man
in keeping with the limitation of the mental faculties, and they may
often be traced to demonstrated structural disorder. Yet some emotions
of joy, fear or rage run very high and are comparatively unchecked by
high mental development or mental training. The effect of training is,
however, very marked in the more educated animals.

=Age= modifies by the sobering that comes from experience and habit. The
frolics of puppies, kittens, lambs, foals and calves are in marked
contrast with the sedateness and stolidity of old dogs, cats, sheep or
cattle.

=Training= is seen in the educated horse which would have been panic
stricken at sight of a locomotive, flag or floating paper, at the smell
of a lion or bear, at the sound of a gun or drum, and which will now
boldly face any one of these with no manifest tremor. The emotional
puppy can be trained to soberly fetch and carry, to drive sheep or
cattle without biting, to lie sentinel by his master’s property, to
point at birds without seeking to catch them, or to carry shot birds
without devouring them.

=Race heredity= comes from the training along the same lines in many
successive generations. Thus the more domesticated breeds of dogs
(shepherd, poodle, and greyhound) are very affectionate; other breeds
(bull, mastiff, bloodhound) are lacking in this character. All trained
races take naturally to the occupations of their ancestors. Some
(horses, cattle and sheep) are easily panic-stricken, (stampeded). Some
(turkeys, roosters) are not easily stampeded. Some (skunks), having
effective sources, of defence, have little fear of man.

=Individual and racial mental dullness and torpor= must also be
recognized. Some are stupid and slow, others alert and quickly
responsive. Some horses are not _level-headed_ and become uncontrollable
in difficult situations. Some dogs are so emotional as to endanger their
lives from sudden heart trouble. Some horses, dogs and cats will pine
and die when separated from their fellows or human friends. Extreme
timidity, or sudden rage may be so marked as to constitute a virtual
morbid phenomenon. Sluggish cerebral and mental action may result from
_exhaustion_, _prostration_, or _dementia_; also from _cerebral
congestion_, _pressure_ and _degeneration_; or from _poisoning by
narcotics_, _ptomaines_ or _toxins_ (opium, hyoscyamus, Indian hemp,
dourine, milk sickness, etc.). It may come from profound absorption in
another object, as when the rabid dog bears whipping without a howl.

=Delusions= or =hallucinations= are shown in the rabid dog snapping at
flies, or attacking his friend or master as an enemy, as well as in
other forms of delirium. Narcotics, such as opium, Indian hemp, etc.,
ptomaines, toxins, and (in dogs) essential oils cause delirium by acting
on the nerve centres.

=Vice= in its various forms may become a genuine neurosis, the animal
losing control of its actions.

=Violence= in the form of self-defence or aggression is seen in mares in
_heat_, in bulls or stallions under sexual excitement, in animals roused
by inconsiderate whipping, or in bulls looking on scarlet clothing.

Some high-spirited animals, under extreme fatigue from overwork,
sometimes become violent but resume their docility under rest and food.

In all cases we must know the normal of an individual animal to enable
us to properly appreciate any apparent deviation from the psychic norm.
No less essential is it to take into account the environment and
treatment of the patient.

With regard to localization of cerebral lesions, Sequin thinks emotions
are probably generated in the basal ganglia such as those of the pons
and thalami, while inhibition depends on the anterior cerebral cortical
convolutions.

DIAGNOSIS, SYMPTOMS AND THEIR IMMEDIATE CAUSES. LOCALIZATION OF LESION
IN SPECIAL SYMPTOMS.

Spasm, pain, numbness—irritation. Paresis, paralysis, anæsthesia
(constant)—destructive lesions. Both combined—variable symptoms,
recurrent. Definite, fixed symptoms—structural lesions, usually
progressive. Symptoms, variable as to place, time, subsidence and
recurrence—functional lesions. Brain lesions. Pressure on brain—pain,
spasm, nausea, dullness, blindness, stupor, coma, palsy. Congestion
and anæmia synchronous. Lesions of cortex. Encephalic
lesions—hemiplegia, with spasms, increased reflexes, spasms follow
cranial nerves, vertigo, apoplexy, epilepsy, dementia, coma, little
muscular atrophy, or dermal sloughing. Spinal lesions, paraplegia
without spasm, reflex reduced or nil, follow spinal nerves, head
symptoms less, much muscular atrophy, bed sores. Sensory and motor
tracts, in crus cerebri, respiratory centres—inspiratory expiratory,
inhibition. Salivation, sneezing, coughing, sucking, chewing,
swallowing, vomiting. Cardiac centres, accelerating and inhibitory.
Vaso-motor centre. Spasm centre. Perspiratory centre. Pons. Corpora
quadrigemini, crura cerebri. Thalamus, corpus striatum. Cerebellum.
Cerebral cortex: in ass; in dog. Spinal lesions: lateral half section:
central anteroposterior, vertical section: superior columns: inferior
columns: cervical lateral columns: respiratory tract: glycogenic
centre: pupillary dilator: cardiac accelerator; vaso-motor,
sudoriparous: centre for anal sphincter: for vesical sphincter:
genital centre: vaso-motor and trophic centres: muscular sense tract:
superior column and Goll’s. Table of phenomena from cord lesions.

In =Irritation= of nervous organs the symptoms (spasm, pain, numbness)
are usually _intermittent_.

In =Destructive Lesions= of nervous organs the symptoms (paresis,
paralysis, anæsthesia) are usually _constant_.

When =irritation and destruction= are associated the symptoms are
variable and frequent. The characteristic symptoms of the two may
coexist or succeed each other.

=Structural Nervous Lesions= have symptoms that are definite in their
area of distribution, nature (spasm, paralysis) and permanency.
_Objective Symptoms_ predominate and the case is likely to be
progressive and fatal.

=Functional Nervous Diseases= have symptoms of indefinite distribution,
variable in character, with intermissions and spontaneous disappearances
(as under marked excitement) and subjective symptoms predominate. They
may, however, last for a length of time without change.

Localisation of Brain Lesions.

Lesions of the cranial nerves and their superficial and deep centres of
origin need not here occupy attention. These may be studied in works on
anatomy and physiology. Attention may be drawn rather to the remoter
effects of ganglia which affect or control distant action, and to
general pressure on the encephalon.

=General Pressure on the Encephalon=, whether through fracture of the
cranium and depression of bone, by acute congestion, by blood
extravasation, by inflammatory exudation, or by acute abscess, will
cause pain, spasms, nausea, dullness, blindness, stupor and coma. After
expulsion of the cerebro-spinal fluid from the cranial cavity, the
increasing pressure compresses the blood vessels, reduces or interrupts
the circulation and abolishes the functions in the parts deprived of
blood. Thus congestion of one portion of the encephalon is usually
associated with diminished circulation in another portion. Disorder in
the first may occur from hyperæmia and irritation and in another part
from a consequent anæmia.

=Destructive Lesions of Cortex of One Cerebral Hemisphere= may or may
not cause permanent symptoms, as shown by the passage of a crowbar
through the front of the left hemisphere, yet the man survived for 13
years and showed no loss of intelligence, his disposition and character
alone having changed for the worse. The one hemisphere may by itself
sufficiently control mental acts, while the other lies dormant or may
even have undergone degeneration.

=Diagnosis of Encephalic and Spinal Lesions.= The following may be taken
as guiding principles:

=Encephalic=: Hemiplegic or bilaterally hemiplegic grouping of symptoms.

=Spinal=: Paraplegic grouping of symptoms.

=Encephalic=: Frequent contracture or spasms of paretic muscles.

=Spinal=: Paralysis more perfect and continuous.

=Encephalic=: Reflexes in affected muscles increased: Cerebral
inhibition absent.

=Spinal=: Reflex abolished or reduced in parts the seat of the lesion.

=Encephalic=: Spasms in areas of distribution of cranial nerves (not
spinal.)

=Spinal=: Spasms and paralysis follow distribution of spinal nerves.

=Encephalic=: Head symptoms frequent (vertigo, apoplexy, epilepsy,
dementia, coma).

=Spinal=: Relative absence of head symptoms.

=Encephalic=: Comparative absence of marked muscle atrophy.

=Spinal=: Atrophy in special muscular groups.

=Encephalic=: Little tendency to form bed sores.

=Spinal=: Tendency to form sloughs and bed sores.

Sensory (Æsthesodic) and Motor (Kinesodic) Tracts in Encephalon.

In the crus and above, the sensory tract lies dorso-laterad of the motor
tract, forming about one-fifth of the crus, and extending upward through
a white layer bending inward to form an angle and finally diverging to
the different cortical convolutions. The motor tract is mainly contained
in the inferior pyramids of the bulb, and constitutes the median two
fifths and basal two fifths of the crus. Without entering farther into
this subject it will be observed that lesions of the outer layer of the
crus and its radiating fibres may cause hemianæsthesia of body or head,
including the eye, while lesions of the median and basal layers and
radiating fibres induce hemiplegia of the head, tongue, fore limb, hind
limb, trunk, etc.

=Respiratory Centres, Inspiratory and Expiratory= are in the floor of
the fourth ventricle between the centres for the vagus and accessory
nerves, and are directly stimulated by the CO_{2} in the blood.
Secondary subsidiary centres are in the optic thalamus, in the corpora
quadrigemini both anterior and posterior pairs, and finally in the
cervical spinal cord, so that disorder of respiration may occur from
lesions in these points as well as in the main oblongata centre.

=Respiratory Inhibition= and arrest depend on the vagus, the superior
and inferior laryngeal nerves.

=The Salivation Centre= also lies in the floor of the fourth ventricle
and stimulation of the medulla causes free secretion.

=The Centres for Sneezing, Coughing, Sucking, Chewing, Swallowing and
Vomiting= are also seated in the oblongata, so that any one of these
phenomena may come from a central irritation. In _bulbar paralysis_ the
loss of power usually extends from the tongue through the lips, cheeks,
jaws, pharynx, larynx, to the respiratory muscles and heart. Coughing
may be roused by irritation of the external auditory meatus, liver,
stomach, bowels, or generative organs as well as from the air passages.

=Cardiac Accelerating and Inhibiting Centres= are both present in the
bulb, the latter receiving its afferent impulse mainly through the vagus
nerve. Stimulation of the vagi, anæmia of the bulb through decapitation
or through tying both carotids, hyperæmia through tying of the jugulars,
a venous state of the blood, and blows on the abdomen all slow or arrest
the heart action. Digitalis or muscarin has a similar effect. The heart
action is accelerated by febrile and inflammatory affections, by a high
or low temperature by section of the vagi, by sipping of cold water, by
atropine or curari, and by salts of soda. Potash salts on the other hand
restore the inhibitory action of the vagi and lower the heart’s action.

=The Vaso-Motor Center= is also in the oblongata and the contraction of
the vessels with increase of arterial pressure may ensue from afferent
currents in the sympathetic nerve and many sensory trunks. The varying
activity is seen in blushing, in the congestion of mucous membranes
under rage or excitement, in the capillary contraction in the early
stage of inflammation, in the second stage of capillary dilation, in
angioma or nævus and in extensive congestions and hæmorrhages in
different organs. The arrest of bleeding under fainting is due largely
to the anæmia of this centre.

=A Spasm Centre= the pricking of which causes general convulsions lies
in the medulla oblongata at its junction with the pons. This is excited
by excess of carbon dioxide in the blood, by suffocation, drowning, by
anæmia of the bulb from bleeding or ligature of the carotids, by venous
congestion after ligature of the jugulars, or by the direct application
to the part of ammonia carbonate, or salts of potash or soda. It may
also be roused by afferent nervous currents from different peripheral
parts (spinal cord, sciatic nerve, etc.).

=A Perspiratory Centre= is found in the medulla, on each side, which may
be roused into action by diaphoretics (opium, ipecacuan, tartar emetic,
Calabar bean, nicotin, picrotoxin, camphor, pilocarpin, ammonia acetate,
etc.).

=The Pons= like the medulla is at once a ganglionic and conducting
organ, and its lesions may lead to arrest of nerve currents generated
above or below it, or to the failure to develop currents in its own
centres. Stimulation of its superficial layers may be without effect,
but if this is carried into the centre epileptiform convulsions ensue.
Lesions of one side of its posterior half cause facial paralysis on the
same side and motor and sensory paralysis on the opposite side of the
body (crossed hemiplegia). Lesions of one side of its anterior half
cause paralysis in both face and body on the same side. This depends on
the crossing of the fibres midway back in the pons, which cross again in
the medulla (motor fibres) and in the spinal cord (sensory fibres).
Lesions of the pons are liable to interfere with the functions of the
trigemini, the oculo motor and the superior oblique, and to determine
epileptic movements and loss of coördination of sensorio-motor
movements. Lesions of the superficial transverse fibres (median
cerebellar peduncles) tend to cause involuntary movements to one side.

=Lesions of the Corpora Quadrigemina= cause disturbance of vision,
failure of the pupil to contract to light, blindness, paralysis of the
oculo-motor nerves, and lack of coördination of movements. Stimulation
of one anterior corpus causes rolling of both eyes to the opposite side,
with, if continued, a similar movement of the head and even of the body
(horse in mill, or index motion, or rolling on its axis).

=The Crura Cerebri= are conducting bodies but contain also different
nerve centres. Lesions of one crus cause violent pain and spasm on the
opposite side of the body, followed by paralysis. The oculo motor may be
paralyzed on the same side, but the face and tongue on the opposite
side, owing to the fibres crossing in the pons. There may be turning
movements.

=The Optic Thalamus= transmits sensory currents to the cerebral cortex.
Lesions in this organ cause sensory paralysis on the opposite side of
the body. Afferent currents that do not traverse the thalamus cause
reflexes only. It contains one of the roots of the optic nerve and its
destruction will impair vision. Its injuries may also produce turning
movements.

=The Corpus Striatum= transmits motor currents originating in the
cerebral cortex. Lesions of its interior (lenticular nucleus) cause
motor paralysis and sometimes anæsthesia on the opposite side of the
body. Electrical stimulation of this nucleus causes general muscular
contractions of the opposite side of the body. Irritation of the surface
layers is painless and symptomless.

=The Cerebellum= has been long credited with coördination, and Flourens,
after its removal from a pigeon, found an utter lack of harmonized
movement in walking, springing or balancing. Luciani removed the organ
from a bitch and, after full healing of the part, found a lack of
muscular tone (a cerebellar ataxy), so that no great muscular effort
could be satisfactorily accomplished. After months, marasmus set in and
proved fatal. The lack of coördination is especially connected with
lesions of the vermiform process, those of the posterior portion causing
falling forward and those of the anterior portion, falling backward.
Injury to the middle peduncle on one side causes turning or rolling to
the opposite side. Under slighter injuries there may be only
unsteadiness and staggering like a drunken man. Nausea and vomiting,
with more or less stiffness of the neck or oposthotonos, may be present.
Rolling of the eyes or squinting may occur.

=Focal Cortical Centers of the Cerebrum. Cortical Localization.= Much
has been done experimentally and by observation of morbid lesions to
locate functions in the different convolutions, and though the
subsidiary implication of adjacent and interdependent parts interferes
with a perfectly confident diagnosis, yet certain fundamental facts may
be borne in mind as contributing to a satisfactory diagnosis.

Arloing, on the basis of his own experiments and those of his
predecessors, gives the following as applicable to the equine (ass)
brain:

1. Stimulation of the origin of the front part of the first frontal
convolution, or of the anterior part of the pre-Sylvian convolution,
causes approximation of the feet on the opposite side of the body.

2. Stimulation of the superior part of the first frontal convolution or
of the superior part of the post-Rolandic convolution causes closure of
the jaws and diduction.

3. Stimulation of the anterior end of the upper orbital convolution, or
of the anterior part of the pre-Rolandic convolution, leads to movements
of the nose and upper lip.

4. Stimulation of the antero-superior part of the lower frontal
convolution, or the union of the post-Rolandic with the Sylvian
convolution causes movement of tongue and jaws.

5. Stimulation of the union of the vertical and horizontal parts of the
orbital convolution or frontal lobe, causes opening of the jaws and
bending of head and neck.

6. Stimulation in the front of the union of the frontal and longitudinal
convolutions, or at the union of the Sylvian and second parietal
convolution causes rolling of the opposite eye.

7. Stimulation of union of the frontal and parietal parts of second
parietal convolution leads to closure of both eyelids or, with a strong
current, of lids on both sides.

8. Stimulation of the second parietal convolution, above and a little
behind the extremity of the Sylvian fissure, causes opening of the eye
and adduction of the ear on the opposite side, or, if a very strong
current, on both sides.

9. Strong stimulation of the posterior part of the first and second
parietal convolutions causes tonic convulsions.

10. Currents through the posterior parts of the third and fourth
parietal convolutions gives similar convulsions with violent trembling
of the trunk and members.

In the =Dog’s Brain= localization is easily made by reference to the
crucial fissure which passes outward, right and left, at right angles
with the longitudinal fissure about the junction of its anterior with
its middle third. Also by four parietal convolutions which run backward
from near the crucial fissure, parallel with the longitudinal fissure.
They are counted from without inward. Fritsch, Hitzig and Ferrier have
mapped out the following motor areas:

1. The convolution in front of the outer end of the crucial sulcus
controls the muscles of the neck.

2. The bend of the same convolution backward, opposite the outer
extremity of the crucial sulcus, controls the extensors and adductors of
the fore limb.

3. The convolution just behind the outer end of the crucial sulcus
controls the muscles which flex and rotate the fore limb.

4. The same convolution behind the middle of the crucial fissure
controls the movements of the hind limb.

5. The second convolution back of the crucial fissure controls the
muscles of the face.

6. The anterior part of the internal (4th) parietal convolution, just
back of the crucial fissure, controls the lateral switching movements of
the tail.

7. The posterior angle of the first post-crucial convolution causes
retraction and abduction of the fore limb.

8. The outer end of the first post-crucial convolution, directly behind
the outer end of the sulcus, causes raising of the shoulder and
extension of the fore limb.

9. The anterior end of the third parietal convolution (the second from
the longitudinal fissure) controls closure of the eyelids, the rolling
of the eyeball upward, and narrowing of the pupil.

10. Stimulation of the anterior end of the second parietal convolution
causes partial opening of the mouth with retraction and elevation of its
angle.

11. Stimulation of the point of union of the first and second parietal
convolutions anteriorly causes opening of the mouth with protrusion and
retraction of the tongue.

12. Stimulation of the median part of the second parietal convolution,
causes retraction and elevation of the angle of the mouth.

13. Stimulation of the convolution directly in front of the outer end of
the crucial sulcus causes dilatation of the eyelids and pupil while the
eyes and head are turned toward the opposite side.

14. Stimulation of the convolution behind the crucial fissure causes
contraction of the muscles of the perineum.

15. Stimulation of the convolution in front of the crucial fissure, on
its anterior and sloping portion, causes movements of the pharynx and
larynx (swallowing).

16. Stimulation of motor areas of the cortex, by scraping, irritation,
or disease tends to produce spasmodic contractions of certain groups of
muscles (Jacksonian Epilepsy). Strong stimulation may cause general
epileptiform spasms, which are at first tonic, then clonic. One such
seizure strongly predisposes to a second. If, during an attack, the
cortical centres presiding over a special group of muscles were sliced
off, such muscles relaxed, though the general spasms in the other
muscles continued.

Localizations of Spinal Lesions.

Being at once a conductor between the brain and nerves, and a reflex
nerve centre, we must consider both rôles in seeking to locate lesions
from symptoms. In passing from the nerves to and from the sensorium both
sensory and motor currents cross so that one side of the brain presides
over the other side of trunk and limbs. This crossing of the motor
fibres takes place in the medulla oblongata, while that of the sensory
fibres occurs in the spinal cord close in front of the nerve from which
they have entered.

=Cross-Section of one lateral half of the spinal cord= therefore causes
motor paralysis and rise of temperature of the whole of that side of the
body posterior to the lesion, while it induces sensory paralysis and
cooling on the opposite side of the body up to the same point. A very
limited sensory paralysis on the same side occurs corresponding to the
few sensory fibres passing outward obliquely through the portion injured
by the cross-section.

=A vertical section of the cord separating the one lateral half from the
other= does not necessarily affect the motor currents, while it produces
a limited anæsthesia on each side in the area of distribution of the
nerves, the sensory fibres of which crossed in the seat of the lesion.

=Transverse section of the superior columns= causes hyperæsthesia and
lack of coördination.

=Transverse section of inferior columns=, or of the inferior horn of
gray matter, if close behind the medulla, causes no motor paralysis, but
if farther back induces motor paralysis on the same side of the body.

=Transverse section of the cervical lateral columns= causes motor
paralysis of the lateral walls of the chest (respiratory tract). If the
section is made in the dorsal or lumbar region it is the same as lesion
of the superior columns.

Among =reflex centres= in the cord the following may be named:

The =Respiratory Tract= in the cervical lateral columns just referred
to.

A =Glycogenic Centre= in the anterior cervical section between the bulb
and the fourth cervical nerve.

=Centres which Dilate the Pupil= between the fifth cervical and the
sixth dorsal nerve.

=Cardiac Accelerator Centres= between the three last cervical and the
five first dorsal nerves.

=Vaso-Motor Sudoriparous Centres= in the central gray matter.

=Centre for Anal Sphincter= between the sixth and seventh dorsal nerves.

=Centre for Vesical Sphincter= between the third and fifth lumbar
nerves.

=Genital Centre=, opposite the first lumbar nerve.

=Vaso-motor and Trophic Centres= are found in the inferior horns of gray
matter, and their degeneration causes progressive muscular atrophy.

The =Muscular Sense Tract= is located near the surface of the superior
columns, so that a certain amount of incoördination and unsteadiness of
progression follows its destruction.

The =Deeper Part of the Superior Columns= and the =Column of Goll= which
bounds the superior median fissure control muscular sense and
coördination, and their disease (posterior lateral sclerosis) entails
locomotor ataxy.

TABLE SHOWING PROMINENT PHENOMENA FROM LESIONS OF THE CORD.

─────────────────┬─────────────────────────────────────────────────────
│ LESIONS IN
─────────────────┼─────────────────┬─────────────────┬─────────────────
„ │Cervical Region. │ Dorsal Region. │ Lumbar Region.
─────────────────┼─────────────────┼─────────────────┼─────────────────
Paralysis in │Neck muscles; │Dorsal, abdominal│Paraplegia.
│ diaphragm; │ and intercostal│
│ trunk; limbs. │ muscles. │
│ │ Paraplegia. │
Sensation │Local │Hyperæsthesia in │Hyperæsthesia in
│ hyperæsthesia │ lower part of │ zone around
│ in fore limbs. │ abdominal wall.│ loins;
│ Anæsthesia in │ │ anæsthesia in
│ rest of limbs │ │ hind limbs.
│ and trunk. │ │
Atrophy │Rare in neck; │Slight in muscles│In hind limbs.
│ common in fore │ behind lesion. │
│ legs. │ │
Electric reaction│Lessened in │Lessened in │Lessened in
│ atrophied │ dorsal and │ atrophied
│ muscles. │ abdominal │ muscles; in
│ │ muscles: │ ratio.
│ │ slightly in │
│ │ wasted leg. │
Bladder │Retention or │Same as cervical.│Incontinence from
│ intermittent │ │ palsy of
│ incontinence │ │ sphincter.
│ reflex, or │ │
│ (later) from │ │
│ overflow. │ │
│ Cystitis │ │
│ common. │ │
Bowels │Involuntary │Same as cervical.│Paralysis of
│ evacuation │ │ sphincter with
│ (reflex spasm) │ │ incontinence;
│ or │ │ costiveness.
│ constipation. │ │
Superficial │Temporary loss; │Same as cervical.│Lost.
reflex │ then rapid │ │
│ increase. │ │
Deep reflex │Temporary loss; │Same as cervical.│Lost.
│ then slow │ │
│ increase. │ │
Priapism │Often present. │Often present. │Absent.
─────────────────┴─────────────────┴─────────────────┴─────────────────

HALLUCINATIONS.

Subjective cerebral impressions projected as real. Rabies. Toxins.
Poisons. Essential oils. Chloroform.

Hallucinations are subjective impressions which the animal supposes to
be real. The disorders in his brain are projected outward and become to
him real objects and occurrences.

They may arise from the presence and proliferation of microbes in the
brain as in rabies in animals. They may proceed from poisoning of the
brain by toxins as in anthrax.

They may be developed, in dogs especially, by the action of certain
essential oils on the cerebral cortex. The first two classes will be
considered with those special diseases. The mental disorders from drugs
have been studied experimentally by Cadeac and Mennier, and may be
noticed in this place.

Lavender, fennel and angelica produce in the dog a condition of extreme
terror, and overcome all disposition to exercise self-defense.

Mints and origanum induce hallucinations of odor. The dog seeks around
with head and nose elevated, sniffs the air, moves cautiously, fixes his
eye on some phantom object, and starts to hunt imaginary game. The love
of catmint seems to amount to a mania in the feline animal.

Kidney vetch evidently causes a sensation of itching or formication; the
dog bites the hair of the tail, the hind limbs or the flank as if to
destroy fleas or other vermin.

Dogs under chloroform have sought to hunt, and stallions under ether
have shown generative excitement with erection of the penis and
movements of coition.

TIMIDITY. PANIC. STAMPEDE.

Timidity. Panic. Timid driver. Impaired vision. Nervous. Irritability.
Gadding. Gregarious habit. Absence of natural weapons. Treatment.
Habit. Substitution. Absolute constraint. Kindness. Boldness. Work.
Moderate diet.

An animal is naturally nervous, and by habit has become timid until it
is virtually impossible to utilize it. In a body of animals, fear is
quickly transferred from one to the other until all join in a wild panic
or stampede. This is common in range cattle or horses, but is found in
army horses as well, and a whole regiment will sometimes refuse to
longer face the enemy and flee in spite of every effort of the rider. On
a smaller scale, two timid horses in a team, scared by some unusual
sight, add each to the sense of fear of the other, as they try to
escape, until they gallop blindly into any danger. This sense of terror
is often fostered by the timid rider or driver, every feeling of
apprehension conveyed through the trembling or uncertain hand, or the
voice which has lost the element of confidence, tending to undermine the
last vestige of trust on the part of the horse. Imperfect sight is one
cause of panic, as the perception of common objects in distorted form or
unwonted situations strikes terror to the timid animal, causing shying
or bolting. Better absolute blindness than such imperfect vision.

A constitutional timidity tends constantly to increase unless the animal
is judiciously accustomed to the object of terror. The horse once
scared, seems to become more and more watchful for other objects of
dread, and even inclined to bolt from such as are common and of every
day occurrence.

Cattle and sheep attacked by the gadfly (œstrus) flee in great terror,
and this dread is communicated from animal to animal so that the whole
herd or flock is suddenly panic-stricken. The bellow of the ox attacked
and the erection of its tail is the signal for every other within reach
to join the stampede.

These panics are associated with the instinct of these races toward a
gregarious life; they mass together for protection and they learn to
heed the slightest indication of approaching danger. This instinct grows
more powerful by constant exercise, and is most marked in those genera
which have the least natural means of protection. Hence, of all animals
sheep are most easily panic-stricken, and once affected, they move in
mass, one following its fellow, without object, without definite
direction or destination, and without consideration of the other dangers
they are to meet. Hence, if one sheep jumps over the parapet of a bridge
to certain destruction, the whole flock speedily follows. If one leaps
over a fallen tree into a snow bank, all at once follow suit and pile
above each other in one suffocating, perishing mass.

While this condition is hereditary in gregarious families, it is
essentially a psychosis in those animals that have been often scared
until they are continually on the watch for objects of fear.

_Treatment._ In the case of horses, the best course is to make the
animal familiar with the object of dread; let him look at it, approach
it slowly, smell it, feel it with his lips. Never turn away his eyes
from it and drive him off, as that confirms the impression of dread, and
the object retains ever after its dreaded appearance. In this way timid
colts become gradually fearless of umbrellas, city sights, street cars,
large vans, flags, music, locomotives and the like,—they become, in the
expressive language of the horseman, _road-wise_. A paddock or yard
beside a railroad will soon accustom a timid horse to the cars, and so
with other things, experience will remove apprehension.

A more speedy removal of the habit of dread may often be secured by the
principle of substitution. The mind of the animal does not readily
attend to more than one matter at a time; if, therefore, we can distract
the attention in another direction, the object of fear may be virtually
ignored until the eye has become habituated to it, and it will be
recognized as harmless. Thus it is that a twitch on the upper or lower
lip, a binding of the chin in upon the breast by a Yankee bridle may
make the horse temporarily heedless of the object of terror. So also in
the bolting horse, the obstruction of the breath by a cord with a
running noose around the neck, or the sending of an electric current
through wire reins and bit will promptly check him in his wild career.

The result is still better when the animal is made to feel his utter
helplessness in the hands of man and the futility of any attempt to
escape. On this are based the method of Rarey and of his various
successors. With fore limbs strapped up, the animal soon exhausts
himself in his efforts to disengage them and escape, and lies down
completely reconciled to his fate. He may now be accustomed to his
objects of terror—the opening and closing of an umbrella, or the waving
of a flag over his head, the discharge of a gun close to his ear, the
passing of car or locomotive, or any other object of his dread. When
allowed to get up he will usually pay no further attention to these
things, especially if patted and spoken to encouragingly, and perhaps
fed apple or sugar, or something of which he is fond. As far as is
consistent with the thoroughness of the subjection, the animal should be
treated throughout with the greatest kindness, so as to retain and even
increase his trust in man and sense of dependence, while at the same
time he is strongly impressed with the futility of resistance to his
will. After the animal has been thus taught to bear with equanimity his
former objects of terror, he should not be at once allowed to forget
them, but by daily experience he should be confirmed in the conviction
that they are harmless, and may be met with safety. This should be
carried out, if possible, in the hands of the bold and kind operator who
has trained him, as, if returned to a timid driver or rider, he may be
easily led back into his former habits of blind terror. A similar and
even easier resort is the process of turning as given under balking.

Constant hard work, for a time, is an excellent form of accessory
treatment, as the plethora developed by overfeeding and temporary
idleness begets an irritability and impatience of control which is quite
likely to beguile him into his old habits.

In case of runaway, beside the electric and asphyxiating treatment
already referred to, the animal may be blinded and quickly brought to a
standstill. Movable blinds may be used which habitually stand well out
from the eyes, but which may be instantly drawn closely over them by the
simple pulling of a cord. The sudden darkness and the impossibility of
directing his course, brings an instant realization of the existence of
other dangers beside the original bugbear.

BALKING. RESTIVENESS.

Definition. Common in ass and mule. Causes: low condition;
overloading; nervousness; sluggish nature; irritable driver; shoulder
sores; poor collar; hard bit; sharp or sore maxilla; sores in angle of
mouth; mares; racial tendency; going from stable; a psychosis.
Symptoms: stands stock still; plunges, but won’t draw; will stamp,
bite, kick, rear, buck, crowd on wall; lie down. Breach of warranty:
sound price; willfulness; balking of raw horse; diagnosis from nervous
disorders; sores, etc. Time in which returnable. Treatment:
preventive; curative; distract attention; cord on ear; whiff of
ammonia or capsicum; closing nostrils; blindfolding; tying up the fore
leg; stroking nose, eyes or ears; tapping flexors of metacarpus; move
in circle with head tied to tail; coax to go.

In general terms this has been defined as a refusal to obey. Usually in
solipeds it is a refusal to move as directed with a load, under the
saddle, or in hand. Though essentially a vice, it may become such a
fixed habit that it appears to dominate the will of the animal and may
thus be called a psychosis—a mental infirmity.

It is much more common in asses and mules than in horses, in keeping
with their more obstinate disposition and too often harsher treatment.

There may be simple refusal to pull. This often comes from overloading,
and especially when the animal has been sick or idle, and comes back to
work with soft flabby muscles unequal to any violent exertion. After one
or two ineffective efforts he sets himself back in the harness refusing
to try again and the vice is started. Ordinary loads on bad roads full
of holes from which it is impossible to drag the wheels have a similar
effect. The danger is greater if the animal is naturally of a nervous or
impatient disposition, and if he makes a desperate plunge forward and
fails at once to move the load. Such a horse hitched with a slow steady
mate is liable to have expended his effort before the latter has had
time to join him in the pull, and it becomes impossible to move the load
because the two cannot be started simultaneously. The conditions are
aggravated if the driver is irritable and by voice and acts further
excites the already too excitable animal.

Lesions of various kinds, such as shoulder bruises, abscesses, abrasions
and callouses, saddle bruises, callouses, abscesses or fistulæ cause
acute pain whenever the effort is made, and render the animal more
impatient and indisposed to try again.

Too small a collar or one that fits badly (too narrow, uneven) has often
a similar effect.

Among other causes may be named a hard bit harshly used, a sharp edge of
the lower jaw bone where the bit rests in the interdental space, sores
of the buccal mucous membrane in this situation, and caries or necrosis
of the superficial layer of the bone. Also chaps, ulcers, or cancroid of
the angle of the mouth.

Young horses, that are as yet imperfectly trained, are more readily
driven to balk than old trained animals.

Mares are more subject to the vice than geldings, by reason apparently
of a more nervous disposition, but much more because of the excitement
to which they are subjected, under the periodic returns of _heat_.

Pench speaks of rare hereditary cases in which the habit is
uncontrollable and the animal incurable.

Friedberger and Fröhner accuse chestnut and sorrel horses as being
especially liable to balk.

However started the continued exercise of the act fixes it as an
incurable habit a virtual psychosis. Yet the inclination of the animal,
his likes and dislikes to a certain extent control its manifestations,
thus a horse rarely balks in going home, and shows it mostly in going in
the opposite direction, and above all on a new or unknown road.

The _Symptoms_ vary greatly in different cases. One animal stands stock
still propping his legs outward and absolutely refusing to budge. This
may occur even in the stall when it is attempted to take the animal out.
When on the road he is usually willing to turn and go back, but no
persuasion by voice or whip can force him forward.

Other horses make ineffective plunges forward but never throw weight
enough into the collar to overcome any resistance.

Still others stamp, bite, throw themselves to one side rather than
forward, rear up, strike with the fore feet, and if whipped kick with
the hind. Some will throw themselves down and struggle in this
condition.

Under the saddle the animal may crowd against a wall, rear, kick, buck
or even throw himself down in his efforts to dislodge the rider. These
violent manifestations however rather belong to vice than mere balking.
Trembling, perspiration, frequent rejection of urine, and general
acceleration of pulse and breathing may manifest a severe nervous
disorder.

_Diagnosis._ It is often important to pronounce upon the exact nature of
this trouble so as to determine whether the seller is responsible for a
breach of warranty given or implied. As regards implied warranty a
_sound price_ for an animal sold to do a given kind of work implies a
mutual understanding that the animal is not physically or psychically
incapacitated for such work.

The balking horse is one that obstinately refuses to perform a piece of
work for which his physical condition seems to be well adapted. The
_willfulness_ of the refusal is the important feature. In case of such a
serious drawback to the value of a horse, the presumption of fraud on
the part of the seller is unavoidable, in case he failed to mention the
habit to the purchaser, but of course this is even more emphatically
certified if he has warranted the animal as a _good worker_, or _kind_,
or _true in work_.

On the other hand he cannot be held responsible for the failure to
perform an act in case the horse has been overloaded when fat or out of
condition, or if he has sores on back, withers or shoulders, a badly
fitting collar, a severe or large clumsy bit, or sores on the lower jaw,
or indeed any temporary physical infirmity, to which the balking can be
fairly attributed.

Balking is not to be confounded with nervous affections (paretic,
spasmodic, congestion) in which the failure to obey is not due to lack
of will, but to lack of power. Nor must it be confounded with the
inability of the paralysis of lead poisoning. It is perhaps most likely
to be confounded with that lack of both sensory and motor power which
attends on ventricular dropsy and other chronic affections of the brain.
In such cases (immobility, coma) the habitual dullness, drowsiness,
general hebetude, and lack of energy contrasts strongly, with the
strength, vigor and general life of the animal which suddenly, willfully
and incorrigibly balks.

The balky horse which has no such nervous disorder as an excuse, no
badly fitting harness, no lesion on shoulder, back, limbs nor mouth, no
unsuitable bit, no special softness nor poverty of condition, no slow,
ill-adjusted mate, no impatient driver, and no excessive load, nor
impassable road, but which jibs without excuse, as a willful
disobedience, may well be cause for annulling a sale. In most European
countries such a horse can be returned to the seller and the sale set
aside within 3 days (Austria), 4 days (Prussia), 5 days (Saxony), 9 days
(Hesse).

_Treatment_. This should be preventive by avoiding the various causes
above enumerated, for if the habit is once contracted it is too often
impossible to establish a permanent cure. The horse is largely a bundle
of habits and the first act of disobedience has given a bias to the
nerve cells of the cortex cerebri which like a planted seed tends to
reproduce itself whenever an opportunity offers. With every successive
act of the kind, the impression on the nerve cells becomes deeper and
more indelible and the habit fixed the more firmly.

In slight recent cases in the milder dispositions the vice may be
overcome by some resort which engages and engrosses the animal’s
attention. Among these may be named tying a cord round the root of the
ear and tying it down; giving an inhalation of ammonia or a sniff of
powdered capsicum; closing the nostrils until the horse struggles to
breathe; blindfolding for a few minutes; tying up one fore leg until
thoroughly tired; even stroking the nose or ears until the fret is
overcome. Immediately following on any one of these methods, move the
horse gently to the right and left and call him confidently to _get up_.
Some will start if gently tapped with the toe below the knee until the
foot is lifted and repeating this a few times in succession, then, after
a few steps, reward with an apple, sugar or piece of bread, and don’t
push too far at a time but repeat the lesson often. If among the first
exhibitions of the vice it may be met by occupying the time in a
make-believe fixing of the harness until the animal ceases to fret, then
standing by his head, tap him on the croup with a whip and call him to
go on. Or he may first be moved to the right and left and then ordered
to move. A rather wearisome treatment is to place in the stall with a
man behind him who taps him on the rump every few minutes, preventing
composure, rest, or sleep, and keeping this up without interval for
twenty-four hours or even double that time if necessary. If he goes well
when hitched, he is driven but if he balks, he is returned to the stall
and the treatment continued.

Magner, who mentions all these methods, reserves his highest
commendation for the method of tying the horse’s head round to his tail
and letting him turn in a circle until he is giddy and falls over. Some
stubborn cases get habituated to turning in one direction and continue
obdurate until the head and tail are tied around on the other side and
the rotatory motion reversed. When thoroughly dazed by this treatment,
the animal is hitched up and will usually move on. If there is still an
indisposition, stand by his head and tap the croup with a whip, calling
on him to start. Or subject him to further rotatory treatment.

DELIRIUM.

A phenomenon in different morbid states; cerebral hyperæmia, anæmia,
congestion, inflammation, intoxication, toxin poisoning. Symptoms:
horse, ox, sheep, swine, dog. Treatment: adapted to primary disease
present, narcotic, poison, and to degree of violence. Anæsthetics,
soporifics, cerebral sedations, cold to head, eliminants, depletion or
tonics and nutritious food.

Delirium or derangement of emotional or mental functions is usually the
result of organic disease of the brain and especially of the cortical
gray matter of the cerebrum. It is seen in hyperæmia, anæmia, faults of
nutrition, intoxications and variations of temperature. The derangements
of circulation may be in the meninges or in the nervous substance. The
intoxications may be with mineral (lead, mercury), vegetable (opium,
Indian hemp, belladonna, hyoscyamus, stramonium, strychnia), or other
poisons, including the toxic products of microbes (as in pneumonia,
scalma, rabies, influenza, Rinderpest, milk sickness, Texas fever,
etc.).

_Symptoms._ These are usually an extraordinary and disorderly nervous
excitement. =Horses= take expectant or ready positions of the limbs,
plunge with feet in rack or manger, rear, turn, kick, bite, spring
violently, neigh, and push or knock the head against the wall. =Cattle=
bellow in a loud or frightened manner, attempt to kick and gore, grind
the teeth and make movements of the jaws, froth at the mouth, dash
themselves in any direction heedless of obstacles, push the head against
the wall breaking teeth or horns, and moving heedlessly against fences,
or trees, or into water or pits even to their own destruction. =Sheep=
stamp the feet, butt, bleat, work the jaws, grind the teeth, leap, and
move in a given direction regardless of obstacles. =Pigs= grunt,
tremble, champ the jaws, run against obstacles, scratch the ground with
their feet or snout and creep under the litter. They may even attempt to
bite. =Dogs= are restless, whine, move in a circle, snap at straw, bars,
doors, and other objects, and may show a disposition to bite. In all the
domestic animals these delirious symptoms may closely resemble those of
rabies. This has been particularly noticed in certain forms of
poisoning. Pascault has found this in cattle that had eaten garlic and
Cadeac in dogs that had eaten tansy.

The animals in such cases become morbid, dull, taciturn, they become
usually hypersensitive, sometimes hyposensitive, have a change of voice,
and show a readiness to resent and bite if interfered with, and even to
wander away by themselves as in rabies. On the other hand they may be
seized with lethargy and torpor as in dumb rabies, and with or without
access of convulsions may pass away in a condition of paralysis.

Among other conditions these symptoms have been found to be associated
with epilepsy, foreign bodies in the pharynx, gullet, stomach or bowels,
with intestinal parasites, or with mycotic poisoning (ergotism, smut,
the fungus of coniferous trees, etc.).

The lack of the extreme hyperæsthesia and excitability of rabies, and
usually of the mischievous disposition to bite, the presence of foreign
bodies in the mouth or gullet, and the evidence of disorder of
digestion, with costiveness, tympany, and tenderness, and the history of
the case may serve to differentiate. In cases of doubt the inoculation
of a rabbit on the brain should demonstrate the absence of rabies by the
absence of the characteristic symptoms after sixteen days.

_Treatment._ As delirium in animals is a deranged innervation from
congestion, narcotic drugs, ptomaines, etc., it must be looked on as in
most cases a mere phenomenon, pointing to a definite disease, or to a
particular intoxication, and treatment must be directed toward the
removal of the primary cause. Thus the remedial measures must be
directed in the different cases to the encephalitis, meningitis,
digestive disorders, contagious disease, or drug to which the affection
may be traced. The patient must be put in a strong enclosure or securely
tied so that he can do no harm: it will often be desirable to secure
shade or cool air, or to apply cold water or ice to the head, and to
quiet the nervous excitement by inhalations of chloroform, or ether,
rectal injections of chloral, or bromides, or full doses of hyoscine,
sulphonal, trional or tetronal. These may be pushed to the extent of
inducing anæsthesia, sleep or quiet, as the case may be, and meanwhile
other measures should be taken to eliminate the poisons, correct the
congestion, or remove the source of irritation. Anæmic cases may demand
iron and bitters, with an aliment rich and easily assimilated, while
plethoric cases may require purgation, diuresis or even bloodletting.
All noise and any cause of excitement must be carefully guarded against.

VICIOUSNESS. AGGRESSIVE VICE.

Subject maliciously using its natural weapons. Horse kicks, bites,
crowds against wall, rears, bucks, plunges, treads upon. Cattle use
horns or forehead, or kick. Dog bites. Cats scratch and bite.
Ticklishness different. Developed or inherited. Revenge. Desperation
in pain. Sexual. A psychosis. Responsibility of owner, in selling,
toward employe, in exposing in a public place. Treatment: remove
source of suffering, treat kindly, secure confidence, castrate, place
under absolute constraint, throw _a la Rarey_, Comanche bridle, tie
head to tail and circle, etc.

This word is employed to cover only those forms of vice in which the
animal shows a malignant disposition to attack or injure man or beast.
Each animal uses its natural weapons according to the occasion.

The =horse= strikes with his fore feet, kicks with his hind, bites,
crowds his rider’s leg against a wall, or his attendant’s body against
the side of the stall, rears, bucks, plunges, or treads his victim under
his feet.

The =ruminants=, large and small, use their horns, and cattle their feet
as well. In the absence of horns they still use the forehead, but much
less effectively and usually only with the purpose of defence.

The =dog= attacks with his teeth and the cat with her claws by
preference, and uses the teeth as a secondary weapon.

=Swine= use their tusks to rip or disembowel their adversary or victim.

A very ticklish horse cannot bear to be touched on the flank or hind
parts, without throwing the ear backward, glancing back, showing the
white of the eye, and lifting the foot. But if this is mere excess of
sensitiveness and begets no disposition to kick it is not viciousness.

The vicious horse will in such cases bite or kick repeatedly and with
well directed purpose. He will moreover show the movements of ears and
eyes and attack his victim in the absence of any such excuse, the simple
approach being a sufficient occasion. He will bite and strike with the
fore feet at the same time, or he may strike out with one hind foot or
with both at once. He may attack indiscriminately all who approach him,
or reserve his ill-will for particular individuals, and then he often
acts under a feeling of revenge for ill-usage from this individual or
some one he conceives him to represent.

In some cases viciousness is inherited and certain families have a bad
reputation in this respect. It may be either a survival of the ancestral
disposition of the wild horse, or it may be a trait developed by
ill-usage of a team of more immediate ancestors.

In other cases the habit is acquired by the individual himself, and in
such cases it may be due to brutal treatment at the hands of man; to a
continuous punishment of a high-spirited horse leading to resentment and
retaliation; to acute pain in boils, abrasions or other sores in the
root of the mane, or the shoulder, or the back, where pressed on by the
collar or saddle; or to the generative excitement of mares in _heat_. In
many such cases the vice lasts only during the persistence of the cause,
in others it becomes permanent. The stallion is much more disposed to
aggressive vice than the gelding.

Whether we may consider the vice a disease or not, it becomes a habit
engrained in the nature, the nerve centres tending to reproduce their
habitual acts indefinitely, so that we may look on the condition as a
psychosis which is too often incurable.

=Responsibility of the owner.= Dangerous aggressive vice is too
self-evident to the buyer to constitute a good cause for annulling a
sale, but it has this legal bearing, that the owner who keeps an animal
known to be vicious, renders himself responsible for whatever injury to
man or beast he may perpetrate. Thus the vicious stallion, bull or dog
in a public place which damages person or property, renders his owner
liable to the extent of such damages. This, of course, must be largely
qualified by the attendant circumstances. The man employed to take care
of a horse, knows his habits as fully as the owner, takes his chances
and should exercise due precautions to avoid danger. The person who
enters a stall carelessly without speaking to the horse, seeing that he
stands over, or otherwise responds to his call, is himself to blame if
he gets kicked. The attendant who does things to a dangerous or
questionable horse for mere bravado cannot blame the owner if he gets
himself injured. If a person teases a horse so as to tempt him to
retaliate, not only is he responsible for his own consequent injuries,
but largely also for the habits of the horse and for such injuries as
others may subsequently sustain from him.

A dog or a bull shown in a public place, and which breaks loose and
injures spectators or others, manifestly renders his master responsible
for all such damage.

_Treatment of aggressive vice._ In mild dispositions in which the vice
is roused by temporary suffering, it may often be cured by removal of
the cause of such suffering. Indeed, without the healing of sores under
the collar or saddle the vice cannot be arrested. Considerate and gentle
treatment, too, will go far to restore confidence and to gradually do
away with the aggressive disposition.

In wicked stallions castration will usually restore to a good measure of
docility. The exceptional cases appear to be those that are hereditarily
and constitutionally vicious, or in which the habit has been thoroughly
developed and firmly fixed by long practice.

Mares, too, which become vicious and dangerous at each recurrence of
œstrum, can usually be completely cured by the removal of the ovaries
especially if this is done early in the disease.

The inveterate cases may usually be subdued and rendered controllable
for a time by one of the methods of subjugation employed by the
professional tamers, but unless they are thereafter kept in good hands
they are liable to relapse into the old habit. Among the more effective
methods are the Rarey mode of throwing which may be repeated again and
again until the animal is thoroughly impressed with a sense of the
domination of man and the futility of resistance; the resort of tying
the head and tail closely together and letting the animal weary and daze
himself by turning in a circle, first to the one side and then to the
other; the application of the Comanche bridle made of a small rope, one
loop of which is passed through the mouth and back of the ears and drawn
tightly, then another loop is made to encircle the lower jaw, and the
chin is drawn in against the trachea by passing the free end of the rope
round the upper part of the neck and again through the loop encircling
the lower jaw and drawing it tight; or a similar small rope is passed a
number of times through the mouth and back of the ears and drawn tightly
so as to compress the medulla and stupify the animal. This is supposed
to be rendered more effective by passing one turn each between the upper
lip and gums and between the lower lip and the gums.

CATALEPSY.

Definition. Tetanic and paralytic forms. Balance of flexors and
extensors Cataleptoid. No constant lesion. Hysterical. Hypnotic.
Subjects: horse, ox, wolf, cat, chicken, Guineapig, snake, frog,
crayfish. Causes: strong mental impression, indigestion, etc., in
susceptible system. Lesion: inconstant, muscular degeneration, etc.
Symptoms: wax-like retention of position given, voluntary movement in
abeyance, mental functions impaired, secretions altered. Duration and
frequency variable. Treatment: shock; cold; ammonia, pepper, snuff,
electricity, amyle nitrite, nitro-glycerine, apomorphine, bromides,
purgatives, bitters, iron, zinc, silver, open air exercise.

_Definition._ This is a functional nervous disorder, characterized by
paroxysms of impaired or perverted consciousness, diminished
sensibility, and above all a condition of muscular rigidity, by means of
which the whole body, or it may be but one or more limbs retain any
position in which they may be placed.

Laycock describes two forms in man—the catochus or tetanic form, and the
paralytic form. Mills would restrict the name catalepsy to cases in
which the muscular tone is such that the affected part may be bent or
moulded like wax or a leaden pipe, and will not vary from this when left
alone. Other forms in which this waxen flexibility (flexibilitas cerea)
is absent or imperfect he would designate as cataleptoid.

The disease is not associated with any constant cerebral lesion, though
it may supervene in the course of other nervous disorders, and therefore
may own an exciting cause in existing lesions of the brain. The
immediate cause must however be held to be functional, and this is in
keeping with its most common form in man (hysterical), and with the
hypnotic form which is observed both in man and animals. This latter may
be looked on as a form of induced or hypnotic sleep, in which the
retention of the position given to a limb or part is the most prominent
symptom. In all cases there is an impaired condition of the sensory
functions of the cerebral convolutions, and an insusceptibility of the
motor centres to the control of the will, or the reflex stimulus.

Hering has recorded the disease in the horse, Landel in the ox, and
Leisering in the prairie wolf. The hypnotic form has been shown in cats,
chickens, and Guinea pigs. The serpent charming of the Indian dervishes
and similar effects on frogs and crayfish have been attributed to
hypnotic catalepsy.

_Causes._ Strong mental emotions and diseases which profoundly affect
the nervous system have been adduced as causes (fear, excitement,
chills). Indigestible food has even been charged with causing it. There
is undoubtedly, to begin with, a specially susceptible nervous system,
and hence it is liable to prove hereditary, and in man to appear as a
form of hysteria, or to alternate in the same family with epilepsy,
chorea, alcoholism, opium addiction and other neurosis.

Hypnotism as a cause is claimed by various writers. Azam says that in
the fairs in the South of France, jugglers hypnotize cocks by placing
the bill on a board, on which they trace a black line passing between
the two feet of the bird. Cadeac adds that Father Kircher, in the 17th
century, employed a similar method to put fowls to sleep. Alix put cats
to sleep by securing them firmly, and then looking steadily into their
eyes. The condition attained varies according to the degree of the
sleep, the will being dominated first, and later, consciousness of
external objects is lost. Hypnotism, however, appears to be difficult
and uncertain in the lower animals, in keeping with the limited
development of intelligence and will, as compared with the human being.
Cadeac states that the very old and the very young are completely
refractory to hypnotizing influences.

_Lesions._ No constant pathological changes are found, though different
nervous lesions may serve to rouse the disease in a predisposed subject.
Fröhner found in the affected muscles granular swelling, fatty
degeneration, hæmorrhages, and waxy (amyloid) degeneration of the
cardiac muscles, corresponding to what has been found in tetanus; also
hæmorrhages on the stomach and intestines.

_Symptoms._ The leading objective symptom is the tonic condition of the
muscles by which a perfect balance is established and maintained between
the flexors and extensors so that the affected part maintains the same
position which it had when the attack began, or any other position which
may be given to it during the progress of the paroxysm. The position is
only changed when the muscles involved have become completely exhausted.
During the attack the affected muscles are swollen and firm, so that
their outline may often be traced through the skin, later as the attack
subsides they become soft and flaccid. Voluntary movement of the
affected muscles is impossible until after the paroxysm. The attack
usually comes on suddenly and in this respect resembles epilepsy; at
other times there are premonitory symptoms of nervous anxiety,
excitement or irritability. There is usually considerable impairment of
consciousness, intelligence, common sensation, and even of the special
senses. In a cataleptic dog Fröhner noted mental and motor troubles,
considerable anæsthesia, and loss of sight, smell, and hearing. The eyes
are fixed, the pupils either contracted or dilated, and the urine passed
may be albuminous or even icteric.

_Course, Duration._ Like other functional nervous disorders this is
extremely uncertain in its progress. There may be but one attack or a
succession; they may last from a few minutes, to 7 days (Fröhner), or
even several weeks (Hertwig); they may end in recovery or less
frequently they may prove fatal usually by inanition.

_Treatment._ During a seizure a sudden shock will sometimes cut short
the attack, douching with cold water, an inhalation of ammonia, of
capsicum or of snuff, or the application of electricity in an
interrupted current through the spine and affected muscles. Ether
anæsthesia will not always relax (Sinkler). Inhalation of a few drops of
nitrite of amyle has proved effective in man, as has also the injection
subcutem of three drops of a 1 per cent solution of nitro-glycerine,
apomorphine hypodermically is usually effective (Sinkler). Bromide of
potassium has also been advised, and in case of coldness of the surface,
a warm bath.

When there is overloaded stomach and gastric indigestion an emetic is
indicated, and in constipation a purgative (for speedy action chloride
of barium or physostigma subcutem).

In the intervals between attacks tonics and general hygiene should be
invoked to build up the weakened nervous system. Quinine, and salts of
iron, zinc or silver with a nourishing diet and out door exercise are
especially indicated.

INSOLATION. HEAT EXHAUSTION. SUNSTROKE. THERMIC FEVER.

Definition: two forms. =Heat exhaustion.= Causes: prolonged heat, and
moisture, overexertion. Impaired vaso-motor centre. Failing heart.
Carbon dioxide poisoning. Symptoms: weak, fluttering pulse,
perspiration, muscles flaccid, prostration, no hyperthermia.
Treatment: stimulant, digitalis, digitalin, subcutem, nitro-glycerine,
warm baths. =Thermic fever.= Hyperthermia excessive. Causes:
insolation, prolonged heat and impure air, furnace heat, moist and dry
heat, electric tension, overwork, muscular exhaustion, coagulation of
myosin, constant heat on one part (head), excess of carbon dioxide,
stiffening of bodies when killed in hot weather, debility, weakness,
fatigue, chest constriction, tight girths or collars, short bearing
reins, plethora, obesity, open cars and yards, fever, privation of
water, heavy fleece. Lesions: right heart and systemic veins full,
blood black fluid or diffluent, left ventricle empty, congested
meninges, effusions in or on brain, or hæmorrhages. Symptoms: =horse=:
dull, stupid, stubs toes, sways quarters, droops head, hangs on bit,
props on feet, breathes rapidly, pants, stertor, dilated nostrils,
gasping, fixed eyes, dilated pupils, tumultuous heartbeats, gorged
veins, epistaxis, perspiration, convulsions: =ox=: parallel symptoms:
=sheep=: open mouth, stertor, fixed eyes, pupils dilated, panting,
swaying, fall, convulsions: =dog=: dull, prostrate, pants, congested
veins and mucosæ, weakness, spasms, syncope, speedy rigor mortis.
Overheating. Diagnosis: early excessive hyperthermia, venous
congestion, shallow panting breathing, violent heart action, loss of
sensory and motor functions, convulsions. Prevention: avoid violent,
prolonged heat, and exertion, especially in case of fat animals or
those new to hot climate, keep emunctories acting, shade head, water
on head and to drink, protect fat cattle, shear sheep, water.
Treatment: shade and laxatives; if severe, cold water from hose, ice
bags to poll, rub legs, acetanilid subcutem, stimulant enemata, later
mineral tonics, iron or zinc.

_Definition._ A morbid condition produced by the exposure to extreme
heat, and marked by profound disorder of the _vaso-motor_ and _heat_
centres.

The single term of _sun-stroke_ or _heat-stroke_ has been replaced by
two,—=heat exhaustion= and =sun-stroke=, indicating two distinct
conditions, brought about by exposure to heat and manifested by
different states of the body and distinctive symptoms.

Heat Exhaustion.

This appears as an exaggerated form of the general sense of relaxation,
weakness and languor which follows on prolonged violent exertion in a
hot atmosphere. There is more or less impairment of the vaso-motor nerve
centre in the medulla, relaxation of the capillary system, and flagging
of the heart’s action, which loses its customary stimulus, by reason of
the defective supply of blood returned by the veins. This may become so
extreme that the patient dies by syncope. In other cases the paresis is
mainly shown in the vaso-motor system, and its centres in the medulla,
the blood is delayed in the distended capillaries and veins, it becomes
overcharged with carbon dioxide, the heart’s action is accelerated and
feeble, the pulse rapid, weak and fluttering, perspiration breaks out on
the skin, and the temperature is normal or subnormal. The muscular
weakness, the flaccid condition of the facial muscles, and general
depression suggest a state of collapse. This condition is not
necessarily due to exposure to the intensity of the sun’s rays, but may
come on in animals subjected for a length of time to artificial heat,
and especially if the air is impure, and if the subject has to undergo
severe physical exertion.

_Treatment._ In slight cases of this kind a stimulant is usually
desirable and ammonium carbonate in bolus or solution will usually serve
a good purpose. In its absence alcohol or spirits of nitrous ether may
be given. Digitalis is of great value in sustaining the flagging action
of the heart and has the advantage that as digitalin it can be given
hypodermically when it is impossible to give ammonia, alcohol or ether
by the mouth. For the same reason nitro-glycerine may be resorted to, or
even atropia as a vaso-motor stimulant. Active friction of the body and
limbs will aid circulation and indirectly stimulate the heart, and in
case of subnormal temperature it may be supplemented by a warm bath in
the smaller animals, kept up until the normal temperature in the rectum
has been restored.

Thermic Fever. Sun-stroke.

This is readily distinguished from _heat exhaustion_ by the predominance
of the hyperthermia. While in =heat exhaustion= the temperature is
usually subnormal, in =sun-stroke= it is excessive, (108°–113° F.).

_Causes._ The immediate cause of sun-stroke is exposure to undue heat,
but this need not be the heat of the sun’s rays direct. A large
proportion of cases in the human subject are attacked during the night,
and again at sea where an attack in a passenger is practically unknown,
it is terribly common among stokers working in a close atmosphere of
100° to 150° F.

The attendant conditions have much influence in determining an attack,
thus it is generally held that heat with excess of moisture is the most
injurious, yet in Cincinnati, statistics showed a greater number of
cases in man when the air was dry. The suppression of perspiration and
the arrest of cooling by evaporation in the latter case would tend to a
rapid increase of the body temperature, and the condition would be
aggravated by the electric tension usually present with the dry air.
With the hot, moist air perspiration might continue, but evaporation
would be hindered, and there would be arrest of the cooling process and
an extreme relaxation of the system.

Again, if is usually found that seizures take place during or after hard
muscular exertion in a hot period, and much importance is attached to
the attendant exhaustion, the excess of muscular waste, and the
alteration of the myosin, which latter coagulates at a lower temperature
in the overworked animal. But on the other hand, experiment shows that
the animal confined to absolute inactivity in the hot sunshine or in a
high temperature (at 90°), dies in a few hours, whereas another animal
left at liberty in the same temperature does not suffer materially. The
explanation appears to be that the dog, kept absolutely still, has the
continuous action of the heat on the same parts and on the same blood,
for the capillaries dilate, and the blood is delayed, overheated, and
surcharged with carbon dioxide, and the result is either syncope from
heart failure, or asphyxia from excessive carbonization of the blood.
Back of these and concurring with them is the paralysis of the
vaso-motor and heat generating nerve centres, from the high temperature
or the condition of the blood.

The excessive carbonization of the blood deserves another word. The
prolonged contact of the blood and air in the lungs is essential to the
free interchange of oxygen and carbon dioxide. Vierordt showed that with
sixty respirations per minute the expired air became charged with but
2.4 per cent. of this gas, whereas with fourteen respirations it
contained 4.34 per cent. Therefore, with violent muscular work (which
charges the blood with carbon dioxide) and rapid breathing (which fails
to secure its elimination), the overdriven animal soon perishes from
asphyxia. Under a high temperature of the external air, this condition
is aggravated since the rarefied air contains just so much the less
oxygen, the absorption of which is the measure of the exhalation of
carbon dioxide.

Dr. H. C. Wood, who has experimented largely on the subject in animals,
finds the cause of heart failure in the coagulation of the myosin, which
takes place under ordinary circumstances at 115° F., but at a much lower
temperature when a muscle has been in great activity immediately before
death. As the temperature of thermic fever frequently reaches 113°, or
even higher, he easily accounts for the sudden syncope occurring during
active work in a high temperature. As an example of such sudden rigor,
he adduces the sudden stiffening of the bodies of some soldiers killed
in battle during hot weather.

Wood further shows that all the symptoms of thermic fever can be
produced in the rabbit by concentrating the temperature on its head,
which seems to imply a direct action on the brain and in particular on
the heat producing and vaso-motor centres. This becomes the more
reasonable that the temperature attained does not impair the vitality of
the blood but, leaves the leucocytes possessed of their amœboid motion.
He found, moreover, that if the heat were withdrawn before it has
produced permanent injury to the nervous system, blood or other tissues,
the convulsions and unconsciousness are immediately relieved and the
animal recovers.

Other conditions may be adduced as predisposing or concurrent causes of
thermic fever. Whatever impairs the animal vigor has this effect.
Fatigue, as already noticed, is a potent factor, in man a drinking
habit; in all animals a long persistence of the heat during the night as
well as the day; impure air in badly ventilated buildings; and
mechanical restriction on the freedom of breathing. In military barracks
with the daily temperature at 118° F. and the night temperature 105, the
mortality became extreme, and in close city car stables the proportion
of sun-strokes is enhanced. In all such cases, the air becomes
necessarily more and more impure continually. The atmosphere has the
same heat as the animal body, so that no upward current from the latter
can be established, to create a diffusion. The carbon dioxide and other
emanations from the lungs, the exhalations from the skin, dung and
urine, accumulate in the air immediately surrounding the animal and
respiration becomes increasingly imperfect and difficult. This condition
is further aggravated by the accumulation of the animal heat in the
body. The blood circulating in the skin can no longer be cooled, to
return with refrigerating effect on the interior of the body, the
cooling that would come from the evaporation of sweat is obviated by the
suppression of that secretion, as well as by the saturation of the zone
of air immediately surrounding the body, and thus the tendency is to a
steady increase of the body temperature until the limit of viability has
been passed.

The mechanical restriction of respiration should not be overlooked. In
European soldiers landed in India and marched in the tight woolen
clothing and close stocks a high mortality has been induced and in
horses with tight girths or collars and short bearing reins, and oxen
working in collars a similar result is observed. Any condition of fever
is a potent predisposing factor.

Horses or cattle that are put to violent or continued exertion when too
fat or out of condition are especially subject to sun-stroke. Fat cattle
driven to market under a hot sun, or shipped by rail, crowded in a car
and delayed on a siding under a hot sun, with no circulation of air,
often have insolation in its most violent form. The same may be seen in
the hot stockyard, with a still atmosphere and the fat animals subjected
to the full blaze of a July sun. The chafed feet caused by travel, and
the muscular weariness caused by standing in the moving car are material
additions to the danger.

Similarly horses suffer on the race track when subjected to protracted
and severe work in hot weather, or again dragging loads in a heated
street under a vertical sun, or on a side hill with the sun’s rays
striking perpendicularly to its surface.

A change in latitude has a decided effect, the Northern horse suffering
much more frequently than the one which is native to the Southern States
and which has inherited the habit of heat endurance.

Finally faults in feeding and above all watering are appreciable
factors. The privation of water in particular is to be dreaded. Tracy in
his experience with American soldiers in Arizona, found that the command
could usually be guarded against sun-stroke when a supply of water was
kept on hand. It should be used guardedly, but nothing would act better
in obviating an attack. On the other hand, when the canteens were empty,
under the hot sun the seizures increased disastrously.

Sheep are especially liable to suffer from heat by reason of their dense
fleece, which hinders the evaporation of perspiration, and the cooling
effect of air on the skin. When the temperature rises, respiration is
accelerated and panting, the lungs seeking to supplement the work of the
skin. When traveling in a heavy fleece, or in the hot sunshine in July
or August sun-stroke is not uncommon among them.

_Lesions._ Among the lesions may be named, vacuity of the left ventricle
and fullness of the right ventricle and veins with fluid blood or a
diffluent clot; congestion of the pia or dura mater, effusion into the
ventricles, hæmorrhages into the subserous tissues, and degeneration of
the muscles.

_Symptoms._ =Horse.= When premonitory symptoms are observed the animal
fails to respond to whip or voice, lessens his pace, stubs with his fore
feet and sways with the hind, depresses his head and hangs heavily on
the bit.

Too often these are omitted or overlooked, and the horse suddenly stops,
props himself on his four limbs, drops and extends the head, breathes
with great rapidity, panting and even stertor, dilates the nostrils
widely, retracts the angle of the mouth and even gapes, has the eyes
fixed, the pupils dilated and the beats of the heart tumultuous. The
superficial veins are distended, the visible mucosæ congested with dark
blood, and blood may escape from the nose. Perspiration usually sets in.

The animal may fall and die in a few minutes in convulsions, or, if
stopped sufficiently early and suitably treated, he may in a measure
recover in 15 to 20 minutes.

_Symptoms._ =Ox.= The premonitory symptoms are like those in the horse:
dullness, rapid, panting breathing, the mouth is opened and the pendent
tongue is covered with frothy saliva, a frothy mucus escapes from the
nose, the eyes are congested and fixed, the pupils dilated, the nostrils
and flanks work laboriously, the heart palpitates, the animal sways or
staggers and falls. Death follows in convulsions, or it may be delayed,
the animal struggling ineffectually to rise, or having periods of
comparative quiet. The rectal temperature is very high, 107° to 114° F.
If able to stand, there is usually blindness and heedlessness of
surrounding objects.

_Symptoms._ =Sheep.= The open mouth, protruding tongue, frothy saliva,
reddened fixed eyes, rapid breathing, beating flanks, stertor, and
unsteady gait are characteristic when taken along with the manifest
causes. Swaying movements followed by a sudden fall and death in
convulsions form the usual termination of the disease.

_Symptoms._ =Dog.= These have been mainly produced experimentally and
consisted in hyperthermia, dullness, prostration, accelerated breathing
and heart action, congested veins, and mucosæ, muscular weakness,
convulsions, and syncope or asphyxia. After death the muscles became
speedily rigid, and the blood accummulated in the venous system, was
fluid or only loosely coagulated. In these animals, if the experiment
were stopped in time the animal could be restored to health.

Slighter cases may occur in the different animals, more particularly
from overdriving in hot weather, and in such cases the _overheated_
animal recovers, but there is liable to remain a special sensitiveness
to excessive heat and a tendency to be dull, sluggish and short winded,
to hang the head in hot weather, and to seek shelter from the direct
rays of the sun.

_Diagnosis_ is largely based on the suddenness of the attack, on the
occurrence of high temperature before the seizure, not after as it is
liable to be, if at all, in apoplexy, on the dark congestion of the
mucosæ, and of the venous system, on the rapidity and shallowness of the
respirations, on the tumultuous action of the heart, and on the general
loss of sensory and especially of motor function, in circumstances
calculated to induce sun-stroke. Localized paralysis or spasm would
suggest the formation of a cerebral effusion or clot.

_Prevention._ This will depend on the class of animal and its conditions
of life and work. In horses care should be taken to regulate the work by
the heat of the season and condition of the animal. When the temperature
ranges from 80° to 100° F. the work should be lessened and every
attention should be given to maintain the healthy functions (bowels,
kidneys, skin) in good working condition. If the horse is young, fat, or
out of condition from idleness or accumulation of fat he must have the
greater consideration. So it is with a horse recently come from a colder
latitude, and with a heavy draught horse that may be called on to do
rapid work. Some protection is secured by wearing a sunshade or a wet
sponge over the poll, and much may be expected from an occasional rest
in the shade, a swallow of cool water and sponging of the head.

Very heavy fat cattle should not be driven far nor shipped on the
hottest days, and the packed car should not be left in the full sunshine
in a still atmosphere. Yards with sheds under which they can retreat
must be secured if possible.

The heavily fleeced sheep must have equal care and the pastures for fat
sheep and cattle should have available shade in form of trees, walls or
sheds. Access to water is an important condition.

_Treatment._ In slight cases (_overheated_) a few days of rest, under an
awning rather than in a close stable, with a restricted and laxative
diet.

In severe thermic fever the first consideration is to lower temperature.
If available turn a hose on the head, neck and entire body for five or
ten minutes, or until the rectal temperature approaches the normal. In
the absence of such a water supply, dash cold water from a well on the
body but especially the head and neck, and if available tie a bag of ice
around the poll. Active friction to the legs and body is often of great
advantage. A large dose of antipyrin or acetanilid may be given
hypodermically. On the other hand stimulants, and especially carbonate
of ammonia, or sweet spirits of nitre may be given as an enema. This may
be repeated in an hour in case the pulse fails to acquire force and
tone.

Should the temperature rise again later it may often be kept in check by
cold sponging and scraping followed by rubbing till dry.

In case of continued elevation of temperature, with heat of the head,
and perversion of sensory or motor functions, meningitis may be
suspected and appropriate treatment adopted.

For the prostration and weakness that is liable to follow thermic fever,
mineral tonics such as the salts of iron or zinc may be resorted to.

EPILEPSY. FALLING SICKNESS.

Definition. Frequency. Susceptibility: dogs, pigs, cattle, horses,
parrots, sparrows. Divisions: slight and severe: Jacksonian (partial):
symptomatic; idiopathic. Lesions: inconstant: of brain, cranium,
cerebral circulation, myelon, poisons in blood, dentition, cortical
and ganglionic lesions, cerebral asymmetry, stenosis of vertebral
canal. Medullar asymmetry, traumas of cranium, anæmia, bleeding,
carotid ligation, spinal reflexes, irritation of skin, creatinin,
cinchonoidin, lead, ergot, nitro-pentan, nitro-benzol, ptomaines,
toxins, parasites, nerve lesions, local hyperæsthesia (withers of
horse, recurrent ophthalmia), indigestion, constipation, sciatic
neuritis. Causes: nervous predisposition, heredity (man, cat, dog,
ox), sexual excitement, fear, sudden strong visual impression, uric
acid in blood, meat diet. Symptoms: =horse=, sudden seizure, bracing
feet and limbs, swaying, fall, convulsive rigidity, jaws working or
clenched, eyes rolling, salivation, stertor, dyspnœa, sensation
absent. Duration. Symptoms of localized epilepsy. =Cattle=, bellow,
stertor, rolling eyes, jerking, rigidity, fall. =Sheep.= =Swine=
premonitory malaise, jerking, champing jaws, fall, trembling,
rigidity, involuntary discharges. =Dog= trembles, cries, falls,
rigidity, clonic contractions, stertor, sequelæ. Diagnosis: sudden
attack, unconsciousness, spasms, quick recovery, no spasms in syncope,
vertigo has no spasms, thrombosis has symptoms developed by exercise.
Jurisprudence: animal returnable after twenty-eight days (Wurtenberg,
etc.,) thirty days (France). Treatment: of susceptible brain, and
peripheral irritant. Correct all irritation or disease, or expel
parasites. Nerve sedations: bromides, opium, valerian, belladonna,
hyoscine, duboisine. Tonics: zinc, arsenic, silver, baths,
electricity. Borax. Vegetable diet. Castration. Avoidance of
excitement. Surgical operations. Trephining. Excision of cortex.
Outdoor life. _During a fit_: amyle nitrite, chloroform, ether,
chloral, warm bath, cold or warmth to head, quiet secluded place.

_Epilepsy_ is the name given to a class of cases characterized by a
sudden and transient loss of consciousness with a convulsive seizure,
partial or general. It appears to be due to a sudden explosive discharge
of convulsive nervous energy, which may be generated by a great number
of causes of morbid irritation—pathological, traumatic, or toxic. As a
rule the epileptic seizure is but the symptomatic expression of a
complex derangement which may be extremely varied as to its nature and
origin.

_Frequency in different animals._ The affection is far less frequent in
the domestic animals than in man, doubtless because of the absence of
the special susceptibility which attends on the more highly specialized
brain, the disturbing conditions of civilization, and the attendant
vices.

Among domestic animals, dogs are the most frequent victims in keeping
with their relatively large cerebral development, their emotional and
impressionable nature and the unnatural and artificial conditions in
which as house pets they are often kept. Their animal food and the
consequent uric acid diathesis is a probable cause, as it is in man. In
ten years of the dog clinic at Alfort they made an average of 3 per
cent. of all cases. Next to the dog the pig kept in confinement is the
most frequent victim, while cattle and horses come last. At the Alfort
clinic epileptic horses were not more than 1 per 1000 patients. It is
not at all infrequent in birds, especially canaries and parrots. Reynal
has seen it in sparrows.

_Divisions._ The disease has long been divided into _petit mal_ and
_grand mal_ (_haut mal_). The =petit mal= (slight attack) is usually a
transient seizure affecting a group of muscles only and associated with
only a momentary or very transient loss of consciousness. The loss of
consciousness is uncertain as to many cases. Under partial epilepsies
must be included the hemi-epilepsy, or Jacksonian epilepsy, which is
confined to one side of the body.

The =grand mal= (severe attack) is one in which the loss of
consciousness is complete, and the convulsions are general in the
muscles of animal life.

Another division is into =symptomatic= and =idiopathic= cases, and if
this distinction could always be made it would be of immense value in
the matters of prognosis and treatment as the removal of the morbid
state of which epilepsy is the symptom will usually restore the patient
to health. Thus the removal of worms from the alimentary canal, of
indigestible matters from the stomach, of a depressed bone or tumor from
the surface of the brain may in different cases be the essential
condition of a successful treatment.

_Morbid Anatomy and Pathology._ The literature of epilepsy is very rich
and extensive and yet no constant lesions of the nervous system can be
fixed on as the local cause of the disease. A review of the whole
literature leads rather to the conclusion that irritations coming from
lesions of the most varied kind, acting on a specially susceptible brain
will rouse the cerebral centres to an epileptic explosion. Thus epilepsy
has been found to be associated with lesions of the following kinds:

1st. Brain lesions of almost every kind, including malformations.

2nd. Lesions of the walls of the cranium.

3d. Disorders of the cerebral circulation.

4th. Lesions of the spinal cord.

5th. Morbid states of the circulating blood (excess of urea, uric acid,
creatinin, lead poisoning).

6th. Reflected irritation, as from dentition, worms, sexual excesses,
injuries to certain nerves, notably the sciatic, or to particular parts
of the skin.

1st. =Brain lesions.= Those which affect the medulla and the cortical
convolutions around the fissure of Rolando would be expected to be
implicated because these centres preside over the principal motor
actions of the body and limbs. Yet though these parts are found to be
affected with various morbid lesions in a certain number of cases of
epilepsy, such lesions are exceptional, rather than the rule. In 20
cases of epilepsy in man, 15 showed no lesion whatever of the brain.
Blocq and Marinesco, pupils of Charcot, recently made a critical
examination of the medulla and Rolandic cortex in nine cases that died
during the fit. All showed granular bodies (degenerated myelin or blood
pigment) in the perivascular sheaths but they found these in
disseminated sclerosis and even in healthy brains as well. The neuroglia
cells of the first cortical layer contained black granules. Otherwise
four cases had no change, while five showed sclerosis of the cortex. The
medulla was sound in all cases excepting one which showed punctiform
hæmorrhages. Visible lesions may be present in other parts of the brain;
Wenzel long ago claimed constant lesion of the pituitary body. Beside
the cerebral cortex, lesions have been found in the bulb, the
hypoglossal nucleus, the olivary body, the hippocampi, the thalamus, the
corpus striatum, the quadrigemini, the cerebellum, etc.
Hughlings-Jackson who made an extended investigation of the subject
concludes that any part of the gray matter of the encephalon may become
over-excitable and give rise to a convulsive attack. Not only may the
lesion be in any part of the brain, but it may be of any kind:
meningitis, cerebritis, softening, tubercle, tumor, hydatid, embolism,
or dropsy. Marie Bra found an extreme asymmetry of the cerebral lobes in
epileptics. Kussmaul and others found stenosis of the vertebral canal
and asymmetry of the two lateral halves of the medulla.

2nd. =Cranial lesions.= These consist largely in blows or falls upon the
head, with osteitis, periostitis, fractures with depressions, fibrous
neoplasia implicating or not the meninges and pressing on the brain,
hæmorrhages from minute arteries, etc. The diagnosis of such lesions
will often open a way to a successful treatment. Baker found most of the
severe cases from head injuries.

3d. =Disorders of the cerebral circulation.= Burrows, Kussmaul and
Turner showed that in animals, loss of consciousness and epileptiform
convulsions followed on cerebral anæmia caused by profuse bleeding or by
compression of the carotids. The same has been observed in surgical
cases after ligation of one common carotid. Hermann caused convulsions
in a rabbit by ligating both anterior and posterior venæ cavæ.

4th. =Lesions of the Spinal Cord.= Brown-Sequard determined epileptiform
convulsions by transverse section of one-half of the spinal cord, or of
its superior, lateral or inferior columns. The later development of the
doctrine of interrupted spinal inhibition, suggests that, many of the
seizures in question are but exaggerated spinal reflexes, which are no
longer restrained by cerebral inhibition. That all are not of this
spurious kind may be fairly inferred from his further demonstration that
bruising of the great sciatic in animals tended to produce epilepsy. In
such cases., the irritation of certain areas by pinching the skin,
served to produce a seizure. Not only so, but the animals in which such
artificial epilepsy had been induced tended to transmit the infirmity to
their progeny. The prevailing view of epilepsy however, would consider
such lesions as sources of peripheral irritation by which the brain is
affected sympathetically, while the real explosion is the result of the
sudden discharge of the pent up excitement caused in the encephalic
centres by the irritation at such distant points.

5th. =Morbid States of the Circulating Blood.= Certain poisons, when
brought in contact with encephalic nerve centres produce epileptic
seizures. Gallerani and Lussana applied creatinin directly to the
cerebral cortex and quickly induced epileptiform convulsions and
choreiform movements. Injected subcutaneously it failed to produce the
same effect. Cinchonoidin acted on the basal ganglia of the brain
producing convulsions but no choreiform movement. Poisoning with lead,
ergot, nitro-pentan, nitro-benzol and a number of other poisons brings
about intermittent convulsive seizures. The same may be inferred of
ptomaines and toxins, in the convulsions that appear in the advanced
stages of infectious diseases (canine distemper, hog cholera, etc.).

6th. =Reflex Irritation.= Perhaps no peripheral irritation more
frequently causes epilepsy, than parasites. In young dogs worms in the
intestines (tænia cœnurus, tænia tenuicollis, tænia serrata, tænia
echinococcus, and ascarides) have been especially incriminated. Also
linguatula tænioides in the nasal sinuses. In young pigs the
echinorrhynchus gigas, ascarides and trichocephalus. In horses ascarides
have been principally blamed.

Wounds implicating nerves, and tumors pressing on nerves, have served as
sources of nervous excitement which accumulates in the cerebral ganglia
and bursts forth as an epileptic explosion. Bourgelat mentions the case
of a horse which fell in a fit the moment he was touched on his tender
withers, also a case in which a seizure coincided with an attack of
recurrent ophthalmia. Gerlach saw a horse which had an epileptic fit the
instant he was touched on his sensitive withers. In kittens and puppies
the irritation attendant on dentition is a common cause of attacks. In
nervous dogs and pigs indigestion or constipation may serve as the
occasion of an explosion. In the experimental cases of Brown-Sequard,
not only did the injury to the sciatic nerve develop in the brain a
latent tendency to epilepsy, but the subsequent pinching of the skin in
certain areas (epileptigenous zones) promptly brought about a seizure.

=Causes.= Most of the causes of epilepsy have been given above under the
head of pathology and morbid anatomy. The nervous predisposition may,
like any other peculiarity or function, become hereditary. In the human
race nothing is more certain than the tendency to some form of nervous
disorder (insanity, dementia, alcoholism, morphinism, epilepsy, chorea,
etc.) in a special family line. Reynal records the case of an epileptic
cat (belonging to an employe of the Alfort veterinary school) the
progeny of which for three generations, became affected with epilepsy
and mostly died before they were a year old. Also four epileptic dogs (3
males and 1 female) which produced a number of epileptic puppies.
LaNotte records the cases of two bulls affected with epilepsy, in the
progeny of which numerous cases of epilepsy appeared; the cows being
attacked after the first calving, and the oxen soon after they were
first put to work. Breeding stallions are particularly liable to
attacks, the high feeding, lack of muscular work in the open air, and
above all the oft repeated nervous excitement attendant on copulation
being directly exciting causes. The heredity of the artificial epilepsy
induced by Brown-Sequard in Guinea pigs, serves to strengthen the
doctrine of heredity in ordinary forms.

Among emotional causes fear easily heads the list. Bernard states that a
horse became epileptic in connection with the terror caused by the
giving way of a wooden bridge over which he was passing. Bourgelat and
Reynal adduce instances, in cavalry horses when first put under fire.
Reynal records the case of another which had his first attack when
facing a moving locomotive, and which never again could see an engine in
motion without suffering another attack. La Notte mentions the case of a
horse attacked when frightened by a sky rocket; Romer, the case of a
horse scared by the sudden display of a white sheet in front of him, and
Friedberger and Fröhner relate cases of attacks caused by intense rays
of light, as in racing toward the declining sun, or the dazzling
reflection from the surface of water. Liedesdorf saw it in a dog scared
by a locomotive.

A strong impression like that caused by transition from bright light
into darkness, by seeing shadows of trees crossing the road, or violent
suffering caused by severe forms of constraint have been named as
causes.

Speaking in “Brain,” of epilepsy in man, Alexander Haig attributes the
fits to the fluctuations of uric acid in the blood. Headache (migraine)
he finds to be very closely allied to epilepsy and convulsions and to be
a result in a susceptible system of a liberal flesh diet. By a vegetable
and fruit diet he reduces the ingestion and formation of uric acid, so
that the largest quantity which a patient is likely to get into his
blood, shall never or only very rarely, affect the blood pressure and
increase the intracranial circulation to a dangerous extent. In
predisposed subjects, all flesh food, soup, and meat extracts must be
avoided, while even tea, coffee, cocoa and other vegetable articles
containing xanthin compounds are to be regarded as producing uric acid,
and to be denied, or employed only as the merest flavoring.

This position is greatly strengthened by the fact that epilepsy is so
much more frequent in the carnivora (dog, cat, bird) than in the
herbivora. It also suggests very strongly a light vegetable diet for
both prophylactic and curative purposes in our domestic animals. In the
same line the frequent and liberal drinking of warm water, the use of
diuretics and the flushing of the large intestine are indicated.

For other causes see under pathology.

_Symptoms in the_ =Horse=. It has been claimed that premonitory
symptoms, such as dullness, lack of energy and quick, nervous or
startled movements herald an attack, but in animals as in man, the
disease usually attacks suddenly without any antecedent indication.

If at work the horse stops suddenly, or if in the stable he ceases
eating, seems frightened, stands for an instant immovable, braces his
feet, sways, trembles, and falls heavily to the ground. Or he may remain
for an instant supported on his rigid limbs, the jaws moving or firmly
closed, the eyes rolling, and the facial muscles drawn or twitching.
When down there are convulsive movements of the limbs, so that the
animal may kick out violently, and tense contractions or twitchings may
occur in the muscles of the croup, chest and abdomen. There is usually
an increase of the salivary secretion with frothy accumulation about the
angles of the mouth. The respiration is stertorous, dyspnœic, and
interrupted, the nostrils widely dilated, the nasal mucosa of a dark
brownish red, and the superficial veins distended. The pulse is weak,
slow, irregular, intermittent and sometimes imperceptible. Sensation
seems to be in abeyance. No attention is paid to loud sounds, nor to
pinching, pricking, or even cauterizing the skin. Perspirations may
break out on the flank or over the whole surface of the body.

The duration of the attack may be from one to four minutes, or
exceptionally ten or fifteen, after which the muscles relax, the
twitching ceases, the horse raises his head, extends his fore limbs and
finally rises.

After rising some are dull and stupid for an hour or so, and may
continue to perspire, some move the limbs, jaws or head automatically,
turn in a circle, or seek seclusion and darkness, while some take at
once to eating and seem as if nothing had happened.

In _partial_ or _localized_ epilepsy the spasms are confined to a
limited group of muscles like those of the jaws, neck, or fore limbs.
These may alternately contract and relax, or they may remain rigid for a
minute or less, the mouth being held open or firmly closed with grinding
of the teeth, the eyes rolled backward and upward, or affected with
strabismus, the face drawn and distorted, the head turned to one side or
downward, or the limbs fixed and immovable.

At the conclusion of an attack it is not uncommon to see a discharge of
urine or fæces, or in stallions, of semen.

The horse often contracts a fear of the place where the attack occurred,
and this contributes, with the re-appearance of the former object of
dread (car, locomotive, rifles, cannon, etc.) to precipitate a new
attack if he is compelled to go to such a place.

_Symptoms in_ =Cattle=. In cattle the animal is attacked without
premonition, bellows, breathes hard and with effort, has dilatation of
the nostrils, and squinting or rolling upward and backward of the eyes
and falls to the ground rigid and trembling. There may be violent
succussions of the limbs, head or neck, movements of the jaws, grinding
of the teeth, and the appearance of frothy saliva and elements of food
about the lips. The beats of the heart are violent, the pulse slow and
small, and sometimes intermittent. Involuntary micturition, defecation,
or discharge of semen may occur. In slight cases one or more of these
symptoms may be absent, and the victim may not even fall to the ground
but support himself against a wall or other object.

The duration of the attack may be from one to five minutes, rarely more,
and there is often a slow and progressive subsidence of the spasms. When
recovered the animal may get up and go to eating or rumination as in
health.

_Symptoms in_ =Sheep=. In sheep the attack is sudden. The animal ceases
eating or stops in its walking, and after turning or other involuntary
movement falls to the ground, head extended, mouth open, eyes rolling or
squinting, and with rigidity or twitching of the muscles of the neck or
limbs. There is the same loss of sensation, frothing from the mouth, and
grinding of the teeth as in the larger animals. The attack may last 40
to 50 seconds.

_Symptoms in_ =Swine=. In pigs a state of discomfort and restlessness
often marks the approach of an attack, referable probably to the
digestive disturbance or to parasites which furnish the occasion of the
disease. Uneasy, wandering movements, jerkings of head or limbs, rolling
of the eyes, and champing of the jaws may first appear. Then the animal
falls, extending its limbs and head, with open mouth, retracted lips,
and a free flow of saliva. Trembling and jerking of the head, neck and
limbs, hurried, short, difficult breathing, and complete loss of
sensation may be noted. Discharges of urine, semen, and prostatic fluid
are not uncommon. The attack usually lasts 2 or 3 minutes, and
exceptionally 10 to 15. In the shorter seizures, frequent repetition is
not uncommon, Delafond having observed 5 or 6 attacks in the course of
an hour.

_Symptoms in_ =Dogs=. The attack is sudden and unheralded by prodromata.
The animal stops, trembles, cries plaintively and falls; he may manage
to rise or to do so in part but instantly falls anew. The limbs stiffen,
tremble or twitch, the head is extended or flexed, or jerked, violently
striking the ground, the mouth open, with abundant saliva, or firmly
closed though the tongue may be between the teeth. The trunk may be firm
and rigid or alternately twisted in one direction or the other. The eyes
roll or squint, and the breathing is stertorous and difficult.
Insensibility is complete. Toward the end of the attack there may be a
discharge of urine, fæces or semen, the stools often containing worms.
The body is often wet with perspiration during or after an attack.

The attack usually lasts for two or three minutes, then the convulsions
gradually lessen in intensity and finally cease, the dog raises his
head, opens his eyes, and gazes inquiringly around. Then he gets on his
feet shakes himself and may at once resume his customary habits. In
other cases the restoration is less sudden. The dog remains for 30 to 60
minutes dull and stupid, or seems to have little power of control over
its muscles and staggers as if intoxicated, or as if the muscles were
benumbed. It may drop on its knees and then fall with the head on the
ground and repeat this several times. In other cases the dog wanders
around, or trots off and may snap at any one interfering with him, so
that the case is often mistaken for one of rabies. Finally the animal
may remain prostrate and fall into a deep sleep marked by stertorous
breathing.

_Diagnosis._ The diagnosis of epilepsy is usually easy. The suddenness
of the attack, the loss of consciousness, the muscular spasms, the
complete temporary recovery and the tendency to recur, form a _toute
ensemble_, which is pathognomonic. The danger of confounding this with
other nervous disorders is on the whole greatest in the slight cases in
which the symptoms are less typical.

From =Syncope= it is easily distinguished by the spasms which are not
present in syncope.

From =eclampsia= it is not so easy to diagnose, but the line between
eclampsia and epilepsy has not been accurately drawn, and some have even
shown a disposition to drop eclampsia from medical nomenclature.
Eclampsia may be defined as general convulsions dependent on some
eccentric irritation, and which do not recur after such irritation has
been removed. This would remove from the category of epileptic attacks
the cases of convulsions in which the attacks were due to intestinal or
nasal parasites, dentition irritation, tumors pressing on nerves, canine
distemper and other infectious diseases. So far the distinction might be
made by the diagnosis of the particular disease on which the convulsions
depend. There remains however a class of cases in which the centric
nervous disorder on which the epileptic seizure depends is present, and
also the peripheral source of irritation (worms, etc.). In such a case
the presence of the worms or other eccentric source of irritation, even
if added to the fact that this was the immediate exciting cause of the
epileptic explosion, could not do away with the fact that the essential
conditions of epilepsy are permanently present in the nervous centres.
The difficulty therefore of making an accurate differential diagnosis,
resides largely in the impossibility of drawing a definite line of
pathological separation between eclampsia and epilepsy.

From =Vertigo= epilepsy is distinguished by the absence in the former of
marked spasmodic contractions. It is only in the milder forms of
epilepsy those in which the spasmodic action is so slight as to be
overlooked, that this disease can be confounded with vertigo.

From =Thrombosis= or =embolism= of the iliac or femoral arteries
epilepsy is easily distinguished by the absence of exercise as the
essential cause in the development of the latter. In thrombosis on the
other hand, the loss of control over the hind limbs is developed at will
by active motion (walking, trotting). In thrombosis too the absence of
pulsation at the fetlocks or at any point below the seat of obstruction
is conclusive.

=Question of Soundness and Jurisprudence.= Manifestly a horse or bull
subject to attacks of epilepsy is _not sound_. It is moreover a disease,
the symptoms of which are only shown for a very short period at one
time, after a long interval of apparently perfect health. It is,
therefore, a disease against which a purchaser cannot be expected to
protect himself and he should have the right to annul the sale and
return the animal in case the infirmity should appear within a
reasonable period after purchase. This is provided for in the laws of
different countries of Europe, thus in Wurtenberg, Baden and Hesse, a
purchased animal may be returned within 28 days; in France within 30
days, and in Bavaria within 40 days. The greatest difficulty arises from
the frequent impossibility of obtaining expert testimony on a seizure
which is likely to occur at any moment, without premonition, and in
which the testimony of a non-expert may easily be misleading. It seems
as if complaint having been made within the specified legal time, an
extension of guarantee should be given by the court, the animal to be
meanwhile kept under the supervision of a veterinarian.

Another question has arisen as to the position of an animal suffering
from reflex epilepsy. If the attacks are caused by intestinal worms or
nasal acarina which are easily removed, it is quite evident that this
cannot be considered as a permanent unsoundness, and one for which a
contract of sale can be justly annulled. But on the other hand, while
the eccentric source of irritation which is easily curable may have been
the active agent in developing the seizures, it may be none the less
true that the central infirmity which determines the abnormal
susceptibility, to excessive generation and epileptic explosion of
nervous force, may also be present and the animal cannot be considered
as _sound_ until a sufficient length of time has elapsed after the
removal of the peripheral irritation and no new seizure has taken place.

_Treatment of Symptomatic Epilepsy._ In cases due to an eccentric
irritant the first step must be the removal of such irritant. In case of
intestinal worms the various vermicides and tæniacides must be resorted
to. (See Intestinal Parasites). For the linguatula tænioides the
injection of benzine or tobacco water into the nose, or into the
sinuses, with or without trephining may be resorted to. In diseased
teeth extraction or filling may be demanded. In dentition irritation,
lancing of the gums. In all other cases in which a peripheral nervous
irritation can be traced every available means should be taken to remove
it.

_Treatment of Central Epilepsy._ Bearing in mind that peripheral
irritation is a frequent exciting cause of a seizure, too much care
cannot be given to the conservation of the general health and especially
to make the diet wholesome in quantity, quality and time of feeding and
watering, and to guard against constipation and indigestion. In dogs a
too stimulating meat diet is to be avoided.

The medicinal agents employed have been mainly such as are sedative, or
tonic to the nervous system. Valerian was long extolled as a valuable
remedy (Gohier, Delafond, Delwart), and this has been improved upon more
lately by substituting valerianate of zinc. Belladonna and its alkaloid
atropia have been strongly advocated (Tisserant, Bernard, Williams,
Friedberger) and it has the recommendation that it causes vaso-motor
contraction and tends to lessen cerebral congestion. Hyoscine or
duboisine may be used as a substitute. Cyanide of iron has been lauded
by Jourdier and Tabourin, as far superior to valerian. Of late years the
nerve tonics, zinc compounds (oxide, sulphate, chloride) and silver
salts (nitrate) and arsenic have been used, often with excellent
results. Borax strongly recommended for man (1 to 1¾ drachm daily) by
Pastena is worthy of a trial for dogs. It is given largely diluted in
syrup to avoid gastric irritation.

Of all agents employed up to the present the bromides still claim a
foremost place. They should be given in a large dose, on an empty
stomach and at such a time as to occupy the system at the hour when the
seizure is expected to recur. Thus for morning attacks the dose may be
given at night, while for night attacks it may be given in the
afternoon. Müller uses sodium bromide in the dog as least liable to
disturb the stomach, while Peterson, for man, advises the potassium salt
for the same reason. For man, McLane Hamilton advocates a combination of
the sodium and ammonium salts, Eulenberg adds the potassium compound,
while Berkley uses strontium bromide, and Bourneville camphor
monobromide.

Given at night in full dose (30 grs. for dog) the bromides tend to
secure a quiet sleep, with brain rest and recuperation. If beneficial
they should be repeated daily until a cure or other sign of bromism
appears. This may be somewhat checked by arsenic or chloral hydrate.

Wesley Mills finds potassium iodide useful in some dogs when bromides
fail. Bromohydrate is advocated by Müller. Flechsig and others have had
excellent results in man from the opium bromide treatment. Full doses of
opium are given three times a day for six weeks, when they are replaced
by full doses of bromides four times a day.

Improvement should be shown in the shortening of the convulsions and the
lengthening of the intervals between them. Should the bromides fail in
this, resort may be had to other treatment.

Toulouse, Clark and others find that privation of salt, in man, allows
the bromine salt to replace the chlorine one in the tissues, and the
hydrobromic acid the hydrochloric in the gastric juice, and in this way
the bromine can be introduced safely in larger amount into the tissues
and is longer retained, though given in half the doses.

A most important element in the treatment is a vegetable diet with or
without milk, to obviate excessive production of uric acid. Anything
which will disagree and produce gastric or intestinal fermentations with
toxins must be carefully guarded against and these will differ in
different individuals.

Stallions and other excitable males, and females may often be cured by
castration. Patients should be very carefully guarded against all
sources of excitement, reports of guns, sight of locomotives or
automobiles, waving flags, instrumental music, sudden exposure to
sunshine or other bright light, reflection from water, snow, or ice, the
contrast of dark shadows, as of trees, alternating with bright light,
etc. Dogs, becoming excited at a show, may have a convulsion if not
removed, and much more so in presence of another dog in a fit.

A surgical operation often places the disease in abeyance for many
months, but, unless in the case of the removal of a diseased organ which
has acted as a factor, this is not permanent. Hence in man transient
benefit has been secured from operations on the eyes, the brain, the
testicles, the ovaries, etc. In local (Jacksonian) epilepsy, which can
be traced to a definite cortical area in the brain, the trephining of
the skull and the excision of the cortex at that point, has given
temporary relief, with a local palsy, but too often the irritation from
the resulting cicatrix has in time aroused the disorder anew. Even
independently of the removal of the cortex, the trephining has been
successfully resorted to, by savage as well as civilized peoples,
securing a temporary relief. Though not in practice in veterinary
medicine it seems as if this were even more applicable than in man. It
would be fully justified if it preserved for a year or more an animal in
usefulness which must otherwise be destroyed, even if the disease should
return at the end of this time.

Plunge or douche baths (60° to 70° F.) and rubbing dry will often tone
up the nervous system, and a course of bitters, or iron, or both, may
prove valuable. An outdoor life and moderate muscular exercise are
important.

=During a convulsion= the animal should be freed from all harness,
halters, girths, etc., that would impair respiration, the jaws may be
kept apart with a cloth to prevent biting the tongue, and the animal
held with head and neck in natural position. To arrest the spasms the
best agent is amyle nitrite inhaled from a handkerchief. It may be
replaced by a mixture in equal parts of chloroform and ether. Or rectal
injections may be given of chloral. Nitro-glycerine will sometimes cut
short an attack or prevent it. Small animals may have the body immersed
in a warm bath, and cold applied to the head. Congested buccal and
conjunctival mucosæ would indicate cold to the head, while pallor would
suggest warm fomentations.

When the fit is over the animal should be kept in a quiet, dark place
until the excitement or stupor has completely passed.

ECLAMPSIA. CONVULSIONS. SPASMS.

Definition: functional convulsions from peripheral irritation. From
dentition, helminths, uterine disease, nursing (anæmia). Treatment.
Injuries to cranial bone.

Eclampsia (convulsions) is difficult to define as distinct from
epilepsy, the present tendency however appears to be to apply this term
to cases in which the spasms are of a purely functional nature as far as
the brain is concerned and caused by peripheral nervous irritation.
Whereas in epilepsy there is some organic disease or disorder of the
brain itself. Therefore the convulsions of anæmia, of teething, and of
parasitism, would come under this heading being curable by the removal
of the distant source of irritation, while the spasmodic seizures, that
are due to central nervous lesions and are not exclusively dependent on
peripheral irritation would be classed as epilepsy. In other words
reflex epilepsies with no central brain disorganization would be classed
as convulsions.

_Eclampsia from_ =Dentition= is seen especially in young cats, dogs and
pigs when cutting-teeth, and may be obviated by lancing the gums,
extracting diseased or milk teeth entangled on the crowns of their
successors, and by a slight laxative with bromides.

_Eclampsia from_ =Helminthiasis= has been already referred to under
epilepsy. The main object is the expulsion of the worms, after which
nerve sedatives and tonics will be valuable.

_Eclampsia from_ =Uterine Disease= has been noticed by Albrecht, in cows
shortly after calving, the symptoms being spasms of the neck, persistent
extension or turning of the head, grinding of the teeth, loss of
consciousness, convulsive movements of the legs, rolling of the eyes,
and slow recovery. The same symptoms have been observed in goats and
have been supposed to depend on a reflex from the irritated womb.
Another supposable cause is the absorption of toxic products from the
womb and vagina. Manifestly the removal of the after birth and the
disinfection of the womb, should be here employed along with the
ordinary nerve sedatives.

_Eclampsia in_ =Nursing Female Dogs= has long been attributed to anæmia
by English veterinarians. It occurs especially in high bred bitches,
when nursing a large litter and some weeks after parturition when the
puppies have grown large and vigorous, with proportionately increased
demands on the maternal source of supply. The dam shows an emaciated
aspect, with restless anxious eyes, a wearied expression, and a
generally exhausted appearance. There is weakness and swaying behind, or
complete inability to use the limbs, the animal goes down, trembles
violently and shows clonic spasms of the extensors of the legs, the
neck, the back, the face and the eye. Breathing is accelerated,
stertorous and labored, the heart beats violently the mucous membranes
are congested, and the mouth is opened with convulsive movements of the
jaws and throat. The attack is readily distinguished from epilepsy, by
the retention of sensation, and by the absence of involuntary passages
from the bowels, or kidneys. Recovery is likely to be secured if the
puppies or most of them are removed early enough and the bitch sustained
by nourishing food, and tonics. The spasms may be combatted by the
antispasmodics and nerve sedatives employed in epilepsy. Chloroform,
morphia, phenacetin, acetanilid, urethane have been specially commended.
Beef teas, cod liver oil, and iron may be resorted to and free outdoor
exercise and sunshine should be secured.

General convulsions are common in connection with direct injury to the
brain and more particularly of its coverings, (cranial bones, meninges).
In such cases the irritation which otherwise starts at a distance and
reaches the brain through the afferent nerves, or the modification of
the circulation acts directly on the gray matter. It is interesting to
note in this connection that the evacuation of the cerebral fluid, which
removes the soft support of the water cushion and allows the brain to
come in contact with the hard bony walls, determines an access of
convulsions. In cases of convulsions attendant on mechanical injury to
the cranium surgical interference will be in order.

CHOREA. ST. VITUS DANCE.

Definition. Susceptible animals. Causes: nervous lesions inconstant,
youth, debility, anæmia, microbian toxins, cerebral embolism,
rheumatism, trophic alterations in nerve cells, fright. Lesions:
variable in seat and character, congestion of perforated space, corpus
striatum, Sylvian convolutions, gray matter at root of posterior horn
of spinal cord, etc., experiments of Chauveau and Wood. Symptoms:
=dog=, local twitching, fore limb, one or both, neck, head, maxilla,
eyelids, eyeballs, hind limbs, trunk, rhythmic, less when recumbent,
usually absent in sheep, roused by excitement: =horse=, head neck,
fore limb, trunk: =cattle=, head, neck, limbs: =swine=, hind limbs,
neck, head: severe cases lead to exhaustion, emaciation, marasmus,
paralysis. Duration: weeks, months, years. Treatment: laxative, tonic,
hygienic, arsenic zinc sulphate, strychnia, sedative, belladonna,
conium, cannabis Indica, chloral, acetanilid, trional, etc., icebags
or ether spray to spine, cold douches, outdoor life.

_Definition._ A neurosis characterized by constant twitching of muscles
or of groups of muscles, and which usually ceases during sleep.

_Animals Susceptible._ This disease is especially common in the dog, but
has been recognized also in the horse, ox, cat and pig.

_Causes._ Much difference of opinion exists as to the true cause of
chorea. In many cases no nervous lesion has been found and therefore the
disease has been pronounced purely functional. The victims are as a rule
the young, weak and debilitated so that anæmia has been held to be the
main causative factor. Then in dogs the affection is a common sequel of
distemper and hence it has been attributed to toxic matters (microbian,
etc.) in the blood. It should be added that European writers attribute
the rhythmic spasms which follow distemper to eclampsia, epilepsy or
tic, and claim that the contractions must be irregular or arhythmic in
order to constitute chorea. English and American writers, however, have
attributed less importance to this point and consider that the constancy
and persistency of the contractions in the dog, differentiate an
affection from both eclampsia and epilepsy and relate it rather to
chorea. Tic as illustrated in cribbiting is certainly not constant nor
rhythmical nor is it a habit beyond the control of the will.

Among other alleged causes of chorea is embolism of the arteries of the
brain or spinal cord. Angel Money went so far as to inject a fluid
containing arrowroot, starch granules and carmine into the carotids of
animals, and produced movements closely resembling those of chorea.
Another theory connects chorea with the rheumatic poison. Some English
writers find more than 80 per cent. of all cases in man associated in
some way with rheumatism, but in Philadelphia, Sinkler found that not
more than 15 pet cent. showed such a relation. D. C. Wood as the result
of necropsies of a number of choreic dogs reached this conclusion:
“Owing to emotional disturbance, sometimes stopping of various vessels
of the brain, or sometimes the presence of organic disease, there is an
altered condition of the ganglionic cells throughout the nerve centres.
If the cause is removed and the altered condition of the nerve cells
goes only so far, it remains what we call a functional disease. If it
goes so far that the cells show alteration, we have an organic disease
of the nervous system.”

In man the element of sudden fright is awarded a high position in the
list of causes.

_Lesions._ Constant morbid changes of structure have not been
established in chorea. On the contrary in the many careful necropsies of
choreic subjects some lesion of brain or spinal cord has been almost
always found. Dickinson always found congestion of some part of the
brain or spinal cord, but most constantly of the substantia perforata,
the corpora striata and the beginning of the Sylvian fissure. In the
cord the cervical and dorsal regions were the most commonly affected,
and preëminently the gray matter at the root of the posterior horn. The
bilateral symmetry of the contractions in cases of unilateral lesions,
has been held to discredit the theory of embolic origin, yet this may be
explained by mutual relation of the ganglia of the two sides and their
coördination of function.

The question of the relative importance of the encephalic and spinal
lesions has been also debated. Chauveau believed that by section of the
cord in choreic dogs, he had proved that the spasms were of medullary
origin. Wood on the other hand found that the choreic movements
persisted after section of the cord, and seemed warranted in the
conclusion that the movements originated in the cord. The probability
is, that with the cord intact, the primary source of the morbid movement
may reside either in the encephalon or the cord. In chorea, following
distemper, I have found marked congestion of the encephalon and its
meninges.

_Symptoms._ In the dog the twitching may be confined to one fore leg, or
it may extend to both and then usually implicates the neck and head. In
other cases the lower jaw, the head, the eyelids or even the eyeballs
may be the seat of the twitching motions and in still others the hind
limbs and trunk are also implicated. In nearly all cases the tendency is
to a continuous rhythmic action, which may moderate without actually
ceasing while the animal lies down, but which usually stops altogether
during deep sleep. When it intermits at other times it can commonly be
roused into activity by exciting the animal in any way.

In the horse the muscles affected may be those of the head and neck, of
the fore limb (Hering), of head, limbs and trunk (Leblanc).

In cattle the movements have affected the neck and head and the fore or
hind limbs (Anacker, Schleg).

In young pigs the hind limbs, the neck and head have been chiefly
involved in the spasms (Hess, Vervey).

If the affection is slight it may not seriously impair the general
health, but in proportion to its severity and the constancy and
generalization of the spasms and the consequent muscular waste and
exhaustion, the animal becomes gradually worn out and emaciated and dies
of paralysis and marasmus.

_Duration._ In favorable cases recovery may ensue in a few weeks; in
others the disease becomes chronic and will last for months or years.

_Treatment._ Among the first indications are fresh air and wholesome
easily digestible food. The removal of any source of intestinal
irritation should be sought by bland laxatives. As the health is usually
low, a course of iron tonics is nearly always in order.

Special nervous tonics are next demanded. No agent has a better
reputation than arsenious acid. Ten drops of a 1 per cent. solution of
arsenite of soda may be given daily to the dog or one ounce to the
horse. If gastric irritation forbids the use of this agent, sulphate of
zinc may be given in 1 to 3 grain doses twice a day to the dog. In other
cases strychine ¹⁄₈₀ to ¹⁄₆₀ of a grain may be given in the same manner.

Nerve sedatives often have a good effect in calming the nervous
irritability and in this way belladonna, conium, cannabis Indica,
chloral, chloroform, acetanilid, trional, etc., have been employed.

In the same line are ice bags or ether spray applied to the spine for
ten minutes at a time, and douche baths of cold water, the animal being
afterward rubbed dry. This last partakes of the nature of a stimulant
and may be classed with gentle exercise which at once distracts the
patients’ attention from the nervous infirmity, trains him to control
the muscles, gives normal exercise and tone to the enfeebled organs and
improves the general health.

CONVULSIVE TWITCHING OF THE FACE.

Nature of phenomenon, arhythmic, hyperexcitability of nerve centres or
skin. Nerve section. Head jerking: =horse=, hard bit, severe check,
internal pain, exertion, hypersensitiveness. Treatment: nerve section.
Tongue lolling, etc. Flapping of lower lip. Nasal rhythmic movements.
Weaving, from impatience, rhythmic. Rocking on hind limbs. Resting
foot on coronet. Pawing. Treatment: eliminate irritation, nerve
tonics, sedatives, hygienic measures.

This has been observed especially in the dog and may be easily
confounded with chorea. The muscles on one side of the face, are
twitched at more or less regular intervals, or in other cases there are
sudden opening and closing of the lower jaw. The affection has not been
satisfactorily connected with any special brain lesion, though as in
chorea proper and epilepsy, we must invoke a special disorder or
hyperexcitability of the nerve centres presiding over the affected
muscles. The clonic spasm may in some cases be due only to a motor
impulse from such excited nerve centre, while in others it may be traced
backward along the afferent nerves to an oversensitive part of the skin
or other organ. In these last purely reflex forms of the trouble it may
be possible to correct it by section of the sensory nerves involved.

Convulsive Movements of the Head.

Convulsive movements of the head as a whole constitute a frequent form
of chorea in the dog. It is especially common in horses and shows itself
in different forms. A horse with a tender mouth, or which has been used
with a hard bit, or with a heavy hand on the reins, or which has been
driven with a check rein so short as to be unsuited to its conformation,
is liable to indulge in annoying elevation and depression of the head
when under the saddle or in harness. The same phenomenon may be shown in
connection with violent internal pains, as in strangulated hernia,
intussusception, or twisting of the bowels. The habit once formed is not
easily corrected, so that careful treatment with the view of prevention
is especially to be given.

Another more objectionable, dangerous, and less voluntary motion is the
sudden jerking of the head upward, or to one side when excited under the
saddle or in harness. The disorderly movements are not, as a rule, seen
while the animal is at rest, but seem to be produced under the stimulus
of exertion. They appear to be quite involuntary, and suggest the dread
caused by the settling or buzzing of an insect about the nose or ears,
but occur in the depth of winter in the absence of insect life, as well
as in midsummer. The suddenness and involuntary nature of the movement
is suggestive of epilepsy, but there is no indication of attendant
unconsciousness. From choreic movements it is apparently distinguished,
by its presence only when ridden or driven. It is unquestionably
associated with hypersensitiveness of the nerve centres, and yet in many
cases it appears to be a reflex originating in a specially tender or
sensitive part of the skin or mucous membrane. In more than one instance
in this college clinic the trouble was corrected by the section of both
facial branches of the 5^{th} cranial nerves as they emerged from the
infra-orbital foramina.

Abnormal Movements of the Tongue.

Some horses double the tongue downward, others upward of the bit; others
protrude the tongue and give it a sinuous, serpentine motion which
causes alternate protrusion and retraction.

Flapping of the Lower Lip.

This habit of rapid opening and closing of the lower lip so as to
produce a disagreeable flapping noise by striking it against the upper,
is seen in many horses and proves a most objectionable trait in harness
or saddle animals.

Rhythmical Movements of the Nose.

Certain horses apply the protractile end of the nose against the lower
lip and spend hours in succession in moving it rhythmically forward and
backward, or from side to side.

Weaving. Movement like a Bear in a Cage.

This consists in a lateral rocking of the head and neck, and sometimes
of the chest as well with alternate stepping on the right and left fore
feet. It has been supposed to represent the movement of the weaver in
working a hand loom, or still better the movement of a caged wild beast
in constant turning toward the right and left of the front of his cage.
The motions are as regular as a pendulum, and involve the contraction of
corresponding groups of muscles on the two sides of the body.

They seem, in some cases, to begin in impatience in waiting for the
feed, while other horses in the same row are being attended to first,
but when the habit has been formed it may be continued most of the time
in the intervals between feeds as well. Nervous horses and those that
are hearty feeders are the most subject to this infirmity.

Disorderly Movements of the Limbs.

Some horses have a habit of continuously raising one hind limb, others
raise the right and left alternately, rocking the hind quarters from
side to side, others stand with the heel of one hind foot resting on the
front of the coronet of the other, while still others paw continuously
with the fore feet while standing in the stall.

_Treatment._ These various conditions even when begun as an expression
of impatience, soon become fixed habits, that prove in the end virtually
uncontrollable by an animal, which has no strong will and no
consciousness of anything to be gained by resisting the impulse. They
become virtual psychoses. In cases in which the habit can be traced to a
peripheral irritation, the cutting off of this by complete section of
the afferent nerves leading to the irritable nerve centre will sometimes
succeed in effecting a cure. In other cases in which the source of the
disorder is probably largely central in the cerebral ganglia, nerve
tonics, and sedatives, and generally corroborative treatment are the
most obvious means of palliation. Such measures are, however, rarely
successful. Nourishing food and invigorating outdoor exercise are useful
auxiliaries.

VERTIGO. MEGRIMS. BLIND STAGGERS.

Disadvantage of lack of subjective symptoms. Causes, varied,
narcotics, overloaded stomach, cerebral anæmia or hyperæmia,
degenerations, parasites, tumors, jugular obstruction, valvular heart
disease, disease of internal ear, plethora. Susceptible animals,
horse, ox, dog, pig, sheep. Direct causes: tight collar, or throat
latch, flexion of head, heart disease, pulmonary disease, embolisms,
gastric distension, hepatic disorder, optic vertigo, aural vertigo,
injections into ear, rhigolene, chloral, acariasis, seasickness,
railroad sickness, cholesteatoma, cœnurus, concussion, degeneration,
softening, œstrus, linguatula, narcotics, essential oils: essential
vertigo. Symptoms: in irritable animal, highly fed, and without
exercise, crowds pole, his mate or a wall, shakes or jerks head,
staggers, trembles, rears, plunges, falls, struggles, sweats, rolls
eyes, recovers. In gastric or hepatic cases, dullness, pendent head,
swaying gait, dull eye, dilated pupil, pendent lids and lips, leans on
adjacent object, staggers, falls. In optic cases are obvious cause in
transition to light, etc., and palliation by covering the eyes. In
aural cases, rolling eyes, constrained position of ear, deafness,
pharyngeal or Eustachian trouble, wax or acari in ear, tender or itchy
ear. Plethoric cases in spring, in overfed, etc. Brain lesions may
have fever and disordered innervation, but retained consciousness, and
no marked spasm. Duration. Sheep: parasitic vertigo. Turning.
Rotation. Treatment: according to cause: restrict ration, give
exercise, purgative, adjust collar, breast strap, check, avoid sudden
transitions of light, overdraw check, blinds, treat nasal, pharyngeal,
ocular or aural trouble; during attack, stop in shade, cold to head,
deplete, bleed, purge, shady pasture or light work, bromides,
blisters, etc.

In dealing with vertigo or giddiness in animals we are confronted by the
impossibility of realizing the subjective feelings of the animal, as we
can so easily ascertain by interrogation in the case of man, and thus
our conclusions are largely inferences drawn from certain unsteady,
reckless or uncontrollable movements, or from an apparent inability to
maintain a stable equilibrium. The condition is rather a symptom of a
variety of morbid conditions, functional and structural, than a disease
_sui generis_. It may be due to alcoholic or other narcotic
intoxication, to overloaded or otherwise deranged stomach, to shock, to
a stroke of lightning, to disturbances—anæmic or hyperæmic—in the
circulation in the encephalon, to degenerations, parasites or tumors in
the brain, to compression of the jugular veins, to valvular or other
disease of the heart, to disease of the internal ear, to the plethora of
spring or early summer, to the qualms of sea sickness, to insolation.

The purely toxic cases are more clearly defined and temporary so that
they may be eliminated from consideration at present, yet their possible
occurrence must always be borne in mind by the practitioner especially
when called to pronounce upon cases of vertigo in connection with
veterinary legal questions. The cases that are due to a persistent
neurosis, or to circulatory troubles may well be placed in a list by
themselves, yet in their legal relations it is highly important that the
practitioner should as far as possible discriminate among these as well.

_Susceptible Animals._ Vertigo undoubtedly exists among all domestic
animals. The symptoms by which it is recognized have been noted
especially in the horse and much less frequently in ox, dog, pig and
sheep.

Among _horses_ it especially attacks the mature or aged, and family
harness horses, pampered and irregularly exercised; (saddle horses
rarely suffer); it is more likely to appear for the first time in spring
though when established it happens at all seasons; it may come on when a
horse is driven in blinders and fail to appear in the absence of these.

_Causes._ 1st. =Compression of the jugular veins= by a too tight collar
is the cause of one of the simplest forms of vertigo and is observed, in
growing or fattening animals in which the neck has become gradually too
large for the collar. The supply of a larger and well fitting collar
will soon confirm the diagnosis by a complete and permanent removal of
the trouble. In other cases the veins may be compressed by undue flexion
of the head, the chin being drawn toward the breast, or by a throat
latch buckled too tightly. The substitution of an overdraw check rein,
or a loose throat latch will show the true source of the trouble.

2nd. =Disease of the valves= _of the heart_ or their insufficiency from
cardiac dilatation is a common cause of vertigo, and may be recognized
by auscultation and by the general symptoms of chronic heart disease.

3d. =Disease of the lungs= interfering with the flow of blood through
the right heart and more distantly with the return of blood from the
brain. It further effects the brain functions through the circulation of
a highly carbonized blood, which fails to maintain the normal functions
of the ganglia.

4th. =Disease of the blood vessels=, it may be by emboli washed on from
clots in the pulmonary veins or the left heart and arrested in the
vessels of the brain; it may be by aneurism of the anterior aorta as
reported of a horse (Lustig); it may be by phlebitis and thrombosis of
the jugulars; it may be by adjacent tumors pressing on the vessels.

5th. =Gastric Vertigo=, =Abdominal Vertigo=, is a complication of
gastric or hepatic disorder with giddiness and unsteady movement. The
abdominal disorder may be at once a cause and result of the vertigo and
it is not always easy to decide which predominates. The unsteady
movements in certain cases of overloaded stomach, in the horse are
illustrations of purely abdominal vertigo, while on the other hand in
vomiting animals nausea, retching, emesis, and other gastric disorders
promptly attend on the primary cerebral disorder. There is also a
special tendency to vertigo in the fat, idle, gorged horse and in those
with torpor or other disorder of the liver occurring in pampered horses
in spring and early summer.

6th. =Optic vertigo= is a reflex disorder, determined in the excitable
nerve centres by the visual influence. Thus it has been seen in horses
and sheep from the intense glare of the sun’s rays, reflected from a
lake or river or from white snow or ice, or even from the glistening
inner surface of the blinds. The effect is intensified if the animal has
just emerged from a dark stable or a darker mine. The overdraw check may
be a factor by reason of its turning the eyes upward and exposing them
continuously to the full glare of the sun. The sense of motion conveyed
through the eyes contributes to bring on giddiness and a sense of
swimming. In man this is notorious, the sense of nausea and vertigo
being precipitated by looking at the nearby, moving objects in cabin or
on deck, while it may be retarded by directing the eyes to steady
distant objects. As dogs, horses and other animals suffer from
seasickness, and even railroad sickness, this attendant factor may be
logically accepted. The mere limitation of the field of vision, by the
use of blinds, and the disappearance in rapid succession of near objects
behind this narrow screen probably has an influence similar to the
visible motions in the ship between decks, in cases in which these
portions of the harness are manifest factors.

7th. =Aural Vertigo= is determined by irritations of different kinds
affecting the external, middle or internal ear. Experimental sections
show that this is especially due to injuries of the semicircular canals.
If the _horizontal canal_ is divided there are pendulum-like movements
of the head alternately to the right and left, also lateral rolling of
the eyes. If the _posterior canal_ is cut there is a vertical movement,
or nodding of the head and vertical rolling of the eyes. If the
_superior vertical canals_ are injured there are pendulum-like vertical
movements of the head and the animal tends to fall forward. Injury to
the _anterior canal_ causes diagonal rolling of the eyeball. In
destruction of _all the canals_ various pendulum-like movements are
performed, and standing often becomes impossible. Stimulation of one
auditory nerve is followed by rotation of the eye and rotation of the
body on its axis toward the injured side. The passage of a galvanic
current through the head _between the mastoid processes_, or _from one
external auditory meatus to the other_, causes rolling of the eyeballs.
_Injection of water violently into a rabbit’s ear_, or of _iced water_
or of a _rhigolene_ jet, causes rolling of the eyes, and rotation of the
body toward the side operated on. Dr. Weir Mitchell had a similar
experience in his own person. If the injections are repeated a permanent
vertiginous condition is induced, and the rabbit or Guinea pig, which
has been kept in darkness for a few hours and is then suddenly exposed
to sunlight, is unstable on its limbs for a few seconds. Lucæ found that
with perforation of the membrana tympani, an _ear air douche_, at 0.1
atmospheres caused abduction of the eyeball, dyplopia, giddiness, sense
of darkness, and disturbed respiration. Vulpain found that a 25 per
cent. solution of _chloral hydrate dropped into the ear_ of a rabbit
caused vertiginous movements. McVey records the case of a music teacher
who had intense vertigo induced by the _low bass notes_ of a piano. Crum
Brown noticed that if a person with bandaged eyes, is rotated for some
time as on a potter’s wheel, he can at first estimate the degree of
rotation, but after a time he fails to do so, and the rotation may be
stopped, without checking his sense of whirling. The familiar method of
subduing an intractable or vicious horse by _running_ him rapidly around
_in a very narrow circular course_, or by tying head and tail together
and letting him circle around until he staggers or falls, is another
manifest example of this aural vertigo. Rabbits and dogs suffering from
_acariasis of the external ear_ move around in a circle, or even turn
somersaults tending toward the affected side. Trasbot has found larvæ of
insects (simulium cinereum?) in the ears of vertiginous horses, which he
successfully treated with injection of chloroform. Even hard pellets of
wax pressing on the tympanic membrane have been found to give rise to
vertigo.

The explanation of cases of aural vertigo, has been sought in the
physiological action of the endolymph and perilymph on the end filaments
of the nerve in the membranous labyrinth, the turning of the head from
one side to the other having the effect of changing the pressure in
different parts and establishing currents by which the change of
position is recognized; on the other hand any injury to the canals, by
disturbing the pressure of the perilymph and interfering with the
relative position of the canals, and the direction and force of the
currents of the endolymph and perilymph, destroys all proper sense of
balance. The rotation of the subject as on a wheel or in turning in a
narrow circle, is held to cause circular currents in and around the
membranous labyrinth which temporarily destroy all sense of equilibrium.
Seasickness and railroad sickness are doubtless in part due to the
swaying motions causing disturbance in the canals. The intimate relation
between the root of the auditory nerve and that of the vagus in the
medulla, may serve to explain the mutual interdependence of derangement
of the stomach and liver on the one hand and the occurrence of vertigo
on the other. Again the relation of vertigo to visual troubles, both as
to cause and effect, has been attributed to the close relations of the
ganglia presiding over the 3d, 4th, 5th and 6th nerves and those of the
nerve of hearing.

There is a degree of deafness in nearly all cases of aural vertigo, a
circumstance which may be utilized in the diagnosis of such cases, the
presence of disease of the guttural pouch, or Eustachian tube, and
evidence of deafness on one side rather than the other, may be taken as
corroborative evidence of the affection. On the other hand James shows
that the stone deaf are much less subject to both seasickness and
vertigo than those that hear. The disorder that leads to vertigo implies
a retention of a measure of the normal function of the internal ear, and
therefore of hearing, whereas the disease that has caused complete
destruction of the internal ear and consequent loss of hearing has
equally destroyed the function of the labyrinth in maintaining a sense
of balance, and has obviated the aural sensations of equilibrium and
loss of balance.

8th. =Cerebral Vertigo= may be associated with derangement of the
circulation, or disease in the brain or its meninges. Anæmias and
congestions resulting from disease or impaired function of heart, lungs,
arteries or veins have been already noticed. It remains to note the
presence of cholesteatomata and other tumors, and of parasites
(cysticercus cellulosa in pig; cœnurus cerebralis in sheep) in the
encephalon, and of injuries from concussion, degeneration and softening
of the brain substance.

9th. =Nasal Vertigo= has been noted by Cadeac in connection with
irritation in the nose and especially by the larva of œstrus ovis
(sheep), and the linguatula (dog, horse). In certain of the cases
manifested by jerking of the head and diverging to one side, the
recovery after section of the pes anserina indicates a nasal origin.

10th. =Vertigo from Narcotics= (alcohol, lolium temulentum, belladonna,
solanum, various essential oils, carbon monoxide, etc.), have been
already referred to.

11th. There remains to be noted cases in which no narcotic poison, no
mechanical disturbance of the circulation, no visual, aural nor nasal
trouble, no gastric nor hepatic disorder, and not even a distant nervous
lesion can be found; the disease may in such cases be ranked for the
present as =essential vertigo=.

_Symptoms._ As usually seen in the horse, vertigo often attacks the
nervous, irritable animal in which the slightest occasion of irritation
or disturbance causes intense suffering and quick response. This is
often aggravated by the plethoric condition of the animal, kept on a
liberal ration of grain and having little exercise. In some forms of the
affection, however, and especially the gastric and hepatic, the subject
is dull, carries the head low, and lacks vivacity and energy.

In the first form (the most common in the horse) the animal which has
been full of life and vigor, slackens his pace and the tension on the
reins, or stops suddenly, shakes the head, vertically or horizontally,
or jerks it to one side, trembles, staggers, props his legs outward for
more stable support, presses against the pole, or the other horse, or a
wall, leans on the breeching or hangs on the breast strap, plunges
forward, or to one side, or rears up and even falls backward, and comes
to the ground. Profuse perspiration ensues, the eyes roll, the face is
pinched and drawn, the prostrate animal may struggle in a helpless way,
and, if the harness is loosened, he may get up in a few seconds and
slowly recover. Often, however, he remains for an hour or more, nervous,
sensitive, bedewed with sweat, trembling and with anxious expression.
Such are the more common manifestations of what is familiarly known as
blind staggers. The symptoms will vary however, with the cause.

In =gastric= or =hepatic= cases there may be more particularly dullness
and lack of energy, low carriage of the head, unsteadiness of gait, lack
of lustre in the eye, pupils dilated, semi-closed eyelids, pendent lips,
a tendency to lean on the stall or hang on the harness, and though the
animal may stagger and fall, there is not the abrupt transition from
life and energy to the active excitement and uncontrollable movements.
The same remarks apply in a measure to narcotic vertigo.

With =optic vertigo=, the attendant conditions will help to a diagnosis.
The animal has come from darkness to full sunshine; there is the white,
icy or snowy reflection everywhere which the animal was facing when
attacked, or the glistening lake or river, the overdraw check rein, or
the blind with perhaps a shining inner surface. The pupil is closed, and
the eye is rolled back or oscillates in one direction or another. The
symptoms are checked by covering the eyes or removing the subject into a
dark building or even into the shade of a tree or shed.

With =aural vertigo= there may be similar rolling of the eyes, without
the pupillary closure, the ear may be drawn down or back, and the
shaking or jerking of the head is likely to be a marked feature. If
there is more motion of one ear than the other, if the head is jerked to
the one side, if there is a measure of deafness in the one ear (to be
ascertained rather in the intervals between attacks), if there is
disease of the pharynx, the Eustachian tube or pouch, or swelling about
the root of the ear, if there is wax, scurf, or acarus in the ear, if
the animal rubs it frequently, aural vertigo may be suspected.

=Nasal vertigo.= Those forms in which the head is jerked horizontally,
vertically, or diagonally, the animal pressing against its mate or the
pole, or outward in the harness, and getting out of its track, even if
it should stop short of falling, and which appear only during work, or
are aggravated by exertion, have been attributed to lesions of the ear
(Fleming), but in some cases they can be warded off by wearing a net
over the nostril, and can be entirely stopped by complete transverse
section of the pes anserina, so that in a certain number at least they
must be accounted nasal. These are not usually attended by sneezing. The
simple expedient of driving with a rather close net over the nostril may
enable one to diagnose many of the purely nasal forms.

=Plethoric vertigo= may be suspected when the attack comes on in spring,
in a fleshy or fat horse, overfed and little exercised, when there is
dark red congestion of the nasal mucosa and conjunctiva, and a
subsidence with rest.

In the _vertigo_ of brain lesions, the acute forms are attended by fever
and marked signs of delirium or disordered nervous functions, while in
the chronic forms there may be permanent hyperæsthesia or anæsthesia,
general or with rather diffuse limits, and the vertiginous attacks
repeat themselves frequently irrespective of weather, though they may be
precipitated by faults of feeding, indigestion, severe exertion, or some
of the other exciting causes above mentioned.

These cases are to be distinguished from epilepsy by the absence of any
spasmodic contraction, aside from the jerking of the head and rolling of
the eyes, and by the fact that consciousness is retained throughout.
During the attack the animal may fail to respond to irritation of the
nasal mucosa, but this appears to be due to the fact that his whole
attention is engaged with a more serious trouble.

The duration of an attack is from one to two, or exceptionally five
minutes. The form which is represented by jerking of the head and
deviation from the direct line of motion may continue so long as
exercise is kept up.

In the =nasal vertigo= of sheep and dogs, due to parasites, sneezing,
and congestion of the mucosa are to be looked for.

In the =cerebral parasitic vertigo= of sheep and pigs, the symptoms vary
according to the seat of the parasite. These may be blindness, turning
in a circle, moving straight ahead regardless of obstacles, jerking
upward of the head with nose protruded, hemiplegia, hemianæsthesia,
cross hemiplegia, cross hemianæsthesia, and any one of the many forms of
paralysis, or exaggerated nervous action. The animal usually turns to
the side on which the parasite lies and is paralyzed on the opposite
side of the trunk. A peculiarity of these cases is that while the
symptoms are continuous, yet there are periodic aggravations which bear
no relation to feeding, exertion or excitement, but depend on the
protrusion at intervals of the heads of the parasites into the brain
substance. If there are several parasites in the brain and they do this
at different times the symptoms are liable to vary according to their
seat, and the special organ which is irritated. This variability of
symptoms is suggestive of parasitism.

While turning around in a circle has been already noticed there remains,
in certain cerebral forms, the peculiar phenomenon of the animal
rotating rapidly on its longitudinal axis. The patient falls on its side
and rolls over and over. Among the brain lesions with which it has been
experimentally identified are injuries to the _middle peduncles of the
cerebellum_, or of the _superoexternal portion of the cerebral
peduncles_, or of the _posterior part of the encephalon_, or of
different parts of the hemispheres.

Cases of vertigo that occur without any appreciable lesion have been
named _essential vertigo._ Guibert has attributed some cases to
irritation of the lower part of the limbs by contact with the litter but
this could only occur in an animal in which the nervous system was in a
morbidly excitable condition.

_Treatment._ The prophylactics and therapeutics of vertigo will vary
with the cause. The diagnosis of the cause is therefore the most
important step. In pampered, overfed, idle horses a reduced ration and
daily exercise or work will often suffice. It is usually desirable,
however, to remove intestinal irritants and deplete the vascular system
by an active purgative. If the attacks appear only in Spring this care
should be especially given at such seasons. A tight or badly fitting
collar should be corrected, also a position of the breast strap which
causes it to press on the jugular veins. A short bearing rein causing
undue flexion of the head must be lengthened or abandoned. A too dark
stable should be avoided, also the sudden exposure to white, dusty roads
and, still more so, to the glare of snow, ice, or water. A short,
overdraw check rein, turning the eyes up directly into the sun’s rays,
or blinds with a glistening inner surface may require correction. It may
be better to abandon blinds altogether, or to cover the eyes by a piece
of leather, 2 to 4 inches wide, extending across the forehead from one
eye to the other; or a sunshade attached to the headstall may be worn so
as to protect the eyes. Horses which become seasick or carsick may
sometimes be helped by covering the eyes. Other indications would be to
treat any existing trouble which interferes with a normal circulation in
the brain (pulmonary congestion, aneurisms, tumors pressing on carotids
or jugulars, phlebitis, etc.), and such as affect the ear (disease of
the pharynx, guttural pouches, adjacent glands, petrous temporal bone,
membrana tympani, external ear). Indurated wax, insects or insect larvæ
may be removed by careful irrigation with warm water, and perhaps by
chloroform. Nasal parasites must be washed out or destroyed by benzine,
and any hyperæsthesia of the nasal mucosa may be met by covering the
nostril with a net, or radically by cutting the facial branch of the 5th
nerve as it emerges from the infra-orbital foramen.

When attacked the horse should be at once stopped and put under the
shadow of a roof or tree, or in their absence a blanket or lap robe may
be used to cover his eyes. If there is danger of falling remove the
harness, and secure a soft piece of ground, free from stones or other
hard bodies. Cold water applied to the head will sometimes check. A
common practice is to bleed from the palate, and in plethoric cases
especially, and in such as are dependent on congestion, tumors or other
lesion of the brain it is to be commended. The action will be rendered
more prompt and effective if the blood is taken from the jugular. A
laxative diet, and carefully regulated work are desirable to obviate the
tendency to the affection, and this may often be accomplished by a run
at pasture. Otherwise daily small doses of Glauber salts in the feed may
suffice. Bromides may be used to calm nervous excitement.

In cases of =gastric vertigo= an active cathartic, followed by smaller
laxative doses or a laxative diet and a course of bitters may prove
useful. Such cases should never be worked on a full stomach but should
be left at rest for at least an hour after a meal.

In =aural vertigo= special attention must be given to the throat, and
external ear. Bromides may often be useful, and sometimes benefit may be
derived from an occasional blister or light firing back of the ear.

In =cœnurus cerebralis= in sheep the only resort is to trephine and
remove the parasite.

CONCUSSION OF THE BRAIN.

Definition. Causes: leaps, trips, falls, blows. Symptoms: fall,
insensibility, flaccidity, suspended respiration, tumors, vomiting,
recovery, signs of cerebral congestion. Pathology: anæmia followed by
congestion. Diagnosis: from fracture, epilepsy. Treatment: quiet,
rubbing of limbs, ammonia, cold to head, or heat; for congestion,
bromides, depletion, ice pack, derivatives.

_Definition._ Concussion is the condition produced by mechanical jar or
shock of the cerebral mass, and manifested by modification of the brain
functions of any grade from a simple dazed condition to that of complete
unconsciousness.

_Causes._ The most familiar cause is the stroke of the butcher’s pole
axe, producing sudden and absolute insensibility. A horse in leaping,
trips and falls on his head or running against a wall sustains a
concussion, which leaves him for some seconds without any signs of life.
The same will happen to other animals, but above all to rams which in
their combats, back for a number of yards and running together meet with
a shock from the effect of which even their thick skulls cannot save
them. Other blows upon the head operate to the same end.

_Symptoms._ Concussion is manifested by different grades of symptoms. At
first there is usually a fall with complete insensibility. The animal
lies flaccid, utterly insensible to external irritation and there is
suspension of respiration. The heart continues to beat and a frequent
weak pulse may be often detected. In slight cases, breathing may be
reestablished at the end of a minute or two, with muscular tremors and
movements of the limbs; then the animal rises, shakes his head, neighs,
and walks at first unsteadily and afterward with greater and greater
firmness. In vomiting animals, emesis occurs.

In some cases this may be followed, after an hour or two, by signs of
congestion, heat of the head, redness of the eyes, irritability, or
dullness and stupor and perhaps muscular twitching. This may improve or
it may terminate in death preceded by spasms, general convulsions,
rolling of the eye balls, and stupor or coma with general muscular
relaxation.

The primary condition is usually an anæmia of the cerebral matter as
seen in the brain of the animal suddenly killed by the blow of a hammer.
The return of consciousness or semi-consciousness is connected with the
resumed freedom of the cerebral circulation. The later convulsions,
stupor or coma, usually imply active congestion or the effusion of blood
on the brain surface, or in its substance.

_Diagnosis_ from fracture must be made mainly by manipulation of the
bone in the seat of the blow, and by the absence of the increasing
stupor and coma which attend on pressure from a gradually increasing
blood clot. From epilepsy it is to be distinguished by the evidence of
mechanical injury, by the absence of spasms at the first, by the
suspension of breathing and the absence of froth about the lips.

_Treatment._ Keep the patient still and prostrate until there are signs
of returning respiration and free cerebral circulation. This may be
hastened, however, by active rubbing of the limbs and body, by giving
guarded inhalations of ammonia, or even by friction of the skin with
ammonia and oil. Sometimes reaction is favored by dashing cold water on
the head, while in other cases hot water to the poll will prove more
effective, or the two may be used alternately with good results.

If, after partial recovery, there is marked restlessness, or
irritability it may be met with bromides. If secondary unconsciousness
supervenes effusion of serum or blood is to be feared, or extreme
congestion, and blood may be drawn from the jugular or by cups from the
cranium, and ice bags or cold water may be applied to the head. Hot foot
baths or mustard embrocations applied to the limbs, and even derivation
toward the bowels may be used. The indications for treatment come to be
for meningo-encephalitis.

LIGHTNING STROKE. ELECTRIC SHOCK.

Fatal. Non-fatal. Herbivora at pasture under tree. Symptoms: dazed for
a few minutes, unconscious for hours, permanent paresis or paralysis.
Lesions: lines of burned hair, skin or muscles, rigor mortis slight,
decomposition rapid, bluish black venous and capillary congestion,
extravasations, blood fluid. Diagnosis. Treatment: ammonia, ether,
alcohol, caffein, nerve stimulants.

While a stroke of lightning is usually fatal, yet in certain cases, the
victim is but temporarily stunned and recovers with more or less
remaining paralysis. The subject has also great importance in connection
with the claim of the owner against a company which may have insured his
stock against lightning.

Any animal may be struck, but the herbivora which are turned out to
pasture are especially liable to such injuries, because they seek
shelter under trees, which operate as lightning rods.

_Symptoms._ In slight cases of shock whether by lightning or the current
of a hanging live electric wire, the subject may be simply dazed and may
or may not fall to the ground, and recover itself in a very few minutes.
In other cases there is a more violent shock which prostrates the animal
to the earth, where it may lie unconscious for some hours and yet
quickly and completely recover. In still other cases after such
prostration recovery is incomplete and the animal remains affected with
paresis or paralysis of one or more, commonly of both hind, or all four
limbs. In the more violent shocks death is instantaneous.

Often the impact and course of the current are marked by visible
lesions. Sometimes the skin is wounded exposing a bluish black tissue
beneath. More commonly there is an area of burnt hair, or straight,
radiating or angular lines of raised and frizzled hair marking the
course of the current. In a horse killed by an electric light wire in
Ithaca recently the current had burned to a depth of several inches in
the muscles of the shoulder which rested on the wire.

_Lesions_ are often rather indefinite. There may be no appreciable
change in the nervous system. Rigor mortis is slight; it passes off
rapidly and decomposition sets in early. The venous system and
capillaries are usually filled with liquid blood of a dark bluish black
color, and at intervals are points, spots and patches of blood
extravasation. The uniformly liquid state of the blood is one of the
most marked phenomena of death from electricity. The dark blue
congestion of the radical veins is also very pathognomonic, the part
struck or traversed by the main current, being the seat of the most
elaborate arborescent network. This arborescent appearance of the dark
colored veins, and the petechiæ are often marked in the internal organs
(brain, kidneys, liver, lungs).

_Diagnosis._ The environment of the animal will often clear the
diagnosis. The patient is found helpless, or dead under a tree, by a
pole, or under a hanging wire, and if a tree there are evidences of the
electric shock in scattered leaves and branches, stripping off of the
bark, or perhaps rending of the tree in pieces. In case of wires
attached to or passing near such a tree, the supporting poles show
similar splitting and rending. Add to these the fluidity of blood in the
carcase, the thickly ramifying network of the minute dark bluish, red
veins, the petechiæ and the comparative absence of cadaveric rigidity,
and we have a picture very significant of lightning stroke.

_Treatment_ in such cases is according to the condition. The primary
unconsciousness is met by inhalations of ammonia or ether, or the
injection of brandy or alcohol subcutem. Caffein, atropine or hyoscyamin
may be used as substitutes. If consciousness returns recovery is usually
rapid and complete. Should paresis or paralysis remain it must be
treated like any ordinary case of these affections.

INTRACRANIAL HÆMORRHAGE AND THROMBOSIS. APOPLEXY. SOFTENING OF THE
BRAIN.

Definition. Causes: Nature: intracranial rupture, with pressure,
serous effusion, excessive congestion, experimental cases, anæmia from
pressure, comparative immunity of horse, heart disease, Bright’s
disease, atheroma, degeneration, emboli, age, blood tension, severe
exertion, excitement, concussion, insolation, venous obstruction,
toxins, neoplasms. Lesions: blood clots, small and multiple, large and
solitary, brain absorption, cavities, cysts. Symptoms: dullness,
swaying, trembling, elevation of head, turning in circle, sudden fall,
spasms, unequal dilated or contracted pupils, eyes turned to affected
side, congested or anæmic mucosæ, stertor, puffing cheeks except in
solipeds, pulse slow, soft, full, vomiting, stupor, coma,
unconsciousness, paralysis, monoplegia, hemiplegia, sequelæ.
Diagnosis: sudden unconsciousness, with little spasm, but paralysis,
history, sign of trauma, deep coma, eyes turned to one side, pupils
unequal, stertor, slow breathing and pulse; from uræmia, pulmonary
apoplexy, œdema or anthrax. Treatment: bleeding, ice pack, snow, cold
water, rest, derivatives to limbs, later purge, bromides, potassium
iodide, tonics, open air life.

_Definition._ Cerebral apoplexy has been defined as a sudden loss of
sensation and voluntary motion, from pressure originating within the
cranium and followed by paralysis, often unilateral. The definition is
somewhat insufficient as regards the early symptoms as the same
conditions attend on convulsions and epilepsy (haut mal), and it is only
by excluding these by their characteristic features of sudden seizure
with clonic spasms and their intermittent and paroxysmal habit that we
reach an easy and satisfactory distinction. Later the paralysis tends to
identify the apoplectic attack.

_Causes and Nature._ The immediate cause and essential lesion of
apoplexy has been generally held to be the rupture of an intracranial
artery and the formation of a considerable blood clot which presses upon
(and abolishes the functions of) the brain. There are cases, however, in
which the characteristic symptoms are present, and yet a complete
recovery ensues at an early date, too early to allow for the absorption
of a considerable clot. Moreover, in fatal cases perhaps no blood clot
is to be found, but in place a serous effusion, or an internal
congestion which exercised the fatal pressure on the brain. So far,
therefore, as clinical phenomena are concerned, we must allow that
apoplexy may arise from any sudden pressure on the brain substance.
Pagenstecher produced the symptoms of the disease by injecting, at a
regulated pressure, melted wax and tallow between the skull and dura
mater in the dog. In the moderate cases there were drowsiness, psychic
depression and general muscular weakness. In the more severe ones there
were added sleep and unilateral paralysis. In the more extreme cases
death followed in a few hours after coma set in, though in some of these
a partial recovery ensued if the waxy mass was scooped out before the
fatal symptoms appeared. Cases ended fatally only when the injection
pressure equalled that of the blood, and convulsions occurred only when
the pressure was unsteady. The temperature fell as it does in apoplexy
in man, at the outset, but it continued falling to the fatal issue
contrary to what takes place in man.

Duret injected water into the cranium of animals so as to produce great
tension of the occipito-atloid membrane causing thereby arrest of the
respiration and slowing of the heart’s action. On tearing the membrane
so as to allow escape of the water, respiration began anew and
consciousness was gradually restored.

Edes sustains the view that apoplexy is directly due to anæmia of a
lesser or greater portion of the brain substance, and that this need not
be in any one particular seat nor of any definite extent. This anæmia is
usually induced by pressure and may be caused by effused blood, or
serum, or by the extreme congestion due to narcotic poisons, or other
cause. Embolism of a cerebral vessel, however, by cutting off the blood
from the part of the brain which it supplies may give rise to the
apoplectic phenomena.

Friedberger and Fröhner found apoplexy quite frequent in sheep, ox. and
dog, and rare in the horse, although more subject to the violent
exertion which they put in the front of all causes. It is probable that
the sluggish, pampered life of the first three animals, and the tendency
to fatty degenerations and heart disease introduces a special
predisposition as it does in man, while the horse, inured to an open air
life and a vigorous muscular condition, is comparatively immune.
Bright’s disease is a common cause in the human subject, with its
resulting cardiac hypertrophy. The degenerations attendant on these
conditions and especially fatty change (atheroma) in the walls of the
cerebral arteries, pave the way for their rupture and for blood
effusion. Emboli also carried from the diseased heart not only cut off
the blood from the parts supplied by the plugged arteries, but increase
the blood tension on the cardiac side of the obstruction and endanger
rupture at any weak part. Thus they may cause apoplexy from anæmia
without rupture or apoplexy from the pressure of effused blood.

=Age= which is such a notorious factor in man is not without its
influence in the lower animals. It is in the old that we mostly see
disease of kidneys and heart and the degenerations of the tissues,
including the brain and its vessels; in these, therefore, rupture and
extravasation are the most frequent.

The other causes are mostly connected with increased blood tension with
or without a debility of the vascular walls. Violent exertions as in
racing, coursing, dragging heavy loads up hill or on heavy ground,
severe excitement, cerebral concussion, insolation, and intense
congestion of the brain substance have all been recognized as causative
factors. The compression of the jugulars by a small collar, the violent
straining attendant on parturition, or constipation, and even the
retrocession of blood from the surface when exposed to extreme cold, may
contribute to the final rupture.

In infectious diseases in which the toxic products tend to produce
profound modifications in the blood and tissues, extravasations are met
with in the brain as in other organs. Thus they are seen in anthrax,
Texas fever, petechial fever, etc.

Then the formation of =neoplasms= in the brain may be the occasion of
the rupture of the vascular walls and apoplexy. =Hæmatoma= of the dura
in the dog (Friedberger and Fröhner), =cholesteatomata= in the horse,
and =carcinoma= may be apparent causes.

The effect of =mechanical injury= must be admitted, as blows on the
head, injuries from an ox yoke, and concussions during the battles of
rams and bulls.

_Lesions._ Blood extravasations may be found at any part of the brain:
a. into the brain substance; b. into the ventricles; c. from the pia
mater; d. into the arachnoid sac; e. between the skull and dura mater.
It is especially common in connection with the ganglia adjoining the
ventricles; the corpus striatum, optic thalamus, the corpora
quadrigemini, the fornix. In other cases the crus cerebri, pons, medulla
oblongata, corpus calosum. In other cases the convolutions of the
cerebrum or cerebellum suffer. The amount of effusion may be limited to
a few drops or it may cover an extensive area and cause considerable
flattening of the brain substance.

When capillary hæmorrhages are present—the size of a millet seed or a
pea—Friedberger and Fröhner have usually found them multiple, but when
large enough to form distinct clots they are usually single and confined
to one side. If a clot, involving the brain substance, is small, it
merely separates the nervous fibres, but if larger, the cerebral tissue
is broken down in the mass of clot, discolored, torn and softened. If
the patient has survived the first attack the clot passes through the
different stages of discoloration, brown, brownish yellow, yellow, and
may become fibrous forming a distinct cicatrix, with loss of brain
substance. In connection with the partial absorption of the effused
blood, cavities may be filled with a serous fluid (apoplectic cysts),
and these may show multiple loculi. The nerve fibres which lead to an
old standing lesion are usually degenerated.

When effused into a ventricle, blood is less readily absorbed and tends
to remain as a flattened discolored layer.

Extravasation between the dura mater and the cranium is probably always
the result of direct mechanical violence.

_Symptoms._ Premonitory indications of apoplexy are less commonly
recognized in the lower animals than in man, doubtless largely because
of the impossibility of appreciating subjective symptoms. The first
observed indications are usually dullness, some lack of coördination of
movement, swaying, unsteady gait, trembling and a tendency to deviate to
one side or to move in a circle. In the majority of cases, however, the
first symptoms noticed are a complete loss of consciousness or nearly
so, a sudden fall and often more or less convulsive movements of the
limbs aggravated by any excitement. The eyes remain dilated, the pupils
enlarged or sometimes contracted, and in case of unilateral effusion the
axis of vision of both eyes is turned to the affected side, right or
left. The pupil of one eye is likely to be more widely dilated than that
of the other. Rolling of the eyeballs is not uncommon. Convulsions may
occur, the head and hind limbs being drawn back forcibly as in
oposthotonos, or the animal may lie flaccid and comatose from the first.
The nasal, buccal and orbital mucous membranes are usually congested,
deep red or livid, yet sometimes they are anæmic and pale (Shock). The
breathing is usually characteristic, being deep, slow, labored,
irregular and stertorous and accompanied by puffing out of the cheeks at
each expiration (except in solipeds). Yet there are cases in which
stertor is absent. The pulse is usually slow, full and soft, and, in the
carotids, throbbing, but it may be weak and imperceptible. There may be
complete unconsciousness, and again from the first, or nearly so, there
may be a slight response to a stimulus, which cannot be referred
altogether to reflex action. In vomiting animals, emesis may ensue.
Stupor and coma are more or less marked, though liable to intermissions
under any cause of irritation.

Along with the above symptoms the spasms and sequent paralysis, are
significant. If confined to given muscles or groups of muscles
(monoplegia) it usually implies pressure on some special cortical
convolutions presiding over these muscles, and convulsions are to be
expected. If there is hemiplegia it is suggestive of implication of the
medulla or pons on the opposite side, or of a clot on the corpus
striatum or extensively on one side of the cerebrum. A clot in the
lateral ventricle tends to profound coma. So liable, however, is
pressure to be extended from one side of the brain to the other, and
irritation on the one side to rouse a corresponding condition on the
opposite side, or in related ganglia, that deductions of this kind
cannot always be implicitly relied on.

Though an animal should recover from an attack there is liable to remain
some modification of the nervous functions, partial anæsthesia,
circumscribed paresis, dullness, lack of energy, irritability, or
muscular atrophy.

Cerebral embolism and thrombosis and their sequelæ, infarction and
softening, give rise to corresponding symptoms, according to the seat of
the lesion, and like lesions of the blood vessels predispose to
subsequent attacks.

_Diagnosis_ is based largely on the appearance, usually sudden but
sometimes slow, of a more or less profound unconsciousness, attended or
followed by paralytic troubles. The history of the case may assist, any
blow on the head, or sustained by falling, striking a wall or post, or
wearing a yoke, is to be noted. Any extraordinary exertion or excitement
must be considered. Any sign of injury about the head; the congestion of
the cephalic mucous membranes in contrast with the pallor of _shock_;
the onset of the attack without convulsions (or with them as in
epilepsy); the deep coma indicating cerebral hæmorrhage or narcotic
poisoning; the absence of the odor of alcohol, opium, or other narcotic
from the breath; the turning of the eyes to one side and the inequality
of the pupils on the two sides; the turning of the head to the same side
as the eyes; the slow, labored, usually stertorous breathing; the slow,
full, soft pulse; the occasionally rigid condition of the muscles and
finally the paralysis, hemiplegic, and less frequently monoplegic or
paraplegic, make up the diagnostic picture.

_Uræmia_ and _diabetic coma_ may be excluded by examination of the
urine, _pulmonary apoplexy_ or _œdema_ by the predominance of
respiratory troubles, and fulminant _anthrax_ by the examination of the
blood and by the fact that this disease does not prevail in the
locality.

_Treatment_ is very unsatisfactory in the lower animals, as the disease
is very fatal, and unless recoveries are complete, they are not
pecuniarily desirable. It is only in the slighter cases, therefore, that
treatment can be recommended. At the very outset nothing is better than
a full bleeding in a large stream from the jugular vein or temporal
artery. Ice, snow, or cold water should meanwhile be applied to the
cranial region. Absolute rest should be given, any harness that would
impede circulation or respiration removed, and hot water or stimulating
embrocations applied to the limbs.

When consciousness returns and the patient can swallow, an active
purgative may be administered, or barium chloride or eserine may be
given subcutem. Any recurring heat of the head may be met by renewal of
cold applications, and the force of the circulation may be kept in check
by small doses of bromides or aconite. In case of the formation of a
clot, iodide of potassium and other alkaline agents may be resorted to.
Quiet and the avoidance of all excitement together with a laxative
non-stimulating diet must be secured throughout. A course of vegetable
or mineral tonics and an occasional blister to the side of the neck may
prove a useful sequel.

CEREBRAL HYPERÆMIA.
MENINGO—ENCEPHALIC CONGESTION.

Passive and active hyperæmia. Causes: _passive_: obstacles to return
of blood: anæmia: _active_: brain excitement, sun-stroke, violent
exertion, fear, abdominal tympany, ptomaines, narcotics, lead, darnel,
millet, leguminous seeds partly ripened, tumors, parasites. Symptoms:
_horse_: variable, vertigo, stupor, convulsions, apoplexy,
irritability, disorderly movements, strong, hard pulse, congested
mucosæ, heat of head, dulness, drowsiness, lethargy, coma, alternating
periods of violence, aggravated by what tends to increase vascularity
of brain, congested optic disc: _cattle_: parallel, with special heat
of horns: _dogs_: similar, with desire to move, or wander, or has
nausea, howls, snaps. Treatment: cold to head, derivation to limbs and
bowels, chloral, bromides, ergot, bleeding, darkness, coolness,
non-stimulating food.

Congestion of the encephalon is treated here as a pathological entity,
though it cannot always be distinguished clinically from some forms of
vertigo on the one hand and from the milder types of apoplexy or
encephalitis on the other. It has been divided into _passive_ or _venous
hyperæmia_ and _active_ or _arterial hyperæmia_.

_Passive hyperæmia_, as shown under vertigo and apoplexy is a common
result of a tight collar, a tight strap used for cribbiting, a too short
bearing rein, dilation or valvular disease of the right heart, or
disease of the lungs, violent efforts in running, draught, etc. It tends
to be associated with arterial anæmia on the principle that the closed
cranial cavity can only admit a certain amount of blood and if an excess
accumulates in the veins and capillaries, this must be compensated first
by the movement backward to the spinal canal of the cerebro-spinal
fluid, and second by the diminution of the blood in the cerebral
arteries.

_Active hyperæmia_ may be brought about by any excitement which
especially affects the brain. This has been already noted in connection
with insolation (sun-stroke). It may result from severe exertion during
hot weather, in a violently contested race, in drawing a heavy load up
hill, or in harsh training. Violent exertion just after a meal is
especially injurious. Also the excitement of travelling by rail, or that
caused by proximity to locomotives, to discharges of firearms and to
other causes of great fear; encreased blood tension in the cerebral
vessels in connection with hypertrophy of the left ventricle, or
obstruction in other vessels (of the limbs) so as to direct the force of
the current into the carotids, the expulsion of blood from the
splanchnic cavities by gastric or intestinal tympany, or overloading of
the paunch, and irritation of the brain by ptomaines and toxins in
certain infectious diseases (rabies, canine distemper, etc.). In the
same way vegetable narcotics (opium, etc.) produce congestion. Among the
most common causes of congestion are lead, poisoning by lolium
temulentum, partially ripened lolium perenne, millet, Hungarian grass,
and partially ripened seeds of the leguminosæ (chick vetch, vicia
sativa.). Other causes are the presence of tumors (cholesteatoma) and
parasites (cœnurus, cysticercus) in the brain.

_Symptoms._ Cerebral hyperæmia, like other brain disorders may give rise
to a great variety of symptoms, according to the condition of the animal
and the susceptibility of its nerve centres. Some cases have the
characteristic seizures of vertigo, others the manifestations of heat
stroke, and others, epileptic explosions or apoplectic symptoms. For
these see under their respective headings. In other cases the symptoms
are those of encephalo-meningitis but moderate in its type and often
tending to a transient duration, or to prompt resolution and recovery.

=Horse.= There is manifest change of the nervous and intellectual
conditions, which may show itself by irritability or restlessness, by
pushing against the wall, by hanging back on the halter, by trembling,
shaking the head, neighing, pawing and, in exceptional cases, by
rearing, biting or kicking. The pulse is hard and full, the heart’s
impulse strong, the beats in the carotids and temporal arteries being
especially forcible, and the buccal, nasal and orbital mucosæ are
strongly congested. Heat of the head is usually a marked feature. While
usually very sensitive to touch, noise or light, the animal may be dull
or drowsy, and in spite of its marked sensitiveness, it is then inert or
lethargic and indisposed to any active exertion. Freidberger and Fröhner
say that the habitual comatose condition alternates at intervals with
periods of violent excitement during which the animal pushes or dashes
against the wall, grinds the teeth, rears, paws, kicks, bites, etc., and
then relapses into the state of coma. When the disease reaches this
stage it may be questioned whether we are not dealing rather with acute
encephalitis.

In active congestion the symptoms are always aggravated by whatever
tends to increase the vascular tension in the brain. Active exertion,
draught, the pendent position of the head, the recumbent position on the
side with the head as low as the body or lower, aggravate all the
phenomena and render the animal more helpless.

The following table slightly modified from Spitzka serves to point out
the distinctions between anæmia and hyperæmia:

─────────────────┬─────────────────┬─────────────────┐
Symptoms. │ In Cerebral │ In Cerebral │
│ Anæmia. │ Hyperæmia. │
─────────────────┼─────────────────┼─────────────────┤
│ │ │
Pupils. │Usually dilated │Usually small or │
│ and mobile. │ medium. │
Respiration. │Often interrupted│Normal or nearly │
│ by a deep │ so. │
│ breath or sigh,│ │
│ even when at │ │
│ rest. │ │
Activity. │Lassitude. │Restless, but │
│ │ indisposed to │
│ │ exertion. │
Temperament. │Lethargic with │Irritable with │
│ exceptions. │ exceptions. │
Intelligence. │Senses impaired. │Impaired. │
Elevation of │Aggravates │No effect, or │
head. │ symptoms. │ improvement. │
Recumbent, │Amelioration. │Aggravation. │
dependent head.│ │ │
Straining. │Not necessarily │Aggravated. │
│ aggravated. │ │
─────────────────┴─────────────────┴─────────────────┘

=Cattle= show the same general congestion and heat of the head, ears and
horns, congested mucosæ, fixed eyes, and pupils, indisposition to follow
the herd, irritability, and dulness with often a disposition to lie
down. This may go on to violent bellowing, pushing against the wall,
grinding of the teeth, working of the jaws, rolling of the eyeballs, and
violent dashing in different directions regardless of obstacles.

=Dogs= show the same restlessness and excitability, congested head, eyes
and nose, frequent movement from place to place, a desire to wander off,
and it may be spasms. If there has been any gastric disturbance vomiting
usually supervenes. As in the larger animals the disease may go on to
more violent symptoms, and the animal howls, rushes in different
directions, and may snap at imaginary objects, or at any one who
interferes with him. His movements are liable to be unsteady, uncertain
and swaying.

In all cases the ophthalmoscope reveals a congestion of the optic disc.

In the different animals too, acute cerebral hyperæmia tends to merge
early into encephalitis with exudation and pressure, attended by stupor,
coma, somnolence or profound lethargy.

_Treatment._ In slight cases of cerebral hyperæmia, it may be sufficient
to apply cold to the head with a stimulating fomentation to the limbs,
and an active purgative, with chloral or bromides. Ergot in full doses
has often an excellent effect.

In the more acute types of the disease, bleeding is the first and most
efficient measure. A full abstraction from the jugular will relieve the
vascular tension and relieve the circulation on the brain. It has been
counselled to avoid this when comatose symptoms have set in, and in some
prostrate conditions a large and rapid abstraction of blood may fatally
increase the prostration. In other cases, however, the less rapid
abstraction will improve at once the intracranial circulation and
nutrition, and solicit the reabsorption of the exudate which produces
sopor and coma.

A purgative is one of the most efficient derivatives, the determination
of an excess of blood to the bowels and of an abundant serous discharge
into their interior acting as a valuable depletion, and abstraction of
blood from the over-excited brain. At least a half more than the usual
dose must be given, and may be supplemented by an injection of glycerine
or a hypodermic exhibition of eserine. It is best to avoid too drastic
or irritant purgatives as the cerebral congestion may be aggravated by
the irritation, as it often is induced in severe indigestions. For the
horse, aloes and podophyllin, or for ruminants, omnivora and carnivora
castor oil may be resorted to.

The patient must be placed by himself in a dark, cool, well aired
building, and when able to resume feeding must receive an easily
digested, non-stimulating diet; for horses or cattle gruels, wheat bran
mashes, pulped roots, or green food; for dogs and pigs, gruels, mush or
milk.

Any sequent paralysis must be treated on general principles.

MENINGO—ENCEPHALITIS. STAGGERS.

Divisions. Causes: traumas, faulty diet, highly nitrogenous,
leguminous seeds, undergoing ripening, cotton seed, gluten meal,
forced feeding, buckwheat, ryegrass, lupins, cryptogams, trefoil,
equisetum, narcotics, microbian ferments, experiments with spoiled
food and epizootics in wet years, high temperature, violent exercise,
railroad travel, climatic change, complex causes, embolisms,
infections, lead, phosphorus, tumors, parasites. Symptoms: with
_meningitis_, fever, hyperæsthesia, active delirium and convulsions
predominate: with _encephalitis_, dullness, stupor, somnolence,
muscular weakness, anæsthesia, paralysis, coma; usually complex,
hyperthermia, periods of benumbing, followed by excitement; drowsy,
stupid, semi-closed eyelids, drooping lips, ears, and head, latter
resting on manger or wall, walks unsteadily, limbs out of plumb, hangs
on halter, won’t back, turns in circle, costive, indigestion,
tympanies, rumbling, abnormal (often slow) pulse and breathing,
congested optic disc; alternate with trembling, excitement, pawing,
rearing, plunging, pushing against the wall, trotting motions, etc.:
uncontrollable violence; severity and frequency of paroxysms indicate
gravity; recovery: sequelæ. Duration: death in 24 to 36 hours: or
weeks. Prognosis: one-quarter recover, with increased susceptibility;
nervous animals worst. Lesions: extravasation, congestion, exudates,
pus, thickened meninges; choroid plexus: brain matter gray or red,
puncta, infiltrated, softened, excess of leucocytes, red softening,
yellow softening, sclerosis, cicatrix, abscess. Diagnosis: from
rabies, cerebral congestion, immobility, influenza. _Cattle._
Symptoms: evidence of trauma, indigestion, lead poisoning, narcotism,
parasitism; dullness, stupor, somnolence, stertor, grinding teeth,
spasms, twitching, restless movements, blindness, violent actions,
bellowing, hebetude, palsy. Relation to causation. _Sheep_: Symptoms.
_Swine_: Symptoms. _Dog_: Symptoms. Diagnosis from rabies. Treatment:
quiet, darkness, coolness, restraint, ice or cold irrigation,
elimination, derivation, depletion, diuretics, potassium iodide,
antipyretics, laxative diet, cool water, evacuate abscess. _Cattle_,
similar, saline laxatives, for lead sulphuric acid, for cœnurus,
operation, for œstrus, benzine. _Dog_, parallel treatment, milk diet
or gruels, for linguatula, benzine.

The inflammatory affections in the cranial cavity have been divided
primarily into the following:

1. _Meningitis._ Inflammation of the coverings of the brain, and

2. _Encephalitis_ (_Cerebritis_). Inflammation of the nervous
substance. These are further subdivided into:

_A._ _Pachymeningitis._ Inflammation of the dura Mater.

_B._ _Leptomeningitis._ Inflammation of the pia Mater.

_C._ _Purulent Meningitis._

_D._ _Serous Meningitis._

_E._ _Tubercular Meningitis._

_F._ _Traumatic Meningitis_, etc.

_G._ _Cerebro-Spinal or Infective Meningitis._

_H._ _Acute Meningitis._

_I._ _Chronic Meningitis._

_J._ _Polioencephalitis Corticalis._ Inflammation of the brain cortex.

_K._ _Polioencephalitis Superior._ Inflammation of convolutions around
the Sylvian fissure, palsy of the eyeball.

_L._ _Polioencephalitis Inferior._ Inflammation of the Medulla, bulbar
palsy.

_M._ _Interstitial Inflammation of the Brain._ Resulting often in
sclerosis.

In the lower animals, however, where we cannot avail of subjective
symptoms, such fine distinctions can rarely be made in diagnosis and
except in case of an uncomplicated meningitis, or a circumscribed
encephalitis, which affects only a limited group of muscles like those
of the eye, arm, or leg, we have to fall back upon a more general
diagnosis. Again meningo-encephalitis is more common than the
uncomplicated affection of the brain, or the membranes, and therefore,
we shall follow Trasbot in dealing with the combined affection, and
noting incidentally the distinctions that can be made in the more purely
limited affections.

_Causes._ =Mechanical Injuries=. Pachymeningitis occasionally results
from blows or other injuries upon the head, especially in stallions and
vicious horses struck with a heavy whip or club, cattle and sheep
injured in fighting, and oxen hurt by the yoke. These injuries may also
affect the brain as in concussion, or by the extension of the disease
into the nervous tissue. In the cranium of a stallion in the New York
State Veterinary College Museum the whole of the meninges are greatly
thickened by a traumatic meningitis of old date and the subjacent
cerebral convolutions of the right hemisphere are deeply encroached on,
flattened and absorbed over an area of 1¾ inches in the longest
diameter.

=Diet.= Among the most common causes of encephalitis in horses is an
injudicious dietary. Overfeeding with grain, but especially with grain
and seeds that are rich in albuminoids deserve the first mention. The
various leguminous seeds, peas, beans, tares, vetches, and the ripened
leguminous fodders, clover, alfalfa, and sainfoin, are especially to be
incriminated. These are usually most dangerous when in the stage of
advanced ripening and yet not fully matured, evidently indicating the
development of narcotic poison at this stage. Such poisons are found
habitually in certain species, like the chick vetch (vicia cicera) which
produces paralysis when fed to the extent of more than one-twelfth part
of the ration. This danger is not, however, confined to the leguminosæ;
an over abundant ration of cottonseed meal has a similar effect, and
indeed this rich alimentary product has been practically discarded from
pig feeding, and largely as the main constituent from the ration of
dairy cows. Gluten meal, another product rich in proteids, is attended
by similar dangers. But it is not alone the seeds that are rich in
nitrogen that are to be dreaded, forced feeding even on the carbonaceous
maize induces disorder of the digestion and brain, especially in dairy
cows. Buckwheat, also, and indeed all the heating carbonaceous grains
tend to similar disorders, and are especially injurious in internal
ophthalmia (recurring ophthalmia) which is so closely related to brain
congestion. With sound judgment and in well balanced rations, all such
agents can be fed to advantage; it is only when fed exclusively or to
excess as the heavy ration that they are to be feared.

=Narcotics.= Next must be noted those alimentary matters which are
hurtful by reason of narcotic constituents. At the head of this list may
be placed the lolium temulentum or intoxicating ryegrass. like the vicia
sativa or cicera, the seeds of this are always poisonous, hence its
significant name. Then the other ryegrasses, perennial and annual
(Italian), though perfectly safe in ordinary circumstances, develop at
the period of ripening a narcotic principle, which produces cerebral
congestion or inflammation in whole stables of horses at a time. The
lolium temulentum is poisonous to man and animals alike. Baillet and
Filhol obtained from the seeds an etherial extract containing a bland
oil to the amount of two fifths and a yellow extract to the extent of
three-fifths. The amount of this extract derived from three ounces of
the seeds often developed the most violent symptoms in the dog, while
that furnished by six pounds of the seeds proved fatal to the horse.
Pigs and cattle seemed to be unaffected by the agent when given by the
mouth. Sheep suffered more but required large doses. Ducks and chickens
were practically immune, being affected only by very large doses.
Rabbits were not poisoned by the yellow etherial extract, but succumbed
to a watery extract. Brydon found that lambs suffered extensively from
eating the heads of the ryegrass.

Lupins on certain lands produces an icteric disorder accompanied by
cerebral symptoms but the result is not the same under all conditions
and it has been suspected that the symptoms were caused by cryptogams
and their products. The same remark applies to the brain symptoms
sometimes produced by trefoil, equisetum and other plants.

A great number of =narcotic= and =narcotico-acrid= plants produce
nervous symptoms indicating cerebral congestion or inflammation such as
ranunculus, wild poppy, digitalis, fennel, œnanthe crocata, hellebore,
veratrum, conium, yew, tobacco, box, aconite, cicuta virosa, even
buckwheat at the time of flowering, vetch and flax.

Fodders affected with =cryptogams= or =bacterial ferments= are
undoubtedly at times the cause of encephalitis. Veterinary records
furnish many instances of wide spread attacks of stomach staggers,
abdominal vertigo, and cerebro-spinal meningitis in wet seasons, when
the fodders have been harvested in poor condition, or when from
inundation or accidental exposure they have become permeated by
cryptogams and microbes. Among comparatively recent accounts of this are
those of Martin and Varnell (musty oats), Lombroso, Depre, Erbe,
Pellizi, and Tireli (smuts), Bouley and Barthelemy (musty fodder), and
Ray (fermented potatoes). One of the most extended local outbreaks of
cerebro-spinal congestion I have seen, occurred in the pit mules of the
Wilkesbarre coal mines, while fed on Canadian hay which had been soaked
with rain in transit and had undergone extensive fermentation. It should
be noted that there were the attendant factors of overwork, in
anticipation of a strike, and a Sunday’s holiday above ground in a
bright summer sunshine.

The experimental administration of moulds, smuts and microbes, have in
the great majority of cases led to little or no evil result (Gamgee,
Mayo, Dinwiddie, etc.) and there is a strong tendency to discredit the
pathogenic action of these agents in reported outbreaks. The safer
conclusion perhaps would be, to recognize the fact that they are not
equally pathogenic under all conditions of their growth and
administration. The oft-recurring epizootics of brain disease in
connection with wide spread spoiling of the fodders in remote and recent
times, probably imply that cryptogams or microbes and their products,
plus some condition not yet fully understood are efficient concurrent
factors. If we can discover this as yet unknown factor and demonstrate
that it operates with equal power in the absence of the cryptogams and
ferments, as in their presence, it will be logical to pronounce these
latter as nonpathogenic under all circumstances. Until then cryptogams
and bacteria must be held as probable factors.

A continuance of =high temperature= is an undoubted factor and becomes
more potent, if conjoined with a close, damp, ill-aired stable.

=Violent exertion= especially in hot weather produces active congestion
of the brain and occasionally merges into meningo-encephalitis. If the
animal has been for sometime confined to the stable on rich aliment the
condition is aggravated.

=Railroad travel= is another recognized cause.

Any considerable =change of the conditions of life= may operate in the
same way. A sale and transport to a distance with change of feed, water,
work, stabling and even of climate is at times a potent factor. Prietsch
has seen a horse attacked three times in a single year, and on each
occasion after a change of ownership and locality. Trasbot quotes an
Algerian veterinarian to the effect that many of the percheron horses
imported into the Mitidja are attacked by encephalo-meningitis during
the extreme heats of summer.

A careful observation of cases will however show that in the majority of
cases an attack comes not from one individual factor alone but from a
concurrence of several operating together.

Other cases are caused by =embolisms= and =infections= from diseases
localized in other parts of the body. Thus we have cerebral abscess in
pyæmia, strangles and omphalitis, and cerebral congestions and
inflammation in canine distemper, equine contagious pneumonia,
laminitis, and angina.

Among mineral poisons, =lead= is notorious as a cause of acute cerebral
disorder often leading to inflammation. Other mineral poisons like
=arsenic= and =phosphorus= may lead to encephalitis symptomatic of
gastro intestinal irritation, or caused by the toxic products of
indigestion.

Rapidly growing =tumors=, like cholesteatomata, are liable to induce
recurrent attacks of encephalitis in connection with periodic
irritation.

Finally =parasites= in the cranium are sufficient causes of attacks. In
the New York State Veterinary College Museum is the brain of a cat with
a nematoid wound round the hypophysis. In equine subjects suffering from
the strongylus armatus the larval worm or clots caused by its presence
in other arteries sometimes invade the encephalic blood vessels causing
disturbances of the circulation, embolism, inflammation or degeneration.
(Albrecht, Von Heill). The larvæ of the œstrus has also been found in
the brain substance producing inflammatory or degenerative foci
(Brückmüller, Megnin, Siedamgrotzky). Their presence in the nasal
sinuses at times cause encephalitis by contiguity. The cestoid worms,
cœnurus in sheep and other ruminants, and cysticercus in swine, find
their natural larval habitat in the brain and by their movements produce
more or less congestion and inflammation. Cases of cœnurus in the horse
have been described by Rousset, Frenzel, Zundel, and Schwanefeldt.

_Symptoms._ The symptoms of uncomplicated meningitis on the one hand and
encephalitis on the other are rarely seen, the disease usually
implicating more or less both brain and meninges, in a common
inflammation or the symptoms of the one involving those of the other
through proximity or interdependence of function. And yet in traumatic
lesions of the cranial walls, the symptoms may be those of pure
meningitis, and in thrombosis, embolism or parasitism of the brain, and
in certain tumors they may be those of simple encephalitis. The
distinction consists largely in the predominance of fever,
hyperæsthesia, active delirium and convulsions in _meningitis_, and
especially in its earlier stages; and the prominence of dullness,
stupor, somnolence, muscular weakness, paralysis, anæsthesia, coma, and
the clouding of special senses, with much less pronounced febrile
reaction, or vascular excitement in _encephalitis._

There is usually, however, a mixing of symptoms so that the benumbing or
paralysis of the nervous functions alternates with periods of their
exaltation, and with both conditions hyperthermia exists, though usually
higher with meningitis.

The manifestations of benumbing or paresis may be continuous or
interrupted, and are exhibited in stupor, coma, somnolence, lethargy,
paresis or paralysis. The manifestations of excitement are not
continuous but occur in paroxysms or at least exacerbations, which may
show in visual or mental illusions, active, violent delirium, trembling,
rigors, clonic or tonic spasms. The onset is usually abrupt, the animal
passing in a few hours from apparent health, to pronounced nervous
disorder. The horse seems drowsy and stupid, standing with semi-closed
eyes, often drooping lower lip and ears, head pendent and resting in the
manger or against the wall in front, the back arched and the limbs drawn
together. When moved, it walks unsteadily and often the limbs are left
out of plumb, one extending unduly forward, backward or to one side, and
often crossing over its fellow. Some cannot be made to back, others back
spontaneously hanging on the halter. Turning short in a circle is
difficult or impossible and tends to throw the patient down. Yet some
exceptional cases will turn around spontaneously to the right or left,
and an animal tied to a post goes around it at the end of its halter in
its effort to pass straight forward. The circling movement may be due to
the irritation on the one side of the brain or to irritation of
particular ganglia and nervous tracts as noticed under cerebral
hyperæmia.

Appetite is usually lost, or, more properly, the animal no longer takes
notice of surrounding things, not even of its food. In some cases,
however, in which stupor or coma is not extreme the animal will eat a
little during his quiescent intervals. In ryegrass and other dietetic
poisoning, the animal may still eat and fall asleep with the month full.
The digestion is impaired or suspended, the bowels costive, and
fermentations with tympanies and rumbling are frequent complications.
When originating from poisonous food this often contributes to these
abdominal complications.

Respirations in the comatose condition are deep and slow, sometimes not
more than four or five per minute. The heart usually beats strongly,
often tumultuously, and the pulse varies greatly—infrequent or frequent,
strong or weak, full or small. With cerebritis it is often abnormally
slow.

Hyperthermia is always present to a greater or less extent, being often
more marked in the more violent forms or those in which meningitis
appears to predominate than in the purely cerebral forms. The
temperature may vary from 101° to 106°.

The optic disc is congested.

Probably in all cases or nearly all there is a preliminary stage of
excitement, in which the eye is clear, the eyelids open, the aspect
alert and the whole skin affected by a marked hyperæsthesia. In some
cases the symptoms of excitement are much more violent at the outset of
the disease, as marked by trembling, nervous movements, pawing, pushing
the head against the wall while the motions of walking or trotting are
performed by the limbs, or those of plunging forward, rearing up,
drawing back on the halter, etc.

But even when the disease seems to have started with stupor and coma,
these paroxysms of excitement almost invariably appear at intervals as
it advances. Some, however, plunged in stupor or coma at the first,
remain in this condition until they end in paralysis or death, or start
in convalescence.

During one of the paroxysms the trembling animal may push his head
against the wall as if pulling a heavy load; at other times he will
plunge with his feet in the manger and recoiling, fall to the ground,
where he struggles violently in an apparent effort to rise; others rear
up, pulling on the halter or breaking it and falling back over; some
pull back on the halter and throw themselves down; some grind the teeth,
or seize the manger, or strike blindly with the fore limbs. When seized
out of doors the horse may be quite uncontrollable and refuse to return
to the stable even when led by two men with double halters. In all such
cases the eye has a fixed, glaring aspect which is the more pronounced
when the pupils are dilated, the conjunctiva is deeply congested, of a
deep, brownish red with a tinge of yellow. This is usually greatly
enhanced by the bruises and extravasations caused by pushing or knocking
the head against the wall. The same violence may lead to serious bruises
and injuries elsewhere, even fractures of the orbital process or zigoma,
of the ilium or ischium, of the poll or the base of the brain; also of
the incisor teeth.

These paroxysms may be so frequent that they seem to be subject to
remissions only, and not separated by complete intermissions. During the
paroxysms breathing and pulsations are both greatly accelerated.

The gravity of the attack may be judged in part by the violence and
frequency of the paroxysms. Yet some cases, marked by profound coma from
the first, prove the most rapidly fatal, and the paroxysms of excitement
and violence are not incompatible with recovery. Improvement may usually
be recognized by the increased length of the intervals between the
paroxysms, and by the shortening and moderation of the periods of
excitement. After the paroxysms have ceased the drowsiness or stupor
gradually disappears, and the hyperthermia subsides.

Even after recovery from the acute or violent symptoms there is liable
to remain some aberration or perversion of function, due to the
persistence of some encephalic or meningeal lesion. The general hebetude
known as _immobility_ may bespeak dropsy of the ventricles, pressure of
a tumor or clot, or degeneration of ganglionic centres. Diseases of the
eyes (amaurosis, glaucoma, cataract), or of the ear (deafness, disease
of the internal or middle ear) are less frequent results.

The supervention of general or facial paralysis or of hemiplegia during
the active progress of the malady, is an extremely unfavorable symptom.

_Duration._ A fatal result may take place at any time by self inflicted
injuries (dashing the head against a wall, or falling backward and
striking the head on a solid body). Apart from this, death may come
within twenty-four or thirty-six hours. If the animal survives two to
seven days recovery is more probable. Hering records a case of recovery
after five weeks illness. Hot weather hastens a fatal result, while
cool, cloudy weather is favorable.

_Prognosis._ Under rational treatment about one-fourth recover. One-half
of the victims make a partial recovery but remain in a condition of
dementia or hebetude, blindness, deafness, local or general paralysis
which renders them more or less useless. Not more than one-fifth or at
most one-fourth of all cases recover. Even in these there is left an
increased predisposition to recurrence. It is noted by Trasbot that the
mortality is higher in highbred, nervous, irritable animals, which show
a tendency to greater frequency, force and duration of the paroxysms of
excitement. When decubitus is constant, death may take place from septic
poisoning starting from bed sores, and gangrenous sloughing. In other
cases there is fatal starvation from inability to eat.

_Lesions._ In =pachymeningitis= due to mechanical injury there is
usually cutaneous and subcutaneous, blood extravasation, and there may
be fracture of the cranial bones. The dura mater is dark red, hyperæmic,
thickened, covered with exudation and small blood clots mixed with pus
cells, and has contracted strong adhesions to the cranial bone. Bony
spicula may project into the fibrous neoplasm.

=Leptomeningitis= usually coexists from extension of the inflammation
into the adjacent arachnoid and pia mater. There is then a reddish
serous effusion into the arachnoid and beneath it, and the substance of
both membranes is thickened by exudate, and discolored by congestion and
minute hæmorrhages. Whenever the pia mater is thus inflamed, the
superficial layer of the brain is implicated, œdematous, soft and
doughy. The extension is also made into the ventricles and a serous
effusion takes place often to two, three or more times the normal amount
(82 grammes Schütz). The choroid plexus forms a yellowish gelatinoid
mass, and the ganglia (corpora striata, optic thalamus, etc.), are
flattened.

In =encephalitis= the affected superficial gray matter of the ganglia or
convolutions, is deepened in color, usually in limited areas
corresponding to the disease of the meninges. Sometimes the color
becomes of a distinctly reddish tinge, and when cut into shows unusually
prominent red points where the capillaries have been cut. Somewhat
larger areas of blood staining indicate hæmorrhagic extravasations. The
nervous substance is more or less infiltrated with liquid and softened.
The nerve cells are swollen, and in process of granular degeneration and
the same is true of the myelin, while the axis cylinder is uneven in its
outline. Apart from the numerous minute petechial hæmorrhages there is
an abundant migration of leucocytes which are found scattered in the
degenerating and softened nervous tissues.

The softening of the nervous tissue may result in a pulpy material,
which in the comparative absence of blood is grayish (=gray softening=),
if abundantly infiltrated with blood is red (=red softening=), if older
and discolored is yellow, as in an old extravasation, (=yellow
softening=), if thick and viscous is =gelatinoid softening=. If the
exudate becomes organized into fibrous material it is a =connective
tissue sclerosis= or a =cicatrix=. If the softening exudate becomes
purulent it constitutes a =cerebral abscess=. Cerebral abscess is
especially common as secondary abscess in strangles or contagious
rhino-adenitis in the horse, but may occur as the result of the presence
of any pyogenic germ.

_Diagnosis._ While there is a certain similarity to =rabies=, the horse
with encephalo-meningitis is distinguished by the absence of the extreme
hyperæsthesia and irritability, of the persistent neighing and
squealing, of the rapid alterations of the voice, hoarse and shrill, of
the hallucinations, as following imaginary objects with the eyes, of the
readiness to attack with teeth or heels when in any way disturbed or
excited, of the disposition to get violently excited when a dog is
brought near, or in the case of a stallion to show generative
excitement.

From =cerebral congestion= it is to be distinguished by the greater
severity of the paroxysms, or the deeper character of the stupor, but
above all by the presence of the hyperthermia and other indications of
fever.

=Immobility= which presents the symptoms of drowsiness, stupor and
hebetude, is also unattended by fever, or anorexia, shows a healthy
condition of the functions, of respiration, digestion and assimilation
and a restful condition when left quiet and still.

The _cerebral excitement_ that sometimes appears in =influenza= is
really an encephalitis complication, but its specific cause is
recognized in the local prevalence of the infectious disorder, and the
inflammatory or catarrhal condition of the mucous membranes.

The diagnostic manifestations of _meningitis_ and _encephalitis_
respectively are given under symptoms.

_Symptoms in Cattle._ In cattle encephalo-meningitis supervenes on
congestion, and sometimes comes on abruptly in connection with traumatic
injuries, acute gastric disorder, leadpoisoning, or narcotism. The cases
of cerebral parasitism are usually slow in their onset.

Upon the preliminary dullness and somnolence there supervenes
excitement, manifested by loud bellowing, pushing the horns, forehead or
teeth against the wall, labored often stertorous breathing, a fixed eye
often with dilated pupil giving it a peculiar glaring appearance,
movements of the jaws, frothing at the lips, tremors, muscular spasms,
twitching, or a restless disposition to move, in a circle, in a straight
line or less frequently backward. The patient seems to see nothing and
is utterly regardless of obstacles. Sometimes the animal plunges
violently into manger or rack, against or through the partition of his
box, through fences, into ponds, pits, quarries and other dangerous
places that may be accidentally in his way. The paroxysms may be
intermitted by intervals of comparative calm, and tend to merge into a
condition of dulled sensation, staggering, stupor, hebetude and
paralysis. The congested conjunctiva and, when it can be seen, the optic
disc will correspond to the cerebral congestion. These cases usually
proceed to a fatal issue in a few hours. Some cases, however, make a
good recovery after a few days of dullness and prostration. In cases
that are connected with lead poisoning, or the toxic action of narcotics
in the fodder, the attendant circumstances will assist in the diagnosis.
From malignant catarrh implicating the encephalon, it may be
distinguished by the absence of the catarrhal inflammation of the
conjunctiva, pituita, sinuses, buccal mucous membrane, and
genito-urinary passages. Also of the tendency to implication of the hair
follicles and the keratogenous tissue of the frontal horns.

In the _Edinburgh Veterinary Review_, Dundas describes a form of
alcoholism in cows caused by feeding these animals on “burnt ales” in
the vicinity of distilleries. The ale is given by steeping straw in it,
and the animals will also drink it freely. They often sleep soundly
after such a beverage or give evidence of intoxication. The head is
turned singularly to one side and slightly elevated. The pupils are
widely dilated, and the eyes have a remarkably wild appearance. On being
approached the animals wink rapidly and tremble. There is marked heat of
head, horns, and ears. When pressed with the finger in the axilla they
fall instantly and when pulled by the head they incline to turn over.
The pulse is 70 to 80 per minute. Delirium and loss of coördination of
the muscular movements set in, and in case of survival various forms of
chronic brain disease are manifested. In one cow the violent symptoms
came on with the near approach of parturition. The post mortem lesions
consisted in ramified redness and punctiform blood extravasations in the
pia mater and meninges. The brain substance was softened and clots of
blood were found in the lateral ventricles. Congestion and
extravasations were also found around the cervical myelon. (See
Alcoholic Intoxication).

_Symptoms in Sheep._ The sheep is often drowsy, dull and stupid, lying
by itself with head low or laid backward. During the periods of
excitement it works the jaws, froths at the mouth, carries the head
turned in one direction, upward or lateral, bleats piteously, pushes
against the wall, has uncertain, stiff or staggering gait, or
convulsions, and finally paralysis. The head is hot, and the eye fixed,
congested or sometimes rolled upward or squinted. Symptoms in the goat
are nearly the same. The cœnurus disease is more gradual in its onset,
and produces periodic paroxysms corresponding to the activity of the
heads of the parasite when protruded into the brain substance. It is
mainly confined to sheep of one year and under and that are kept where
dogs have access.

_Symptoms in Swine._ Pigs may at first have a period of dullness or
restlessness, the latter merging into active delirium. The patient
champs his jaws, froths at the mouth and nose, sometimes vomits,
squeals, raises himself with fore feet on the wall, walks round and
round, or falls and rolls over, has tremors or convulsions.

_Symptoms in the Dog._ There may be preliminary indications of illness,
anxiety, restlessness, irritability and a desire for seclusion. Vomiting
may occur. This is liable to merge into prostration, a dullness of the
special senses, utter inattention to calls, yet a disposition to resent
any interference, a readiness to bite, at least to howl, when handled.
Some will constantly howl or moan. The eye is fixed, the pupils dilated,
the conjunctiva deep red, the head and roots of the ear are hot. The
expression of the face is pinched and drawn, the muscles may twitch, the
eyes roll, twitching of the neck or limbs may appear, and even
epileptiform attacks. In exceptional cases the symptoms approximate to
those of rabies, in the tendency to seek seclusion, to wander off, to
bite on any interference, and even to gnaw the bars of the cage or any
object within reach. After more or less of such excitement, the period
of stupor, coma, paresis, or paralysis comes on, and the animal dies in
a state of complete nervous prostration. In cases associated with the
linguatula tænioides the sneezing, nasal discharge and nasal congestion,
even in the early stages, betray the true character of the disorder.

The rabiform cases usually lack the intense heat of the head, the deep
conjunctival congestion, the depraved appetite, the alteration of the
voice, and the mischievous desire to attack without reason which
characterize rabies.

_Treatment._ In all cases of phrenitis, quiet, darkness, and coolness
are especially demanded. For the horse a roomy, loose box or a well
fenced yard may be secured, and if he can be secured by a halter from a
point above the level of the head and in the centre of the box it will
obviate the increase of congestion by hanging of the head. The
application of cold to the cranium in the form of wet cloths, ice bags
or irrigation is always in order, and should be continued so long as
heat of the head and other indications of cranial hyperæmia last.

In the _horse_ suffering, as is so often the case, from narcotic
poisoning an active purgative is one of the first considerations to
clear away any remains of the poison from the _prima viæ_. An ounce of
aloes may be safely given, as there is in this case little danger of
superpurgation, and, to secure an even more prompt response, eserine (1½
grain) or barium chloride (½ drachm) may be given subcutem. Or an ounce
or two of glycerine by the rectum might be used as a substitute for
these last. The action of the purgative proves not only eliminant and
therefore antidotal, but it is a most effective derivative from the
brain. When the restlessness or excitement is very great we may use
acetanilid, trional, sulphonal or some one of the many brain sedatives
and antithermics. Sedatives, or anodynes like opium, which tend to
increase cerebral congestion are dangerous.

Bleeding from the jugular or temporal artery, has been objected to on
the ground that it tends to increase the exudate and therefore the
pressure and cerebral anæmia. On the other hand it often proves of great
value in vigorous, muscular and plethoric horses in temporarily
lessening the blood pressure in the brain, and affording the walls of
the overcharged capillaries an opportunity to resume a more normal tone
and to control that very exudation which is so much dreaded. It is most
effective in the early stages when little or no exudation has taken
place and may then be pushed to the extent of producing a perceptible
softening of the pulse (4, 6 or 8 quarts). Even in the advanced stages
when exudation has led to stupor or coma a moderate and carefully
guarded bleeding may favor reabsorption of the liquid exudate. In weak
and anæmic cases in which general bleeding appears to be
contra-indicated the shaving of the cranial surface followed by leeching
or wet cupping can be safely resorted to.

Counter-irritants like bleeding are denounced and advocated by different
practitioners. In cases of extreme hyperæsthesia where excitement and
fever would be dangerously increased by their use, they must be
discarded, or used only in the modified form of soothing hot
fomentations to the extremities. Where there is less sensitiveness
mustard poultices or pulp applied on the sides of the neck, or upon the
limbs, or even more energetic blisters will be of great service.

After the action of the purgative the bowels may be kept free by calomel
in ½ drachm doses twice daily and as much sulphate of soda as may be
necessary.

Iodide of potassium (1–2 drs. twice a day) is beneficial as an
antithermic a circulatory sedative, an eliminant, and probably at times
as an antidote but it cannot be given while calomel is used. Certain it
is that it often seems to act well in succession to the purgative, in
cases of poisoning by ryegrass and leguminosæ.

When fever runs very high it may sometimes be admissible to give
aconite, but the coal tar products are much more prompt and powerful,
and may therefore be more hopefully employed for a short time.

In conditions of extreme prostration, stupor, or coma, stimulants are
resorted to, but too often with no good effect, the exudation and
compression which many times cause such symptoms being rather aggravated
than benefited by such agents.

During convalescence a restricted, non-stimulating laxative diet (bran
mashes, gruels, apples, potatoes, carrots) is demanded. Pure cool water
should be always accessible.

In other forms of meningo-encephalitis the same general principles
should be applied, due attention being paid to the removal of the active
cause when that can be discovered.

When indications point unequivocally to abscess, and its seat can be
accurately located by a circumscribed paralysis, an operation for its
evacuation is fully warranted. Otherwise death or permanent uselessness
is almost certain.

In _cattle_ and _other ruminants_ the same general principles of
treatment must be applied. As a cathartic Epsom or Glauber salts are
preferred to aloes and may be supplemented by barium chloride or
eserine. Croton, sometimes useful, is liable to dangerously increase the
gastric irritation in cases in which this is a marked determining
factor. When the animal is down, raise the head by bundles of straw, or
by a halter tied to a beam overhead. In lead poisoning, sulphuric acid
largely diluted may be added to the sulphates so as to precipitate the
insoluble sulphate of lead. Potassium iodide is of value to dissolve the
lead in the tissues and lead to its elimination. Cases of cœnnrus
require trephining and extraction; the larvæ of the œstrus should be
washed out with tobacco water or destroyed by benzine.

In _dogs_ the stomach is usually emptied spontaneously by emesis. A
purgative of castor oil, followed by daily doses of calomel may be
given, and attention given to the cooling of the head and general
system. Antipyrin or acetanilid may be usefully employed. The diet
should be restricted to milk or thin, well-boiled gruels.

The linguatula in the nose must be met as are the œstridæ of the sheep,
and intestinal worms must be got rid of by active vermifuges.

CHRONIC HYDROCEPHALUS. DROPSY OF THE VENTRICLES. IMMOBILITY.

Horse especially suffers. Enzootic in given Alpine Valleys, along
Rhone, in Mississippi Valley and bottom lands. Acclimatizing fever.
Old, lymphatic, large heads, narrow foreheads predisposed. Geldings.
Causes, heredity, cerebral and meningeal congestion, cranial traumas,
venous obstruction, tumors, false membranes, fodder or water
poisoning, overwork, insolation, prolonged moist heat, hepatic,
gastric, and pulmonary disorders. Symptoms: form of head, stupid
expression, irresponsive ears, pendent lips, sluggish movements,
crossed legs, slow mastication, dips face in water, intractable by
halter or rein, unable to back with rider, or wagon, drags back fore
limbs, worst in hot damp weather, in sunshine, or after work, or with
full stomach. Paroxysms of excitement. Lesions: excess of arachnoid,
subarachnoid or ventricular fluid, atrophy of ganglia and
convolutions, ependyma thick, opaque, sclerosis, brain anæmic. Tumors,
nature. Experimental cases. Prognosis, incurable, better in cool
season. In cattle, sheep, swine and dogs. Treatment: derivatives,
nerve stimulants (nux), puncture, pilocarpin, purgatives,
Jurisprudence. Notify seller in 9 days (France), 15 (Bavaria), 21
(Wurtenberg, Baden), 28 (Hesse, Prussia), 30 (Austria). Examination by
expert.

Dropsy of the ventricles is common in the horse in certain countries and
districts, yet even there it is uncommon in cattle, sheep, swine and
dogs, save as a congenital affection. It is reported as enzootic in some
Alpine valleys and along the Rhone, attacking especially the mares and
immature horses so that breeding becomes impossible. Mauener who reports
this says that in the same localities encephalic diseases are more
common in man. In America it appears to be most frequent in the rich
bottom lands of the Mississippi valley and of the Southern States.
Northern horses taken to the Gulf States though they may not suffer to
this extent, are liable in the first year to show weakness, debility,
and lack of vigor which is spoken of as the =acclimatizing fever=.
Elsewhere the affection is one of the old horse in which the vital
powers begin to fail. Common breeds of horses with lymphatic
temperament, large head and narrow forehead have been found to be
especially predisposed. Geldings are said to be most liable on account
of the arrested development of the brain, but with the great
preponderance of geldings among work horses, it is dangerous to
generalize too far.

_Causes._ Acute encephalitis may lapse into the chronic form and then
assumes the symptoms of this disease. Cases that come on slowly and
imperceptibly appear at times to be hereditary, as might be expected
from the fact that it usually goes with a lymphatic temperament. The
conditions which cause cerebral or meningeal hyperæmia in chronic form
conduce to the affection. Injuries to the cranial vault from traumatism
or disease are infrequent causes. Renault records a case associated with
two bony tumors, each as large as an egg, projecting inward from the
frontal bone and which had produced extensive absorption of the
convolutions and increase of the cerebro spinal fluid. In a case of my
own with an abscess in the diplöe above the frontal sinus, and pressing
inward on the brain a similar condition existed. In other cases Renault
noticed that the cerebro spinal fluid was largely in excess.

Much more commonly, however, the accumulation of liquid takes place in
the ventricles, and is associated with different causes: as tumors or
false membranes near the base of the brain pressing on the veins
returning blood from the ependyma, tumors in the ventricles
(cholesteatomata, etc., of the ependyma or choroid plexus) obstructing
the circulation or giving rise to local hyperæmia and chronic
congestions from the other causes such as faulty conditions of fodders,
or water, exposure to undue heat, overwork, etc. The enzootic prevalence
of the disease in certain localities, (Alps, Rhone Valley, bottom lands)
would suggest that local conditions in food or water are factors, though
we cannot as yet fully explain the mode of causation. In the same way we
must recognize the influence of hepatic and gastric disorders, which
arise from such faulty regimen and affect the brain by nervous sympathy
and by the action of toxic elements thrown into the circulation. Then
again we must take sufficient account of the congestions resulting from
obstructions in the lesser circulation, disease of the lungs, and of the
right heart, and compression of the jugulars by a tight or badly fitting
collar, or compulsory curving of the neck as set forth under vertigo and
cerebral congestion.

_Symptoms._ Among the symptoms must be recognized the conformation with
which it is usually found associated. The predisposed animals are
usually low bred, common horses, with narrowness of the cranium and
space between the ears and with a retreating of the head from the orbits
to the poll. Other horses suffer but the majority are of this
conformation, and thus the disease acquires a hereditary basis.

The expression of the face is characteristic. The eye is dull, often
sunken, lacking in vivacity and life, the eyelids are semi-closed, the
ears do not prick up to sounds, the muscles of the face are relaxed, so
that the lips hang flaccid, and the nostrils fail to dilate freely and
rhythmically. The animal is apparently unconscious of all that goes on
around him, and is not aroused by the entry or exit of men or horses, by
voice or slap, by food or water. His head is probably dropped and
resting in the manger, and he raises it sluggishly when compelled; when
moved from side to side of the stall his legs may retain a position
turned outward or crossed one over the other; if energetically roused he
wakes up slowly, and almost immediately relapses into his former
lethargy, without accomplishing what was called for. When left with legs
crossed he often remains so until wearied by the constrained position,
or in danger of falling from loss of balance. Not only the legs but the
head will retain for a time an abnormal position given to it,—bent,
dropped, turned to one side or the other.

This same lethargy extends even to mastication, which is usually
performed slowly and indifferently, and is often interrupted in the
middle of the trituration of a morsel which remains in the cheek, on the
tongue, or between the teeth, and perhaps hanging out of the mouth.
Hence the horseman’s expression, _he smokes his pipe_.

His mode of drinking is no less singular. Usually the lower part of the
face is dropped deeply into the water, and he will only withdraw it when
it becomes necessary to breathe. He may continue to masticate while
drinking.

When walked or trotted he may move a short distance all right; he may
even hasten his progress for a short distance without refusing meanwhile
to respond to the rein, then he may stop and for a short time longer
resist all efforts with voice, whip, or spur to start him anew. In other
cases he will turn to one side, getting into ditches or fences by an
apparently involuntary action and in defiance of whip or reins.

One of the most striking features of the disorder is the difficulty of
backing. In some cases he will back a few steps and then prove unable to
back farther; in others he will show it best when heated with a journey;
in other cases still he will back well enough under his own weight, but
prove utterly unequal to the act if a heavy man is placed on his back,
or if hitched to a loaded wagon. In backing with or without a rider the
horse, pulled back by the reins, inclines backward with his hind limbs
extended forward beneath the abdomen, his forefeet extended in front,
and his back arched; he extends his head or turns it to one side, and
when the change in the centre of gravity endangers his equilibrium, he
draws back his forefeet without lifting them, each making a groove in
the ground, and at the same time he makes a disorderly motion of the
hind limbs to one side to restore the balance. In default of this he may
drop his quarter on the ground and perform a back somersault on his
rider. Even when he succeeds in balancing himself after dragging the
forefeet back, the difficulty of further backing is rather increased, as
the nervous irritability is enhanced by a continuance of the excitement.

When hitched in a carriage the phenomena are virtually the same; when
backed he extends or flexes the head, inclines the body backward, and
after a time loses his equilibrium, sometimes executes a few disorderly
steps backward, or throws himself violently to one side, or turns over
backward in the shafts.

The symptoms are always worse during hot, damp weather, and when the
animals are exposed to the full glare of the sun. The milder cases can
be worked without great inconvenience in winter, while they become
utterly useless in summer.

Active exertion and increased rapidity of the circulation has a
similarly injurious effect. After a period of rest nothing amiss may be
noticed, while after a period of work in the sunshine the symptoms
become well marked and the difficulty of backing pronounced. Plethora or
full feeding aggravates, while spare, laxative diet, laxatives, rest or
bleeding relieves.

The affection may become complicated by more active inflammatory action
leading to paroxysms resembling those of meningo-encephalitis;—pushing
against the wall, rearing up with the fore feet in the manger, acting as
if walking or trotting, etc. In other cases the paroxysms resemble those
of vertigo; the animal plunging forward, starting to one side, or
rearing up and falling back.

_Lesions._ The pathological anatomy of this disease is that of chronic
hydrocephalus. Renault records cases in which the subarachnoid and
arachnoid fluids were under the normal while the fluid in the ventricles
was increased to a marked extent. This accumulation is often so great
that the whole of the surrounding nervous matter is greatly attenuated,
the convolutions of the cerebral hemispheres are flattened so that the
sulci are all but effaced, the water may shine through at points and
even bulge after the manner of a hernia, the ganglia in the ventricle
(corpus striatum, optic thalamus, hippocampus) are flattened and
atrophied, the base of the cerebrum is thinned and bulges downward, and
the olfactory lobes may have their internal cavity greatly distended so
that they look like little bladders of fluid. The ependyma may have lost
its normal thinness and translucency, having become thick and opaque,
and sometimes its surface is granular and rough. The choroid plexus is
congested and swollen with infiltration. The brain tissue adjacent is
firmly adherent and there is a hyperplasia of its connective tissue
constituting a veritable sclerosis. At some points, however, the
compressed nervous tissue has undergone degeneration and softening. As
might be expected from the pressure of the liquid, anæmia of the brain
tissue is a marked feature of the morbid condition.

Other conditions have at times been found in chronic hydrocephalus.

Renault found two long tumors each as large as a hen’s egg projecting
from the dura mater into the cerebral hemisphere. In other cases there
have been fibrous thickening of the dura mater, exudations on the pia
mater, and false membranes on the arachnoid (Röll). Chabert and more
recent writers have observed cysts and tumors of the choroid plexus in
such cases, but these have been met with not unfrequently in the entire
absence of the characteristic symptoms of this disease.

_Nature._ The affection before us is evidently one in which the majority
of the higher brain functions are profoundly depressed or debilitated,
and this is accounted for by the accumulating intraventricular liquid
pressing on the ganglionic centres in the cerebral hemispheres, and in
the floor of the lateral and third ventricles.

Experimentally an approximate loss of sensation, intelligence,
spontaneity, will, and muscular power is produced in birds or mammals
deprived of their cerebral hemispheres. Colin’s heifer, which had been
thus mutilated, would lie in torpor, and though it could be made to get
up and walk, it struck its head heedlessly against the wall, and
retained in its mouth unchewed, the food that had been placed there. He
says of such cases: “they live a long time, move automatically, respire,
digest, but they lose, with the sensations, memory, judgment, will, and
the most vital instincts of their kind.”

In the dropsy of the ventricles the attenuation and atrophy of the
cerebral convolutions produce symptoms which approximate closely to
those resulting from their experimental ablation, so that one may fairly
attribute the general symptoms in the two cases to the loss of their
function. Many of the attendant symptoms, and especially the aberration
of smell, sight, hearing and taste, may be referred to the concomitant
injuries of the basal ganglia of the brain.

We need not seek in one general answer to resolve the question whether
the dropsy or inflammation is the initial lesion. For our present
purpose it must suffice, that dropsy with anæmia and atrophy of the
cerebral convolutions and basal ganglia produce the symptoms of
immobility.

At the same time it is only logical to conclude that any morbid
condition of the cerebral circulation or of the brain or membranes which
leads to a corresponding amount of ventricular effusion, or atrophy or
destruction of the nerve centres already designated, will produce the
symptoms characteristic of this disease. Thus the different forms of
meningitis, traumatic injuries to the cranium, chronic encephalitis,
cerebral softening or degeneration, sclerosis, neoplasms of all kinds
affecting the brain (cysts, cholesteatoma, psammoma, melanoma, etc.),
and parasites may occasion this disease.

_Prognosis._ The disease is essentially incurable. It may last for years
with little change except the winter improvement, but it rarely subsides
permanently. It is only in those cases in which the symptoms have been
determined by a transient or removable cause, as a moderate exudation or
a parasite with a short term of life that a favorable result may be
looked for. Usually the improvements seen in cool seasons or stables,
under good hygiene, are not recoveries but temporary amelioration only.

_Symptoms in other animals._ Corresponding conditions produce similar
symptoms in cattle, sheep, swine and dogs, but the disease receives less
attention in these animals because they are not called on for steady
work. The animals are lazy, dull, insensible to excitement, stupid, show
a lack of muscular power and control, stagger or move disorderly and
show tympanies or other indications of indigestion.

_Treatment._ Majendie and others had a few apparent recoveries after
violent counter-irritation over the spinal cord (cervical and dorsal).
Coculet and Lafosse claimed recoveries from the prolonged use of nux
vomica in large doses (up to 5 drachms). Hayne attempted evacuation of
the fluid by puncture through the perforated plate of the ethmoid bone,
but had evil results from the ensuing hæmorrhage and encephalitis.
Aseptic puncture through the plate of the frontal bone would be much
more promising. Klemm suggested hydrochlorate of pilocarpin (15 grains),
and this would promise better than any other measure to induce
absorption of the liquid. The fatal drawback to this as to other
measures is that it is not applied until the slow, steady pressure has
caused such extensive cerebral atrophy that, even if the liquid could be
removed and its reproduction prevented, the lost functions can never be
restored. If the disease could be diagnosed and treated before this
change of structure had taken place, the hope of recovery would be much
better founded. Even in cases which make a temporary recovery during
cold weather one would be warranted in using active derivatives toward
the bowels and kidneys, also pilocarpin, counter-irritation to the spine
and even tapping of the ventricles.

Legal Aspect of Chronic Hydrocephalus.

To claim relief in case a horse affected in this way is sold as sound,
the seller must be notified at an early date. In the different countries
of Europe a limit is set after which such notification will have no
legal value. The seller must be notified, in France in 9 days, in Saxony
in 15 days, in Bavaria, Wurtenberg and Baden in 21 days, in Hesse and
Prussia in 28 days, and in Austria in 30 days.

_Diagnosis._ The veterinarian called to act as expert in such cases must
examine the suspected animal along the different lines in which the
cerebral aberration is manifested in the disease. He will see the animal
standing quietly in the stall apart from all sources of excitement. See
if there is a defect in the breadth of the cranium, or a deflection
backward of this region from the straight line of the front of the face,
together with a heavy clumsy head. Is the head pendent, resting on the
manger, with dull eye, drooping lids, lack of expression, loose hanging
lower lip? Does he hold morsels unchewed projecting from the mouth or
over the tongue, or in the cheek? Does he plunge both mouth and nose in
the water to drink, and masticate meanwhile? Are his legs found crossed
or in abnormal positions, and if put in such positions, does he fail to
rectify them at once? Is the head left in an abnormal flexed, depressed
or lateral position if placed in it? Does the subject find it difficult
or impossible to back? Does he pay the customary attention to the going
or coming of other horses, to feeding, etc.?

If no distinct symptoms are found he should then be examined under other
conditions. In taking out of the stable how does he turn in the stall or
back out of it, and in what way does he approach the door, clumsily or
with difficulty? When moved in a circle, does he sway or stagger? Can he
back when mounted or attached to a heavy carriage? Can he execute all
these movements satisfactorily after the respiration and circulation
have been excited by walking, trotting or galloping in hand or
otherwise? In case of difficulty in backing, in the absence of the other
diagnostic symptoms, he must see that this does not arise from other
causes. Some untrained horses have not been taught to back and cannot be
made to do so at once. Some refuse to back from indocility or
stubbornness, but can perform the act if induced in other ways, as in
having a narrow stall. Sometimes a sore mouth, from a hard bit may make
a horse nervous and obstinate so that he will seek to escape in any
other way rather than by backing under steady pressure of the bit.
Sometimes he will back all right under a halter. In all such cases of
simple obstinacy or fear of pain, the absence of the other symptoms is
strongly suggestive. If the horse has a well-developed cranium, a full
bright, alert eye, firmness of lips, intelligent expression, readiness
to appreciate and respond to all noises, words, touches or other causes
of excitement, plenty of fire and spirit, and an absence of any apathy,
dulness, awkwardness of movement or position of the limbs, or of any
other sign of failing nervous power he may be considered free from this
affection, even if he refuses to back in a docile manner. In other cases
there is a distinct physical incapacity quite apart from any brain
disorder. Sprains or anchylosis of the back or loins or anchylosis or
painful arthritis of the hocks, may hinder backing.

The diagnosis from encephalitis and other inflammatory affections
associated with stupor, rests on the absence of hyperthermia, of the
congestion of the orbital and nasal mucosæ, of the heat of the head and
of the paroxysmal attacks of excitement which characterize these
diseases.

CEREBRO-SPINAL MENINGITIS.

Definition. Epizootic manifestations. Faulty hygiene, insanitary
stables, impure air, defective drainage, fermenting food, overwork,
overfeeding, excitement, heat exhaustion, electric tension. Probably
complex. Horse, ox, sheep, goat, dog. Microbian factors in man and
rabbit. Lesions: meningeal, brain and spinal congestion, effusion,
suppuration, circumscribed necrosis, softening, petechiæ. Blood dark,
fluid or a diffluent clot. Symptoms: _horse_: paresis, anorexia,
dysphagia, mucous congestion, reddish brown: in severe cases, chill,
stupor, apathy, debility, palsy, tonic spasms of neck, back or loins,
hyperæsthesia, twitching, trismus, hyperthermia, delirium, coma,
convulsions, and early death. Duration averages 7 to 15 days. _Ox_, as
in encephalo-meningitis. _Sheep_, microbes. _Dog_, dulled senses,
stupor, coma, palsy, hyperthermia, heat of head, spasms, etc.
Diagnosis: by brain and spinal symptoms; cases in groups. More sudden
than tetanus, or rabies, and shows no mischievous purpose, nor
depraved appetite: from tubercular meningitis. Treatment: Avoid
suspected stable, food, water, or suspicious environment, disinfect,
correct local diseases, unload bowels, belladonna, atropia, chloral,
bromides, ergot, phenacetin, potassium iodide. Bleeding. Cold to head
or back. Derivatives. Sling. In convalescence, regulated diet and
tonics.

_Definition._ Concurrent inflammation of the meninges of the brain and
spinal cord.

This appears at times in many horses in the same locality, as in New
York in 1850 (Large), in Denmark since 1852 (Stockfleth, Bagge), and in
Egypt in 1876 (Apostolides). In Cairo alone about 6,000 horses, mules
and donkeys perished. Hence the disease is known as _epizootic cerebro
spinal meningitis_. But again it is often seen in scattering or sporadic
cases. Add to this that no evidence has ever been adduced that the
disease is communicated from one animal to another, and in these days of
the parallelism of _epizootics_ and _pathogenic microbes_, we may well
hesitate about continuing to use such a qualifying term. Friedberger and
Fröhner claim “that a large number of clinical facts have been
erroneously reported under the name of spasm of the neck. Rabies,
tubercular basilar meningitis, apoplexy, simple encephalitis, and
certain poisonings have been confounded with that disease.” They assure
us that “cold, damp, chilly weather, hot stables, clipping and
overfeeding are of but secondary importance,” but they fail absolutely
to tell us what is of _primary importance_ in a causative sense.
American writers who have attempted to account for the disease have
groped somewhat blindly for causes in the idea of poison. Large charged
it on insanitary conditions, poisonous gases, and defective sewerage in
cities, and lack of drainage and deficient stable ventilation in the
country. J. C. Michener attributes it to foods undergoing fermentation
and considers it as a paralysis due to toxic fungi. W. L. Williams, in
Idaho, found the greatest number of cases in winter had been fed hay
made from alfalfa (lucerne) and timothy, though some had small grains
and native grasses. The soil was dry, porous, gravelly, devoid of humus,
and lying on lava rock. The altitude and clearness of the atmosphere
were supposed to exclude the idea of cryptogams, yet the crops generally
were raised by irrigation. The water was from clear mountain streams.
Stables were generally low and full of manure, with thatched roofs, but
hardly tight enough to be called close. In these cases the defective
stable room, the irrigation, the leafy hay (lucerne), and the probable
presence of ferments (bacteria), are the only suggestive conditions. In
a fatal outbreak which I saw among the Wilkesbarre, Pa., pit mules,
rain-soaked and badly fermented timothy hay, overwork in view of a
strike, and a Sunday’s holiday in an unshaded yard under a hot July sun,
in contrast with the previous darkness and coolness of the pits,
coincided to disturb the general health. In several of the Southern
States it is attributed to worm-eaten corn. Trumbower thinks it should
be traced to the parasitic fungi that grow on plants, grains, and
vegetation. In many instances the disease has appeared simultaneously
with the feeding on certain specimens of brewer’s grains, oats and hay,
so that to use Trumbower’s words these were the carriers if not the
prime factors of the disease.

In recognizing how much cryptogams and bacteria vary under different
conditions of life, and what various products they elaborate at
different stages of their growth, we can theoretically explain the
absence of the disease at one time and its presence at another under
what seem to be identical circumstances, as also the variety of symptoms
shown in different outbreaks. While this causation cannot be said to be
absolutely proved, it is not antagonistic to the facts in many of the
best observed outbreaks, and may serve as a hypothetical working theory
until actual demonstration can be furnished. The affection suggests a
narcotic poison introduced from without, rather than a disease due to a
germ propagated in the system.

This need not, however, exclude the operation of attendant conditions
such as overwork, plethoric feeding, excitement, close stables, heat
exhaustion, etc., which tend to bring about cerebro-spinal congestion.
Even the electric tension of Idaho, of the United States generally, and
of Egypt, in connection with their comparatively dry atmosphere, should
not be overlooked in considering the possible causative factors.

In all probability as we learn more of the true pathology of the
disease, we shall come to recognize not one, but several toxic
principles, and several different affections each with its
characteristic phenomena in the somewhat indefinite affection still
known as cerebro-spinal meningitis.

The malady has been described in horses, oxen, sheep, goats and dogs,
attacking by preference the young, which are not yet inured to the
unknown poison, and by preference in winter and spring, the periods of
close stabling, dry feeding and shedding of the coat.

In the absence of bacteriological data from the horse, it may be noted
that in man cerebro-spinal meningitis, has been commonly found to be
associated with the presence in the meningeal exudates of the
_micrococcus pneumoniæ crouposæ_, (Micrococcus lanceolatus
encapsulates). This is frequent in the mouths of healthy persons so that
some additional accessory cause must be invoked to increase the
susceptibility or lessen the protective power of the tissues. This has
been thought to be found in the concurrent presence of other bacteria,
the staphylococcus pyogenes aureus, pneumobaccillus of Friedländer and
the streptococcus pyogenes. Mosny appears to have established this for
the staphylococcus in the case of rabbits. With a given dose of the
micrococcus pneumoniæ death was always delayed for a fortnight, while
with the same dose thrown into one thigh, and the staphylococcus aureus
in the other, the rabbit died in one day. This enhanced potency
resulting from the presence of the golden staphylococcus has been
invoked to account for the germ making its way from the mouth to the
brain in cases of otitis, suppuration of the Eustachian tube, tonsilitis
or nasal catarrh. These remarks are intended to be suggestive, rather
than conclusive, as we have as yet no certainty that cerebro spinal
meningitis in the horse is caused by the same germ as it is in man.

_Lesions._ The lesions are usually those of leptomeningitis, or
congestion of the brain and spinal cord and often effusion into the
ventricles, with a serous exudation under the pia mater or into the
arachnoid cavity. This may be transparent and yellowish, or grayish and
turbid, or milky. In the sheep, Roloff has found purulent products under
the pia mater, around the roots of the spinal nerves, and in the surface
layers of cerebral gray matter. The marked hyperæmia on the surface of
the gray matter is a striking feature, and circumscribed areas of
necrotic nervous tissue and softening are not uncommon. Petechiæ are
frequent on the meninges, the brain, heart, lungs and kidneys. Granular
and fatty degenerations are also met with in these parenchymatous
organs. The blood may be dark and liquid or diffluent.

_Symptoms in the_ =Horse=. The mildest attacks are manifested by
paresis, or loss of perfect control over the limbs, or loss of power
over the tail, impairment of appetite and some difficulty of swallowing,
together with some congestion or reddish brown discoloration of the
orbital and nasal mucosæ. In other cases paralysis of one or more limbs
may supervene but without marked fever or coma.

The more severe forms are ushered in by violent trembling, or by stupor,
apathy, and extreme muscular weakness, or actual paralysis. In such
cases the animal may stagger or fall. Dysphagia or inability to swallow
is often a marked symptom, the saliva falling in strings from the lips.
Another common phenomenon is the rigid contraction of the muscles of the
neck, back and loins, the parts becoming tender to the touch and a more
or less prominent oposthotonos setting in. Twitching of the muscles of
the shoulders and flanks may be noticed. Trismus also is sometimes seen.
The breathing is usually rapid and catching and the temperature 104° to
106°. The pulse may be accelerated and hard, or weak and soft, or
alternating. The eyes are violently congested, of a brownish or
yellowish red color, and the eyeballs may be turned to one side.
Paroxysms of delirium may set in, when the animal will push against the
wall, or perform any of the disorderly movements described under
meningo-encephalitis. Sooner or later coma and paralysis supervene, and
death occurs in from five to forty-eight hours. In the most acute
(fulminant) cases the animal falls and dies in convulsions. On an
average the disease lasts from eight to fifteen days. In the more
favorable cases, without any supervention of coma, recovery may begin on
the third or fourth day.

_Symptoms in the_ =Ox=. These are largely those of encephalo-meningitis.
If they do not come on with the customary violence, there may be at
first difficulty in prehension, mastication and swallowing of food; a
rigid condition of the muscles of the neck, back, and sometimes of the
jaws, and twitching of the muscles of the limbs, neck, lips, or eyes.
For a time there may be hyperæsthesia, restlessness and irritability,
stamping of the feet or shaking of the head, then there is liable to
follow, dullness, apathy, stupor, coma and paralysis. As in the horse,
the distinction from ordinary encephalo-meningitis will at times rest on
the prevalence of the epizootic disease in the locality.

_Symptoms in_ =Sheep=. The attack is described as coming on with
weakness, dullness, lethargy, salivation, convulsions, oposthotonos,
grinding of the teeth, succussions of the body and limbs, heat of the
head, and stupor or paralysis unless death ensues during a paroxysm. The
congestion of the head and of the encephalic mucous membranes, and the
deviation of the eyes are constant features. Wischnikewitsch describes
an extended outbreak in sheep in which the brain lesions were
complicated by hepatization of the lungs, and bacilli were found in the
various exudates. This reminds one of the presently accepted cause in
man, which is, however, a micrococcus rather than a bacillus.

_Symptoms in_ =Dogs=. These are described as some aberration of the
senses, which gradually merges into stupor, coma and paralysis. While
the animal is able to keep on his feet he sways and staggers, runs
unconsciously against objects, or walks in a circle. There is heat of
the head, injected eyes, sometimes drawn back or squinting,
oposthotonos, and general spasms occurring in paroxysms. The duration of
the disease is about the same as in the horse.

_Differential Diagnosis._ From other forms of meningitis this is easily
distinguished. Fulminant cases almost all belong to this type, the fact
of the coincident implication of brain and spinal cord is strongly
suggestive of this form, and the occurrence of many cases at once,
without any demonstrable toxic or thermic cause, is tolerably
conclusive. From tetanus there is this added distinction, that the
disease does not set in so slowly, the spasms of the neck and back are
not so persistent, and stupor sets in early, in a way that is unknown in
lockjaw. Rabies is recognized by the slow onset, the characteristic
prodromata, the mischevious disposition, the depraved appetite, and by
the history of its local prevalence. Tubercular meningitis in cattle has
a similar association with tuberculous animals in the same family or
herd, and often by the local indications of tubercle elsewhere,
emaciation, unthriftiness, cough, flocculent and gritty nasal discharge,
enlarged lymph glands, pharyngitis, mammary disease.

_Treatment._ With a disease so fatal _prevention_ should be the first
consideration and especially when it appears in an enzootic form. Even
in the absence of a definite knowledge of its germ or toxin, it is
logical to avoid the locality, condition, food or water by which such
germ or toxin has presumably entered the system, together with every
unhygienic condition, which may have reduced the resistance of the
system and laid it open to the attack. The animals should be removed to
a clean, airy, building and the old one should be thoroughly emptied,
purified and whitewashed, the lime-wash containing 4 ozs. of chloride of
lime, or 1 dr. of mercuric chloride to the gallon. Drains and gutters
should have special attention and the animals should not be returned
until the stable is thoroughly dry. A change of feed is imperative when
there is any suggestion of damp, mustiness or fermentation, and even in
the absence of such indications, since the ferments and their products
may still be present in a dried condition. It should also be an object
to correct any morbid or pyogenic condition of the pharynx, Eustachian
pouch, nose or ear, by appropriate measures and the inhalation of
sulphurous acid or chlorine may be resorted to with advantage.

As medicinal treatment Large advises to give at the outset 1 oz. aloes
with one or two drs. of solid extract of belladonna and as an eliminant,
derivative and nervous sedative there is much to be said for it. In case
the difficulty of swallowing should prove a serious barrier a hypodermic
injection of ½ dr. barium chloride, 1½ to 2 grs. eserine, or 2 grs.
hydrochlorate of pilocarpin together with ¼ grain of atropin, may be
employed. As a substitute for atropin, ergot, potassium bromide, chloral
hydrate, chloroform, or phenacetin have been tried in different cases
with varying results. Iodide of potassium has been employed with
advantage in the advanced stages and in convalescence, and may be
usefully employed in the early stages as a sedative to the nervous
system, a deobstruant and an eliminant, if not as a direct antidote, to
the toxins.

Bleeding is generally condemned, yet in acute cases where there are
indications of active brain congestion, threatening convulsions or coma
it may tend to ward off a fatal result.

Cold applications to the head are generally commended. Bags of ice or
snow, irrigation with cold water, or cooling by running water at a low
temperature, through a pipe coiled round the head or extended along the
spine, will meet the purpose. Applied continuously this constringes the
blood-vessels within the cranium as well as on its surface, lessens the
exudation, and controls the pain and spasms. This may be advantageously
associated with warm fomentations to the feet and limbs, friction, or
even the application of stimulating embrocations to draw the blood to
these parts. In the smaller animals even warm baths may be resorted to
as a derivative, cold being meanwhile applied to the head and spine.
This not only lessens the vascular pressure within the cranium, but
secures elimination of toxic matters by both skin and kidneys. Cold pure
water should be constantly within reach.

A most important thing in the horse is to put him in slings, if he is at
all able to stand with their assistance. In decubitus he rests on his
side, with the head on the ground, and lower than the splanchnic
cavities. The result is a gravitation of blood toward the head. In the
sling, with the head fairly raised the gravitation is the other way and
the head is depleted. If the patient is too ill to be maintained in the
sling, he may be packed up with bundles of straw on each side, so that
his breast may lie on a thickly littered bed, and his head may be
elevated.

When convalescence sets in care must be taken to nourish with
non-stimulating, easily digested food, gruels, soft mashes, pulped or
finely sliced roots. In vomiting animals rectal alimentation may become
necessary. The rise of cranial temperature or the aggravation of brain
symptoms should be met as needed by the local application of cold, and
potassium iodide and iron or bitter tonics may be given if they do not
interfere with digestion.

ABSCESS OF THE BRAIN.

Infection, in traumas, meningitis, encephalitis, strangles, etc.
Symptoms: evidence of trauma, chill, hyperæsthesia irritability,
drowsiness, giddiness, stupor, spasms, paresis, coma, dilated pupils,
congested mucosæ, vomiting. Location indicated by muscular groups
involved. Treatment: As in meningitis: trephining in hopeful cases.

The formation of abscess in the cranial cavity has been referred to in
connection with injuries to the cranium and meningo-encephalitis. It may
here be said in general terms that this abscess is a product of
infection. In the horse the most common cause is strangles, and
especially such cases as run a tardy or irregular course with imperfect
softening and limited suppuration in the submaxillary or pharyngeal
region. It is to be looked on as an extension of the purulent infection
so as to cause a secondary abscess. The same may occur in case of
ordinary abscess in any distant organ. In the brain as elsewhere
suppuration may result from direct local injury as in the case of blows
by clubs, or yokes, running against walls or posts, falls, the effects
of butting, injuries by bullets and otherwise. In these cases, as
noticed under concussion, there may be two points of injury (and two
abscesses) one, in the seat of the injury, and one in a deeper part of
the brain, at the opposite wall of the cranium. Again abscess may result
in the brain from extension from a similar process going on in the
vicinity. Thus otitis extends through the middle and internal ear to the
brain, and its starting point may have been more distant, namely, in the
Eustachian tube, or pouch, or in the pharynx.

The _symptoms_ vary according to the size of the abscess, the rapidity
of its formation and the amount of attendant congestion. In the common
cases resulting from strangles, I have usually found the animal down,
unable to rise, blind, amaurotic, with dilated pupils, congested mucous
membranes, and occasional spasmodic movements of the limbs, neck and
head. The symptoms may, however, vary through hyperæsthesia,
irritability, drowsiness, giddiness, stupor, local or general paralysis
with occasional spasms or convulsions. There may be an initial
shivering, and a rise of temperature, yet as pressure on the brain
increases it may become normal or subnormal. In circumscribed abscess
the symptoms may be much less severe, not perhaps exceeding
irritability, drowsiness, and some paresis or local paralysis.

In some such cases one can trace the connection to some primary disease,
(traumatic injuries to the cranium, abscess of the diplöe or sinus,
parasites in the sinus, otitis, or pharyngeal disease) which serve as an
indication of the true state of things. In others there may be
circumscribed local manifestations, (anæsthesia, hyperæsthesia,
hemiplegia, paralysis of special muscular groups, or spasms of the same
) which may indicate more or less accurately the exact seat of the
lesion. When well defined, this localization of the resultant phenomena,
serves to distinguish this and other local lesions, from meningitis
which is apt to be much more general in its diffusion. In the carnivora
and omnivora vomiting is a marked symptom.

_Treatment_ of brain abscess is usually hopeless, yet the attendant
inflammation may be met as in other cases of meningitis. If the seat of
abscess can be ascertained surgical interference is fully warranted.

TUBERCULAR MENINGITIS.

Little seen in cattle. Acute and chronic cases. Miliary tubercles in
pia. Hydrocephalus. Progresses slowly. Irritability, hyperæsthesia,
photophobia, congested conjunctiva, grinding teeth, spasms, squinting,
dilated pupils, congested disc, drowsiness, stupor, coma, palsy.

Tubercle of the encephalon has been little noticed in the lower animals,
partly because it is especially a disease of early life, while animals
usually contract tubercle later in life, and partly because subjective
symptoms are inappreciable, and the cranium is seldom opened in post
mortem examinations. As the affection usually appears as a secondary
deposit, the tubercles elsewhere go a long way toward identifying the
nature of the disease in the brain. It has usually been found
consecutive to pulmonary tuberculosis.

In a case reported by Fischœder as seen at the Bromberg abattoir, in a
350 lbs. calf, the animal had shown weakness, stupor and a tendency to
fall toward the right. The brain lesions consisted of small foci of
tubercle on the posterior pillars of the fornix (trigone) and adjacent
parts. The left eye had on its inner aspect, near the junction of
sclerotic and cornea, a firm mass with tubercular centres, extending
inward as far as the retina. The bronchial mediastinal, prepectoral,
brachial and precrural glands were tuberculous.

In a case in a cow reported by Lesage there were unsteady gait, impaired
vision, and great timidity. Necropsy showed a suboccipital tubercle
extending into the frontal sinus and cranium, and invading the brain
near the parietal lobe for more than an inch. There were
retro-pharyngeal and pleural tubercles as well.

In a case of Routledge’s, with extensive recent exudate, the condition
advanced from apparent health to extensive paralysis in three days,
while in a case which the author obtained in slaughtering a tuberculous
herd no special nervous symptoms had been noticed during life. Much
therefore depends on the rapidity as well as the seat of development.

The primary lesions in the brain are of the nature of miliary tubercles
in the pia mater which becomes congested, rough, granular, and throws
out a free serous secretion. Thus hydrocephalus is a usual concomitant
of the affection.

The disease is characterized by its slow advance in keeping with gradual
increase of the tubercle and is thus distinguishable from the more acute
congestions and inflammations. The earlier stages are usually marked by
nervous irritability, hyperæsthesia, intolerance of light, closed
eyelids, congested conjunctiva, grinding of the teeth and even spasms
partial or general. The second stage shows somnolence, deepening into
stupor or coma, or there may be going in a circle or other irregular
movement. Squinting usually convergent, dilated pupils and congestion of
the optic disc frequently occur. The sleep, stupor, paralysis or coma
may set in early and is usually largely due to the amount of exudation
and the rapidity of its effusion.

TUMORS OF THE BRAIN. NEOPLASMS.

Existence inferential with similar external tumors. Cholesterine
tumors on plexus of lateral, third or fourth ventricle: pea to egg: in
old; concentric layers with abundant exudate. Symptoms: slight, or
excitability, dullness, vertiginous paroxysms with sudden congestions,
as in encephalitis, sopor, stupor, paresis, coma. Melanoma: mainly
meningeal; pea to walnut; with skin melanomata in gray or white
horses. Cases. Pigmented sarcomata. Diagnosis, inferential. Psammoma:
advanced cholesteatoma, melanoma, fibroma, etc.: osteid tumors.
Nervous irritation, delirium, spasms, nervous disorder, and paroxysms.
Myxoma: contains mucin: cells (in homogeneous matrix) round,
spindle-shaped or stellate. Changes to fat (cholesterin). Œdematous
connective tissue, neoplasm. Myxolipoma. Myxo-cystoid. Symptoms.

Tumors in the brain are not marked by distinct pathognomonic symptoms,
so that their presence is to be inferred as a probability rather than
pronounced upon as a certainty.

The most common forms in the horse are cholesterine (cholesteatoma),
melanotic (melanoma), sandy, gritty (psammoma), and fibrous (fibroma).

CHOLESTEATOMA.

These are tumors formed largely of the peculiar fat which is found in
bile and brain matter, and that crystallizes in flat oblong scales with
a notch at one corner. The tumors are usually connected with the choroid
plexus and developed beneath the pia mater, and may be of any size from
a pea to a hen’s egg, or in exceptional cases a sheep’s kidney. As a
basis there is a stroma of connective tissue permeated by blood vessels
from the plexus. Groups of spherical or polygonal cells fill the
interstices while fusiform cells are found in the stroma. There is a
variable amount of phosphate or carbonate of lime which in oldstanding
cases may give a cretaceous character to the mass. These constitute
sandy tumors (psammomata).

Cholesteatomata are especially common in old horses and are manifestly
connected with congestion of the choroid plexus and exudation. In a
recent case or in a case which has shown a recent cerebral hyperæmia, we
may find a central mass of yellowish cholesterine, and surrounding this
an abundant yellow gelatinoid exudation. This latter is rich in
cholesterine which fails to dissolve along with the rest of the exudate
on the occurrence of resolution, and is therefore laid up as the solid
fatty material. For the same reason the fatty element is usually laid on
in layers, one corresponding to each access of local hyperæmia and
exudation. The great tendency to calcareous degeneration has been
attributed to the abundance of phosphate of lime in the cerebral
exudate.

The _symptoms_ of these tumors are exceedingly uncertain. Many such
tumors of considerable size have been found after death in animals in
which no disease of the brain had been suspected during life. In these
it is to be inferred that the accretions were slow, gradual, and without
any serious congestion. In other cases the tumor is attended by
paroxysms of vertigo, or indications of hyperæmia or meningitis, which
will last for several days and gradually subside. It is reasonable to
suppose that the tumors are largely the result of such recurrent attacks
of encephalitis, and are no less the cause of their recurrence. The
intervals of temporary recovery correspond to the subsidence of
hyperæmia and the reabsorption of the liquid portion of the exudate. The
manifestations during an access correspond directly to those met with in
encephalitis. As in that affection there is usually an initial period of
excitement and functional nervous disorder tending to more or less
somnolence, stupor, paralysis or coma, with long intermissions of
apparently good health. In other cases the stupor or paretic symptoms
may persist up to the fatal issue.

MELANOMA OF THE ENCEPHALON.

Black pigment tumors have been found in connection with the brain and
especially the meninges, varying in size from a pea to a walnut, and as
a rule, secondary to similar formations elsewhere. They are most common
in gray horses which have turned white, and may give rise to gradually
advancing nervous disorder. Bouley and Goubaux record a case of this
kind attended with general paralysis. W. Williams reports the case of an
aged gray stallion with melanomata on the meninges and in the brain
substance which were associated with stringhalt of old standing.
Mollereau in a vertiginous horse found a pigmented sarcoma in the right
hemisphere between the gray and white matter, and like an olive in size
and shape. There were melanomata around the anus. (Annales de Medecine
Veterinaire, 1889). So far as such have been examined they follow the
usual rule in melanomata in having a sarcomatous structure.

While it is impossible to make a certain diagnosis without opening the
cranium, the condition may be suspected, in gray horses, when melanotic
tumors are abundant in the usual external situations (anus, vulva, tail,
mammæ, sheath, lips, eyelids, etc.), and when brain symptoms set in and
progress slowly in such a way as to suggest the gradual growth of a
tumor.

_Treatment_ is hopeless, since if they have invaded the brain, the
tumors are likely to be multiple in the organ, and numerous and widely
scattered elsewhere.

PSAMMOMATA (GRITTY TUMORS) OF THE BRAIN.

As already noted these sandy tumors are often the advanced stage of
cholesteatomata, the abundance of the phosphate of lime leading to its
precipitation in the neoplasm. The same cretaceous deposit often takes
place in old standing tumors of other kinds, as in melanoma, and fibroma
so that the sandy neoplasm may be looked upon as a calcareous
degeneration of various forms of intracranial tumors. The same tendency
to calcareous deposit is seen in the tuber cinereum (pineal body) of the
healthy brain which has taken its name from the contained gritty matter.
This tendency to the precipitation of earthy salts may be further
recognized in the osteid tumors which occasionally grow from the dura
mater.

The gritty tumors are especially found in the older horses in which the
tendency is greatest to extension of ossification and calcic
degenerations.

Like other tumors these may attain a considerable size before they give
rise to any very appreciable symptoms, but having attained a given
development—often the size of a walnut, they become the occasion of
nervous irritation, delirium and disorder, as indicated under encephalic
hyperæmia and inflammation, cholesteatomata, etc. There may, however, be
drowsiness, stupor, coma, or paralysis as the exclusive symptom, or
there may be spasms and convulsions.

MYXOMA OF THE BRAIN.

Myxoma is a tumor in which mucoid elements or a gelatinoid degeneration
and infiltration containing mucin is a prominent feature. The _mucous
tissue_ which constitutes the tumor may differ little from ordinary
connective tissue except that the intercellular spaces contain mucin.
Histologically the tissue consists of cells embedded in a homogeneous
matrix. The cells may be of various forms, round, (in recent formations)
and spindle-shaped or star-shaped, but especially the latter, in the
older. When incised a fluid containing mucus escapes in greater or less
abundance. While this has properties resembling albumen it is
distinguished by the fact that the precipitate thrown down in it by
alcohol is softened and redissolved on the addition of water. The
precipitate thrown down in an albuminous liquid is insoluble in water.

The formation of this mucous exudate is liable to be followed by fat so
that Virchow considered it as antecedent to fat formation. This is
especially noticeable in the early stages of the cholesteatomata of the
choroid plexus of the horse, in which, as observed by Fürstenberg,
Lassaigne, and Verheyen, the new formation is at first a myxoma, which
later becomes filled up with cholesterine.

Recent observations tend to discredit the alleged distinctive character
of myxoma. The meshes of all connective tissue contain a perceptible
amount of mucin. Œdematous subcutaneous connective tissue contains this
mucin in greater proportion and approximates to the condition of mucous
tissue. The umbilical cord, which has been long advanced as the
physiological type of mucous tissue, has been shown to consist of
ordinary connective tissue with an abundance of fluid in its meshes.

Koster denies that the myxoma is a special type of tumor, and holds that
it is only a condition that may arise in any tumor which contains
connective tissue. In other words, myxoma is only an œdematous condition
of the connective tissue neoplasm—fibroma, sarcoma, carcinoma, etc.—due
to passive congestion or other circulatory disturbance.

As seen in the brain of the horse the formation is usually of the nature
of a myxo-lipoma, as the final outcome is usually the cholesterine
bearing mass. In other cases the connective tissue spaces become further
distended with the viscous, gelatinoid liquid and form veritable
cysts—myxoma-cystoides.

In tumors of this kind affecting the choroid plexus the chain of
symptoms is essentially the same as given under cholesteatoma and the
prognosis is nearly equally grave. It need only be said that in recent
cases in which there is as yet little permanent tissue, measures may
sometimes be hopefully adopted, to secure the reabsorption of liquid
constituents, and even perchance to remove some obvious cause of passive
congestion upon which the effusion depends.

ACROMEGALY. HYPERTROPHY OF THE PITUITARY BODY.

Like other portions of the brain the pituitary body is subject to
degenerations and diseases of various kinds. This is particularly
mentioned here because of the occasional association of its hypertrophy
with the trophic processes of different parts of the body. Along with an
over-development of the limbs, and less frequently of the body, an
enormous increase of the hypophysis has been found, and the one
condition has naturally been set down as the result of the other. In
some such instances, of overgrowth, however, some other blood glands,
such as the thyroid or thymus, have been found to be hypertrophied, so
that at present it is difficult to do more than notice the association
observed between the two conditions.

CEREBELLAR DISEASE.

Cerebellum and coördination. Pressure on adjacent parts renders
results uncertain. Generic symptoms, ataxia, titubation. Marked
symptoms with rapid morbid progress. Treatment: tonic, hygienic.

Whatever functions are exercised by the cerebellum there is no doubt of
its control over muscular coördination. It is quite true that disease of
any other part of the brain causing effusion, exudation or intracranial
pressure will more or less completely arrest the functions of the
cerebellum just as disease of the cerebellum producing intracranial
pressure will derange the functions of other parts of the encephalon.
The general symptoms produced in this way cannot therefore be accepted
as indicating the precise localization of an intracranial disease.
Dullness, stupor, coma, dilated pupils, choked discs, optic neuritis,
and vomiting, are in this sense generic symptoms, which may in the
absence of fever indicate dropsy, exudation, apoplexy, tumor, concussion
or other lesion, and with hyperthermia may indicate encephalitis or
meningitis. But if in the absence of these symptoms and of aural disease
there should appear ataxia, swaying unsteady gait, and staggering, there
is a strong presumption of cerebellar disease. This may also be
manifested by the other and generic symptoms already mentioned only the
diagnosis is not then so certain. Again cerebellar disease may exist
without the ataxia and lack of balance, but probably only in cases in
which the progress is slow and the organ has had ample time to
accommodate itself to the as yet comparatively restricted lesions. The
result may be a mere defect of muscular tone, or it may extend to an
almost absolute loss of contractility, or it may be of any intermediate
grade.

_Treatment_, which is eminently unsatisfactory, consists in improving
the general health and tone, by corroborant medicines and conditions of
life, and training the muscles by carefully graduated exercise and even
electricity.

BULBAR PARALYSIS. DISEASE OF MEDULLA OBLONGATA.

Impaired innervation of bulbar nerves. Paresis of lips, tongue, and
larynx. Roaring. Rapid pulse. Glycosuria, albuminuria. Ptosis.
Twitching eyelids. Dysphagia. Paralysis. Treatment, rest, cold to
head, laxatives, nerve stimulants, tonics, electricity.

The bulb is intimately connected with the origin of the hypoglossal,
glosso-pharyngeal, spinal accessory, vagus, facial, and trifacial nerves
and active disease in the bulb is therefore likely to entail impairment
of the function of several of these nerves. In man this is recognized in
_chronic progressive bulbar paralysis_, which almost always affects the
lips, tongue and larynx advancing steadily though slowly to a fatal
termination. In degenerative lesions there is modified voice, difficulty
of swallowing, rapid pulse, and laryngeal paralysis (especially of the
arytenoid muscles). The implication of the root of the vagus may be
inferred from the arrest of inhibition of the heart, and from glycosuria
or albuminuria. Occasionally the ocular and palpebral muscles are
involved causing ptosis, or twitching of the muscles. When the facial
(7th) nerve is implicated, paralysis of one or both sides of the face
may be marked, including often the ears. When the glosso-pharyngeal, the
difficulty of swallowing is a prominent feature, and when the spinal
accessory, spasm or paralysis of the neck. In the worst cases death
supervenes early, by reason of interference with the respiratory and
cardiac functions.

The _treatment_ of these affections is usually very unsatisfactory,
though in meat producing animals it may sometimes be desirable to
preserve them in preparation for the butcher. Rest, in hyperæmic cases,
cold to the head and purgatives, and in those in which fever is absent,
small doses of nerve stimulants (strychnia) and tonics (phosphorus,
phosphates, ammonia-sulphate of copper, zinc sulphate, silver nitrate)
may be tried. A course of arsenic and carefully regulated electrical
stimuli may at times give good results.

LOCO POISONING. OXYTROPIS LAMBERTI. ASTRAGALUS MOLLISSIMUS

Astragalus Hornii: A. Lentiginosus: A. Mollissimus: Oxytropis
Lamberti: O. Multifloris: O. Deflexa: Sophora Serecia: Malvastrum
Coccinium: Corydalis Aurea. In dry regions. Cause, a psychosis.
Emaciation. Lassitude. Impaired sight. Illusions. Vice. Refuses other
food. Contradictory views. Experiments by Dr. Day.

The term _loco_ is of Spanish origin and has come to us through the
Spanish speaking residents on the cattle raising plains and the Pacific
Coast. The word is defined to mean _mad_, _crazy_, _foolish_. It has
been applied indiscriminately to a disease in stock manifested by these
symptoms, and to a variety of leguminous plants, found growing on the
western lands and supposed to cause the disease in question. The plants
complained of are Astragalus Hornii, and A. Lentiginosus (Griesbach) in
California, A. Mollissimus (Torrey) and Oxytropis Lamberti (Purshiana)
in Colorado and New Mexico. Other allied species, and like these found
also in the other Rocky Mountain States, Sophora Serecia, Oxytropis
Multifloris, O. Deflexa, Malvastrum Coccinium, and Corydalis Aurea var.
Occidentalis have been less confidently charged with producing the
disease.

These plants grow on poor, dry, sandy or gravelly soils, and having
great power of resisting drought, are often in fair growth, and present
an abundant mass of leaves when surrounding vegetation is withered up.
Hence, it is alleged, the animals are driven to use it when nothing else
is obtainable and once accustomed to it, the desire for more becomes a
veritable craze or neurosis, and the victim searches for it and devours
it to the exclusion of other food.

The following quotations may serve to illustrate the effects alleged:

Among the symptoms first noticed are loss of flesh, general lassitude
and impaired vision; later the animal’s brain seems to be affected; it
becomes vicious and unmanageable and rapidly loses both flesh and
strength. Frequently when approaching some small object it will leap
into the air as if to clear a fence. The patient also totters on its
limbs and appears as if crazy. After becoming affected it may linger
many months, or a year, but usually dies at last from the effects of the
complaint. (Dr. Vasey. Report of Dept. of Agriculture, 1884).

“I think very few if any animals eat the loco at first from choice; but
as it resists the drought until other food is scarce they are first
starved to it, and after eating it a short time appear to prefer it to
anything else. Cows are poisoned by it as well as horses, but it takes
more of it to affect them. It is also said to poison sheep. As I have
seen its actions on the horse, the first symptom apparently is
hallucination. When led or ridden up to some little obstruction, such as
a bar or rail lying in the road, he stops short, and if urged, leaps as
though it were four feet high. Next he is seized with fits of mania in
which he is quite uncontrollable and sometimes dangerous. He rears,
sometimes even falling backwards, runs or gives several successive leaps
forward, and generally falls. His eyes are rolled upward until only the
white can be seen, which is strongly injected and as he sees nothing, is
as apt to leap against a wall or a man, as in any other direction.
Anything which excites him appears to induce the fits, which, I think,
are more apt to occur in crossing water than elsewhere, and the animal
sometimes falls so exhausted as to drown in water not over two feet
deep. He loses flesh from the first and sometimes presents the
appearance of a walking skeleton. In the next and last stage he only
goes from the loco to water and back, his gait is feeble and uncertain,
his eyes are sunken and have a flat, glassy look, and his coat is rough
and lustreless. In general the animal appears to perish from starvation
and consequent excitement of the nervous system, but sometimes appears
to suffer acute pain, causing him to expend his strength in running
wildly from place to place, pausing and rolling, until he falls and dies
in a few minutes.” (O. B. Ormsby, Report Dept. of Agriculture, 1874.)

“Animals are not fond of it at first, or don’t seem to be, but after
they get accustomed to the taste they are crazy for it and will eat
little or nothing else when loco can be had. There seems to be little or
no nutrition in it as the animal invariably loses flesh and spirit. Even
after eating of it they may live for years, if kept entirely out of its
reach, but if not, they almost invariably eat of it until they die.”
(Mrs. T. S. Whipple, San Luis, Cal. Report Dept. of Agriculture, 1874).

“Cattle, after having eaten it,” Oxytropis Lamberti, “may linger many
months, or for a year or two, but invariably die at last from the
effects of it. The animal does not lose flesh apparently, but totters on
its limbs and becomes crazy. The sight becomes affected so that the
animal has no knowledge of distance, but will make an effort to step
over a stream or an obstacle while at a distance off, yet will plunge
into it or walk up against it on arriving at it.” (Dr. Moffat, U. S.
Army.)

“The term _loco_, simply meaning foolish, is applied because of the
peculiar form of dementia induced in the animals that are in the habit
of eating the plant. Whether the animals (horses chiefly) begin to eat
the plant from necessity (which is not likely) or from choice, I am
unable to say. Certain it is, however, that when once commenced, they
continue it, passing through a temporary intoxication, to a complete
nervous and muscular wreck in the latter stages, when it has developed
into a fully marked disease, which terminates in death from starvation
or inability to digest more nourishing food. The animal, toward the
last, becomes stupid or wild, or even vicious, or again acting as though
attacked with blind staggers.” (Dr. Rothrock, Report of Dept. of
Agriculture, 1884).

Dr. Isaac Ott, of Easton, Pa., gives the following as the physiological
action of the Astragalus Mollissimus: “It decreases the irritability of
the motor nerve, greatly affects the sensory ganglia of the central
nervous system, preventing them from readily receiving impressions. Has
a spinal tetanic action. It kills mainly by arrest of the heart.
Increases the callory secretion. Has a stupifying action on the brain.
Reduces the cardiac force and frequency. Temporarily increases arterial
tension, but finally decreases it. Greatly dilates the pupil.” (_Amer.
Jour. of Pharmacy_, 1882).

In opposition to these statements Professor Sayre, of Kansas, after an
extended observation, arrived at the conclusion that “it is a grave
question whether loco weed is a poison at all; upon chemical examination
no poisonous principle of any kind was discovered; no toxic effect was
observable when administered to frogs, cats, dogs, or the human
species, ... the point cannot be accepted as a settled one whether loco
is poisonous to cattle or not.”

Dr. G. C. Faville found in _locoed_ sheep in Colorado bunches of
tapeworms in the gall ducts. Dr. Cooper Curtice, who subsequently
studied the subject, found the tænia fimbriata, and believes that to
these the symptoms are exclusively due. “The affected lambs are large
headed with undersized bodies and hidebound skins. Their gait is
slightly like that of a rheumatic. They seem to have difficulty in
cropping the shorter grass; they also appear to be more foolish than the
other sheep, standing oftener to stamp at the sheep dogs or the herder
than the healthier ones. Others do not seem to see as well, or are so
affected that they seem to appreciate danger less. In driving, they are
to be found at the rear of the flock.” (Animal Parasites of Sheep.)

It is altogether probable that the tæniasis of sheep has been mistaken
for _loco_, but this can hardly account for the remarkable symptoms
found in other genera of animals, as a concomitant of an acquired and
insatiable fondness for these leguminous plants. The tænia fimbriata has
been found in sheep and deer, but there is no record of it as a parasite
of cattle and horses.

Dr. Sayre’s failure to find any poisonous principle in the plants, or
any toxic action on frogs, dogs or cats, cannot be received as
conclusive in face of the results reached by others. Perhaps Dr. Sayre’s
specimens were not grown under the proper conditions, or were not
collected in the proper season to secure the toxic ingredient.

Miss C. M. Watson, of Ann Arbor, Mich., succeeded in separating a small
amount of alkaloid from the root of Oxytropis Lamberti, but did not
apply the crucial test of physiological experiment. In the Report of the
Department of Agriculture for 1879, are given analyses of Oxytropis
Lamberti, Astragalus Mollissimus and Sophora Speciosa, in each of which
a small amount of alkaloid was found.

In 1888–9, Dr. Mary Gage Day, of Wichita, Kansas, made careful
experiments on cats and rabbits, under the supervision of Dr. Vaughan in
the Michigan Laboratory of Hygiene. She used a decoction of roots, stems
and leaves of plants gathered in September and gave 60 to 70 c.c. of
this to a half-grown vigorous kitten daily, along with abundance of milk
and other food. In two days the kitten became less active, showed rough
coat, increased desire for the _loco_, with partial loss of appetite for
other food, diarrhœa came on, and retching and vomiting occasionally
occurred. The expression became peculiar and characteristic. These
symptoms increased, and emaciation advanced, and on the 18th day periods
of convulsive excitement supervened. These were sometimes tetanic, the
head being thrown backward and the mouth frothing. At other times the
kitten stood on its hind limbs and struck the air with its fore paws,
then fell backward and threw itself from side to side. There were short
intervals of quiet, life being indicated by breathing only. After 36
hours of these intermittent convulsions paraplegia set in, and the
kitten died in two hours. There was no apparent loss of consciousness
before death.

Post mortem examination revealed gastric and duodenal ulcers, some of
which were nearly perforating. The heart was in diastole; brain and myel
appeared normal; the entire body anæmic.

To a _vigorous adult cat_ 60 c.c. to 70 c.c. of a more concentrated
solution were given with other food. The results were essentially the
same. By the twelfth day the cat was wasted to a skeleton and very weak.
Paralysis of the hind limbs came on and the cat died on the thirteenth
day.

As a test experiment, two strong young cats were confined in the same
place, fed from the same dish, and treated in every way the same, except
that the one was fed daily a decoction of the _loco_. The one fed _loco_
acquired the _loco_ disease with the symptoms described above while the
other, eating ordinary food only, remained healthy.

Subcutaneous injections of the concentrated decoction thrown into frogs
and chickens at the Michigan Laboratory of Hygiene, under direction of
Dr. Victor C. Vaughan, caused nervous twitching and in large doses,
death in 1 or 2 hours from heart paralysis. The same symptoms were
produced in frogs by injection of an alcoholic extract of the residue
left after evaporation to dryness of the decoction.

The loss of appetite, acquired liking for the “_loco weed_”, rough coat,
emaciation, peculiar expression, rearing, plunging, and a staggering
uncertain gait are among the symptoms given in the earliest published
observations on the loco disease, and agree with the statements
universally made by ranchmen. An ulcerated condition of the intestines
was also pointed out by Professor Sayre in a locoed cow upon which he
made a necropsy (Dodge City Times, July, 1887): but the diarrhœa which
was so marked a symptom in the cats experimented on, is not mentioned as
a characteristic symptom in horses and cattle.

“From the close agreement of the symptoms in the cats with those
universally recognized in locoed horses and cattle, I conclude that the
cases described above were genuine cases of the “loco disease” and are,
so far as can be ascertained, the first that were ever experimentally
produced.”

“The craving for the “loco” is soon acquired. The kittens would beg for
it as an ordinary kitten does for milk, and when supplied would lie down
contented. To determine whether a herbivorous animal would easily
acquire the “loco habit” a young “jack” rabbit was captured and fed a
few days on milk and grass; then fresh “loco” was substituted for the
grass. At first the “loco” was refused, but soon it was taken with as
much relish as the grass had been. After ten days of the milk and “loco”
diet the rabbit was found dead, with the head drawn back and the stomach
ruptured.”

“With reference to the character of the plants at the different seasons
of the year, I am convinced by numerous experiments, on material
gathered in different months, that the greatest amount of poison is
present in the autumn and winter.” The scarcity of other food at that
period of the year is only a partial explanation of the number of deaths
occurring at that season.

Conclusions:

“1st. There is some poison in “loco weed” which may cause the illness
and, if sufficient quantity is taken, the death of an animal.”

“2d. This poison is contained in the decoction obtained from the plants,
and by systematically feeding it to healthy cats cases of “loco” disease
may be produced.”

“3d. Taste for the green “loco weed” may be experimentally produced in
the jack rabbit.”

“4th. From the large quantity of the plant or the decoction required to
produce the disease, the poison must be weak, or if strong, it must be
in very small amount.”

LEAD POISONING. PLUMBISM.

Physiological action on nervous system. Sources: near smelting
furnaces on vegetation; paints; paint scrapings in manure and on
soils; lead packing of pumps, engines, etc.; sheet lead; bullet spray;
wall paper lead; leaden water pipes or cisterns; lead acetate; painted
buckets; painted silo; lead compounds in arts. Experiments on animals.
Accidental poisoning: =horse=, fever, gray nasal discharge,
salivation, convulsions, paralysis, dyspnœa. =Cattle=, emaciation,
dyspnœa, palsy, tonic spasm of flexors of limbs, swollen carpus, death
in a few months. Young worst. =Sheep=, lambs paretic. =Swine= in pens
escaped, those at large suffered. Post mortem; lead or lead compounds
in stomach, or shown by analysis, in gastric contents, liver, spleen,
kidney, etc. Tests. Treatment: hydrosulphuric or sulphuric acid,
sulphate of magnesia or soda, antispasmodics; in chronic cases,
potassium iodide, bitters.

The physiological action of lead is exerted on the nervous system, so
that lead poisoning may be appropriately enough treated of as a disease
of the nervous system.

_Sources._ The sources of lead as a poison for animals are extremely
varied. In England in the vicinity of lead mines and smelting furnaces
it is deposited from the air in a fine powder, and consumed with the
vegetation. Herapath found that the deposit, in dangerous amount, began
half a mile from the chimney of the smelter and extended about half a
mile further.

A second source is in lead paints used about farms and the scrapings of
paint pots thrown out with manure and spread upon the fields. These lead
combinations will last for years in the soil or on the surface, being
plowed under one year and turned up again the next when the occasion of
their presence has been completely forgotten. In one case I found the
red lead paint marked by the tongues of cattle at the back of an
abandoned cottage the fence around which had been broken down. In
another the scrapings were found in an orchard which had been near and
convenient for throwing them out. In a third case a paint can hung on
the branch of an apple tree, well out of the way of the stock as the
owner fondly supposed, showed in its contents the marking of the barbed
tongues of the cattle. In a fourth case a barrel of paint was set under
the barn where there was not height enough to admit the matured cattle,
but it bore the marks of licking by the young stock, and they alone died
but in such numbers that the owner concluded it must be the
“Rinderpest.”

The lead packing from the joints of pumps, engines and other machinery,
thrown away around works and mines, is a common source of the trouble. I
once found large quantities in the gastric contents of cows that had
died around a coal mine in Ayrshire, Scotland.

Sheet lead—tea-chest lead—is another common source of the poison. This
is thrown out, scattered with the manure on the field, and will resist
the elements for years but dissolves when taken into the acid stomach of
the animal.

The spray from bullets in the vicinity of rifle butts is another common
cause of the poisoning.

In one instance I have seen a cow poisoned by eating some
lead-impregnated wall paper which had been carelessly left in the
stable.

Less frequently the poisoning comes from drinking water carried in
leaden pipes, or left to stand in a leaden cistern. The softest
waters—rain, snow, distilled water—are the most liable to this
impregnation. The hard waters containing carbonates, sulphates or
phosphates, tend to be decomposed, the acid uniting with the lead to
form comparatively insoluble carbonates, sulphates or phosphates of
lead, which protect the subjacent lead against solution. The hardness of
the water is not, however, a sufficient safeguard, as iron, solder, and
other agents present in the lead as an impurity or merely resting upon
it, are sufficient to set up a galvanic action resulting in solution.

The salts of lead may find direct access to the animal, as in the case
reported by Gamgee in which a farmer used a barrel which had contained
acetate of lead for mixing the feed given to his stock. A somewhat
similar source of poisoning is found in the use of buckets or silos
which have been painted inside, and scale off in contact with hot water,
etc.

Blythe enumerates the following compounds of lead as employed in the
arts:

1st. Hair dyes which have a basis of litharge, acetate or carbonate of
lead in combination with lime and other agents.

2nd. White lead in its various forms is carbonate of lead.

3rd. Newcastle white is white lead made with molasses vinegar.

4th. Nottingham white is white lead made with sour ale.

5th. Miniature Painter’s white is lead sulphate.

6th. Pattison white is an oxychloride of lead.

7th. Chrome Yellow is impure chromate of lead.

8th. Turner’s Yellow, Casella Yellow, Patent Yellow is oxychloride of
lead.

9th. Chrome Red is a bichromate of lead.

10th. Red Lead is the red oxide of lead.

11th. Orange Red is an oxide obtained by calcining the carbonate.

12th. Nitrate of Lead is much used in calico printing.

13th. Pyrolignite of Lead is an impure acetate used in dyeing.

14th. Sulphate of Lead is a by product in the preparation of acetate of
aluminium for dyeing.

_Forms._ Lead poisoning occurs in acute and chronic forms. The two
forms, however, merge into each other and are largely convulsive and
paralytic.

_Experimentally._ Harnack found that 2 to 3 mgrms. in frogs and 40
mgrms. in rabbits caused increased intestinal peristalsis, diarrhœa, and
paralysis of the heart. Dogs had choreic symptoms. Gusserno gave 1.2
grm. to rabbits and dogs respectively, and produced emaciation,
shivering and paralysis of the hind extremities. Rosenstein with 0.2 to
0.5 grm. obtained in dogs similar symptoms with epileptiform
convulsions, and Heubel had symptoms of colic in a few cases.

=Casual or Accidental Poisoning.= Metallic lead is slowly dissolved and
therefore large doses of this may be taken in without visible ill
effect. Shot has often been given to relieve the symptoms of broken wind
in horses, and a dog at the Lyons Veterinary School took four ounces
without visible ill effect. When finely divided, however, as in sheet
lead or the spray of bullets it presents a much more extended surface to
oxygen and acids, and in the acid stomach of monogastric animals, or
even in the organic acids of the rumen it is dissolved in quantity
sufficient to prove poisonous.

_Symptoms in Horses._ Shenton thus describes his cases. “There was a
rough, staring coat, a tucked up appearance of the abdomen, and a
slightly accelerated pulse; in fact, symptoms of febrile excitement
which usually, however, passed away in about a week. About this time
large quantities of gray colored matter were discharged from the
nostrils, and saliva from the mouth, but at no time was there any
enlargement of the submaxillary, lymphatic, or salivary glands. Nor was
there constipation of the bowels, which appears to be nearly always
present in cases of lead poisoning in man. Fits and partial paralysis
came on at intervals; and when the animals got down they often
struggled, for a long time ineffectually, to get up again. The breathing
up to this time was pretty tranquil, but now became so difficult and
labored that the patient appeared in danger of suffocation. The pulse
was in no case above 60 or 70, and I ascribe the difficulty of
respiration to a paralyzed state of the respiratory apparatus. The
animals did not live more than two or three days after these symptoms
appeared. The _post mortem_ appearance varied but little. The lungs and
trachea were inflamed; the lungs engorged with large quantities of black
blood; the trachea and bronchia filled with frothy spume. In all cases
but two the villous part of the stomach presented isolated patches of
increased vascular action, and in all cases the intestines, and
especially the large ones, were inflamed. The blind pouch of the cæcum
was nearly gangrenous. There was nothing remarkable about the liver,
spleen or kidneys, except that they were of a singularly blue
appearance.”

_Symptoms in Ruminants._ These are described by Herapath as following
the erection of lead smelting furnaces in the Mendip Hills in
Somersetshire. There were stunted growth, emaciation, shortness of
breathing, paralysis of the extremities, particularly the hinder ones,
the flexor muscles of the fore limbs affected so that the animals stood
on their toes, swelling of the knees and death in a few months. Even if
removed to a healthy locality the victims failed to thrive. The effects
were most pronounced in the young. Lambs were born paralytic; at three
weeks old they could not stand, and palsy of the glottis rendered it
dangerous to feed from a bottle. Twenty-one out of twenty-three died
early. The milk of cows and sheep was reduced in quantity and quality,
and contained traces of lead. The cheese had less fat in it. The dead
showed the mucous surfaces paler than natural and the lungs had large
areas with abruptly circumscribed margins of a dark red color,
surcharged with fluid. A blue line appeared on the gum close to the
teeth, and from this a globule of lead could be melted under the
blowpipe.

In the cases that have come under my observation paralysis of the hind
limbs, emaciation and low condition, have been most prominent in the
chronic forms, while these have been complicated by torpor of the
bowels, blindness, stupor, coma, and more or less frequent paroxysms of
delirious excitement or convulsions in the acute. In the chronic cases
the blue line on the gums is an important symptom.

Herapath noticed that near the smelting furnaces pigs escaped if kept in
the pen but suffered if allowed to go at large. This is explained by the
presence of lead in the forms of oxide, carbonate and sulphate on the
herbage, hay and hedge rows, and in short, on all vegetation.

In _post mortem_ examination the stomach should be carefully searched
for lead in the metallic form as sheet lead, bullet spray, etc., for the
different forms of paint of which lead forms an ingredient, for the
discarded white lead packing of pipes and machinery, and even for solid
masses of metallic lead. This is especially necessary in the case of
cattle in which the morbid habit of eating non-alimentary matters is so
common, and for which the sweet taste of some of the lead compounds
seems to offer an attraction. The lead being long retained in the first
three stomachs in contact with acetic and other organic acids is
especially liable to be dissolved and absorbed in dangerous amount.

In the chronic cases especially, the test by electric current may
furnish a valuable pointer. In lead poisoning the muscles respond much
less actively to the stimulus than in the normal condition.

In resorting to analysis the following table from Heubel of the amount
of lead in the different organs of a dog may offer a guide to the
selection of an organ for examination:

Liver .03 to .10 per cent.
Kidney .03 to .07 „ „
Brain .02 to .05 „ „
Bones .01 to .04 „ „
Muscles .004 to .008 „ „

Professor George Wilson found the lead very abundant in the spleen, and
used it for analysis. He dissolved it in aqua regia over a slow fire,
cooled, filtered, evaporated, cleared, and boiled with dilute nitric
acid. Then filtered and dried again, dissolved in dilute muriatic acid,
and finally applied the color tests. With hydrosulphuric acid it gives a
black precipitate, with sulphuric acid, a white, and with potassium
iodide or bichromate a bright yellow. Or from the solution of the
chloride the lead may be obtained as a metallic deposit on zinc from
which it can be fused into a minute globule on charcoal.

In the _treatment_ of lead poisoning the first object is to prevent the
further solution of lead in the alimentary canal and to carry it off. To
fill the first indication, hydrosulphuric acid or sulphuric acid may be
administered to form respectively the insoluble sulphide or sulphate. As
a purgative, sulphate of magnesia or soda should be preferred, as
favoring at once elimination and the formation of an insoluble
precipitate. Large doses are usually desirable, especially in ruminants,
because of the bulky contents of the stomach and the torpor of the
alimentary canal. If griping is a prominent symptom opium or other
antispasmodic must be added.

In chronic cases, after the evacuation of the contents of the alimentary
canal small daily doses of potassium iodide will serve to dissolve the
lead out of the tissues, while sulphates may be given in small doses to
assist in elimination from the bowels and to prevent reabsorption. The
treatment by potassium iodide is equally applicable, to assist in the
elimination of the lead that has passed into the circulation and
tissues. The doses, however, should in any case be small to avoid the
sudden solution of a large amount of lead which had been deposited in
the tissues in a comparatively insoluble form. The sudden entrance into
the circulation of any large amount of such lead would induce a prompt
return of the toxic symptoms. A continuous exhibition of small doses is
the course of wisdom and safety. The bowels should meanwhile be kept
somewhat relaxed by small doses of sodium or magnesium sulphate. As a
general tonic a course of bitters may be called for, especially when
torpor or emaciation is pronounced.

ALCOHOLIC INTOXICATION.

Beer in pigs, alcohol in dogs, absinthe in horse, alcohol and burnt
ales in cows, alcoholized grain in fowls, also fermented raisins.
Symptoms, lack of coördination, staggering, flushed mucosæ, full
pulse, stertor, sopor, coma, alcoholic breath, chill, muscular
twitching, delirium. Treatment: ammonia acetate, or carbonate,
apomorphia, pilocarpin, warm water, coffee, stomach pump, electricity.

Poisoning by alcohol is less common in the lower animals than in man,
yet the veterinary journals record a considerable number of cases. We
have seen pigs suffer from drinking soured beer; the smaller breeds of
dogs (English terriers) which are systematically dwarfed by feeding
alcohol are often kept for a length of time in a condition of
semi-intoxication. Bissauge records the case of a horse inebriated by a
glass of absinthe and a pint of white wine, and that of a cow which died
intoxicated 24 hours after she had been given three quarts of pure
alcohol (Rec. de Med. Vet. 1895). Dundas records intoxication in cows
fed on _burnt ales_. Intoxication of barnyard fowl and wild birds from
eating grain soaked in strong alcoholic liquids has been frequently
noticed, and Bissauge reports fatal drunkenness among our domestic fowls
from eating raisins and other fruits which had undergone fermentation.

The _symptoms_ are too suggestive to require notice in detail. There is
a lack of coördination of movement, a staggering gait, a disposition to
lie, dilated pupils, dark red flushing of the visible mucous membranes,
a full pulse, stertorous respirations, drowsiness, stupor, and finally
coma. The breath exhales the odor of alcohol, and the temperature
usually falls, especially if the subject has been exposed to cold. It
may rise later in connection with inflammation of the stomach or brain.
Muscular twitchings and delirium are sometimes found, and may occur
paroxysmally.

_Treatment._ A pint of liquor of the acetate of ammonia to horse or ox
may quickly relieve the symptoms, or 1 oz. carbonate of ammonia may be
given in solution in a pint of vinegar. If more convenient the
hypodermic injection of 1 or 2 grains of apomorphia, or of 5 grains of
pilocarpin may be employed. Warm water is of the greatest value in
securing elimination. A strong infusion of coffee is very effectual. If
the patient is a vomiting animal an emetic may be employed, and in case
of coma the stomach pump may be resorted to. Cold applied to the head or
galvanism may be used to rouse the patient.

In case of gastritis or encephalitis following the attack these must be
treated according to indication.

ANILINE POISONING.

Composition. Source. Uses. Toxic action on skin, by inhalation, and by
stomach. Symptoms: acute: chronic. Test. Treatment: emesis,
purgatives, stimulants, tonics, enemata, bleeding, normal salt
solution.

Aniline (Amidobenzene, Phenylamine, C_{6}H_{7}N) is a product of coal
tar produced in the manufacture of benzole and of aniline dyes. Being an
object of large production and consumption in the arts, its toxic action
is seen not infrequently in man, and less so in animals. As used in
confectionery it is so diluted that it is rarely or never injurious. On
textile fabrics, however, it often causes cutaneous irritation, and when
eaten by animals may be toxic. Workmen in the factories usually suffer
from its inhalation.

Turnbull gave ½ dram sulphate of aniline to a dog, inducing vomiting in
2½ hours and purging one hour later. There were accelerated pulse,
labored breathing and paraplegia, followed by recovery in five hours.
Other objective symptoms are coldness of the surface, and a bluish or
purple color of the visible mucosæ, the blood failing to take up oxygen.
In chronic aniline poisoning in man the following symptoms have
appeared: papular, vesicular or pustular skin eruptions, or ulcers on
hands feet and scrotum; an odor of coal tar; anorexia, nausea and
vomiting; headache, vertigo, stupor, ringing of the ears, amblyopia,
muscular spasms, muscular weakness, anæsthesia and motor paralysis
especially of the extremities. The fatal dose is 1½ dr. and upward.

Aniline may be extracted from the tissues by petroleum ether, and on the
evaporation of the solution, it is left as an oily yellowish mass which
gives the following reactions:—with a few drops of sodic hypochlorite a
blue or violet blue; with acids a rose red; with bromine a flesh red.

The _treatment_ must be by elimination by emesis, or purgation, by
removal from aniline fumes or mixtures, and by stimulating and tonic
agents. In place of emesis a stomach tube and lukewarm water in large
amount may be employed to wash out the stomach. For vomiting animals
ipecacuan may be employed. Copious enemata may be given, along with
purgatives, to clear out the bowels. As stimulants strong coffee,
caffein, camphor, or strychnia may be employed. In case of profound
stupor, prostration, or paresis it may be desirable to reduce the amount
of aniline in the system by free bloodletting, care being taken to
inject subcutem, or into a serous cavity, a nearly equivalent amount of
normal salt solution.

POISONING BY NITRO-BENZOL.

Composition. Source. Uses. Characters. Toxic qualities. Convulsions:
paralysis: cyanosis; weak pulse; bitter almond odor; dark red urine;
sopor, giddiness; reduced size of red blood globules; congested brain,
stomach, intestines. Treatment: emesis, purgation, stimulants,
electricity, derivatives, bleeding, normal salt solution.

Nitro-benzol (Nitro-benzine, C_{6}H_{5}NO_{2}) is a coal tar product,
formed in large quantities in the manufacture of aniline dyes and
extensively used as a flavoring agent for soaps, sweet meats, etc. It is
formed by the addition of strong nitric acid to benzine, and appears as
a yellow fluid with an odor resembling, yet somewhat different from,
that of prussic acid or oil of bitter almonds. It may prove deadly to
man or dog in a dose of fifteen drops, though most commonly it enters
the system by inhalation. In animals the prominent symptoms are
convulsions and paralysis, supervening on a period of weak circulation
and pulse, and blueness of the visible mucous membranes. The
characteristic odor resembling the oil of bitter almonds exhales from
the lungs and skin. In man there are dilatation of the pupils, blueness
of the lips and nails, pallor of the face, weak pulse, slow breathing
(often in the end Cheyne-Stokes respiration), a dark maroon or port wine
color of the urine, and amblyopia. In the chronic cases the skin is
yellowish, and there are weariness, a dragging walk, headache, morning
anorexia, drowsiness, giddiness, numbness of the hands or other parts
and emaciation. The blood is chocolate color with red globules reduced
in size, in number and in hæmoglobin, but containing an excess of carbon
dioxide. The brain is often congested and the gastro-intestinal mucosa
like the skin may be yellow (from alleged formation of picric acid). In
chronic cases disseminated sclerosis may be seen.

In _treatment_ emesis, purgation, stimulants (ammonia, camphor),
galvanism, sinapisms to the chest, and phlebotomy, with injection of
normal salt solution, may be resorted to, as in aniline poisoning.

POISONING BY CARBON DISULPHIDE.

Used to kill insects in grain, etc., in barns. Locally anæsthetic, and
irritant. Inhaled, toxic, causing excitement, anæsthesia, collapse.
Large doses, excitement, reckless movements, incoördination,
giddiness, sleep, stertor, paraplegia. Small doses, weakness,
emaciation, tremors, paraplegia, polyuria, mellituria; convulsions,
death. Distortion and varicosity of axis cylinder, and unequal
staining of cytoplasm. Treatment: pure air, good diet; massage,
electricity, tonics, phosphorous.

This agent is largely used in vulcanizing and other factories where the
employes are liable to suffer, and also in granaries, barns, etc., for
the destruction of insects in grain and other objects and where animals
are liable to suffer.

_Locally_ it acts like chloroform, when confined to the surface, as
under a glass or covering, producing very active irritation with
anæsthesia.

_Inhaled_ it produces intoxication, excitement, general anæsthesia and
finally collapse. In rabbits it causes intense excitement, giddiness,
swaying from side to side, and reckless leaps forward, followed by
profound sleep with deep stertor, and paraplegia for half an hour after
the return of consciousness (Oliver). When taken for a long time in
smaller quantity it caused weakness, emaciation, tremors, paraplegia,
and death in convulsions. There was polyuria, with excess of sugar but
neither urea nor albumin. The large cells in the motor areas of the
brain, when stained by Golgi’s method, showed the axis cylinder
distorted and varicose, and the cytoplasm stained unequally. The action
on dogs was essentially the same, and in neither animal were changes in
the blood globules observed (Oliver).

In man slow poisoning caused headache and exhilarate intoxication,
followed by depression, mental apathy, dullness, loss of memory,
impaired vision, hearing, sexual desire and muscular power. Cramps are
common (Delpech, Curtis).

_Treatment_ consists in giving pure air, good food, massage, galvanism,
tonics, and for the persistent nervous failure phosphorus.

TETANY.

Definition. Casual and experimental cases in animals. Causes: Excision
of the thyroid, indigestions with fermentation, rheumatism, infection,
malaria, rachitis, want of hygiene, hereditary or developmental
irritability, microbian poisons. Symptoms: intermittent spasms with
semi-flexed limbs, tremors. Diagnosis: by the complete intermissions
of spasms, and by pressure on nerve or artery, rousing them. No fever.
Like spasms of ergot. Treatment: thyroid extract, grafting thyroid;
remove sources of irritation, antispasmodics, warm or tepid baths,
electricity.

_Definition._ Tetany is the name given to a limited contraction of a
group of muscles usually in the extremities occurring paroxysmally with
intervals, during which it may usually be roused into activity by
compression of the nerve or artery proceeding to the muscles in
question.

The disease has not been accorded a place in systematic works on
veterinary medicine, though cases have been recorded which are supposed
to have been of this nature, and in cases occurring in man and
associated with dyspepsia and gastric dilation, Bouveret and Devic have
extracted from the contents of the stomach a toxic substance which
caused tetanic convulsions in animals. The total removal of the thyroid
gland, or even of four-fifths of it (Eiselsberg), in the cat is found to
be invariably followed by tetany.

_Causes._ Beside the origin from the removal or general disease or
degeneration of the thyroid, it has been attributed to digestive
troubles, associated with fermentations and the production of toxic
matters, to rheumatism, infection and malaria, to rachitis and
unhygienic conditions. The systemic changes and trials of growth and
development, of pregnancy and lactation, seem to be factors in certain
cases. A peculiar irritable nervous organization transmitted by heredity
is undoubtedly a potent cause, and upon this, bacteridian, leucocytic
and other poisons operate so as to rouse the paroxysms.

_Symptoms._ There are usually prodromata in the shape of dullness,
prostration, weariness, and some dullness of the special senses. Fever
is commonly absent and the contractions tend to affect both flexors and
extensors, but as the force of the first predominates, the affected
member is usually held more or less rigidly semi-flexed. The spasm
appears suddenly, often taking occasion of some voluntary movement, and
may last for several minutes or hours. It is followed by an interval of
relaxation of equally uncertain duration. Though usually attacking the
limbs and causing the victim to walk on the toes, it may extend to the
face, neck or trunk, and constitute an intermittent trismus,
oposthotonos, or emprosthotonos.

_Diagnosis._ Tetany is to be distinguished from tetanus by the complete
intermissions of the spasms, and by the voluntary development of these
by compression of the presiding nerve or artery. Pressure on the nerve
arouses its excitability, and compression of the artery shutting off the
supply of blood from the disordered and susceptible muscles, tends to
increase their irritability. Ligature of an artery supplying healthy
muscles causes simple trembling of such organs. From the spasms of
cerebral, spinal or meningeal inflammation tetany is distinguished by
the absence of fever, and the complete intermissions of the paroxysms.
The spasms of ergotism bear the closest relation to those of tetany and
in the absence of proof of the ingestion of ergot, might well be
confounded with them.

_Treatment._ This consists mainly in doing away with the causes, when
these can be ascertained. Portions of thyroid may be grafted if complete
thyroidectomy has been performed, or thyroid extract may be given. In
the human subject recoveries have followed the expulsion of intestinal
worms, the cure of gastric dilation, dyspepsia, fermentations, diarrhœa,
rachitis, menstrual irregularity, or auto-intoxication. Fíré has seen
recovery follow the extraction of a carious tooth.

The spasms may be met by the internal administration of antispasmodics
(chloral, belladonna, bromides, opiates), and the external application
over the affected muscles of anodynes and antispasmodics (belladonna,
opium, chloroform, oil of cajeput, oil of peppermint, menthol, etc.).
Warm or tepid baths are often of great value and a mild electric current
has been found useful.

CONGESTION OF THE SPINAL CORD IN THE HORSE AND COW.

Under this heading Trasbot describes hæmoglobinuria and parturition
paresis, but this tends to cover up the more important causes and
phenomena of these diseases, which should be kept in the foreground.
Spinal congestion is undoubtedly a feature of both these affections, and
the sudden onset and rapid recoveries often seen, indicate the absence
of inflammatory action, yet this is but an accompaniment of a
constitutional morbid state which we think fully warrants a special
consideration of each elsewhere (see Hæmoglobinuria; Parturition
paresis).

Apart from these affections congestion habitually merges into myelitis
or spinal meningitis, and may be considered as the initial stage of
these disorders. It owns the same causes and is manifested by closely
allied symptoms, but these are less persistent, and may subside abruptly
into a condition of health. The treatment will be on the same general
lines as for myelitis, but with much better hope of success.

ACUTE MYELITIS. POLIOMYELITIS. INFLAMMATION OF THE SPINAL CORD.

Causes: Stimulating food to excess, sexual over-stimulation, violent
overexertion, hot sun, chill, rheumatism, traumas, injury to spinal
nerves, vertebral caries, microbian infection, narcotics, vegetable
poisons, cryptogams. Lesions: discoloration of white or gray matter,
swelling, friability, softening, extravasations in points, leucocytes
in excess, nerve cells cloudy, granular, nucleus enlarged, stain
highly, chromophile granules irregular, neuroglia thickened. Symptoms:
Hyperthermia, rigor, hyperæsthesia, tonic contractions in neck and
limbs, intense lameness, paresis, palsy, muscular atrophy, areas of
heat followed by coldness, such parts may not perspire, palsy less
complete than in broken back, circulation and breathing accelerated or
slow, paraplegia in large herbivora. Diagnosis: progressive onset,
hyperæsthesia or rigidity merging into palsy, retention and later
incontinence of urine, extreme spinal tenderness, rapid atrophy of
affected muscles, skin sloughing. Prognosis, always grave. Treatment:
purgation, bleeding, hot fomentations, ice bags, compresses,
derivatives, bromides, chloral, potassium iodide, atropia, ergot,
electricity, strychnia, soft laxative food, bitters, phosphates.

_Causes._ Like congestion this may be a result of =plethora= in overfed
animals, in those subjected to specially stimulating food like gluten
meal, cotton seed meal, beans, peas, vetches in excess, animal food for
herbivora (the waste of hotels and restaurants for cows, compressed meat
products for pigs), a period of absolute rest on full rations in horses
habituated to hard work and full feeding; of =sexual over-stimulation=
in males (stallion, bull, ram); of =violent overexertion=, especially if
=under a hot sun=; of =sudden chill= when over-fatigued and perspiring;
of =cold rain storms= (Freirier); of =rheumatism= (Kowalski); of
=traumatism= (fractures, sprains, slipping with overdistension); of
=falls upon the point of the ischium=; of blows upon the back (Cruzel,
Trasbot); of =tumors implicating the cord=; of =too violent efforts in
serving= by stallions; of =injuries of the great nerve trunks= passing
off from the cord (Gull, Trasbot, etc.); of extensions from =caries or
suppurations of the vertebræ= (Decoste, Trasbot); of =microbian
infection=, as in rabies, distemper, tubercle, dourine, louping ill,
milk sickness, contagious pneumonia, influenza, and suppurations; of
=narcotic poisoning=, as from ergot, smut, the poisons of the cryptogams
and bacteria of mouldy bread, musty fodder, spoiled meats, fish, etc.;
also the poisons of =lolium=, =vetch=, =lupin=, =astragalus=,
=oxytropis=, =arsenic=, etc.

_Lesions._ These consist in a yellow or pink discoloration of the white
and especially of the gray matter, and a special prominence of the
puncta vasculosa in the affected part. Swelling or distortion of the
part is not usual. This may involve only a single gray horn, the two
horns on the same side, the two inferior horns, or all four at once, or
the white matter adjacent may also show the rosy tint, the large puncta,
and a characteristic softness and friability. Minute blood
extravasations are very significant. Microscopically examined leucocytes
are found in abundance in the perivascular spaces and in the neuroglia.
The neurons (nerve ganglion cells) are degenerated, being cloudy,
swollen, with enlarged nucleus, stain highly, and show enlargement of
the chromophile granules. In a more advanced stage the cell has an
indefinite outline and the nucleus is indistinct and may fail to take a
stain; the chromophile granules are irregular and do not radiate evenly
from a centre and many vacuoles appear. This may lead to fatty
softening, or to fibrous increase of the neuroglia, and sclerosis.

_Symptoms._ These vary greatly in different cases according to the part
involved, the meninges or some special region of the cord, to the
essential cause of the inflammation and its acuteness. Usually the
attack sets in slowly in contradistinction to the abrupt attack of
congestion. =Hyperthermia= and =rigor= are usually among the first
symptoms, though in many cases =hyperæsthesia= is the most marked early
symptom. The skin covering the muscles which derive innervation from the
affected section of the cord is the most sensitive. This is often so
extreme along the vertebral column that percussion on the spinous
processes or pinching between the fingers and thumb causes the most
pronounced wincing and dropping of the back. Copland and Laposso have
noticed that a sponge of hot water drawn along the line of the vertebræ
causes acute pain and contractions of the muscles of the back and limbs,
which are almost tetanic in their force. This probably implies the
existence of meningitis, since the absence of rigidity of the muscles of
the neck, back and limbs, usually implies the absence of meningeal
inflammation. It may, however, occur in localized or commencing
myelitis. The existence of unilateral lesions and rigidity determines
intense lameness, which is further characterized by the most marked
hyperæsthesia.

The =morbid phenomena of the motor system= are more characteristically
paretic or paralytic than spasmodic. When rigidity or spasm ushers in
the attack it is superseded in a few hours or in two or three days by
flaccidity of the muscles of the affected part, with imperfect control
or even complete paralysis. The muscles affected will depend on the seat
of the spinal lesion. If in the neck it may affect fore and hind limbs,
and even the chest and abdomen; if in the back or loins it will induce
paraplegia, the anterior limit of which will correspond to the seat of
the lesion; if near the caudal extremity of the cord, (lumbar portion),
paralysis of the tail and of the sphincters ani and vesicæ may be
prominent features. Retention of urine and fæces (spasm) may precede
incontinence (palsy).

=Common sensation= may be dull or abolished on one or on both sides. If
on one side only, the other may show hyperæsthesia.

=Trophic modifications= are very marked though they may not be
noticeable at first. The paralytic muscles waste rapidly and the
impaired nutrition is manifested in the rapid formation of sloughing and
intractable sores where pressure comes in recumbency (the hips, stifles,
hocks, shoulders, etc.). This is especially noticeable on parts supplied
by the cord at or behind the seat of the lesions.

=Vaso-motor changes= are usually marked by a preliminary hyperthermia of
the affected parts, followed by a corresponding hypothermia. Sometimes
the affected part of the skin will remain quite dry while the rest of
the body is covered by perspiration.

=Choked optic disc= and retinitis are sometimes present.

The =febrile reaction= which is at first moderate, gradually increases
in force; the animals become dull, drowsy, careless of food, and the
hyperæsthesia merges into paresis or paralysis. This is rarely so
complete as in fracture of the vertebræ. If the inflammation is
restricted to the lower columns only, there may be akinesis without
change of the sensitiveness or with hypersensitiveness. If restricted to
the upper columns there may be sensory paralysis only on the opposite
side.

The =heart sounds and pulse= are usually altered, palpitations may
appear early with acceleration and sharpness of the pulse, and this may
alternate with a tardy slow pulse with intermissions. =Breathing= also
becomes accelerated and in violent cases with trembling, though in
moderate inflammation with effusion, softening and degeneration, it is
liable like the heart beats to become slow and tardy.

When =vertigo= appears it may be attributed to extension to the bulb or
cerebellum, or to the sympathetic implication of these organs.

The frequency with which paraplegia occurs in the large herbivora
suggests a special susceptibility of the lumbar portion of the cord,
probably in connection with severe muscular effort of the hind limbs.

In protracted cases the fever may run very high, being complicated by
septic poisoning from the numerous cutaneous sloughs and sores, as well
as by cystitis and nephritis.

_Diagnosis._ This may be based on the progressive onset, unlike the
sudden attack of congestion; on the occurrence of primary fever with
hyperæsthesia or even muscular rigidity, merging into a later paresis or
paralysis; on the retention of urine, followed by incontinence; on the
torpor of the rectum; on the extreme tenderness of the spine in the
region of the inflammatory lesion; and on the tendency to rapid atrophy
of the affected muscles, and the death and sloughing of the skin under
pressure over the prominent parts of the body. The definite localization
of the muscular symptoms, and the different temperature and secretion of
the affected part of the skin, from the unaffected, are further
confirmatory of myelitis.

_Prognosis._ While always grave, myelitis induced by narcotic elements
in the food which can quickly be eliminated from the system, and that
which has not caused compulsory decubitus, or persistent retention of
urine and fæces, may be considered as hopeful. When, on the other hand,
the nature and extent of the lesions have entailed a prolonged
paralysis, or in the large animals, (especially solipeds), a
persistently recumbent position, there is little to be hoped for. The
degenerated myel, and the badly wasted muscles, combine to prevent
rising and the use of the limbs, the sloughing bed sores quickly poison
the blood and general system, and the animal sinks beyond hope of
remedy. Again, if the fæces accumulate in the rectum causing general
retention of the bowel contents and fermentation, the shock to the
nervous system and the toxins absorbed add materially to the prostration
and danger. Finally the retained urine infected through the blood or by
a catheter, quickly passes into ammoniacal fermentation, with softening
and detachment of the cystic epithelium, septic infection of the mucosa,
and the extension of this infection through the ureters of the kidneys.
The complication of infective inflammation of bladder and kidneys
introduces one of the most dangerous conditions possible.

_Treatment._ In an acute case, at the outset, elimination of any
extraneous poison should be sought as the first step toward a
restoration of the normal spinal functions. Purgatives may be employed
to this end, and if the case is urgent and without spasms immediate
action may be sought by a hypodermic injection of 1½ gr. eserine and 2
grs. of pilocarpin. Meanwhile the horse may receive a dose of aloes or
the cow one of Epsom salts. Abundance of watery or demulcent liquids
given by the mouth, or as enemas, should not be omitted.

When plethora has been a prominent factor and symptoms are urgent, a
free bleeding (4 to 5 quarts for horse or cow) from the jugular vein may
serve to relieve the vascular tension, dilute the vital fluid, and
moderate the inflammation. Hot fomentations or sinapisms to the limbs,
and even cupping on the neck and chest, may contribute to relieve the
tension on the spine. When the temperature is already high, bags of ice
may be applied to the tender parts of the spine or those indicated to be
the inflamed parts by the groups of rigid or paretic muscles. Wet
compresses or evaporating lotions may be substituted. In the absence of
mustard, tartar emetic, biniodide of mercury, or euphorbium may be used,
or even croton oil in a carefully guarded manner, but cantharides, oil
of turpentine, and other agents calculated to irritate the kidneys are
to be avoided.

Bromides, hydrobromic acid, potassium iodide, chloral, or belladonna may
be availed of. Some prefer ergot, but this, like strychnia, is of
doubtful effect or positively injurious in most cases in the early
stages. Even in the early stages electricity may be used in the form of
a constant current, which tends to vaso-motor contraction and a better
tone of the capillaries. The electrodes may be applied along the
affected side of the spine so that the current may traverse the affected
part. It may be kept up for ten to twenty minutes at a time and repeated
daily. Any undue suffering under the current may be accepted as a demand
for the reduction of its force or its suspension for the time being.

When the hyperthermia has subsided and the occurrence of paresis or
paralysis demands nervous stimuli, these may be sought in
counter-irritants, strychnia, and interrupted currents of electricity.
The blisters already mentioned may be used. Strychnia may be used
internally (horse or ox 2 grs., sheep ¼ gr., dog ¹⁄₅₀ to ¹⁄₁₆ gr.) or
hypodermically (horse 1½ gr., sheep ⅛ gr., dog ¹⁄₁₀₀ to ¹⁄₃₀ gr.).
Should this excite the animal or aggravate the symptoms it must be
stopped and deferred until the inflammation shall have more completely
subsided. The same remark applies to electricity which may be tried in
the interrupted current, and graduated to the endurance of the patient
or entirely abandoned for the time.

If the patient is able to support itself on its limbs, it is best kept
in a sling to avoid the formation of sloughs and sores. If it cannot so
support itself a very thick soft bed of litter is essential to avoid the
sloughing and septic poisoning. Food must be laxative and easily
digestible such as mashes, hay tea, and boiled or pulped roots. Fresh
green grass may be employed when obtainable.

During convalescence a course of bitters with calcium phosphate and
carefully regulated exercise are important. In tardy cases Trasbot
especially recommends cauterization.

SPINAL MENINGITIS.

Complex cases. Microbian invasion. Lowered vital tone. Traumas.
Poisons, parasites, tubercle, rheumatism, neoplasms, poisonous food.
Symptoms: Stiffness, tonic contraction, spasms, hyperæsthesia with
warmth, enuresis, paralysis later. Treatment: parallel to myelitis;
cold, anodynes, nerve sedatives, and antispasmodics, saline
purgatives, diuretics. Iodine, electricity, cauterization.

It is often difficult to distinguish between spinal myelitis and
meningitis in the lower animals, and the danger of confusion is greater
because the two affections are often conjoined. Attacks appear to be
often associated with microbian invasion of the membranes, but in its
turn this is often favored by the lowered tone of the membranes through
mechanical injury, circulatory disorder, trophic changes, or the action
of poisons in the blood. Thus the condition may supervene on fractures,
partial dislocations or sprains of the neck, back or loins, abscesses
pressing on the spine, extension of septic inflammation from poll evil,
fistulous withers, or arthritis of the vertebræ, penetration of the
membranes by sharp pointed bodies (Reindl found a darning needle in a
cow’s spinal canal), invasion by microbes in influenza, brust-seuche,
dourine, rabies, milk sickness, distemper, pyæmia, septicæmia,
strangles, louping ill, or Texas fever. The toxins of tetanus may start
similar trouble. The larva of cysticercus cellulosa may cause meningitis
in dogs or pigs, the sclerostoma in the soliped, the filaria in dogs and
strongle in a variety of animals. Tubercle of the meninges is not
unknown, and rheumatism is alleged as a cause. Neoplasms commencing in
the cord act in a similar way, and the poisons of rye grass, millet,
loco, lupins, tares and vetches may act on the membranes as well as on
the myel.

_Symptoms._ In the main these resemble those of myelitis and are often
present at the same time, and it is only necessary to note those which
are especially pathognomonic. The early rigors are followed by stiffness
of the back shown in rising or walking and aggravated by motion. There
may be tonic contraction of the dorsal and lumbar muscles amounting at
times to oposthotonos. The muscles of the limbs, chest or abdomen or
some part of them may be the seat of tonic or clonic spasm. The skin is
usually hypersensitive and this is aggravated by heat. The urine is
liable to be retained because of the pain of stretching to micturate.
Paralysis usually follows and implies extension to the myel, compression
of the cord by reason of exudation, or implication of the spinal nerves
at the points of exit. In myelitis on the other hand the spasms may be
entirely absent, and paralysis sets in early and extends rapidly
according to the seat and extent of the lesion.

_Treatment._ This will be along the same lines as in myelitis, being
aimed at elimination of toxic matters, and the counteracting of the
existing inflammation. Anodynes such as bromides and chloral and cold
water or ice are especially called for to alleviate pain and
hyperæsthesia, and antispasmodics like ether, chloroform, chloral,
belladonna, etc., to allay the spasm. Saline purgatives too, and
diuretics may be availed of to limit effusion and favor reabsorption. In
the advanced stages iodine may be freely applied to the spine, and an
occasional electric current, or cauterization may be availed of.

ACUTE MYELITIS IN THE DOG. MENINGO-MYELITIS.

Causes: distemper, in long-haired pets, pyæmia, exposure to cold,
violent overexertion, traumas, vertebral caries or abscess. Lesions:
in lumbar enlargement, horns yellowish, red, friable, pultaceous,
leucocytes in excess, punctiform extravasations, neurons opaque;
granular, filaments diffluent, varicose, sclerosis. Meninges
congested, thickened. Symptoms: as in horse, extreme hyperæsthesia,
later anæsthesia, tremors or twitching, later paraplegia. Treatment:
Laxatives, ice bags, sedatives, later derivatives, cauterization.
During convalescence, phosphates, iron, zinc, strychnia. Attend to
bladder and rectum, light, laxative diet, pure air and water.

_Causes._ This disease is a common result of distemper and according to
Trasbot, is much more frequent in long-haired and pet dogs than in the
short-haired and mongrels. The shelter of the hair, like the warm indoor
atmosphere, seems to contribute to a special sensitiveness of the
cutaneous and nervous tissues. The infective inflammation of the myel is
also seen in pyæmia, rabies and milk sickness. It appears to be further
induced by exposure to cold draughts when heated, or excited, by
plunging into ice cold water, by lying on cold, damp, stone pavement or
metallic plates. Violent overexertion, excessive fatigue, and a variety
of traumatisms are further factors. Kicks, blows on the back, concussion
from falling from a window or other height, and sprains received in
fighting or otherwise, are common causes. Disease of the vertebræ or
abscesses in their vicinity will sometimes extend to the meninges and
cord.

_Lesions._ These are like those in the larger animals, being to a large
extent determined by the cause and nature of the lesion, concussion,
sprain, fracture, pyæmic, septicæmic, or other infection. The
implication of the myel to the exclusion of the meninges is very
frequent and the lumbar enlargement is the most common seat of disease.
Localization in the brachial enlargement or in one lateral half of the
cord is uncommon. The gray matter towards the extremity of the horn is
the most commonly involved, reflecting a yellowish, grayish red or deep
red color, and breaking down into a pultaceous mass on the slightest
pressure. At an advanced stage the altered coloring matter gives to the
tissue a brownish yellow color without altering its consistency. The
still vital and vascular area around the centre of softening may be
slightly swollen and abnormally firm. The neuroglia is the seat of
leucocytosis, and minute (usually punctiform) extravasations of blood.
The red globules are crenated or otherwise distorted and the white are
granular and opaque. The neurons are swollen, granular and opaque and
the nerve fibres are more or less diffluent, moniliform and in their
substance show no clear outline of white substance and axis cylinder.
Interruptions by granule masses and vacuoles are common. In old standing
or chronic cases the liquid exudate and granular debris have been
largely absorbed and the thickening of the neuroglia by fibrous
neoplasm, has restored the firmness or even approximated the part to a
condition of sclerosis.

In case the meninges are involved there is thickening by exudation into
their substance or on their surface, there may be adhesion between the
outer and inner layers of the arachnoid and a serous fluid, red, milky
or clear, distends the arachnoid or subarachnoid space. The false
membranes, here as elsewhere, are usually red if recent, and increase in
pallor with age.

_Symptoms._ These are in the main the same as in the larger animals. The
early excitement usually takes the form of hyperæsthesia. When lifted,
pressed, touched or only approached the dog may growl, howl, snap,
cringe, cower or tremble, glancing up meanwhile with anxious or pleading
eyes. When later, this gives place to anæsthesia no such interference
will draw a response. The motor disorders at the outset are mostly of
the nature of tremors or twitching of the muscles of the limbs or of
those parts of the trunk corresponding to the seat of the lesion. In
exceptional cases spasms or convulsions may be shown. Trasbot records a
case of very acute myelitis of the brachial enlargement in which there
were clonic contractions of the muscles of the neck, jaws and eyeballs,
and grinding of the teeth, which condition lasted for thirty-six hours.
When this motor excitement merges into paralysis it usually attacks the
hind limbs which are extended backward helpless while the animal pulls
himself forward by his fore limbs. Some such cases are restless and in
continual movement while others are dull, apathetic and indisposed to
move. The precise seat of the paresis or paralysis will be determined by
the seat of the lesion as in the larger animals. Thus paraplegia is most
common, less frequently hemiplegia, palsy of the fore limb, palsy of a
single limb, and monoplegias, about in the order named. Palsy of the
tail and sphincters implies a lesion of the lumbar section of the cord
and is very offensive in the incontinence of urine and fæces especially
in long-haired subjects.

_Treatment._ The abstraction of blood is rarely called for in myelitis
in the dog. If admissible at all it is in the case of strong, vigorous,
plethoric animals which have been attacked in connection with sudden
exposure to cold or accidental concussion, and which are presented for
treatment at once. Then leeches may be applied to the abdomen or inside
of the thigh, or the jugular may be opened with a lancet. Usually on the
other hand the patient is fat, lymphatic, and, if a few days have
elapsed, even anæmic, while if he has been the victim of an accident the
shock and prostration would forbid any depressive measures.

Derivation toward the bowels may be sought by purgative doses of calomel
or jalap. In case of high fever, cold may be applied (in the form of
icebags, evaporating lotions or wet cloths) to the tender portion of the
spine. If the attack has followed exposure to cold, salicylate of soda
may be given, otherwise the bromide of potassium or camphor. Acetanilid
and other antithermic agents may be used with caution.

With the abatement of the high fever and the supervention of paresis, if
not before, counter-irritants are demanded.

Owing to the propensity to lick and the danger of absorption, poisonous
agents are virtually proscribed. Yet Möller advises cantharides, croton
oil, mercuric iodide, and oil of mustard, and Trasbot restricts the
choice to tartar emetic one part to sixteen parts of lard. This the
latter rubs softly along the spine for several minutes. If the dog is
closely watched or muzzled this or the mustard or croton oil may be
admissible. If otherwise, a long-haired dog may be rubbed on the spine
with a combination in equal parts of strong aqua ammonia and olive oil;
or it may have applied for some minutes wet cloths rather hotter than
the hands can bear; or a light cauterization may be made with a Paquelin
cautery. At this stage, too, bitters and phosphate of lime may be given.
Trasbot has long used with the best results 1 grain doses of neutral,
gelatinoid phosphate of lime, repeated two or three times a day. Iron
may also be resorted to, or sulphate of zinc. Strychnia and electricity
are also of great value as soon as the irritability of the spinal
centres will allow of their safe employment. Massage and gentle exercise
are important.

From the first, attention must be given to obviate the retention of
urine and fæces, and the strict antisepsis or asepsis of the catheter
adopted to prevent infective cystitis and nephritis.

Throughout the disease abundant nourishment of an easily digestible
quality is demanded. Cleanliness, pure air and general comfort must not
be forgotten.

CHRONIC MYELITIS. SCLEROSIS.

Sequel to acute. Result of sprains and spinal injuries. Symptoms:
paresis on exertion, lameness in one or more limbs, knuckling,
circumductive movement of feet, uncertain planting, dropping, worse if
blinded, phenomena progressive. Lesions: sclerosis of cord; absorption
of nerve cells and fibres, in gray horns, and columns, superior,
lateral and inferior, cord, altered in color, unduly firm, in points
softening. Stains deeply in carmine, lightly in osmic acid or
hæmatoxylin. Meninges thickened, nerve roots atrophied. Diagnosis:
previous acute myelitis; later muscular weakness, and paresis, under
exercise; from embolism. Treatment: hopeless if advanced: progress
delayed only. Good hygiene, tonics, open air, gentle exercise, pure
water, grooming, succulent pasture, nourishing food, alkalines, common
salt, phosphates.

Cases of this kind have not been satisfactorily diagnosed, and as a rule
domestic animals affected with partial paralysis are rarely allowed to
live in a condition in which they are offensive to themselves and
owners, a source of constant expense with little or no hope of recovery
nor profit. Again, in the case of the large mammals, the prolonged
recumbency and the low grade of nutrition in the semi-paralyzed parts,
usually entail unhealthy sores and septic poisoning which sooner or
later prove fatal. It is only, therefore, in the slighter cases, in
which a fair measure of control over the limbs remains, that these cases
are likely to survive. Trasbot suggests that many cases which pass for
lumbar sprains are really chronic myelitis and on careful examination
will show spinal sclerosis.

_Causes._ These are largely speculative, yet doubtless the same causes
which determine the acute form, will produce the chronic when acting
with less force and greater persistency. The lesions that are left after
an acute attack are calculated to keep up a measure of vascular and
trophic disorder which will be found associated with more or less
sclerosis.

_Symptoms._ In Weber’s case in the horse (Recueil de Med. Vet., 1884, p.
432) the advance was slow, so that for nearly a year the manifestations
were not diagnostic. At first there was weakness of the hind limbs when
worked to fatigue. Perfect rest led to improvement, and work, to
aggravation which became steadily worse and worse. For a length of time
the horse maintained good condition, glossy skin, elevated head, alert
expression, keen sight and hearing, and normal breathing and pulse.
Standing in the stall there was no abnormal position of the limbs, nor
evidence of lack of perfect control.

But when moved all this was changed. He showed first lameness in the
right fore limb and soon in all four members. The feet were swung and
planted uncertainly, the animal swayed and staggered, the limb would
knuckle over at the knee or fetlock, or bend at the hock, and be
recovered with difficulty. After going slowly for a few steps he moved
with greater freedom though still with difficulty, and the trouble was
greatly aggravated when the eyes were blindfolded. Then every step
threatened to precipitate him to the ground. The symptoms were
essentially those of locomotor ataxy.

The tactile sensibility was unimpaired, the loins had the normal
sensibility, urination and defecation were natural and the appetite
remained good. After ten months he showed loss of condition, dullness of
the special senses, stupor, and a special sensitiveness about the head,
and resented its handling.

_Lesions._ Thirteen months after the commencement of the attack this
horse was destroyed and the cord was found to be profoundly altered by
fibroid degeneration of the neuroglia and absorption of the nerve
elements (cells and fibres), the lesions affecting different portions of
the gray horns, and the columns—superior, lateral and inferior. The
affected portion of the cord usually shows in man a grayish, opaque or
translucent appearance, with in some cases a shrunken aspect and undue
firmness of texture, with at points, centres of softening. If hardened,
the sclerosed sections take the carmine stain deeply, but the osmic acid
or hæmatoxylin stain very slightly, contrary to what holds in health. In
recent cases there is only slight thickening of the neuroglia, but when
the disease is advanced the trabeculæ are thick, dense, and firm, and
the nerve fibres have largely disappeared. The coats of the blood
vessels adjacent to the sclerosis are thickened and their lumen is
narrowed. Thickening of the meninges is not uncommon, either confined to
those covering the diseased portion of the cord or extending completely
around it. Atrophy of the nerve roots is often appreciable by the naked
eye.

_Diagnosis._ This depends largely on the fact that the condition follows
an acute attack of myelitis, on the supervention of muscular weakness
and lack of muscular control, whenever the animal is exercised to
fatigue, the morbid symptoms subsiding promptly when he is allowed to
rest, the aggravation of these symptoms when the patient is blindfolded
and a gradual though slow advance of the symptoms with the lapse of
time. From arteritis and embolism it is to be distinguished by the
absence of the local symptoms of pain and tenderness, and by the absence
of pulsation in the same artery distal of the obstruction and of
improvement by the lapse of time or a run at grass.

_Treatment_: Unless in the very early stages even a partial recovery is
not to be looked for. By a run at grass or by gentle well regulated
exercise the impaired nerves and muscles may be educated to a better
control for a limited period but the progress of the disease is not
really arrested and the final issue is likely to be ruinous. Even in
man, where 90 per cent. of the cases are connected with syphilis, the
fibroid hyperplasia (sclerosis) is not remedied asgummata are, by
mercury and iodides. In the soliped, where no such specific disease can
be charged, the repair of the structural changes is no more hopeful. The
many different methods of treatment in man,—electricity, blisters,
firing, stretching of the spine, stretching, of the sciatic and crural
nerves,—though inducing transient improvement in many cases, produce no
real permanent benefit, and are to be remanded to the region of psychic
inferences which have little or no place in the therapeutics of the
lower animals. Strychnia, veratrin and other spinal stimulants are of
little permanent value. A general hygienic and corroborative treatment
may be used with the view of retarding the progress of the disease
rather than of curing it. Open air exercise, sunshine, succulent
pasturage, an ample supply of pure water, and active grooming are
valuable. Nourishing food is all important. Lecithin or the hypodermic
injection of spermin or other rich albuminous animal product is useful.
A course of bicarbonate of soda and carbonate of iron with or without
bitters may be tried. When the animal must be kept on dry winter food,
he should have free access to common salt and water. This favors at once
absorption, assimilation, and elimination, and by fostering nutrition
and the removal of waste matters, it contributes to keep the disease in
abeyance. Phosphoric acid and the various phosphates have been largely
used and largely rejected, their main value being in the tonic effect on
the spinal centres. Trasbot especially recommends the neutral gelatinoid
phosphate of lime as having proved especially valuable in his hands. He
gave from 1 grain upward to dogs twice a day.

ARTERITIS (THROMBOSIS, EMBOLISM) OF THE SPINAL CORD AND MEMBRANES.

Conditions of spinal circulation favorable to embolism and microbian
invasion. Slow currents. Blood stasis. Free anastomosis a
compensation. Symptoms. Treatment.

Facts are wanting with regard to these lesions in the domestic animals,
but anatomical, physiological and pathological consideration are
strongly suggestive of their occurrence. The vascular network of the
spinal cord favors a tardy circulation, and this in turn is favorable to
the arrest of solid bodies and the delay, proliferation and colonization
of microbes. The median spinal artery receives a supply of blood by two
trunks, right and left, entering by the intervertebral foramina at each
intervertebral articulation. It has not, therefore, one continuous,
equable, onward flow, but rather numerous independent currents
corresponding to the entering vessels, and with intervening eddies or
areas of comparative stagnation. The nervous material of the cord admits
no large arteries but only capillary trunks which anastomose freely in
its substance. This would seem to entail a sluggish flow, which would
favor microbian arrest and colonization, even if the small size of the
vessels serves to shut out clots of any material size. Finally the
abundant venous plexus, and especially the two lateral venous sinuses,
communicating freely with each other and, through each intervertebral
foramen, with the extra spinal veins determine a similar tardy flow that
should be favorable to morbid processes. If we pass back of these
vessels, we find the posterior aorta to be at once the largest and the
most direct channel for the entrance of emboli coming from the left
heart or lungs. This danger is counteracted in greater part by the fact
that the greater part of this blood passes into the large vessels which
supply the liver, spleen, kidneys, stomach, bowels, and hind limbs, and
while embolism is well known in these parts it has not been demonstrated
as yet in the spinal cord. The toxins produced in infectious diseases
and circulated in the blood can often lead to destruction of the
endothelium, and inflammation of the deeper structures. In this way any
circulating microbes find a ready infection atrium. Hektoen seems to
have demonstrated this in the case of tubercular meningitis. By pressure
of the neoplasm on the vessel or by fibroid thickening and contraction
of the walls of the vessel, the subsidiary cord is denied its full
supply, and degeneration of the nervous substance is invited. In the
human subject degeneration of the cord has been shown to follow the line
of such diseased arteries. Thrombosis follows in every case in which the
serous coat is involved, and embolism can easily occur from clots small
enough to enter the capillary vessels. Lamy’s experiment of blocking the
small arteries with inert powder, shows that this will give rise to foci
of hemorrhagic softening, which commence in the gray substance. The
blocking, however, must be multiple to produce any material effect, as
the free anastomosis of the spinal capillaries otherwise secures an
abundant blood supply to adjacent parts. In case of an infective
embolism the disease will advance even if the obstruction is single.

The general symptoms of these conditions would depend on the exact seat
of the lesion, and treatment would have to proceed on general
principles, the object being to check the inflammatory conditions, and
trust to the _vis medecatrix naturæ_ in connection with rest and good
hygienic conditions.

HEMORRHAGES INTO THE SPINAL MEMBRANES.
MENINGEAL SPINAL APOPLEXY. HÆMATORRACHIS. HEMORRHAGE INTO THE SPINAL
CORD. SPINAL APOPLEXY. HÆMATOMYELIA.

Definition. Causes: violent exertion, blows, falls, morbid blood,
fractures, caries, tumors, tubercle, aneurisms. Lesions: Clot between
or outside membranes in meningeal hæmorrhage, in gray matter and even
in white in myelon bleeding. Cord bulges. If survives, nervous matter
absorbed. Symptoms: Sudden stiffness or palsy of given areas; spasms
more common in meningeal extravasation. Rapid muscular wasting. No
fever at first. Treatment: cold to part; slings; atropia, ergot, lead
acetate. Later as for myelitis. Large clot may warrant surgical
interference.

In the first of these forms the bleeding takes place between the
arachnoid and the two contiguous membranes—pia and dura, or outside the
dura. In the second it takes place into the substance of the cord though
it may encroach on the pia mater. Both conditions have been attributed
to violent muscular efforts or contractions as in draught, racing,
fighting, leaping, tetanic convulsions, also to blows on the back, or
falls from a height. Morbid states of the blood in which there is a
hemorrhagic tendency (scurvy, purpura, hæmophilia, anthrax) may be
contributory causes. Spinal fractures, aneurisms, caries, tumors, and
tubercle may be additional causes.

_Lesions._ In meningeal bleeding the clot is found outside the dura, or
between the dura and arachnoid which may or may not be ruptured. A clot
on the pia mater may press seriously on the cord or may cause rupture of
the arachnoid. In hemorrhage of the cord, the effusion usually begins in
the gray matter, though it may extend far into the white. It may be
circumscribed to half an inch in diameter or affect almost the entire
length of the cord. The cord may be distinctly enlarged at the point of
effusion, and in exceptional cases the blood may have broken through to
the membranes. If the patient survives, absorption and degenerations of
the cord are inevitable.

_Symptoms._ In both forms there is a sudden attack, with stiffness or
paralysis of given muscles and without hyperthermia. Rigidity and spasms
of the muscles are more characteristic of meningeal hemorrhage, and
early paralysis of the spinal. An early hyperæsthesia is also most
significant of an effusion in the cord. Rapid muscular atrophy is also
characteristic of this. The two conditions resemble meningitis and
myelitis but come on much more suddenly and are unattended by fever.

_Treatment._ Such cases are not hopeful. Cold to the affected part of
the spine, keeping the patient in slings to solicit the good effect of
gravitation, and giving ergot or lead acetate internally are among the
first indications. Later, the treatment would be practically the same as
for meningitis or myelitis. In case of complete paralysis from the
sudden formation of a large clot, it has even been advised to cut down
on the seat of the injury and evacuate the blood, using antiseptic
precautions.

SPINA BIFIDA.

This is an elastic swelling consisting of the spinal meninges enclosing
a liquid, and in some cases the spinal cord as well, and protruding
between the unclosed laminæ of the vertebral rings, usually in the
region of the sacrum or loins. It is essentially an arrest of
development on the part of the vertebræ and enveloping muscles and skin,
and an extension of the cord and effusion of the meningeal and central
spinal liquids, in the absence of their bony and muscular support.
Hydrocephalus is no uncommon complication.

The _diagnosis_ may be based on the presence of an elastic, somewhat
transparent tumor, projecting from the vertebral spines, at birth. If it
contains a segment of the cord it is usually flattened, depressed on the
summit and often associated with paralysis.

As occurring in the lower animals this need not be treated. In man,
careful antisepsis and evacuation followed by injection of a solution of
iodine 10 grs., iodide of potassium 30 grs., and glycerine 1 oz., have,
in favorable cases, secured obliteration of the sac, but even then the
recovery has rarely been complete and permanent. Paralysis and death
have usually supervened.

SPINAL CARIES. TUBERCULAR OR OTHER INFECTIVE DISEASE OF THE VERTEBRÆ.

Spinal caries in old horses, sprains, fractures, infections; caries
often confined to articulating processes: anatomical form:
Axoido-atloid caries from poll evil, concussions, fights, rachitis.
Tubercle of bone and intervertebral cartilage in cattle. Symptoms:
distortion, stiffness, rigidity; stands day and night, sensory and
motor paralysis: localization of lesion; dyspnœa; spastic palsy back
of lesion; effect on tail, sphincters. Diagnosis: progressive
tenderness and stiffness of spine, distortion, localized exaltation or
depression of nervous function, osteoporosis, rachitis, caries,
tubercle, melanoma, abscess, infectious disease. Treatment: Sling in
narrow stall, good food, pure air, sunshine, tonics, phosphates.

As seen in the human subject spinal caries is usually tubercular and is
known as “_Pott’s disease_.” As seen in old horses it appears to be
rather a result of other infections, especially purulent, and may have
started in connection with traumatic or mechanical injuries to the bones
and ligaments. In such cases I have seen it repeatedly in hollow backed
horses in which the line of the spine descended abruptly and extremely
from the withers and rose again to the sacrum. The distortion was so
great that the back appeared as if it could barely sustain the weight of
the animal and yet the patients were kept at work and proved useful for
light driving. Post mortem examination showed extensive caries and
suppuration of the vertebral bodies, confined, however, to one or two
segments as if due to a mechanical lesion. In the region of the loins it
is much more likely to affect the articulations of the vertebral rings,
because of the manner in which these are wedged into each other when the
spine is pressed downward. In the neck where the normal movement is so
much freer such injuries are much less common. Caries affecting the
articular surfaces of the axoido—atloid joint is by no means uncommon.
It may follow poll evil, or injuries sustained when a horse runs against
a wall, or in the fights of bulls or rams. Disease of the vertebræ may
be of the nature of rachitis occurring in this case in early life.

In cattle the disease is liable to be tubercular in which case, not only
is the bone invaded but the morbid process extends to the intervertebral
cartilage and projecting, presses on the spinal meninges and cord. It
may even encircle the entire spinal cavity and strangle the cord. If the
pus should extend downward it may form abscess under the spine, and
rupture into an internal cavity or externally.

_Symptoms._ Injuries and disease of the vertebræ may last for a length
of time without implicating the spinal cord or nerves. They may then
cause only distortion, with stiffness or rigidity of the spinal column.
When, however, the displacement of the injured, carious or tubercular
bones, the distension of the abscess or the increase of the hyperplasia
leads to pressure on the nerve roots, the meninges or cord, nervous
symptoms are likely to be developed. Compression of the nerve
roots—sensory or motor—may cause sensory or motor paralysis or both,
limited to particular areas the outline of which will point to the
precise seat of the lesion. If in the recti of the head and other
muscles of the neck, it points to the anterior cervical vertebræ. If in
the fore limbs, it points to the posterior bones of the neck. The
implication of the diaphragm would incriminate the fourth and fifth
cervical vertebræ. If in the crural muscles or those of the quarter and
thigh, the lumbar vertebræ must be looked to. The implication of the
nerves of the back, while impairing the functions of the intercostal and
abdominal muscles, produce less marked symptoms than when the limbs are
involved.

When the disease extends deeper so as to implicate the meninges and
especially the cord, there is evidence of impairment or interruption of
conduction in the cord in addition to the simple involving of the nerves
that emerge at that point. Thus serious disease or pressure on the
cervical part of the cord in front of the fourth vertebra will make
respiration difficult or impossible and speedy asphyxia may ensue. The
paralysis of all parts behind the lesion is overlooked, in view of the
fatal nature of the paralysis of the intercostals and diaphragm. If the
interruption of conduction is incomplete there may be spastic paralysis
and hyperæsthesia in the limbs and trunk back of the lesion.

If the dorsal cord is involved so as to render conduction imperfect
there will be at first imperfect control of parts posterior to the
lesion, and when still further implicated, flaccid or spastic paralysis,
especially of the hind limbs and tail. When it implicates the lumbar
region in addition to the paralysis named for the dorsal, there will be
incontinence of urine and even relaxation of the anal sphincter. In a
case of acute tuberculosis in a cow, supervening on an ancient
tuberculous lesion, as seen by the author, there were imperfect control
of the hind limbs and uncertain gait, with tenderness of the dorsal
region as if the animal had sprain of the back.

_Diagnosis_ of these cases of vertebral disease may not always be
possible in the early stages, yet the symptoms of progressive tenderness
and stiffness in the region of the spine, the distortion in some
instances of the spinal column, the subsequent appearance of localized
motor and sensory symptoms, and later still the spasms or spastic
paralysis in all parts behind the seat of the lesion, will be strongly
suggestive of such a disease. When indications exist of osteoporosis,
rachitis, or tuberculosis, of caries, abscess, or infectious lesions of
the cervical or dorsal spinal region, the inference is still stronger.
Then if reaction occurs under the tuberculin test, or if the urine
contains an excess of phosphates in the herbivora, the case may be
diagnosed with certainty.

_Treatment._ This will rarely be admissible on account of the expense
and uncertainty of result. Some meat animals may be killed for food. If
otherwise, keep in narrow stall where the animal cannot turn even the
head, feed from moderate level to avoid movement of the spine by the
upward and downward movements of the head. Gentle brushing is useful as
a means of cleanliness, and of toning up the muscular system. Nourishing
food of an easily digestible kind is essential, and pure air and
sunshine are important auxiliaries. A course of cod liver oil with
bitters may be given to improve the general health, calcium sulphide may
be tried in case of suppurative caries, and calcium phosphate will
usually be desirable to improve the nutrition and consistency of the
osseus system. In case of a valued patient which it is desirable to
preserve for reasons of sentiment or affection, or for breeding
purposes, one might be warranted in continuing a long and expensive
course of treatment, but in the regular run of cases considerations of
humanity and economy would counsel the prompt destruction of the animal.

SLOW COMPRESSION OF SPINAL CORD. PARALYSIS.

Causes: Caries, vertebral diseases and lesions, neoplasms,
actinomycosis, tubercle, abscess, organizing exudates, parasites.
Melanoma, cholesteatoma, sarcoma, papilloma, lipoma, glioma,
chrondroma. Symptoms: advance insensibly, or by sudden leap with
exudate, spasm, paresis, transverse, senses clear, muscular atrophy,
advance from behind forward. Cervical, dorsal, lumbar lesions.
Bladder, sphincters, tail. Symptoms increased by movement. Treatment:
according to lesion. Tumors, hopeless. Blood clots, Actinomycosis.
Analgesics. Electricity.

_Causes._ Slowly progressive compression of the cord has been already
noted as resulting from caries and other diseases of the vertebræ. It
remains to notice such as result from the growth of tumors and other
neoplasms in the spinal canal. In the horse these are commonly melanoma
(in white horses), sarcoma, encephaloid, papilloma, cholesteatoma, and
osteoma; in cattle, beside tubercle and actinomycosis, have been found
sarcoma, lipoma, osteoma and glioma; and in dogs sarcoma and
chondro-sarcoma. Chronic abscesses may be met with in all animals
determining the same class of symptoms by slow pressure. In the same
manner exudates in process of organization contract, and are liable to
compress the myelon. Cadeac draws attention to a calcic degeneration of
exudates in the dura mater of the dog (ossifying pachymeningitis), and
of ossification of the intervertebræ cartilages with vegetations on
their surfaces. Parasites also exercise a growing pressure, especially
echinococcus, in cattle cysticercus mediocanellata, in sheep and dogs
cœnurus, and in pigs and dogs cysticercus cellulosa.

=Melanoma.= In gray and white horses, with disseminated melanosis, the
spinal canal is often involved, the pigmentary sarcoma appearing in
small formations and sometimes large enough to determine injurious
pressure. In the early stages these may cause stiffness and lameness
referable to particular muscles or groups, varying in situation, even as
to the limbs affected, at successive dates, and finally merging into
paraplegia.

=Cholesteatoma= is less common than in the encephalon, yet one is
reported by Dexler as attached to the pia mater and possessed of great
firmness, crisply crackling under the knife. It doubtless secures
accretions under meningeal exudates like those of the choroid plexus.

=Sarcoma= and =encephaloid= are usually found in connection with the
dura mater, and of small size, but numerous. They often surround the
roots of the spinal nerves, and here as on the cord exert sufficient
pressure to impair nervous function.

=Papilloma= has been found connected with the pia mater and of marked
vascularity. The author has found one in the ewe in a case of the
neurasthenia of advanced gestation.

=Lipoma= is also rare. Osseous growths are common, being favored by
sprains and injuries. All show a marked predilection for the lumbar and
last dorsal vertebræ. This may be partly explained by the liability to
injury and to disease invasion through the interlocking of the joint
surfaces of the rings. _Osteophytes_ growing from the intervertebral
cartilage are common in the dorsal region as well.

=Glioma= has been found in cattle, occupying the substance of the cord
itself and growing to the size of a hen’s egg or even of the closed
fist. The cord is gradually atrophied and paraplegia is inevitable.

=Chrondro-sarcoma= has been found growing from the intervertebral fibro
cartilage of dogs.

The _Symptoms_ may be deferred for a length of time on account of the
accommodation of the myelon to the slowly increasing pressure. When they
do become manifest, it is usually at first by insensible gradations so
that for a time their existence is questionable. Yet a case will
sometimes reach a sudden climax, by reason of a blood extravasation or
inflammatory exudate, and the signs of sudden pressure or acute myelitis
or meningitis supervene. In the absence of sudden access of trouble, the
symptoms are those of a slow increase of _motor troubles_ (local
paresis, paralysis, paraplegia), or _sensory_ (hyperæsthesia,
anæsthesia). Spasms may occur early or even later in the disease. From
disorders due to cerebral lesions the morbid phenomena are distinguished
by being paraplegic rather than hemiplegic; sensori-motor rather than
sensory or motor; local rather than general; with intelligence and
special senses clear, rather than dull or abolished; associated with
marked muscular atrophy in the affected parts; advancing from behind
forward rather than uniform throughout the body.

The area of nervous disorder points more or less clearly to the seat of
the lesion. Early implication of the fore limbs, and then later of the
hind, suggests lesion of the cervical region. Dyspnœa tumultuous heart
action, or vertigo may coincide. Tardy movements of the hind limbs,
imperfect balancing, dragging, swaying, knuckling, involuntary flexions
of stifle or hock, flexor contractions, standing on toe, cramps,
paraplegia, indicate lesion in the dorsal or lumbar region. There may be
palsy of the rectum, anus, bladder, sphincter vesicæ, penis, and vulva.
Paralysis or other nervous disorder of the tail and sphincters ani and
vesicæ, without implication of the hind limbs or quarters, may bespeak
lesion in the terminal end of the spinal cord.

With paralysis of the bladder the penis may be pendent out of the
sheath, or being retained within it, the urine may dribble constantly
into and from that cavity, and the vulva may be soft and flaccid. When
the anus is involved, the adjacent part of the rectum usually
participates becoming overloaded, the sphincter is soft and lax and
allows a constant oozing, and the exposure of the mucosa. The paralytic
tail hangs between the thighs, limp and flaccid, and becomes saturated
with manure and in females with urine.

Even in the earlier stages the symptoms are usually greatly aggravated
by compulsory movements like turning in a circle, walking up hill, or
(in dogs) up a stair, the arched back, the pendent head, and hesitating
planting of the foot suggests walking on pins. For a more exact
localization of the lesion the reader may consult the table indicating
the functions of the different parts of the spinal cord. The early
fatigue under exercise grows as in other progressive spinal lesions.

_Treatment._ In most cases this is hopeless. Tumors, bony and calcic
growths, tubercles, degenerations and absorption of nervous tissue are
practically beyond remedy. A blood extravasation may be largely
absorbed, leaving only the permanent changes in the nervous tissue. In
this time is the main element. Actinomycosis may sometimes be
successfully met by a course of potassium iodide, when, if the nervous
lesions are slight, a fair recovery may be secured. In the majority of
cases, however, the practitioner is limited to measures for palliation
of suffering by atropia, chloral, phenacetin, etc., or by nerve
stimulants like nux in small doses, or by weak currents of electricity.
In meat producing animals, it is often the best course to fatten
rapidly, or to turn over at once to the butcher.

DILATATION OF THE CENTRAL CANAL OF THE SPINAL CORD. SYRINGOMYELIA.

This means literally a cavity in the spinal cord but is applied to
cavities formed by dilatation of the central spinal canal, or by an
excavation in the nervous tissue immediately adjacent and usually
communicating with a dilated segment of the canal. In man it is usually
the result of an active proliferation of the epithelial cells of the
canal, blocking the same, or extending into the adjacent nervous tissue
in the form of a glioma. In different cases in dogs it occurred as the
result of pressure. It has been seen in dogs, cats and Guinea pigs, as a
casual lesion and as the result of experiment.

In a case reported by Lienaux it extended for practically the whole
length of the cord, varying in form and size at different points. In the
lumbar portion it was only slightly dilated, in the dorsal it was very
irregular with prolongations into the gray matter, toward the cervical
enlargement, its transverse section resembled an inverted V, and in the
anterior cervical part it was unevenly rounded. Notable changes were
cell proliferation and subsequent degeneration with the formation of
cavities, thickening of the neuroglia, and compression and even
obliteration of the vessels with circumscribed areas of necrosis,
terminating also in cavity formation.

_Symptoms._ These vary with the nervous structures invaded, atrophied or
destroyed. Invasion of the anterior horns of gray matter, causes
trembling and muscular wasting. The implication of the superior horns
determines more or less marked anæsthesia. Hyperæsthesia, spasms,
paresis and paraplegia are also seen but no symptom nor group of
symptoms is diagnostic of the exact lesion.

_Treatment_ is manifestly hopeless.

NEURASTHENIA IN PREGNANT EWES.

Causes: inactivity, lowered muscular and nervous tone, twin pregnancy,
approach of parturition, dry (clover hay) ration, concurrent diseases.
Symptoms: moping, anorexia, depression, stupor, blindness, paresis,
lethargy. Prevention: open air life, exercise, high muscular
condition, avoidance of debilitating and relaxing conditions.
Treatment: hygienic, nerve tonics, attend to concurrent diseases.

Neurasthenia has been defined as an incompetency of the nervous system,
leading to early fatigue, and inability to recuperate from the prostrate
condition. Pending a better knowledge of the affection, I have given
this name to an asthenic affection seen in pregnant ewes when nearing
the completion of the period of gestation.

_Causes._ In a large number of cases I have found several conditions so
constant, not to say invariable, that they seem to deserve special
attention in the list of causes:

1st. =Enforced inactivity.= In every instance that has come under my
notice the ewes have been confined for several months to a barn or at
most a confined yard so that exercise became impossible. The muscular
system was flabby and soft, although as a rule there was abundance of
fat, and the number of red globules did not vary much from the normal.
In an animal that is naturally so active, and so accustomed to outdoor
life the reduction of tone and vigor is to be expected. The same evil
shows in other directions, thus after a snowy winter and close
confinement the crop of lambs will sometimes perish of goitre without
exception, while in subsequent years, with enforced exercise of the
ewes, practically all escape.

2d. =Twin lambs= have been found in the womb of almost every case
examined. The extra drain upon the system, and the depressing action of
the load on an atonic ewe together with the symptomatic irritation are
to be noted.

3d. The near approach of the =completion of gestation=, the cumulative
effect of a long pregnancy, and perhaps the absorption of metabolic
products from the fœtal membranes in course of preparation for
detachment, and of leucomaines from the physiologically active or
developing mammæ, doubtless have a prostrating influence on the
susceptible nervous system.

4th. All had been fed on =clover hay= either as an exclusive diet or as
part of their ration. This is sufficiently nutritive, as testified by
the fat condition of the patients, but it may be that it was too
nitrogenous for such an inactive life. Again the clover hay usually
abounds in cryptogams and bacteria and their products, which may have
contributed somewhat to the asthenia.

5th. =Concurrent diseases=, in individual cases or flocks, manifestly
contributed to the general loss of nervous power. In some the bowels
were studded with the nodules of the œsophagostoma, in others œstrus
larvæ had extensively invaded the nasal sinuses, one had congestion of
the mucosa of the small intestines, some had congestion and fatty
degeneration of the liver, others had fatty kidneys, and one had a
papilloma pressing on the spinal cord. Manifestly diseases and
degenerations of various kinds would still further undermine nervous
energy and add to the atony.

Cold and heat did not seem to dominate, as most were kept in warm barns,
and wore heavy winter fleeces, while one clipped early in December, and
kept in an atmosphere of 40° to 55°, was attacked in the second week of
January.

As this experience was had in a goitre district it may become a question
whether the poison of this disease was a causative factor. Goitre was
not a prominent feature in either ewes or lambs.

_Symptoms._ Variable. The most prominent are, leaving the flock, moping
alone, grinding the teeth, drooping and trembling of head and ears,
temperature normal or subnormal (100.5°), respiration 24, pulse 80,
feeds and ruminates sparingly, bowels normal, buccal mucosa pale,
conjunctiva hyperæmic, in some cases stupor and partial blindness, the
animal walking against racks or fences, walk is slow and unsteady, the
muscles feel soft and flabby, the abdomen may be full, but its walls are
quite flaccid so that the lambs can be easily felt. As the disease
advances all symptoms are aggravated, food is no longer taken,
rumination ceases, the ewe remains recumbent, cannot be made to rise,
and when lifted and carried makes no struggle. After 24 hours of this
helpless condition death supervenes. In some instances labor pains have
come on and the ewe has perished in a vain effort at delivery. Illness
lasted about a week.

Prominent _lesions_ have been noted under causes. It need only be added
that no notable difference from the normal was found in making a count
of the red globules, and the size of the individual globule was normal
or only perceptibly smaller as is to be expected in a dense plasma. In
different cases there was found congestion of the abomasum, small
intestine, liver and brain.

_Prevention._ The most important measure is to maintain a strong,
well-developed muscular system, and a vigorous nervous tone by a
sufficiency of out door exercise during the winter months. Half a mile
or a mile at least should be given daily to the breeding ewes, no matter
what the attendant difficulties. If clover hay is musty it should be
replaced in whole or in part by another kind. Parasites and other
diseases which tend to lower the general tone should be appropriately
treated.

_Treatment._ When once established, the disease has not been
successfully treated. Nerve tonics are indicated.

NEURITIS. PERINEURITIS.

Definition. Causes: traumas, poke, stanchions, collar, yoke,
interfering, neurectomy, fractures, tumors, callus, rheumatism, gout,
violent overdistension. Lesions: nerve sheath red, swollen, exudate,
leucocytes in excess, fibroid thickening, nerve atrophy, degeneration,
axis granular, myelin in oily globules, peripheral extension. Muscular
degeneration and atrophy. Symptoms: tenderness, swelling, muscular
atony, wasting, spasms, twitching, decreased excitability, paralysis,
in section swelling on proximal end. Prognosis: disability for weeks,
months or year; response to electric current, operability of tumors,
curability of rheumatism or gout, hopeful conditions; long standing
degeneration, etc., unpromising. Treatment: rest, soothe, anodynes,
splint with soft pad, essential oils, lead and opium lotion, ice,
snow; derivatives; laxatives; diuretics, anti-rheumatics,
Faradisation.

_Definition._ Inflammation of a nerve leading to paralysis of the parts
to which it is distributed.

_Causes._ Traumatism is the most common factor. Among the common
examples are injury of the seventh nerve above the angle of the lower
jaw, by a poke worn in pasture by the horse, or by stanchions in the
cow. Hogs may suffer from blows of the triangular neck gear worn to
prevent them from breaking through fences. Blows by the yoke, incised
and contused wounds implicating the nerve, such as neurectomy, and the
blows received in interfering, and compression by tumors or bony
growths, are familiar examples. Fractures with displacement, notably
those of the sacrum and proximal end of the coccyx with caudal
paralysis, are not uncommon. In fractures of the limbs the pressure upon
or wounding of a nerve. Again, the callus on the seat of fracture may
induce neuritis by pressure, as may also the projection of the end of a
bone in luxation. Rheumatism affecting the nerve sheaths and, in birds
and swine, gout, are additional factors. Violent overdistension, and
even chronic muscular spasm, are quoted as causes.

_Lesions._ The early changes are mainly in the connective tissue sheath,
which becomes hyperæmic, red and swollen, with a gelatinoid exudate and
a great multiplication of leucocytes. Later, the interfibrillar
connective tissue is involved and the nervous substance proper undergoes
hyperæmia and degeneration. The axis cylinder undergoes granular
degeneration and the myelin breaks up into oil-like globules. The
lesions are at first limited in extent, though there may be more than
one focus, and the resulting degeneration of the nervous filaments
advances toward the periphery in accordance with Waller’s law by which
disease changes proceed rapidly in parts cut off from their trophic
cells.

The muscles supplied by the inflamed nerves also rapidly degenerate. The
fibres shrink in size, and lose their striated appearance, becoming
distinctly granular, and pale. Round cells are formed in excess in the
sarcolemma and muscular fibre, and if the morbid condition persists
there is fibroid degeneration, cirrhosis and contraction.

_Symptoms._ In the absence of the subjective element of pain, which is
the most constant symptom in man, we must rely mainly on the exquisite
tenderness on pressure along the line of the nerve, but localized at
some particular point, on the swelling at such tender point and on the
loss of muscular power or even of sensation in the tissues corresponding
to its peripheral distribution. The muscles may be hypersensitive and
are usually flaccid if not from actual paralysis, still from the pain
which attends on their contraction. In some cases they are the seat of
clonic spasms or twitching. Under a current of electricity they show a
decreased irritability which bears a direct relation to the grade of
degeneration which has occurred in the nerve fibres. In cases of
deep-seated neuritis paralysis may be the only appreciable symptom. In
traumatic injuries like bruises of the seventh nerve or fracture of the
sacrum the local swelling and tenderness are marked initial symptoms,
upon which supervene the paralysis and atrophy of the muscles cut off
from full innervation. In neurectomy the tender swelling in the stump
which is still in connection with the nerve centre may amount to a
distinct neuroma, while the peripheral and detached portion of the nerve
steadily loses its irritability as shown by electric stimulus.

_Prognosis._ This will depend on the nature of the lesion. A single
transverse section of a nerve, without loss of substance may be repaired
in a few months, while with loss or degeneration of a considerable part
of its substance it may maintain a paralysis for years or even
permanently. Lesions due to slight bruises may recover in a few weeks,
while the more severe ones will persist for months or years. The
response to electric stimulus distal of the lesion, is a guarantee of
the absence of degeneration and a feature hopeful of recovery. Pressure
by bony displacement or neoplasia must be done away with as the first
condition of improvement in such cases. Rheumatic and gouty cases will
persist until these constitutional infirmities are corrected.

If the neuritis and paralysis have lasted for any length of time, the
degeneration of the muscles will keep up a degree of muscular weakness
(and if in the limbs lameness) after the repair of the nerve has been
completed.

_Treatment._ Rest is the first consideration accompanied by soothing and
anodyne application to the inflamed nerve. When neuritis exists in a
limb a softly padded splint may be useful at first. The skin over the
inflamed nerve may be rubbed by one or a combination of the anodyne
essential oils, (oil of cajeput, oil of peppermint, oil of lavender). If
the pain and tenderness are extreme, a bag of ice or snow may give
relief and should be kept applied for a length of time. Or hot
fomentations with a lotion of lead and opium may be preferred especially
in rheumatic cases. If blisters seem to be called for, aqua ammonia and
oil of turpentine may be added to the essential oils, or muriatic acid
may be applied with a glass rod in points along the line of nerve. A
laxative of Epsom or Glauber salts will often prove of great value at
the outset and may be followed by diuretic doses of potassium iodide,
potassium nitrate or acetate, and in rheumatic cases sodium salicylate.
In these last forms, as also in gout, the carbonates and acetates of the
alkalies, colchicum, and salicylates are especially to be persisted
with. In these, too, rubefacients and blisters are often of essential
value and may be repeated again and again.

Faradism is of little account during the active stage of neuritis
excepting as a test of the progress and extent of the degeneration, but
when inflammation has subsided nothing contributes more to the
restoration of the tone and healthy nutrition of both nerve and muscle.
The current is to be sent along the line of the paretic nerve and
muscles for ten or fifteen minutes at a time and not less than once a
day.

NEURALGIA.

Intermittent or remittent pains, in line of nerve without
inflammation, or other structural lesion. Diagnosis: lameness,
stiffness of particular muscles having a common nerve. Unnatural
position habitual. Pain of inflammation and of neuralgia. No
functional change. Rheumatism. Tumors. Causes: lead, rheumatism, gout,
auto-poisons, cold, anæmia, reflex. Facial neuralgia,
occipito-cervical, dorso-intercostal, lumbo-abdominal, sciatic.
Treatment: elimination, of lead, etc.; intestinal antiseptics, tonics,
hot water, anodynes, arsenic.

This is characterized by pain paroxysmal, intermittent or remittent
situated in the course of given nerves. It must be a pure neurosis and
unaccompanied by any specific structural lesion like inflammation,
degeneration, atrophy, hypertrophy, tumor or the like. It is therefore
manifested subjectively and cannot be easily identified in the lower
animals. Nevertheless, Lafosse, Zundel, Genée, and others have recorded
cases, their conclusion being deduced from symptoms which were held to
indicate nervous suffering in the absence of any structural lesion
whatever. _A priori_ one can with difficulty escape the conviction that
neuralgia must exist in the lower animals as in man, and the only
drawback to its recognition is the difficulty of diagnosis.

The first step in such diagnosis must usually be the presence of
lameness, stiffness or indisposition to free movement of some particular
muscle or group of muscles deriving their innervation from a particular
nerve. Or there may be a particular position habitually assumed such as
semi-closed eyelids, drawn back ears, laterally inclined neck which
strongly suggests nervous suffering. Next, there must be the exclusion
of any appreciable structural cause and especially of inflammation. The
three prominent features of the pain of inflammation is that it is
aggravated by pressure, it is heightened by movement, and it is
accompanied by some decided alteration of the function of the part. If
there are at the same time exudation and swelling, inflammation is all
the more certainly indicated. In a neuralgic pain on the contrary
pressure does not increase the pain: it may even alleviate it: movement
of the part may be rather satisfactory to the patient than painful; and
the disturbance of function, contractile, secretory, trophic, is not
perceptible. There is no local exudation nor swelling to account for the
nervous disorder.

The liability to confound the affection with a neuritis more centrally
situated, but the pain of which is referred to the periphery of the
nerve, is to be obviated by a tracing of the nerve along its course to
the nerve centre so as to identify any centre of tenderness, and also by
the implication of all the peripheral branches coming off ectal of that
point.

Again, rheumatism may be easily confounded with neuralgia, but here the
affected nerve and muscle and even the skin over it is liable to be very
tender to the touch or pinch, and if at all acute some hyperthermia is
present. Like rheumatism, neuralgia shows a tendency to shift from place
to place.

Pains due to pressure on the nerves by tumors, aneurisms, and other
swellings, are constant, whereas neuralgic pains are marked by
remissions and aggravations and even by intervals of complete relief.

_Causes._ The toxic neuralgias are illustrated by chronic lead
poisoning, in which, in man, there are wandering pains like those of
rheumatism, and in the lower animals muscular stiffness and contractions
which suggest a similar condition. In man, too, gout is a common factor,
and in pigs and birds in which this condition exists, stiffness and
evidence of suffering may well be at times attributed to a similar
cause. How many other forms of chronic metallic poisoning and poisoning
by morbid autochthonous products of indigestion are attended by
disorders of innervation and nutrition, it is as yet impossible to say.
The direct action of cold, an anæmic condition of the nerves, and reflex
action from distant sources of irritation are among the other invoked
causes. Inflammation in the _nervi nervorum_ is also invoked as a
factor, but in this case the symptoms would not accord with the rule
given above, since the nerve trunks would be very tender to touch or
pressure, and the suffering would be unshifting and shown permanently in
the one seat.

=Facial Neuralgia.= Lafosse and Zundel describe as cases of this kind
those in which periodically the horse’s eyes are fixed and shining, the
ears drawn back and depressed as in vice, the head at intervals bent on
the neck, with plaintive neighing, rubbing the head on the stall and
pawing. Those cases of twitching of the head or rapid jerking of the
ears in horses, when they have been driven for some distance, and which
are relieved by wearing a close net over the nostril or by section of
the trifacial nerve at the infra-orbital foramen, manifestly partake of
this character.

=Cervico-Occipital Neuralgia.= Lafosse speaks of this as often mistaken
for torticolis, the head being turned to the affected side during the
paroxysms. In man this is often a result of cold draughts on the back of
the head, and associated with tender points on the course of the nerve,
between the mastoid and the median line.

=Dorso-intercostal neuralgia= causes pain in deep inspiration, and
=lumbo-abdominal neuralgia= develops tenderness in the loins, in one
testicle, or in one lip of the vulva according to Lafosse. Diagnosis
between such cases and neuritis, spinal disease, and other obscure
nervous affections must be very problematical.

=Sciatic Neuralgia.= This is described by Zundel as causing jerking and
lameness in the affected limb, sometimes aggravated and sometimes
improved by work and associated with muscular weakness or paresis.
Sciatica in man is, however, rarely a simple neuralgia, but partakes
rather of the nature of a neuritis, and there is no good reason for
supposing that the disease of this nerve in the lower animals is other
than an inflammatory condition.

Leclainche after consideration of the testimony adduced, is of the
opinion that we still lack absolute evidence of uncomplicated neuralgia
in the domestic animals.

_Treatment._ For =toxic= cases elimination of the poison is the first
consideration. For _lead_ carefully graduated doses of iodide of
potassium to carry off the offending agent without increasing its
poisonous action must be continued as long as the metal is passed by the
urine. It may be followed by a course of strychnia, by electricity,
massage and blisters. Gouty subjects may be treated with salicylate of
soda, alkalies, or colchicum. The victims of Bright’s disease must be
treated for the kidney affection.

Where there has been =trouble of the digestive organs=, intestinal
antiseptics (salol, sodium salicylate, bismuth-salicylate,
beta-naphthol) and small doses of arsenious acid will sometimes benefit.

In =anæmic conditions= a course of tonics (cod liver oil, iron, quinine,
nux vomica) are indicated, and, to improve the local blood supply,
nitro-glycerine. A rich stimulating ration, currying, an open air life,
and sunshine (in summer a run at grass) are called for.

In man with a suspicion of =traumatic origin=, W. H. Thomson strongly
advocates a persevering use of the hot water douche to the parts first
affected, the hypodermic use of morphia and atropia, and in case of
local anæmia nitro-glycerine every three hours. Where there is a
suspicion of inflammation he successfully employs absolute rest, with
opium narcotism so as to abolish the pain, for twenty days if necessary.
Aconite, antipyrin, acetanilid, phenacetin, exaglin, and gelsemium have
their advocates, and may benefit in individual cases. A course of
arsenic is often successful, and phosphorus and ergot have each proved
of value.

ATROPHY OF NERVES.

From arrest of function, from lesions, pressure, distal, but at times
central of lesion. Symptoms: Loss of function advancing to paralysis.
Muscle atrophy. Prognosis: in absence of incurable cause, is hopeful.
Union of divided ends, restoration of function. Treatment: time,
ligature of divided ends.

This is usually the result of arrest of function. It may be due to
transverse section of the nerve, as in surgical neurectomy when the
separated peripheral end of the nerve gradually wastes. It may come from
contused wounds implicating the nerve and causing destruction of its
substance. It may be from tumors or other neoplasms pressing on the
trunk of the nerve and preventing the passage of nerve currents. Or,
inflammatory effusion may press on the nerve, as happens often to the
crural in hæmoglobinuria. Or the pressure may come from enlarged
mediastinal glands, or even from the distended posterior aorta under
habitual violent exertion so as to permanently incapacitate and atrophy
the left recurrent laryngeal nerve as in chronic laryngeal paralysis
(roaring). Similar wasting occurs in other nerves under corresponding
conditions. Atrophy may, however, extend centrally from the peripheral
end of a nerve when it can no longer remain functionally active. We find
an example of this in the atrophy of the optic nerve up to the
commissure when the eyeball has been excised. A similar condition is
often seen in horses in which the integrity of the eye has been
completely destroyed in connection with recurring ophthalmia.

The _symptoms_ attendant on atrophy of a nerve are those of impaired
function gradually advancing to complete paralysis of motion or
sensation. In cases of a complete breach of continuity as in section or
severe traumatism the entire loss of function necessarily precedes the
atrophy. Again, when it comes from destructive changes in the coats and
media of the eye, and of the ganglionic cells of the retina, the atrophy
of the nerve trunk proceeds simultaneously with the lesions of the organ
of vision.

The _diagnosis_ will in many cases be easy as deduced from the traumatic
or surgical lesion. In other cases it may be made with certainty from
the complete muscular paralysis, wasting and degeneration of the muscles
supplied by the nerve, and by the history of the case (hæmoglobinuria in
atrophy of the triceps extensor cruris, roaring in atrophy of the
laryngeal muscles and recurrent nerve). In other cases, as in the eye,
we have the atrophy of the eyeball, the distortion or complete paralysis
of the iris, the opacity of the lens, or the exudation into the
vitreous, choroid and retina when these can still be observed.

_Prognosis_ will depend on the cause. With a nerve severed with a knife
or crushed in a part of its course and atrophied, without destructive
changes in the organs in which it is distributed, repair is possible and
to be expected in time.

_Treatment_ is expectant, yet inflammation must be subdued, tumors
removed, divided ends ligatured, etc.

DISEASES OF THE URINARY ORGANS.

Relative prevalence in man and animals. Causes of difference. Kidneys
as eliminating organs for nitrogenous material, toxins, bacteria,
mineral, vegetable and animal poisons, diuretic drinking water,
condition powders, cantharides, urea, etc. Suppression of urine,
precipitation of urine. Filtration through kidney. Secretion. Urinary
solids. Nervous control of secretion. Excess.

Diseases of the urinary organs are less prevalent in the lower animals
than in man, owing largely no doubt to the greater simplicity of their
habits of life and to the comparative shortness of the lives of those
that are kept for meat producing. It is a mistake, however, to suppose
that they are so infrequent as would appear, since the absence of
subjective symptoms in the animal allows a number of the milder forms of
renal disease to be passed over without recognition.

In man the excessive consumption of animal food, the lack of exercise,
the abuse of alcohol, the prevalence of venereal diseases, conduce
largely to renal troubles, while animals in general escape. Yet animals
suffer much more extensively than is generally supposed. The kidneys
are, as in man, the eliminating organs for superfluous and waste
nitrogenous matter, and in overfed animals may be overcharged with this
work. They are the general emunctories for the soluble poisonous
products of bacteria and plants, which may stimulate the urinary
secretion, and from these irritation may result. It is through the
kidneys that the bacteria themselves largely leave the animal body, and
trouble is liable to come during their passage. Further, exposure to
cold tends to =increase the urinary secretion=, over-stimulating the
kidneys, and the same may come from diuretic drinking waters and
condition powders, also from cantharides and other diuretic agents
applied to the skin. Urea and many toxins are diuretic, hence the
occurrence of polyuria at and after the crisis of fevers.

On the other hand =suppression of the urinary secretion= may occur in
connection with profuse perspirations in hot weather, with prolonged
diarrhœa, or with privation of water, and in such cases the liquid
becomes concentrated and irritating and there is a disposition to
precipitate its solids under slight disturbing causes. As conducive to
such precipitation may be named foreign solid bodies, bacterial ferments
and probably the goitre poison since gravel and calculus are common in
goitrous regions.

There are two forms of elimination through the kidneys. 1, _filtration_;
2, _secretion_.

1. _Filtration_ is referred to the glomeruli, and is determined by the
relative blood pressure. Increase of pressure causes increase of watery
transudation. Digitalis increases heart action and arterial pressure,
and accidently urination. Excessive consumption of water and watery
liquids increases intravascular tension, and the amount of urine.

2. _Secretion_ is referred to the columnar epithelium of the convoluted
tubes. It is by the elective affinity or selective power of this
epithelium that the solids of the urine are abstracted from the blood
and passed into the urine. Crystals of uric acid have been found in
these cells and it is supposed that the abundance of water furnished by
the glomeruli, irrigating these convoluted tubes, dissolves and washes
on the various solids and other products with which the epithelial cells
are charged. The protoplasm of the cells becomes saturated with the
urea, uric acid, hippuric acid coloring matter (indican, urochrome,
etc.), and this is washed out, passing by exosmosis to the liquid of
lesser density with which the tubes are filled.

Nervous Control of Urinary Secretion.

An electric current through the renal plexus of the sympathetic
(vaso-motor) lessens, or suppresses urinary secretion (inhibition).

Cutting the nerves of this plexus causes excessive vaso-dilation, renal
pulsations synchronous with heart beats and arterial pulse, and great
increase of urine. A similar increase comes from the application of cold
to the surface, from fatigue, from heat exhaustion, from irritation of
the floor of the fourth ventricle just in front of the origin of the
vagus and from section of the splanchnic nerve. This last is, however,
much less marked and more transient than from section of the renal nerve
noted above; the latter causing dilation of the renal vessels only, and
increased pressure, whereas the former causes dilation of the abdominal
organs generally, diverting the blood largely to other parts than the
kidney and preventing the same increase of pressure in the vessels of
the latter. For the same reason transverse section of the medulla
oblongata, or of the spinal cord as far back as the seventh cervical
vertebra, lessens or interrupts the urinary secretion, the pressure in
the kidney being reduced by the diversion of much of the blood
elsewhere. This influence of the nervous system on the urinary secretion
seems to be mainly or entirely one of increase or decrease of blood
pressure in the kidney. For this reason a weak heart tends to lessen
urinary secretion.

=Excessive increase= of urine is only important when continuous and in
the absence of visible cause, such as diuretics.

PHYSICAL PROPERTIES OF THE URINE.

Color, yellow, red, brown; horse, ox, calf, sheep, goat, dog, cat,
bird. In disease: pale yellow, with water in excess; deep yellow, red,
brown with solids in excess, urobiline, biliverdin, hæmoglobin.
Extraneous colors. Bilharzia. Translucency: Turbidity: horse,
ruminants, carnivora, pig. In disease, horse, other animals.
Consistency, viscous, stringy, tarry; odor, horse, dog, cat,
ammoniacal, fœtid, drug odor. Specific gravity, estimate of solids;
reaction, acid, alkaline, neutral; morbid chemical changes, sodium
chloride, phosphate, alkaline, earthy, indican, urea, uric acid,
hippuric acid, phenol, creatinin, acetone, oxalic acid, allantoin,
xanthin, hypoxanthin, cyanuric acid, leucin, albumen, glucose, bile
salts and pigments, blood, hæmoglobin, epithelium, pus, casts.

=Color.= In estimating the color we must note the various shades of
yellow, red and brown and compare these with the normal in different
genera of animals, on different food and water, and in different
conditions of health. Grades of color may be stated as follows:

=Yellow=: Pale, clear and deep yellows.

=Red=: Reddish yellow, yellowish red, and red.

=Brown=: Brownish red, reddish brown and brownish black.

=Color of Normal Urine.= This varies with the species of animal, food,
quantity of water drunk, and time of retention in the bladder.

=Horse=: Urine is normally clear yellow, brownish yellow, or deep citron
yellow, and the color is deepened by rich and abundant food (excess of
solids) and by exposure to the air (changes in pigments). It may be
sulphur white and sedimentary from precipitation of CaCO_{2} when on
green food.

=Ox, Calf, Sheep and Goat=: Normal urine clear yellow to wine yellow. In
the ox especially it is a pale straw tint, but varies to a deep brown on
nitrogenous food (clover, peas, beans, cotton seed, lentils, pea or bean
straw). Color may be due to indican and sometimes to indicanin or indigo
blue, which explains the blue urine sometimes described.

=Dog=: Normal urine is yellow, straw colored, aniline yellow, honey
yellow, to brownish yellow in hot season or on dry nitrogenous food. Is
always relatively deeper than in ruminants.

=Cat=: Straw yellow to honey yellow, with variation as in the dog.

=Pig=: Very pale yellow, more highly colored on dry feeding, nuts, peas,
etc.

=Birds=: White or yellow, sedimentary. Mixed with fæces in cloaca.

=Color of Pathological Urine=: =Pale yellow= with excessive secretion
glycosuria, polyuria, cryptogamic polyuria, chronic interstitial
nephritis, under diuretics, or after excessive drinking. The free
secretion of a crisis in a fever is pale yellow.

=Deep yellow=, =deep red=, =deep brown color=, indicates excess of
urinary pigment (urobiline) and is deepened by nitric acid. This is seen
in all hyperthermias with suppressed or diminished secretion, in
privation of water, or food. This urine is _acid_ even in herbivora.

=Yellow=, =saffron yellow=, =brownish yellow=, =greenish=, =olive=, =or
brownish red= indicate the presence of bile pigments (biliverdin,
bilirubin) as in jaundice or cholyuria. Bile salts should be tested for.
A similar coloration may come from free consumption of carrots, or other
yellow pigmentary matters.

=Red=, =brownish red=, =blood red=, =or deep brown color= implies the
presence of blood or blood coloring matter in the urine (hæmaturia,
hæmoglobinuria). Exposed to the air this becomes brown or chocolate in
ratio with the amount of blood or blood pigment present. Some such cases
are complicated by blood clots.

Color due to Foreign Constituents.

=Bronze or black color= may come from injection of =phenic acid=.

=Deep green or olive green= may come from =tar=, =carbolic acid=,
=salol=, =creosote=, or =derivatives of benzine= taken in.

=Brownish green= comes from =thallin= and reddens with iron chloride.

=Brown or blood red= from =rhubarb= or =senna=.

=Purple red from santonin=, if alkaline (if acid, is reddish yellow).

=Red= from =madder= (it is alleged from indigo).

=Yellow= from =carrots=.

=Blue= (indigo blue) may occur in urine of horse or ox when exposed to
the air.

=Bluish green= will come from feeding =indigo=.

=White or yellow color= will result from the presence of =pus=.

=White, chylous urine= occurs with a hæmatozöon (=Bilharzia Crassa=) in
the blood of cattle.

=Translucency.= Urine may be passed clear and become turbid by standing.
The presence of colloids hinders precipitation and prevents clearing.

=Horse=: Urine is generally turbid, especially what has been long in the
bladder, and that which is last passed. The turbidity is largely due to
precipitation of calcium carbonate and bicarbonate, and increases on
green food, or if the liquid stands exposed to the air and is cooled.
Not unfrequently the salts are thrown down as fine spherical granules,
or there may be a white pultaceous mass. They are sometimes entangled in
extremely mobile cylindroid masses coming from the uriniferous tubes
during convalescence from fevers or during fasting. A fine pellicle on
the surface is normal in horse’s urine left in the air.

=Ox, Sheep and Goat=: Urine is passed clear. May become turbid through
the change of lime carbonate into bicarbonate in cattle but always more
slowly than in the horse.

=Carnivora=: Urine is passed clear but becomes turbid on decomposition,
or if concentrated. With excess of fat in the food it may become opaque
from floating oil globules, apart from the classic chyluria.

=Pig=: Fed on raw fresh vegetables the urine is clear, but if on cooked
or dried vegetables, and especially if nitrogenous, it may show opacity.

=Pathological=: The =horse’s= urine is limpid and acid in polyuria;
limpid and alkaline or neutral with modified phosphates. It may be
morbidly turbid from excess of lime phosphate or sulphate, urea or other
acid salts, exudates, leucocytes or pus. These usually indicate
nephritis. Mucus and muco-purulent exudate suggest pyelitis or pelvic
nephritis. Blood elements indicate nephritis, cystitis or urethritis.
Debris of kidney tissue may indicate tuberculosis; tumors, etc.

Turbidity in =other animals= than solipeds is abnormal: examine the
urine.

=Consistency of Urine.= Morbid urine may be gluey, sizy, syrupy, mucous,
oily. If a =horse’s= urine is scanty a =slight siziness= may be normal
and due to tenacious mucus from the pelvis of the kidney, and from the
solution of mucin and epithelium in the alkaline fluid. =Viscous=,
=sizy=, =stringy=, and =tarry= (=pitchy=) urine is found in pyelitis,
pyelo-nephritis, or cystic catarrh, but not in polyuria owing to the
presence of the solvent acid.

=Odor of Urine.= This is somewhat =aromatic= in =horse= and =ox=,
=disagreeable= in the =dog=, and =repulsively heavy= in the =cat=. With
polyuria the odor is less. If the urine has been =retained= and
=fermented= it is =ammoniacal=, if there are =ulcers= or =tumors= it is
=fœtid=, in =diabetes= it smells of =acetone=, after taking =turpentine=
it has a =violet odor=, and after phenic acid, camphor, ether and other
drugs it is variously modified.

=Specific Gravity of Urine= in ratio to water 1000:

Horse, 1020 to 1050 (1040)
Ox, 1025 „ 1045 (1030)
Sheep; Goat, 1015 „ 1065 (1040)
Dog, 1020 „ 1060 (1040)
Pig, 1005 „ 1015 (1010)
Cat, 1020 „ 1040 (1030)

In the horse the urine may be 1001 to 1010 in polyuria, in chronic
interstitial nephritis, and in a crisis of fever attended by diuresis.
It may be 1050 to 1060 in glycosuria. Undissolved solids that are merely
suspended in the urine do not affect its density.

A rough estimate of solids may be made by multiplying the last two
figures of a specific gravity expressed in four figures by 2.33. The
result approximates to the number of grammes of solids in 1000 cc.

=Chemical Reaction of Urine.= The liquid is tested by litmus paper, red
and blue, weakly impregnated. The normal reaction is determined by the
food: the urine of =carnivora= and =sucking herbivora= is =acid= turning
blue litmus red: the urine of =vegetable feeders= is _alkaline_ turning
reds blue. In the =horse= the =alkalinity= is mainly due to excess of
lime bicarbonate, passing, with standing, into lime carbonate, the
carbon dioxide being derived from organic acids (lactic, malic, citric,
etc.), by oxidation. The hippurates are also alkaline in reaction. In
=dogs= the acidity is due to lime and soda phosphates, sulphates, urates
and oxalates.

=Pathologically= we find the urine strongly =alkaline= from the
evolution of ammonia from urea, in fermentations occurring with
prolonged retention in the bladder or in cystitis. The urine is =acid=
even in herbivora in all fevers in which appetite is lost or seriously
impaired, and in which the metabolism is excessive.

=Chemical Changes in the Urine in Disease.= =Sodium Chloride=, is
present in large amount in health (horse 25 to 35 grammes, dog 0.25 to 5
grammes daily) is =diminished= in fever, anæmia, visceral and exudative
inflammations. It is =increased= during the absorption of false
membranes and exudates. It is thrown down by adding solution of nitrate
of silver, the curdy white precipitate being insoluble in nitric acid.

=Phosphates of lime, soda, potash and, scantily, of magnesia= are
normally present (horse 0.08 to 0.60 gramme phosphoric acid daily) and
are present in excess in digestive disorders and in malnutrition of
bones (rachitis, osteoporosis and rheumatoid arthritis). The =alkaline
phosphates= are very soluble and never precipitated. =Earthy phosphates=
dissolve in acid urine, but are precipitated from alkaline. To a little
of the urine add a few drops of acetic acid, followed by a few drops of
uranium acetate. A yellow precipitate of uranium and ammonium double
phosphate is thrown down.

=Indican= (C_{8}H_{7}NSO_{4}) is formed from indol which passes
successively through the forms of indoxyle and indoxylid
potassio-sulphate. This is normally present in the urine, the horse
excreting 1 to 2 grammes daily, the dog 0.15 gramme. It is present in
excess in intestinal indigestions, constituting indicanuria. It is
tested by adding a drop of muriatic acid and one of a solution of
chloride of lime to the urine, when it will show a blue ring, the depth
of which indicates the relative amount.

=Urea= (CON_{2}H_{4}) the principal waste product of nitrogenous matter,
is always present in considerable amount. The sound horse may eliminate
100 to 200 grammes daily, the dog 5 to 180 grammes. It is present in
excess in all fevers and inflammations unless urination is suspended or
impaired, in cryptogamic diuresis, in mellituria, uræmia, nephritis and
cystitis. Test: The addition to a filtered solution of urine, freed from
phosphates, of solution of acid nitrate of mercury, precipitates it as
nitrate of urea. A simpler test is to add to a drop or two of urine on a
glass slide a drop of nitric acid and heat gently. The nitrate of urea
is precipitated in the characteristic rhombic or hexagonal crystals as
seen under the microscope. Heat urea crystals in a test tube: biuret is
formed and ammonia escapes. Add a trace of a copper sulphate solution
and a few drops of a 20 per cent. solution of caustic potash: a rose-red
color is produced—the biuret reaction.

=Uric Acid= (C_{5}H_{4}N_{4}O_{3}). Traces only of this are found in the
normal herbivorous urine, yet it is more abundant when on a full dry
grain diet, on milk (suckling) or on animal food. The dog kept on animal
food has a large amount.

=Pathologically= it is produced in the dog and even in the horse in
fever, overwork and starvation, the animal living on his own tissues.
Interference with oxidation in the lungs seems to produce it as an
arrest in the transformation of albuminoids to urea. The neutral urate
of soda remains in solution: the acid urate of soda is precipitated.
_Test_: To the urine add one-fourth its volume of muriatic acid and set
aside for 24 hours in a cool place. On the bottom and sides of the glass
and on the surface of the liquid will be found the yellowish red
acicular crystals of uric acid.

=Hippuric Acid= (C_{9}H_{9}NO_{3}) is normally present in all urine, but
is especially abundant in that of herbivora. The horse eliminates 60 to
160 grammes daily. It has been found to be increased by feeding on
dandelion, carrots, clover, asparagus, apples, plums, benzoic acid, oil
of bitter almonds, toluol, cinnamic or kinic acid. It is absent in
sucking calves, and horses fed on grain devoid of husk. =Pathologically=
it is increased in hyperthermia, icterus, some liver diseases and
diseased kidneys. Test: Precipitate any albumen by nitric acid and
boiling, then add hydrochloric acid which precipitates the hippuric acid
in long needle-like crystals. Heated in a small glass tube it forms an
oily liquid, and heated to redness gives off an odor of hydrocyanic acid
(nitro-benzol) and carbon is left. This distinguishes alike from uric
acid and benzoic.

=Phenol= is produced by intestinal fermentation. The horse normally
excretes about 3 grammes daily. Pathologically it appears in excess in
indigestions, abscesses, softened discharging tubercle, pyæmia, and
septicæmia. Test: Dilute solutions of ferric salts give a blue
coloration.

=Creatinin=, a product of metabolism of albuminoids, is found especially
in the urine of carnivora and omnivora in health. It is pathologically
increased when oxidation is interfered with, as in diseases of the
lungs. Test: Add to the urine a very dilute solution of sodium
nitro-prusside and then drop by drop some solution of caustic soda, when
a ruby red color is shown and disappears again on boiling. Acetic acid
changes to blue.

=Acetone= (C_{3} H_{6} O) is found in the urine of healthy omnivora and
carnivora and increased by excess of nitrogenous food. Pathologically it
has been found in fevers with much blood change, in inanition, in
cancer, in indigestions, and auto-intoxications. Test: To several c c.
of urine add a few drops of iodo-potassic iodide solution and caustic
potash when iodoform will be abundantly precipitated with its
characteristic color and odor.

=Oxalic Acid= (C_{2} H_{2} O_{4}) appears to be secreted in small amount
by healthy kidneys and it may also come from the splitting up of uric
acid after secretion. It is augmented by feeding agents rich in oxalic
acid (beets, fresh beans, asparagus, tomatoes). Pathologically it
abounds in certain indigestions, and is associated with lameness and
emaciation. Test: Add lime water to the urine, and the white oxalate of
lime is precipitated.

=Allantoin= (C_{4}H_{6}N_{4}O_{3}) is found in the urine of sucklings
(calves) during the first few weeks of life, in pregnancy and when on a
meat diet. It diminishes with the increase of vegetable food.

=Xanthin= (C_{5}H_{4}N_{4}O_{2}) is found in urine as a result of
imperfect oxidation of nitrogenous matters especially, which would
otherwise pass into uric or hippuric acid. Its immediate antecedents in
such transformation are guanin and hypoxanthin or sarkin. It is a rare
constituent of urinary calculus.

=Hypoxanthin= (C_{5}H_{4}N_{4}O) is produced from fibrine in gastric and
pancreatic digestion and in putrefaction, and is especially abundant in
leucæmic subjects.

=Cyanuric Acid= (C_{20}H_{14}N_{2}O_{6}) occurs in dog’s urine.

=Leucin= (C_{6}H_{13}NO_{2}) and =Tyrosin= (C_{9}H_{11}NO_{3}) are
products of pancreatic digestion of proteids, and the former occurs
normally in the spleen, thymus, thyroid, liver, salivary glands, and
urine. Both are present in large amount, in the urine, in acute atrophy
of the liver. Test for leucin: Evaporate carefully to dryness with
nitric acid: the residue, if leucin, will be almost transparent and turn
yellow or brown on the addition of caustic soda. If now heated with the
soda it forms an oily drop. Test for tyrosin: treated with strong
sulphuric acid, gently warmed and chloride of iron added, it gives a
violet color.

=Albumen= is an important morbid constituent of urine, which appears in
a great variety of diseases (nephritis, pneumonia, epilepsy, anæmia,
leucæmia, diabetes, hæmaturia, hæmoglobinuria, hydræmia, infectious lung
diseases, cardiac obstruction, venous stasis in the kidney, dermatitis,
burns, lesions of the crura cerebri, floor of the fourth ventricle,
spinal cord, or renal vaso-motor nerves). It also occurs after violent
exertion, in poisoning by strong acid, phosphorus, arsenic, lead,
mercury, opium or alcohol, and when an excess of albumen is injected
into the blood. All forms of albumen may enter the urine, but the most
common are serum albumen, globulin of serum, propeptone and peptone. A
simple test is to acidulate the urine with acetic acid and boil: if the
precipitate does not dissolve on addition of nitric acid, it is albumen.
Sulphosalicylic acid added to the urine will cause a precipitate in
urine containing only ¹⁄₅₀₀₀₀ of albumen.

=Glucose= (C_{6}H_{12}O_{6}) is often normally present for a short
period in small amount after a full meal of farinaceous material. It is
permanently present in excess in glycosuria, which may result, among
other conditions, from diseased liver, punctured medulla, suppression of
milk secretion on weaning the calf, oil of turpentine, nitrobenzole,
nitrotoluol or amyle nitrate. Test: Add yeast to the urine and keep at
15° to 20° C. when if glucose is present, it becomes cloudy and gives
off carbon dioxide, or add a little caustic potash solution, and a few
drops of cupric sulphate solution until it is blue: then heat and a red
precipitate of cupreous oxide is thrown down. The amount gives the ratio
of glucose. Uric acid, hypoxanthin or mucus causes brown precipitate in
the absence of glucose: peptone, creatin, creatinine, pepsine and
urinary pigment prevent its formation though glucose be present.

=Bile Salts and Pigments= are present in excess in cases of icterus,
where these characters may be studied. See Icterus.

=Blood and Hæmoglobin in Urine.= In a variety of diseases (anthrax,
hæmaturia, nephritis, Texas fever, hæmoglobinuria, etc.) blood or blood
coloring matter escapes in the urine. When blood escapes one finds the
reddish color, and under the microscope red globules, normal or crenated
(especially in alkaline urine), free, aggregated in masses, in small
clots, or embedded in casts of the uriniferous tubes. Under the
spectroscope the spectrum shows two dark absorption bands, one in the
yellow and one in the green. When the color is due to hæmoglobin the
urine shows under the microscope numerous masses of amorphous brown
pigment, and the spectrum shows one dark line in the yellow, and three
others less deep, (but one of them very broad) on the limit of the green
and blue. Urine which contains the elements of blood is usually turbid
and thick or glairy, by reason of the presence of salts, albumen and
fibrine. There may also be crystals of urinary salts (calculi),
fragments of broken down tissue (tumors) or the ova of worms.

=Epithelium in Urine.= The slight cloud seen in healthy urine contains
epithelial cells. The source of these may be often determined under the
microscope. The _bladder epithelium_ are the most numerous, the largest,
and are squamous. Those from the _ureters_ and _renal pelvis_ are also
squamous, but neither so large nor so numerous. The _epithelium from the
uriniferous tubules_ are polyhedral with large nucleus or columnar. The
cells from the _male urethra_ are also largely columnar. In cases,
however, in which these cells are passed in large amount because of
catarrh of the mucosa all alike tend to assume the globular form with
large nucleus so that their true source cannot be certainly stated. It
is only from such cells as have become detached without change of form
that the seat of desquamation can be determined. If an excess of cells
approximating to the kidney type are associated with albuminuria and
cylindroid casts they become diagnostically significant. Polygonal cells
darkly granular with large oval nucleus and nucleolus suggest kidney
inflammation. If the granules are freely soluble in ether there is
probably fatty degeneration. If hard, tough and glossy they suggest (but
don’t prove) amyloid degeneration.

=Pus Cells in Urine.= Pus cells, with multiple nuclei revealed by adding
dilute acetic acid, may be found in small numbers in apparently healthy
urine. When present in large numbers, they usually indicate a catarrhal
affection of the mucosa, and especially pyelitis, cystitis, or
urethritis. There is always cloudiness, excess of mucin, and, in the
alkaline herbivorous urine, the liquid may be glairy or stringy.

=Casts of the Uriniferous Tubes.= These usually indicate the existence
of nephritis, yet they may be present in small numbers in the urine of
healthy individuals under a slight toxic action such as alcohol.

_Unorganized casts_ of urinary salts or hæmatoidin found in sucklings
appear to have no pathological significance. _Organized_ casts, on the
other hand, usually imply renal troubles, and especially inflammation.
As these will be fully described under Bright’s disease, it need only be
noted here that they may be composed in great part of _red globules_,
_leucocytes_, _epithelium_, _bacteria_, _granules_, a _homogeneous
wax-like matter_, _fat globules_, _hyaline matter_, or _urinary salts_.
The predominance of one or other of these determines the nature of the
cast.

The observations of Mayer, Knoll, Bovida, Von Jaksch and others seem to
show that the basis substance of urinary casts differs from all our
familiar proteids and must be considered as a distinct nitrogenous
compound, a derivative of one of the common proteids.

GENERAL SYMPTOMS OF URINARY DISEASE.

External symptoms, arched back, stiff gait, straining, tender loins,
backing, turning, dropping under weight, urine checked, dribbled; in
dogs and cats, palpation of kidney; bladder, urethra, pains in
different animals. Internal symptoms, rectal exploration, vaginal,
urethral, straining, ureters, bladder, calculi, neoplasms, prostate,
urethritis.

=External Symptoms.= With inflammatory or painful affections of the
urinary organs the animal tends to roach the back or loins, tuck up the
abdomen, move the hind limbs stiffly and with a straddling gait,
protract and withdraw the penis which may be semi-erect, retract and
drop the testicles alternately, and stretch himself and strain to pass
urine without success. Lying down and rising may be accomplished with
marked effort and groaning. The loins along the spines or beneath the
outer ends of the transverse processes may prove tender to tapping or
pinching, the animal drooping to excess. Backing or turning in a narrow
circle may be accomplished awkwardly and stiffly though usually more
easily than with lumbar sprain. The animal drops when mounted but less
than with sprained back. Urine may be passed in excess or in diminished
amount, or it may be entirely suppressed. It may be abruptly interrupted
when in full stream, suggesting calculus or polypus, or it may be passed
often in mere dribblets, or finally it may ooze away constantly partly
lodging in the sheath and partly trickling down the thighs.

In dogs or cats with flaccid walls of the abdomen external manipulation
may detect in the kidneys, differences in size, position, and tenderness
as well as the presence of tumors. The distended bladder also may be
distinctly felt, and the pyriform area of flatness on percussion will
serve to map out its size and outline.

In the horse the urethra is superficial and easily traced over the
ischiatic arch and for some distance downward, when it becomes deeper
and is less easily felt. In the bull the urethra is deep over the
ischiatic arch but becomes more superficial lower down and can be easily
felt at the sigmoid flexure and below. In sheep and dog it is easily
followed from the ischium to the end of the penis.

As a rule the penis is easily drawn from its sheath in the horse and
dog; this is more difficult in the sheep and goat and still more so in
the bull and boar. In the small animal protrusion is favored by setting
him on his rump, with his back between the operator’s legs, and the
pelvis doubled forward toward the sternum. The penis of the bull may be
extended in presence of a cow in heat, and promptly seized, or it may be
seized through the sheath back of its first bulging part and skillfully
worked out. In the ruminant, calculi may be felt at the sigmoid curve,
and in the ram, in the vermiform appendix at the fore end of the penis.

=Internal Exploration.= This is accomplished in the larger animals with
the oiled hand in the rectum, the nails having been pared short and even
to avoid injury to the mucosa. In ponies and yearlings the kidney may be
felt, and this may be true also of mature animals of larger species in
cases of hypertrophy or floating kidney. The ureters, bladder and
intrapelvic urethra are easily felt in the male. The empty bladder lies
on the anterior border of the pelvis; when full, it projects forward
into the abdomen but retains its pyriform or, in the very young animal,
its fusiform shape. In the female the sensation is somewhat modified by
the presence on its upper surface of the uterus dividing into its two
horns anteriorly. The single enlarged horn of pregnancy is especially
misleading.

The female urethra, cervix and bladder may be explored through the
vagina. To explore the cervix vesicæ and urethra the fingers are slowly
drawn back from the bladder along the median line of the floor of the
vagina. In the _mare_ the cervix and adjacent portion of the bladder can
be further explored with the index finger introduced through the opening
of the urethra in the floor of the pelvis and at the junction of the
vagina and vulva. In the cow the urethra is too small to be readily
explored from within, and the orifice is still further guarded by the
two lateral blind canals of Gærtner, into which the unskilled fingers
more readily pass. Success only attends the careful search for the small
central lower orifice. In the _smaller animals_ the finger only can be
introduced into vagina or rectum and the urethra, cervix and bladder
only can be felt. _The result of such exploration_ is straining even in
healthy conditions but which becomes excessive in nephritis, pyelitis,
renal, urethral, vesical or urethral calculus, cystitis, rectitis or
enteritis.

The _ureters_ are tender when inflamed, and they are swollen in calculus
obstruction with an elastic feeling in front of the stone.

The _bladder_ is very sensitive when overdistended, inflamed or pendent
on the abdominal floor, or when the seat of calculus. In the absence of
any liquid contents a calculus is felt as a hard solid mass firmly
clasped by the contracted vesical walls. If liquid is present the solid
hard calculus is felt movable in the fluid. An empty contracted bladder
is firm and pyriform. An empty flaccid bladder, resulting from rupture
or exhaustion, is flabby, with indefinite form and, if the seat of a
lesion, tender. It varies in consistency with neoplasms (papilloma,
sarcoma, carcinoma, or epithelioma). These have not the free mobility of
the calculus floating in urine, and their point of connection with the
wall may often be made out. When a solid body is felt, or suspected to
be in the contracted bladder, an injection of sterilized water will
usually facilitate diagnosis, and a differentiation of calculus and
neoplasm.

_Hypertrophy_ of the prostate is felt as a swelling of uneven outline
over the cervix vesicæ. It is to be looked for especially in old dogs.

_Urethritis_ is indicated by swelling and tenderness along the median
line of the pelvic floor, back of the cervix. With a _calculus_ in the
urethra the swelling is more strictly localized and the canal in front
of it may be full and elastic.

HEMATURIA.

Symptoms of different lesions of kidneys and constitutional states, of
poisoning by irritant plants, common on moors and in woods. In
puerperal cow fed on turnips raised on mucky, unreclaimed, sour lands.
Bacteria. Toxins. Anæmia. Poor wintering. Limed new soils. _Symptoms_:
in plethoric, congested mucosæ, vascular tension, hurried breathing,
colics, straining, red urine; in vegetable irritants, depression,
weakness, coldness, trembling, stiffness behind, scanty red or black
urine, diarrhœa, constipation; in anæmia, poverty, debility, red
urine, pink tinge in milk, emaciation, hidebound, anorexia, colics.
Chronic or intermittent. Lesions: in plethoric, congested enlarged
kidney, without softening; in irritant poisons, congestion also of
throat, stomachs, intestines, liver with hæmorrhagic extravasations;
in anæmia, kidneys pale, flaccid, hydroæmia, liver enlarged, softened,
reddish liquids in serous cavities. Treatment: avoid the injurious
soils, drain, cultivate, feed products of such soils with other food,
oleaginous or saline laxatives, antiferments, tonics, astringents,
flax seed, farinas.

The passage of blood or blood elements in the urine.

_Causes._ A symptom of a variety of diseases, producing lesions of the
secreting structures of the kidneys; acute congestion, tumors, calculi,
parasitism. Also as a manifestation of diseases of distant
organs—hæmoglobinuria, southern cattle fever, anthrax, poisoning by
irritant diuretics, wounds of the bladder, pelvic fracture with injury
to bladder or urethra, cystitis with varicose cystic veins, etc.

Among the irritant plants charged with producing the affection are the
young shoots of oak, ash, privet, hornbeam, alder, hazel, dogberry,
pine, fir, and coniferæ, generally. Also ranunculus, hellebore,
colchicum, mercuriales annuus, asclepias vincetoxicum, broom, etc. The
disease is common in spring in cattle turned out too early to get good
pasturage and which, it is alleged, take to eating the swelling buds and
young shoots of irritant plants.

The disease has occurred mostly in woods and wild lands and has
accordingly been vulgarly named the wood evil, (maladie de bois,
holzkrankheit), and moor ill.

In England, as occurring in the puerperal cow, Cuming, of Ellon,
attributes it to a too exclusive diet of turnips. His analysis showed
that turnips contained 10% sugar and 1 to 1½% vegetable albumen. The
sugar is held to stimulate unduly the milk secretion, but fails to
supply the nitrogenous materials needful to form it, and the cow is
speedily rendered anæmic, with solution of the blood globules or of the
hæmatin and its excretion by the urine. No attempt was made to produce
hæmaturia by an exclusive or excessive diet of sugar, and cows fed on
turnips grown on well drained lands never suffered from the disease.

Williams says that urine in such cases had a strong odor of rotten
turnips. This argues not an anæmia determined by sugar, but rather an
intestinal fermentation, perhaps superinduced by ferments introduced
along with the turnips. Add to this the notorious fact that the
offending turnips are usually such as are grown on wild, damp,
undrained, swampy, or mucky lands, and we have the suggestion of a
bacteridian poison, or a toxic product of bacteria. Williams and Reynal
practically agree on the point that the common hæmaturia is the result
of anæmia. It has long been noticed that the herds which suffer from the
affection are those which have come out of the winter in low condition,
the victim is the poor man’s cow, and the symptoms are most likely to
appear when turned into the fields in spring before the pastures have
come up. The anæmic condition of the carcasses is quoted in support of
this view, but perhaps without making sufficient account of the
extraordinary destruction of blood globules during the progress of the
malady.

Pichon and Sinoir see in the liming of soils and the production of
larger crops, a cause of anæmia in the rank and aqueous growth of the
meadows, and their overstocking in order to eat them down, or to consume
their products. They found that an abundant artificial feeding was the
most efficacious mode of treatment.

Reynal, who endorses this view, tells us that in the anæmic and liquid
blood the globules become smaller and can pass more readily through the
walls of the vessels. But this is exactly the opposite effect from what
we see when the blood is diluted with water. The globules in such a case
are distended and enlarged, and may finally have their protoplasm and
hæmatin dissolved and diffused through the liquid. If the blood globules
are shrunken, then we must look for a cause very different from anæmia.

Reynal further assures us that plethora is a common cause of hæmaturia
in cattle. “Under the prolonged influence of a very assimilable diet,
the blood becomes more plastic, circulates with difficulty in the
capillaries, and may even rupture them, with a resulting capillary renal
hæmorrhage, and bloody urine.” He further intimates that this occurs
especially in spring after the animals have been turned out on very rich
pastures, and that in Normandy certain pastures of unusual richness are
notorious for producing hæmaturia.

Apart from the fact that the rich grasses of spring produce at first
intestinal congestion, and diarrhœa, with consequent disorder of the
liver and kidneys, this spring affection on particular pastures suggests
some special poison in the pasture as the unknown cause of the disease.

In all forms alike of this affection the nature of the soil appears to
have a preponderating influence. It is the disease of the woods, and
waste lands, of damp and undrained lands, of dense clays, of lands
underlaid by clay or hard pan, of lands rich in vegetable humus, or
vegetable moulds the decomposition of which has been hastened by the
application of quicklime.

Pottier, Salomé, Wiener, and Reynal especially testify to the prevalence
of hæmaturia on soils that are either dense and impermeable, or that
have a subsoil of clay or hardpan.

The disease has not been traced to any definite microbe nor toxin, but
there is much to suggest the necessity for inquiry in that line. The
special susceptibility of animals that may be plethoric on the one hand,
or in low condition on the other, would be entirely in keeping with such
a view, as the debility or derangement of health would lay the system
open to attack.

_Symptoms._ In the plethoric animal there are congested mucosæ, full,
strong pulse, forcible heartbeats, full veins, accelerated breathing,
colicy pains, dullness, straining frequently and the discharge of thick,
red or bloody urine.

If from irritant buds and shoots, or plants, there is more depression,
weakness, fever, dry skin, staring coat, coldness of the surface,
tremblings, stiffness or weakness of the hind limbs, diarrhœa, followed
by constipation, frequent straining and the passage of colored urine
with pain. In violent cases the expulsion of bloody urine may be
excessive, and the cow may die in 24 hours. From irritant plants however
the quantity of urine is liable to be small, but frequently passed.

As occurring irrespective of plethora or irritants there may be at first
only poor condition and debility with the passage of blood. A pink tinge
may show on the froth in the milk pail, and a red precipitate on its
bottom. If not anæmic at the outset they soon become so, and the pulse
which was at first bounding becomes small and weak, the heart
palpitates, the red mucosæ become pale. The subjects become tucked up,
emaciated, weak, rough coated, the skin adherent to the bones, and the
appetite and rumination impaired or lost. Sometimes colics are present.

In the milder anæmic forms it may continue for months before it causes
death. In such cases it may prove intermittent.

_Morbid Anatomy._ In the hæmaturia of plethora the kidneys are large,
congested and of a dark red, but, preserve their normal consistency and
texture.

In the form associated with ingestion of irritant plants, there is
congestion of the pharynx, stomachs, and intestines with hæmorrhagic
spots, congestion of the liver, violent congestion of the kidneys which
are of a blackish red color, and enlarged to perhaps twice the normal
size, with hæmorrhagic exudations, the convoluted tubes filled with
fibrinous exudate and blood globules, the pelvis red and like the
bladder containing some reddish urine. The vesical mucosa may be black.

In anæmic cases the kidneys are pale, flaccid and colorless, with a
reddish liquid in the pelvis and bladder. The vascular system is
comparatively empty, and the blood, thin, and watery, and often
coagulates loosely or not at all. As noted by Herland globules are
greatly reduced in numbers and size, and often crenated or partially
broken down. Slight serous effusions in the serous membranes are common.
The liver is softened and enlarged, the lacteals have reddish contents,
and the ingesta are dark colored.

_Treatment. Preventive._ Avoid hæmaturia pastures and the fodder grown
on such lands. Drain and cultivate such soils. When animals must feed on
the products of such soils supplement the food by grain, oil cake,
cotton seed meal, etc. Avoid stagnant waters draining from such soils.

_Therapeutic Treatment._ Give oleaginous or saline laxative to clear out
poisons and ferments from the bowels and may add an antiferment (salol,
salicylic acid, carbolic acid, turpentine oil, chlorate of potash,
sulphites or hyposulphites), no matter if diarrhœa is present. Follow
with tonics (copperas, chloride of iron) and stimulant antiseptics (ol.
terebinth, potass. chlorate), and sound food. Flax seed, linseed meal,
farinas. Bitters may be added (gentian, quinine, quassia). As a
calmative, camphor (2 to 4 drs.) 2 or 3 times a day has proved useful.

In case of nephritis treat as for that affection.

Weiner lauds empyreumatic oil and oil of turpentine with camphor.

In chronic cases, nourishing food with change of locality and water are
very important.

A course of iron tonics should wind up the treatment.

ACUTE CONGESTION OF THE KIDNEYS IN SOLIPEDS.

Definition. Causes: bacteria, toxins, irritant diuretics, musty oats
or fodder, foul water, cantharides, turpentine, aqueous grasses,
onions, moulting, cold, chills, injuries to loins, over-driving.
Lesions: kidney enlarged, red, black, softened, capsule loose, cut
surface drops blood, brown, softened necrosed areas, gorged
capillaries of glomeruli and convoluted tubes, granular or fatty
changes in epithelium, may be ruptures. Symptoms: sudden; weak tender
loins, slow dragging straddling gait, accelerated pulse and breathing,
anxious countenance, colics, sweating, urine from limpid to black,
with red globules, and casts. Prompt recovery or nephritis. Diagnosis:
from nephritis, hæmoglobinuria, laminitis, indigestion. Prevention:
Treatment: bleeding, laxatives, diffusible stimulant diuretics,
bromides, diluents, mucilaginous agents, fomentations, sinapisms,
rectal injections, clothing, friction to the skin, restricted laxative
diet.

_Definition._ Active congestion of the renal capillaries, especially of
those of the glomeruli and convoluted tubes, with colicy pains, and free
discharge of urine, in some cases bloodstained.

_Causes._ It may be determined by local irritation caused by the passage
of the bacteria and toxins of infectious diseases such as influenza or
contagious pneumonia. In the same way irritant diuretics, medicinal,
alimentary and toxic, operate. Diuretic balls and condition powders
given recklessly by stablemen and grooms, saltpeter, resin, oleo resins,
turpentine, rue, savin, colchicum, squill, anemone nemorosa, adonis,
cynanchum vincetoxicum and other species of ascelepias, hellebore,
mercurialis annua and bryony are examples. The young shoots of the
coniferous plants, fir, balsam fir, pine, white and yellow, and hemlock,
are at times injurious.

In the same way, damp moldy oats or fodder produce renal congestion and
excessive polyuria, also corrupt, stagnant water and that of marshes
which often contains complex toxic products of fermentation. Water of
ponds in which cantharides or potato beetles have been drowned, is
dangerous. The cantharides, euphorbium or oil of turpentine applied too
extensively to the skin as a counter-irritant, is another factor.

Even the rich aqueous grasses of spring succeeding to the dry winter
diet, stimulate the kidneys, determining an active congestion with
polyuria and in bad cases hæmaturia. In many such cases there are
superadded the acrid diuretic plants already referred to. In Denmark
where onions are grown on a large scale, the tops fed to animals have
produced renal congestion.

There appears to be an extra susceptibility in spring when the winter
coat is being shed, and at this time especially, but also independently
of this and at other seasons, exposure to cold and the occurrence of
chills tend to induce an attack. Exposure to cold storms of rain or
sleet when perspiring or fatigued, standing tied out of doors in zero
weather without a blanket, wading or swimming deep rivers in cold
weather and while fatigued, standing wet and unblanketed in a cold
stable when returned from work, exposure to draughts between open
windows or doors, the continuous falling of cold rain, from a leaking
roof, on the loins, the cold of a damp stable newly finished in brick or
stone, the cold and damp of an undrained floor in a wet retentive soil,
all have a tendency to drive the blood from the surface, to increase the
tension of the blood in the heart and internal organs, to stimulate the
kidneys to extraordinary secretory activity, and at the same time to
temporarily debilitate the whole system and lessen the power of
resistance and recuperation. The factor is especially potent when it
involves the nervous interdependent sympathy between the chilled loins
or abdomen and the kidneys. Sprains and other injuries of the loins have
long been charged with producing renal congestion and inflammation, and
even Trasbot, who doubts the reality of this, acknowledges that the
already diseased kidneys are seriously injured in this way. Cadeac and
Schmid record cases of actual rupture of the horses’ kidney from violent
movement, and other cases of congestion and bloody urine have been
traced to kicks on the loins, falls, sprains and the carrying of unduly
heavy loads. The overexertion which produces albuminuria, casts and
sanguineous transfusion in athletes has a similar effect on the
overdriven race horse, trotter or draught horse.

_Lesions._ The congested kidney is enlarged, sometimes to two or three
times its natural size, softened, and red, especially in the cortical
portion which may be so dark as to appear cyanotic. The capsule is also
the seat of ramified redness, and is very loosely adherent to the
cortex. Beneath it may be considerable yellowish exudate especially
abundant in the vicinity of the hilus. On section the cut surface is
very bloody, the cortex literally dropping blood, though brownish spots
may appear at intervals representing areas of necrosis, which under
pressure break down into a pulpy debris. Microscopically the glomeruli
appear hæmorrhagic, the capillary vessels being gorged to excess, while
blood globules and even minute blood clots are found in the
intervascular spaces. The epithelium covering the glomeruli and lining
the convoluted tubes show granular or fatty changes, and granular matter
is found outside the vessels.

The congestion is less in the medullary portion and even in the
convoluted tubes and the tubes of Henle, though these may be the seat
both of hyperæmia and exudation.

In case of very violent congestion, extensive sanguineous extravasation
may occur, leading even to rupture of the capsule and the escape of
blood into the perirenal adipose tissue or into the abdominal cavity.
Cases of this kind in the soliped are recorded by Caroni, Cadeac,
Moussu, Kitt, Zundel, Mollereau and Porcher. Averons describes in the
_Revue Veterinaire_ (1897) a case in which both kidneys were surrounded
by an immense black clot, and weighed no less than 36 lbs. Leblanc
records a similar case affecting the one kidney. The mass measured about
10 inches by 8.

_Symptoms._ These are liable to appear suddenly, often while the patient
is at work, and are manifested by weakness in the loins, slow gait or
sudden stopping, the hind limbs are held in abduction, and advanced with
apparent stiffness and pain. There is much excitement and anxiety, the
face is pinched and strained, the respiration accelerated, the pulse
hard, tense and rapid, and the eyes or nose may be turned toward the
flank or loins. There may be colicy pains, with uneasy movements of the
tail and hind limbs, pawing, and even lying down and rolling. The
visible mucosæ are strongly injected and in bad cases the skin may be
drenched with sweat. There is at first little or no hyperthermia.

At first there may be no micturition but in an hour or more, urine may
be discharged in excess, sometimes as much as 25 quarts, and of a low
specific gravity (1001 to 1005). If there has been no blood
extravasation it is usually clear and limpid but with extravasation it
may be of all shades of pink or red to black. In the latter case the
suffering is liable to be acute (Cadeac), and contrary to the condition
in hæmoglobinuria, the urine contains blood globules and even tubular
coagula representing the uriniferous tubes and entangling the blood
cells. This is complicated by albuminuria.

_Course. Duration._ The congestion is short lived. It speedily undergoes
resolution with the passage of normal, clear urine, and the recovery of
appetite and spirit, or it becomes rapidly aggravated, with continuous
suffering and colic, complete loss of appetite, dullness, constant
decubitus, weakness, debility, small or imperceptible pulse,
palpitations, darker color and perhaps complete suppression of urine,
and stupor or other nervous disorder. Death may occur on the fourth to
the sixth day. It may be delayed by a partial recovery followed by a
relapse.

_Diagnosis._ Acute renal congestion is distinguished from _nephritis_ by
the suddenness of the onset, the absence of fever and the comparative
absence of tenderness of the loins, and of tubular casts.

From _hæmoglobinæmia_ it is distinguished by the absence of the
conditions under which that affection appears:—the previous heavy work
and full rich feeding, the day or more of complete rest on full ration,
and the sudden exercise following. The hind parts in hæmoglobinæmia are
benumbed, paretic, or paralytic and not unfrequently rigid and swollen,
and the brownish or reddish urine contains hæmoglobin in amorphous
particles, and not red blood globules and sanguineous tubular casts as
in renal congestion.

From _laminitis_ it is distinguished by the absence of high fever, by
the absence of the advance of the fore feet resting on the heels, of the
heat and tenderness of the feet, by the ability to bear the lifting of
one fore foot, or the tap of a hammer on the toe, by the lack of
improvement after the first few steps as is seen in laminitis, and by
the absence of the strong pulsations in the digital arteries.

From _indigestion_ it is distinguished by the absence of the history
which leads up to that condition, of abdominal tympany, of rumbling, of
impaction and of frequent attempts to defecate, and by the presence of
the stiffness, straddling, and the blood globules and albumen in the
urine of low density.

_Prevention._ This must be sought by the avoidance of all the factors of
causation:—auto-intoxication in contagious diseases, excessive renal
irritation from the injudicious use of diuretics, or the accidental
ingestion of irritant or acrid diuretic plants or waters, or musty
fodders, or the sudden change to the succulent, watery, first vegetation
of spring, or of exposure to cold, wet, or damp, in all their forms, or
of direct injury to the back or loins by blows, shocks, or violent
exertions.

_Treatment._ Trasbot and Cadeac strongly recommend venesection, and at
the very outset in specially acute cases the sudden lessening of the
arterial and capillary tension, by this potent means, may furnish the
opportunity for the capillaries of the glomeruli and tubes to regain
their normal tone, and thus contribute to a speedy abortion of the
affection. If resorted to at all it should be made in a full stream from
the jugular, so as to secure the fullest and most prompt result with the
least possible effusion of blood.

Much, however, must depend on the attendant conditions. In toxin
poisoning following on an infectious fever, the already existing
debility will sufficiently forbid a resort to the lancet, and we must
seek elimination by the bowels, the skin or even the kidneys.
Antiseptics, too, are in order if there appears any ground for suspicion
of the action of infecting agents. Some cases will recover promptly
under diffusible, stimulant diuretics such as spirits of nitrous ether,
which by stimulating the circulation in other organs and especially the
skin, appears to relieve the kidney and solicit normal secretion. But
most veterinarians dread the stimulus and irritation and prefer small
doses of refrigerant diuretics: bicarbonate of soda 4 drs., saltpeter 2
drs. or the tartrates, citrates or acetates of the alkaline bases. In
case of irritation by acrid diuretics, but especially by cantharides,
camphor 2 drs., has been found to be particularly soothing, and next to
this, bromide of camphor or bromide of potassium 1 to 2 drs. may be
resorted to. Zundel prescribes acidulated camphorated drinks. The free
use of mucilaginous drinks, such as boiled flax seed; and the persistent
application of fomentations or wet compresses to the loins are of equal
value in soothing irritation. Sinapisms may advantageously follow the
local emollients.

Laxatives act with less promptitude than diuretics, but on the whole
constitute a safer treatment, since they secure elimination and
derivation without risk of irritation to the kidneys. The oils: castor 1
to 2 pints, linseed 2 pints, or olive 2 pints, are especially to be
recommended in this respect, but l’Homme advises manna, and calomel may
also be used as a substitute. Injections of warm water are valuable in
unloading the rectum and colon, soothing the kidneys and soliciting
peristalsis.

A restricted amylaceous diet is essential, and a warm stall or abundant
clothing. Grooming or active rubbing of the skin tends to active
derivation and often materially relieves. The case should not be
abandoned until a day or two after the urine has returned to the normal,
and for some time special care should be taken of the diet, stabling and
work.

ACUTE CONGESTION OF THE KIDNEYS IN CATTLE.

Causes: infection, toxins, etc., irritant diuretics, chills, moulting,
swill. Lesions: cortical kidney congestion, red to black, softening
friability; urine limpid to red, with blood globules, albumen, and
crystals. Symptoms: chill, tender loins, colic, straining, recovery in
four days. Diagnosis: from hæmoglobinuria, cystitis, calculus.
Prevention: diet, etc. Treatment: laxatives, flax seed, wet
compresses, bromides, camphor, disinfectants, bitters.

_Causes._ In cattle this malady is largely traceable to the same causes
as in the horse, and is very often but a complication of some other
affection. The renal congestion of infectious diseases is seen in the
advanced stages of lung plague, in anthrax, in malignant catarrh, in
hæmoglobinæmia, and implies an accumulation of irritant toxins in the
system. The abuse of diuretics, the ingestion of acrid diuretic plants,
including the early shoots of the coniferæ, the introduction through any
channel of cantharides or potato beetles, the drinking of stagnant water
charged with deleterious fermentation products, the consumption of musty
or spoiled fodder, and the sudden change to the succulent grasses of
spring, operate as in the horse. So it is with cutaneous chills, cold
stone floors, cold wet storms, draughts and dropping from a leaky roof.
The shedding of the coat in spring is an undoubted predisposing cause.

Cattle in the swill stables of breweries and distilleries are the
subjects of a constant renal congestion and polyuria, which, however,
does not prevent rapid fattening. This diet, however, unfits the animal
for a future vigorous life, and any concurrent injurious influence may
easily bring on active kidney disease.

_Lesions._ There is redness and swelling of the kidney, it may be to two
or three times its normal size, the enlargement being especially
referable to the cortical portion, which may be mottled in different
shades of red up to black extravasations. The lack of firmness in its
connection with its sheath, and the softening and friability of the
parenchyma resemble the same conditions in the horse. The urine may be
clear or more or less tinged with blood, and contains blood globules,
albumen, and crystals of carbonate of lime and urate of ammonia, which
seem to indicate the presence of a bacterial ferment.

_Symptoms._ The patient usually shows some indication of chill, with
staring coat and arched back, which is very sensitive to pinching. There
is impairment of rumination and appetite, decrease of milk in dairy
cows, uneasy movements of the hind limbs and tail, frequent straining to
urinate, and the passage of urine often in small amount and sometimes of
a pink or reddish tinge. In bad cases this may become deep red, or
black, and the pulse becomes weak, with palpitations, marked muscular
weakness and a tendency to lie down most of the time.

With early improvement recovery may be complete in from four to six
days. In the more severe and fatal cases death may occur as early as the
sixth day. Unless under the influence of violent irritants or a
persistence of the original poison the prognosis is favorable.

_Diagnosis._ It is especially important to distinguish this from
=hæmoglobinæmia=, which shows an uniform red or brown discoloration of
the urine and an entire absence of blood globules as such. In congestion
the reddish material tends to precipitate and is found to consist
largely of blood globules. It is further associated with albuminuria.

=Hæmorrhagic cystitis= and =cystic calculi= are both chronic affections,
and identified on rectal exploration by the tenderness of the bladder
and the presence of the stone.

_Prevention_ consists in the avoidance of the various causative factors,
and especially those that find access among alimentary matters. Cattle
turned out in early spring should be fed before going and should be
returned from the pasture in an hour or two. This repeated day by day,
allows the digestive and urinary organs to accommodate themselves to the
fresh spring grass and to any vegetation to which the animals have not
been accustomed. Chills, draughts, injuries and other disturbing
conditions must be guarded against.

_Treatment._ Bleeding is strongly recommended by Cruzel and Cadeac. In
Germany, England and America derivation toward the digestive organs is
more generally relied on. Laxatives should be, as in the horse,
oleaginous (castor, olive, linseed) or manna, rather than agents that
may perchance act on the kidneys. Free purgation should be secured.
Flaxseed tea, and wet compresses over the loins are valuable adjuncts,
and anodyne agents like camphor, bromide of camphor, or other bromides
may be added, and when there is any suspicion of infection, salicylates,
or iodide of potassium may be employed. Finally a course of bitters
(salicin, quinine, nux,) may be employed to restore tone and iron
carbonate with sodium carbonate as a reconstructive tonic. The diet must
be changed to wholesome food, but not too stimulating, and the animal
kept quiet.

ACUTE CONGESTION OF THE KIDNEYS IN SHEEP AND GOAT.

Causes: irritant food. Lesions: Symptoms: separates from its fellows,
arched back, stiff straddling gait, straining, muscular weakness,
recumbency, urine red, with blood globules and albumen. Prevention:
care in feeding and watering, change of pasture and treatment as in
the ox.

_Causes._ As in cattle, the smaller ruminants appear to suffer
especially from an alimentary renal congestion, showing itself mainly in
animals that are unaccustomed to the particular toxic aliment. Thus,
Cornevin finds that the Pyrennean sheep thrives on the leaves of the
Quercus tosa, while Southdown sheep taking it in any considerable
quantity perish of renal congestion or nephritis. Similarly Weith fed
four sheep on cynanchum vincetoxicum and developed renal congestion in
the course of three days. Other causes doubtless contribute in
individual cases but have not been specially traced to their effects.

_Lesions_ are in the main the same as in cattle, the kidneys being
bluish red, soft, flaccid and friable.

_Symptoms._ The sheep lags behind the flock, frequently lies down and
rises, strains to urinate, and passes often considerable quantities. The
back is arched, the loins tender, the walk stiff and straddling, the
pulse small and weak. If the disease advances, there come on extreme
muscular weakness, a disposition to lie, an uncertain, gait, with
frequent stumbling, dullness, stupor, and it may be coma. The urine is
usually tinged with blood or of a deep red or black, and contains
well-formed blood globules and more or less albumen.

_Prevention and treatment_ should proceed on the same lines as in the
ox, but in dealing with a large herd it becomes difficult to treat each
separate case with special care. The avoidance of sudden change of food
as in turning out in spring, the feeding of grain before turning out,
the return to the fold after a short freedom, and the gradual transition
to the new food are important. When the disease has developed, an entire
change of pasture or food, the use of roots, ensilage, or grain, or of
freshly cut meadow grass, is indicated, and an oleaginous laxative
(castor oil 2 to 3 ozs.) are indicated. Oilcake or flaxseed meal will
often prove a most valuable article. Beyond this the same agents would
be indicated as for the ox.

ACUTE CONGESTION OF THE KIDNEYS IN SWINE.

Causes: infection, toxins, fermented food, traumas, crowding, cold.
Symptoms: stiff loins and quarters, frequent micturition, urine limpid
or red. Treatment.

Renal congestion in pigs has been seen mainly as the result of toxin
poisoning in swine erysipelas, hog cholera or caseous pneumonia. It is
also liable to occur from putrid or overfermented food, and in fat,
heavy animals from injuries sustained in shipping by rail by trampling
on or squeezing each other. Kicks and other injuries may at times
contribute to its occurrence. Exposure to cold storms, to which swine
are especially sensitive, a wet, cold bed, or a leaky roof, are
additional causes.

The _symptoms_ are more or less stiffness of the loins and hind parts,
frequent urination, the secretion being often passed in excess, and
though at times clear yet at others pink or bloody and precipitating
blood clots or at least containing blood globules.

_Treatment_ is mainly prophylactic. If therapeutic measures are
desirable for valuable animals, they should follow the same lines as for
sheep: rest, fomentations, aqueous food, anodynes, weak alkaline
diuretics, laxatives, and balsams.

CONGESTION OF THE KIDNEYS IN CARNIVORA.

Causes: acrid diuretics, loss of kidney, catheterization, dermatitis,
burns, traumas, overexertion. Lesions: enlarged, blood-gorged kidney,
red or black, petechiated. Symptoms: stiff, arched, tender loins,
tardy, dragging of hind limbs, urine passed often, clear to bloody,
albuminous, anorexia, nausea, vomiting, diarrhœa, dullness, stupor.
Treatment: stop cause, give emetic, laxative, in surgical cases
antiseptic, for cantharides, camphor, bromides, vegetable food. Warm
clothing or building.

_Causes._ This comes most commonly from the ingestion of acrid or
diuretic agents, saltpeter, turpentine oil, cantharides and, according
to Cadeac, various essential oils including oil of mustard. It takes
place in the remaining kidney after the one has been extirpated, or had
its functions abolished by disease or urethral obstruction. Again,
surgical operations on the urinary organs, even the simple passing of a
catheter, will cause sympathetic renal congestion. Extensive acute
dermatitis, and burns of the skin may have a similar sequence.

Falls, kicks, blows, or crushing beneath a wheel or otherwise are
additional causes.

Finally violent overexertion as in coursing, causes congestion with
albuminuria, and blood globules and even casts in the urine. This is
common to the human athlete, who undergoes a violent and continued
overexertion, race and draught horses, and dogs.

_Lesions._ When congestion is produced experimentally by cantharides the
kidneys are found to be enlarged and the cortex gorged with blood so
that it has a deep red or blackish port wine hue, with here and there
spots of ecchymosis. The veins, capillaries and glomeruli are especially
congested, and the epithelial cells of the convoluted tubes have become
laterally distended, so that they approximate to a globular form. A
loose coagulum containing blood globules may be found in the capsule of
the glomerulus and in the convoluted tubes.

_Symptoms._ These are arching and stiffness of the loins, a tardy,
dragging movement of the hind limbs and tenderness of the loins. The
urine may be scanty or in excess, and tends to be passed frequently, in
small quantities and with evidence of pain. It may be clear, pinkish or
bloody, and shows albumen and frequently casts, and blood globules or
small clots. There is some impairment of appetite, and, in severe cases,
nausea and vomiting, with, it may be, diarrhœa, nervous depression,
dullness and stupor. When due to poison or other transient cause the
symptoms improve when this factor has been stopped.

_Treatment._ When due to poison taken by the stomach this must be
stopped, and the stomach and bowels evacuated by an emetic (ipecacuan)
and laxative (sodium sulphate). Appropriate treatment must be made in
case of burns or skin eruptions. When surgical cases are due to
infection rather than simple shock or sympathetic irritation, antiseptic
injections of the bladder are indicated. In all cases alike a warm bath
is an important adjunct. When irritation is due to cantharides, it may
be calmed by camphor, 2 grains every three or four hours. Other anodynes
may be given as required. Rest is essential and, as appetite is
recovered, a moderate amount of amylaceous puddings. A warm building or
comfortable clothing is desirable.

NEPHRITIS.

The renal inflammations have not been fully investigated in the domestic
animals, and even in man, the pathology of several of the forms is still
enveloped in some measure of doubt. _In man_ the following conditions
have been noted:

1st. _Acute parenchymatous nephritis_ with enlarged kidney and
degenerated tubules.

2d. _Chronic parenchymatous nephritis_ with enlarged kidney and
degenerated tubules.

3d. _Acute diffuse_ (_desquamative, interstitial_) _nephritis_ with
enlarged kidney and glomeruli, tubules and connective tissue
degenerated.

4th. _Chronic diffuse_ (_desquamation, interstitial_) _nephritis._

5th. _Suppurative nephritis and pyelo-nephritis_, infection may be from
injury.

6th. _Perinephritis_: infection of connective tissue with adjacent
disease.

_In domestic animals_ the following distinctions have been made:

1st. _Acute nephritis._

2d. _Chronic nephritis._

3d. _Purulent nephritis and pyelo-nephritis._

4th. _Perinephritis._

ACUTE NEPHRITIS. ACUTE BRIGHT’S DISEASE.

Animals affected. Causes: hyperæmia, traumas, cold, chill, fever,
bacteria, toxins, overfeeding, nitrogenous food, raw potatoes, xanthin
products, acrid diuretics, diuretic insects, suppression of
micturition, skin lesions, burns, embolism, calculus. Symptoms: colic,
trembling, rigor, arched, stiff, tender loins, stiffness in quarters,
drags hind legs, urination frequent, movements of penis and testicle,
costiveness, grinding teeth, anorexia, vomiting (in dogs, cats and
pigs), fever, dropsies, uræmic convulsions, urine scanty, high
colored, red or bloody, thin, cloudy or turbid, albuminous, purulent,
oxalates, urates, hippurates, hæmatoidin, epithelium, mucus, casts.
Prognosis: resolution in three days, or uræmia, suppuration,
degenerations. Lesions: kidney enlarged, softened, friable, red,
yellow, black, purulent, glomerulitis, tubular nephritis, interstitial
nephritis. Treatment: rest, warm building, warm clothing, green or
sloppy, amylaceous food, bleeding, cupping, skin friction,
fomentations, warm bath, hot air bath, sinapisms, anodynes, laxatives,
diaphoretics, heart tonics, alkaline diuretics, paracentesis, bitters,
iron, phosphates, hydrogen peroxide, cubebs, etc.

_Genera affected._ This has been seen in horse, ox, dog, sheep and pig.

_Causes._ It is ascribed to the most varied causes, such as: hyperæmia,
blows and injuries on the back and loins, sprains of the loins, abrupt
wheeling when in galop, exposure to cold winds, and storms, especially
when perspiring and fatigued, sudden suppression of perspiration,
extreme terror, bacterial infection and infection by toxins (in
septicæmia, pyæmia, influenza, contagious pneumonia, uterine sepsis,
omphalitis, infectious angina (Friedberger), bronchitis (Siedamgrotzky),
glanders, tuberculosis). Among dietary causes are named: a rich
nitrogenous food (grains, beans, peas, vetches, cotton seed, clover),
raw potatoes in excess, cotton seed meal, agents that increase the
nitrogenous and xanthin bodies in the urine.

Dr. Alfred C. Croftan, in his experiments with xanthin bodies on
rabbits, found that xanthin and hypoxanthin produced great increase of
arterial pressure, atheromatous changes in the vessel walls consisting
in thickening of the intima, with small celled infiltration and necrotic
changes in different areas of the vessel walls. This in the kidney
produces the primary interstitial form of nephritis known as gouty
kidney and associated with retention of uric acid and other xanthin
bodies. The accompanying cardiac hypertrophy, so common with such
kidneys, he attributes to the increased intravascular pressure.

Irritant vegetables that are resinous or diuretic, and irritant diuretic
insects are incriminated (cantharides, caterpillars in grass, or on
plants, etc., lice on cabbages particularly,—Cruzel, Neubert). Irritant
drugs that are eliminated by the kidneys have been equally charged (tar,
carbolic acid, iodoform, chlorate of potash, nitrate of potash,
phosphorus, arsenic, lead, mercury). Compulsory suppression of
micturition is undoubtedly injurious in house dogs shut up, mares kept
long in harness, or horse on railway car, above all if this follows a
diuretic or drinking abundantly. In such cases it is altogether probable
that bacteria already exist in the blood or kidneys and take occasion to
attack the tissues weakened by the overdistension or other inimical
cause. This is all the more probable seeing that the kidneys are a
favorite channel for the elimination of bacteria present in the system.
It should be noted that nephritis is liable to supervene on extensive
skin burns, chronic dermatitis and other skin diseases. Some cases are
traceable to embolism, the clots coming from the lungs, heart or
arteries, in others the irritation is due to calculi in the renal pelvis
or tubules, and their attendant bacteria. These are especially common in
cattle that are winter fed on dry food. Again, the infection may have
travelled forward through the ureters from a pre-existing infective
cystitis.

_Symptoms._ There may be obscure or intense colic; trembling or rigor
may occur, yet is often omitted or unobserved; the loins are arched; the
hind feet are advanced under the belly, or there is frequent shifting of
the weight from one foot to the other; the walk shows stiffness of the
back and hind limbs which appear to straddle or drag behind; urination
is frequent in small amount, or there are frequent ineffectual attempts
to urinate; the patient is indisposed to lie down, and if he does so it
is carefully, with difficulty and groaning; the testicles are drawn up
and dropped alternately, the penis is often protruded from and retracted
within its sheath, the loins are sensitive to pinching, percussion, or
electric current; when mounted the animal drops under the weight; he
carries the head low and refuses to go fast. In bad cases there is
constipation, grinding of teeth, anorexia, and in dogs, vomiting.
Temperature may be normal or there may be considerable fever. Dogs may
lie curled up, with occasional tremors. Dropsical effusions are frequent
in the form of anasarca under the chest or abdomen, or beneath the lower
jaw, or as stocking of the limbs, or the effusion may occur into an
internal serous cavity. Convulsions may occur from brain poisoning by
urea or other retained urinary product.

In the slighter forms the severe symptoms may be absent, and the
_condition of the urine_ must be investigated as affording _the most
constant and characteristic_ phenomena.

The _urine_ is usually scanty, high colored, of a high specific gravity
and is passed often with pain and groaning. At the outset of an acute
attack it may be bloody; later it may be only cloudy or turbid from the
excess of epithelial and pus cells, leucocytes, salts and albumen. Early
in the disease the casts may contain red blood cells, and renal
epithelium, later leucocytes, nuclei, granules, pus cells, crystals and
other matters. Albumen is usually abundant as demonstrated by boiling
and nitric acid.

_Soda carbonate crystals_, rhomboid, rosette-shaped or spherical and
effervescing with acetic acid, abundant in normal herbivorous urine may
be greatly reduced or absent in nephritis.

=Soda oxalate crystals=, tetrahedral and insoluble in acetic acid, and
normal in herbivora and carnivora, are increased if the urine is acid as
in severe nephritis, but also in rheumatism, tetanus, septicæmia,
angina, heaves, and other affections with defective æration of the
blood.

=Ammonio-magnesian phosphate crystals=, rhomboid but insoluble in acetic
acid, are found in alkaline (ammoniacal) or neutral urine, and appear to
be often due to intestinal fermentations.

_Cystine crystals_, flat hexagonal plates, precipitated in healthy
urine, but dissolved by ammonia are absent in retained and fermented
specimens.

=Uric acid crystals=, rhomboids and plaques, brick red, and normal in
the urine of carnivora and flesh-fed omnivora, may be present in
herbivora not only in acute nephritis, but in other extensive
inflammations attended with anorexia and the consumption of the animal
tissues.

=Hippuric acid crystals=, right rhombic prisms and their derivatives,
and insoluble in hydrochloric acid or ether, are greatly increased in
all febrile diseases in herbivora, nephritis included.

=Hæmatoidin crystals=, fine needles or bundles of the same, yellowish
red, are found in nephritis, hæmaturia, heaves, etc.

=Epithelium, if columnar=, points to disease of the kidney tubes, though
very similar cells are derived from the urethra in both male and female.
Squamous epithelium points to the cystic mucosa and is not increased in
nephritis.

=Mucus= in cylindroid form may point to nephritic congestion or
inflammation, but this may be present in health, and may show in
irregular masses derived from the renal pelvis or the bladder. Mucous
casts are always extremely elastic and mobile, and lack the even clear
cut margins of the casts of nephritis. They are much more common in
horses urine than in that of other animals.

=Tube casts= are especially indicative of nephritis and exudation into
the uriniferous tubes. They are much firmer than the mucous cylinders
and have smoother and more even margins. If relatively thick and
straight they probably come from the straight tubes; if sinuous or
twisted, from the convoluted tubes. With a similar basis substance they
often enclose different solid bodies and have been named
accordingly:—=epithelial casts= when containing cylindroid, or
polyhedral cells may be unhesitatingly referred to the uriniferous
tubules:—=granular casts= in which the homogeneous cast is impregnated
with granular cells and free granules of proteid, fatty, or mineral
matter, point directly to inflammation affecting the uriniferous tubules
and their epithelial lining:—=blood casts= enclosing red blood globules
imply hemorrhage, or congestion or inflammation of the tubules, with
blood extravasation or diapedesis:—=casts containing leucocytes and pus
cells bespeak= suppurative inflammation of the tubules:—=calcareous
casts= entangle numerous crystals and granules, mainly of lime
carbonate, and effervesce with acetic acid:—=hyaline casts= are
homogeneous, clear, so transparent that it is sometimes necessary to
stain them with iodine or aniline to make them distinct; they are found
in nephritis and especially in the chronic forms:—=colloid casts= or
=waxy casts=, or =amyloid casts= may designate a class of firmer
cylinders, clear, homogeneous and refractive, and often bearing fatty or
blood globules, crystals or fungi. They may have a yellow color, or they
may give the amyloid mahogany reaction with the iodo-potassic iodide
solution (even in the absence of amyloid degeneration of the kidney;
Jaksch).

_Progress._ Acute nephritis may advance for three days or more and then
terminate in resolution, or go on to complete anuria with coma, to
suppuration, gangrene or chronic nephritis.

=Resolution= is marked by general improvement of pulse, breathing and
expression, clearing of the urine, and return of appetite. The urine may
remain albuminous for eight days longer.

=Complete suppression of urine= has persisted five days in cattle
(Funk), and seven days in horses (Friedberger), accompanied by intense
fever, dullness, stupor and coma ending in death from uræmia.

=Purulent urine= is white, milky, albuminous, granular, with epithelial
cells and casts and pus cells, showing their double nuclei with acetic
acid. There are usually rigor, hyperthermia (106° F.), thirst,
intermittent colics, diarrhœa, perspiration, uncertain walk, and stocked
legs. Convulsions have been noticed in the horse (Didie), cow (Pflug)
and bitch (Trasbot). The horse may turn in a circle (Friedberger) or
have amaurosis (Didie). Death usually occurs in two weeks.

=Gangrene= is likely to prove fatal. Berger has seen death occur in
three days in the horse, and Trasbot in four days in a cow, after a
large cantharides blister.

_Pathological Anatomy._ The kidney is enlarged, soft, friable, dark red,
yellow with red spots, or having areas of hemorrhage. When fatty it is
marbled, pale yellow or white and red. The capsule is easily detached.
On section it is bloody, oozing or even dropping blood, or a pale creamy
fluid. The pelvis contains urine, thick, gelatinoid, bloody or purulent.
The latter condition must not be confounded with the thick pus-like
mucus which normally occupies the renal pelvis in the horse.

The lesions of the secreting portions of the kidney will vary with the
concentration of the inflammation in one or other of the separate
tissues.

In =glomerulitis= from toxic irritants, the capsules enclose an
albuminous liquid exudate, the capillaries are overdistended, their
walls thickened and cloudy, and thrombi with an excess of red globules
and leucocytes block them at intervals. This capillary obstruction
extends to the plexus surrounding the convoluted tubules.

In =tubular nephritis= there is congestion of the plexus covering the
convoluted tubes, and the epithelium shows cloudy swelling, with fatty
granules and hyalin droplets in the desquamating cells.

With =interstitial nephritis= there is an exudate into the interstitial
connective tissue between the tubules, and into the tubules, forming
hyalin casts. The epithelium of the tubules are swollen, granular,
opaque and desquamating.

In =suppurative nephritis= may be found all stages of abcedation from
minute points, gray or yellow, and only just visible to the naked eye,
in the midst of the deep red congested tissues, through the larger white
suppurative areas, to the extensive abscess formed by a coalescence of
the many, the intervening tissue having broken down by a necrotic
disintegration. In the earlier stages the pus infiltrates the parenchyma
so that it may be comparable to a sponge filled with this liquid.

_Treatment._ The first consideration is rest, with a warm building or
clothing to solicit the action of the skin and lessen the work of the
kidneys. Warm summer weather is favorable, or we should secure a sunny,
comfortable, loose box, or a building heated by a stove. In default of
this, warm woolen blankets, hood and leg bandages should be secured. If
the case is mild enough to allow of appetite, the food for herbivora may
be green food in summer and carrots, beet, turnip, potato or ensilage in
winter. The dog may have buttermilk or sweet milk or mush and milk. Meat
is objectionable because of the amount of urea and other urinary
products which it produces.

Trasbot strongly recommends general bleeding in strong, vigorous horses
and cattle, attacked by the disease in an acute form, but deprecates it
in the lymphatic, fat, or debilitated.

Omitting the general bleeding, one can always find a good and safe
alternative in bleeding the animal into his own tissues. Shaving the
loins and cupping has often an excellent effect. An approach to this may
be had by vigorous rubbing by several men at once, of the limbs and the
whole surface of the body, by warm fomentations over the loins by means
of spongio-piline or surgeon’s cotton covered with dry blankets, or by
winding a hose round the body through which warm water is forced, or
finally by a bath of steam or hot air, or in small animals of warm
water. The dog may be placed in a bath of 80° or 90° F., which is
allowed to gradually cool to 65° or 70°. In all these cases the greatest
care must be taken to avoid chill when the animal is taken out. He
should be quickly rubbed dry in a warm room and blanketed.

Counter-irritants act in the same way, and mustard or hot water hotter
than the hands can bear may be applied. Turpentine, cantharides and
other diuretic counter-irritants must be carefully avoided. An old
practice of laying a freshly removed sheep skin over the loins, with the
flesh side inward, often causes a distinct exudation, thickening of the
skin and derivation.

A damp cloth, laid across the loins and thoroughly covered with dry to
prevent any evaporation and chill, will usually give great relief and
may be kept on for days.

Internal medication must at first be mainly anodyne, laxative and
diaphoretic. The two latter classes are at once derivative and
eliminating, carrying out through other channels, waste products that
would otherwise have taxed the kidneys.

Among anodynes, the bromide of camphor (horse, 1–2 drs., dog, 2 to 5
grs.), bromide of potassium (horse, 1 dr., dog, 1 to 3 grs.), or
hyoscyamus may be used, and repeated twice daily.

Purgatives must be restricted to such as have no tendency to act on or
irritate the kidneys. Castor oil, or sweet oil for the larger animals,
or for the dog senna or jalap, may be given every morning to secure free
movement.

As diaphoretics, ipecacuanha, Dover’s powder, tartar emetic, and even
pilocarpin may be used. The last named agent is especially useful when
dropsy sets in, or uræmic stupor or coma threatens (horse 3 grs., ox 7
grs., dog ½ to ⅓ gr. according to size). If the heart shows weakness it
must be sustained by digitalis, strophanthus, caffein or
nitro-glycerine, and the pilocarpin withheld.

In a sufficiently strong subject the stupor or coma may be met by the
abstraction of blood, which benefits by the dilution of that which is
left.

Eclampsia may be further met by the inhalation of ether or chloroform,
or the rectal injection of chloral or bromide solution.

As the inflammation abates, if the action of the kidney is still
insufficient in spite of the free drinking of pure water, alkaline
diuretics may be given in small doses (tartrate, acetate or citrate of
potash, bicarbonate of soda, saltpeter).

In excessive dropsy avoid sloughing by lancing the most tensely swollen
parts to allow drainage, and keep the parts disinfected with carbolic or
other antiseptic lotion. For ascites or hydrothorax, aspirate, and apply
a compressory bandage.

During convalescence a course of bitters (cinchona, salicin, gentian,
nux vomica) and iron (phospho-tartar, iodide or phosphate) will often be
called for. Anæmia may be met by doses of peroxide of hydrogen or the
inhalation of oxygen.

In the advanced stages benefit may accrue from the use of small doses of
cubebs, copiaba, oil of turpentine or buchu, which have a tonic action
on the renal mucosa.

PURULENT NEPHRITIS.

Causes: general, traumatic, metastatic, infective, wounds, shocks,
strains, blows, falls, crowding, heavy loads, calculi, infective
embolism. Lesions: miliary or large abscesses, diffuse suppuration,
softening, disintegration, fistula. Symptoms: obscure, nephritic
symptoms following distant abscess, chill, hyperthermia, general
symptoms of nephritis, pus in urine, anæmia, emaciation. Treatment: to
external wound, antiseptics, evacuate abscess, extirpate kidney with
pyonephrosis, in dog or pig, calcium sulphide, sulphites, copiaba.

_Causes._ Aside from the main causes of nephritis, the suppurative form
may be determined by traumatic or metastatic infective conditions. Under
_traumatic_ factors may be named punctured or gunshot wounds, shocks and
strains connected with falls, blows, crowding, compression, too heavy
weights on the back (pack, rider, two wheeled cart loaded too heavily
forward and going down hill), and finally calculi in the uriniferous
tubules. Under _metastatic_ factors come all infections, pyæmia,
omphalitis, any suppurative affection of the lungs, (abscess, pneumonia,
broncho-pneumonia), pharyngitis, etc. Embolic renal abscess may start
from endocarditis, arteritis, or pulmonary phlebitis.

_Lesions._ There may be a circumscribed renal abscess like a good large
orange, or many small gray spots like millet seeds, peas or hazel nuts,
having purulent centres and containing pus cocci or bacilli. In other
cases a diffuse inflammation suppurates throughout till the whole gland
becomes a pulpy mass of pus, blood and broken down kidney tissue
(pyonephrosis). In traumatic cases the pus centres around the wound or
injury, perhaps invading adjacent parts, and even communicating through
the skin externally along the line of the original wound. The pus may
burrow in different directions in the cortex or under the capsule with
abscess at intervals (perinephritis), or along the vessels to the
medullary structure.

_Symptoms._ These are often obscure. The sudden appearance of kidney
disease in the course of a suppurative affection elsewhere, the
extension being ushered in by a chill or rigor or attended by a
succession of these, and the course marked by a variable hyperthermia is
very suggestive. Stiffness and weakness of the hind parts and tenderness
of the loins are significant; also, in carnivora and omnivora, nausea
and vomiting. When the kidney can be felt by the hand in the rectum or
in the small animals, through the flaccid abdominal walls, the manifest
enlargement, the tenderness, and in some cases even fluctuation will
assist in diagnosis. In such cases, puncture by a large hypodermic
needle, or a small trochar may betray the presence of pus and complete
the diagnosis. If the pus escapes into the pelvis of the kidney it may
be recognized in the urine. The case is very liable to become chronic,
and is then marked by anæmia and emaciation.

_Treatment._ When an external wound exists it must be treated,
antiseptically, with boric acid, potassium permanganate, or other
antiseptic lotion. If a single large abscess exists, puncture evacuation
through needle or trochar, and washing out with an antiseptic solution
is the obvious resort. Any foreign body must of course be removed. If
the suppuration is diffused through the whole mass of softened kidney,
the resort of extirpation may be considered. This is always dangerous as
provocative of infectious peritonitis, but it is less so in dogs and
swine than in other animals owing to their natural antagonism to pus
microbes. The operation should be attempted extraperitoneally, the
incision being made beneath the anterior lumbar transverse processes and
carried inward through the sublumbar connective tissue. The renal artery
will require ligature with antiseptic catgut and all manipulations
should be aseptic or antiseptic. Even if successful, this operation
leaves the subject in a dangerous state, as in case of kidney disease at
any future time, there is no second kidney to compensate for the
temporary loss of function and uræmic poisoning is to be dreaded.

Apart from surgical measures the general treatment would be largely the
same as for acute infectious nephritis. As antiseptics calcium sulphide,
the different sulphites, copiaba, etc., will be indicated.

PERINEPHRITIS.

Definition. In cattle on low damp lands, acrid plants, sprain, blow,
calculus, from purulent nephritis, in anæmia. Symptoms: of nephritis,
soiling of tail or prepuce, albumen, pus or blood in urine, lameness,
unilateral or bilateral, lumbar swelling, in small animals
fluctuation, history. Lesions: abscesses around kidney, under capsule,
intercommunicating. Treatment: as in purulent nephritis.

Suppuration in the connective tissue between the kidney and its capsule
is seen in cattle in low condition, on damp, unimproved soils like
undrained river bottoms and estuaries, abounding in acrid and diuretic
plants. Even among such animals it is rare and has probably a directly
exciting cause in a sprain or blow on the loins, or the presence and
movement of a renal calculus. It may extend from suppurations in the
substance of the kidney and to such extension the weak or anæmic
condition materially contributes. In man, in which such conditions have
been more frequently observed, a weak or cachectic condition is
considered as an essential accessory factor along with the traumatic
lesion (R. Harrison). Similar conditions may be expected to bring about
perinephritis in any one of our domestic animals. The author has
observed it especially on the low lands on the banks of the Ouse in
Yorkshire, England.

_Symptoms._ These are mainly those of nephritis in general, shivering,
stiff movement in the hind limbs, straddling, frequent passage of urine,
straining, difficulty in lying down and rising, tenderness of the loins,
dropping when mounted, groaning when turned in a short circle. If the
suppuration communicates with the pelvis of the kidney there may be, in
females, soiling of the tail, and in males of the prepuce. Blood may be
passed with the urine, and pus cells and albumen are found when it is
examined. If one kidney only is affected, there is lameness in the
corresponding hind limb, the special feature being inability to extend
it backward. A swelling on the one side of the loins, and beneath the
lumbar transverse processes just posterior to the last rib, is likely to
be a marked symptom, and if this persists and is especially prominent at
one point, an exploratory incision or puncture will detect the presence
of the pus. Fluctuation can rarely be detected, yet in small animals
with very flaccid abdomen, the swollen, tender kidney and even
fluctuation should be detected at times. The history of the case, the
low, damp pasturage, the access to acrid plants, the alimentation with
hay or grain covered with cryptogams, the fact of an injury and the low,
weak, anæmic condition of the animal should contribute to a satisfactory
diagnosis.

_Lesions._ In bovine kidneys affected in this way we have found general
inflammation and exudation around the entire kidney and inside the
capsule, with numerous small abscesses, in many instances communicating
with each other. They may extend through the capsule and invade
surrounding organs.

_Treatment._ In the treatment of cases of this kind the general
principles of therapeutics for nephritis are about all that can be
attempted in the lower animals. Fomentations over the loins are
especially desirable as a means of relieving the suffering, and
moderating inflammatory action. To the same end is the allowance of
plenty of pure water as a diluent. Then the various agents that
antagonize suppuration may be thought of, and some one selected for use.
Beside the antisuppurants already mentioned one may use copiaba, cubebs,
or turpentine in small doses, salicylates, or the sulphide or sulphite
of calcium. Surgical interference by puncture or incision and antiseptic
irrigation can only be thought of when the abscess is single and
circumscribed; never when the whole periphery of the organ is involved.
In the latter case the only rational surgery would be the desperate
resort of the removal of the entire kidney.

PYELITIS. PYELONEPHRITIS. INFLAMMATION OF THE RENAL PELVIS.

Definition. Causes: primary from vegetable irritants in food, toxins,
cryptogams, pelvic calculus, strongylus gigas; secondary from renal
calculus, parasite, tubular urethral or vesical infection, infecting
deposits, metastasis. Symptoms: as in nephritis, pus, blood, or
albumen in urine, tender, arched loins, purulent polyuria, with
spheroidal epithelium. Diagnosis. Lesions: inflammation, calculus,
etc., in pelvis. Treatment: pure water, sodium bicarbonate,
antiseptics, balsams, fomentations, piperazin, extraction of calculus.

Suppurative inflammation of the mucosa lining the renal pelvis may occur
in the acute or chronic form.

_Causes._ It may be either primary or secondary. As a =primary= disease
it may be the result of poisoning by irritant diuretics such as
cantharides, turpentine, colchicum or balsams, or shoots of the
coniferæ, it may be due to the passage of the irritant products of
cryptogams found in musty fodder or grain, or it may come from the
irritation caused by the toxins of bacteria developed in the system or
in food or drink. Cases that develop from the irritation of a pelvic
calculus or precipitate, and from the presence of the strongylus gigas
(in dogs) may also be placed in this class.

As =secondary= causes are those in which the inflammation starting in
the uriniferous tubes extends down to and implicates the pelvis, and the
still more frequent instances of extension of purulent infection upward
from the ureter, bladder or prostate, so as to involve the pelvis. So in
blocking of the urethra by strongylus, stricture, clot or calculus, and
in spasm of the sphincter vesicæ, the delayed urine is liable to undergo
fermentation with evolution of ammonia, and not only the bladder but the
ureter and renal pelvis may suffer. Again, the occurrence in the kidney
of the hyperplasia of cancer, glanders (horse) and tuberculosis (cow)
may be the direct cause of pyelitis. Similarly foci of infection in the
kidney may be found in distemper in the dog, and in the contagious
pneumonia and influenza of the horse. In man infection from the bowel
through the migration of the bacillus coli communis to the devitalized
kidney and contents in hydronephrosis, has been traced, and the
liability to this must be still greater after the surgical insertion of
the ureters in the rectum as a substitute for the obliterated bladder
and urethra. Again, in the intra-arterial migrations of the strongylus
(sclerostoma) armatus pus microbes may be carried to the kidney and
reach the pelvis.

_Symptoms._ These are in the main those of nephritis with marked rigors.
The presence of pus cells and albumen in the urine may come from
suppuration in the substance of the kidney itself, or sub-capsular
abscess opening into the pelvis, or it may come from cystitis,
prostatitis or urethritis. The special stiffness and tenderness of the
loins, polyuria in which the liquid is purulent, but free from
uriniferous casts, and in which it is charged with the spheroidal
epithelium of the pelvis (not the columnar of the tubules), may afford
presumptive evidence of pyelitis. But pyelitis is usually combined with
nephritis or cystitis and the complications prevent diagnosis. In some
cases the urine is scanty and strongly albuminous, and in others a round
calculus will block, at intervals, the opening of the ureter giving rise
to obstruction of the flow from that kidney and the occurrence of
violent renal colic lasting until the stone is again dislodged backward.

_Diagnosis_ cannot often be certain. Purulent urine, with a considerable
number of the spheroidal cells of the pelvis, and the general signs of
nephritis may be taken as diagnostic. A great excess of such epithelial
cells would on the contrary point to cystitis.

_Lesions._ In the early stages the mucosa of the pelvis is congested,
red, and sometimes, with calculus, hæmorrhagic. Later it becomes
thickened by exudate, which fills also the submucous tissue. In some
instances the pelvis is distended by an impacted calculus, in others the
obstruction of the ureter by an impacted calculus or a swelling has led
to overdistension of the pelvis, and ammoniacal fermentation of its
contents. Coincident inflammatory lesions of the kidney, ureter, or
bladder are common.

_Prognosis_ is not hopeful. Where it has resulted as a descending
infection from the kidney, the severity of the primary lesion renders
the case a grave one, while if it has been an ascending inflammation
from the bladder it is no less so.

_Treatment._ Diluent (watery) diuretics are especially indicated. Pure
water may be given _ad libitum_. To this may be added if necessary
moderate doses of bicarbonate of soda or potash with such non-irritating
antiseptics as salicylic acid, salicylate of soda, sulphite of soda,
sulphide of calcium, quinia or chamomile. Trasbot even recommends small
doses of vegetable astringents, balsam of Tolu, or Peru or of Copiaba,
or oil of turpentine or tar water. Apart from simple water, the diuretic
agents may be used with greater freedom if the solid parts of the kidney
are little or not at all involved and if the urine contains no casts of
the uriniferous tubes.

Benefit may also be obtained from fomentations, or cupping of the loins,
and even from the application of mustard and counter-irritants.

If the active symptoms subside the continued use of tonics would be
indicated, especially quinia, and also of the balsams with the view at
once of antisepsis and toning up of the mucous membrane.

In case of calculus of the pelvis surgical extraction is virtually the
only resort, though a very desperate one. Its increase may be retarded
or prevented by antisepsis, a liberal use of water, and the exhibition
of piperazin or some of the essential oils.

CHRONIC NEPHRITIS.

Cases destroyed as eating their heads off. Causes: sequel of acute
nephritis, swill, lead, experimentally, microbian invasions, toxins,
metastatic embolism, extension from aortic disease, sclerostoma,
nitrogenous overfeeding, toxins of putrid food, or cryptogams,
valvular disease of the right heart, rheumatism, heaves, calculus,
starvation, debility, retention of urine. Symptoms: emaciation, flabby
muscles, lack of vigor, stiff loins and quarters, short step,
straddling, fatigue under slight exertion, groaning in trot, or in
turning, droops when mounted, slow to rise on hind limbs, poor
capricious appetite, anæmia, stocked legs, dropsies, urine of lower
density, albuminous, with granular epithelium and casts, abundant in
early stages, scanty with weakened heart and degenerated kidneys.
Secondary palpitations, bronchial catarrh, pneumonia, hemorrhage,
stupor, lethargy, vertigo, etc. Lesions: recent cases, kidney large,
cortex firm, capsule adherent, with granular fatty debris, and tubular
casts; old cases, kidney contracted, fibroid, glomeruli and tubules
atrophied. Bronchitis, pneumonia, hepatic cirrhosis, heart enlarged,
fatty, dilated, insufficient valves. Prognosis unfavorable. Treatment:
gentle exercise, warmth, succulent food, amylaceous, tonics, iron,
bitters, mineral acids, heart tonics, for polyuria bromides or
iodides, balsams, pilocarpin, fomentations or sinapisms to loins.

Chronic nephritis has received little attention in the lower animals for
various reasons. The lower animals largely escape the causative factors
of alcoholism and chronic lead and copper poisoning, and when suffering
from any chronic affection that disqualifies the animal for use and
renders it anæmic and emaciated it is naturally sacrificed to save the
cost of maintenance. In spite of this a considerable number of cases
have been recorded in horses, and cattle and especially in dogs and
cats.

_Causes._ Cases of acute nephritis sometimes improve and give promise of
recovery without completing the work of convalescence. Trasbot notes
such cases in the dog, and Dickinson in the ox. Alcoholic nephritis and
degenerations are to be sought for especially in cattle kept on
distillery and brewery dregs. Lead taken in small quantities in soft
water that has run through lead pipes or stood in leaden cisterns
produces in cows and other animals chronic affections of the kidney.
Ellenberger and Hofmeister have produced the disease experimentally with
lead and copper respectively.

Microbian invasions of the kidney that advance slowly like glanders and
tubercle are further causes of chronic nephritis. Other secondary
microbian infections of the kidney are complications of infectious
diseases in other parts, including abscess, pyæmia, septicæmia,
ulcerative endocarditis of the left heart, bronchitis, pneumonia
(Fröhner), and of others less directly in the line of the circulation,
as omphalitis, uterine phlebitis (Lustig), abscess of the nasal sinuses,
bones, and fistulæ (Trasbot).

In other cases the nephritis is evidently a result of the irritation
caused by toxins in process of elimination by the kidneys, as there is
no evidence of a nephritic infection.

In some instances minute emboli originating in the lungs or heart,
become the starting point of the nephritis, which slowly extends by
reason of infection or low condition and special susceptibility. Disease
of the aorta or renal artery may lead to this condition as noticed by
Cadeac and Lustig. Cadeac has also noticed its association with aneurism
of the mesenteric arteries so that the strongylus (sclerostoma) armatus
may be considered as a factor. Again in old horses and dogs it has been
associated with atheroma of the aorta and renal vessels (Trasbot).

Overfeeding is not without its influence, especially when on animal
food, which charges the kidneys with excreting an excess of the
irritating urea and uric acid, and this is one reason why it is far more
frequent in house dogs than in other domestic animals. When the meat is
already decomposing and putrid there is the added evil of a quantity of
toxins and even of microbes to be eliminated from the system by the much
abused kidneys. Add to these that the dog’s urine is even in the normal
condition more dense and contains more irritating ingredients than that
of herbivora, and that owing to the slight activity of his perspiratory
apparatus he can obtain less relief from the skin, and we find a
substantial ground for the prevalence of chronic nephritis in this
animal.

Disease of the valves of the right heart or dilatation with
insufficiency of the auriculo-ventricular valves is a potent cause of
nephritis, the reflux of blood into the veins and the increased venous
tension, speedily producing passive congestion and a slow type of
inflammation in the kidney. This factor is especially liable to operate
in dogs, which are particularly obnoxious to rheumatism and valvular
ulceration, and are very subject to nervous cardiac disorders; in horses
that have contracted heaves; and in beef breeds of cattle which suffer
from fatty degeneration of the heart with dilatation.

The influence of calculi must not be overlooked, whether they are lodged
in the pelvis, the chalices, or the uriniferous tubules. Their tendency
is to induce local irritation and exudation, with fibroid degeneration
and thickening of the walls of the tubules or pelvis and of the adjacent
tissue.

When to one or more of the above conditions there are added overfeeding
or what is worse a low condition from starvation or unwholesome food
(permeated by bacteria or cryptogams or containing vegetable acids), and
when to crown all there are frequent exposures to cold or wet, we have a
vicious combination especially conducive to kidney trouble.

Habitual retention of urine in mares in harness, in house dogs, or in
horses in railway cars, and violent exertion, or sprains of the back are
among the remaining accessory causes.

_Symptoms._ These are often slight or obscure, so that not only owners
and attendants but even veterinarians are liable to overlook them. Loss
of flesh, flabbiness of the muscles and a lack of spirit and energy are
among the first symptoms. The _horse_ appears stiff, especially in his
loins and hind limbs, and fails to advance the hind feet as far under
the belly as formerly, and straddles more. When put to work he is early
fatigued and appears unfit for sustained exertion. His movements are
slow and if urged to a trot he may even groan with every step and
quickly settles back to his sluggish pace. If turned sharply round on
himself he does so with difficulty and often groans. When he is mounted
or when the loins are pinched he may droop to excess. If you come on him
lying down, and urge him to rise he may rise on his fore limbs and sit
on his haunches until urged before he makes any attempt to raise himself
on his hind. The _dog_ may spend most of his time in the kennel, and
show little disposition to run, play or hunt. On the contrary the owner
may have to call him several times before he will come out and then he
moves listlessly, wearily and even weakly.

In all animals the appetite is poor or capricious, and the patient
gradually loses condition, at first slowly and later, after a few weeks
or months, more rapidly. The advance of anæmia is also steadily
progressive.

Dropsical effusion is not uncommon. It is often prominent in the horse
as stocked limbs, but may be absent for a length of time. In other
animals it is more likely to appear later in the disease and under the
chest or abdomen or in one of the internal serous cavities. Trasbot has
found it absent for months in the nephritic dog.

The exploration of the kidney through the flaccid abdominal walls in
small animals, and through the rectum in small horses and cattle, may
reveal renal tenderness and even swelling. If there is a tendency to
frequent passage of urine in small quantities, or to straining without
micturition, the indication is of value.

There may be little or no fever, and, when left at rest, little evidence
of discomfort.

Any indication of urinary trouble, and especially with dropsy, weakness,
flabbiness and anæmia and a subnormal temperature, should lead to
examination of the urine, as a crucial test. A high density is good
ground for suspicion. But this is not constant. In advanced cases
(chronic interstitial nephritis, small white kidney, atrophic nephritis)
it may be 1015 to 1025, in exceptional advanced cases with polyuria, it
may be 1010, 1005, or even 1001. With such a condition, however, there
is great anæmia, pallor of the mucosæ, and prostration. Tested with
nitric acid and heat, the urine throws down an abundant precipitate of
albumen. Under the microscope it shows a profusion of granular,
degenerating epithelial cells, and casts of the uriniferous tubes.

_Progress._ The course of the disease is usually slow, extending over
several months, but with a tendency to constant advance. The thirst
increases and the urine increases in amount, clearness and levity. There
may supervene extreme sluggishness, dropsies, anæmia, and weakness,
irritability of the heart, and palpitations on slight exertion. So long
as the heart’s action is strong, elimination may be maintained and life
prolonged for months (in cow, Dickinson), or years (Friedberger and
Fröhner). When the heart’s action becomes weak, elimination is rendered
imperfect and the animal shows catarrh of the lungs or bowels (common in
dogs), local inflammation of the lungs, pleura or pericardium, or
œdemas, or hæmorrhages. The toxic effect on the nerve centres is shown
by stupor or lethargy, or vertigo. When an abscess forms it is
associated with a temporary rise of temperature (Trasbot). The patient
may die in convulsions, in a state of coma, or by gradually advancing
debility and failure of the heart.

_Lesions._ In cases of comparatively =short standing= the kidney is
usually of full size, or somewhat enlarged, with firmly adherent capsule
and rough or even nodular surface. The surface of the cortex may be red
or grayish or parti-colored, pink and gray. The cortical portion is firm
and it may even be attenuated somewhat, while the medullary portion,
naturally lighter, has often grayish streaks converging toward the
hilus. When the gray streaks are scraped with the knife a serous fluid,
mixed with fatty granules or globules, is obtained. The glomeruli may be
still about the normal size with some increase of the epithelial tuft
cells. The tubules contain casts (colloid, hyaline, granular), and their
epithelium normally columnar, are flattened down to cubes and are
swollen, granular or fatty.

In cases of =older standing= the connective tissue has usually undergone
a marked increase. The capsule is thick, dense and adherent. The
cortical substance is shrunken with a great increase of the fibrous
elements, and the same holds true of the medullary portion. In
consequence of this, even in the cortical substance the white or gray
color predominates. The parenchymatous tissue (glomeruli, tubules) have
greatly shrunken. In connection with the contraction of the forming
fibrous hyperplasia, there is a general shrinkage of the kidney in size,
it may be to one-half its original volume. Trasbot reports a case of
nephritis, of 8 months standing, in the dog, with a kidney half the
normal size. In the end the parenchyma may have practically disappeared,
and the kidney may have shrunken to a small, firm, white, fibrous mass.
Abscess of the kidney is exceptionally met with (Laurent, Lafosse).

_Lesions of distant organs_ are not uncommon. Bronchitis, pneumonia,
pleurisy, insufficiency of the tricuspid or mitral valves, dilated
heart, hypertrophied or fatty heart, congested or fibroid liver,
arteritis, and dropsies are among such morbid conditions.

_Prognosis._ This is almost always unfavorable. Death may be delayed for
months or years, and partial transient recoveries may take place but a
restoration to normal structure and function is not to be looked for.

_Treatment._ This cannot be expected to be much more than palliative.
The avoidance of overwork, and of the exposure to cold and wet, and the
securing of a free action of the skin by warm buildings and clothing,
are essential. The diet should be easily digested and non-stimulating,
for _herbivora_ green food, carrots, roots, apples, silage, with a
moderate allowance of oats to counteract weakness and anæmia; and for
_carnivora_, milk, buttermilk, mush made of oat, wheat or barley meal,
with, if necessary, a slight allowance of tender raw meat. Tonics fill a
similar need. Iron and bitters may be combined. Or hydrochloric acid or
nitromuriatic acid with bitters (nux, calumba, salicin, quassia) may be
tried. These acids are especially valuable when the case has originated
in or is maintained by calculi, indigestion or hepatic disorder. When
the heart is defective in tone, it may be stimulated by small doses of
digitalis, strophanthus, sparteine, caffein, or nitro-glycerine, or to a
certain extent by strychnia or nux. These, however, must be used with
judgment, if it is found that they aggravate the case by increasing the
arterial tension. In those cases in which there is an excessive
secretion of watery urine, the possible source of this in musty aliment
should be avoided, and the flow checked by nux vomica, in moderate
doses, and bromide or iodide of potassium in full doses. When, on the
other hand, the urine becomes scanty and dense, the great danger of a
toxic action must be met by agents that favor excretion. Pure water at
will is perhaps the least objectionable of such agents, but potassium or
sodium acetate or citrate, or even sodium chloride, in weak solution,
may be given. In some cases benefit will come from a moderate use of the
balsam of copiaba, or the leaves of buchu, which may improve the tone of
the secretory elements. The most promptly effective of these agents is
pilocarpin (Friedberger and Fröhner), but it has the serious drawback of
inducing profuse and dangerous depletion and debility. Yet in careful
hands, and with good cardiac tone, it may often be used to advantage.

Fomentations over the loins, warm baths and mustard embrocations, may at
times be beneficial. Attempts have been made to check the hyperplasia by
the use of arsenic, mercury or the compounds of iodine, but their use in
such cases is based on theory rather than accomplished results.

HYPERTROPHY OF THE KIDNEY.

Hypertrophy of both kidneys has not been recorded in domestic animals.
On the other hand the extraordinary development of one in compensation
for the loss or atrophy of the other is not uncommon. In this the organ
follows the general law of adaptation, seen in the double symmetrical
organs (testicle, etc.) and the more so that its functional activity is
indispensable to life. Among _causes_ are: blocking of an ureter by
calculus, worms, neoplasm, nephritic abscess, gangrene, etc. The
enlargement of the remaining kidney is a vicarious act and essentially a
physiological one.

If compensation is perfect, it may be impossible to detect symptoms
apart from those of the primary disease.

_Prognosis._ Life is endangered in case of any subsequent kidney
disease.

ATROPHY OF THE KIDNEY.

Result of hyperplasia of connective tissues and compression and
absorption of parenchyma. Unilateral or partial. Causes: chronic
productive inflammation, calculus in tubes, ureter, or pelvis, tumor,
retention cyst, embolism. Lesions: sclerosis of kidney, firmness,
pallor, anæmia, lack of glomeruli and tubules, cysts, congenital,
urinous retention, colloid. Symptoms: reduced secretion, palpation of
kidney. Treatment: Prevention: arrest conditions, abundance of water,
succulent food, parasiticides, operation on cysts, counteract
nephritis.

Unlike hypertrophy, this is constantly the result of a pathological
process. So long as a normal functional activity of the secreting
elements is carried on, such parts must maintain their size and healthy
characters. But with the compression of such secreting elements
(glomeruli and convoluted tubes) by a hyperplasia of connective tissue,
by pressure from without or from the damming back of the urine in the
pelvis and tubes, the secretory elements are absorbed and removed, and
the final result is a general atrophy. If such atrophy appears in both
kidneys at once it can only be very partial in extent, as extreme
atrophy of both, with loss of their secretory function, would entail
poisoning and death from the retained urinary products. The comparative
frequency of the disease may be inferred from the reports of the numbers
of specimens found by Barrier and Moussu in old horses in the dissecting
rooms. The latter observed a dozen cases in a single winter, other
examples are recorded by Cadeac (horse), Soula (swine) and Trasbot (in
various animals).

_Causes._ The most common source of the condition is the occurrence of
chronic productive inflammation. The new product in such cases, if not
pus, or a growth that rapidly passes into fatty or granular
degeneration, or into gangrene, tends to form tissue of a low
organization, especially fibrous. The resulting increase of the fibrous
trabeculæ, in undergoing subsequent contraction necessarily compresses
the secretory tissue and the final result is a visible and, it may be,
extreme wasting. Hence any slowly advancing productive inflammation is
liable to result in absorption and removal of the kidney parenchyma, and
distinct atrophy of the gland.

Again the obstruction of the ureter by a calculus in the pelvis which
falls into the infundibuliform entrance, or a stone arrested at any part
of the duct (or even of the urethra) or by worms, hydatids, cysts or
tumors, throws back on the kidney the secreted urine, which distending
the pelvis and uriniferous tubes leads to direct compression and
absorption of the secretory parenchyma. Direct compression of the kidney
by an adjacent tumor will act in a similar manner. Retention cysts by
their gradual increase and augmenting pressure cause absorption of the
gland tissue.

The blocking of individual uriniferous tubules by minute calculi, which
is so often seen in cattle, kept on dry feeding in winter, is a cause of
partial nephritis, and absorption, as noted by Röll.

A somewhat rare cause of atrophy is the diminution of the blood supply
by arteritis and embolism of the renal artery, or by pressure of tumors
on that vessel. Arteritis and blocking suggests at once the possible
agency of the strongylus (sclerostoma) armatus in the horse. Trasbot
records a striking instance of compression of the renal artery and
kidney by an enormous sublumbar melanoma. This occurred in an aged horse
and led to atrophy.

_Lesions._ In cases due to productive inflammation with sclerosis of the
kidney, the firmness, pallor and bloodlessness of the organ is a marked
feature. When incised it is found to be composed mainly of fibrous
tissue, while the glomeruli and tubuli have to a large extent
disappeared.

If there has been simple lack of circulation the kidney becomes flaccid,
pale and small in size. The secretory elements (glomeruli and
uriniferous tubes) are first absorbed, leaving the fibrous network,
which tends to shrink and form a hard resistent mass. In extreme cases
there may be absolutely no glandular tissue left, and the dense shrunken
mass represents only the hyperplasia of the original fibrous network. In
the different successive stages of this process the glomeruli and
tubules become flattened, the epithelial cells become granular, or
contain colloid casts and refrangent elements like oil globules and
finally they are represented by a small mass of fibrous material.

Of all the atrophies caused by the pressure of tumors perhaps that
caused by cysts is the most characteristic. There may be a single cyst
or they may be multiple; they may range in size from a pea to the size
of the two fists the total size exceeding that of the normal kidney. In
all such cases the cysts project visibly from the surface of the organ.
They vary according to their origin and nature. Congenital cysts are
said to have resulted from distension by retained urine of the capsule
of the glomerulus. The arterial tuft is atrophied and flattened against
the wall. Serous cysts with clear contents are found in the old. Urinous
cysts again form by distension of the tubules that are obstructed by
cysts or minute calculi. Colloid cysts are found in certain forms of
nephritis formed by the dilatation of the capsule of the glomerulus or
of the uriniferous tubules. The liquid often contains leucin, tyrosin
and cholesterine. In all such cases the walls of the cyst become thick,
and the glandular parenchyma is compressed leading to progressive
degeneration and atrophy.

_Symptoms_ of atrophy of the kidney are necessarily those of suppression
of urine, with, in certain cases, the passage of casts of the
uriniferous tubes and of crystals of salts. There are, however, no
absolutely pathognomonic symptoms. When the kidney can be reached
through the flaccid walls of a comparatively empty abdomen, or through
the rectum, its hard, shrunken condition may assist in diagnosis.

_Treatment_ is not successful in advanced cases. _Prevention_ is to be
sought by obviating or treating the conditions on which the atrophy
depends. Nephritis must be treated on general principles. Calculi must
be avoided by a liberal supply of water, by soiling, or by pasturage.
Strongylus parasitism should be dealt with by destroying the parent
worms in the bowels, and by securing pure drinking water free from their
eggs and embryos. Cysts, and tumors are only amenable to surgical
measures and not often open even to these.

FATTY DEGENERATION OF THE KIDNEY: STEATOSIS OF THE KIDNEY.

Causes: age, overfeeding, idleness, atony, retention of urine.
Lesions: kidney enlarged, pale yellow, capsule loose, cut surface
glistening unctuous, oil globules in scrapings, granules soluble in
ether. Symptoms: in idle, overfed, obese, improved meat producing
breeds, closely confined, starchy or saccharine food, fatty granules
in urine, finally dropsies, anæmia, debility, sluggishness. Prognosis
unfavorable in advanced stage. Treatment: butcher, restricted regimen,
open air exercise, nitrogenous diet, crossing, diuretic food or drugs,
oil of turpentine, balsam copiaba. Palliation only.

Fatty degeneration of the kidneys is by no means unknown in the domestic
animals. It has been observed in dogs and cats (Rogers, Goubaux,
Vulpain, Trasbot). In dogs it has been erroneously set down as a
characteristic lesion of rabies. Like fatty degeneration of other
organs, it is also met with in old and overfed individuals of meat
producing breeds of animals, in which the tendency to early maturity and
rapid and excessive fattening has been fostered from generation to
generation. In man small, granular, fatty kidney is a common result of
chronic parenchymatous nephritis, and often coincides with fatty liver.
Chronic poisoning by arsenic or phosphorus is another cause, as it is of
fatty degeneration in other organs.

Vulpain has attributed it to a lack of active exertion and of general
tone, associated with excessive amylaceous feeding, sluggish, shallow
breathing and tardy elimination. Goubaux and Trasbot attach great
importance to the compulsory retention of urine in house dogs, cats and
horses. The damming back of the urine in the convoluted tubes and
glomeruli, temporarily arrests secretion, and the inactive and
compressed cells tend at once to granular and fatty degeneration.

_Lesions._ The gland is sensibly increased in size, and pale, yellowish
or straw yellow. The capsule is easily detached from the cortical
substance, contrary to what is the case in chronic productive
inflammation. The cortical substance is increased in thickness, and
pale, the pallor being largely in ratio with the duration or extent of
the fatty degeneration. The cut surface may be glistening and unctuous
to the touch. It is softer than usual, rather friable, and if scraped,
furnishes a serous or grayish pulp in which oil globules are prominent
features, together with granular epithelium and free granules that
dissolve readily in ether. Tubules are varicose and unequal at different
parts. The medullary portion has undergone little change. It may be
paler at certain points, with some shrinking of its substance and
increase of firmness.

_Symptoms._ As a rule the disease occurs in pampered, overfed and obese
animals, and in those of the improved breeds which have great power of
digestion, assimilation and fattening. It is especially to be looked for
after close confinement on full, stimulating, amylaceous diet. Symptoms
are not usually recognized during life. There is, however, a lessening
of the urinary secretion, and, as the disease advances, albuminuria.
When examined microscopically this is found to contain characteristic
elements, such as granular epithelial cells, the granules soluble in
ether, oil globules, and at times crystals of cholesterine (Beale). A
diagnosis based on the mere presence of oil globules may, however, be
fallacious, as these may be present in animals that have just been
heavily fed on oleaginous food, and again the oil used to smear the
catheter may float in the urine and prove misleading. Under such
circumstances vaseline or glycerine may be substituted on the catheter.
Scriba induced fatty urine by injecting fat or oil emulsion into the
blood, and Chabrie by ligating the large intestine. Trasbot says that
cylindroid casts may be present. As in other grave kidney affections,
dropsies supervene as the disease advances. These may show in the limbs,
in the abdomen, or in other serous cavities. A steadily advancing anæmia
with pallor of the mucosæ, listlessness, weakness, debility and
sluggishness are to be noted.

_Prognosis._ Since the disease is rarely diagnosed until it has reached
an advanced stage, it usually progresses steadily to a fatal issue. If,
however, it can be detected at an earlier stage, it may be palliated, or
held in abeyance, for a length of time varying with the extent of the
lesions. As it is very largely a disease of meat producing animals and
as the subject is at first in a condition of marked obesity, it can
usually be turned over to the butcher without material loss.

_Treatment._ If the disease has resulted from the inbred propensity to
fattening, the family that shows the disposition must be subjected to a
somewhat different regimen, open air exercise must take the place of
confinement in warm stables, a rather bare pasturage is valuable for
herbivora, and a restricted diet in which the oleaginous, saccharine,
and amylaceous constituents do not predominate, is strongly indicated.
Crossing with a strange male having many of the desirable qualities of
the herd, but which is more vigorous may be resorted to. When the
secretion of urine becomes scanty an abundance of pure water, or a diet
of succulent grass or roots or ensilage or even small doses of alkaline
diuretics may be resorted to. Any source of arsenic or phosphorus
poisoning should be cut off, and as an antidote to phosphorus, oil of
turpentine may be given in small doses. This agent may, indeed, replace
the alkalies as a diuretic, bringing in an element of tone for the
mucosa which is not to be despised. Or balsam of copaiba or buchu leaves
may be substituted.

When the small white kidney (granular, fatty) results from chronic
nephritis, the prevention and treatment would be as for that disease.
Little hope is to be entertained of entire restoration to health.

AMYLOID KIDNEY. LARDACEOUS OR WAXY KIDNEY.

This condition of the kidney has been found in the ox (Gerlach) and dog
(Rabe, etc.). There are usually similar degenerative lesions in the
liver, pancreas, intestines and other organs. It is usually a
concomitant of some chronic wasting disease (chronic nephritis,
tuberculosis, etc.).

_Morbid Anatomy._ The kidney is usually enlarged, pale and on section
waxy or glistening. Soaked in dilute compound tincture of iodine it
shows spots of a walnut or mahogany brown color. The glomeruli are well
marked and show the earlier changes, later the tubes do so excepting the
epithelium. The latter is swollen, granular, fatty.

_Symptoms._ There may have been those of chronic nephritis. Rabe has
noticed in dogs dropsy of the limbs, ascites, emaciation, anorexia,
followed by uræmia, coma, weakness, vomiting, and if the kidney alone
was affected great lowering of temperature (35.9°C). With hepatic
complication there was greater weakness, giddiness, and higher
temperature (39.6°C). Urine is usually increased (in man albuminous) and
the casts have shown the anyloid reaction. They tend to be fatty or
finely granular. Casts may, however, show anyloid reaction when the
kidney, post mortem, does not (Jaksch).

_Diagnosis_ from Bright’s disease is often impossible.

_Treatment_ is essentially the same as in chronic nephritis, and is not
hopeful.

Trasbot recommends KI 3 to 7 grs., or tinct of iodine 3 drops for
shepherd dog. Ol. terebinth and alkaline diuretics are also commended.

RENAL CALCULUS.

This is much more common than is supposed. Small calculi formed in the
tubuli uriniferi of cattle on dry winter feeding often pass without
recognition, and habitually disappear on rich spring and summer grass.

If retained in the pelvis until increasing size forbids their passage
through the ureter they form pelvic calculi.

If retained in the bladder so that they cannot enter the urethra they
form cystic calculi.

Pelvic calculi or concretions are often (in cattle and swine) mere
scales lying in chalices. They may fill the whole pelvis and send
branching processes into chalices.

_Causes._ They are attributed to phosphaturia, lithæmia or uric acid
diathesis, oxaluria, etc. In cattle they are associated with dry feeding
and are common on all magnesian limestone soils. There are usually
catarrh of the kidney and the presence of bacterial ferments and
colloids (pus, albumen, etc.). (Sharing and Ord.) Calculi or gravel is
preceded by renal catarrh, but this is aggravated by the crystalline
deposit. Bacteria act also in producing NH_{3}O, which instantly
precipitates ammonio-magnesian phosphate. Retention of urine greatly
favors the precipitation.

_Symptoms._ A white or brownish yellow deposit in the last urine
discharged collects on the floor. Cloudy urine. Passage of
crystals—round—or angular. Colic. Lameness in one or both hind limbs.
Arched back. Sensitive loins. Pain paroxysmal. Attempts to urinate.
Little passed but often with drops of blood. Sudden relief when the
calculus enters the bladder.

Retained in the kidney it may cause no suffering in meat producing
animals, but in horses it usually causes stiffness or lameness
especially under violent effort. Also hematuria; blood globules are
found in the deposit when placed under the microscope. There may be
sepsis and specially cloudy offensive urine.

_Diagnosis_: May be confounded with renal tuberculosis, or sarcoma or
oxaluria. Examine for bacillus, small cells, or oxalate of lime or
oxalic acid.

_Prophylaxis._ In the early stages give succulent, watery food,
ensilage, roots, potatoes, spring grass, and water ad libitum.

_Treatment._ Salt may tempt the patient to drink. Nitro-muriatic acid is
a solvent and antiseptic. Or alkalies with salicylate of soda. Also
tonics. Quiet pain by morphia and other anodynes. Use piperazine.

These failing, an operation on the kidney may be considered.

HYDRO-NEPHROSIS.

A common result of calculus or other obstruction, causing increasing
pressure of urine in the pelvis and absorption of the parenchyma, and
finally leaving a mere urinous sac.

RENAL TUMORS.

1. _Non-malignant_: Fibroma.
Lipoma.
Angioma.
Adenoma.
Papilloma.
2. _Malignant_: Sarcoma.
Carcinoma.

RENAL PARASITES.

Echinococcus: Herbivora, Omnivora.
Bilharzia Crassa: Egyptian cattle.
Strongylus Gigas: Horse, ox, dog, man.
(Cysticercus Tenuicollis: Ruminants: Pig).
Tænia serrata: Dog. Pelvis.
Sclerostoma equinum: (renal arteries, _kidney pelvis_), soliped.
Stephanurus dentatus: Pig, (pus cavities).
Trichosoma plicata: (Urinary bladder), dog.
T. felis: (Cat), bladder.
Indetermined embryos: Kidneys, dog; small tumors.
Cytodites nudus: Kidneys; hens.
Œstrus, (Gast. Hemorrhoidalis): Bladder walls: horse.
Mucorimyces: Kidneys; dog.
Coccidia: Kidney, Horse, dog, goose.

INJURIES OF THE URETERS.

Lesions by bullets, arrows, stabs, bruises and lacerations in
parturition, treads, wheels, tumors, ulcers, calculi, tubercles,
parasites. Course. Pathology: transverse division may cause
hydronephrosis, or septic peritonitis. Symptoms: uncertain,
traumatism, bloody urine, arched, stiff, tender loins, straining,
recumbency, groaning in turning or rising, rectal palpation of
distended ureter, of ascitic fluid, pitting on pressure of loin, flank
or groin, liquid drawn through a cannula is urinous, urine still
discharged by normal channel. Crystals in urine, worm ova. Treatment:
compresses, fomentations, sinapisms, anodynes, balsams,
antispasmodics, extraction of calculus, lateral implantation of
urethra.

From their deep and protected position it might be plausibly concluded
that the ureters were secure against every kind of traumatism. This
however, is not the case, since in both man and animals they have been
known to have been injured by bullet wounds, arrow wounds, and stab
wounds of various kinds. In dystokia with laceration of the womb, vagina
or bladder the ureter is liable to be injured. By blows and kicks it may
even be ruptured or torn across, and also by sudden and severe
mechanical compression of the abdomen as when run over by a wagon or
trodden on by a horse, ox, or other large animal. Tumors of various
kinds may grow in, or press upon the ureter, ulcers with thick indurated
margins or base may obstruct the passage, or calculi, or worms may block
and give rise to overdistension and even rupture. Kopp describes
obstruction by multiple calculi with saccular dilation in front, close
to the kidney in a cow. Cadiot records cases of thickening of the mucosa
by numerous cysts as small as hempseed. Intra-abdominal tumors of the
spermatic cord have been known to block the passage. Again tubercles
have formed on the urethra, and polypi on the trigonum vesicæ have
blocked the ureter and produced all the evil consequences of calculus,
parasites, etc.

_Course._ The progress of the disease will vary greatly according to the
nature of the lesion. With complete rupture of the ureter the urine as a
rule escapes into the peritoneal cavity. If the urine is aseptic this
may not lead to serious results and the edges of the wound cicatrizing,
the urine is imprisoned in the ureter and pelvis of the kidney, and
leads to final atrophy of the kidney and hydronephrosis. When on the
other hand infecting matter escapes with the urine, as in perforating
ulcer, tubercle, glanders, cancer, infective catarrh of the kidneys or
ureter, such infection is brought in contact with the whole peritoneal
surface, where secondary infections follow. In cases associated with
penetrating wounds, wounds resulting from dystokia, calculus or
parasitic obstruction, similar infection is to be dreaded.

The _symptoms_ are by no means clear, unless the injury result from
external traumatism, or when it can be detected by rectal exploration.
There may be blood staining of the urine, stiffness of the loins,
lameness in one hind limb, tenderness of the lumbar vertebræ and of
their transverse processes on pinching, frequent straining to pass
urine, a disposition to remain recumbent, pain and groaning when rising,
or when turned in a narrow circle. Under rectal examination the blocked
ureter may sometimes be recognized, its cystic end shrunken and empty,
up to the seat of obstruction, and its renal end, from the
hypersensitive seat of obstruction forward, full, rounded, elastic and
firm. If the ureter has been ruptured, it may be impossible to
distinguish it, but the presence of urine free in the peritoneum may be
detected through the rectum as it may often be through the abdominal
walls. Sometimes the urine infiltrates the subperitoneal connective
tissue, and forms a pasty swelling on the loin or flank. In either case
a hollow needle inserted will draw off a liquid having an urinous odor.
That this urine has escaped in front of the bladder may be safely
inferred from the continued discharge of urine by the urethra and by the
absence of cystic swelling, heat and tenderness. If the kidney can be
reached by rectal exploration it is felt to be firm and resistent up to
the period of rupture of the ureter.

In case of obstruction by calculus, crystals and even small calculi may
be passed in the urine, there is usually a history of previous attacks
of renal colic, and the suffering is manifestly extreme. In case of
worms (strongylus gigas) the use of the centrifuge on the urine, may
possibly secure in the sediment specimens of its ova. The existence of
tumors or tubercles can usually be clearly made out.

_Treatment_ will be as varied as the lesion. Simple ureteritis may be
met by wet compresses, sinapisms, and internally by balsams and
anodynes. Calculi and parasites may be passed with some aid perhaps from
fomentations, antispasmodics, and diluents. Obstinate cases can only be
successfully met by surgical interference. The resulting wounds in the
ureter, like ruptures, perforating ulcers and strictures may be met by
Van Hook’s “_lateral implantation_”: the divided cystic end of the
ureter is ligatured and on the cystic side of the ligature a
longitudinal incision is made, large enough to admit the divided
extremity of the renal portion, and through each of the two sides of
this last a fine ligature is passed; these ligatures are then passed
into the lumen of the cystic portion of the ureter through its
longitudinal incision and brought outward through its walls; next the
renal end is inserted into the incision in the cystic end and the two
are firmly sewed together by the two ligatures. When a small portion of
an ureter must be excised it may sometimes be possible to save a
valuable animal by such an expedient.

In some cases of rupture into the vagina or uterus an available fistula
may sometimes be established into one of these.

URETERITIS.

From wounds, calculus, parasites, infection, injuries in parturition.
Symptoms: in wounds of ureter. Course: danger of infection of kidney
or bladder. Treatment: for calculus, antispasmodics, anodynes,
fomentations, for parasites arsenious acid, for catarrhal conditions,
balsams, buchu, salicylates, etc. Operation. Uretero-vaginal fistula.

This may arise from the passage of a rough calculus, from wounds of the
ureter sustained in kicks and blows or by being run over by wheels
(dogs, cats), it may be due to the blocking of the tube by a parasite
such as strongylus gigas, echinococcus, etc., or it may be the result of
extension of an infectious inflammation backward from the kidney or
forward from the bladder. Again it may be the result of a lesion of the
ureter in cases of dystokia.

The _symptoms_ are obscure but there is likely to be frequent straining
and passage of urine, tenderness of the loins, all the more significant
if confined to one side, lameness or halting on the corresponding hind
limb, and on examination through the rectum the swollen and tender cord
representing the ureter may be recognizable. In case of calculus or
other obstruction the ureter may be felt to be swollen, elastic and
tender back to a slight nodular, painful, firm swelling at the seat of
obstruction.

_Course._ In all such cases there is always danger of inflammation
(infections or otherwise) of the kidney with degeneration and loss of
structure and function, the organ being reduced to a simple urinous cyst
(hydronephrosis). In some cases, however, the obstruction (calculus,
parasite) may escape into the bladder and a recovery follow. Slight
infections, too, may improve and advance to complete convalescence.

_Treatment_ will depend much on the causative factor: Calculus must be
treated by anodyne antispasmodics, and fomentations, and in case of
relief by measures calculated to prevent its formation anew: parasites
may be treated by arsenious acid, oil of turpentine, and other
parasiticides which are secreted by the kidneys: catarrhal and infected
conditions may be met by balsams, buchu, salicyclic acid and even
peppers. In case of calculus which does not give promise of passing,
even a surgical operation may be thought of, especially in the smaller
house animals.

In rupture of the ureter in dystokia the walls of the womb or vagina
have usually suffered, and a recovery with a ureterouterine or
uretero-vaginal fistula is not unknown.

ACUTE CATARRHAL CYSTITIS.

Acrid diuretics, by mouth or skin, microbian infection, retention of
urine, urethral calculus, parasites, spasm, enforced suspension of
micturition, unclean catheter, adjacent infection, chill. Lesions:
hyperæmia of mucosa, thickening, vascular distention, clouding of
epithelium, muco-purulent secretion, alkaline fermentation, ammonia,
liquefaction of cells, erosion. Symptoms: Slight fever, stiff,
straddling gait, urine scanty, cloudy, alkaline, penis or clitoris
semi-erect, smearing of tail or prepuce. Crystals of triple phosphate.
Treatment: Antiseptics, boric or salicylic acid, gum arabic,
astringent antiseptics, laxatives, flax seed, slippery elm, anodynes,
diluents, piperazine, drainage, rest, restricted laxative diet,
warmth, avoid stimulants.

_Causes._ Cystitis is caused in all animals by irritant diuretics like
cantharides, copaiba, or oil of turpentine given by the mouth or applied
to an extensive cutaneous surface. It is an error, however, to conclude
with Williams that this is the sole cause. The very existence of calculi
virtually implies bacterial infection, and fermentation. The presence of
free ammonia in the urine usually implies fermentation, and fermentation
must be looked upon as practically synonymous with microbian invasion.
That bacteria may be present without serious injury is undoubted. The
protective power of the healthy mucosa is very great. But when the
mucosa is weakened, microbes that would otherwise be harmless, find a
ready infection atrium, and triumph over the weakened tissues. Hence
retention of urine and overdistension of the bladder as in urethral
calculus, blocking of the urethra by a parasite, spasm of the sphincter
vesicæ, compulsory retention as in the mare in harness, the dog kept
indoors, or in railway car on a long journey, or in mares so travelling,
may become the occasion of cystitis. Even in cases in which no microbe
is present at first, this reaches the bladder by the introduction of an
unclean catheter, or by extension from an uretheritis, vaginitis or
metritis, or even from a peritonitis, or infected urachus. Or the
infection may descend from a suppurating kidney. Another occasion of
microbian invasion is the congestion which attends on exposure to cold.

_Lesions._ Hyperæmia of the cystic mucosa, with dilation and tortuous
deviations of the larger vessels, thickening of the membrane, and
distension and clouding of the epithelial cells, with a thick covering
of tenacious mucus containing epithelial, pus, or white blood cells. As
the disease advances epithelium is desquamated abundantly, and
degenerates with production of free nuclei and pus. Along with these are
microbes, usually the bacillus coli communis, and various cocci. In the
fully established disease there is liable to be alkaline fermentation,
and the liberated ammonia dissolves the epithelial cells, leading to
extensive desquamation and raw granulating surfaces, so that the disease
tends to run in a vitiating circle, the alkali dissolving the epithelium
and increasing the microbian development and fermentation, which in its
turn produces an increasing quantity of ammonia.

_Symptoms._ There is slight hyperthermia or none, stiff or straddling
gait, frequent passage of urine in small quantities and cloudy, or
straining without passage, the penis or clitoris is semi-erect, eversion
of the lips of the vulva is frequent, and the bladder is tender (through
prepubian wall, vagina or rectum). If a finger is inserted into the
bladder in the mare the thickening of the walls can often be recognized.
The urine often contains precipitated crystals of ammonio-magnesian
phosphate, and even clots of blood. It has an alkaline reaction even in
herbivora.

_Treatment._ The danger centres around the bacteridian fermentations,
and a main object must be to disinfect the bladder. This will be all the
more effectual if the lotions used are of an acid reaction. Thus boric
acid or salicylic acid in 3 per cent. solution, injected after
evacuation of the bladder and repeated a number of times a day may soon
establish a healthy action. If the bladder is especially irritable a
boiled weak solution of gum arabic will form a suitable medium. Other
antiseptics are often used as creosote (0.5:100), carbolic acid (3:100),
chloride of zinc (3:100), chlorate of potash (3:100), mercuric chloride
(1:5000), silver nitrate (0.5:100), or astringents are often better:
PbA, ZnSO_{4} tannic acid, ferri chloridi in dilute solution so as not
to cause pain.

The bowels should be kept open by an occasional saline laxative, pain
moderated by codeine, and abundance of pure water and a laxative diet
enjoined. Linseed tea, and infusions of slippery elm or marsh mallow
have long been employed, and by soothing and relaxing the bowels they
act favorably on the urinary mucosa. Stimulants of the urinary track
like buchu, uva ursi or copaiba in small doses, or antiseptics like
creosote, boric acid, salicylic acid, piperazine, are available in
slight cases or when the acute symptoms have subsided somewhat. With
prior infection of the kidneys, the latter may be used. Constant
drainage may be necessary to avoid distension.

Perfect rest is absolutely essential, a restricted laxative diet, and a
careful avoidance of cold, and stimulants.

When urine is retained it should be removed with a thoroughly aseptic
catheter.

In case of blood clots in the bladder, wash out with a boiled normal
salt solution.

ACUTE CROUPOUS CYSTITIS.

This has been found to follow the use of cantharides and other irritant
diuretics, and to follow on certain specific diseases. Its nature is
that of catarrhal inflammation, but with a fibrinous product or false
membrane formed more or less extensively on the inflamed mucosa.

_Symptoms_ are essentially those of catarrhal cystitis from which it is
distinguished by the presence in the urine of flakes of the fibrinous
membrane.

_Treatment_ is essentially the same as in the catarrhal form, to which
may be added the injection of a solution of 4 grains scale pepsin to the
ounce of sterilized water. The boric acid solution may be of the
strength of 20 per cent. Irrigate two or three times a day.

CHRONIC CATARRHAL CYSTITIS.

This may begin as such or it may continue after an acute attack. It has
been noticed in horse, ox, and dog.

It may be associated with calculi, gravel, papilloma, and bacterial
invasion especially by the colon bacillus.

_Lesions._ The mucosa and muscular coat are thickened, corrugated,
puckered and contracted so that the bladder will not contain more than a
few ounces of urine. The surface of the mucosa is discolored, mottled
and variegated, slaty blue, brown, red, purple, or even black, with
ulcers, encrustations of triple phosphate, and fungoid elevations. In
dogs especially, the prostate is often enlarged.

_Symptoms._ Frequent urination accomplished with pain, groaning, or
whining and it may be with sudden arrest. There may be incontinence, the
urine dribbling almost continuously from the penis or vulva and in the
latter case trickling down the thighs. The presence of pus and mucus
tends to mat the hairs, and a strong urinous and ammoniacal odor is
emitted.

Palpation of the prepubian region often, and of the vagina or rectum
always causes pain and wincing. Temperature is normal.

Urine is albuminous in ratio to the amount of pus, or above that, and is
then suggestive of kidney disease and likely to be complicated by casts.

Complicating lesions of the womb, vagina, prostate, and kidney are to be
carefully looked for, also cystic papilloma.

_Prognosis._ Recovery though not uncommon is too often but partial and
it is usually desirable to fatten the animal.

_Treatment._ Rest, moderate laxative diet, pure drinking water ad
libitum, warmth, antiseptic irrigation.

CYSTITIS IN THE OX.

_Special Symptoms._ Beside general disorder there is a disposition to
decubitus, but with frequent rising to urinate though the bladder is not
filled to repletion. Then the urine is passed in a slow stream by
abdominal contraction, and without pulsating contractions of the urethra
at the ischium which are so marked in calculus. Cystitis is greatly
aggravated by overdistension, and if the bladder is paralyzed is very
liable to go on to rupture.

Galtier considers enzootic hæmaturia as essentially a hæmorrhagic
cystitis, due to marshy soils, disordered liver, often distomatosis, and
irritation of the urinary organs by the poisons which the liver was
helpless to destroy or eliminate.

The _treatment_ of cystitis in cattle does not differ materially from
that of the horse.

The hæmorrhagic form demands prevention by drainage, cultivation and the
use of phosphates to the soil.

CYSTITIS IN DOGS.

The _special symptoms_ in dogs are uneasiness and frequent changes of
place. The patient passes urine often in small quantity, and with whines
or cries. He walks slowly and stiffly with the back arched, and
compression of the abdomen and especially of the prepubian region is
painful to a marked degree. The tense elastic bladder may often be
distinctly felt through the abdominal walls. The inflamed bladder is
liable to paresis and paralysis with great overdistension, and
aggravation of the general symptoms, the eyes sunken, and dullness,
stupor and coma betraying uræmic poisoning. Some claim rupture of the
bladder as is so common in the ox.

In the main, _treatment_ is as for the horse. Rest, warm bath, or
fomentations, catheterism with aseptic catheter, draw urine through
hypodermic nozzle in prepubian region. Antiseptics: boric or salicylic
acid by the mouth and bladder. Laxatives, and plenty of water are
important. Free access to open air where the animal can urinate, is very
essential. In chronic cases, buchu, copaiba, balsams, or piperazine may
be employed. Mustard blister. Electricity. Small doses of belladonna to
give tone to the bladder.

ATONY AND PARALYSIS OF THE BLADDER.

_Causes._ This comes usually from troubles of innervation. Paraplegia,
dorsal and lumbar fractures with injury to the spinal cord, brain
lesions, hæmoglobinuria with effusion pressing on the cystic plexus,
overdistension of the viscus, from cervical spasm, urethral stricture or
calculus or parasite (strongylus gigas), acute or chronic cystitis. In
dogs it may come from obstruction by enlarged prostate. Polypus blocking
the cervix and chronic disease of the walls of the organ are additional
causes.

_Symptoms._ More or less complete retention of the urine. The bladder
cannot be completely emptied except by powerful contractions of the
abdominal muscles. Habitually it may escape in drops, or in jets at
intervals during exercise. Palpation will show overdistended bladder as
a tense, elastic mass. But as overdistension may occur without
paralysis, no case can be certainly diagnosed without catheterization to
show that the urethra is free.

When the paralysis affects the cervix, the urine escapes continually and
trickles down the insides of the hips in mares, or from the sheath in
males.

_Diagnosis_ demands catheterism and rectal examination.

Complication. Cystitis by retention. Infection by catheter.

_Treatment._ Corresponds to causes. These corrected, use aseptic
catheter often. After extreme distension empty partially, or inject a
few ounces of borax or boric acid solution. Thus avoid collapse and
inflammation, and secure antisepsis. Give tone by a course of strychnia,
(ergot, belladonna), mustard blister; turpentine in small doses. Better
electricity, 1 pole in bladder, 1 on pubic symphysis. Apply for 5
minutes.

TUMORS OF THE BLADDER.

Recorded cases of sarcoma (Mauri), carcinoma (Cadeac, Hink,
Friedberger), and tuberculosis can be adduced. Papilloma is perhaps as
frequent as any of the above. The author has treated two cases of
papilloma in mares complicated with multiple small calculi and gravel.
_Treatment_ is exclusively surgical and in the mare with the widely
dilatable urethra this is sometimes possible through that channel. In
the same animals _diagnosis_ may be accomplished by introducing the
finger into the urethra and bladder. In other females and males, vaginal
or rectal palpation must be resorted to.

VESICAL PARASITES.

Eustrongylus gigas. Dog, horse, man.
Trichosoma plicata. Dog.
Œstrus Hemorrhoidalis. Mare.

SPASM OF NECK OF BLADDER.

Spasm of the cervix vesicæ has been doubted, save as the result of local
inflammation, yet it not uncommonly takes place in horses and other
animals in connection with irritation attendant on the retention of
urine during work, or in dogs during a period passed indoors. Trouble
and suffering continues, with ineffectual efforts to micturate, but
practically complete relief is secured by catheterization or by a
spontaneous abundant discharge. The neurosis which leads to it is
produced or aggravated at times by enlarged prostate, or lesions in the
urethra. Intense fear may cause it.

_Treatment._ Remove cause. Give antispasmodics, valerian, musk,
bromides, chloral hydrate, opium, stramonium, hyoscyamus, codeine, etc.,
may be given as injections or suppositories. For the horse spread the
litter and soothe by whistle or song. Or use the catheter and correct
any local irritation.

RUPTURE AND LACERATION OF THE BLADDER.

This occurs most commonly in oxen from obstruction of the urethra by a
calculus. Similar obstruction in the horse causes most acute symptoms,
calling for immediate relief, and rupture is a comparatively rare
occurrence. Pench mentions a case resulting from a fall during an attack
of colic, and with a full bladder. It has happened during lithotrity, or
lithotomy, and even during parturition. Perforation by parasites has
been noted and in one case by an osseous tumor of the pubic symphysis.
In horses a fatal result is prompt, in cattle from 6 to 48 days.

Treatment surgical.

EVERSION OF THE BLADDER.

This is really invagination into the female urethra and bladder. It has
only been seen in mares, and then by reason of the extreme dilatability
of the urethra. A pyriform, red, perhaps rugose tumor shows between the
lips of the vulva, during straining. It is covered by mucosa, and on its
upper surface near to its neck are two small orifices from which urine
oozes or comes in jets during active expulsive efforts. It soon becomes
muco-purulent on the surface, and even excoriated. Urine escaping
continuously trickles down the thighs with much fœtor. It occurs
especially during violent expulsive efforts as in parturition or
constipation.

_Treatment_ essentially surgical consists in uniform compression to
expel blood and exudate followed by the pushing of the fundus through
the bladder and urethra. The more recent the case, the easier is the
process. Pressecq claims to have cured an obstinately recurring case, by
cauterizing the urethra up to the cervix vesicæ with a round iron rod an
inch in diameter. The resulting loss of substance, with the neoplasia
and constriction effectually prevented renewed eversion even during
parturition. Other veterinarians have successfully excised the bladder,
but this entailed incontinence and constant offensive soaking of the
thighs with urine.

HERNIA OF THE BLADDER.

This is commonly seen in the mammalian female in connection with rupture
of the floor of the vagina during dystokia. It has also been observed
without such lesion in both male and female dogs and horses, the bladder
forming a cystocele of the vagina, or bulging between the anus and the
ischium.

_Diagnosis_ is confirmed by careful palpation through the rectum. The
folding of the bladder backward obstructs the exit of urine.

_Treatment_, essentially surgical, might include replacing of the organ
and suturing of the wound, or, in the absence of a wound, evacuation of
the bladder by a hypodermic needle, and replacing by palpation through
the vagina or rectum. Sometimes suture of the vulva is desirable.

ANOMALIES OF THE BLADDER.

=Persistent urachus.= Seen in the new born and mainly in males.
Antiseptic closure is essential after having ascertained that the
urethra is pervious.

=Imperforate cervix vesicæ.= A case reported by Lapotre, in a calf, had
no cervix, and the ureters were blocked by pea-shaped nodules.

=Recto-vesical fistula.= In a calf 13 days old the rectum opened into
the bladder and the fæces and urine escaped by a pervious urachus.
(Kaufmann and Blanc).

URETHRAL ANOMALIES.

_Imperforations._ In the new born male, foal, lamb, etc. Usually at the
outer end, and it may be for some distance back. In one case the sheath
was firmly adherent on the wall of the abdomen, thus shutting off all
exit of urine. If the canal is absent only at the orifice or for a short
distance, the urethra beyond this can be felt full of liquid and
fluctuating. The patient being properly fixed a fine trochar is pushed
from the end of the penis into the blind end of the urethra, which will
be ascertained by the overcoming of resistance. The trochar is now
withdrawn and the urine flows through the cannula. A catheter or sound
is now tied in the passage to maintain it pervious until cicatrization
shall have taken place.

_Hypospadias._ Short urethra opening backward on the lower surface of
the penis. Considered irremediable.

_Epispadias._ Urethra opening on the upper surface of the penis. Much
more rare.

ACUTE URETHRITIS. CATARRH OF THE URETHRA.

This occurs in all genera of domestic animals, and may be either acute
or chronic. It is most common in the entire males, not only because of
infections sustained in copulation, but because frequent erection
exposes the opening of the urethra to injury and inflammation, and to
the entrance of pathogenic germs.

_Symptoms._ Pruritus of the penis, and difficulty and pain in urination
and straining are frequent, but a single small jet may be all that is
passed at a time. The papilla on the end of the penis is red and angry
and somewhat swollen. Later a few drops of muco-purulent fluid may be
pressed from the orifice. In the bull, dog and boar this oozes from the
retracted penis into the sheath, so that a collection is found in that
canal, and the mucosa becomes infected causing a balanitis.

The infection may be conveyed from male to female and _vice versa_. Dr.
Horand of Lyons even found that the muco-purulent discharge of gonorrhœa
in man caused an urethral catarrh in the dog, which however did not
persist for any great length of time.

_Diagnosis_ is based on frequent and painful urination in jets,
tenderness of the urethra under palpation or catheterization, redness
and swelling round the urethral orifice, and the oozing of pus. In the
absence of any external injury one should always ascertain if cystitis
is present.

_Prognosis_ is favorable under appropriate treatment. Spontaneous
recovery will usually occur early.

_Treatment._ Dilute the urine. Give pure water to drink at will, or
flaxseed gruel, or gum or barley water. Alkaline carbonates. In the
early stage foment and use injection of potassium permanganate (2 grs.
to 1 oz.). Later may be used more astringent agents (boric acid 1:100,
zinc sulphate 1:100, lead acetate 1:100, potass. chlorate 3:100. In the
presence of great pain cocaine muriate 2:100). There is danger of
stricture from the stronger astringents or caustics in the early stages
before suppuration. To complete the cure give copiaba, buchu, resin, or
essence of turpentine.

WOUNDS OF THE URETHRA.

Actual wounds occur in surgical operations, or accidentally as by
shafts, poles, forks, hooks, bites, etc., or from calculus or a catheter
forced into a false route. An arrested or slowly moving calculus has
been known to induce several perforating ulcers causing infiltration of
urine and infecting germs into the connective tissue. This determines
rapidly increasing œdematous fluctuating tumors. Gangrene and septic
intoxication are common results, especially in cattle.

Longitudinal wounds keep more open and heal more readily than transverse
wounds, probably because the circular muscular fibres in contracting,
pull the edges apart and counteract stricture, the breach being filled
up by granulations. The perineal wound in lithotomy will heal thus in 20
days, while that made in amputation of the penis is exceedingly liable
to circular contraction and stricture or occlusion.

Contusions of the perineum, may cause lacerations of the urethra and
hæmorrhages, with bloody discharge or sanguineous swelling.

_Treatment._ Will vary. Calculi must be diagnosed and removed. Breach of
the walls of the urethra may necessitate frequent catheterization or,
better, the wearing of a catheter. Escape of urine into the connective
tissue should be met by a counter opening in the skin to drain the part
and allow free antisepsis. Similar resorts are required for urinary
infiltration, accompanied by antiseptic injection subcutem. Abscesses
must be located, punctured with trochar and cannula, evacuated and
injected antiseptically.

FOREIGN BODIES IN THE URETHRA.

Apart from calculi, may be found straws, glumes, chaff and catheters and
even stones and small bodies which must have been introduced
deliberately. An irritation corresponding to the offending mass and its
seat, ensues, and must be treated by soothing and antiphlogistic
measures while the offending body must be found and completely
extracted.

STRICTURE OF THE URETHRA.

This may be suspected when in spite of much straining the urine is
habitually passed in a very fine stream, which has become finer and
finer for a length of time, without complete arrest as in calculus. The
introduction of a catheter will confirm the diagnosis and show the exact
seat of the stricture.

It is determined by irritation caused by calculus, urethritis, ulcer,
wounds, etc., which tend to the formation of a cicatrix encircling and
narrowing the canal. One efficient cause is the injection of strong
astringent or slight caustic solutions in the early stages of
urethritis.

_Treatment_ is by dilation, by bougies pointed and gradually thickening,
or simply by an elastic staff which at first passes with some force and
is replaced by a larger one as the urethra stretches under daily use.

=Catheterization.= In connection with diseases of the bladder and
urethra the passing of the catheter is a most important operation which
requires considerable skill on the part of the operator. A short
statement of the method to be adopted for each of the domestic animals
will therefore be in place.

=Catheterization in the male Soliped.= The catheter, a hollow, gum
elastic tube, must be proportioned to the size of the animal, but for
the average adult horse about 3½ feet in length and ⅓ inch in thickness.
To give it the requisite solidity and resistance it is usually furnished
with a stilet of whalebone or cane.

The operation is performed with the animal standing, in quiet animals
without any restraint, but in the more sensitive or restive, with one
fore foot held up; or with both hind feet in hobbles furnished with
ropes passing between the fore limbs and tied over the neck in front of
the withers; or finally with a twitch on the nose.

The rectum is emptied, and with the oiled or soapy hand the penis is
found and slowly withdrawn from the sheath by steady traction. This is
usually easy, though in certain cases, with a short penis and specially
strong retractors, it will seriously tax the operator’s skill and
address. In a specially obstinate case a hypodermic injection of
morphine may be resorted to.

If the horse is down, as in paraplegia or hæmoglobinæmia, he may lie on
his right side while the operator stoops over him from the loins; or his
feet may be drawn together by hobbles, and the subject turned on his
back, the operator placing himself as before on the left side.

The catheter must have been previously cleansed and disinfected outside
and in. A mercuric chloride solution 1:2000, or boric acid 1:50 or
permanganate of potash 1:50 may be employed. Then it must be smeared,
preferably with vaseline but, in case of necessity, with sweet oil,
glycerine, borated lard, or even castile soap.

The penis being withdrawn from the sheath, the catheter containing its
stilet is introduced into the urethra and pushed on slowly and carefully
until its point can be felt over the ischiatic arch. The stilet is now
drawn out a few inches and the point of the catheter is bent forward
over the ischium by the finger. The stilet is further drawn out and the
catheter can easily be pressed on into the bladder. If any difficulty is
experienced it may be guided by the hand introduced into the rectum.

In one extraordinary case, I found that the catheter entered a dilated
seminal vesicle and failed to evacuate the bladder. This untoward
occurrence must be rectified by the aid of the hand in the rectum.
Usually the penetration of the bladder is signalized by the overcoming
of resistance, and when the stilet is withdrawn the urine flows in a
steady stream. If it fails to flow, a slight compression of the fundus
of the bladder by the hand engaged in the rectum will start the stream.

The catheter should be withdrawn slowly and carefully.

=Catheterization in the Bovine Male.= Most veterinarians suppose that
this is impossible, owing to the narrowness of the sheath interfering
with the extraction of the penis, and the S shaped curve in the penis
preventing the introduction of the catheter. Both obstacles can,
however, be overcome in many cases. The bull may be tempted to protrude
the penis by the presentation of a cow in heat, or in bull or ox the
bulging anterior part of the organ may be protruded by careful
manipulation through the sheath. Then the free extension of the penis
can be made to efface the S shaped curve. The catheter must be small,
not much over a line in caliber, and a metal stilet is employed. The
animal may have to be placed under restraint, and the same antiseptic
precautions are demanded as in the horse.

=Catheterization in the Ram and Wether.= These must be dealt with like
the bull, the only additional difficulty being in the vermiform
appendix. This is small and sinuous but the longitudinal opening on its
lower surface is favorable to the introduction of the catheter.

=Catheterization in the Dog.= The fact that the urethra traverses the
groove on the lower aspect of the bone of the penis, is held to prove an
obstacle to the catheter, yet the introduction of the latter is in no
sense difficult. Small or moderately sized dogs, may be held upright,
the body resting on the rump and the pelvis inclined forward, which will
favor the spontaneous protrusion of the penis. Or it may be pressed out
by manipulation through the sheath. The catheter ⅔ ds. to 1 line in
diameter may be 1¼ to 2 feet in length according to the size of the
animal. It should be used aseptic.

=Catheterization of the Mare.= Nothing can be easier than this operation
in the mare. The shortness and dilatability of the urethra, and the
accessibility of its external orifice in the center of the floor of the
vulva, 4 or 5 inches in front of the lower commissure, favors the
introduction of the catheter. The latter may be a foot in length,
perfectly straight and it may be constructed of silver or some other
metal, which may be readily boiled and rendered aseptic. In the absence
of a catheter the germ free nozzle of a rectal syringe may be used, or
two fingers may be passed through the urethra and parted from each other
so as to allow the exit of the urine.

=Catheterization of the Cow and Heifer.= The operation is often very
difficult in the cow, by reason of the small size and undilatability of
the urethra, and by the presence of two blind ducts (canals of Goërtner)
above and to the two sides of the urethral opening. The thin rigid upper
margin of the orifice projects down over it in a valvular manner so that
the catheter will almost always find its way into one of the blind sacs.
By introducing the tip of the index finger beneath the valvular fold and
into the opening of the canal, the catheter may be directed beneath it
and into the bladder. An apparatus consisting of a series of ribs of
spring wire arranged in the form of a funnel and converging at one end
to a point has been devised to insert into the urethral orifice, and
guide the catheter which is passed through it.

=Catheterization of the Bitch.= The operation is rendered difficult by
the narrowness of the passage, and the puckers and folds of the vaginal
mucosa which serve to hide the urethral orifice. A small catheter like
that used on the male is used or a short metallic catheter may be
substituted. By directing this forward exactly in the median line of the
floor of the vulva, with gentle pressure downward it may be made to
enter the urethra. In case of special difficulty a bivalve speculum may
be resorted to, to efface the mucous folds and reveal the orifice.

ACUTE PROSTATITIS AND HYPERÆMIA OF THE PROSTATE.

Causes: In dogs, house life, overfeeding, compulsory retention of
urine, and fæces, constipation, proctitis (rectitis), piles, calculi,
strangury, uric acid, urethral ulceration or stricture, rude
catheterization, chill, generative excitement to excess, secondary
abscess or infection. Forms. Lesions: follicular, interstitial,
circumscribed and diffuse suppuration. Symptoms: frequent straining
urination, rectal palpation, incontinence of urine, costiveness,
tender perineum, dullness, recumbency, fever, pus in urine, collapse
of swelling, fistula. Diagnosis. Prognosis: grave. Treatment:
laxatives, mercurials, salines, leeches, acid laxative,
non-stimulating, camphor, bromides, ergot, witch hazel, opium,
belladonna, enemata of cold water, or ice suppository,
catheterization, perineal incision, antiseptics.

_Causes._ This is most commonly seen in dogs, in which it may depend on
house life with overfeeding on stimulating, spiced, albuminous food,
compulsory restraint of urination and defecation in obedience to the
demands of cleanliness, distended bladder, and rectum, constipation,
proctitis, piles, and other sources of local irritation. In all animals
its origin is favored by the formation or arrest of calculi in the
prostate, the pelvic urethra or even the bladder; by drug strangury from
cantharides or other irritant diuretic; by excess of urea, uric acid or
other irritant in the urine; by infection extending from the urethra or
bladder; by ulceration or stricture of the urethra; by rude or
incautious catheterization, or injection; by exposure to cold; and by
local infection in pyæmia and other general zymotic disorders. Most of
these conditions conduce to local excitement and hyperæmia, which from
adjacent organs, are sympathetically transferred to the prostate. The
same is true of frequent, and intense generative excitement which
according to Lafosse and Cadiot is a common cause of prostatitis in stud
horses. Again the abscess of strangles may become localized in the
prostate, or the nodule of glanders, or the tubercle of tuberculosis
(cattle, pigs, dogs). Cadiot suggests that in animals, divested of the
tail, external injuries to the perineum may extend by continuity to the
prostate, as happens to man from horseback or bicycle riding. He adduces
no cases however. The habit of masturbation acquired by certain males
may also be adduced theoretically as both cause and consequence of
prostatitis but future observation must show how frequently this really
operates.

_Forms. Lesions._ According to the nature of the lesions the affection
has been divided into different forms 1st, =Follicular= or
=Parenchymatous=; 2d, =Diffuse= or =Interstitial=; 3d, =Circumscribed
Prostatic Abscess=; 4th, =Multiple Miliary Abscesses=.

=Follicular Prostatitis= implicates primarily the follicles and gland
ducts and finally the entire gland tissue. It is usually associated with
and doubtless often proves an extension from an adjacent infective
urethritis, and tends, in persistent cases, to go on to interstitial
inflammation and abscess, or hypertrophy. This is characterized by more
or less swelling of the prostate, with increased vascularity of its
mucosa and the oozing from its openings and gland ducts under pressure,
of a thick, yellow, gelatinoid fluid containing pus and granular
epithelial cells and sometimes striæ of blood.

=Diffuse= (=Interstitial=) =Prostatitis= shows, in addition to the
general swelling and muco-purulent discharge, a considerable exudate
into the interstitial tissue, with increased tension and resistance of
its substance. It is associated during life with more fever and
constitutional disturbance than the simple catarrhal or follicular form.

In =Circumscribed Prostatic Abscess= we find, in addition to the general
hyperæmia and swelling, a much more prominent local swelling, the seat
of intense inflammation, at first firm and resistant and later softer
and fluctuating in the centre, which is filled with pus. This may have
its origin in the follicular form, the pus becoming shut up in a
follicle and gradually increasing until it bursts into the urethra, the
bladder, the rectum, the peritoneum, or pelvic fascia and perineum. In
other cases it becomes complicated by pyæmia and secondary abscesses.

=Miliary Abscesses= may be comparatively few in number or generally
diffused through the prostate, and are often the result of a
pre-existing general infection.

_Symptoms._ As the disease usually begins as a local infection the first
symptoms are, as a rule, unattended by fever, which, however, appears in
two or three days as the local lesions increase. The urine may be passed
frequently in small amounts, or there may be frequent straining without
passage of urine, the pressure of the swollen prostate, with or without
spasm of the sphincter vescicæ, causing retention. It is no uncommon
thing to find the last urine passed of a milky or glairy character and,
coagula moulded in the prostatic canals may at times be found. The
presence of spermatic crystals, fusiform, with very pointed extremities,
and precipitated on the addition of ammonium phosphate, is
characteristic of prostatic fluid, (Fürbringer). In other cases there is
incontinence, the urine dribbling away involuntarily as the animal
walks, and especially if anything occurs to excite him. Micturition may
be painless or attended by acute suffering, which causes a sudden arrest
of the flow. Defecation is attended with difficulty and more or less
pain, and obstinate constipation is likely to set in. The animal is
dull, spiritless and seeks to lie undisturbed. Pressure on the perineum
is painful and exercise aggravates the symptoms. Rectal examination by
the hand or finger according to the size of the animal, reveals the
enlarged, tender prostate lying on the cervix vesicæ. This swelling may
be unilateral but most commonly it is bilateral or general. When fever
sets in with a temperature of 102°–104°, thirst, anorexia and weakness
or stiffness in the hind parts may be noticed. In case of abscess, the
urine may be perfectly clear until it bursts into the urethra or bladder
when there is an abundant flow of pus, and rectal examination shows that
the swelling and tension have notably diminished. Should it burst into
the rectum, the pus shows in the fæces. Reinemann records a case in a
bull with dysuria, œdema of the sheath and a swelling like the fist in
the perineum, containing pus, and which communicated with the prostate
and urethra. With the rupture of the abscess there is a marked
amelioration of the symptoms.

Not infrequently the affection subsides into the chronic form and the
abscess, having a restricted channel for evacuation, remains as a
suppurating cavity.

_Diagnosis._ The enlargement and tenderness of the prostate as felt on
rectal examination is pathognomonic. If the body of the urine is clear
there is further corroboration, as in cystitis it is more or less turbid
and flocculent or even bloodstained. Micturition is likely to be much
more frequent in cystitis than in prostatitis. Catheterization is much
more painful when the catheter passes the prostate in prostatitis than
in cystitis.

_Prognosis_ is always grave. Some cases recover completely, while others
run on to a fatal termination, and still others merge into the chronic
form. Cases that are complicated by abscess are always to be dreaded, as
chronic suppuration, or pelvic or peritoneal infection, or pyæmia, or
septic poisoning is liable to supervene. As the disease is more common
in the old so it is liable to prove more severe and redoubtable.

_Treatment._ In acute cases active derivation toward the bowels is
desirable. A mercurial purge (calomel—horse or bull 1 to 2 drs.; dog, 2
to 5 grs.) may be followed a few hours later by salines (sodium
sulphate—horse or bull 1 lb.; dog 1 oz.). Sodium sulphate or magnesium
sulphate may also be given with glycerine as an enema. Great benefit may
often be obtained from the application of leeches on the perineum or
around the anus. The diet must be restricted and non-stimulating, mainly
of amylaceous materials, and with the water, flaxseed tea may be
liberally mixed. When the suffering is severe it may be met by camphor,
camphor bromide, ergot, hamamelis, gelsemium or potassium bromide, given
by the mouth or rectum. With violent strangury, opium, belladonna or
hyoscyamus may be used. Some cases may be relieved by the use of enemata
of cold water or pieces of ice in the rectum. In retention of urine,
careful catheterization is imperative, the hand or finger in the rectum
being employed to guide the point of the catheter under the prostate.

In case of abscess an opening by the side of the anus is preferable to
one by the urinary passages or rectum, and will obviate the danger of
rupture into the peritoneum. A pasty or fluctuating swelling in the
perineum should be incised until the pus flows. A tense elastic
fluctuating prostate may be transfixed by a cannula and trochar from the
side of the anus, guided by the hand or finger in the rectum. When the
pus has been evacuated a drainage tube may be inserted through the
cannula and left in place when the latter is removed so as to allow free
drainage at all times and frequent antiseptic injections. Punctures and
even incisions have been made from the rectum, but they make badly
infected wounds, and a rupture into the urethra, determines infection on
that side, without any possibility of any effective antiseptic injection
or perfect drainage. As injections may be used permanganate of potash
1:10000, or boric acid, a saturated solution. Poisonous agents must be
eschewed or used with the greatest circumspection.

CHRONIC PROSTATITIS.

Causes. Follows acute. Same causes less potent. Lesions: as in acute,
or sclerosis, and abscess. Symptoms: delayed urination, last glairy or
purulent, constipation, defecation followed by urethral discharge,
little genital ardor, rectal palpation, tenderness of prostate to hand
or catheter, atony of hind limbs. Treatment: open air life, idle, milk
or succulent diet, saline laxatives or enemata, avoid generative
excitement, castrate, check masturbation, iodine, camphor, antiseptic
irrigations.

_Causes._ The acute disease often subsides leaving an indolent chronic
inflammation of the organ. Apart from this, the causes are essentially
those of the acute, but acting with lessened force or on a less
susceptible system. Thus indoor life and overfeeding, with constipation
and urine of a high density, calculus, irritant diuretics, the frequent
incautious use of the catheter, infection from the catheter or
otherwise, intense and frequent generative excitement, and exposure to
cold are all occasional factors. Old age is a common concurrent cause.

_Lesions._ As in the acute form these indicate three successive,
independent or concurrent forms, follicular, interstitial and
suppurative.

With the distinctively =follicular= form the gland is usually enlarged
and of a deep red color, but soft and friable, and when compressed
exudes from its follicles and gland ducts a whitish muco-purulent glairy
liquid. With the =interstitial= changes, which are often an advance on
the follicular, the organ may be enlarged or shrunken, but the
connective tissue has undergone a thickening and sclerosis which renders
the mass firm and resistant, and which may have extended to the tissues
in the immediate vicinity. In the =suppurative= form or stage, foci of
suppuration are found throughout the gland substance, bulging out on its
surface and even encroaching on surrounding tissues.

_Symptoms._ These are by no means obtrusive. There may be some delay in
the discharge when the animal attempts to urinate, and the last drops of
the urine, white and purulent or glairy, may be passed with evident
pain. There is a tendency to constipation with painful straining to
defecate. Compression of the prostate during defecation presses out its
muco-purulent contents so that there is a greater urethral discharge
following this act than at other times. This is also more abundant from
the compression of the abdomen when the animal is lying down. This
discharge is easily distinguished from semen by the absence or almost
complete absence of spermatozoa and _the abundance_ of spermatic
crystals, precipitated by ammonia phosphate. In the earlier stages there
may be undue generative excitement, erections, and even seminal
discharge, with or without the movements of masturbation but in advanced
cases genital ardor is usually defective or there may be practical
impotence. Conclusive evidence is obtained by rectal exploration, when
the enlarged, or irregularly shaped and tender prostate can be easily
recognized. If a sterile catheter is passed the pain caused as it
touches the prostate is significant.

In the dog the affection may last for years, and tends to advancing
atony of the hind limbs. A temporary arrest of the affection is often
misleading, though the urine may be clear and normally discharged, yet
manipulation may show a gradually advancing abscess, and when this
bursts, usually into the urethra, all the symptoms become aggravated and
cystitis, urethritis and general infection are to be dreaded.

_Treatment._ This is far from satisfactory yet in certain purely
follicular or catarrhal cases it may prove successful. An open air life,
without exertion, and a milk and farina diet are desirable, yet any
tendency to costiveness must be obviated by saline laxatives and
enemata. The avoidance of generative excitement must be secured, not
only by restraining stud animals from service, but by keeping them well
apart from all females of the same species. Even castration may be
sometimes resorted to with advantage. Stallions given to masturbation
must be restrained by net or otherwise. Any disease of the rectum, anus,
urethra or bladder should be corrected, and undue exposure to cold
prevented. Lafosse advises to slaughter butcher animals for food.
Hertwig recommends iodine ointment on the anus and perineum of affected
dogs. It must be borne in mind that the affection is maintained by
infective microbes yet it is difficult to reach and deal with these
thoroughly and effectively.

As an anaphrodisiac may be given camphor, or camphor bromide, ergot or
potassium bromide, along with the mild stimulating antiseptic eucalyptol
or copaiba. But the irrigation of the urethra, bladder and as far as
possible the prostate with such antiseptic solutions as potassium
permanganate (1:10000) or silver nitrate (0.5 to 1:100) or zinc chloride
(1:100) is desirable. These should be injected into the urethra so as to
reach the bladder, the contents of which they will render antiseptic and
thus protect the organ against the transported microbes of the prostate.
In man iodoform, europhen, and ichthyol are made into a bougie with gum,
palm butter or other soluble liquifiable agent and inserted in the
urethra as far as the prostatic part. Similar agents are used as
suppositories or enemata. Hertwig’s iodine ointment on the perineum may
be advantageously replaced by sinapisms.

HYPERTROPHY OF THE PROSTATE.

In old dogs. Causes: age, overfeeding on albuminoids, rectal impaction
or irritation, calculus, cystitis, urethritis, productive
inflammation, trophic derangement when function declines. Lesions:
hypertrophy general or partial, hard or soft, condensed or with sacs
of pus, red or pale. Infective cystitis. Calculi. Symptoms: straining
before urine comes, small or weak stream, sudden check, last part
purulent or mucous, incontinence, triple phosphate, ammoniacal odor,
crystals and dark color imply calculus. Diagnosis: by rectal
exploration, and catheterization. Treatment: palliative, moderate,
farinaceous, laxative diet, warmth, correct contiguous troubles,
iodine, castration, extirpation of prostate.

This has been seen almost exclusively in old dogs, among the domestic
animals.

_Causes._ Age and good living, more particularly on highly albuminous
food, may be adduced as the most prominent. Perhaps even more important
are continued irritation in adjacent organs such as the rectum, bladder
and urethra. It is the old, pampered dog that above all suffers from
atonic, overloaded rectum, proctitis, piles, calculus, cystitis, and
stricture, and the constant local pelvic congestion caused by one or
other of these tends to a hyperplasia of the prostate. Again atheroma
which is especially a disease of the aged is regarded as a cause of both
cystitis and prostatic hypertrophy. Chronic inflammation in the prostate
has been claimed as a factor, but contested on the ground that
inflammation never increases normal growth though it may cause
degeneration. The exudate of inflammation, tends, however, on its
temporary arrest, to undergo organization, and such organization
inclines to assume the structure which is normally built up by the
adjacent trophic cells. The products of inflammation may, therefore,
well contribute to hypertrophy, and above all to the increase of the
simpler tissue represented by the fibrous framework of the gland. The
congestion attendant on excessive venery has also been incriminated, and
this too has been denied on the ground that the hypertrophy is not found
in the young animals and men in which the generative ardor is greatest
and most frequently aroused and gratified. Thompson’s idea is that the
prostate, like the ovaries and womb, is especially prone to morbid
growths and developments at the time when in advancing age, the normal
generative functions are undergoing a rapid decline. The two conditions
may well be recognized without considering them as mutually excluding
each other as causative factors.

_Lesions._ The enlargement is usually general, but it may predominate in
the right, left or median lobe, the latter as a rule exercising greater
compression of the urethra so that this is often marked in the worst
cases. The hyperplasia may feel firm and resistant or it may be more or
less soft from sacs of muco-purulent fluid imprisoned by the obstruction
of the outlet canals. On the surface and on section the general
appearance of the gland is pale, bloodless and uniformly solid. This
comes from the great hypertrophy of the fibro-muscular stroma which has
in many cases compressed the parenchymatous or secreting structure so as
to cause its atrophy. The presence of calculi (mainly phosphatic) in the
follicles is not uncommon.

The complication of infective cystitis is frequent, the congestion,
redness, ecchymosis, maculation, puckering and thickening of the mucosa,
the granular degeneration and desquamation of the epithelium, the
exposure of a raw vascular surface, the discoloration of the urine by
mucus, pus and blood, and the formation of ammonia and other products of
decomposition, becoming marked phenomena. Vesical calculus is not
uncommon, the slowness of the exit current of the urine retarded by the
enlarged prostate, tending to prevent its impaction in the orifice and
thus minimizing one of the most prominent symptoms.

_Symptoms._ Among the earliest symptoms, is some modification in the act
of micturition. Straining a few seconds before urine comes, retention,
incontinence and dribbling, discharge in a small or weak stream, and
sudden arrest of the flow and the last few drops may contain muco-pus
showing abundance of spermatic crystals, on the addition of ammonia
phosphate. Impaction of the rectum tends to occur sooner or later, the
animal making little effort to unload the viscus, and the overdistended
organ becoming more and more atonic, congested and catarrhal and
reacting injuriously on the urinary organs. Incontinence may be
especially marked during sleep, the sphincter being sufficiently
controlled by volition during waking hours. Retention may be at first
temporary from excitement and later more continuous by reason of the
greater compression of the neck by the enlarged and indurated prostate.
With the advance of the disease the urine shows abundance of triple
phosphates, and becomes ammoniacal and fœtid. A dark or bloody color of
the discharge and the presence of crystals suggest calculus.

An accurate _diagnosis_ can only be had by rectal examination. The great
enlargement of the prostate, in the absence of heat and tenderness is
characteristic. Enlargement is usually uniform, though it may be
concentrated on the right, left or central lobe. The passage of the
catheter may be obstructed, but is not specially painful at the
prostatic region as in prostatitis. From =vesical calculus= it is
distinguished by the fixity of the swelling on the neck of the bladder
as contrasted with the mobility of the stone inside that half-filled
organ. From =stricture= it is differentiated by the fact that the
obstruction offered to the catheter and the swelling of the prostate
exactly correspond in position, that the stream is lessened in force
rather than simply reduced in size, and that the history of the case
shows no antecedent cause for stricture.

_Treatment._ This has been considered as mainly palliative. Special care
of the general health and above all of the diet which should be
moderate, farinaceous and laxative, protection against cold and wet, the
correcting of any coexisting trouble of the urinary or generative
organs, and the removal from all sources of generative excitement are
important elements. Occasional small doses of Epsom or Glauber salts in
draught or enema obviate rectal hyperæmia. Ergot, potassium iodide
internally, and iodine or mercurial ointment to the perineum have had
little good effect. Möller claims to have secured improvement from the
injection into the prostate at intervals of fourteen days, of a solution
of two parts each of tincture of iodine and iodide of potassium, and
sixty parts of distilled water. A small hypodermic syringe is used and
the injection is made through the rectum directly into the substance of
the prostate. Glass has adopted the recent surgical alternative of
castration, with the result of marked relief from the active symptoms in
a number of cases, but with a more rapid advance through emaciation and
marasmus to death in three or four weeks in others. We would suggest a
careful antiseptic castration in such cases, to obviate any added
trouble from absorbed toxins or sepsis.

For the human subject, Lydston strongly advocates removal of the
enlarged prostate by surgical means in strong, vigorous subjects, with
healthy bladder and kidneys. The difficulty of such an operation in the
dog is greatly enhanced by the relatively greater length of the
pubio-ischiatic symphysis, and the lessened diameter of the pelvic
cavity. Yet with the comparative immunity of the dog from suppuration,
and the hopelessness of the case without such radical measure, and with
the rigid application of an antiseptic technic, the operation would
appear to be fully justified. It would be contra-indicated in all
advanced cases, in which the prostate was the seat of active suppuration
with discharge into the urethra, in cases complicated by urethritis,
cystitis or nephritis, in cases in which there is marked prostration
from sepsis or absorbed toxins, and generally in old, worn out and
cachectic animals.

Short of this, in cases complicated by cystitis, antiseptics by the
stomach and as injections into the bladder are desirable. Eucalyptol in
doses of ten minims four times a day, or beta naphthol, guaiacol, or
phenol have been used in man. As injections mercuric chloride 1:20,000;
boric acid, saturated solution; or carbolic acid ·5:100 (Lydston) may be
used warm several times a day.

TUBERCULOSIS OF THE PROSTATE.

This is a common seat of tubercle in generalized tuberculosis in cattle,
and may give rise to the same urinary troubles as chronic prostatitis or
hypertrophy of the organ. In a remarkable case recorded by Frauenholz
the tuberculous prostate of an ox weighed 10½ lbs. and had contracted
adhesions to surrounding pelvic organs. Section of the mass showed
numerous centres of extensive caseous degeneration. In such cases the
generalized tuberculosis is the important fact and the prostatic disease
is only an unusually intractable complication. If less generalized, the
implication of the testicle or epididymus is strongly suggestive, and
examination of the urine may detect the tubercle bacillus, or the
tuberculin test may develop the characteristic febrile reaction.

CANCER OF THE PROSTATE.

Lafosse records as colloid cancer a case of diseased prostate in an ox,
in which the mass approximated to the size of the human head, and was
made up of numerous cavities the largest not over 1½ inch in diameter,
and all intercommunicating, and containing a gluey, or gelatinoid liquid
with numerous small round cells and a few multinucleated giant cells. No
evidence is given of the implication of even the adjoining lymph glands,
so that the case was probably only an enlarged cystic prostate.

Fournier records a case in a three year old horse, which on necropsy
showed a ruptured bladder, general peritonitis, and an enlarged
prostate, involving Cowper’s glands. Nocard identified its cancerous
nature by microscopic examination. Yet there is not a word of the
implication of adjacent lymph glands.

Goubaux says prostatic cancer is common in dogs.

PROSTATIC CYSTS.

These are not at all uncommon as a complication of hypertrophy of the
prostate, the ducts having become obstructed and the follicles
indefinitely distended. The case described by Lafosse as cancer of the
prostate of a bull is strongly suggestive of such retention cysts.

CALCULUS OF THE PROSTATE.

Two forms of calculi have been found in the prostate in domestic
animals: 1st, small, round, angular or branched bodies made up in
concentric layers and formed of organic nitrogenous bodies: and 2nd,
genuine calculi of calcium phosphate or ammonia magnesian phosphate.
These may cause pressure on the parenchymatous tissue and atrophy, but
in the lower animals they are seldom the direct cause of prominent
morbid symptoms. They must, however, be recognized as one of the causes
of chronic irritation that contribute to prostatic inflammation and
hypertrophy.

DISEASES OF THE FEMALE GENERATIVE ORGANS.
MALPOSITION OF OVARY AND WOMB. HERNIA OF THE OVARIES.

Inguinal or crural hernia of ovary or womb. Bitch. Long uterine horns,
loose broad ligaments; Sow; Ewe; Cow. Other openings. Symptoms: not
marked: strangulation: inflammation: abscess. Gravid hernial uterus.
Treatment: reduction: surgical means: Cæsarian section.

The most common displacement of the ovary in the lower animals is
through the inguinal or crural arch. It is most frequent in the bitch
doubtless for the reason that the horns of the womb are long, and widely
separated from each other, and in any case of inguinal or crural hernia,
or of undue dilatation of the openings they are liable to pass through.
A relaxation of the broad ligaments is another condition of such
displacement. The laxity of these ligaments in the normal condition in
the sow favors ovarian hernia, and Dupont found the ovaries in the
perineal region in five sows examined. Laux found the condition in ewes,
and Müller in cows, one ovary lying on each side of the mammæ. With
relaxation of the uterine ligaments the hernia might occur in any female
mammal, and not only through the orifices named, but through any normal
or adventitious opening in the abdominal walls.

_Symptoms._ In the bitch the hernia is often overlooked although an
examination of the inguinal region will reveal the presence of a small
nodule and vermiform body which may usually be returned into the
abdominal cavity. In some cases it becomes strangulated by the gradual
contraction of the neck of the hernial sac, followed by swelling, heat
and tenderness of the hernial mass, which may go on to abscess
formation. In exceptional cases impregnation occurs with the womb in
this position and the steady nodular increase of the mass, and finally
the automatic movements of the contained fœtuses become very
characteristic.

_Treatment_ consists in passing the womb and ovary back into the
abdomen, and if adherent or incarcerated, in exposing and releasing, and
if necessary extirpating them. In case of advanced pregnancy with the
gravid womb on the inner side of the thigh, a modified Cæsarian
operation is required without the attendant danger of laying the
peritoneal cavity directly open. Inflammation and abscess must be
treated on general principles.

UNDEVELOPED OVARIES. ABSENCE OF OVARIES.

The absence of ovaries has been often noticed in twin heifers, and most
commonly associated with deficiency or absence of the womb, and even of
the anterior part of the vagina. The condition is especially common,
though not constant as some have supposed, when the other twin was a
male. Such females are known as _free martins_ and fail to breed. Even
when the ovaries are present in such twins they remain undeveloped, and
are no larger than a bean or hazel nut. These usually have a firm,
fibrous structure, and though there may be interspaces filled with a
transparent fluid, no true Graafian follicles are formed. In birds, the
left ovary only is developed and physiologically active. The absence of
ovary has been noted also in the ewe, and less frequently in the mare
and other species, and appears to be more common in twins than in single
pregnancy. In cattle only has the influence of the male on the female
twin of the same pregnancy been specially noted.

It has been noted that females with ovaries undeveloped, tend to show
many male characters, in head, horns, and neck in cattle, in plumage in
birds, and in voice in both.

ATROPHY OF OVARIES.

This is observed as a physiological result of having passed the breeding
age, and may also take place from disease and degeneration of the organ.
The fibrous stroma is usually increased and the cell elements reduced,
yet in some cases, a cystic development occurs, giving the appearance of
hypertrophy, while the ovarian parenchyma has actually been diminished.

SUPERNUMERARY OVARIES.

Extra ovaries have been found in different cases in the human female,
the additional organ being furnished with a fallopian tube, and in some
instances an extra uterine horn. No facts are at hand concerning the
lower animals, but the occurrence of gestation and the birth of a single
puppy a year after careful castration, would seem to suggest that the
condition occurs in the bitch. There is no embryological reason why the
lower animals should not at times show this deviation from the normal.

IRRITABLE OVARY. NEURALGIA OF THE OVARY.

This has been noticed most commonly in the mare, which from a quiet
docile animal, has become very ticklish, especially in the region of the
flank, kicking on the slightest touch, or even when approached and
showing an amount of nervous apprehension, that may render her useless,
for work. The ovaries are usually found to be enlarged, diseased and
very sensitive. Œstrum may be in some cases constant and excessive and
in others entirely suspended. Such cases are difficult or dangerous to
shoe. In one case recorded by Thierry, handling of the flank promptly
induced an epileptic attack. Cows with nymphomania (bullers) are often
victims of this condition. The only remedy is castration, which is best
performed by the vagina. The shorter the period of the irritability the
more perfect is the cure. In some old standing cases the vicious habit
may have become so fixed, that it is continued in spite of the
operation.

HÆMORRHAGE ON THE OVARY.

Mare and Cow: genital excitement, mechanical injury, diseased ovary in
unimpregnated, ovulation with bleeding, falls, slings. Lesions: old
degenerations, productive inflammation, varicosities, aneurisms,
torpid vessels, blood staining, clots, follicular or not, ruptures
into peritoneum, amount, microbes usually absent. Symptoms: obscure,
arched, stiff loins, colics, recumbency, large tender ovary.
Shivering, fever, anorexia, anæmia, surface coldness, unsteadiness,
blood from vulva, liquid in abdomen fluctuates. Treatment: cold, ice,
snow, on loins, cold acid drinks, tannin, iron chloride, matico,
gelatine, subcutem atropin, ergotin, viburnum, derivatives,
castration.

This has been seen in the mare and cow especially in connection with
genetic excitement and mechanical injuries, and more especially
pre-existing disease of the ovary. Trasbot notes that it has always been
in the absence of pregnancy, a fact which we can easily explain on the
ground that most active diseases of the ovary render the animal barren.
Gestation like castration, calms the genetic instincts, and prevents the
recurrence of œstrum with its vascular excitement, general and ovarian,
which characterizes the unimpregnated condition. The normal rupture of
the Graafian follicle and escape of the ovum is attended by some
effusion of blood which passes through a series of changes preparatory
to absorption. A more extensive bleeding, at the time of œstrum or
otherwise, into a follicle or intrafollicular, and with or without
rupture of the albugenic tunic constitutes the morbid hæmorrhage. Among
mechanical causes may be named violent exertion, falls, and suspension
in slings.

_Lesions._ Some cases in mares and cows show old standing lesions, to
which the extravasation is secondary: a productive inflammation of the
ovarian stroma; varicosity of the ovarian veins; aneurism of the
utero-ovarian artery: the presence of emboli or thrombi. In the area of
the effusion there is a general turgescence of the vessels, and blood
staining of the stroma. Or there are distinct blood clots in the
follicles or between them, a few lines or an inch in diameter, buried in
the depth of the organ, or standing out in rounded swellings on its
surface, and sometimes with a rupture two or three inches in length, and
the escape of blood into the peritoneal cavity. This may be sufficient
merely to stain the peritoneal fluid, or it may amount to one or two
bucketfuls as in cases recorded by Barrow and Palat. In the absence of
rupture the effused blood may completely surround the ovary, or may
accumulate in one or several of its distended follicles. The effused
blood is rarely septic, being usually free from microbes, and it may
remain fluid in the peritoneum, or coagulate in the ovary. The enlarged
follicle may contain a dark red fluid, in which floats a solid clot,
varying in color from dark red to light yellow, according to age.

_Symptoms._ These vary greatly with the extent of the lesion, and are
always somewhat obscure. With slight interstitial or intrafollicular
effusion, there may be only some general disorder, with, it may be,
arching and stiffness of the loins, colicy pains, a desire for
recumbency, and enlargement and tenderness of the ovary on rectal
examination. In more severe cases as noticed by Cordonnier, Saucour and
Palat in mares, by Laponsée in the ass, and Renault in the cow, there
were shivering, hyperthermia, respiratory and cardiac acceleration,
congested mucosæ, dull colicy pains, and anorexia, followed by
indications of anæmia, small, weak, rapid pulse, pale mucosæ, coldness
of ears and legs (in cows, of muzzle and horns), violent heart action,
indisposition or inability to rise, unsteadiness on the limbs when up,
and in some cases the escape of blood from the vulva. By rectal
examination the enlarged, tender, doughy ovary may be characteristic and
the fluctuation of liquid in the peritoneal cavity, which may also be
recognized by manipulation of the flank.

_Treatment._ This should be directed toward checking the hæmorrhage:
Cold water or ice, on loins or flank: injections of cold water: cold
water or acids or astringents by the mouth: tannic acid: iron chloride:
matico: gelatine: atropine, ergotin. By way of quieting ovarian
excitement, viburnum prunifolium or opium may be tried. Sterilized
solutions of gelatine may be given subcutem. Mustard or ammonia may be
applied to limbs or flank. In case of survival, castration will be
indicated.

INFLAMMATION OF THE OVARIES. OÖPHORITIS. PERIOÖPHORITIS.

Mares, cows, sows, etc. Causes: traumas, œstrum, parturition,
leucorrhœa, pus infection, strangles, dourine, glanders, abortion,
tuberculosis, chill, poisons. Lesions: Ovary enlarged unequally, red,
congested, exudate, extravasation, fibroid, caseated, purulent,
abscess single or multiple, indurations, cretefactions, cysts,
blocking of Fallopian tube, adhesions. Symptoms: mare: genital
erethism, soiling of vulva and tail, colics, tender loins and mammæ:
fever, dullness, emaciation, decubitus, paraplegia, swollen tender
ovary: cow: bellows, paws. Sterility, anæmia, pyæmia. Treatment: Cold
to croup, mustard, anodynes to vagina, calmatives, antiseptics.
Castration.

This has been frequently seen in mares, cows and sows, but it may occur
in any of the female mammals or even in birds.

_Causes._ The condition has been ascribed to blows on the flanks,
pressure on the abdomen and the congestion of the ovary which attends on
frequent œstrum in the absence of the physiological quiet which comes
from conception. In a large proportion of the cases, however, the attack
has followed on parturition, abortion, a preëxisting leucorrhœa or
metritis, or a suppurating process in some other part of the body. These
cases therefore, must be looked upon as secondary and infective, the
microbes having been transferred from the womb, along the Fallopian
tubes, or through lymph vessels, or peritoneal cavity, or finally
through the circulating blood. In mares strangles, abortion, leucorrhœa,
dourine and glanders, and in cows and sows abortion, metritis,
leucorrhœa, and tuberculosis, may prove the starting point of the
infection.

Sudden chills when heated, perspiring or exhausted and especially
exposure in inclement weather just before or after parturition, have
been regarded as effective causes, and doubtless these lower vitality
and power of resistance, but back of these we must look for infection
coming from the parturient womb.

Bivort records an extensive epizootic of oöphoritis in sows kept on
waste ground which had been used for herding swine years before. He
attributes the trouble to poisonous plants, without, however, attempting
to identify them, and the probability is even more strongly in favor of
infection left over from the former herds.

_Lesions._ The inflamed ovary is swollen slightly, or to a great size,
in mare or cow like the fist or even an infants’ head. The swelling,
however, is unequal throughout, and the surface may bulge in rounded
masses at different points. In the early stages the organ is firm,
elastic, red and on the cut surface bleeding, with here and there a
distended follicle with bloody or gelatinoid liquid contents. The
exudate into the fibrous stroma may become coagulated, and later may be
organized into fibrous substance giving a hard resistant sensation to
the finger (sclerosis). In some cases this may become partly
cartilaginous. In other cases the distended follicles may have their
contents coagulated and transformed into a caseous mass, while much of
the stroma has become liquefied and absorbed. When suppuration has set
in, the gland is softened at this point, the parenchyma giving way
before the pus. The pus may be in multiple sacs, as if formed in the
Graafian vesicles, or it may be in one undivided abscess. In the ovary
of a cow, Eléouet counted no less than sixty-three separate abscesses.
In cases complicated by ovarian glanders, tuberculosis or actinomycosis,
the gross, microscopic, and mycotic characters of the lesions will
afford the means of diagnosis.

In chronic forms indurations, cretefactions, cystic degenerations,
caseations, and sclerosis may be met with.

Lesions in adjacent structures are common, such as thickening and
stenosis of the Fallopian tube; congestion, thickening and puckering of
the mucosa in the adjacent part of the womb; peritonitis; adhesions of
the ovary to the abdominal walls or to an adjacent organ.

_Symptoms. Mare._ In many cases the early phenomena are those of
excessive genital erethism: the animal is restless, feverish, whinnies
to attract other horses, snuffs the males on their approach, contracts
the vulvar muscles constantly, exposing the congested mucosa and
clitoris, and ejecting a glairy liquid which soils the tail, hips,
thighs and hocks. She strains frequently, passing small jets of high
colored turbid urine, and rubs the tail and hips against available
objects, twisting and breaking the hair and abrading and excoriating the
surface. The croup may be alternately drooped and raised and the tail
switched. These phenomena are not abated by copulation, nor by time,
like ordinary heats, but will last for one or more weeks when a new set
of symptoms set in. Meanwhile dull colicy pains cause restless
movements, arched back, frequent moving from place to place, crouching
by partial bending of the limbs, twisting of the hind parts from side to
side. The loins are tender to pressure, and the middle of the flank to
pressure or percussion. The mammary glands are usually hot, swollen and
tender. The genital erethism may last from four to seven days. Then it
subsides, with coincident improvement of the general symptoms and a
recovery ensues. Relapses are to be expected sooner or later.

In fatal cases the erethism subsides, but fever, dullness and emaciation
continue, the case becomes aggravated at intervals, weakness and
exhaustion increase, decubitus may become constant or paralysis ensue.
The patient dies in marasmus in one to three months.

In some the genital erethism is absent from the first. There is
dullness, prostration, anorexia, fever, hurried breathing, small rapid
pulse, colicy pains, tender abdomen, difficult defecation, coated dung,
a glairy (perhaps reddish or fœtid) discharge from the vulva, hot, tumid
tender mammæ, arched and sensitive loins, and stiffness of the hind
limbs.

In all cases alike a rectal examination detects the ovary swollen and
exceedingly tender.

_Cow._ The same general symptoms appear with characteristic
modifications. Restlessness, bellowing, pawing, inappetence, arched,
tender loins, swollen vulva with discharge, shiny and perhaps fœtid but
without contractions, abdomen pendent and flanks hollow and tender,
udder turgid, hot and painful, movements of the hind limbs stiff,
halting, straddling. There is greater tendency to salacious movements of
the croup. The diagnostic feature is palpation of the ovary through the
rectum.

In _chronic cases_ more or less of the above symptoms are shown in a
greatly mitigated form, but oftentimes there are long intervals of
apparent health. Palpation through the rectum is the final test in this
as in the more acute cases.

_Prognosis._ This is very uncertain. Unless complete recovery takes
place in a few weeks, the inevitable consequence is sterility, or death
from hæmorrhage, peritonitis, pyæmia, or marasmus.

_Treatment._ In acute cases Trasbot strongly urges bleeding in the
larger races and leeching of the flanks in the smaller. Mustard plasters
to the loins and abdomen, and cold or damp applications to the croup are
in order. Vaginal and rectal injections of mucilaginous liquids,
containing anodynes and antiseptics are indicated. Opium, belladonna,
hyoscyamus, chloral, borax, acetate of aluminium may serve as examples.
If needful to quiet the excitement, morphia, atropia or hyoscyamine may
be given subcutem. Or the anodynes may be administered by the mouth. As
a last resort, and by far the most radical treatment, castration may be
performed. With small ovaries this is best done through the vagina in
the larger animals, while with large and adherent ones the flank
operation is imperative. If the peritoneum is involved, careful
antisepsis of the cavity is desirable. In case of adhesions the
operation may be risky, but if successful it will obviate secondary
infections and establish a permanent cure. Complications must be treated
according to their nature.

OVARIAN CYSTS.

Mare, cow, ewe, sow, bitch, hen. Forms. Histogenesis. Dilated
vesicles, egg tubes, blood obstruction. Lesions: Ovary large, smooth,
lobulated, vascular, size, connective tissue, epithelium, liquid
contents. Abscess. Symptoms: impaired portal circulation,
muco-enteritis, piles, intestinal torpor, impaction, constriction,
obstruction, congestions, inflammation. Urinary disorder.
Strangulation. Sterility. Abortion. Dystokia. Indigestion. Anorexia.
Colic. Genital erethism. Straining. Altered Urine. Peritonitis. Septic
infection. Collapse. Rectal palpation, enlarged, sensitive ovary.
_Treatment_: Castration. Tapping cyst. Rupturing cyst by compression.

These have been met with in all races of domestic animals, mare, cow,
ewe, sow, bitch and hen. They vary greatly in their characters, being
unilocular, multilocular, rounded or lobulated, serous, albuminous,
colloid or hæmorrhagic, strictly ovarian or parovarian (in broad
ligaments), in one ovary or in both.

_Histogenesis._ The source of these cysts has been much debated. Many
have held with Spencer Wells that they have their origin in dilated
Graafian vesicles, and the discovery of an ovum in the contents, by
Rokitansky and Ritchie showed at least that this follicle had formed
part of the cyst. On the other hand Foster, Rivolta, Klebs, Malassez and
others, constantly failed to find ova or other distinct elements of the
Graafian follicles, but did find epithelial elements, and note that the
cysts are at an early stage connected with the surface of the ovary like
the egg tubes. These embryonic tubules of Pflueger are therefore held to
be the starting point for the cysts, which because of their mixed
epithelial as well as liquid contents, seem allied to adenoma. From
observations on the ovarian cysts of the lower animals Galtier, attaches
great importance to vascular obstructions. Obstruction by pressure or
otherwise led to hæmorrhages and transudation of blood, and the cavities
formed in this way became the seats of epithelial growth, and liquid
effusion. The blood remained for a time as distinct clots, and was later
indicated by the pigmentation of the walls of the cyst.

_Lesions._ The enlarged ovary may be uniformly rounded and smooth, or it
may be marked by irregular bosses, giving it a lobulated appearance. It
is very vascular, and is often covered by a thickening of peritoneum.
When multiple they are usually closely adherent and may even be included
one within another. The individual cysts may be of the most varied
sizes. The cystic ovary has at times reached enormous dimensions: in the
mare 46 lbs. (Bouley, Rivolta, Thiernesse): in the cow 250 lbs.
(Reynolds, Meyer): in the ewe 7 lbs. (Willis): in the sow 7 lbs.
(Reyer): in the bitch 15 lbs. (Bovett). The walls of the cyst are formed
of connective tissue more or less perfectly organized, arranged it may
be in several superposed layers (Galtier) and lined or not by epithelial
cells (cylindroid, nucleated, or of various forms). They may be reddened
by hæmorrhages or pigmented from former blood extravasations. The liquid
contents may be clear and watery, white, straw yellow, or of a deeper
yellow, brown or red. Among other constituents there are alkaline
chlorides and sulphates, albumen in solution or flakes, mucin, fibrine,
fatty granules and cholesterine crystals. In some instances they contain
pus cells (chronic abscess).

_Symptoms._ Small, tardily growing cysts may cause no appreciable
symptoms. The larger ones or those that increase rapidly are liable to
cause disorders of circulation, innervation and digestion. The mere
pressure of a considerable cystic ovary may interfere with portal
circulation so as to entail muco-enteritis, rectal congestion, piles, or
intestinal torpor or impaction. Adhesions of the diseased ovary to
adjacent intestinal viscera, tend to produce constrictions, obstructions
and local congestions or inflammation. In adhesions to the womb or
bladder, ureter or kidney, the symptoms will indicate disorder of these
respective parts. The weight of the enlarged ovary causing extension of
its ligamentous connections will allow of its winding around a loop of
intestine and producing strangulation. In those unusual cases in which
pregnancy occurs it may interfere with its completion, causing abortion
or, failing in this, with parturition, by becoming imbedded in the
pelvis. In the line of innervation, disorder is especially common in the
digestive organs, anorexia, nausea, impaired rumination, and colicy
pains resulting. Again, in many subjects the genesic instinct is
stimulated, the patient is more or less constantly in heat, cows become
_bullers_, and mares _switchers_, they cannot be impregnated, and under
the continuous excitement undergo rapid emaciation. There is often
urinary disturbance, frequent straining with the passage of a small
quantity only of turbid or glairy liquid, colored, it may be, by blood,
or fœtid. The colics are liable to be dull and slight, the patient
moving uneasily, switching the tail, moving the weight from one hind
foot to the other, pawing, looking at the flank, but seldom lying down
or rolling. In other cases, with adhesions, impactions, obstructions,
and congestions, all the violent motions of the most intense spasmodic
colic may be shown. Where there has been rupture of the obstructed
bowel, these symptoms may merge into those of peritonitis, septic
infection, or collapse. When with these symptoms of intestinal disorder,
there are tender loins and flank, abdominal plenitude and tension,
genital excitement, frequent straining to pass urine, the discharge of a
glairy or fœtid liquid, and when all these symptoms have increased
slowly for weeks or months in a female, the ovaries may be suspected and
a rectal examination should be made. Usually the outline of the womb can
be made out with the enlarged and irregularly shaped ovary anteriorly
and adherent to it through one of the broad ligaments; it may be
sensitive to touch, tense, or even fluctuating. Difficulty may be
encountered when the enlarged ovary is so great as to fill the whole
region, or when adherent to or wound round the rectum, thus hindering
the advance of the hand or the movement of the gut, or when it has
become pediculated and displaced to a distant part of the abdomen. Even
the obstructed and distended intestine, may prevent a satisfactory
diagnosis. Yet in the great majority of cases rectal examination gives
conclusive results.

_Treatment._ Medicinal measures are useless: surgical alone are of any
avail. Castration is the natural resort, and in all recent cases,
uncomplicated by adhesions, is to be preferred. In the large females it
may often be performed through the vagina, but if the ovary is very
large the flank operation becomes imperative. Sometimes the evacuation
through a cannula of the contents of one or more large cysts will so
reduce the mass as to allow of the safer vaginal operation.

A less radical measure is the evacuation of the cyst with cannula and
trochar and the injection of tincture of iodine. With a hand in the
rectum the ovary may be held against the abdominal wall to facilitate
the operation. The results, however, are not satisfactory, for, although
re-accumulation of the liquid is delayed, it is not entirely prevented.
Moreover, when the cysts are multiple, the punctures also must be
numerous, or remain ineffective. Nor is the operation unattended by
danger as deaths often occur from resulting inflammation, infection, or
iodine poisoning.

Zannger, in 1860, introduced the method of rupturing the cyst without
incision, and met with considerable success. With the hand in the rectum
the cystic ovary is pressed against the wall of the pelvis or abdomen,
until the attenuated wall of the cyst gives way, the fluid is left in
the abdominal cavity, to be absorbed and many animals will afterward
become pregnant. In a large proportion of cases in which the symptoms
are marked, the walls of the cyst are sufficiently attenuated to allow
of rupture by pressure, and, if the escaping contents are free from
infecting microbes, no immediate harm comes to the peritoneum. It should
be avoided in case of abscess, following perhaps on a shivering fit and
constitutional febrile reaction, and when there is a fœtid discharge
from the vulva, suggesting microbian infection likely to dangerously
infect the serosa. In appropriate cases it is a resort of very great
value, in restoring to use animals that are especially valuable for
their progeny and which become utterly useless when rendered barren.
According to different observers an average of 70 per cent. can be
restored to usefulness in this way. Friedberger and Fröhner claim 90 per
cent. Some febrile reaction may be noted for twenty-four hours,
demanding rest, restricted, cooling, laxative food and sometimes
laxatives and anodynes.

DERMOID CYSTS OF THE OVARY. PILOUS CYSTS.

Closed cutaneous sacs, with hair and sebum. Causes: enclosure of
dermoid tissue in embryo: aborted ovum: virgin gestation. Symptoms.
Treatment: Castration.

These are much less common than are simple cysts. They are closed sacs,
lined by a tissue essentially representing skin, and containing
sebaceous matter and hairs, some growing from the dermoid surface, and
others detached and formed into a loose mass.

_Causes._ These cysts have been attributed to the enclosure, in the
forming embryo, of the formative elements of dermoid tissue, which may
or may not remain latent and inactive until maturity, or until the ovary
becomes physiologically active.

Another theory is that an impregnated ovum has remained imperfect,
developing only the elements of the skin, instead of the whole fœtal
body. Many cases cannot by any possibility be included under this head,
seeing that the cyst is found at much too early an age, and its bearer
has never had sexual intercourse.

Another doctrine is that the dermoid cyst is derived from the normal
plastic or formative powers of the ovary, and the product becomes
suggestive of parthenogenesis or virgin gestation. The fact that these
cysts are not confined to the production of skin and hair, but at times
form bone, teeth, nervous and other tissues as well, corroborates this
view. On the other hand we must bear in mind that dermoid cysts are much
more common in other tissues than they are in the ovaries. Thus they are
common in the subcutaneous connective tissue and between the muscles.

The _symptoms_ do not differ essentially from those of simple cysts and
_treatment_ is mainly by castration. As the escape of the contents into
the peritoneal cavity is especially provocative of infection, the
greatest care must be taken to extract the mass whole, or to use the
most thorough antiseptic precautions.

SOLID OVARIAN TUMORS.

These are much more rare than cystic tumors. They seldom maintain the
character of perfect solidity, for whether fibrous, sarcomatous,
melanotic, cretaceous, myomatous, cancerous, epithelial, tubercular,
glanderous, or actinomycotic, they are usually associated with cysts to
a greater or less extent. Not only are they liable to stimulate the
formation of cysts, but the special heteroplasia may become engrafted on
the walls of pre-existing cysts, as well as on normal tissues.

The _symptoms_ of the solid tumors are in the main, those of the cystic
form, and _treatment_ resolves itself into extirpation by castration.
Its success will vary according to the nature of the tumor, sarcoma,
melanoma and carcinoma being especially liable to recur in the same or
in distant situations, and the same is true of the colonizing with
infectious germs (glanders, tuberculosis, actinomycosis) which are
presumably already present in other parts of the body. Castration has,
however, this recommendation, it secures the removal of the entire
diseased organ, and if the morbid process or infection is confined to
that only, it holds out the best prospect of recovery.

INFLAMMATION OF THE FALLOPIAN TUBES. SALPINGITIS.

This condition is met with in the female mammals of all species and
mainly as the result of an infection extending from diseased womb or
ovary. The results are degeneration of the epithelium, exudation into
the mucosa with thickening, stenosis of the tubes, the formation of
cysts along the line of the canal, with pink or straw colored contents,
including fibrine, leucocytes, epithelium and granular debris. As in
oöphoritis there may be blood extravasations and clots and abscess. In
the cow they are at times calcified and create a suspicion of
tuberculosis.

The _symptoms_ are essentially those of metritis or ovaritis, and as
these are usually more prominent the attendant salpingitis is generally
overlooked during life. Careful rectal examination may detect the
enlarged, tender or sacculated tubes. _Treatment_ may be laxative,
diuretic, derivative, and antiseptic toward the womb. Ablation of the
ovaries, tubes and even the womb is often required.

DISEASES OF THE OVIDUCT IN BIRDS.

Imperforate tube near cloaca. Polypus: snare and twist off. Egg
impaction: from atony, inflammation, stricture, congenital smallness,
exhaustion, large eggs, thick end first, broken egg. Symptoms: mopes
alone, feathers erect, wing and tail drooping, large, solid swelling
around anus and abdomen. Rupture into abdomen. Treatment: oil cloaca
and oviduct, manipulate, turn, break egg and scoop out, incise and
extract, antiseptic oils. Excision of ovary.

_Imperforate oviduct_ usually occurs in the lower part of its course,
the tube being connected with the cloaca by a short, fibrous cord. In
the case of a very valuable bird it may be incised and the walls of the
duct may be brought down and fixed to those of the cloaca.

_Polypi of the oviduct_ may seriously impede laying, and start
obstruction and impaction. The seat of the tumor having been
ascertained, it may be seized and twisted off by a snare. An elastic
wire is passed through a small metallic tube so that a loop protrudes
large enough to pass over the polypus. When fixed around the pedicle, it
is tightened, and the tissues twisted through.

=Egg Impaction in the Oviduct.= From weakness or lack of tone in the
bird, by inflammation and loss of contractile power in the oviduct, by
stricture of the duct as a sequel of inflammation or abrasion, by
congenital narrowing, by weakening of the oviduct through constant
laying, by excessive size of the egg, by double yolked eggs, by
presentation of a large egg with its thick end first, or by an egg with
broken shell, the oviduct may be rendered incapable of passing the egg
on and out, and as others continue to press down from above an excessive
and dangerous impaction ensues. The bird refuses food, mopes around with
ruffled feathers and drooping head, wings and tail. The region of the
anus and in front of it hangs downward and feels firm and solid, and the
oiled finger introduced into the cloaca comes in contact with the
impacted mass. The bird strains violently but ineffectually and rubs its
anus on the ground. The swelling goes on steadily and rapidly
increasing, and the bird becomes more prostrate and hopeless. Sometimes
the overdistended and congested oviduct gives way and the eggs escape
into the abdomen. Reul has counted as many as 24 eggs that had thus
escaped into the abdominal cavity. Or without rupture of the oviduct,
the soft eggs pack together into a solid, dry yolk-like mass, the watery
parts having been pressed out or absorbed. In bad cases this may weigh
1½ lb. in the hen (Weber). In the way of _treatment_ the cloaca and
oviduct should be thoroughly lubricated with a bland oil, which might be
injected with a syringe, so as to pass it, if possible, around the
impacted egg or mass. By careful manipulation the egg may now be brought
away. If the thick end is presented it is sometimes possible to turn it
so that the thin end will come first. Should all fail the egg may be
broken and its contents together with the other impacted matter may be
dislodged with a looped wire or small spoon. The oviduct should be
lubricated for some time with a bland antiseptic oil (olive oil and
boric or salicylic acid). In obstinate cases the abdomen and oviduct may
be laid open and both evacuated of any egg matter that may be present.
After suitable antisepsis the wounds in the oviduct and abdominal walls
are to be sutured. If there appears to be danger of the further early
descent of eggs into the weakened oviduct the ovary may be removed.

_Eversion of the Oviduct._ This appears at times as a result of the
intromission of the penis (ducks) being shown immediately after
copulation as a pink, lax membrane one or more inches long, dragging
from the anus. In other cases it appears to result from the paresis that
occurs in old birds from prolonged laying, or from inflammation and
impactions. It may appear abruptly or gradually, and after a few hours
becomes the seat of exudation, swelling and redness, forming a pyriform
mass. In some cases it is carried out around an egg which does not glide
through its canal and may be felt through its walls, and through its
terminal opening. A partial eversion may take place as an invagination
into the cloaca, without showing externally. When an egg is impacted, or
when the protruded organ is inflamed and swollen, violent straining
continues, which tends to aggravate the condition, and the bird gets
rapidly exhausted, resting on its breast, later upon its back, and dying
in convulsions.

In slight cases following copulation, the vermicular movement of the
duct, of the cloaca and anus may serve to secure speedy spontaneous
reduction. In the partial cases, of eversion into the cloaca, the free
local use of oil, may secure the passage of the presenting egg and the
return of the oviduct. If necessary the egg may be broken and its shell
thoroughly extracted. This last method is imperative when the egg
enclosed in the oviduct has already passed through the anus. The oviduct
should then be cleansed in tepid water, and laudanum, oiled and
returned.

_Inflammation of the oviduct_ is a common condition resulting from
debility, from impaction of an egg or of egg-material, from scratching
with the shell of a broken egg, and from microbian invasion. The
frequent passage of large eggs is an accessory cause, and the egg
becomes an important factor in the maintenance and aggravation of the
inflammation. The mucosa becomes red, dry, infiltrated, thickened and
friable, and the muscular coat increasingly paretic. The egg, becoming
impacted, and subjected to constant pressure in the vain efforts at
expulsion, hinders circulation and nutrition, and favors necrotic and
ulcerative processes, and too often the fragile membranous walls yield,
and the mass drops into the abdominal cavity. Short of this, the exudate
at a particular point, the main seat of inflammation, contracting in
undergoing organization, forms a distinct stricture, which renders the
further laying of fully formed eggs difficult or impossible, and further
impaction, inflammation and rupture may follow. Sometimes the irritation
causes undue peristalsis in the anterior and less actively inflamed part
of the tube, and the eggs are laid prematurely without albumen or
without shell, yet with much effort and suffering. Or the bowels become
irritable and a profuse diarrhœa sets in, hastening the exhaustion of
the patient.

_Treatment_ should be applied early. A cooling diet of vegetables or
slops, the careful removal of all irritating contents from the oviduct,
and its frequent injection with bland oils medicated with mild
antiseptics (boric or salicylic acid, or potassium permanganate) will
usually serve a good purpose.

HYDROMETRA AND PYOMETRA.

Cause: chronic metritis, tumors, microbian infection. Symptoms:
ill-health, low condition, vulvar swelling or discharge, swelling and
fluctuation of womb. Rectal exploration. Treatment: evacuate liquid,
disinfect womb and passages, creolin, iodine.

As a rule these conditions belong to obstetrics and would not come under
the scope of this volume, but when in chronic cases, with closure of the
neck of the womb, the liquids accumulate and distend the uterus, they
may deserve mention in a medical work.

The _cause_ is usually a chronic metritis, originating it may be at the
time of a now distant parturition, or associated with tumors or
microbian invasions of the womb. In the deadly cases that follow upon
parturition and abortion streptococcus is usually present, in the more
chronic forms the staphylococcus or other pus microbe.

The _symptoms_ are those of general ill-health, low condition, pallor of
the visible mucosæ, sometimes swelling of the vulva with discharge,
serous or purulent, lessened milk yield, enlargement of the abdomen with
fluctuation felt in the right flank, or still better with the hand in
the rectum. Rectal exploration will further detect the distended uterus
connected with the vagina behind and dividing in front into two horns.

_Treatment_ consists in the evacuation of the liquid through a catheter
or cannula introduced through the os, or through the vaginal wall
immediately above, followed by a systematic disinfection. By placing the
patient upon her back, gravitation of the liquid is more marked, but
when this is not convenient it may be done with the animal standing. The
flow may be favored by raising the abdomen with a sheet held by two
assistants. The womb may be thoroughly cleansed by a normal salt
solution which has been boiled, and then daily injected with a creolin
solution (1 ∶ 100). In hydrometra an iodine lotion may be used. A course
of tonics is often indicated.

UTERINE TUMORS.

These are somewhat rare in the domestic animals, yet they have been met
with in the form of cysts, fibroma, fibro-myoma, sarcoma, and carcinoma.
In a number of cases the nature of the tumor has not been clearly made
out. Mangot saw a mare with two pediculated uterine tumors having an
aggregate weight of 12 lbs. These were expelled with much straining and
suffering. LaMaitre and Rodet record other cases. Stockfleth describes
multiple pediculated fibroid tumors in the womb of the cow. Cysts have
been especially seen in the cow and bitch, and carcinoma in the bitch.

_Symptoms._ These may for a length of time be overlooked, though
breeding animals usually fail to conceive. Then a slimy, muco-purulent,
serous, bloody or fœtid discharge may escape habitually from the vulva,
smearing the tail and hips and collecting on the floor. If the os is
sufficiently patent to admit the hand vaginal and uterine exploration
will detect the tumor. In other cases it may be felt by rectal
examination.

_Treatment_ is essentially surgical and will consist in dilatation of
the os, and the removal of the tumor by twisting, ecraseur, or curette,
and with careful antiseptic precautions before and after. In malignant
tumors in the uterine walls it may be expedient to remove the entire
organ.

UTERINE TUBERCLE.

This has been seen especially in sterile cows, the subjects of
nymphomania, and it may be associated with a muco-purulent or bloody
discharge from the vulva, nodular swelling on the uterine horns, perhaps
also on the broad ligaments, one or both ovaries, and the mesentery, to
be recognized by rectal examination. The presence of tuberculosis in the
lungs or throat, and the response to the tuberculin test will confirm
the diagnosis. As a rule it is not desirable to institute treatment.

IMPERFORATE HYMEN.

Cases of this kind have been described in mare and cow, preventing
copulation and conception, and leading to a distension of the vagina,
with a glairy fluid, which obstructed defecation, irritated the bladder
and caused violent but fruitless straining, under which the mass would
project from the vulva. The centre of the swelling may be penetrated
with a trochar or bistuory and enlarged by incisions in several
directions. Relief is prompt and lasting.

VAGINITIS. LEUCORRHŒA.

Inflammation of the vaginal mucosa is usually a concomitant of metritis
and like that follows parturition. It will however occur independently
from direct injury or infection or from the presence of neoplasms. In
dourine and horsepox, vaginitis is a common symptom, to mare, cow and
bitch infection is conveyed by coition. Dieckerhoff quotes old chronic
cases, also acute ones which extended to the peritoneum and proved fatal
in a few days. The common symptom of muco-purulent discharge having a
heavy or fœtid odor is together with the discharge from the womb known
by the common name of leucorrhœa. The frequent irrigation of the whole
passage with antiseptic solutions is usually successful in putting a
stop to the affection, unless in case of constitutional infection, or
the presence of some neoplasm.

TUMORS OF THE VAGINA.

The vagina is the seat of different forms of neoplasms in the various
domestic animals. Thus cystoma, lipoma, adenoma, fibroma, fibro-myoma,
sarcoma and epithelioma have been noted. They are essentially surgical
and to be dealt with as such. They are mainly important in this
connection as inducing a leucorrhœa, which in the absence of careful
examination might be mistaken for that of uterine or vaginal infective
inflammation.

PARTURITION FEVER (COLLAPSE). MILK FEVER. PARTURIENT APOPLEXY. CALVING
FEVER. PARTURITION PARESIS.

Definition. Predisposing causes: genus, breed, great milking capacity,
heredity, mature age, vigor, high feeding, powerful digestion and
assimilation, sudden plethora, drying up of milk, parturition, easy
delivery, warm season, chills, idiosyncrasy, cardiac hypertrophy,
contraction of womb, emotional excitement: Supposed causes: absorption
of toxins from womb, colostrum, Schmidt treatment its significance,
microbian infection and intoxication, effect of change of stable.
Microbiology. Nature: Theories of nervous explosion, vaso-motor
cerebral anæmia from exaggerated excitability of the uterine nerves,
or from dilatation of the portal system and womb, metro-peritonitis,
cerebral anæmia from congestion of the rete mirabile, etc., palsy of
the ganglionic nerves, plethora, intracranial arterial tension,
narcotic poisons from leucocytic or microbian source. Lesions:
variable, cerebral and spinal congestion, pulmonary congestion,
collapse, septic inhalation, bronchitis, dessication of ingesta in
omasum and large intestine, black thick blood, yellowish gelatinoid
exudates in cranium and spinal canal and under spine, glycosuria.
Symptoms: time, post parturient, plethoric subject, sudden onset,
comatose and violent forms, discomfort, restless movements,
inappetence, moaning, mental dullness, unsteady walk, muscular
weakness, compulsory recumbency, retained urine and fæces, drowsiness,
somnolence, unconsciousness, stertor, venous pulse, tympany, sudden
recovery, complete, with paralysis, fatal cases, violence, tossing
head, trembling, cramps, convulsions, temperature. Mortality.
Prevention: bleeding in plethoric, heavy milkers, purging, low diet,
exercise, comfort, milking, blisters, sucking by calf, disinfection,
iodine solution in udder. Treatment: in early stages bleeding,
purgatives, peristalsis stimulants, antiseptics, injections,
stimulants, rubefacients or cold sponging, elevation of the head,
udder massage, milking, iodine injection of the mammæ.

_Definition._ A nervous disorder which develops suddenly in plethoric
cows, heavy milkers, after calving, and is characterized by loss of
senses, of consciousness and of muscular control, by hypothermia or
hyperthermia, convulsions, coma, and mellituria.

_Causes._ While one cannot speak positively as to the essential cause of
this disease, certain conditions are so constant and prominent that they
must be given a high value as _predisposing causes_.

_Genus and Breed. Milking Capacity._ This is essentially a disease of
cows, probably largely because of all domestic animals, cows only have
been long and systematically bred to secure the greatest power of
digestion and assimilation and the highest yield of milk. It is the
disease not only of cows, but of milking breeds, and preëminently of
individuals that give the most abundant dairy product. It is rare or
unknown in scrub or common herds, while common and fatal in the best
milking breeds, in advancing ratio about as follows: short horn, red
polled, Normand, Swiss, Ayrshire, Flemish, Dutch, Alderney, Jersey,
Guernsey, and Holstein. Heredity may be claimed, as the special
predisposing qualities are hereditary.

_Age_ has a marked influence, but this is subsidiary to the milking
qualities. The disease rarely attacks a cow after the first or second
calving when the system is as yet immature, and the milk yield has not
reached its maximum: nor one that is past its prime and already failing
in vital energy and milking qualities. The following table is from
statistics compiled from veterinary records in Denmark and Bavaria:

Age, yrs Cases
—3 —8
4 21
5 65
6 160
7 171
8 202
9 117
10 124
11 44
12 70
13 78
and over.

It will be noted that it is in the period of the most vigorous, mature
life, from the 6th to the 10th year inclusive that the great majority
suffer. In a judiciously managed dairy it is the best cows that are
carried at these ages, and although the very best are kept on into old
age they show a steadily decreasing number of cases as they begin to
fail. The disease is all but unknown in primipara.

_High Feeding._ Heavy and rich feeding prior to calving and immediately
after, is a most prominent cause of the affection. This is so well known
to owners of milking breeds, that they usually hold to the principle
that the cow that is a heavy milker, should be all but starved for a
fortnight before calving and for a week after. In herds where this rule
is acted on the disease is rare and may be altogether unknown, and when
it is neglected the malady is often very destructive.

_Plethora. High Condition._ Heavy feeding and high condition usually go
together, and the majority of the victims are fat or in good flesh, yet
a certain number are actually thin. The predisposing condition is
plethora rather than fat or flesh, and this may be present in the
comparative absence of flesh. The cow that is from a stock famed as
heavy milkers, does not tend to lay on flesh, but, on succulent diet
especially, the greater part of the nutritive matter assimilated goes to
the production of milk, and she remains thin in flesh no matter how
heavily she may be fed. Many such cows never go dry, but give a liberal
yield of milk up to the day of calving, and if measures are taken to dry
them up, it is done at the expense of a sudden plethora, as the milk
giving system does not at once accommodate itself to the laying up of
fat and flesh.

The _drying up of the milk secretion_ sometime before calving in a cow
which is normally a heavy milker is therefore a potent factor.

_Parturition_ is an almost indispensable factor as the disease occurs
one to seven days after that act, and only in rare and somewhat doubtful
cases before it.

_Easy Delivery_ with little nervous outlay or loss of blood, and no
exhaustion is a special feature. The attack almost never occurs after a
difficult parturition with considerable loss of blood and much nervous
exhaustion. This should to a large extent exclude such alleged factors
as _shock_ or _wearing out of nervous energy_. The nervous prostration
which figures so prominently in the disease, seems to be less the result
of wear and tear, than of the supply of an excess of blood, which is
either over-enriched, or charged with some injurious toxic matter. At
the same time there is a manifest susceptibility at the parturient
period which is not present at other times, and the plethora or toxin
takes occasion to operate when this predisposition renders such an
attack possible. _The Warm Summer Season_ has been claimed to induce a
greater number of cases, and doubtless exposure to continuous heat,
tends to prostrate the nervous system and predispose to congestion, this
fails to take into account the still more important element of the rich
spring and early summer pastures, where the already plethoric animal is
left to feed without stint, or the tempting red clover, alfalfa and
other fodder crops, rich in albuminoids, which are fed liberally in a
succulent condition.

_Chills in cold winter weather_ have been similarly invoked as driving
the blood from the surface to collect in internal organs, including the
brain. That chills do act in this way cannot be denied, but there is no
demonstration that any number of cases have been materially affected by
cold.

_Idiosyncrasy. Constitutional Predisposition._ This must be allowed,
inasmuch as that it covers all those individual conditions, functional
and structural, which belong to the heavy milker, or the animal with
extraordinary powers of digestion and assimilation. The same shows in
the predisposition to a second attack of an animal which has survived a
first one. The structural changes in the nerve centres, which occur in
the primary attack, leave traces, which render these parts more
susceptible at the next calving. In my own experience the violence of
the disease is liable to increase with successive attacks, so that a
second or third cannot be hoped to be as mild as was the former one.

_Cardiac Hypertrophy._ Cagny draws attention to the fact that in man and
beast alike the heart undergoes hypertrophy during gestation and, above
all, during its later stages. In improved breeds of cattle, and
especially in milking breeds, a great development of the whole
circulatory system is seen, and a large heart is a constant feature of
this. This implies an increased force of cardiac systole, an increased
blood tension in the arteries and capillaries, a condition which tells
with special force on the soft tissues of the brain, as the violent
abdominal compression in the expulsive efforts of parturition, tends to
drive the blood from the great vascular viscera situated back of the
diaphragm.

_Parturition_ and the subsequent _contraction of the womb and expulsion
of the great mass of blood_, must be accorded a prominent place among
causative factors. The disease is almost restricted to the first week
after parturition, and its gravity is greater the more it is related to
the parturient act. Cases occurring in the first three days are usually
fatal. The gravid uterus contains a very large amount of circulating
blood, and when the womb contracts, the greater part of this is suddenly
thrown upon the general circulation, already plethoric to an undue
extent. As yet the mammæ are congested and there is no free depletion
through that channel, so that there is a marked temporary plethora and
vascular tension, before the system can establish free elimination and,
as it were, strike a healthy balance. In this period of transient
plethora there lies a source of great danger to the general system and,
more particularly, to the brain.

_Emotional Excitement_ connected with the removal of the calf is urged
by Günther, Jaumain, Félizet and others as a prominent cause. This,
however, must be rare, at the most; the disease does not attack the
primipara that should be most susceptible to this influence, but the
mature animal, at her third calving or later when she is already well
accustomed to this treatment; it supervenes so quickly on parturition in
many cases, that there was no opportunity for such emotion; it occurs
also in cows, the calves of which have remained with them or have
received no attention from them.

_Absorption of Toxic Matters._ The theory of a poisoning of the nerve
centres is indicated in the familiar name of _milk fever_, suggesting an
absorption, or poisonous condition of the milk. Lafosse charged the
trouble on the _uterine milk_ secreted in the cotyledons and reabsorbed
in quantity. Abadie and Kaiser attributed it to the products of
gastro-intestinal ferments, which acted on the nerve centres like a
deadly organic alkaloid. Hartenstein incriminated the products of
muscular contraction in the womb and systemic muscles during
parturition. Ehrhardt invoked a similar auto-intoxication, going on
before parturition and only reaching its climax in connection with that
act.

Allemani and Gratia attribute the disease to the absorption of the first
milk (colostrum), and there are several considerations that strongly
favor this hypothesis. The disease sets in always in connection with the
parturient development and congestion of the udder and the secretion of
the first milk. In exceptional cases it may even appear just before
parturition. Even upon the calf the colostrum operates as an irritant
and purgative. Is it wonderful that, in the parturient cow, with a high
state of plethora, a highly susceptible state of the nervous system, and
the various concurrent conditions already referred to above, a direct
poisoning of the nerve centres should appear? It is worthy of notice
that the absorption from the mammæ takes place without any metabolic
change, such as occurs in the stomach and liver in the case of materials
digested. It is to be presumed that the hypothetical mammary poison is
delivered in the brain in its pristine condition and possessed of its
full force.

The doctrine is corroborated even more strongly by the successful
results of treatment by the injection of a solution of potassium iodide
into the udder. The iodide solution may presumably act in one or more of
several ways. It is unquestionably an antiseptic, and would tend to
arrest or control microbian growth and activity, thus preventing the
further formation of toxins. It has a potent deobstruent action on
glandular tissue, tending not only to dry up the milk, but to hold in
check the leucocytic function of producing dangerous leucomaines. There
is reason to believe that with regard to some poisonous ptomaines iodine
acts as a direct antidote, probably uniting with these and forming new
and comparatively harmless compounds. It manifestly acts in this way in
the case of cryptogamic diuresis, and in cerebral congestions arising
from spoilt fodder. The iodide tends further to act as a calmative to
the nerve centres, and as a diuretic, serving to eliminate the poison
that may be present in the blood.

_Microbian Infection or Intoxication._ The doctrine has been advanced
that the disease is either a microbian infection of the nerve centres or
a process of poisoning by the absorbed toxins of microbes. Of the two
hypothesis the latter is the more acceptable, in view of the fact, that
cows in a condition of coma will sometimes recover with extraordinary
rapidity. This is more likely to occur in connection with the
elimination or exhaustion of a transient narcotic poison, than with a
deadly microbe colonized in the brain. This hypothesis is in full accord
with the acknowledged success of the iodide injections; with the
observation of Bissauge, which I can endorse, that certain villages and
hamlets habitually furnish cases of parturition fever, while neighboring
ones, with the same breeds and apparently the same management escape;
and with the observations of Russell and Wortley Axe, that the malady
will sometimes be suddenly prevented in a herd, by the simple expedient
of having the cows moved to a new and previously unoccupied stable, for
calving and the first nine days thereafter.

In support of the doctrine of a microbian origin is recalled the fact
that the disease almost invariably follows parturition, which opened the
way for the introduction of bacteria by the genital passages. This is
somewhat invalidated by the fact that it follows the easy parturition,
in which there was no chance for the introduction of germs on hands or
instruments, and does not follow dystokia in which, without question,
germs have been planted abundantly in the interior of the womb. Undue
weight should not be given to this objection, as the essential accessory
conditions of plethora, etc., are usually largely modified in cases of
dystokia.

The _microbiology_ of the affection leaves much to be desired. Coureur
and Pottiez and later Van de Velde found a streptococcus in the blood.
Trinchera, Nocard, and Cozette found the common pus cocci
(staphylococcus pyogenes aureus, citreus and albus) a streptococcus and
a colon bacillus in the liquid squeezed from the cotyledons, and in the
liquid debris on the uterine mucosa. These microbes were not found in
other organs. They grew readily in artificial cultures, but we lack the
final proof of a successful inoculation on a susceptible parturient
subject. The whole subject is therefore still a plausible theory.

We are not however limited to the womb as the only possible field of a
pathogenic microbian growth. The frequent presence of microbes in the
sphincter of the teat, in the galactophorous sinus, and in the milk
ducts inside the mammæ is absolutely proved. Guillebeau found on the
mucosa in cases of mammitis three forms of bacillus, to which he
attributed the disease. In the New York State Veterinary College we have
found mammitis usually associated with a streptococcus in the milk. In
one cow in the University herd which gave abundance of good milk, and
rarely showed any sign of congestion, streptococcus was constantly
present. In cows producing “gassy” curd, V. A. Moore and A. R. Ward
found in the milk a bacillus which morphologically and in cultures
resembled the colon bacillus (evidently one of the colon group). In the
milk and mammary gland tissue got from other (slaughtered) cows, a
micrococcus growing in yellow or buff-colored colonies predominated.
(Moore and Ward). That the colon bacillus, so constant in the intestines
and manure, is not always found in the milk ducts, would show that in
its normal condition it is not adapted to this habitat, but when a
variety appears that is so fitted, it appears to be able to maintain its
place indefinitely.

With such facts before us, we must allow the possibility of poisoning by
toxins of bacteria in the udder, or by compounds formed by the synthesis
of such toxins and the leucomaines of the expanding udder, or by the
union of the udder toxins with those from the womb. The whole subject of
microbian and leucocytic causation of parturient fever is still
hypothetical, yet enough is known to show the high probability of such
source, and to demand a thorough investigation which will place the
subject on a substantial and assured basis.

_Nature._ Theories of the nature of this disease are numerous and
varied, and are largely based upon some restricted or one-sided view of
phenomena and lesions. Coutamine considers it as the reaction of the
surplus of nerve force, which was not used up in the easy parturition.
The theory is somewhat fantastic as an explanation of the rapidly
developing asthenia and paralysis. Billings explains the cerebral anæmia
as due to vaso-constriction of the nervous capillaries produced by the
exaggerated excitability of the uterine nerves. But with the easy
parturition, and delivery, and the moderate contraction of the womb,
without violence or spasm, the theory seems rather insubstantial.
Trasbot looks on the affection as a congestion of the myelon, apparently
shutting his eyes to the far more prominent encephalic symptoms. Haubner
considers it as a cerebral anæmia induced by the vaso-dilatation in the
portal system and abdominal viscera generally, the result in its turn of
the vacuity of the abdomen, from the expulsion of the fœtus and its
connections. But the womb is often found contracted and comparatively
exsanguine, the plethoric condition of the cow, suddenly increased by
the great mass of blood from the uterine vessels, maintains a marked
general blood tension, and finally, the closed box of the cranium cannot
have its blood so completely drained from it as can a part outside such
a cavity. Stockfleth attributed the malady to a metro-peritonitis, and
the absorption of the morbid products and poisoning, but neither a
metritis nor peritonitis is a common accompaniment of the affection.

Franck who accounts for the asthenia by an anæmic condition of the
brain, explains the anæmia by a pre-existing congestion and œdema of the
rete mirabile at the base of the brain. He claims that sows which have
also a rete mirabile in this situation sometimes suffer from parturient
fever. He fails to adduce cases in the sheep and goat which also have
retia mirabilia. The pregnant sheep may die of an asthenic affection,
but usually before parturition. Franck’s theory is plausibly based on
the anatomical and physiological conditions, for the elaborate network
of vessels at the base of the brain, undergoes great distention under
increased arterial tension, and with the serous effusion, compresses the
brain and drives out its blood.

Palsy of the ganglionic system has been invoked, with succeeding
congestion of the myelon and encephalon (Barlow, Kohne, Carsten Harms,
etc.). Explanation is made that the supposed excess of nervous force
fails of distribution through a lack of conductility of the nerves, and
the nerve centres suffer. Binz has even found the spinal roots of the
sympathetic surrounded by a thick gelatinoid exudate. The theory is,
however, essentially speculative and fails to explain the origin of the
disease or its connection with the recognized conditions of its
occurrence.

_Plethora with Arterial tension_ and all conditions contributing to
this, as already set forth under causes must be allowed a prominent
place in considering the nature of the disease. The blood globules in my
experience are somewhat smaller than normal, implying the density of the
plasma, and implying a direct influence on trophic and metabolic
processes. Under these influences the congestion of the encephalic
circulation, and notably of the rete mirabile, and a serous effusion,
tend first to prostrate the nerve force, and second to render the other
intracranial structures anæmic.

The direct action of a _narcotic poison_, leucocytic or microbian,
though as yet a hypothesis merely, has much in its favor, on
considerations drawn from the observed immunity in particular buildings,
the sudden prostration, the promptitude of certain recoveries and the
favorable results of the iodine mammary injections. The presence of
sugar in the urine, most abundantly in the worst cases, implies a
profound disorder in glycogenic centres (medulla, liver), and primarily
no doubt in the bulb.

_Lesions._ These are exceedingly variable in successive cases.
Congestion and effusion in the meninges, cerebral or spinal, in the rete
mirabile and choroid plexus have been often noticed, and exceptionally
clots of extravasated blood. In certain cases congestion and pink
discoloration of portions of the brain substance (cerebral convolutions,
bulb, ganglia) with marked puncta vasculosa, are found, while in others
the greater part or the whole of the encephalon is anæmic. The puncta in
such cases, large and dark, on the surface of the section, promptly
enlarge until they may form distinct drops.

In the _lungs_ areas of collapse, and of dark red congestion and
infiltration are common, mostly as the result of the entrance of
alimentary or medicinal matters into the bronchia owing to palsy of the
pharynx. Such materials can be found in the bronchial tubes.

The _third stomach_ and the _large intestine_ may be impacted, the
contents more or less baked and glossy on the surface, and coincident
congestions of the mucosa are not uncommon. In some instances, however,
the contents are soft and pultaceous and the absence of mucous
congestions is remarkable.

The _womb_ rarely shows characters differing from the condition which is
normal to the first few days after parturition.

The _blackness and thickness of the blood_ has been noted by practically
all observers. This is partly the result of its density, but doubtless
also of the undetermined toxins which are operative in the disease.

Yellowish _gelatinoid exudates_ have been found in the subdorsal and
sublumbar regions, as well as the cranium and spinal canal.

_Glucose_ appears to be constantly present in the urine, and in excess
in the more violent and fatal cases: from 1.19 grm. per litre in slight
cases to 41.8 grms. in a fatal one (Nocard). Albumen may be present,
though probably only when local inflammation has supervened.

_Symptoms._ The conditions of the attack should be noted. This is a
disease of the first six days after parturition, rarely seen in the
second week, and never after the fourteenth day. It is very exceptional
before parturition, yet Müller quotes 47 cases in 1107 births. The
breed, condition, milking qualities, plethora, feeding, etc., of the
patient are, as already noted important data in diagnosis. The onset is
sudden without premonitory symptoms.

Two very distinct types are met with, the _comatose_ and _violent or
spasmodic_, which, however, merge into each other by insensible
gradations, and may follow each other.

From twelve to seventy hours after an easy parturition there suddenly
appear signs of discomfort. Feeding and rumination cease, the calf is
neglected, there may be plaintive moaning, the eyes seem dull and
clouded, the eyelids drooped, the conjunctiva red, the pulse normal for
parturition, sometimes extra strong, the breathing excited often with
moans or grunts. The senses are dulled, the walk is unsteady, the feet
being abducted and planted like clumps, or the legs sway, perhaps cross
each other, remain semi-bent, and soon give way leaving the animal
prostrate, resting on the sternum and abdomen, or later on the ribs,
with head extended. Attempts may still be made to rise, but this is
rarely accomplished unless when improvement sets in. This is the
condition in which the patient is usually found, being the first to be
noticed by the owner. The bowels are torpid, the urine retained in the
bladder, and the animal may remain thus in a drowsy condition, without
changing from the sterno-ventral decubitus, or dropping the head on the
ground until improvement sets in. The head rests on the shoulder or
upper flank. If held outward or forward the upper border of the neck has
an S shaped outline.

More commonly the somnolence increases, passing into a complete torpor
and insensibility, the eye may be touched without causing winking,
pricking or other injury causes no further response, the patient turns
upon its side, with its head extended on the ground. She may lie in this
condition with no sign of vital activity save pulsation and breathing,
and the latter is liable to be slow and stertorous by reason of the
paralysis of soft palate and larynx. The jugulars usually show a venous
pulse. Fermentations in the inactive paunch cause the evolution of gas
with tympany, which still further obstructs the breathing, and reacts
injuriously on the nerve centres. The normal eructations from the rumen
may continue, with liquids and floating solids, and in the paralytic
state of the throat these too often pass in part into the bronchia,
causing septic bronchitis and pneumonia. The same is liable to follow
the administration of liquids, the irritant drugs passing into the
larynx, trachea and lungs. The pulse becomes soft, small and finally
almost imperceptible. It may be 50, 60 and upward.

In favorable cases, defecation may still occur, or the rectum once
emptied may fill again through the continuance of peristalsis, the milk
continues to be secreted, and in one to four days, spontaneous
defecation and micturition may be resumed, and the patient may get on
its limbs and commence feeding. There is usually at first a little
weakness of the limbs, but this is transient and health is restored in a
very short time. The suddenness of the improvement is often as marked as
of the attack. The patient is left prostrate and insensible, without
giving any response when the eyeball is touched and in two or three
hours it is found on its feet, eating, with eyes bright and clear.

Some patients, however, are restored to ordinary sensation, intelligence
and appetite, while the hind limbs remain paralytic, or paretic, and the
station and gait both weak and uncertain for days or even weeks. In such
cases there have been presumably structural changes in the nerve
centres, which require time for repair.

In fatal cases, death may occur quietly from apoplexy, cerebral
compression, or narcotism, or it may be preceded by a period of marked
excitement or disorderly muscular movements. Lifting of the head,
throwing it alternately on the shoulder and on the ground, trembling of
head, members and body, cramps or jerking of the limbs or of other
parts, drawing the hind limbs up against the abdomen, and again
extending them, rolling of the eyes, loud, noisy, irregular, embarrassed
breathing and a running down pulse are often marked features.

The temperature range is peculiar. At the start there may be some
hyperthermia 103° or 104°; with the advance of the disease it tends to
become lower, 98°, 96°, or 94°. When improvement sets in, it rises again
promptly to the normal.

Cadeac describes a special form which is ushered in by great
restlessness, bellowing, throwing the head to right and left, grinding
the teeth, sucking the tongue, salivation, licking of certain parts of
the body, spasms in the neck, back or limbs, and prompt recovery, or
lapse into the comatose condition as above described. It proved less
fatal than the ordinary comatose type, but seems to depend on similar
conditions.

_Prognosis. Mortality._ The disease is very deadly, the mortality in
time past having reached 40, 50 or even 60 per cent., the gravity
increasing as the disease set in nearer to parturition. Cases occurring
on the first or second day were mostly fatal, those at the end of the
first week were hopeful, and those occurring during the second week were
very hopeful. With the Schmidt (iodine) treatment the mortality is
claimed to be reduced to 16 or 17 per cent.

_Prevention._ Measures directed toward the lessening of plethora tend to
remove one of the most fruitful causes of the disease and though not
invariably successful, are yet of great value. The most direct is the
_abstraction of blood_ in the last fortnight of pregnancy, to the extent
of 6 or 8 quarts. This tends to secure a lessening of the blood tension,
and blood density, but there is the drawback of a created tendency to a
subsequent increase in blood formation to make up the loss. This measure
should be reserved for cows that are very plethoric, extra heavy milkers
and such as have already suffered from the disease.

_Purgatives_ will measurably secure the same end without the same degree
of danger. One to two pounds of Epsom or Glauber salts in the last week
of gestation, or at latest when labor pains set in, tend not only to
remove solid or impacted masses from the first and third stomachs, and
inspissated contents from the large intestines, but to secure a free
depletion from the portal system. If not before, this should always be
given immediately after parturition to cows in extra high condition,
heavy milkers, and that have had a short and easy delivery.

_Restriction of food_ for a week before and as long after parturition is
of equal importance. A very limited supply of aqueous, easily digested,
and laxative food (roots, sloppy bran mashes, fresh grass, ensilage)
will meet the demand.

_Exercise in the open air_ is of great value in giving tone to the
muscles, and especially the nervous system, and in stimulating the
emunctories and other functions.

In the cold season _protection against cold draughts and chills_ must be
seen to, and in the hot season the avoidance of an excess of solar heat
and above all of the confined impure air of the barns.

At midsummer and later, there is often great danger in the rich clover
and alfalfa pasture, or soiling crop, with which the cow will
dangerously load her stomach, and the only safe course is to remove
predisposed animals and shut them up in a bare yard or box-stall. Under
such simple precautions herds that had formerly suffered severely, have
had the disease virtually put a stop to.

In individual cases other measures are indicated. When the udder has
reached an enormous size and development, and is gorged with milk, days
before parturition, it should be systematically milked. The irritation
in the gorged gland is quite as likely to induce premature parturition,
as is milking, and, at the worst, the result is not so bad as an attack
of parturition fever.

Basing his advice on the fact that parturition fever does not follow a
case of severe dystokia, Cagny applies sinapisms on the loins, croup and
thighs of a fleshy, plethoric, heavy milking, parturient cow. Proof of
their efficacy is not obtainable.

Félizet advises leaving the calf with its dam for one week. Kohne doses
the cow with nux vomica: Harms, with tartar emetic.

In view of the probability of a bacterial infection the cow should be
taken to a clean, pure, well-aired stable a day or two before calving,
having been first cleansed from adherent filth, and sponged all over
with a 4 per cent. solution of carbolic acid.

To prevent diffusion of infection Bournay recommends antiseptic
injection of the womb immediately after calving. Bissauge adds that the
stable should be disinfected after every case of parturition fever, the
manure carefully removed and the ground scraped and well watered with a
disinfectant.

For fleshy, plethoric, predisposed cows, the iodine injection of the
udder should be applied immediately after calving. A measure of this
kind which is so successful as a curative agent, and which brings such
circumstantial evidence of the production of a poison (leucomaine or
ptomaine) in the mammary gland, can hardly fail to be even more
effective as a prophylactic than as a therapeutic resort.

_Treatment._ With the state of plethora and congestion about the head in
the early stages the question of _bleeding_ at once arises. If early
enough while there is a full bounding pulse, and as yet no sign of great
loss of muscular control it is often very beneficial, as much as 6
quarts or more being withdrawn. It is well however to avoid cording the
neck, which must increase the vascular tension in the brain, and to
trust rather to digital compression of the vein. The blood should be
drawn from a large opening in a full free stream, and may be stopped
when the pulse softens. In the more advanced condition, with paralysis
and more or less dulling of the senses, or coma, bleeding may be
dangerous rather than useful. There is then serious pressure on the
brain, with serous effusion, and perhaps blood extravasation, and in any
case anæmia, and this latter may be dangerously or even fatally
increased by the lessening of the blood pressure, without any
compensating advantage in the way of reabsorption of the effusion. In
such cases eliminating agents are a safer resort.

_Purgatives_ commend themselves, but with the drawback of a too tardy
action. Now however with the peristaltic stimulants given hypodermically
this objection is largely obviated. Pilocarpin 1½ gr., and eserine 3
grs. will often secure a noticeable movement of the bowels in the course
of fifteen minutes, implying a corresponding motion onward in the bowels
more anteriorly, and even of the contents of the gastric cavities. If
there is already palsy of the muscles of deglutition, this may be
repeated several times at intervals of four or five hours. If however
deglutition is still well performed a purgative of one or two pounds
Epsom salts, with 10 drops croton oil, and 1 oz. oil of turpentine may
be given by the mouth. Should this operate, it will supplement and carry
on even more effectively the work of the hypodermic agents, and even
lessen the density, plasticity and tension of the blood and act as a
potent derivative from the brain.

A compromise may be made by giving aloes 2 ozs., croton oil 20 drops in
bolus; or 1 to 2 ozs. sulphate of soda in solution may be injected
subcutem.

In any case oil of turpentine or other antiseptic is of great value in
the stomach in preventing fermentation and tympany, and thereby
obviating a whole series of troubles such as: cerebral disturbance by
nervous shock and blood pressure; impaired respiration and hæmatosis by
pressure on the diaphragm; and eructations of food to the pharynx and
its inhalation or gravitation into the lungs.

It is always well to clear out the rectum by injections, when if there
is any indication of pharyngeal paralysis most of the remedies may be
given by this channel.

Stimulants (ammonia carbonate, alcohol, anise, fennel, ether, nux, etc.)
have been largely employed by the mouth and may be by the rectum. In the
absence of spasms I have relied largely on nux or strychnia.

When the skin chills, some have sought to heat it by enveloping the
posterior half of the body in cotton or wool soaked in turpentine, by
applying sinapisms, or by moving over the surface a warming-pan
containing red hot charcoal.

More generally _cold_ in the shape of cold water, ice or snow has been
applied _to the cranium and spine_. Theoretically the anæmic brain might
be thought to forbid this, but clinically it often operates well,
possibly by inducing a sympathetic contraction of the vessels in and
around the nerve centres and thus indirectly favoring the resumption of
active circulation and the reabsorption of effusions.

An _elevated position of the head_ is no less important. It favors the
return of blood from the brain by gravitation, and in this way improves
the intracranial circulation, and the resumption of normal function. A
halter, or a rope around the horns, may be tied to a beam overhead, or
the head may be laid on thick bundles of straw which will keep it up to
or above the level of the chest, and in this way not only is gravitation
ensured, but the brain is protected against the violent blows and
concussions, which come from dashing the head on the ground.

Frequent _rubbing of the udder and drawing of the milk_, is an excellent
means of depletion, a removal of a source of irritation, and presumably
an extraction of part of the offending poison. It should never be
neglected. But of all known methods of treatment the iodine injection
furnishes the greatest hope of success.

_Injection of the mammæ with Iodine._ Iodide of potassium 100 grains
(200 grs. in the case of a very large udder) are dissolved in a quart of
water which has been boiled for 15 minutes, the solution cooled to 104°
F. and injected in equal parts into the four quarters, which have been
just milked out clean. The glands are then manipulated so as to work the
solution into all the recesses of the milk tubes and follicles. If the
patient does not get on its legs at the end of twelve hours, the glands
may be milked out and injected anew. In nearly 2000 cases the recoveries
reached an average of nearly 83 per cent. In serious or advanced cases
with structural changes of a grave nature, a good result cannot be hoped
for. The injection does not forbid the concurrent use of other approved
measures.

The injection is easily made with a caoutchouc tube of five feet long
fitted to a teat tube at one end and to a funnel at the other. The tube
is inserted in the teat, and the funnel at a height of five feet
receives the liquid, which readily passes into the teat. When ready to
pass the tube from one teat to another, an assistant pinches the
caoutchouc tube just below the funnel, until the insertion has been
made. Every precaution must be taken against sepsis. The udder, teats
and hands, must be washed with soap, and treated with a 3 per cent.
solution of lysol. The teat tube and funnel are boiled. The caoutchouc
tube is washed and irrigated with a solution of mercuric chloride
(1:1000), and then with one of boric acid (3:100).

DISEASES OF THE EYE.
DESIRABLE FEATURES IN THE EYE.

The eye in the physiognomy. Broad forehead. Full eyes. Both eyes
alike. Iris smooth, lustrous. Media translucent. Pupil sensitive to
light. Convexity median, uniform. Pupil black in ordinary light. Lids
open and mobile. Sclera light pink. Tears clear, limpid without
overflow. Lids thin, delicate, margins evenly curved. Whole eye
responsive to moving objects. Defects: small eye: semi-closed, thick,
sluggish lids; convex cornea: sunken eye: projecting eye: weeping eye:
blear eye: watch eye: irresponsive iris: dilated pupil: unequal eyes:
flat cornea; ovoid cornea.

Much of the expression of the face depends upon the eyes, and in animals
as in man it is difficult to find compensations for a forbidding
countenance. Perfect, sound, intelligent eyes are always pleasing;
imperfect, defective, sunken or lifeless eyes mar the whole expression.
The following points may be specially noted:

1st. =Ample breadth between the orbits.= This is of great importance in
the horse, in which we seek for intelligence, courage and indomitable
energy. This confirmation does not indicate the size of brain, as the
cranium is situated higher up, but by placing the eyes well outward, it
indicates a wider range of vision, and usually implies large, clear
eyes, and since interdependent parts tend to correspond in development
and quality, this commanding vision bespeaks a large, active brain,
intelligence, docility and activity.

2d. =Full, prominent eyes.= This may be excessive, either through
primary conformation or disease. Abnormal convexity of the cornea
implies myopia. But within normal limits the prominent eye suggests good
health, condition and vigor, with ample cushions of fat under the bulb
and a sound, well-developed condition of the eyeball and its muscles.

3d. =Both eyes equal in all respects.= Any variation in size, shape,
color, fullness, clearness or in any other respect is at best unsightly,
and implies not only defect but often disease as well.

4th. =The iris should be lustrous, uniform in color and even in
surface.= Whether dark brown as in the horse, or yellow as in the dog,
it should be brilliant. Any part that lacks lustre, being lighter brown,
or yellow and dull like a dead leaf, usually indicates previous disease
and a tendency to further trouble. Albinos and those in which the
pigment is congenitally absent in patches must be considered as
exceptions, yet, even in them, the peculiarity cannot be held to add to
the beauty.

5th. =All the Media (Cornea, aqueous humor, lens and vitreous) must be
perfectly clear and translucent.= The slightest cloudiness or opacity in
any of these is a serious blemish and usually indicates disease, past or
present.

6th. =The pupil should promptly and freely respond to light and darkness
by contraction and expansion.= Absence or tardiness of movement
indicates impaired vision, from disease of the eye, its nerves, or their
nerve centres.

7th. =Each cornea should have a median convexity, uniform in all
directions implying the absence of myopia, preshyopia and astigmatism.=
Any deviation from this will interfere with the perfection of sight, and
endanger shying and other troubles.

8th. =Under ordinary light the pupil should appear black throughout.= In
the larger animals such dilation of the pupil as to expose the tapetum
lucidum under such circumstances implies impaired vision (amblyopia,
amaurosis), inflammation of the iris or undue intraocular pressure. A
white color or spot shows cataract.

9th. =The lids must be open and mobile without excessive dilation.=
Tardily moving or semi-closed lids, distorted by scar or angle, everted
or inverted, are unattractive and usually imply disease in the eye,
nerves or brain.

10th. =The unpigmented portion of the sclera should be light pink.= The
dark red of congestion and the pallor of anæmia are equally
objectionable.

11th. =The tears must be clear, limpid and confined within the lower
lid.= Any milkiness, flocculency or overflow is indicative of disease.

12th. =The eyelids must be thin, delicate, evenly and uniformly curved
along the borders, and fringed by an abundance of strong, prominent and
well directed lashes.= Puffiness or swelling betrays inflammation,
dropsy, anæmia, parasitism or other disorder, angularity of the upper
lid an internal ophthalmia, and depilation or wrong direction of the
lashes, local disease.

13th. =The eye should respond instantly, by movement, to new objects and
noises, without showing undue irritability or restlessness.= The
intelligent apprehension of the objects will introduce an aspect of
calmness and docility.

DEFECTS, BLEMISHES AND ABNORMALITIES OF THE HORSE’S EYE.

Some of these may be present in the absence of actual disease, and yet
prove so objectionable that they disqualify the animal for any use, in
which style or æsthetic appearance is demanded. Among such sources of
disqualification may be noted:

1st. =The small eye.= One or both eyes may appear small because of
internal pain and retraction within their sockets, or from actual
atrophy or contraction of the eyeball, the result of deep seated
disease, or the organ may be congenitally small, and deep seated in the
orbit, and the thick tardy eyelids may have a narrow opening through
which they can only be partially seen. This last condition usually
implies a dull lymphatic constitution, low breeding and a lack of
intelligence, docility and vigor.

2d. =The semi-closed eye with thick, coarse, sluggish lids.= In this
case the bulb may be not unduly small, yet as it is not freely exposed
it conveys the same general expression to the observer. Like the small
eye it indicates low breeding, lack of intelligence or docility and
often stubbornness or even vice.

3d. =The convex eye.= In this the transparent cornea describes the arc
of an unduly small circle, suggesting a conical form and projecting
unduly beyond the margins of the lids. It implies imperfect vision,
myopia, and, it is alleged, low breeding and lack of alertness.

4th. =The sunken eye.= This has been already referred to under =the
small eye=. The eyelids are usually flaccid, the upper being drawn in by
its levator so as to form an angle, and the edges of the orbit are
somewhat prominent. It is seen in old, worn out animals, which have lost
the pads of fat in the depth of the orbit, and more commonly in animals
that have suffered several attacks of recurrent ophthalmia.

5th. =The projecting eye.= In this case the lids are unduly contracted
and the eye protrudes between them so as to show a large amount of
sclerotic around the transparent cornea. This may be due to nervous
strain and suffering but, however produced it is decidedly unsightly and
objectionable.

6th. =The weeping eye.= This is always a condition of disease. It may be
due to irritant gases, or solid particles, to inturned cilia, everted
lids, conjunctivitis or a variety of other conditions. A careful
examination may show whether it is only a transient and remediable fault
of a good eye or a permanent and irremediable defect.

7th. =The blear eye.= With swelling and scabbing of the edges of the
lids and Meibomian glands, and congestion of the adjacent conjunctiva,
there is usually some blurring of the surface of the transparent cornea.
The trouble is mostly chronic and constitutes a serious objection.

8th. =The watch eye.= In this, as in the albino, there is a lack of
pigment, so that the iris and sclerotic are white or bluish white in
part or in whole. Such an eye may be good and durable, but not beautiful
nor attractive.

9th. =Blindness of one or both eyes.= In all such cases the pupil
remains fixed and immovable, showing no accommodation to light and
darkness, and there is a lack of prompt responsiveness on the part of
the eye to sounds and objects. In amaurosis, glaucoma and cataract
especially, the pupil remains widely open, and alert movements of the
ears are employed to make up for the lack of sight. The condition often
comes from internal ophthalmia, such as the recurrent form, and is
associated with atrophy of the bulb.

10th. =Eyes of unequal size.= This usually implies serious disease in
one, not infrequently recurring ophthalmia.

11th. =Too flat corneal surface.= In this case there is a manifest lack
of the normal projection, the anterior surface of the cornea describing
the arc of a larger circle, the visual rays coming from a distance alone
converge on the retina and presbyopia occurs. In this as in myopia and
other visual imperfections a horse is liable to stumble and, if nervous,
to shy.

12th. =Ovoid Cornea.= In such cases the front of the transparent cornea
has an ovoid outline the arc formed by it in one direction being that of
a greater circle, than the arc which crosses this at right angles. In
consequence of this, the rays impinging on the outer portions of these
respective arcs do not converge to the same point on the retina and a
blurred and imperfect image results. This astigmatism causes the subject
to stumble and, if nervous, to shy.

SYSTEMATIC INSPECTION OF THE EYE.

System in Examination. Eyelids: cilia: lachryneal puncta: mucosa,
light pink, brick red, yellow, puffy, dropsical: Ciliary vessels deep,
immovable; nictitans; transparent cornea equally smooth, glossy, with
clear image at all points: foreign body on cornea: corneal ulcer:
opacities in aqueous humor: iris and pupil: corpora nigra: changes in
passing from darkness to light: pupillary membrane: adhesions of iris:
intraocular pressure: contracted pupil: hole in iris. Oblique focal
illumination of cornea, aqueous humor, iris, lens, Purkinje-Sanson
images.

In examining animals for soundness and especially the horse or dog, the
condition of the eye must be made one of the most important subjects of
inquiry, as a disease or defect may render the animal altogether
unsuited to the object to which it is destined. As in every other field
of diagnosis thoroughness is largely dependent on the adoption of a
system which will stand in the way of any flaw being too hastily
overlooked. Many of the points to be noted will be decided at a glance,
yet this does not obviate the necessity of turning over in the mind, in
succession, the different points of inquiry, and directing the necessary
attention, however hastily, to each in turn. The following points should
be observed:

1st. =Are the eyelids swollen, hypertrophied or faulty in form, position
or movements.= Faults as thus indicated may imply any one of a great
variety of disorders which should be followed out to their accurate
diagnosis. It may be bruises, lacerations, punctures, parasites,
conjunctivitis, keratitis, dropsy, anæmia, hepatic or intestinal
parasitism, nephritis, paresis, entropion, ectropion, etc.

2d. =Inspect the cilia as regards form, size and direction.= Absence or
wrong direction may imply disease of the Meibomian glands, infective
inflammation, demodex or other acarian infesting, or turning in or out
in inflammatory conditions.

3d. =See that the lachrymal puncta are open and that there is no
overdistension of the sac.= The overflow of tears and the swelling of
the caruncle and of the area beneath it will often indicate such
trouble. In its turn it may imply inflammation of the duct, and
obstruction by the tenacious muco-purulent product, or it may imply
merely obstruction of its lower end by a dried scab. This last may be
seen in the horse, on the floor of the false nostril at the line of
junction of the skin and mucosa, and in the ass, higher up on the inner
side of the ala nasi. In exceptional cases it may be desirable to pass a
stilet through the canal from the puncta downward or from below upward
to determine whether it is pervious.

4th. =Determine the vascularity of the conjunctiva.= When free from
pigment as it habitually is in pigs and birds this is easily done, while
in animals like the horse, in which the bulbar portion, which covers the
sclerotic, is largely pigmented, we can scrutinize only the pigment free
parts. =In health= there should be only a few, fine, pink vessels which
move with the mucosa when pressed aside on the bulb. =In congestion= the
surface may appear brick red, and the vessels are irregular, large,
tortuous and are seen to anastomose at frequent intervals. These move on
the bulb when pressed. The congestion is usually deepest on the
palpebral mucosa and in the _cul de sac_, and may be whitened for an
instant by pressure through the eyelid. To expose the conjunctiva the
right fore finger and thumb may be pressed on the upper and lower lids
respectively of the left eye, and the left finger and thumb for the
right, allowing them to slide backward above and below the eyeball.
Another method is to seize the cilia and edge of the upper eyelid
between the finger and thumb, and draw it downward and outward from the
bulb, and then deftly invert it over the tip of the finger. In the old
the unpigmented conjunctiva may appear yellow from the presence of
subconjunctival fat, or this may appear at any age from hepatic disease
(distomatosis) or icterus. It is swollen, or dropsical in anæmia,
distomatosis, etc.

5th. =Examine the ciliary vessels whether they are congested or not.=
These are distinguished from the conjunctival vessels in that they
radiate in straight lines outward from the margin of the transparent
cornea and do not move on the sclerotic under pressure. They are
enlarged and very red in congestion of the ciliary circle and in iritis.
In eyes devoid of pigment over the sclerotic, there is usually a
circular, narrow, white zone between the congested area and the margin
of the transparent cornea.

6th. =Examine the Membrana Nictitans.= See that its free margin is
uniformly smooth, even, and thin and that there is no swelling,
congestion nor morbid growth on any part of the structure.

7th. =See if the transparent cornea is perfectly and uniformly smooth,
transparent and glistening and if it reflects clear, erect images of all
objects in front of it.= The image of a round object which shows any
irregularity in the curvature of its margin implies a deviation from an
uniform curvature of the cornea: the image narrows in the direction of
the smaller arc and broadens in the direction of the larger one (see
keratoscopy, and corneal astigmatism).

8th. =A foreign body on or in the cornea= may be recognized in a good
light, but better and more certainly under focal oblique illumination
(see this heading).

9th. =A corneal ulcer= may be similarly recognized. It is made more
strikingly manifest by instilling into the lower _cul de sac_ a drop of
a solution of fluorescin and rubbing it over the eye by moving the
eyelids with the finger. This will stain the whole cornea. If now the
excess of stain is washed away by a few drops of boric acid, the healthy
part of the cornea is cleared up and the ulcer retains a bright
yellowish green tint.

10th. =Opacity or Floating objects in the aqueous humor= (flocculi of
lymph, pus, pigment, blood, worms) are always to be looked for. They may
be detected by placing the eye in a favorable light. They may be still
more clearly shown under _focal illumination_ (see below).

11th. =Changes in the iris and pupil= may also be noticed in a good
light. The surface should be dark in the horse, and of the various
lighter shades in the smaller animals, but in all alike clear, smooth
and polished, without variation of shade in spots or patches and without
bulging or irregularity at intervals. Apart from the congenital absence
of pigment in whole or in part, which may be found in certain sound
eyes, a total or partial change of the dark iris of the horse to a
lighter red, brown or yellow shade implies congestion, inflammation, or
exudation. The =corpora nigra= in the larger quadrupeds should be
unbroken, smooth, rounded, projecting masses outside the free border of
the upper portion of the iris. It should show a clear, polished surface
like the rest of the iris. =The pupil= should be evenly oval with its
long diameter transversely (horse, ruminant), circular (pig, dog, bird),
or round with an elliptical outline on contracting and the long diameter
vertical (cat). It should contract promptly in light and dilate as
quickly in darkness. Place the patient before a window, cover one eye so
as to exclude light, then cover the other eye with the hand and quickly
withdraw. The pupil should be widely dilated when the hand is withdrawn
and should promptly contract, and it should actively widen and narrow
alternately until the proper accommodation has been secured. Any failure
to show these movements implies a lesion in the brain, optic nerve, or
eye which impairs or paralyzes vision, interferes with accommodation or
imprisons the iris. In locomotor ataxia the pupil contracts in
accommodation to distance, but not in response to light.

12th. =Other causes of pupillary immobility= include: (a) Permanence of
a pupillary membrane, which has remained from the fœtal condition and
may be recognized by oblique focal illumination and invariability of the
pupil: (b) Adhesion of the iris to the capsule of the lens—complete or
partial—in the latter case the adherent portion only remains fixed,
while the remainder expands and contracts, giving rise to distortions
and variations from the smoothly curved outline: (c) Adhesion of the
iris to the back of the cornea—complete or partial—and leading to
similar distortions: (d) Glaucoma in which intraocular pressure
determines a permanent dilatation of the pupil and depression of the
optic disc: (e) The pupil is narrowed in iritis, and is less responsive
to atropia or other mydriatic: (f) Lesions of the oculo-motor nerve may
paralyze the iris and fix the pupil. The first three and the fifth of
these conditions may be recognized by the naked eye, alone, or with the
aid of focal illumination, the fourth may require the aid of the
ophthalmoscope and the sixth which cannot be reached by such methods,
might in exceptional cases be betrayed by other disorders of the
oculo-motor nerve (dropping of the upper eyelid, protrusion of the
eyeball, squinting outward).

13th. =Coloboma= (_fenestrated iris_), and =lacerated iris= are
recognizable by the naked eye in a good light, or by the aid of focal
illumination.

14th. =Tension of the eyeball= (_Tonometry_). Elaborate instruments
constructed for ascertaining ocular tension are of very little use in
the lower animals. The simplest and most practicable method is with the
two index fingers placed on the upper lid to press the eyeball downward
upon the wall of the orbit using the one finger alternately with the
other as if in search of fluctuation. The other fingers rest on the
margin of the orbit. All normal eyes have about the same measure of
tension and one can use his own eye as a means of comparison. The
educated touch is essential. In increased tension, the sense of hardness
and resistance, and the indisposition to become indented on pressure is
present in the early stages of internal ophthalmias (iritis,
choroiditis, retinitis), phlegmon of the eyeball, glaucoma,
hydrophthalmos, and tumors of the bulb.

Oblique Focal Illumination.

This is so essential to clear and definite conclusions and is so easily
practiced on the domestic animals that every veterinarian should make
himself familiar with the method. The method is based on the fact that
when two perfectly transparent media touch each other a reflection of
luminous rays takes place only at the surface. But in case any opacity
exists in any part of the thickness of one of these media, it reflects
the rays from its surface no matter what may be its position in the
medium. Thus corneal opacities appear as gray blotches and under careful
focal illumination it may be determined whether these are on the
conjunctival surface, in the superficial or deeper layers of the cornea
or in the membrane of Descemet. Similarly cloudiness or floating objects
in the aqueous, reflect the luminous rays, and so with opacities in the
lens or its capsule, or in the vitreous. In the same way the surface of
the iris and corpora nigra may be carefully scrutinized. For
satisfactory examination of the media, back of the iris, the pupil
should be first dilated, by instillation under the lid of a drop or two
of a 3 per cent. solution of atropia, and the examination proceeded with
twenty minutes later. Homatropin is preferable to atropin as being less
persistent in its action, and less liable to produce conjunctivitis. If
it fails to produce the requisite dilatation, it may be followed by a
drop of a 4 per cent. solution of hydrochloride of cocaine, which will
secure a free dilatation, lasting only for one day in place of seven
days as with atropin. The cocaine further removes pain and favors the
full eversion of the eyelids.

The instruments required for focal illumination are a biconvex lens of
15 to 20 diopters, and a good oil lamp or movable gas jet. The light of
the sun is not satisfactory. The examination ought to be conducted in a
dark room, or less satisfactorily in semi-darkness. The lamp is held by
an assistant at the level of the eye to be examined, either in front or
behind, or first one and then the other, so that the rays of light may
fall upon the eye obliquely. If the lids are kept closed it may be
necessary to expose the cornea by pressing on the lids with the finger
and thumb. The light is held 8 or 10 inches from the eye and the lens is
interposed between it and the eye and moved nearer and more distant
until the clearest illumination has been obtained of the point to be
examined. In this way every accessible part of the eye may be examined
in turn. The examiner may make his results more satisfactory by
observing the illuminated surface through a lens magnifying three or
four diameters. It is important to observe that the eye of the operator
must be in the direct line of reflection of the pencil of light.

=Cornea.= By focusing the light in succession over the different parts
of the surface of the cornea, all inflammations, vascularities,
opacities, ulcers, and cicatrices will be shown and their outlines
clearly defined. By illuminating the deeper layers of the cornea proper,
the lesions of keratitis, opacities, ulcers and cicatrices will be
shown. To complete the examination of the cornea the light should be
focused upon the iris so that it may be reflected back through the
cornea. This will reveal the most minute blood-vessels, any cell
concretions on Descemet’s membrane, or any foreign body in the cornea
which may have been overlooked.

=Aqueous Humor.= Unless the cornea is densely opaque, the anterior
chamber can be satisfactorily explored by the oblique focal
illumination. The cloudiness or milkiness of iritis or choroiditis
furnishes a strong reflection from its free particles of floating
matter, its blood and pus globules, and its flocculi of fibrine. The
latter have usually a whitish reflection, the blood elements a red
(hypohæma), and the pus a yellow (hypopion). The writhing movements of a
filaria scarcely need this mode of diagnosis. Sometimes, and especially
in the horse, detached flocculi of black pigment are found floating free
in the aqueous and are highly characteristic.

By this illumination one can easily determine the distance of the cornea
from the iris and lens (depth of anterior chamber) which is lessened by
the forward displacement of iris and lens in undue tension in the
vitreous (glaucoma, retinitis, tumors, bladderworms), or of the iris
alone, in irido-choroiditis with accumulation of exudate in the
posterior chamber of the aqueous. The depth of the anterior chamber may
increase in cases of luxation or absence of the lens or softening and
atrophy of the vitreous.

The adhesion of the iris to the back of the cornea may be satisfactorily
demonstrated by focal illumination.

=Iris.= The lesions of the iris are exceedingly common in connection
with recurring ophthalmia in the horse, and examinations in the
intervals between attacks are of the greatest importance. The eye should
be examined as already stated, at a window or door, and if available by
the aid of a mirror. Any changes in form or color, or luster should be
carefully noted, any tension of the eyeball, or angularity of the upper
lid, and any slight blue opacity round the margin of the cornea. Then
the prompt or tardy response of iris and pupil to light and darkness
must be made out. To complete the test the eye should be treated with
homatropin for three-quarters of an hour and with cocaine for ten or
fifteen minutes, and then subjected to oblique focal illumination.

With partial posterior synechia the rest of the pupil is found dilated
while the attached portion extends inward remaining fixed to the capsule
of the lens. If the synechia is complete no dilatation whatever has
occurred. The edges of the adherent iris extend inward as adherent
projections, and any exposed portion of the lens is likely to show black
points, the seat of previous adhesions that have been broken up. In such
cases the periphery of the iris bulges forward from the accumulation
behind it of aqueous humor or inflammatory exudate which cannot escape.
The discoloration of the iris as the result of inflammation, stands out
more definitely under the fuller illumination.

=Crystalline lens.= In exploring the crystalline lens or its capsule for
opacities (cataracts) oblique focal illumination can be employed to the
very best advantage, if the pupil has first been widely dilated by
homatropine and cocaine. The light is concentrated on all parts of the
anterior capsule in turn, then in succession on the different layers of
the lens at all points and finally on the posterior capsule. The
striking reflection from any points of opacity whether pigmentary, gray
or pearly white is diagnostic, not only of cataract, but of its exact
position—anterior or posterior, capsular or lenticular.

=Purkinje-Sanson images.= If the flame of a candle is passed in front of
the eye, at a suitable distance, in a darkened room, and the observer
looks into the eye obliquely from the opposite side, he observes three
images of the flame, reflected respectively from the front of the
cornea, from the anterior surface of the lens and from the back of the
lens. The image from the cornea is erect, bright and clearly defined:
that from the front of the lens is still erect, but larger and dimmer,
because the difference between the index of refraction of the aqueous
and lens is very slight: the third image, which is smaller and clearer
than the last, is inverted, because the surface of reflection on the
back of the lens acts as a concave mirror. The beginner may at first
find it difficult to make out the image from the front of the lens but
with a little care he can do so, and then by moving the light he should
cause each image to pass over all parts of the reflecting surface in
turn. Any unevenness or opacity at any point of the reflecting surface,
will cause the image reflected from it to become blurred or diffused as
it passes over it and thus, not the existence only, but the exact seat
of such opacity is easily demonstrated. Opacities on the cornea cause
blurring of the bright, erect image of the flame as it passes over that
part: opacities on the anterior capsule of the lens blur the dim, erect
image when passed over them: finally, opacities in the body of the lens
or on its posterior capsule, blur the small inverted image as it passes
over them.

Add to this method the oblique focal illumination and the images of the
flame reflected from the three mirror surfaces (cornea, anterior and
posterior lens surfaces) are made much clearer and more distinct than in
any other way. To do this effectively the convex lens should be held so
as to focus the flame in the air nearly in front of the cornea. The
Purkinje-Sanson images are made very definite and clear. If the lens is
approached nearer to the eye so as to throw the image of the flame
within or behind the lens, a gray phosphorescent streak of light is seen
in the depth of the pupil. This is due to the laminated structure of the
lens as well as to the fact that the lens itself is not perfectly
transparent even in its normal condition. The absence of the lens or its
dislocation and displacement downward, below the line of vision may be
inferred from the absence of this gray luminous reflection under this
test.

OPHTHALMOSCOPE.

Principle of ophthalmoscope: Angle of incidence and angle of
reflection in same line, light close to one side of the eye, reflected
into it by a mirror, having a hole in the centre for eye of observer.
Opacities show a dense white in transparent media: if in front of lens
move with rolling of eye: if behind in opposite direction. To see
fundus must use biconvex lens. Emmetropic eye: myopic: hypermetropic.
Static refraction. Mydriatics: Atropine, homatropine, daturine,
duboisine, hyoscyamine.

In the healthy eye, the pupil and iris, and in cataract, even the opaque
anterior capsule of the lens, can be clearly seen. The reflection of the
pupil, however, is dark and no object back of the iris can be observed.
The reason of the difference is that the rays of light, entering through
the whole cornea, are reflected at the same angle at which they strike
the surface of the iris. The angle of incidence is the same as the angle
of reflection. In the hollow fundus of the eye, however, the light
entering through the narrow pupil, strikes the fundus at a point which
is hidden from the observer, behind the iris, and being reflected by the
concave fundus, in exactly the same line along which it entered, it
remains invisible. To illuminate the fundus of the eye, for the
observer, his line of vision must be made exactly the same as that in
which the pencil of light enters the fundus. This is best effected by
reflecting the light into the eye by the aid of a small plane or concave
mirror having a hole in the center through which the observer looks into
the pupil. The concave mirror gives the stronger illumination, but the
plane article is more easily manipulated and tends to cause less active
contractions of the pupil. This is the simplest form of ophthalmoscope.
For careful examination of the fundus of the eye, it is best to have the
subject in a dark chamber, with a single large flame of an oil lamp or
gas (electric light with an obscure globe may answer). The light is held
behind and on the same side as the eye to be examined, at the level of
the eye and the perforated mirror and the eye of the observer are kept
from 10 to 20 inches in front of the eye and also at the same level. For
the horse or ox under favorable conditions in a stall, the light of day
coming from a fansash over the door may serve the purpose. Nicholas
assures us that it may be accomplished even under the shadow of a shed
or a tree. In such a case it is better not to have too much glare of
light as the reflection from cornea and lens may prevent accurate
observation. A somewhat cloudy day may therefore prove advantageous.

In focusing the reflected light on the cornea, and then on the pupil and
lens, any opacities in these will be shown as a grayish nebular
reflection or a denser white according to their degree of opacity. The
opacities in the cornea or aqueous, in front of the axis of vision in
the lens move in the same direction and to the same degree as the eye
rolls, while opacities on the posterior capsule or in the vitreous, move
in a direction opposite to the motions of the eye, and to a degree
corresponding to their distance back of the lens. Thus if the eye looks
downward such opacities move upward; if it looks upward they move
downward; if it looks inward they move outward; and if it looks outward
they move inward.

To secure an image of the fundus of the eye, including the entrance of
the optic nerve (optic papilla), the tapetum, the pigmentary surface and
retina and vessels, accommodation must be made for the normal refraction
of the eye of the patient, and even for that of the observer.

In the =emmetropic= (normal) eye, the rays leave the surface of the
cornea parallel to each other and it may be possible for the observer to
secure a good image on his retina, without the aid of lenses. In the
=myopic= (short sighted) eye they assume a convergent course on leaving
the cornea, and to secure a satisfactory image a biconcave or
plano-concave lens must be interposed between the cornea of the patient
and the eye of the observer.

In the =hypermetropic= (long sighted) eye, the rays diverge in leaving
the cornea of the patient, and a convex lens must be interposed between
this and the eye of the observer, in order that the rays may be focused
on the eye of the observer.

To adapt the vision to the different eyes the modern ophthalmoscope is
furnished with a series of lenses concave and convex, any one of which
can be moved behind the hole in the mirror to suit the demands of the
particular case.

To make a satisfactory examination the pupil should be dilated as for
oblique focal illumination. A 1:200 solution of apomorphia may be
instilled into the eye (a drop or two) and in 20 to 25 minutes a
satisfactory dilatation will have been secured. The effect of the
homatropin will usually have disappeared in twenty-four hours.

Determination of Static Refraction.

This can be best done in the lower animals by determining the strength
of the lens required to render clear the image of its fundus. By knowing
the refracting power of the lens, we may ascertain what deviation from
the normal refraction there is in the eye under observation.

In making this test the mirror of the ophthalmoscope must be brought
closely to the eye of the patient—1 to 2 inches.

If in such a case and without the use of any lens a distinct image of
the fundus is obtained, and if this is rendered less distinct by
interposing the lowest convex lens in front of the eye of the observer,
the eye is =emmetropic=.

If the ophthalmoscopic mirror without a lens gives an indistinct vision
of the fundus, and if the image is rendered clear by interposing one of
the convex lenses, the eye is =hypermetropic=. The strength of the
convex lens, +1, +2 or +3, dioptrics will give the measure of the
hypermetropia.

If, on the contrary, the ophthalmoscopic mirror gives an indistinct
image of the fundus, which is rendered even more indistinct by the
interposition of a convex lens, but is cleared up and rendered definite
by a concave lens, the patient is myopic. The strength of the concave
lens used will give the degree of _myopia_, –1 dioptric, –2 dioptrics,
etc.

The tendency in the horse is constantly to slight long-sightedness, but
the deviation is rarely found to be serious either in this direction or
in that of astigmatism.

Mydriatics.

Dilation of the pupil by mydriatics (mydriasis dilation of the pupil) is
a most important means of diagnosis, and therefore a knowledge of the
action of the different mydriatics is essential. The mydriatics in
common use not only dilate the pupil, but also paralyze the ciliary body
and the power of accommodation in ratio with the strength of the
solution employed. This determines an adaptation of the eye to the
farthest point of vision and holds it there until the action of the
mydriatic passes off and normal power of accommodation is restored. In
short it renders the subject long sighted, during its action.

=Atropine= the alkaloid of atropa belladonna is the most generally
available and persistent of the mydriatics, and is in most common use.
It is usually employed as sulphate of atropine, though some prefer the
nitrate, the salicylate or the borate to obviate the danger of
atropinism. This form of poisoning may show in the occurrence of
conjunctivitis and in case of one attack the susceptibility to atropine
is greatly to be dreaded, so that it should never again be used on the
same subject. The real cause of atropinism is uncertain, it has been
variously ascribed to too great acidity or alkalinity, or to
micro-organisms growing in the solution. Hence the importance of using
the antiseptic salts of atropine, and of testing the solution to see
that it is exactly neutral before it is applied.

The strength of the solution of atropine is an important consideration.
Donders found that 1:120 of water produced a full effect, while Jaarsma
obtained the full effect in one hour from a drop of a solution of one to
twelve hundred of water. The action on carnivora (dogs and cats) is
equivalent to that on man, while on the herbivora (rabbit, horse, ox,
sheep) it is somewhat less, and on birds very slight indeed. On diseased
eyes a large amount may be required, and with synechia (adhesion of the
iris to the capsule of the lens) dilatation may be impossible. The full
effect may last 24 hours, and accommodation may remain very imperfect
for 11 days.

The direct action of atropine on the eye is shown in dilatation of the
pupil of the frog after the eye has been detached from all connection
with heart or brain, by excision. It acts also in the normal system
through reflex nervous action, since, after division of the sympathetic
trunk going to the eye, that eye does not dilate so much under atropia
as the opposite eye.

Atropine is usually employed by lodging a drop in the pouch of the
conjunctiva (inside the lower lid), and from this it makes its way into
the aqueous humor, for if that liquid is transferred to the conjunctiva
of another animal it causes dilatation. Puncture of the cornea with
evacuation of the aqueous humor lessens the action of the atropine.
Atropine dilatation is increased by following it with cocaine which
causes contraction of the iridian vessels, the antithesis of the
dilatation of the vessels which occurs when the cornea is perforated and
the pressure of the aqueous humor is removed.

Atropine is one of the most potent poisons and must be used with caution
especially in the carnivora and omnivora. The danger lies not alone in
the absorption from the conjunctiva, but also from the escape of the
liquid through the lachrymo-nasal duct, to the nose and later to the
actively absorbing mucosæ of the lungs and stomach.

The symptoms of general poisoning are: rapid pulse, vertigo, weakness of
posterior limbs, general prostration and thirst or dryness of the
throat.

=Homatropine= is an oily liquid produced by the action of muriatic acid
on the cyanate of atropine. With hydrobromic acid it forms a readily
crystallizable salt, the solution of which acts on the eye like
atropine, but more promptly and transiently. One drop of a solution of
one to one hundred and twenty, usually gives in twenty minutes, full
pupillary dilation and complete paralysis of accommodation which lasts
only for twenty-four hours. Add to this that there is little danger of
constitutional disturbance and poisoning, and homatropine must be
accepted as a more desirable agent than atropine. It is especially to be
preferred in cases of senility with shallow anterior chambers, and in
glaucoma, in which atropine tends to aggravate the lesion.

=Daturine=, the alkaloid of datura stramonium is a potent mydriatic,
causing pupillary dilatation in a solution of one to one hundred and
sixty thousand of water. It appears to be identical with atropine.

=Duboisine= the alkaloid of duboisia myoporoides is also a potent
mydriatic. Jaarsma found that a solution of the sulphate, of one to
three thousand, paralyzed accommodation for twenty-four hours. It acts
more promptly than atropine but is more poisonous.

=Hyoscyamin=, the alkaloid of hyoscyamus niger, is also strongly
mydriatic. One drop of an one to three hundred solution of the sulphate
paralyzed accommodation for from seventy-five to one hundred hours.
Risley found it to act more promptly than atropine, and to be less
dangerous than duboisine.

WOUNDS OF THE EYELIDS.

Traumas: bites, lacerations, blows, penetrating wounds, gunshot,
scratches, kicks. Upper lid or commissure. Reparatory power of eyelid.
Danger of distortion. Treatment: sutures, plaster, shellac, collodion,
gelatine, Frick’s gelatine, birdlime, sterilisation: Quilled and
twisted suture. Position in stall. Metallic guard for eye.

_Causes._ Traumatic injuries of the eyelids are especially common in the
horse mainly because of his exposure in connection with the services
required of him. In a team he is liable to be bitten by one of his
fellows, or the lid may be caught on nails, in turning, or on hooks upon
harness, chains or wagons. It is sometimes injured by a blow from a club
or whiplash, or by knocking the head against solid objects that he
failed to see on account of the blinds. Again the injury will come from
running against prongs of bushes or trees, or of stump fences.
Occasionally a blow with the horn of an ox or cow is the cause, but this
is much more frequent with the bovine races. Then again gunshot wounds
are found in all animals. In sheep the eyelids sometimes suffer from
bites of dogs, while in dogs and cats, the teeth and claws are the main
causes of injury. These smaller animals also suffer from brutal blows
and kicks.

_Nature._ Wounds of the eyelids almost invariably affect the upper lid,
because of its extra size and prominence. Sometimes one commissure or
the lower lid is the injured part.

Clean incised wounds are rare, while lacerations with or without
contusions are the common experience. The laceration often extends
through the free margin of the lid, and then to one side, mostly the
outer, in a direction more or less parallel to the tarsus. The result is
that the detached flap drops downward exposing a greater or less portion
of the bulb covered with blood. The conjunctiva, the cornea, the
sclerotic or iris may be implicated in the lesion in different cases, so
that such wounds are of the most varied degree of gravity. If, however,
the lesion is confined to the lid, and in the absence of absolute
detachment of the flap, or severe contusion, a good repair may be
confidently hoped for. The vascularity and reparatory powers of the
eyelid are unusually great, and the looseness of the skin, connective
tissue, mucosa, and even the muscles is such that they do not draw
injuriously upon the edges of the wound to disturb the process of
cicatrization. If the two opposing ends of the divided tarsal cartilage
are kept in accurate opposition, the elasticity of his structure serves
to preserve the even contour of the palpebral margin, and the adhesion
or granulation process between the edges of the wound, soon becomes firm
enough to prevent further displacement. Even when one-half of the eyelid
is torn loose, remaining attached only by a narrow portion, reunion
without any unsightly distortion is not to be despaired of. In case of a
mere vertical laceration on the other hand, the case is very simple and
hopeful. Even when a portion of a lid has been completely torn off and
lost, the loose textures of the remaining part, often appear to stretch
in the process of healing so that a fairly serviceable, though by no
means an æsthetic covering for the eye may remain. This may serve for a
common work horse, but the unsightliness would necessarily debar him
from use in a carriage or as a saddle horse. The imperfect protection
too, exposes the eye to rainstorms, hail and snow, as well as to dust,
and greatly predisposes to conjunctivitis.

_Treatment._ One can trust implicitly to the extraordinary reparatory
power of the eyelids, yet so unsightly is any distortion of these parts,
that the greatest pains must be taken to obviate loss of substance, or
unevenness or puckering in healing. The points to be mainly sought for
are the perfect coaptation of the divided edges, and the restraining of
the patient from interrupting the healing process and breaking loose the
forming adhesions, by rubbing the eye.

Inconsiderable wounds of the skin may be simply stitched together with
sterilized catgut. Then the intervals between the stitches may be
approximated, dried, and covered with strips of sticking plaster, or
with shellac, collodion or gelatine. Frick’s gelatine is made by
dissolving fine gelatine in a 1 per cent. solution of corrosive
sublimate and adding about 10 per cent. of glycerine, perfecting the
admixture by the aid of heat. When wanted for use it may be melted by
heat and applied on the skin with a camel’s hair brush. Bird lime may be
used as a substitute. Sterilization must be sought by the use of
sublimate lotion 1:2000, or boric acid 2:100. Formerly the edges were
kept in close opposition by the use of quilled sutures, the stitches
passed around the quills being inserted at the usual distances while the
quills, applied against the edges of the wound kept them smooth and even
and obviated puckering. Or, perhaps better, the twisted suture may be
employed, the edges being brought together by pins placed close together
and a silk thread carried around each in figure of 8, and spirally from
pin to pin along the entire length. If one pin comes out it ought to be
promptly replaced and the whole left in place until a firm adhesion is
established. The points of the pins are cut off short so that there may
be no risk of their pricking.

With any method the horse or ox may be turned in his stall so that his
tail may be toward the manger and his face outward, and he may be tied
by two halters to the two posts, right and left. His food may be
furnished in a sack hung from the ceiling and cut down one side. In this
way the animal may be absolutely prevented from rubbing the itching sore
against any solid body, and thereby interrupting the healing process.
Another method is to apply a hood of stiff material with a metallic
guard for the face, having bars extending from above downward and arched
outward so that they shall effectually protect the eye in any attempt at
rubbing.

DEFICIENCY OF THE EYELIDS. COLOBOMA PALPEBRARUM.

The term coloboma representing merely a hiatus or deficiency is
applied to different parts of the eye according as there may be a lack
of substance of the part in question:—=Coloboma palpebrarum=
(deficiency of the palpebræ or lids), =C. iridis= (perforation of the
iris), and =C. choroideæ= (partial absence of the choroid).

=Coloboma palpebrarum= is usually congenital and takes the form of a
vertical notch on the upper lid, separating its two lateral parts into
independent flaps. According to the breadth and depth of the notch are
the extent of the exposure of the bulbar conjunctiva and the liability
to irritation and infection by foreign bodies. The same condition of
things will occur traumatically and require identical measures of
repair. These consist in paring the edges of the notch and bringing them
accurately together with catgut, silk or quilled suture, the
approximation being rendered more perfect by the application of
collodion, shellac or gelatine mixture (see wounds of eyelids). The
vascularity and extensibility of the tissues of the lids greatly favor a
kindly healing. Rubbing of the eye must be guarded against as advised
under wounds of the eyelids.

ORGANIC UNION OF THE EYELIDS. ANKYLOBLEPHARON. NARROWED FISSURE BETWEEN
THE LIDS. BLEPHAROPHYMOSIS.

Complete closure of the palpebral fissure has been seen as a congenital
infirmity in sheep, dogs and cats, while the partial closure has been
found in all classes of animals as the result of chronic conjunctivitis
and contraction of the exudation in undergoing organization. Narrowing
of the fissure gives the appearance of a small eye, so that a
progressive diminution is usually supposed to come from a reduction in
size of the bulb, though no actual atrophy of that organ has taken
place. In drooping of the upper lid (ptosis) too, the fissure is reduced
and the illusion of an atrophy of the eyeball is induced. The closure of
the fissure may come from _blepharospasm_, as the result of irritants in
the eye, or even of nervous disorder.

_Treatment._ In case of complete closure of the palpebral fissure, the
skin is picked up with forceps and an incision is made between the two
tarsi into the conjunctival sac. Then with probe pointed scissors, or a
grooved director and bistuory the incision is carried between the tarsi
to the proper position for the internal and external canthi. During
healing the lids should be frequently bathed with a boric acid solution,
and an ointment of the same with vaseline should be applied to prevent
adhesion.

When the trouble consists in a drawing together of the skin at the outer
canthus, the result of inflammation, the adhesions are separated by a
horizontal incision leading outward from the line of the angle. The
edges of the conjunctiva and skin are then sutured together, so as to
prevent further adhesion and the part treated as an ordinary wound. This
is known as _canthoplasty_.

Ptosis coming from tumors on the lid, or excess of fat in its substance,
or from oculo-motor disease must be treated according to indications.
The same remark applies to _spasm_ of the orbicular muscle
(_blepharospasm_), whether clonic or tonic. In domestic animals the
removal of the cause (foreign body, eyelash), will usually succeed.

WIDENED PALPEBRAL FISSURE.

After wounds of the outer canthus the union of the edges may remain
imperfect so that the fissure is enlarged and the eye unduly exposed.
The case is still worse if the wound has deviated from the horizontal
and has involved the orbicular muscle, the divided ends of which
continue to draw the edges apart, and cause a constant overflow of tears
(epiphora). Enlargement of the bulb or its protrusion by reason of a
swelling beneath it may give rise to the same appearance (exophthalmos).

_Treatment._ Pare the edges of the upper and lower lids at the outer
canthus and bring them together by sutures.

LAGOPHTHALMOS. INABILITY TO CLOSE EYELIDS.

This is called _hare-eye_ (lagos, hare) from the fact that the hare
habitually keeps the eyelids open. It is mostly due to spasm of the
levatores palpebræ, or to undue size of the orbicular opening. It may,
however, accompany ectropion, exophthalmos, and enlargement or swelling
of the eyeball from any cause. Bayer has seen cases in diseases of the
trifacial nerve, in neoplasms in the orbit and in buphthalmus.

Cases of the kind are especially liable to irritation, inflammation and
ulceration due to foreign bodies falling on the exposed bulb.

The _treatment_ is largely that of the attendant condition ectropion,
tumor, etc., which may be consulted.

ADHESION OF THE EYELID TO THE BULB. SYMBLEPHARON.

Causes: Conjunctivitis, burns, operation and other wounds. In front of
or behind the reflection of the mucosa from eye to lid. Prevention.
Treatment: section of adhesion, and vaseline, etc., Two edges of
healthy mucosa sutured together over the sore. When fornix is
implicated mucosa is transplanted.

This is liable to occur to a greater or less extent, in all animals, in
connection with violent conjunctivitis, burns and operation and other
wounds. It has been divided into _anterior_ and _posterior
symblepharon_, the former being an union in front of the normal
reflection of the conjunctiva from the lid upon the bulb (fornix), and
the latter involving the fornix in the substance of the adhesion. The
_anterior_ form by anchoring the lid to the eyeball is much more likely
to induce blindness, but it has the compensation that the union may be
broken up and the parts healed without subsequent reunion. In the
posterior form the eye can be better exposed and vision retained, its
repair is much more difficult demanding transplantation of skin or
mucous membrane on to the sore, and even then the granulation tissue
being continuous from bulb to eyelid may so contract in healing as to
leave matters no better than before.

These adhesions not only restrict the movements of the lids, preventing
their opening and the exposure of the bulb, but they also anchor the
bulb itself, and hamper its movements, necessitated for vision. In all
cases therefore of wounds, burns, abrasions and ulcers, of the palpebral
and bulbar mucosæ it is highly important to take precautions against the
formation of such connections. Any forming adhesions must be broken up
day by day and the surfaces must be kept apart in the intervals by
borated or iodoformed vaseline.

In a small anterior symblepharon the connections may be cut through and
subsequent adhesion prevented by the frequent introduction of iodoformed
vaseline, and if need be, by the daily separation of the surfaces by a
probe. When this fails a plastic operation may be resorted to, the
mucosa on the inner side of the lid being incised in a vertical
direction a short distance on each side of the sore and the inner edges
accurately stitched together. The raw surface left on the bulb thus
comes in contact only with the healthy mucous strips on the eyelid,
which have been drawn together over the seat of the former sore, and the
two new raw surfaces formed on the lid are well to each side of the sore
on the bulb, and are in contact with its healthy mucosa only. Thus no
two raw surfaces can come in contact, and adhesion is obviated.

When the fornix is implicated mucous membrane from the mouth, vulva, the
bronchia of the rabbit, or the skin of the frog must be transplanted
after the requisite incision of the cicatrix has been made.

INFLAMMATION OF THE EYELIDS. BLEPHARITIS.

Phlegmon. Causes: traumas, skin disease. Symptoms: swelling, redness,
distortion, infiltration, semi-closed lids, scabs, sloughs, abscess.
Tenderness. Itching. In eczema papules, vesicles, weeping eye.
Treatment: antiseptic astringent lotions, almond oil, vaseline, zinc
oxide, salicylic acid, boric acid, starch, xeroform, pyoktannin; for
eczema, mercury oxides, silver nitrate.

Conjunctivitis will be treated later, and under the present head there
will be considered only the phlegmon of the outer structures.

_Causes._ This lesion may come from two distinct causes, traumatism and
skin disease. The traumatisms in _horses_ and _cattle_ are bruises
sustained in rolling, especially during colics, in striking the head
against posts, poles, shafts and other solid bodies, in enduring blows
with horns or clubs, or frictions by the halter or in putting on a
collar. _Dogs_ suffer especially from blows with clubs and kicks from
men or animals. _All_ may suffer from wounds of the lids, and from
extensions of eczema and other skin diseases.

The _symptoms_ consist in swelling, redness, distortion, and often
extensive infiltration of the lid, sometimes eversion with exposure of
the reddened conjunctiva, usually abrasion, contusion, puncture or
laceration, semi-closed eye, the upper eyelid being comparatively
immovable (ptosis), and the formation of scabs, sloughs, or abscess.
There may be extreme tenderness, or, more commonly, intense itching.
Where eczema exists there may be found minute shot like papules at times
surmounted by small vesicles and the skin disease is continuous backward
upon the face. When abscess forms, the rounded swelling and manifest
fluctuation will betray its presence. Usually the eye waters and the
side of the cheek is wet and the hairs matted by a whitish coagulated
lymph and mucus.

_Treatment._ In the early stages without scabs, sloughs, or abscess,
antiseptic astringent lotions are in place. Weak solutions of zinc
sulphate, boric acid and morphine may be kept applied on a light
bandage. Or silver nitrate 1 gram to 1 oz. water may be applied daily
with a fine brush.

When scabs and crusts have formed they may be softened by the
application of almond oil, and then removed. The surface may then be
dusted with a bland antiseptic powder such as: zinc oxide 10 parts,
salicylic acid 1 part; or boric acid and starch equal parts; or
iodoform; or xeroform. Or unctuous applications may be used; zinc oxide
10, salicylic acid 1, vaseline 10; or iodoform 1, vaseline 5. Or a
watery application may be used, such as the silver lotion or that of
pyoktannin 1:1000.

For eczema yellow oxide of mercury 1, to vaseline 10, has an excellent
reputation. It may be alternated with pyoktannin.

When abscess has formed it should be excised in a line parallel to the
free border and the resulting cavity injected with the silver or the
pyoktannin solution.

In all cases the patient must be fastened as for wounds of the lids so
that he cannot rub the eye.

For eczema and other skin diseases the special treatment appropriate to
the disease should not be omitted.

ŒDEMA OF EYELIDS.

In anthrax, malignant œdema, disease of heart, kidney or liver,
distomatosis, trichiniasis, wasp stings, urticaria, petechial fever.
Treatment: correct general disorder, remove local irritant, antiseptic
astringents.

An œdematous condition of the eyelids with or without inflammatory
conditions may be due to local disease or it may be the result of more
general disorder. In anthrax districts any of the herbivora, but
especially cattle and sheep, are liable to a diffuse anthrax of the
eyelid with a special petechial or brownish condition of the palpebral
conjunctiva. Malignant œdema and other local bacteridian affections
affect the loose textures of the eyelid in a similar manner, but with
extrication of gas and crackling under pressure. Such cases are
complicated by local inflammation. When in the absence of inflammation
the lids pit on pressure, one should seek for some disease of the heart,
kidney or liver, also for indications of similar dropsical effusions in
other parts of the body. Distomatosis and, to a less extent, pulmonary
and duodenal strongylosis are especially common factors in sheep. In
distomatosis (liver rot) a simultaneous dropsy is often present in the
intermaxillary space, the chest or the abdomen. The puffiness of the eye
is especially marked in the palpebral conjunctiva, and is exposed by
everting the eyelid over the tip of the finger. In trichinosis in man
and less frequently in swine, dropsy of the eyelid is often present at
the end of the first week. Other swellings of the lids partaking more of
the nature of inflammation, result from the stings of wasps, hornets and
other insects, from urticaria (in horses especially) and from petechial
fever in solipeds.

In _treating_ such cases the general disorder, if present, must be first
attended to, then the removal of any local irritant, and finally the
antagonizing of any local inflammation or infection. Astringent and
antiseptic lotions are especially called for.

EMPHYSEMA OF THE EYELIDS.

This has been already referred to as occurring in malignant œdema, black
quarter and other gas producing infections. It may also come from
lacerations made in puncturing the lachrymal sac, and from fracture of
the margin of the orbit—the air entering the connective tissue in this
case from the cavities of the nasal sinuses. The lid feels puffy and
crackles when pressed and apart from a general infection it requires
only soothing and antiseptic dressings.

DISEASE OF THE MEIBOMIAN GLANDS. BLEPHARADENITIS. SEBORRHŒA.

This is a blepharitis of the edges of the lids which are swollen, red,
and incrusted along their margins with scabs and sebaceous concretions.
When this scurf is removed the skin is found to be red, tender and
glistening. The glands are the seat of congestion, and produce a
modified secretion in excess, which dries into crusts instead of
preserving its normal oleaginous consistency. As these glands open into
the follicles of the eyelashes, their walls are implicated and shedding
of the lashes is a common result. It may be assumed that this affection
is often associated with the proliferation of microbes in the glands and
gland ducts, while in other forms the presence of acari is the
controlling factor. Wilson found the demodex folliculorum in the
Meibomian glands of the horse, and Oschatz in those of the sheep.

_Treatment._ Smear the margins of the lids with vaseline and when the
crusts have been thoroughly softened wash them off with Castile soap and
warm water. Then dress the margin with the ointment of the yellow oxide
of mercury 1, in vaseline 10. If demodex is suspected they may be
squeezed out and the lids washed frequently with spirits of wine as a
solvent.

HORDEOLUM. STYE. ACNE.

Like acne of the skin in general, this consists in inflammation and
suppuration of a hair follicle and sebaceous gland. The whole lid or a
large part of it may be swollen, but by stroking it with the finger, a
hard, rounded, very tender spot will be detected and as the disease
advances this develops a minute collection of pus. A specially wide
orifice favors the entrance of the pus microbes, and the onset of the
disease. It has been noted in dogs (Fröhner).

For abortive _treatment_ Fick recommends dry heat from a pocket
handkerchief or a heated teaspoon. If pus is present it must be
evacuated, and recurrence guarded against by cleanliness and
antiseptics. Use pyoktannin solution (1 ∶ 1000), or mercuric chloride (1
∶ 5000) or yellow oxide of mercury ointment.

CHALAZION.

This is a pea like tumor growing from the tarsal cartilage, its
flattened side toward the mucosa, which is red and angry, and its round
surface toward the skin. When manipulated between the fingers it moves
with the tarsus. It is usually of slow growth and may continue for years
apparently unchanged. Some have thought it tuberculous, but its true
nature is uncertain. Warner records the disease in the horse.

_Treatment_ consists in incision and removal of the tumor, curretting of
the cavity, and after antiseptic douching, suturing the lips.

TUBERCULOSIS OF THE EYELID.

Described by Jewsejenke in the lower lid of birds, this is manifested by
small, hard round knots, covered by bluish red, or yellowish red skin,
and when incised showing a characteristic miliary tubercle, with bacilli
and sometimes a caseated centre. It is treated by incision, curretting
and caustics.

TURNED IN EYELASH. TRICHIASIS.

Sometimes an eyelash grows inward so as to impinge upon the front of the
eyeball, or even to extend between this and the eyelid. The condition
exists in _entropion_ but _trichiasis_ is rather the deviation of one or
two cilia by reason of their false direction, individually. It may occur
as the result of a pre-existing inflammation affecting the edge of the
lid and the follicle, and the offending hair is not only badly directed
but small and shrunken as well. On this account it is not always easy to
recognize it, and accordingly in cases of conjunctivitis without
apparent cause it is well to examine carefully with the aid of oblique
focal illumination.

_Treatment_ consists in pulling out the offending hair with ciliary
forceps, avoiding bending it lest it break off short and become at once
more irritating and more difficult of extraction. In case the hair grows
anew in the same direction extract it anew and destroy its root with the
electric cautery.

ENTROPION. TURNING IN OF THE EYELID.

In foals, puppies, hounds, with narrow fissure, and conjunctivitis, or
tarsitis. Permanent bandaging, orbicularis spasm. Symptoms:
disappearance of tarsus and lashes by involution. Treatment: in spasm
fix by plaster; suture skin; excise elliptical section of skin and
suture edges together. Release cicatrices.

Inversion of the eyelid or a portion of it, with consequent trichiasis,
conjunctivitis and lachrymation has been met with congenitally in foals
(Aubry, Bourdeau, Hamon) and puppies (Cadiot, Almy). Hounds have
especially suffered. In the older animals it is largely determined by
abnormally narrow fissure, and by old standing disease of the
conjunctiva or tarsus, with cicatricial contraction or adhesion.
Persistent bandaging turns in the cilia and contributes to entropion.
Finally a persistent spasm of the orbicularis muscle may bring it about.

_Symptoms._ Trichiasis is usually, though not always, present.

In any case the tarsus is turned inward so as to press upon the front of
the bulb, or even to disappear completely. Thickening and distortion of
the lid is a not infrequent condition.

_Treatment._ In case of simple spasm clip or shave the hairs from the
lid corresponding to the lesion, and close to the tarsus attach a strip
of plaster. When firmly adherent draw it sufficiently to efface the
entropion and attach it to the skin of the face.

This failing, Gaillard’s sutures may succeed. With a pair of forceps
with looped, transversely elongated blades, pinch up skin and muscle
sufficient to correct the entropion, and passing a needle twice through
this fold with an interval of 3 mm., tie the suture over a small roll of
cotton. The stitches may be removed in two days and the cicatrices may
permanently obviate the deformity.

The older plastic operation is more trustworthy: The skin of the
affected lid is pinched up to such an extent in length and breadth, as
to correct the entropion and is then excised with sharp scissors or
bistuory so as to leave a long elliptical sore. The edges of this are
then carefully sutured together and the resulting union corrects
deformity. In case the entropion is caused by an old standing cicatrix,
it may be necessary, first, to make a careful incision along the edge of
the lid so as to separate the tarsus and conjunctiva from the cilia and
Meibomian ducts, and then to proceed with the plastic operation on the
skin.

TURNING OUT OF THE EYELID. ECTROPION.

In large dogs, in old age, debility, conjunctival swelling, cicatrized
skin of lids, distortions of lids. Symptoms: exposure of palpebral
mucosa, weeping eyes, conjunctival hypertrophy (chemosis). Treatment:
scarify or excise a fold of mucosa, astringent antiseptics, Snellen’s
suture, Diefenbach’s operation, Wharton-Jones operation.

This is much more common than entropion, but much less injurious as the
tarsi and lashes do not irritate the conjunctiva. It is especially
common in large dogs (hounds, mastiff) and usually affects the inner
part of the lower lid. Old age and debility contribute materially to the
condition, the lack of tone or paresis being an important factor. It
may, however, occur in any animal, from conjunctivitis and swelling of
the mucosa, from cicatrices or old standing disease of the skin of the
eyelids, or from imperfectly healed wounds leaving distortions of the
lower lid. It is most frequent in the lower lid, and the slightest
pendulous condition, which detaches the tarsus from the bulb, and
exposes a narrow zone of the conjunctiva is considered to be an
ectropion.

_Symptoms._ Beside the exposure of the zone of mucosa, there is the
overflow of tears, and in old standing and bad cases a hypertrophy of
the exposed conjunctiva, which projects as a fleshy-looking mass, and
weighs down the lid, with a continual tendency to aggravation.

_Treatment._ Where the main factor seems to be the infiltration of the
mucosa this may be reduced by scarification, or by the complete excision
of a fold of the membrane. Use an antiseptic wash (boric acid) and the
retraction of healing tends to brace up the lid against the bulb.

Snellen’s suture is sometimes employed successfully. A silk thread is
armed at each end with a needle, and the needles are passed into the
conjunctiva just inside the tarsus and brought out through the skin near
the margin of the orbit, where they are tied round a small roll of
cotton. Several of these may be inserted side by side so as to extend
the whole length of the ectropion and they should be drawn tight enough
to correct the deformity. If left some days they will usually determine
cicatrices which will overcome the deformity.

The most common operation (Dieffenbach’s) is the excision of a
triangular portion of skin from just outside the lower lid and having
its base or upper side running horizontally outward from the outer
canthus. Then pare the margin of the lower lid for a distance equal to
the base of the triangle. Then bring together and suture the skin
forming the right and left sides of the triangle, and the raw edge of
the lid to the skin that formed the base of the triangle. In this way
the triangular sore formed by the operation is completely covered and
the margin of the lower lid is shortened so as to brace it up against
the bulb.

In case of cicatricial ectropion the Wharton-Jones operation is to be
adopted. A V-shaped incision is made in the skin of the lower lid
commencing just beneath the tarsus and carried down so that the two
lines of incision meet well down beneath the cicatrix. The triangular
flap of skin thus made, is detached by a bistuory from the cicatricial
tissue beneath, and allowed to shrink upward toward the tarsus. Finally
the two edges are sewed together from the angle upward, as far as may be
necessary to allow the proper application of the tarsus against the
bulb, and the remainder of these edges are sutured to those of the
triangular flap.

TUMORS OF THE EYELIDS.

=Warts.= The most common tumors of the eyelids in horses, cattle, and
dogs are warts. These are most simply disposed of by seizing them with
rat-tooth forceps and clipping them off with sharp scissors curved on
the flat. Any bleeding may be checked by a pencil of silver nitrate.

=Sarcoma=, =melanoma=, and =epithelioma= are common in solipeds,
especially in the gray and white. They usually form a cauliflower-like
mass red and angry and bleed easily. They may occupy any part of the
lid, the skin, the dark tarsal margin, the connective tissue or the
mucosa, and not unfrequently they involve the eyeball, and the
surrounding tissues, even the bones of the orbit.

_Treatment._ These may be excised like warts taking care to remove every
vestige of disease. In these cases I have usually found it necessary to
remove the entire bulb.

FRACTURE OF THE ORBIT.

_Nature and Causes._ The usual seat of fracture is the orbital process
of the frontal bone, yet any portion of the orbital margin may suffer,
and even the inner wall or floor of the orbit may be broken by a
penetrating instrument. Horses and polled cattle and sheep are
especially exposed to the injury, while in horned stock the region is in
a measure protected. Carnivora, which have no bony orbital process, are
less liable but may still sustain fractures of the remaining parts.
Horses and polled ruminants suffer mainly from beating the head on the
ground or other solid body in the paroxysms of colic and enteritis, or
in nervous affections; horned stock suffer from concussions in fighting
and direct blows by the horns. All animals suffer from blows with clubs,
kicks and other mechanical injuries.

_Symptoms._ With (and less frequently without) a skin wound, there may
be indication of depression, or mobility of the detached segment, or its
sharp edge may be felt, through the skin, or by the sterilized finger
introduced into the orbit. In case of a penetrating or stab wound, which
cannot be followed by the finger, it may be followed by an aseptic probe
and any fracture recognized. The conjunctival sac must be first
thoroughly washed out with an antiseptic lotion, as the introduction of
any septic germs into the osseous wound, is likely to cause a dangerous
infection or abscess.

_Treatment._ Simple, slight fractures with blunt instruments are treated
by rest and cooling, disinfectant lotions. If foreign bodies or detached
particles of bone are found in the wound they should be extracted. Shot
that are difficult to find, may be left, as they are often aseptic and
tend to become encapsuled. Should they cause abscess they will usually
be found in the pus sac and may then be removed. Displaced bones may
often be replaced by the finger in the orbit. Sometimes they can be best
reached by trephining the frontal or maxillary sinus and introducing a
lever through the cavity (Hendrickx). If the sinus has been involved it
must be opened in any case. Cadiot advises bandages impregnated with
black pitch to fix the bones in certain cases. Antiseptic washes
(sublimate 1 ∶ 5000) and antiseptic cotton packing are demanded for all
wounds.

BRUISES AND WOUNDS OF THE ORBIT.

These may come from the same _causes_ as fractures and though less
violent may occasion inflammation which involves the eye or even the
brain with fatal results. Thus in horses it has been a cause of
infective inflammation, with a fatal extension (Robellet); in cattle a
similar inflammation has extended to the cerebral meninges and caused
death (Leblanc), and in dogs an advance to the eyeball threatens its
destruction (Möller). Short of this necrosis is not uncommon (Rey).

_Treatment._ This does not differ materially from that demanded by
penetrating wounds with fracture. A perfect cleansing and antisepsis of
the wound is the first demand. A solution of boric acid (4 per cent.) or
of mercuric chloride (1 ∶ 5000) liberally applied, and maintained
thereafter on soft pledgets of surgical cotton, will often have the best
results. All foreign bodies must be carefully removed, lacerated flaps
and shreds may require suturing, dead portions excision, and finally
abscesses or excessive exudate may require the lance, but cooling,
antiseptic lotions and an elevated position of the head, are among the
most prominent resorts.

RETRO-BULBAR ABSCESS.

Schindelka has observed this in the horse, in connection with petechial
fever. If connected with meningeal abscess it will be necessarily fatal.
In favorable cases evacuate the pus as soon as detected and dress with
pledgets of cotton saturated with a mercuric chloride solution (1:2000)
or other antiseptic.

PERIOSTITIS OF THE ORBIT.

This may be shown by the firm swelling of the bone and, in case a wound
has been formed, by the contact of the probe with the denuded, hard,
rough bone. When thus exposed or necrosed on the surface, or when an
exostosis has formed, the bone may be laid open and scraped down to the
healthy tissue, and then dressed with antiseptic pledgets.

TUMORS OF THE ORBIT.

These may be of different kinds, as =sarcoma=, =encephaloid=, =osteoma=
and =actinomycosis=. They demand thorough surgical treatment, except
perhaps in the case of the latter, which may recover under iodide of
potassium. Emmerich records an extensive sarcoma of the orbit in a cow,
weighing six pounds and extending into the nasal sinuses, and chambers,
and implicating the cerebral meninges. Möller records cases of sarcoma
and carcinoma of the orbit in horses and dogs, and Leblanc in cattle.
Melanosarcoma is not uncommon in the orbits of gray horses which are
changing to white.

Exotoses are common around the orbits of cattle.

If such growths do not show on the surface they cause a more or less
unsightly protrusion of the eyeball, owing to the presence of the
neoplasm in the depth of the orbit, and the removal of the bulb becomes
a necessity.

DISEASE OF THE LACHRYMAL GLAND AND DUCTS. DACRYO-ADENITIS.

Even in man these parts are remarkably free from disease, while in the
lower animals, we have literally no record of such conditions.
Inflammation of the gland (dacryo-adenitis) would be manifested by a
sensitive swelling under the outer part of the orbital process, and
upper eyelid and by lachrymation, and obstruction of the gland duct and
by a tense transparent rounded swelling inside the lid. A fistula is
possible from a penetrating wound of the lid in the same situation. In
both of the latter conditions an opening made through the palpebral
conjunctiva will allow the discharge of the tears in the proper place,
and healing of any external wound may be hastened by suture or plaster.

OBSTRUCTION OF THE LACHRYMAL PUNCTA. ATRESIA. INFLAMMATION.

Congenital atresia of these puncta has been recorded in foals, by
Hollmann and obstruction as the result of inflammation, by Lafosse,
Verjaus and Tyvaert, and of the entrance of the seeds of bromus by
Stockfleth.

Apart from congenital atresia and impaction of foreign bodies the
_symptoms_ are those of conjunctivitis, with escape of tears over the
face (epiphora). Injection of aseptic water into the lower puncta and
its escape by the upper, and by the nasal orifice, will determine the
patency or otherwise of the various channels.

_Treatment_ consists in astringent collyria to check the inflammation,
in the removal of any foreign body, in the dilation or slitting of the
lachrymal canaliculi, and in case of complete atresia, in incising the
lachrymal sac. Slitting of the canaliculi is accomplished by a small
probe pointed bistuory (canaliculus knife). The lid is drawn away from
the carnucle, and the probe point inserted at first downward, then
inward and backward, and when it is well inside the sac the handle is
brought to the vertical and the walls of the duct slit open.

In case of atresia Leblanc recommends to seize the inner canthus with
rat tooth forceps so as to include the structures about the sac and to
plunge the bistuory directly into the sac. Then by the aid of a
whalebone staff he passes three silk threads through the duct and fixes
them in place by attaching them to a copper ring at each end. This is
retained in place and moved daily until the passage has been definitely
healed and its permanency assured.

WOUND AND FISTULA OF THE LACHRYMAL SAC.

The lachrymal sac, which receives the tears from the canaliculi, is
situated in the infundibulum at the upper end of the lachrymal canal and
is in great measure protected against external injuries by the prominent
orbital edge of the lachrymal bone. Yet violent blows with or without
fracture, sometimes lead to rupture of the mucous walls and the
formation of a fistula. Wounds made with penetrating bodies, more or
less pointed are also liable to involve the sac. The fistulous orifice
may be through the skin at the inner canthus or through the mucosa by
the side of the carnucle. The cutaneous opening may be a minute orifice
from which tears and muco-purulent matter escapes, to mat together the
hairs on the side of the face. Sometimes there is a reddish elevation,
the size of a pin head, and in fistula through the mucosa this is the
rule, and the orifice is elevated so that the tears flow out over the
face. For the symptoms of the attendant catarrh of the sac see below. In
infected cases with obstruction of the lachrymo-nasal duct, it has been
known to extend to the bone and even to open into the sinuses, or tooth
follicles. (Gerard, Leblanc).

The condition is found in horses, cattle and dogs.

_Treatment._ In fistula resulting from simple traumatism, nothing more
may be requisite than rest and soothing astringent applications. Sutures
are sometimes resorted to but are liable to cause itching and do more
harm than good. It is above all important to keep the lachrymo-nasal
duct patent, and for this purpose a lead or silver stilet, or a thick
catgut suture may be worn in the canal until healing has ensued.

CATARRH OF THE LACHRYMAL SAC. DACRYOCYSTITIS.

Connected above through the canaliculi with the conjunctiva, and below
through the lachrymal duct with the nasal chamber this cavity is liable
to be more or less implicated in all cases of nasal catarrh and
conjunctivitis, (strangles, canine distemper, influenza). If the
lachrymal duct is obstructed so that the tears accumulate in the sac,
the tendency to catarrh is further enhanced by the distension and
weakening of its walls, and by the propagation of bacteria which have
entered with the tears, and find in them a favorable and abundant
culture medium; the diameter of the sac in the horse being about ⅔rds.
of an inch. The presence of foreign bodies is another cause.

_Lesions. Symptoms._ Swelling at the inner canthus, which raises the
carnucle above the normal level, and the escape of tears over the lower
lid are the most prominent symptoms. If the swelling is pressed it
subsides, the contents, clear or purulent, escaping through the
lachrymal duct, to the nose, or through the puncta and accumulating in
the inner canthus or flowing over the cheek. The hair beneath the inner
canthus is matted together, or drops off leaving bare patches. Wolff
found in one case, a distension of the sac to over two inches in
breadth, and 1⅔ inches long. To the swelling there is soon added
conjunctival inflammation, closure of the puncta by swelling and the
escape of all tears over the face. Suppuration supervenes in the sac,
and in the larger animals the pent up pus often makes its way outward,
causing destructive ulceration of the walls of the canaliculi and
puncta, or of the walls of the sac, the skin, or even the subjacent
bone. In this way fistula results. Caries of the bone and penetration of
the molar alveoli may ensue. (Girard, Leblanc).

_Treatment._ The first object must be to secure a free drainage into the
nose. The evacuation of the sac by compression having been accomplished,
an astringent solution may be injected through the nasal opening of the
lachrymal duct. If the canal is pervious the sac will be re-filled and
will swell out as before. The injection may be 0.5 per cent. sulphate of
zinc, 1 per cent. acetate of lead, 0.3 per cent. nitrate of silver, 1
per cent. tannic acid, 2 per cent. boric acid, or 0.02 per cent.
corrosive sublimate. Cocaine may be added in the proportion of 5 per
cent. The injection may be repeated thrice a day at first, then twice,
and finally once as the catarrh subsides.

If the injection fails to reach the sac, thoroughly sterilized, flexible
probes may be used, increasing the size as they can be passed without
too great pressure.

Or the puncta and canaliculi may be injected as in the human subject,
the conjunctiva having been first anæsthetized by cocaine, or general
ether or chloroform anæsthesia having been induced. The slitting of the
puncta and canaliculi may be resorted to, as spoken of under atresia.

The frequent passage of a sound is usually resorted to, and a stilet may
even be worn, but there is always danger of resulting thickening and
narrowing of the duct, and, if healing can be secured without this
measure, it is to be preferred.

STENOSIS OF THE LACHRYMO-NASAL DUCT.

Obliteration of the lachrymal duct may occur from stricture of the
canal, the result of wounds or other irritants: from pressure by the
inflamed mucosa in nasal catarrh or strangles: from polypus or osseous
tumor in the nose: from actinomycosis or other disease of the bones.

The one manifest _symptom_ is the escape of the tears on to the face. To
complete the diagnosis, injection of one punctum will cause distension
of the lachrymal sac.

_Treatment._ This may be attempted by bougies. In the _horse_ a small
sound, metallic or whalebone bougie, thoroughly sterilized and smeared
with aseptic vaseline, or oil, is inserted from the nasal opening and
carefully passed on into the sac. In the _dog_ the nasal opening cannot
be reached and the bougie must be passed by the puncta and lachrymal
sac. To secure the requisite dilation, it is usually necessary to probe
the passage daily, using a larger probe when the first passes easily,
until the canal has been sufficiently dilated.

A second resort is to distend the canal by a liquid injection thrown
into the nasal opening. This will succeed when the obstruction is only
caused by concretions in the canal.

A somewhat similar resort is the insufflation of the duct by means of a
finely pointed tube inserted from below into the nasal orifice of the
duct.

Still another method is to make a new opening for the escape of the
tears into the nose. When the stenosis is at or near the nasal opening
of the duct, an artificial opening is easily made and usually
satisfactory. Under anæsthesia, a sterilized silver probe is passed
through the upper punctum, the sac and canal. When it meets definite
obstruction its position is ascertained inside the nose, and an incision
is made so as to allow its escape. The constant escape of tears tends to
prevent it from closing up again, but it is well to examine into this
until it has thoroughly healed. A silk thread worn in the duct and held
in place by a copper or aluminum ring on each end may be resorted to.

Attempts have been made to establish a new outlet by boring through the
lachrymal bone into the nose, but without a permanent success. It has
also been advised to obliterate the lachrymal ducts and sac, on the one
hand and to excise the lachrymal gland on the other, but the proposed
cure is worse than the disease.

DISEASE OF THE LACHRYMAL CARUNCLE.

The caruncle is inflamed in conjunctivitis. When this inflammation leads
to hypertrophy it is known as _encanthis_. This is a common condition in
_dogs_ and the caruncle may increase to the size of a pea or acorn, and
by compressing the canaliculi it leads to a profuse overflow of tears on
the cheek. At first there is the acute congestion of conjunctivitis, but
later there may be induration and pallor.

The _treatment_ of this condition consists in astringent and sedative
collyria in the early inflammatory stages, and later in the ablation of
the hypertrophied mass. The caruncle is seized with a pair of rat-tooth
forceps and snipped off with curved scissors, the free bleeding being
afterward checked by cold water.

In cases that seem, by reason of excessive vascularity ill adapted to
this method, the hypertrophied mass may be tied at its base with a stout
silk thread so as to cut off the supply of blood, and cause it to slough
off. A collyria of boric acid (4 per cent.) or mercuric chloride (0.02
per cent.) may be used to prevent infection.

=Tumors= of the Caruncle are met with, such as fibroma (Wörz), Sarcoma
and Melanosarcoma. For all alike the complete extirpation of the
neoplasm is demanded.

WOUNDS AND INFLAMMATION OF THE MEMBRANA NICTITANS.

Like other parts of the ocular apparatus, the third eyelid and gland of
Harder are subject to accidental injuries of various kinds. What is
worse, ignorant persons seeing the cartilage and membrane projected over
the eye in ophthalmias and tetanus, have mistaken it for a morbid
product and deliberately cut it off in part. The condition of the organ
may be ascertained by parting the lids with the fingers and pressing
gently on the front of the eyeball, when the nictitating membrane will
be fully exposed.

If detached portions cannot be restored, but threaten to slough, or
cause distortions or unsightly and irritating neoplasms they should be
seized with forceps and snipped off with scissors. Otherwise the
treatment consists in soothing astringent and anodyne Collyria as in
conjunctivitis.

TUMORS AND HYPERTROPHY OF THE MEMBRANA NICTITANS.

Neoplasms of this organ may occur in any quadruped or bird and may be
recognized by the swelling of more or less of its substance, by the
unevenness of its free margin, or by distinct outgrowths from its
surface. They are especially common in dogs and pigs and may be fibrous,
epithelial or otherwise. The treatment is purely surgical and in case of
a malignant neoplasm should demand the removal of the entire organ.

ADENOMA OF THE GLAND OF HARDER.

Cases in dogs have been recorded by Fröhner and Schimmel, and it might
be expected in other carnivora, ruminants, pigs, rabbits and birds. The
treatment is by excision with forceps and scissors, and subsequent
treatment with an antiseptic zinc lotion.

FOREIGN BODIES IN THE CONJUNCTIVAL SAC.

Frequency: seeds, glumes, awns, dust, sand, wood, metal; exudate; in
conjunctival pouch, under nictitans, in puncta. Filaria lachrymalis.
Symptoms: closure of lids, epiphora, congestion, inflammation,
infection. Treatment: local anæsthesia, forceps, lead pencil, pin’s
head, collyria.

So common are foreign bodies in the conjunctival sac of the domestic
herbivora, that in any case of epiphora, hyperæmia or inflammation of
the mucosa, the first care should be given to see that the condition is
not caused by the presence of such an irritant. In animals fed from high
racks, seeds and glumes of the gramineæ, awns of barley, and dust of
various kinds often get into the eye and stick fast. Under other
conditions, insects, particles of sand, dust, wood, metal, etc., prove
equally injurious by their presence. Awns and chaff are particularly
liable to adhere to the mucosa and even to become covered by an exudate,
which renders them more firmly adherent. Other objects lodge under the
eyelids, or membrana nictitans, or in folds of the mucosa. Their
entrance into the lachrymal puncta has already been referred to. The
larger and more rounded bodies are likely to be washed off by the
excessive flow of tears, assisted by the movements of the nictitating
cartilage, but flat glumes, or awns stick too closely to the surface,
while the smaller objects become entangled beneath the lids, or hair, or
in the folds of the mucous membrane. The filaria lachrymalis may be the
cause of trouble.

_Symptoms._ There is closure or semi-closure of the lids, the escape of
a profusion of tears over the cheek, and active congestion or hyperæmia.
A careful examination with everted lids, or even with raised nictitans
will usually reveal the foreign body. If overlooked or neglected the
hyperæmia rapidly advances to active inflammation, with or without an
infective complication. Foreign bodies blown into the eye, as a rule
carry with them more or less bacteria, and, if these have any tendency
to pathogenesis, the irritation of the mucosa easily paves the way for
their colonization. Thus, any grade or form of conjunctivitis may
supervene upon the introduction of a foreign irritant.

_Treatment._ Nearly all such bodies are most easily and certainly
removed by a pair of fine forceps. It may be necessary to first
anæsthetize the eye with a 5 per cent. solution of cocaine. The clean
tip of the finger passed under the lid and nictitating membrane is a
safe and effective method. Less effective methods are to pick up the
offending body on the point of a lead pencil, or a small, blunt metallic
spud, or with a pin’s head covered with a clean pocket handkerchief.
This may be followed by an antiseptic (boric acid) collyria, with or
without cocaine or morphia.

WOUNDS OF THE CONJUNCTIVA.

These occur in all domestic animals, but are especially frequent in dogs
and cats from scratching with the claws. In clumsy handling of the
eyelids, the mucosa is wounded by ragged and uneven nails. Injuries and
stings by insects which are attracted by the reflection from the eye
constitute a specially grave lesion, often proportionate to the nature
of the poison instilled.

_Symptoms._ There are usually closure of the eyelids, with exudation and
thickening of the conjunctiva especially in the vicinity of the wound, a
free flow of tears, mingled it may be with blood, and the visible
evidence of the lesion on the exposure of the injured part. If the
cornea is implicated, even the pupil is contracted, showing photophobia.

_Treatment._ Slight noninfected wounds will heal readily under simple
astringent collyria, following upon the removal of any cause of
mechanical irritation. A solution of corrosive sublimate, 1:5000, or of
boric acid, 4 per cent. may be used. If photophobia exists ½ per cent.
of atropia sulphate or 1 per cent. of cocaine hydrochlorate will usually
give relief. Extensive wounds may require sutures, and sloughing tissue
may be excised with fine curved scissors. Excessive granulations may be
removed in the same way. For stings use a potassium permanganate
solution (2 grs. to 1 oz). Violent inflammation may be met by a laxative
and by leeching the periorbital region.

BURNS OF THE CONJUNCTIVA.

Burns may occur in all domestic animals from acids, alkalies, quicklime,
carbolic acid, boiling liquids, etc. The cornea usually suffers, being
the part most exposed. The caustics cause swelling, blanching and
finally exfoliation of the epithelium, or even of the superficial layers
of the cornea. In burns by hot liquids vesication may be present. If the
destruction extends deeply into the cornea there may be escape of the
aqueous humor and destruction of vision. If less penetrating, there may
still develop vascularity, and permanent opacity by reason of the
formation of a cicatrix or a change of structure in the layers of the
cornea, or, in dogs especially, adhesion of the cornea to the eyelids
(symblepharon). In the early stages there is closure of the eyelids,
with swelling, profuse lachrymation, and photophobia.

_Treatment._ The first object is to remove or neutralize the offending
body. Thus sulphuric or other mineral acid would demand a free
irrigation with a 1 per cent. solution of carbonate of soda or potash.
For alkalies, carbonated water, or a 4 per cent. solution of boric acid
may be employed. For lime, Gosselin recommends free irrigation with
saccharated water. The first step, however, should be to wipe out the
particles of lime with a soft rag soaked in oil.

The pain may be met by a solution of cocaine (1 per cent.), or atropia ½
per cent. In addition, we may irrigate with cold water or apply weak
antiseptic collyria, and employ derivation by the bowels or the skin.

SIMPLE ACUTE CATARRHAL CONJUNCTIVITIS.

Causes: irritant gases, smoke, dry air, dust, pollen, microbes,
insects, seeds, chaff, awns, sand, dust, quicklime, coal dust, hairs,
whips, canes, branches, stubble, fences, nails, claws, teeth, iodine,
chlorine, bromine, formalin, turpentine, rain, hail, sleet, glare of
sun, ice, snow, white sand or clay, filaria, acari, infectious
diseases. Symptoms: closed lids, epiphora, redness diffuse on lids,
ramified on sclera, projected nictitans, milky flocculent discharge,
later purulent, matted lashes or tarsi. No photophobia. Fever
variable. Lesions: exudate: cell proliferation: papillæ enlarged:
desquamation: swollen lymphoid bodies: hyperplasia: abscess: ulcer.
Treatment: remove cause, sterilized syringing, antiseptic and
astringent collyria, sublimate, zinc sulphate, lead acetate,
pyoktannin, silver nitrate, morphia, atropia, cocaine, vaseline,
cupping, leeching.

Under this head may be noted the simple forms of conjunctival
inflammation, which result from direct injuries, irritant gases from
manure, smoke, very dry air, dust, pollen, and in which no specific nor
contagious element is a prominent feature. Strictly speaking, all
purulent conjunctivitis are probably infecting, as all may be held to be
associated with the presence of pus microbes. As early as 1864, de
Graefe said every inflammation of the conjunctiva which “secretes, is
inoculable and therefore transmissible,” and Warlomont concurs, saying
that “conjunctival ophthalmias have one character in common: all can
produce a secretory product which, when brought in contact with a sound
conjunctiva, is capable of provoking the different affections of this
mucosa.” The exposure of the conjunctiva of man and beast alike, to the
germs borne on the dust or carried in liquids or on solids, renders this
structure preëminently susceptible to infection, while the lachrymal and
mucous secretions furnish a favorable culture medium. Fortunately in the
lower animal the danger of infection is greatly reduced, since there are
comparatively few opportunities for the transference of the germ through
water, soap, sponge or towel, to which man is exposed, not only in
public lavatories but even in private families. Thus in the animal the
single case remains isolated and in a sense sporadic, only because there
have not been the means of transferring and inoculating the morbid
product.

_Causes._ The contact of mechanical and chemical irritants of all kinds,
insects, seeds of gramineæ, chaff, particles of fodders, barley and
other awns and spikes, grains of sand, dust, quicklime, coal dust,
smoke, hairs, blows with whips, canes, branches, stubble, fences, etc.
Also erosions caused by nails, claws, teeth, and by falls must be
considered.

Irritant gases and vapors whether from accumulation of manure in the
stables, or from chemical products of fires and factories are direct
causes. The mere exposure for some time to the warm, dry air from a
furnace is injurious to the mucosa, and the emanations from certain
medicines, iodine, chlorine, bromine, formaline, turpentine are strongly
irritant.

Exposure in a cold draught, or in a blast of cold rain or hail, or even
to a cold dry wind, in the case of hunting dogs working much in water,
are potent factors.

The glare of the sun through a window at the front of a stall, or from
a white surface of snow, ice or water or even from white sand, lime or
clay is an active cause. The overdraw check exposing the eyes directly
to the sun is often injurious. We must include the irritations caused
by the filaria lachrymalis and by various lesions already
described—trichiasis, entropion, ectropion, stenosis of the lachrymal
duct, etc.

In certain animals a distinct predisposition exists, often as the result
of a previous attack, and such are readily attacked under slight
disturbing causes.

It should not be forgotten that hyperæmia and even inflammation of the
conjunctiva, often accompanies different infective diseases—strangles,
influenza, contagious pneumonia, rinderpest, canine distemper, etc.

_Symptoms._ The discharge of tears and the closure more or less complete
of the eyelids are among the earliest and most marked symptoms. The
general conjunctiva is congested and that on the inner side of the lids
especially, so as often to hide the individual vessels, while on the
sclerotic portion they usually remain distinct, tortuous and freely
movable with the mucosa upon the sclera beneath. The membrane is more or
less infiltrated, swollen and opaque. In two or three days this has
increased so that the lids are visibly swollen, and completely closed,
or the paw is projected over the cornea. The discharge has become milky
or flocculent, and mats the cilia together, or holds the eyelids closed.
Unless the cornea has been directly injured it usually remains clear,
and there is no photophobia nor contraction of the pupil. The lids,
however, are tender and nervous animals show active resistance to any
attempt to examine the eye. In aggravated cases a free muco-purulent
discharge takes place, and the red, swollen mucosa projects between the
eye and the tarsus, constituting _chemosis_. In such circumstances the
inflammation may extend to the cornea causing opacity and photophobia or
to the iris and choroid or other deep-seated parts.

In the milder forms of the affection there may be little or no
hyperthermia, while in severe attacks the febrile reaction may be
considerable.

_Lesions._ The non-traumatic cases which are not complicated by varied
wounds and injuries, show exudation and cell proliferation in the
palpebral conjunctiva and to a less extent in the bulbar. The
conjunctival papillæ are swollen and become visible to the naked eye and
in aggravated cases stand out like fungous masses. The superficial layer
of cylindroid epithelium is found swollen, opaque and sometimes
desquamating. The lymphoid bodies which are most abundant in the depth
of the conjunctival sac, are infiltrated, swollen, and bulging in
reddened masses.

Other lesions in the nature of granular or follicular hyperplasia,
abscess and corneal new growth and ulcers may follow, but will be better
considered under separate headings.

The tendency of simple uncomplicated conjunctivitis is to recovery which
may be completed in a week or ten days. In case of contused wounds,
abscess, ulcer, special infection in a lymphatic subject like the ox,
the affection is more likely to be prolonged or followed by grave
lesions.

_Treatment._ The first object must be to remove the cause, hence foreign
bodies, displaced lids or cilia, irritant gases, excess of light, cold
draughts or exposure, etc., must be sought and corrected. For the
removal of the foreign bodies, fine forceps or various common articles
(hair pin, lead pencil, a pin head, a folded clean handkerchief, or even
the clean finger) may be used. In case of wounds especially, they should
be first sterilized. Boiled water which has been cooled to luke warm may
be used from a sterilized syringe.

Locally antiseptic and astringent collyria (sublimate solution—1:5000),
zinc sulphate—1:1000, lead acetate, alum, tannin, silver nitrate, etc.,
are valuable and may even be thrown under the eyelids from a syringe
with a finely rounded nozzle and many orifices. Even a 2 per cent.
solution of silver nitrate may be applied in the conjunctival sac twice
daily, or as being less irritating, a solution of pyoktannin (1:1000).
If the irritation is great a soft rag wet with the solution may be
attached to the headstall of the bridle and hung loosely over the eye,
care being taken to prevent drying. A few grains of morphia added to the
collyria will be specially soothing. Irrigation of the eyelids or
bathing for ten or fifteen minutes at a time with luke warm water, will
often greatly relieve. When the eyelids become agglutinated during sleep
or prolonged closure, as in the small animals, cleanse with a tepid
sublimate solution, and smear with vaseline. In severe cases local
depletion may be resorted to. The hair may be shaved off from an area of
2 inches below the orbit, and a cup applied for ten minutes.
Scarification may or may not be resorted to. Or a leech may be applied
to the same part.

A laxative often proves an excellent derivative especially useful in
costive conditions.

CHRONIC CONJUNCTIVITIS.

Sequel of acute. Same causes. Old horses, young foals, damp lands,
night dews, frosts, eczema, follicular scabies. Lesions: swelling of
lymph bodies in conjunctival pouch, general congestion, chemosis,
hypertrophied papillæ, clouded cornea; Symptoms: as in acute form but
less intense. Treatment: Remove cause, irritants, damp soils, stables,
etc., glare of light, heat, etc., astringent antiseptic lotions,
atropia, mercury oxide, counter-irritation, setoning, cupping,
leeching.

This is generally recognized by veterinary writers as a sequel of the
acute form, though it may begin _de novo_, from slight persistent causes
of irritation. Habitual exposure to fierce light, dusty roads,
ammoniacal and other gaseous emanations, and at other times to the dust
from musty fodders in a high rack, trichiasis, entropion, ectropion, and
indeed any continued irritation may start the disease or keep it up.
Leblanc says it is especially common in _old horses_ and _young foals_
pastured on low damp grounds, bottom lands and lake shores, and in worn
out work oxen which have been exposed to cold night dews, or frosts. In
this respect it resembles the recurring ophthalmia of the horse which
prevails especially in lymphatic subjects. In _dogs_, Leclainche has
observed it associated with eczema or follicular scabies of the lids.

_Lesions._ Besides the general congestion of the mucosa, there are
liable to be special lesions in the depth of the conjunctival sac at the
point where the mucosa passes from the eyelid to the sclerotic, causing
uneven swellings from infiltration in this region. The lymph bodies or
follicles in this part are swollen and project as small red or grayish
nodules visible when the eyelid is everted, and at other times the whole
infiltrated conjunctiva projects between the lids constituting the
condition known as =chemosis=. The papillæ conjunctivæ are also
hypertrophied, so as to become visible to the naked eye, and ulcers may
be present on the mucosa. The cornea is often clouded blue or milky, or
it may have become in part vascular and reddish, or even ulcerated. A
more or less abundant muco-purulent discharge is always present.

_Symptoms._ The inflammation is usually moderate in degree, the eyes
water without being habitually closed, the hairs are lost from the
cheek, which is habitually wet, the lids are swollen, and like the cilia
tend to stick together after sleep, and the whole mucosa is visibly
infiltrated and congested, but usually especially at given points, as in
the _cul de sac_, on the lids or membrana nictitans. Unless the animal
has been treated with irritant dressings, there is much less pain on
manipulation than in acute conjunctivitis. On everting the lids the
folliculitis in the _cul de sac_ and the circumscribed swellings become
apparent. The membrana nictitans is partly projected over the cornea,
and the eyeball usually appears smaller by reason of its retraction
within the orbit.

In cases of eczema, or demodectic mange, the lesions of the skin of the
eyelids will furnish the key to the trouble.

_Treatment._ The first object must be to remove the cause which tends to
keep up the malady. Foreign bodies, musty hay fed from high racks, dusty
roads, excess of light, windows in unsuitable places, damp stalls or
pastures, and local parasitism must be corrected. In case of persistent
chemosis keeping up the inflammation, and which will not subside under
the usual astringent lotions, the hernial mucosa may be excised. (See
chemosis.)

The usual astringent lotions may be employed, sulphate of zinc (2:100),
sulphate of copper (1:200), alum (5:100), tannin (10:100) to which may
be added sulphate of atropia. In place of being simply applied to the
surface of the lids, or the cornea, it is usually desirable to inject it
into all parts of the cul de sac beneath the upper and lower lids and
beneath the nictitating membrane. Alum 4 grs. and boric acid 3 grains,
in water 1 oz. make a good combination. As the mucosa becomes accustomed
to one agent, we may change for another. Thus in addition to the above,
silver nitrate (2:100), and lead acetate (2:100) are often useful as
alternates. In obstinate cases red or yellowish oxide of mercury in
vaseline (5:100) may be applied inside the lids and on their margins.

Counter-irritation is often desirable, in the horse a blister of
cantharides or mercury biniodide to cover a spot as large as a silver
dollar above the anterior end of the maxillary spine (zygomatic), or a
stout silk thread as a seton inserted in the same place. In the dog the
blister may be applied on the temporal region.

Cupping or leeching beneath the eye, or phlebotomy from the angular vein
of the eye may prove useful. Great care should be taken to prevent
further injury by rubbing.

PURULENT CONJUNCTIVITIS. BLENNORRHŒA.

More purulent and more infective through dust, tongues, rubbing posts,
kennels, swill; a class due to different microbes. Prevalence in dogs,
swine, horses, sheep, goats, cats. Symptoms: acute conjunctivitis with
excess of pus, follicular swelling and enlarged lymph bodies in cul de
sac. Diagnosis. Treatment: Astringent and antiseptic lotions, injected
often: silver nitrate: pyoktannin.

The forms of conjunctivitis in which there is an abundant production of
pus are usually relatively more inoculable and therefore more liable to
pass from animal to animal in a casual manner. Infection takes place
through the dried up discharges floating as dust, but more directly by
means of the tongue when the animals lick each other, and through posts
against which they rub the head. Animals smelling or licking the
infected genital organs and then the eyes of their fellows may convey it
readily. Dogs occupying the same kennel successively, contract the
disease (Guilmot). Swine feeding from the same trough and plunging the
face into swill up to the eyes are especially subject to infection. In
speaking of such infections one must be understood to refer to a group
and not to one specific disease, as that will vary with the particular
pus microbe present, and with the virulency of such microbe in the
particular case. In keeping with the greater fertility of microbes in
the warm season, these affections have been more commonly met with in
summer than in winter, and where the animals are kept in filthy
surroundings rather than otherwise. This is above all true of swine.
Möller records a wide spread epizootic of gonorrhœal ophthalmia in dogs
in Berlin and environs in 1883. In different cases, however, he failed
to induce disease in the eyes by direct inoculation with the preputial
secretion. Heinman equally failed with the gonococcus of man in
inoculations on the eyes of rabbits, and dogs. Fröhner, however,
succeeded in infecting the eye of the dog by applying the gonorrhœal
discharge of man.

Infecting inoculable, purulent ophthalmia has been reported in the horse
(Vermast, Sobornow, Blazekowic, Menard, Möller, Leclainche), in sheep
(Repiquet), and in goats (Mathieu). Again Blazekowic found in an
infectious ophthalmia of horses, dogs and cats a microbe which was like
that of malignant œdema.

The _symptoms_ are those of conjunctivitis with especially free
production of pus, and a tendency to chemosis or to follicular
inflammation in the depth of the conjunctival sac, with irregular
swellings of the lymph bodies. The pus accumulates in the inner canthus,
inside the lids and along their margins, and tends to mat them together.
The diagnosis depends on the rapidity and severity of the course of the
malady, on the depth of the congestion and on the profuse suppuration.

_Treatment._ Astringent and antiseptic lotions are especially indicated.
Mercuric chloride (1 ∶ 5000), boric acid (2 ∶ 100), creolin (1 ∶ 100),
salicylic acid (1 ∶ 1000), silver nitrate (1 ∶ 200). It is not however
enough that these should be applied externally; they should be freely
injected under the lids at all points so as to act on the deepest
portions of the conjunctiva, and this should be repeated once or twice
daily. Or they may be applied with a soft brush. In a specially virulent
outbreak silver nitrate (2 ∶ 100) or pyoktannin (1 ∶ 1000) solution may
be used. Setons and blisters, laxatives and cooling diuretics may be
employed as in the severe types of simple conjunctivitis.

INFECTIOUS CONJUNCTIVITIS IN HERBIVORA. ENZOOTIC OPHTHALMIA.

Causes: infection, pollen, soil emanation, winter or summer; cases of
extension by infection. Cattle, sheep, goats, ponies. Accessory
irritants. Symptoms: severe purulent conjunctivitis. Papillary and
follicular hypertrophy, uniform redness, protruding head, opacities,
erosions, ulcers, photophobia, staphyloma. Treatment: rest, darkness,
coolness, elevated head, purgative, diuretics, sedatives; locally
solutions of pyoktannin, sublimate, silver nitrate, boric or salicylic
acid, atropia, puncture.

_Causes._ This affection which attacks at once or in rapid succession a
large portion or the whole of a herd or flock, is by many held to be
infectious while others attribute it to irritant pollen or soil
emanation. Its origin from vegetation in flower is held to be supported
by its greater frequency in summer than in winter, and the few outbreaks
seen in winter are attributed to pollen preserved in the hay. But other
things being equal, organized germs are preserved, multiplied and
diffused to a greater extent in the hot season so that the origin of the
disease from a purely microbian source is at least equally plausible.
Certain outbreaks indeed show the transmission of the infection in a
most unequivocal manner. A cow suffering from the affection was brought
into a stable occupied by a herd previously sound, and in a few days the
cow standing next her was attacked, and thereafter a number of others in
rapid succession. A small number of cattle from the Buffalo Stock Yards,
but which had sore eyes on their arrival in Tompkins Co., N. Y., were
placed in a sound herd and the disease spread rapidly to the other
members of the herd. Similarly in both sheep and cattle the writer has
seen the disease prevail in one herd or flock, while the adjacent herd
or flock, separated only by a good stone wall and subject to exactly the
same condition of soil, water, exposure, vegetation and pollen has
entirely escaped. Kaiser has seen it introduced into a herd by a bull;
Fünfstück saw a herd of 300 head attacked in a few days, and Klink 20
out of a herd of 40 head in 14 days. Trumbower has never seen an animal
suffer a second time. This is the common experience and would suggest an
acquired immunity, yet the comparative rarity of the disease forbids a
positive conclusion, without further experience. Menard saw an outbreak
among the ponies in the Jardin d’Acclimatation, and as many as fourteen
weeks later in the same gardens it attacked the bovine animals.

In sustaining the doctrine of infection, however, we must not altogether
ignore accessory causes. Like other affections of the eye, this has
seemed to appear especially in low, damp lands, bottom lands, deltas,
marshy borders of lakes and level prairies, so that a general lack of
tone or a lymphatic constitution may be held to predispose. Nor is it
necessary to ignore the influence of pollen, dust and other irritants,
which though they may not cause the specific disease, yet prepare the
way for its attack by reducing the resisting power of the tissues.

_Symptoms._ These are the phenomena of severe purulent conjunctivitis.
Closed eyes; profuse secretion of tears, sometimes mixed with blood,
changing in a few days to a thick, purulent, white or yellow secretion,
which collects in masses inside the lids, along their margins, in the
inner canthus and on the cheeks, gluing together the cilia, lids and
hairs. When separated the lids show a mucosa of an uniform deep red,
covered with pus, and irregularly swollen according to the amount of
infiltration. Papillary and follicular hypertrophy are marked features,
and the nictitans projects excessively over the eyeball. In many cases
the cornea becomes opaque and in some instances erosions occur which may
cause perforation or loss of the eye. In other instances the ulcers heal
with the formation of cicatrices, or the weakened portion of the
membrane yields under the internal tension and staphyloma supervenes. In
such cases the pupils are contracted.

The disease is usually attended by marked hyperthermia, the secretions,
including the lacteal, are materially decreased, appetite and rumination
are impaired and the animal leaves the flock or herd. The disease
affects cattle and sheep, and Menard and Hoffmann add horses and goats.

_Treatment._ This must be primarily antiseptic, but without neglecting
constitutional disorder. Rest in a dark, cool stall, with the head
elevated by tying to a high point. Give at once an active purgative 1½
lb. Glauber salts in 4 quarts warm water, and follow up with cooling
diuretics and sedatives (saltpeter ½ oz. and tincture of aconite 20
drops, thrice a day). If the temperature runs very high a few doses of
acetanilid or phenacetin may be given. Locally use silver or other
antiseptic collyrium.

_Locally_ use pyoktannin solution (1 ∶ 1000) or mercuric chloride (1 ∶
5000) injecting under the lids so as to bring it in contact with the
whole diseased surface. A cloth wet with the same solution may be hung
over the eye. Boric acid (1 ∶ 100), salicylic acid (1 ∶ 1000), or silver
nitrate (1 ∶ 100) may be substituted for the above when they seem to be
losing their efficacy.

Ulcers are treated by pyoktannin or silver nitrate solution applied
daily with a soft brush. Keratitis will demand atropia. Abnormal tension
or staphyloma will demand puncture of the cornea. Improvement may be
expected in a few days and recovery in a week or ten days.

VARIOLOUS CONJUNCTIVITIS.

In cow pox, horse pox, and above all sheep pox, the infection sometimes
falls on the conjunctiva, giving rise to the formation of the specific
eruption on that membrane. The coexistent eruption on other parts of the
body (udder, heels, hairy portions of skin) of the specific variolous
eruption, furnishes the means of a satisfactory diagnosis. The lesions
in the eye develop rapidly to an extreme severity. The lids are swollen
and closed, lachrymation abundant, and early mixed with pus, and when
exposed the conjunctiva is strongly congested with circumscribed areas
of elevation. In cow pox these are circular in form, raised above the
surrounding mucosa, having a deep red areola and a paler, flattened
center. In _sheep pox_ the elevations have the same general character,
but are liable to be more numerous and confluent, and tend to permanent
opacities, cicatrices, and perforations of the cornea with loss of the
eye. Short of perforation, internal inflammations are not uncommon.

_Treatment._ At the outset this form may be aborted by the application
of silver nitrate solution (2 ∶ 100) or sodium hyposulphite (1½ ∶ 100).
Otherwise the local treatment is like that for simple conjunctivitis,
cooling astringent and sedative lotions, and if need be, derivatives and
eliminants.

APHTHOUS CONJUNCTIVITIS. PHLYCTENULAR CONJUNCTIVITIS.

Closely allied to the last, are those cases in which vesicles appear on
the conjunctiva. In exceptional cases these are seen during an epizootic
of foot and mouth disease, while in other instances they are associated
with eczematous eruptions on other parts of the body, particularly in
dogs. In the human subject conjunctival vesicles are often associated
with tuberculosis, but this has not been recorded of animals so far. The
disease usually makes a rapid eruption, with symptoms of extreme
inflammation, and its duration is largely determined by the general
disease.

Beside the local _treatment_ by astringent or antiseptic and sedative
collyria it may be desirable to correct the hepatic, digestive or other
disorder on which the eczema depends, or to improve the general health
by a course of bitters or even of cod liver oil.

DIPHTHERITIC CONJUNCTIVITIS IN BIRDS.

Hens, ducks, pigeons. Local inflammation, fibrinous exudate,
concreting or becoming cheesy, necrotic, sloughy. Beneath the mucosa
red, raw; without epithelium, but excess of lymphoid cells, some only
muco-purulent, gravity varies. Grave cases inoculable on birds, mice,
rats and rabbits. Bacillus diptheriæ avium, morphology and biology.
Pathogenesis. Prevention: exclude germ; cleanliness; pure air; pure
food; pure water. Quarantine strange fowls, keep flocks apart, seclude
manure, segregate sick, disinfect. Treatment: Antiseptics; boric acid;
sublimate: ichthyol; silver nitrate. Infection to man.

A disease of the mouth, fauces, nose and eyes, associated with the
formation of false membranes, has been long recognized in birds (hens,
ducks, pigeons, etc.), and is known to bird-fanciers by the names of
roup, and diphtheria. The disease is characterized by the presence of a
local inflammation in patches, associated in the early stages, with a
free serous discharge, but, later, with the formation of white, or
grayish, fibrinous exudate, which may be at first firm and smooth, later
soft and cheese like, and still later in many cases more or less
necrotic and sloughing. In Dr. Moore’s experience this is more common on
the conjunctiva than on the nares or fauces. The interior of the eye was
not involved in the inflammation. Beneath the false membrane the mucosa
was devoid of epithelium and the underlying tissue was red, raw and
angry, bleeding readily when handled, and infiltrated with an excess of
lymphoid cells.

The lesions however were by no means constant. In some even of the fatal
cases, the exudate was merely muco-purulent, while in others the false
membrane was quite abundant.

The gravity of the affection also varies in different outbreaks or in
the same outbreak at different times. Sometimes it runs a very rapid and
fatal course, while at others it becomes chronic and comparatively
dormant and the great majority recover.

In its more virulent form it is readily inoculable on birds, mice, rats,
and rabbits, while the milder cases are not easily propagated in this
way.

The false membrane contains a variety of saprophytes, and among them the
pathogenic bacillus, which may be obtained in pure culture by
inoculating it on a rabbit or mouse. Emmerich believed this bacillus to
be identical with the Klebs-Löffler bacillus of diphtheria in man, but
Löffler recognizes it as essentially distinct.

The _bacillus diphtheriæ avium_ is 0.8 to 1.5μ long, by 0.8 to 1.2μ
broad. The ends are oval so that short specimens seem round. In bouillon
cultures they form chains or clumps. They stain in aniline dyes, most
deeply at the poles. Are not stained by Gram’s method. They are
non-motile, ærobic, grow in agar, and alkaline bouillon, but render the
latter acid in one or two days. Do not grow on peptone gelatine, nor
produce gas with sugars. Are killed in 5 minutes at 58° C. (137° F.).
Are killed by dryness in 24 hours, by sulphuric acid (0.25 ∶ 100) in 10
minutes, by lime water in 1 minute, and by sulphur fumes.

_Pathogenesis._ Eight rabbits inoculated subcutaneously with 0.1 cc. of
the bouillon culture died in 18 to 36 hours. Of several white and gray
mice inoculated only one died. Inoculations of mature hens subcutem and
on the nose had no effect. Inoculation of a six weeks old chicken caused
death in 4 days with bacilli in the liver and blood (Moore). Inoculation
of pigeons produced the disease (Löffler). It seems doubtful whether the
milder forms part with their virulence to birds, when cultivated
artificially, or whether a special susceptibility is required in order
to render the inoculation effective.

_Prevention._ Besides the general conditions of good hygiene,
cleanliness, pure air, and pure water, the strict exclusion of the germ
is the great desideratum. New fowls should not be taken into a flock,
when they show any indication of disease in the mouth, throat, nose or
eyes, nor when they come from a flock in which such signs of disease can
be found. When examination of the flock, from which they are sold,
cannot be made, the new fowls should be placed by themselves in
quarantine until proved sound. Sound flocks should not be allowed to
wander at large and mingle with the birds that are unsound, or open to
suspicion. Neither should they be allowed to come in contact with manure
from suspected poultry yards. If disease of air passages, mouth or eyes
appears, separate at once the diseased fowl, and sprinkle roost, house
and yard with dilute sulphuric acid, quicklime, or other disinfectant.

_Treatment._ Beside separation and disinfection the local use of
antiseptics to the surface divested of the false membrane gives the best
promise. Boric acid solution (4 ∶ 100) or sublimate solution (1 ∶ 5000)
may be applied to the eye. For the nose and mouth somewhat stronger
applications may be made.

_Prevention of infection to man._ The essential difference of the
Klebs-Löffler bacillus of diphtheria in man, and the microbe of this
affection in fowls does not exclude the necessity of avoiding contagion
from birds to man. Among reported cases of such infection are: (1) That
at Wesselhausen, where 4 attendants on the fowls contracted the disease
from the sick fowls at a time when no other cases existed in the human
population: (2) That of Sebdon where 6 persons suffered and 10 fowls fed
by a hospital attendant also suffered: (3) That of Tunnis in which
diphtheria prevailed in fowls, and soon also in those who fed them
producing an extended epidemic: (4) That of Jacksonville, Ill., where a
diphtheritic chicken, conveyed the disease, with fatal effect, to a
child which fondled it (Moore).

These and other similar instances seem to show that the disease of the
bird may become so virulent as to be communicated to man, and the
disease of man so potent as to be transmissible to the bird. Every
precaution therefore should be taken to prevent infection passing from
one to the other.

FOLLICULAR CONJUNCTIVITIS.

Common in dogs. Violent congestion with enlargement of lymph
follicles, or beneath the nictitans, dark red, like millet seed, also
over sclera and lids. Enlarged lymph follicles with excess of lymphoid
cells. Often chronic. Entropion. Infection. Treatment: astringent and
antiseptic lotions: lunar caustic: cocaine and crushing of follicles:
pure air: excision of nictitans.

Fröhner has drawn attention to the frequency of this affection in the
dog, which according to him attacks 40 per cent. of the race. It is
especially liable to begin on the inner surface of the membrana
nictitans, and though it may be at first somewhat hidden by the severe
congestion, yet when that subsides in part, the swollen follicles can be
seen as dark red elevations, the size of a millet seed, when the
nictitans has been everted. It may extend over the sclerotic and
palpebræ. Microscopically these swellings are found to be enlarged lymph
follicles, with an excess of lymphoid cells.

The disease tends to assume a chronic course and may cause entropion and
other troublesome lesions. The diagnosis depends on the recognition of
the swollen follicles, and especially in the depth of the conjunctival
sac.

It is presumably infective yet all Fröhner’s inoculation gave negative
results.

_Treatment._ In the earlier stages the common astringent and antiseptic
lotions may be used. Sublimate, or boric acid lotions are especially
valuable for their antiseptic properties. Should these fail, the eyelid
and nictitans may be inverted and the individual follicles touched with
a fine pencil of lunar caustic, the resulting smarting being lessened by
application of cold water. In case they should still prove obstinate,
the conjunctiva may be cocainized and the follicles individually crushed
with ciliary forceps. Pure out door air is a prime essential in the
treatment.

In extreme cases Fröhner counsels the excision of the membrana
nictitans.

NEOPLASMS OF THE CONJUNCTIVA.

Pinguecula: fatty growth: Lipoma: Melanoma: Dermoid tumor in young
dogs, calves, sheep. Cocainize the part and excise. Cold water: silver
nitrate. Polypus. Pterygium.

A pale fatty looking elevation on the sclerotic at the inner side of the
cornea is not unknown in the dog, resembling =pinquecula= of man. It has
not been seen to prove harmful and may be safely ignored.

=Lipoma= has also been observed (Müller) and when troublesome may be
removed by excision with scissors.

=Melanosis= is met with in gray horses in connection with the same
disease of the skin of the lids, and usually with generalized pigment
tumors. In the latter case surgical interference is useless unless it is
to secure a very temporary relief.

=Dermoid Tumor of the Conjunctiva.= This consists in a cutaneous
product, consisting externally of a mass of epidermic cells, beneath
which are connective tissue, fat cells, and muscular fibres, glands and
growing hairs. It usually extends inward from the outer portion of the
sclerotic conjunctiva and may encroach on that of the cornea. It is
firmly adherent to the sclera, and sometimes to the cornea by its base
and deeper aspect, but the apex is free and more or less projecting. The
color is yellow, or more or less blackened by pigment or even reddened
by blood. It has been observed, above all, in dogs, Prince reports a
case in a calf and Zundel in a sheep. The Cornell Veterinary College
clinic has furnished cases in ox and dog. They have, however, nearly
always been seen in young animals and are probably congenital.

These are easily removed from the eye anæsthetized by a 4 per cent.
solution of chloride of cocaine. The inner projecting end of the tumor
is seized by rat-tooth forceps, and carefully snipped off with sharp
scissors curved on the flat. Where adherent to the cornea it must be
carefully handled, but where attached to the thicker and more resistant
sclerotic it can be dealt with more freely. A pencil of silver nitrate
may be used to check the bleeding, or that may be effected by cold water
freely applied.

=Polypus=, a small, pale, pediculated tumor of the conjunctiva is
described by Lafosse and should be removed by scissors, and bleeding
checked by cold, wet applications.

PTERYGIUM.

This name is employed to designate a triangular conjunctival fold
broader at its sclerotic end and gradually narrowing to its corneal
extremity, with loose, slightly overlapping borders, and firmly fixed to
the structures beneath. It is more vascular than the surrounding
conjunctiva, and its comparatively large blood-vessels have suggested
the veins of an insect’s wing—hence its name. The growth may extend from
either canthus toward or partly over, the cornea.

Möller and Leclainche claim its existence in dogs, though rarely to such
an extent as to demand surgical interference. Dunewald operated on a
case in the cow.

Unless growing, it need not be interfered with. It may be dissected up
with scissors the narrow end being dragged on by forceps. Another method
is to cauterize the narrow end with the electric cautery which leads to
material contraction of the entire mass.

XEROSIS CORNEÆ (EPITHELIALIS). DRY KERATITIS.

This is described by Mayer as following distemper in dogs. It seems to
begin in the epithelial layer of the conjunctiva, which becomes dry,
lustreless, spotted, opaque and fatty so that water runs over it without
wetting it. It may extend deeply into the substance of the cornea and
lead to the development of a scar. When scraped and examined under the
microscope the scrapings are found to consist of epithelium undergoing
fatty degeneration and myriads of _xerosis bacilli_. As the disease
takes occasion to attack by reason of the debility of the system, the
_treatment_ is mainly corroborative and tonic, including the arrest of
the affection on which the weakness depends. The early application of
antiseptics is desirable (iodoform 1, vaseline 10; mercuric chloride 1,
vaseline 3000). Warm compresses and a bandage may be tried.

WOUNDS OF THE CORNEA.

Causes: harness, whip, nail, hay, straw, stubble, thistles, spikes,
twigs, pine needles, cones, burdocks, stones, gravel, glass, splinters
of wood or metal, scratches, stings. Symptoms: closed lids, epiphora,
sight of lesion, soon cloudy swelling, opacity. Treatment: antiseptic
bandage and lotion, boric acid, sublimate, potassium permanganate,
avoid lead or zinc, atropia, cocaine, with perforation, bandage,
eserine, excision. For foreign body, antiseptic cotton, spud or
curette.

_Causes._ Corneal wounds are common in working animals by reason of
contact with harness, canes, whips, etc., and in the stable from contact
with nails or with the hard ends of hay or straw. At pasture the cornea
is injured by the ends of long stubble, the sharp points of thistles,
the spikes of various thorny plants, and twigs of bushes and trees. The
last named factors are especially operative in hunters and horses worked
in forests. Punctures with pine needles and cones, and with burdocks,
are other common causes. Stones, gravel, pieces of glass, and splinters
of wood or metal, produce traumas of the cornea, and, in cats and dogs,
scratches and even perforations with the claws are common. In this
connection the stings of insects are not to be forgotten.

_Symptoms._ There is always a prompt and complete closure of the eyelids
and a profuse secretion of tears. Then on parting the eyelids with
finger and thumb, the lesion of the cornea, its nature and extent should
be recognizable. In case of a small, punctured wound, however, as with a
smooth thorn or other conical body, the normal elasticity of the corneal
tissue may lead to such a perfect coaptation of the divided edges that
the lesion may escape even a close scrutiny. If the case is seen early,
before time has been allowed for cloudy swelling and opacity the wound
is all the more likely to escape observation. In incised, scratched and
torn wounds, on the other hand, the seat and nature of the lesion are
made out with the greatest ease.

_Treatment_ of a slight wound which is at once recent and free from
infection, is by a simple antiseptic bandage and lotion. Boric acid (1 ∶
100), sublimate solution (1 ∶ 5000) or potassium permanganate solution
(1 ∶ 100) may be used. Lead and even zinc salts, are liable to
precipitate in the abraded tissue and cause a lasting opacity. If the
pain is severe it may be moderated by the addition of atropia sulphate,
or a solution of 1 to 100 water may be instilled into the eye several
times daily. Cocaine makes an excellent substitute. In deeper wounds,
perforating the cornea and allowing the escape of aqueous humor, there
may be prolapse of the iris through the wound. It may be pressed back
with a flat sterilized spatula, and retained by bandage and a course of
eserine. Should it still escape, it must be seized with forceps, drawn
out and snipped off with a sharp pair of sterilized scissors. The
greatest care must be taken to avoid infection which may cause
panophthalmitis and destruction of the entire eyeball.

FOREIGN BODIES IN THE CORNEA.

In case of penetration of the cornea by thorns, thistles, glass, metal,
etc., there usually follows inflammation with a red area around the
offending object. If the foreign body is a piece of iron there is a
brownish area caused by iron oxide. Focal or transillumination will
usually reveal the object. Should both fail, a solution of fluorescin
when applied will develop a greenish area around it.

_Treatment_ may be made as advised by Gould by pressing a little
antiseptic cotton to the front of the eye, so as to entangle and
withdraw the foreign body when the eyeball is rolled. Failing in this we
may cocainize the eye and remove the offending object with a small
curette or spud. A careful focal illumination of the eye will enable the
operator to see and remove the smallest particles without injury.
Subsequent treatment is that of wounds.

ACUTE KERATITIS. INFLAMMATION OF THE CORNEA.

Extension from conjunctivitis, wounds, foreign bodies, bites, stings,
blows, infections, filaria. Symptoms: eye tender, closed, epiphora,
red, pannus, photophobia, congested sclera, opaque or ramified red
cornea, or diffuse red, exudation, suppuration, corneal abscess,
ulcer, perforation, prolapsus iris, panophthalmia. Focal illumination.
Recovery. Permanent cicatrix or opacity. Lesions: exudates of lymph
and leucocytes into corneal layers: embryonic tissue: vascularization:
abscess: ulcer: cicatrix: opacity: staphyloma: hypopion: prolapsus
iridis: panophthalmia. Treatment: antiseptic astringents, atropine,
leeching, derivatives, blister, seton, opacities; in severe cases
antiseptic puncture, sublimate lotion, silver nitrate, potassium
permanganate, boric acid, pyoktannin: in perforations antiseptic
bandage and eserine, iridectomy: in chronic cases mercury oxide.

Keratitis occurs in all domestic animals as a primary disease, or as an
extension from conjunctivitis.

_Causes._ Extension from acute, enzootic, infectious conjunctivitis in
sheep and cattle has been noticed by a great number of observers. Bayer
and Lohoff have studied maculated keratitis of the superficial layers in
horses. Again it has followed wounds by foreign bodies, spikes of
vegetables, particles of iron and glass, blows of whips, or insects,
stings, etc. It also occurs in connection with the local action of
particular poisons, such as variola (foot and mouth disease), canine
distemper, etc., and from the local irritations caused by trichiasis or
entropion or by the filariæ lachrymalis (ox) and palpebralis (horse).

_Symptoms._ The eye is extremely sensitive, and habitually closed, with
a profuse flow of tears, and a disposition to resist opening of the
lids. When exposed the cornea is seen to be more or less clouded and
perhaps reddened by the formation of vessels proceeding from its
sclerotic margin. This is known as _pannus_. If the anterior chamber is
still visible the pupil is found to be contracted showing photophobia.
The congestion is first visible in the sclerotic and in the absence of
pigment is most intense near the margin of the cornea. Upon the cornea
itself it is preceded by a deep white opacity, into which the
vascularity gradually extends. The whole cornea may finally become of a
bright pink hue.

The congestion of the cornea may advance to fibrinous exudation, or the
formation of pus between its layers, to molecular degeneration and the
formation of ulcer, or even to perforation and escape of the aqueous
humor. In this case prolapsus iris, panophthalmia and destruction of the
eye are likely to ensue.

Ulcer if not readily seen with unaided vision can be easily recognized
by the aid of focal illumination, and abscess can be detected by the
presence of a sharply circumscribed centre of intense opacity, white or
yellow, and some bulging of the membrane.

The pus may be absorbed, or it may escape by rupture and discharge
externally, or into the anterior chamber when the resistance is least in
that direction, and when this takes place, a dangerous internal
infective inflammation is the result.

In the slighter forms of keratitis the inflammation may come early to a
standstill, and recede, tenderness and photophobia pass off, the eyelids
may be opened, and the corneal opacities gradually disappear. If any
portion of the cornea has become vascular, that portion is liable to
remain opaque or even pink.

_Lesions._ Under the influence of an irritant on the cornea, the vessels
in the margin of the sclerotic become actively congested and pour out
lymph freely, leucocytes also escape and with the lymph pass through the
lymph channels into the substance of the corneal tissue. Here they
undergo active fission and increase, and the normal cells of the corneal
tissue multiply in like manner, so that in a short time there is an
extraordinary production of embryonic cells. Into the embryonic tissue
so formed, blood escapes from forming loops of new vessels, and this
goes on extending until the whole cornea may have become vascular.
Degenerations in the newly formed structure may result in suppuration,
(_hypopyonkeratitis_) or molecular decay and ulceration, (_ulcus
corneæ_) or organization may take place into the fibrous tissue with
contraction and permanent opacity, (_macula_) or a hyperplasia may form
in the shape of a staphyloma.

Among the other complications may be named pus in the anterior chamber
(hypopion), prolapsus of the iris, iritis and panophthalmia.

_Treatment._ In the milder form of keratitis, antiseptic astringents
with atropia sulphate are often effectual: zinc sulphate, boric acid or
alum (1 ∶ 100). Any direct mechanical cause of the irritation must be
removed, and the eye rendered as far as possible antiseptic or aseptic.
Derivatives also may be of service, and Trasbot especially advises
bleeding from the angular vein of the eye but only in the very earliest
stages. Cupping, leeching or setons may be employed. Excessive tension
may be relieved by puncture of the cornea near its margin. The remaining
opacity after the inflammation has subsided may usually be removed by
touching it daily with a camel’s hair brush dipped in a solution of
silver nitrate (1 ∶ 200).

In the more severe cases antiseptic lotions are even more essential,
mercuric chloride (1 ∶ 5000), potassium permanganate (1 ∶ 100), boric
acid (1 ∶ 100), silver nitrate (1 ∶ 200). Careful massage is of value.

Ulcers may be touched daily with a solution of silver nitrate (1 ∶ 400),
or of pyoktannin (1 ∶ 100).

Perforations must be treated by antiseptic bandage, eserin, and in case
of necessity, iridectomy as advised under perforating wounds.

Abscesses of the cornea should be opened with a flamed needle and
treated with antiseptic lotions.

Obstinate cases are often benefited by ointment of yellow oxide of
mercury 1, vaseline 10, or by the red oxide of mercury or calomel.

POISONING WITH COTTON SEED OR COTTON SEED MEAL.

Poisons in cotton plant: on man, pig, cow, stock cattle. Symptoms in
latter: Nervousness, debility, exhaustion, in-cöordination, paresis,
dyspnœa, dullness, anorexia, drooping head, trembling, lachrymation,
corneal ulcer, opacity, vesiculation; unilateral or bilateral; with
rest and change of food recover in five days except eye lesions.
Treatment: suspend cotton seed, purge, and treat eye lesions.

The cotton plant develops poisons for various genera of animals. The
bark of the root is a favorite abortifacient for woman and may be used
for the same purpose in the domestic animals. The seed when fed
continuously to swine will destroy life with symptoms of scorbutus, and
grave constitutional disorders. Cotton seed meal fed in excess to dairy
cows has a bad reputation for inducing garget and mammitis. In stock
cattle it has the reputation of producing diarrhœa, running from the
eyes, abscess and ulceration of the cornea, staphyloma, hyperthermia
(103° to 109° F.), swelled legs, congestion of the liver and spleen, and
high colored urine. As described by Dr. F. C. McCurdy, of Kansas City,
the southern cattle arrive in poor condition, seem nervous, weak and
exhausted, move with an uncertain, staggering gait, and may fall and
make convulsive but ineffectual efforts to rise. Dyspnœa, blue mucosæ,
and protruded tongue are noticeable in such cases. In the slighter
cases, dullness, inappetence, suspended rumination, drooping head, and
trembling limbs are characteristic features, and profuse lachrymation is
constant. In some eyes there is a small opaque spot around a minute
ulcer containing small granules like dust or sand, and situated in the
centre of the cornea on the line of approximation of the two eyelids.
Larger opaque areas when present were generally confined to the corneal
surface, without any areola of distended vessels, and without a vascular
zone at the junction of cornea and sclera. In certain cases the whole
transparent cornea stood out in the form of a vesicle, so prominently as
to interfere with closure of the eyelids. The affection might attack
both eyes or only one.

An important feature is that cattle coming from the cars in this
condition and left at rest for five days on hay without cotton seed
recovered rumination and appetite, and the weakness and nervous
excitement or depression disappeared. There remained only the lesions of
the eye which progress tardily according to their extent or severity.

The southern origin of the cattle, together with the congested liver and
spleen and the high colored urine would have suggested the southern
cattle fever, but from the promptitude of the recovery under a change of
regimen and the prominence of the lesions of the eye.

The important point in connection with this subject is the prophylaxis
by avoidance of the too liberal diet of cotton seed. When the disease
has actually set in, the true course is to suspend this aliment, clear
the bowels of any that may remain therein, and treat the lesions of the
eyes according to their respective conditions.

CHRONIC KERATITIS.

Sequel of trichiasis, entropion, eczema, etc. Age. Symptoms: moderate,
lids partly closed, cilia matted together, crusted, cornea clouded,
dull, with ramifying vessels. Resolution. Fibroid degeneration,
permanent opacity. Treatment: tonic regimen, outdoor exercise, iron,
bitters, calcium sulphide, astringent antiseptic collyria, atropia,
mercury oxide.

This is especially common in dogs in warm latitudes. Trichiasis and
entropion are perhaps the most common of the direct causes. Eczema and
other skin eruptions affecting the lids are additional causes, while old
and debilitated dogs are especially subject to the affection. It is less
frequent in horses.

The _symptoms_ are much less severe than in the acute form. The lids are
usually partially but rarely completely closed, lachrymation may be
absent and is never excessive, the secretion usually sticks together the
cilia and lids, and always forms crusts on them, the palpebræ are less
sensitive than in acute keratitis, the cornea is habitually clouded of a
bluish-white color, yet in the main partially transparent and without
the disc opacities of the acute type of disease, and the pupil, which is
usually visible in a good light or under oblique illumination, may be
slightly but is not excessively contracted. The surface of the cornea
seems to have lost some of its polish, and in its substance blood
vessels can usually be made out.

Under favorable conditions these cases may end in resolution and
especially under a change of food and environment. In less fortunate
cases they result in a fibroid degeneration of the cornea and deep
permanent opacity.

_Treatment._ It is usually desirable to change the regimen so as to
improve the general health, and to allow a fair amount of outdoor
exercise. In the very old and debilitated the case is rather hopeless. A
course of iron or bitters will sometimes have a good effect. In other
cases sulphide of calcium ⅒ grain thrice a day will prove useful. Eczema
must be treated secundum artem.

Locally astringent and antiseptic collyria may be used as in the acute
form. Atropia, 5 grs. to the oz., is a valuable adjuvant, to be
instilled in drops. Ointment of yellow oxide of mercury, a piece like a
pin head rubbed inside the lids once or twice a day often acts well.
Finally Trasbot strongly commends liquor of Van Swieten.

OPACITY OF THE CORNEA. NEBULA. MACULA. LEUCOMA.

Nebula, macula, leucoma, pigment spots, infiltration, cicatrix,
vascular or not, result of lead, silver or cocaine. Treatment: silver
nitrate solution in young and vigorous; calomel: iodoform: avoid
mercury and iodine at the same time. Tatooing.

As a sequel of inflammation of the cornea, persistent opacities are very
common occurrences. These may last only a short time after the
subsidence of the inflammation, or they may be persistent and chronic.
They are of all degrees of severity from a mere bluish haze to a dense
white cloud, or a dark pigment spot.

The term nebula is given to the slightest form which appears as a
grayish blue but still transparent blue and may be so slight as to pass
without recognition except under focal or oblique illumination. It
shades off gradually into the adjacent healthy cornea, and is often seen
as a marginal zone when the centre of the cornea is clear.

=Macula= is more marked, requiring no special illumination to detect it,
especially when the dark pupil forms a background for the affected area.
It is not, however, of a clear white, but of a grayish blue tint.

=Leucoma= is a dense white spot or patch which reflects all the light
falling upon it, and has usually a sharply circumscribed margin.

=Pigment spots= are usually on the membrane of Descemet and are the
result of a previous adhesion of the iris and detachment of a portion of
its pigment.

The white opacity may be merely a remnant of inflammatory infiltration
or it may be a fibrous cicatrix with or without a remaining minute
ulcer. It may be the result of an insoluble deposit of lead or silver in
the tissues. Sometimes it will form as the result of the application of
cocaine.

_Treatment._ A case of slight inflammatory infiltration can usually be
cleared up by touching it daily with a solution of 2 grs. silver nitrate
in an ounce of distilled water. This is especially satisfactory in the
young and healthy, in which the power of repair is greatest. Finely
powdered calomel or iodoform applied to the cornea will often prove
effective. In case potassium iodide has been given by the mouth, calomel
or corrosive sublimate is liable to form mercurous or mercuric iodide
and cause ophthalmia. The same is true of iodoform if mercury has been
given internally. As a last resort tatooing the spot has been resorted
to, to hide the opacity.

ULCER OF THE CORNEA.

Infection of abrasions may cause ulcer. Age. House dogs. Puppies on
vegetable food. Exhaustion. Starvation. Improper, insufficient diet.
Specific microbes and toxins. Symptoms: Ulcer with peripheral zone of
opacity. Photophobia. In marasmus little other local trouble.
Diagnosis by oblique focal illumination or fluorescin. Granulation of
Descemete’s membrane. Escape of aqueous. Keratitis. Panophthalmia.
Staphyloma. Prognosis in debilitated, vigorous. Treatment: tonics,
fresh air, good food, sunshine, exercise, silver nitrate, mercuric
chloride, iodoform, alcohol, chlorine water, boric acid, cocaine,
eserine, atropine, warm antiseptic compress, juice of fresh cassava.

_Causes._ Wounds of the cornea making an infection entrance for pus
microbes, are liable to lead to ulceration, and a corresponding
destruction of the epithelium and superficial layers by inflammation,
may start a similar ulcerative process. Apart from these conditions,
ulceration is especially liable to occur in very old dogs, in closely
confined house dogs, in puppies raised on an exclusive diet of vegetable
food, and in animals worn out by disease, exhaustion, starvation, or
improper and insufficient diet. Majendie’s dogs fed on sugar, starch and
other imperfect diet, suffered in this way. Finally, the local action of
certain specific disease poisons, enzootic purulent ophthalmia, canine
distemper, dogpox (Trasbot), equine influenza (Schindelka), sheep pox,
and blennorrhœa (Möller), leads to ulceration.

_Symptoms._ In keratitis there is usually a marked local opacity in the
centre of which the breach of the surface may be found. The attendant
photophobia with closure of the lids and pupil is strongly suggestive of
ulcer. In the specific diseases, the local inflammation, the rapid
progress of the lesion and the coexistence of the particular infective
disease are characteristic. In cases due to debility and marasmus the
disease may appear with little indication of attendant irritation,
lachrymation, tenderness, photophobia, or even opacity. At one
circumscribed point only is there a grayish cloud, perhaps no more than
a thirtieth of an inch in diameter, and slightly projecting. This
becomes soft and gelatinous and finally drops off, leaving a shallow
excavation or abrasion, surrounded by a narrow grayish zone. This
necrobiosis may extend inward and even penetrate the membrane, before
the lesion has enlarged to more than a hemp seed in diameter. In other
cases lateral extension occurs.

It is always important to recognize the ulcer at an early stage, and
this may be done by oblique focal illumination and the use of a
magnifying lens. In case of doubt a drop of solution of fluorescin
placed on the cornea and at once washed out, will promptly reveal the
lesion by the high color given to the tissues which have been denuded.

When perforation has taken place the membrane of Descemet may bulge out
of the orifice and undergo granulation, or it may open and allow the
escape of the aqueous humor. Active keratitis and even panophthalmia are
liable to follow perforation. Again, the escape of aqueous humor tends
to the approximation or contact of the iris with the cornea, where it
may become adherent and staphyloma may ensue.

_Prognosis_ is unfavorable in debilitated subjects, and when the lesion
is extensive and in the line of vision. In slight recent cases in good
constitutions it is favorable.

_Treatment._ Debility must be met by tonics and rich diet, fresh air,
sunshine and exercise. Specific diseases must be met according to their
nature.

Locally the daily application of silver nitrate lotion (1 ∶ 200) is
often very effective, proving an excellent antiseptic, checking the
microbian proliferation, and coagulating the albumen in the wound so as
to form an antiseptic barrier to further invasion. A mercuric chloride
solution (1 ∶ 5000) is an excellent substitute. Iodoform powder though
less antiseptic, is especially valuable in favoring the healing process.
It is dusted over the cornea, and the upper lid immediately drawn down
and held over the cornea for several minutes. If this is neglected the
dry powder is removed by the flow of tears, and the movement of the lids
and membrana nictitans. Trasbot recommends dilute alcohol (5 ∶ 100).
Möller advises chlorine water reduced to one-third the standard
strength, or boric acid solution (2 ∶ 100). Bouley found good results
from a cocaine solution. Cadiot and Almy get the best results from
creolin (.5 to 1 ∶ 1000) 5 or 6 times a day, with eserine.

In all cases great relief can be obtained from a strong atropia lotion
(1 ∶ 100). Indolent cases may often be helped by warm antiseptic
compresses, which seem to stimulate the circulation and nutrition of the
part. The juice exuding from the scraped fresh cassava and concentrated
to a syrupy consistency, is strongly antiseptic, and used with atropia
or pilocarpin is the best agent known for senile ulcer (Risley).

In perforation use eserine, and antiseptic bandages and in case of
prolapsus iris, excise as already advised.

CORNEAL STAPHYLOMA.

Bulging corneal scar with adherent iris: from perforation, escape of
aqueous, intraocular pressure, vascularization of cornea. Diagnosis by
central cicatrix, vascularisation, pigmentation. Oblique illumination.
Treatment: iridectomy, eserine. Suture. Enucleation.

This is a bulging forward of a corneal scar with the iris adherent to
its internal surface. It may originate in perforation of the cornea and
escape of the aqueous humor, or in intraocular pressure that advances
the iris until it comes in contact with the cornea, which becoming
adherent and receiving an abnormally large supply of blood or plasma,
softens and bulges outward. It may grow out to a great length in some
cases, Eck has seen it two inches in the horse, and somewhat smaller in
an ox. May records a case affecting both eyes in the dog.

_Diagnosis_ is not usually difficult. The scar in the midst of a
granulating projection of the cornea is nearly conclusive, but the
recognition of pigmentation of the growth and the adherent iris often
revealed by oblique illumination will nearly always show the true nature
of the case.

_Treatment_ is by iridectomy and eserin if the disease can be recognized
in its earliest stages, but it is rarely satisfactory. Later the choice
may be between excision of the staphyloma and coaptation of the edges of
the wound by suture, and the enucleation and removal of the eyeball. The
last resort is preferable to the continued irritation of the staphyloma
by the lids and cilia under the ocular movements.

ECTASIA CORNEÆ. KERATOCONUS. CONICAL CORNEA.

This consists in a thinning and protrusion of the cornea in the form of
a blunt cone, without loss of transparency. It has accordingly been
called _staphyloma pellucida_. There is a gradual attenuation and
distension of the corneal tissue from some unknown cause. It has been
seen mainly in the young and is manifestly due to a trophic defect.
Stockfleth records a case in a foal and Bayer in a cow. No satisfactory
treatment has been proposed, but as the trouble usually comes to a
standstill without perforation, it can be left to take its course. With
rapid increase and manifest tension antiseptic puncture of the cornea or
even iridectomy might be tried.

KERATOGLOBUS.

This is a variety of _ectasia_ in which the clear, pellucid, protruding
cornea is more globular and less conical in outline. It is seen
especially with enlargement of the entire eyeball (_buphthalmus_).

TUMORS OF THE CORNEA.

Various tumors may grow from the cornea. Dermoid cysts may implicate the
cornea and demand excision. Malignant growths demand extirpation of the
eyeball.

WOUNDS OF THE SCLERA.

Covered as it is by the bones of the orbit, and by the palpebræ the
sclera is little liable to traumatic lesions. Wounds with swords,
needles, nails, splinters of wood, and other sharp pointed bodies are
not unknown, however, and penetration by shot is especially common in
setters. Rupture from blows of clubs, beams, poles, stumps, etc., are
also met with.

The _symptoms_ are profuse lachrymation with more or less of blood, and
when the eyelids are separated the wound may be discovered and its
gravity estimated by protrusion of the vitreous. Slight injuries which
are not infected heal readily under the treatment recommended for
keratitis. Infecting and penetrating wounds are liable to cause
panophthalmitis and destruction of the eye. Foreign bodies, if present,
should be removed when possible. Pyoktannin is especially recommended by
Stilling.

EPISCLERITIS. INFLAMMATION OF THE SCLERA.

Scleritis in man is described as a manifestation of rheumatism, gout, or
tuberculosis. It occurs in animals in connection with traumatic lesions,
with iritis, cyclitis and choroiditis and is manifested by more or less
congestion, swelling and tenderness of the sclerotic, but is always
subordinate in importance and the treatment demanded is for the more
serious disease.

ECTASIA (BULGING) OF THE SCLERA.

Cases of this kind are adduced by Schleich and Mayer, in dogs, in which
there was a corresponding bulging or even an absence (_coloboma_) of the
choroid and retina. With a large protrusion of the sclera behind, there
was a shrinkage of the front of the globe (_microphthalmos_), so that an
atrophy might be suspected. The condition is irremediable.

PROLAPSE OF THE IRIS.

This has been already referred to as a complication of perforating ulcer
or wound of the cornea. If it cannot be returned and maintained by a
compression bandage and eserin, the only resort is to draw out the
prolapsing portion and cut it off with scissors, the eye and instruments
having been rendered thoroughly aseptic.

INTERNAL OPHTHALMIA.

Diagnosis of internal ophthalmias difficult. Causes: as in
conjunctivitis, extension of conjunctivitis or keratitis to iris,
choroid, ciliary circle, retina; Lymphatic constitution, damp soil,
air and stable, pit life, dentition, grain feeding, training.
Symptoms: ophthalmic symptoms generally, enlarged ciliary vessels in
sclera not movable; white zone around corneal margin; iris dull,
brownish, sluggish; intraocular tension increased: flocculi in aqueous
humor: photophobia: oblique focal illumination: sudden change from
darkness to light: synechia: ophthalmoscope. Cyclitis. Diagnosis: from
keratitis, recurrent ophthalmia. Lesions: according to chief seat of
the disease: inflammation of Descemet’s membrane, iris, choroid,
ciliary circle, lens, vitreous and retina in variable degree. Opacity
of aqueous, lens, capsules, or vitreous. Prognosis: always grave,
often vision impaired or lost. Treatment: rest, pure air, apart from
strong sunshine, removal of causes, local bleeding or cupping,
derivation, purgative, cooling diuretics: locally astringent
antiseptic lotions, cocaine, homatropine, blister, undue tension
antiseptic puncture, mercury oxide ointment; in rheumatic cases
salicin or sodium salicylate.

In the domestic animals it is not always possible to distinguish between
inflammations affecting different portions of the inner and middle coats
of the eye (iritis, cyclitis, choroiditis, retinitis), so that it is
convenient to give in general terms the phenomena and treatment of the
class known as _ophthalmia internus_. This is all the more appropriate
that inflammation of one of these divisions so frequently extends to the
others producing _panophthalmitis_, that the disease in one usually
implies an early implication of all.

_Causes._ Many of the causes of conjunctivitis, when acting with special
intensity, or for too long a time, may cause internal ophthalmia. Severe
blows, bruises, punctures, lacerations, sand, cinders, dust, lime,
foreign bodies inducing traumas, sudden transitions from darkness to
bright sunshine, habitual exposure to sunshine or to the reflection from
snow, ice or water, through a window in front of the stall, the abuse of
the overdraw check rein, the glare of electric light or of lightning
flashes, draughts of cold damp air between windows or doors, the beating
of cold storms on the eyes and skin, a sudden chill from plunging in
water or standing in a cold draught when perspiring, blows with
branches, pine cones or needles in the eye, the constant irritation from
entropion, trichiases, burdocks or thistles in the forelock, irritant
gases, etc., are among the factors which coöperate in setting up the
disease. Again diseases of the digestive organs, rheumatism, influenza,
canine distemper, brust-seuche, petechial fever, variola, eczema, and
aphthous fever may be direct causes. Conjunctivitis and keratitis are
liable to merge into irido-choroiditis by extension, and above all when
owing to perforation of the cornea a direct channel is opened for the
easy entrance of infective, pathogenic microbes. A lymphatic
constitution, connected with low breeding, or living in a low, damp,
cloudy region, or in dark, damp, impure stables, has a strongly
predisposing influence. The period of dentition, connected as it usually
is with domestication, stabling, grain feeding, and training is often a
potent accessory cause.

_Symptoms._ With the general phenomena of superficial or external
ophthalmia there are some indications which may be called pathognomonic.
These may be summarized as follows: in eyes devoid of pigment the
_enlarged ciliary vessels run deeply and are not tortuous, nor mobile
when rubbed; the scleral redness increases toward the margin of the
cornea, but leaves a white zone in front of the penetration of the
ciliary vessels; the iris has lost its clear reflection, appearing dull
or brownish; the pupil is contracted and sluggish in response to light
and darkness, it may be fixed or may show marked unevenness in its
margin: the tension of the eye ball is often increased, flocculi of
lymph may be seen in the aqueous humor settling into the lower part of
the anterior chamber_. This deposit may be white or yellowish or it may
even be reddened by extravasated blood especially in traumatic injuries.
In traumas, too, the cornea and even the aqueous or vitreous humor may
be opaque. In cases resulting from exposure to cold or from internal
causes, the media of the eye are at first clear and transparent. The
condition of the interior of the eye is usually to be learned by
examining the patient as he stands facing the light from a dark back
ground. A stable door or window will afford the requisite amount of rays
falling from above and from each side upon the interior of the eye. The
observer looks indirectly or obliquely and under favorable conditions
can see the iris and through the pupil. If the pupil is unduly closed it
may often be dilated by instilling a few drops of a 5 per cent. solution
of atropia and waiting for fifteen or twenty minutes.

The examination is made more satisfactorily with a candle or other
single source of light in a dark chamber. If this light is surrounded by
a chimney opaque except at one side which is directed toward the eye,
the results are much more satisfactory. Focal illumination with a
biconvex lens, or oblique illumination will show a swollen condition of
the iris with uneven bulging swellings at different points, and
generally a lack of the clear dark surface which marks the healthy iris.
It may be yellowish or brownish, rather than dark, or blue, or yellow,
but is always duller than normal. The pupil may be contracted or
dilated, but is always uneven at the margin according to the degree of
congestion of the different portions. It may be quite immovable under
the stimulus of light and darkness, and is always sluggish as compared
with the healthy condition. To test this reflex action, the one eye may
be bandaged, and the other eye covered with the palm of the hand for one
or two minutes. When exposed the pupil will be found to be widely
dilated, and in the healthy eye it will rapidly contract and dilate
alternately until it has reached a condition of adaptation to the
intensity of the light when it will remain immovable. With the inflamed
iris these contractions and dilatations will be lacking altogether, or
they will be sluggish and imperfect in various degrees according to the
intensity of the inflammation, the degree of congestion or the tension
of the liquid media of the eye. Restricted movement may also be due to
adhesion to the cornea, (_synechia anterior_) or to the capsule of the
lens (_synechia posterior_).

When viewed with the ophthalmoscope properly focused the choroid may
show a lack of its normal lustre and an unevenness due to the formation
of small rounded elevations in connection with congestion, or exudation,
and patches of yellowish red or whitish discoloration together with
lines of the same color following the course of the blood-vessels. It
may also reveal dark spots of opacity in the lens (_cataract_) or clouds
in the anterior region of the vitreous, the result of exudations. The
blood-vessels may appear enlarged and tortuous.

In some cases the exudate may form a false membrane which completely
closes the pupil.

A special tenderness around the margin of the cornea is suggestive of
_cyclitis_. Internal ophthalmia is usually accompanied by a variable
amount of fever.

_Diagnosis._ From simple keratitis, it is distinguished by the
thickening, discoloration and sluggishness of the iris, by the absence,
in many cases, of corneal opacity, and of free lachrymation, and in some
instances by increased tension of the eyeball.

Recurring ophthalmia, which is usually also an internal inflammation,
appears more abruptly and often at first with greater severity, and
accompanied by more hyperthermia. There is almost always a bluish white
opacity around the margin of the cornea, the eye is retracted in its
sheath so as to appear smaller, and the upper lid usually shows a marked
angle between its inner and middle thirds in place of the evenly curved
arch of the healthy palpebra. It usually appears for the first time in
the young and in those that have inherited the susceptibility and have
been kept on damp soils, in cloudy districts, or dark buildings.

_Lesions._ These are necessarily varied according as the inflammation is
concentrated on particular parts of the interior of the eye. The
secreting membrane of the aqueous humor is nearly always inflamed giving
rise to an exudate and a milky opacity of the aqueous humor. The iris is
the seat of congestion exudation, thickening, cell proliferation and
investment by false membranes. The capsule of the lens is early clouded,
may be covered by exudate and is rendered vascular in some cases. The
choroid is also the seat of congestion, exudation and discoloration with
the covering up at points of its pigmentary layer. The vitreous and lens
finally become the seat of exudation and opacity which is liable to
prove permanent.

_Prognosis._ The internal ophthalmias are always to be dreaded. In other
organs exudates may take place and become organized as permanent
structures without abolishing the function or rendering the organ
physiologically useless, but in the delicate and transparent tissues of
the eye, any such permanent product almost infallibly causes opacity and
loss, or serious impairment of vision. In the retina the displacement,
derangement, or covering up of the cones and rods necessarily interferes
with or abolishes sight, the opacity of the cornea, lens, capsule, or
vitreous interrupts the rays of light, and the destruction, or coating
over of the pigment of the choroid leads to undue reflection and
destroys vision. Beside this the destruction or impairment of one part
of the eye, changes the refraction and blurs the vision, or interferes
with accommodation and destroys the utility of the organ. Unless
therefore the disease can be cut short in its early stages and a
complete resolution effected it is likely to leave the patient very much
deteriorated in value. Fortunately it is only in the most violent cases
or in very susceptible animals that the disease in the one eye is
transmitted to the other by sympathy and leads to destruction of that
eye as well.

In the _treatment_ of internal ophthalmia, rest in pure air and moderate
warmth, away from a fierce glare of light is imperative. The causes
should as far as possible be removed. Next, it is desirable to establish
derivation. Leblanc and Trasbot attach great importance to phlebotomy
from the jugular on the same side. A more direct local action with less
loss of blood may be obtained from opening the angular vein of the eye
or applying a leech beneath the lower lid. In most cases a sufficient
derivative action can be secured by an active purgative which may be
followed by daily doses of cooling diuretics. Locally astringent lotions
(lead acetate or zinc sulphate 1 dr. to 1 qt. water; mercuric chloride,
1 ∶ 5000; boric acid, 2 ∶ 100; pyoktannin, 1 ∶ 1000) in combination with
cocaine hydrochlorate, homatropin, atropia sulphate, duboisia or
hyoscyamin (1 ∶ 1000) would be appropriate. These may be applied over
the eye on a soft cloth, and in cases of infective inflammation the more
antiseptic agents may be injected under the lids. When the inflammation
is very severe the atropia or other sedative agent may be made of the
strength of 1 ∶ 100 and a drop or two placed inside the lids with a
dropper every two or three hours.

A blister of biniodide of mercury may be applied to a space the size of
a dollar above the anterior end of the zygomatic ridge, or in dogs back
of the ear on the side of the neck: or a seton may be passed through the
skin in the same situation.

When the eyeball is unduly tense, puncture through the margin of the
cornea with a fine aseptic lancet will relieve the tension and in some
cases induce a more healthy action. Assiduous antisepsis is needful
until the wound has healed.

In other cases benefit can be obtained from the use of an ointment of
yellow oxide of mercury 1 part, in vaseline 10 parts, or of iodoform of
the same strength. A small portion the size of a grain of wheat is put
under the lid, and the latter manipulated with the finger to bring it in
contact with all parts of the surface. In case of a rheumatic origin
salicin and salicylate of soda are demanded.

SIMPLE IRITIS.

Causes. Symptoms: redness of sclera, in dogs, cats, birds, pigs, with
a narrow zone of white next the cornea, red scleral vessels immovable,
iris dull gray or brown, uneven, sluggish in response to light,
synechia anterior or posterior, lens and capsule clouded or clear,
pupillary margin uneven, myosis or midriasis, black cataract.
Treatment: rest, dark stall or covering, head elevated, midriatics,
cocaine, antiseptic puncture, purgation, leeches, seton, cooling
astringent lotions, diuretics, for tension in convalescence
iridectomy. In traumatic cases careful antisepsis.

This may come from any one or more of the _causes_ of internal
ophthalmia above named. The inflammation, however, concentrates itself
on the iris so as to overshadow the disease in the adjacent organs.

The more distinctive _symptoms_ are the redness of the sclerotic in
unpigmented organs (swine, birds, dogs, cats), the redness increasing as
it approaches the margin of the cornea but leaving a narrow white zone
surrounding the edge. The red vessels on the sclerotic are not moved
with the conjunctiva when the lid is moved over the front of the eye.
The front of the iris is dull, grayish or brownish, it is thickened
unevenly and very sluggish in response to light and darkness. Not
infrequently it is adherent to the back of the cornea (synechia
anterior) or to the front of the lenticular capsule (synechia
posterior). The lens and its capsule may or may not be clouded, but if
the interior of the vitreous can be seen it is found to be clear. The
pupil is more or less uneven in outline and sometimes it is torn at its
inner edge so as to form shreds and projecting tongues. Myosis
(contraction of the pupil) or midriasis (dilatation) may be present. If
the latter has been preceded by adhesion a portion of the uvea may
remain attached to the lenticular capsule constituting =black cataract=.
The lens or its capsule may become opaque, and a fibrinous membrane may
form over the pupil.

_Treatment._ Rest for body and eye are essential. A dark stall, or a
thick covering for the eye is desirable. The head should be kept
moderately elevated to facilitate the return of blood. The pupil should
be kept widely dilated to prevent adhesions to the lens. Sulphate of
atropia 5 grs. to the oz. of water should be applied a few drops at a
time, thrice a day, or as often as may be necessary to secure
dilatation. In case the atropia fails to secure dilatation a 5 per cent.
solution of cocaine should be dropped into the eye every three or four
minutes for four or five times and then another application of atropia
may be tried warm. Should it still fail and should there be indications
of extra congestion and swelling of the iris or of excessive tension of
the eyeball, relief may be obtained by puncturing the cornea. With the
reduction of the tension the iris will often respond to the midriatic.
Benefit may also be obtained from an active purgative, or the
application of leeches in the vicinity of the eye.

Cooling astringent applications may be kept up over the eye, or warm
antiseptic applications will often give great relief.

In obstinate cases the yellow oxide of mercury ointment may be applied
as advised for _internal ophthalmia_.

Cooling diuretics may also be of essential advantage.

If, after a fair recovery the bulb remains unduly tense, iridectomy may
be resorted to as a prophylactic measure for the future. An incision is
made with a lancet close in front of the margin of the cornea, and the
iris seized and withdrawn with a pair of fine forceps, and a portion
snipped off with fine scissors. The eye and instruments must be rendered
absolutely aseptic by carbolic acid and boiling water, and the
antisepsis of the eye must be carefully maintained until the wound is
healed. This tends to relieve congestion in the iris and to moderate the
secretion in the anterior chamber, so that the former extreme tension
does not recur. In making choice of the seat of the iridectomy a
selection may be made which will do away with adhesions, or one that
will expose a portion of the lens which is still transparent, and which
may restore vision when obscured by a cataract.

In traumatic cases there should be extra care in maintaining a thorough
antisepsis of the eye as the great danger is that of infective
panophthalmitis. The injection of antiseptic liquids under the eyelids,
and the covering of the eye with antiseptic cotton wool or with a soft
rag wet with an antiseptic lotion are important factors in treatment.

SYMPTOMATIC OR METASTATIC IRITIS.

Complications of infectious diseases, influenza, contagious pneumonia,
strangles, tuberculosis, omphalitis. Symptoms: exudation of fibrine
and blood, with those of simple iritis. Treatment: as in iritis, plus
measures for the specific primary disease. When second eye is
threatened enucleation.

Under this head Möller describes those forms of iritis which occur as
complications of various infectious diseases. It has long been observed
that iritis and other ophthalmias, occurred as complications of the
acute infectious diseases of the respiratory organs of the horse
formerly known under the general name of “influenza.” More recently many
veterinarians and others have classed these influenza iritis separately
under the name of “pinkeye.” The same can be said of “contagious
pneumonia” (brustsenche) of horses which is distinctly caused by the
_diplococcus_ (_streptococcus_) _pneumoniæ equina_. Attention was called
to the iritic complication of this disease in 1881 by Siedamgrotzky and
it has been often noticed since. Conjunctivitis is however a more
frequent complication of this disease than iritis. In both influenza and
contagious pneumonia the iritis often supervenes when convalescence has
apparently set in. Strangles is another affection in which the iris
occasionally suffers. Mathieu has described tuberculosis of the iris in
cattle, and Möller mentions with some hesitancy cases of iritis which
complicated the infection of the navel in new born animals.

The _symptoms_ of symptomatic iritis vary according to the particular
infection. In addition to the fibrinous exudate the infections of the
respiratory organs are liable to be complicated by blood extravasations.
In influenza this may show as deep blotches on the bulbar conjunctiva
and in chemosis. In contagious pneumonia Schütz met with iritis of a
distinctly hæmorrhagic character.

In Matthieu’s cases of tubercle of the iris there was first a slight
lachrymation, and soon the iris assumed a grayish tint, and became
uneven and unduly approximated to the cornea though it failed to become
adherent to it. The swellings of the iris increased and became of a
grayish yellow color, and the pupil was usually contracted and varied
little in size. Post mortem examination showed the presence of
tubercles. The same condition has become familiar in connection with
experimental inoculation in the eye. As in ordinary iritis adhesion to
the capsule of the lens and cataract are common results.

Apart from the _treatment_ of the specific primary disease this type of
iritis demands the same treatment as other forms. Strong atropia lotions
to prevent or break up adhesions and antiseptic astringents are
especially indicated. When implication of the second eye is threatened
it may be desirable to remove the first by enucleation. (See
Panophthalmitis).

FOREIGN BODIES IN THE IRIS.

These are sometimes fine shot particularly in dogs, and splinters of
iron and steel in other animals. Their presence can sometimes be made
out by careful focal illumination. If septic they cause violent iritis
and panophthalmia. If aseptic they may sometimes cause little trouble.
If they can be exactly located, they should be removed at once before
the aqueous humor and cornea become clouded. If the offending body is a
piece of iron or steel and can be reached by a magnet introduced through
the original wound or through one made with a lancet in the edge of the
cornea it may be extracted by this means. If it is shot or other body
that is not attracted by a magnet the portion of the iris in which it is
entangled may be drawn out with forceps and snipped off with fine
scissors. Due antiseptic precaution must be exercised.

COLOBOMA IRIDIS. CONGENITAL APERTURE IN IRIS.

This is a congenital defect in which there is an aperture in the iris.
Hering figures the two eyes of a horse in which these appeared in the
direction of the outer canthus. Renner records a case in a foal in
connection with intra-bulbar enchondroma. Dochtermann and Berlin record
that among 64 pigs the result of breeding a boar on his daughters and
grand-daughters no less than 36 showed coloboma. Möller figures a dog
with the same affection.

The condition is not known to prove hurtful to the affected animal so
that it may be wisely let alone.

DOUBLE PUPIL.

Mayer notes a case of congenital double pupil in the horse, a bridge
extending across the space from the upper to the lower border and
cutting off the outer third of the opening. The present writer has seen
a similar condition as the result of union of the corpus nigrum in
severe iritis. Section of the bridge is possible, though rarely
desirable, seeing that it opens a door to possible infection.

ALBINISM. WATCH EYE.

The albino is an animal in which there is a complete absence of pigment
in the eye. It is usually seen in white races of rats, rabbits and dogs,
and both the iris and choroid reflect a pink tint. It may cause
photophobia and some weakness of vision but, in the main, it seems to be
harmless to the lower animals. In horses it is occasionally seen as a
partial defect, a portion only of the iris and adjacent sclerotic
appearing of a brilliant white color. It does not usually seem to impair
the vision, so that at the worst, it is only looked on as a blemish. It
is needless to attempt a remedy.

PERSISTENT PUPILLARY MEMBRANE.

The persistence of this embryonic membrane has been noticed in the horse
(Schindelka), ox (Meyer), rabbit (Mayerhausen), and dog (Möller). It
tends to disappear with the growth of the animal and rarely does any
perceptible harm.

OCCLUDED PUPIL.

This has been frequently found in horses as a sequel of iritis, and
permanent adhesion of the contracted iris to the front of the lens
capsule. It is in short, a posterior synechia with closure of the pupil.
The lens and its capsule are usually opaque so that there would be no
gain in detachment of the iris. If, however, there is reason to conclude
that any part of the lens is still transparent, the performance of
iridectomy over this portion, would produce a new aperture for the
entrance of light.

CYCLITIS.

This is described by Möller as occurring in the domestic animals, but he
fails to furnish instances of its diagnosis during life, and it is not
likely to be often recognized in the living animal. Beside the usual
signs of iritis, there is extreme tenderness to pressure around the
anterior border of the sclera, increase of intraocular pressure,
followed later by its diminution, and a cloudiness of the anterior
portion of the vitreous humor. This last condition can only be detected
by a full illumination of the vitreous, and its examination with the
ophthalmoscope. It is quite liable to be complicated by suppuration and
to go on to panophthalmitis.

The _treatment_ does not materially differ from that of iritis, yet
atropia must be used with caution as it is liable to increase the
suffering. The preparations of mercury have been especially recommended.

CYSTS OF THE IRIS AND CORPORA NIGRA.

Mayer speaks of these lesions in horses, but it is very difficult to
diagnose them correctly, even with the aid of the ophthalmoscope. The
very manifest bulging at the part may be due to excess of pigment,
especially in the corpora nigra, and an exploratory puncture would only
be warranted when the protrusion became excessive and injurious. One
such puncture by Eversbusch led to infection and loss of the eye.

TUBERCULOSIS OF THE IRIS.

This has occurred as the result of inoculation of the aqueous humor in
the smaller animals, and as a spontaneous localization of the disease in
cattle (Hess, Röder, Fischöder, etc.). In Hess’s case, the left eye was
shrunken to half the size of the sound right eye, and small caseated
tubercles were present in both iris and choroid. There are usually
coincident tubercles in other organs, and these with the nodular
appearance of the iris swellings, if visible in life, may assist in
diagnosis. (See _Symptomatic Iritis_, and _Tuberculosis_.)

CHOROIDITIS.

Causes: as in iritis: traumatic and infective. Exudative. Suppurative.
Symptoms: as in iritis: less change in iris and of flocculi in the
aqueous humor; opacity of lens and vitreous. Lack lustre choroid under
ophthalmoscope, uneven, detached. Suppurative form: early profuse
weeping, bleeding, later suppuration, pus oozing from orifice;
panophthalmitis. Treatment: as in iritis; atropia; cocaine;
astringents; purgatives; diuretics.

_Causes._ These are largely the same as those of iritis and cyclitis.
Blows, traumas, foreign bodies, sand, cinders, dust, lime, fierce light,
reflection from snow, water, etc., chills, draughts, storms, irritant
gases, and a number of specific diseases like influenza, contagious
pneumonia, canine distemper, rheumatism, omphalitis, pyæmia, etc., may
be named. It is a common lesion of recurrent ophthalmia in horses, and
is not unknown in tuberculous cattle. It is usually more or less
involved in iritis, as the iris is in choroiditis. The name given to the
disease which involves both, will depend mainly on whether the
inflammation predominates in the iris or choroid. Mayer divides it into
exudative and suppurative, the latter being a common result of trauma,
and likely to issue in panophthalmitis.

_Symptoms._ These are largely those of iritis. The congestion and
redness of the sclerotic around the margin of the cornea, the fact that
the enlarged vessels are firm in the sclera and not easily moved as in
conjunctival congestion, and a certain partial blindness, without much
change in the brilliancy of the iris, or opacity or flocculi of the
aqueous humor, would suggest choroiditis. Later some opacity of the
lens, or its capsule or of the vitreous humor would be equally
significant.

The only certain manifestations would be such as are found on
ophthalmoscopic examination. Swelling and unevenness of the inner
surface of the choroid, and a loss of luster, a change of its dark
surface to light colored spots and patches, (dull-red, yellowish red,
grayish green) and of the tapetum lucidum to a dirty grayish green in
solipeds. Areas of minute blood clot may also be seen. But these are
rarely recognized or indeed skillfully sought during life, and it is
mainly to necropsies that we owe most of our diagnosis of choroiditis in
the lower animals.

In the _suppurative form_ there is early profuse lachrymation more or
less tinged with blood, and later oozing of pus from between the lids.
The redness and swelling of the conjunctiva and lids are very prominent
features, and if the lids can be separated the corneal or scleral
orifice may be seen oozing pus. If visible at all the anterior chamber
shows yellowish opaque contents, and the symptoms of panophthalmitis
supervene.

_Treatment_ of the exudative form is essentially the same as for iritis.
Atropia lotions with or without cocaine, also astringents, which may be
used warm, and generally purgatives, diuretics, local bleeding, cupping,
and counter-irritants are in order. In obstinate cases ointment of the
yellow iodide of mercury, and in cases of extra tension puncture of the
cornea may be the means of relief. Iridectomy may be advantageous under
careful antiseptic precautions. In case of extensive or general
suppuration (_panophthalmitis_) enucleation of the eye may be the only
resort, and may contribute to save the other eyeball. (See
Panophthalmitis).

DETACHMENT OF THE CHOROID.

The choroid is detached from the sclera by exudates, blood effusions, or
blows with blunt articles. The lesion is especially common in recurrent
ophthalmia, choroiditis, and cyclitis. The ophthalmoscope will show the
detached portion as a rounded elevation on the otherwise smooth concave
surface, with normal or diminished intraocular tension. A _tumor_ of the
choroid is usually associated with increase of tension. After
inflammation has been subdued these cases may be left to rest and time,
and will often recover through absorption of the exudate. =Rupture of
the choroid= from violence is to be similarly dealt with.

RECURRENT OPHTHALMIA OF SOLIPEDS. PERIODIC OPHTHALMIA. MOONBLINDNESS.

Definition. Causes: wet impermeable soil, clay, river bottoms, deep
valleys, inundations, enclosing forests, damp air, lack of sunshine,
rank fodders, wet seasons, damp, cold, basement stables, heating
constipating fodder (corn, buckwheat, wheat), dentition, training, age
of domestication, sale, etc., spring, shedding coat, heredity,
debility, ill health, worms, debilitating infectious diseases, over
work, insufficient, indigestible food, local irritants. Microbes.
Rheumatism. Parasitism. Symptoms: fever variable, lack of vigor,
sudden attack, irritation, photophobia, lachrymation, closed lids,
contracted pupils, retracted eye, redness, swelling of lids,
conjunctiva, haw, sclera, slight corneal opacity, with vascularity,
aqueous turbid, flocculent, iris of dull color, sluggish, pupil
contracted, hypopion, posterior chamber yellowish green, intraocular
tension, crisis seventh to tenth day, convalescence fifteenth day.
Recurrence. Obscurity of vision. Eye between attack: blue zone around
cornea, eye seems smaller, retracted, prominent haw, angle in upper
lid, dull iris, tint lighter, contracted pupil, cataract, alert ears.
Lesions: exudates back of cornea, narrowed anterior chamber, sizy
aqueous, thickened iris, adhesions of lens capsule, or iris, torn
iris, lens opaque, fibroid, calcareous, atrophied, black cataract,
vitreous opaque, yellow, black, shrunken, choroid uneven, discolored,
detached, retina with exudate, detached, posterior chamber contracted.
Prevention: drainage, mature horses for damp lands, liming soil, get
fodder from dry locality, don’t breed in cloudy regions, good diet and
regimen, avoid corn, wheat and buckwheat, Glauber salts, pure dry
stable, exclude debilitating diseases and parasites, keep in hard
muscular condition, change to dry locality, don’t breed from blind
stock, legislation. Treatment: remove causes, cure rheumatism or other
morbid factor, darkness, antiphlogistics, laxative, diuretic, local
bleeding, cupping, blister, seton, locally atropine, cocaine,
pyoktannin, sublimate, lead, puncture, tonics, treat corneal
opacities. Jurisprudence: return a newly bought horse in 30 days,
(France) or more: extend the time if suspected.

_Definition._ This is an inflammatory affection of the interior of the
eye, intimately related to certain constitutions, soils, climates, and
systems of management, showing a strong tendency to recur again and
again, and usually ending in blindness from cataract or other
destructive lesion.

_Causes._ A =wet, impermeable, swampy or undrained soil= is a potent
cause of this disease. Heavy clays, which absorb and retain moisture,
river bottoms and deltas which are frequently overflowed and constantly
wet, hollow basins where no effective drainage has been secured, and the
coasts of seas and lakes which scarcely rise above the level of the
water and are submerged at intervals, are the especial homes of the
affection. In time past the disease was very prevalent in the low
districts of France (Reynal), Belgium, Alsace-Loraine (Zundel,
Miltenberger,) Germany, Holland (Möller), the English fen country and
above all the damp lands of Ireland. Lafosse mentions a whole family of
horses in South Western France which were characterized by blindness.
Reynal records the terrible devastation which it caused in former times
in the government studs at Limousin and Pompadour. It also prevails on
the low banks of the Guadalquivir near Seville (Hurtrel d’Arboval),
around Ostend, Cassel and Frankfort (Hofgeismar). Wet soils surrounded
by forests or hills, which hinder free circulation of air, are
especially injurious (Reynal). At Schlestadt, Alsace, at the beginning
of this century, Miltenberger found 75 per cent. of the horses of the
environs affected, whereas after great drainage works and the removal of
all stagnant water Zundel found in 1870 not more than 2 per cent. In
many localities in England, Ireland, France, Belgium and Germany the
disease has greatly diminished in connection with land drainage and
improved methods of culture. Harmon tells how in different parts of
Brittany, drainage supplemented by the free use of marl and lime on the
soil has caused a striking decrease in the prevalence of the malady. In
the department of Ain a ratio of 333 per 1000 was thus reduced to 100
per 1000 (Reynal). On the contrary in the absence of such drying of the
soil the previous high ratio of attacks was maintained. This has been
notorious in the damp lands of Northern France and Belgium (Picardy,
Artois, Flanders, where it often reaches 40 to 70 per cent. Reynal):
Alsace-Loraine, Holland, Hanover, Mecklenberg, North and East Prussia,
Lithuania, the low parts of Austria and Hungary and the Danubian
Principalities—Moldavia and Walachia.

Reynal further shows that dealers are in the habit of taking young
horses, which have so far escaped, or which have suffered but one
moderate attack, away from the low damp soils of the low Pyrenees or of
the Jura Valley in France to the dry elevated lands of Dauphiny,
Provence and Languedoc in France, or to the mountainous regions of
Catalonia in Spain in the well justified confidence that few of them
will suffer a second attack.

As a direct test the French Government sent ten yearling foals from the
affected depot at Limousin to the healthy depot at Tarbes, retaining an
equal number at home as test animals: it also sent ten yearlings from
Tarbes to Limousin, retaining an equal number at Tarbes as test cases.
Then the twenty yearlings at Limousin were divided, five of the home
bred and five drawn from Tarbes having been sent into a very low wet
country at Lariviere, and the rest were sent to a high dry location at
Maraval. The result was that but one of the ten yearlings sent from
Limousin to Tarbes contracted the disease, while on the damp land at
Lariviere one Limousin-bred and four Tarbes-bred colts suffered; and
finally on the dry soil at Maraval not a single colt, from either
Limousin or Tarbes was attacked.

The other conditions that usually attach to a low, damp soil are
important factors. =Damp air and a cloudy, rainy climate= are potent
accessory causes. Hence the great prevalence of the disease formerly in
Ireland, on the west coast and in the fen country in England, in
Belgium, in the Low Pyrenees, in the valleys of the Loire, Jura, Meuse,
Moselle, the Guadalquivir, etc., (Reynal). Such an atmosphere relaxes
the system, induces a heavy lymphatic temperament, with coarse bones and
muscles, an excess of connective tissue, thick hide and hair, and thick,
shaggy and often gummy legs. All this implies a low tone of health which
will less effectually withstand inimical influences.

The =rank, aqueous fodders= grown on such damp localities have a similar
effect. These are more bulky and less nutritive and fail to maintain the
highest tone and vigor. The animals must overload the stomach and
intestines in order to obtain the requisite amount of nutriment, so that
with a large, pendent belly they are still in poor condition. The case
is even aggravated when they go on the succulent grasses of early
spring, as they continue to gorge and may even make fat, but they lack
in muscle and tone and in this condition even the rapid formation of
blood seems to favor the attack. Möller records the great prevalence of
the disease in Central Germany in 1884, in connection with excessive
rainfall, inundations, and spoiled fodder.

Dard records that a low, overflowed meadow in the Soane bottom near
Chalons, caused blindness in nearly all horses put upon it. Bouin quotes
a case of a sewage irrigated meadow in Vendée which almost infallibly
produced recurrent ophthalmia in the horses fed on its products. On the
other hand, oats and hay from a dry, rich soil and well harvested, are
the most trustworthy food when the disease is to be dreaded.

=Damp night air on wet, impermeable soils= is to be especially feared as
not only relaxing the system and lowering its power of resistance, but
also producing a chill and thereby increasing the susceptibility.

=Damp, cold basement stables= are concurrent causes acting like the wet
soils, the damp air, and the attendant relaxing conditions. Thierry long
ago noticed that improved stable hygiene around Strassburg led to a
notable decrease of recurrent ophthalmia. In 1807 horses were blind to
the extent of 16.5 per cent., in 1821 to 8.5 per cent., and in 1870
Zundel found but 1.79 per cent., and few of the latter from recurrent
ophthalmia.

Again the ventilation, lighting and drying of close, low, dark damp
stables where the disease had previously prevailed has often practically
banished the affection. Hofgeismar states that during the prevalence of
the disease in a detachment of the German army in Alsace, out of 84
attacks in 700 horses 52 appeared in February and March, the period of
severe weather and close stabling.

=Fodders of a heating, or starchy nature=, like =Indian corn=,
=buckwheat=, or =wheat= strongly predispose to the disease, probably by
inducing costiveness, slight impactions and indigestions, and in bad,
frequently recurring cases the writer rarely fails to find that the
animal is being fed on corn. Beans, peas, vetches and other leguminous
fodders are less injurious and when grown on high, dry soils and fed
judiciously they are as a rule harmless. When grown rank, badly
harvested, and used to excess they become distinctly hurtful. Any fodder
which has been allowed to become musty is to be avoided, since any
condition which lowers the general tone of health strongly predisposes
to an attack. The same remark applies to irregularities and faults in
feeding. The best food and the most abundant supply will fail under such
circumstances to maintain the condition, and the horse that is losing
condition is becoming increasingly susceptible to this malady.

The period of =dentition= and =training= is the most common occasion for
the attack, partly because this is the time when the colt is taken from
the pure air and exercise of the field, into the hot, close, impure
atmosphere of the stable, partly because he is made to exchange the
cooling succulent grass for the stimulating ration of hay and grain,
partly because he is subjected to severe constraint and much excitement
in the hands of the trainer, and partly because of the irritation of the
gums, the jaws and the whole head in connection with the shedding and
eruption of the teeth. When injudicious biting is resorted to, to give a
special curve to the neck, the consequent obstruction of the jugulars
and capillary congestion in the head is another potent cause. Heavy
draught and overdriving have a similar effect. In 53 cases Schmidt found
that 3 occurred under one year old, 5 in the 2d year, 10 in the 3d year,
16 in the 4th, 15 in the 5th, and 4 from the 5th to the 9th years.

=Influence of Season.= Mayer gives a statement of the percentages seen
in the various months of the year as follows: January 4.9%, February
4.7%, March 10.1%, April 15.1%, May 13.4%, June 9.9%, July 11.9%, August
6.4%, September 4.9%, October 6.2%, November 6.7%, December 5.2%. The
high rate in March, April and May may have a significance in connection
with the debility connected with shedding the coat, and the resumption
of more active work, when somewhat out of condition, it must also be
noted that this is in Germany the season of the most active trade in
horses and consequent change of ownership, stabling, feeding, work and
management.

=Heredity= must be accepted as one of the most potent accessory causes.
The lymphatic constitution is of course transmitted and with it the
special susceptibility. This is notorious in the case of both parents,
and is of course more potent if both sire and dam were predisposed, and
have themselves suffered. In the latter case the heredity of the
lymphatic temperament, and of the impaired organ of vision combine to
render transmission more certain. A mare may have borne a number of
sound foals before suffering from the malady and then have offspring
that do contract the disease. So with the stallion. Möller quotes the
case of the eastern horse Turk-Mayn-Atty which served for a length of
time in Prussian Studs and left a great stock of blind progeny. Lafosse
records the existence of a family of horses in Southern France all of
which went blind. The same cause has greatly extended the disease among
fast American horses in which the great strain of the track served to
intensify the tendency. The writer has seen a colt which was born blind,
by a blind dam and got by a sire with diseased eyes, but still held at
$300 for service. Mangin, Marimpocy and Hamon record congenital cases
from parents with affected eyes.

This hereditary susceptibility is so strong and pernicious that
intelligent horsemen everywhere refuse to breed from either horse or
mare that has once suffered from recurrent ophthalmia, and at the
Government studs in France not only is every unsound stallion rejected
but the service of the healthy stallion is refused to any mare which has
suffered from disease of the eyes. A consideration for the future of our
horses would demand that no stallion shall stand for the public service
of mares unless he has been examined and licensed as a sound animal.

Yet, as already stated, heredity is not the one controlling factor,
since the offspring of the victims of this disease will often escape
when brought up in a high, dry locality.

Reynal records the appearance of the disease in =alternate generations=,
the stallion offspring of blind parents remaining sound himself but
producing foals which became victims of the disease in large numbers. A
partial explanation may be found in the better conditions under which
the stud horse was kept, while under less favorable surroundings his
offspring developed the disease.

It must be added that every condition which induces =debility= or =ill
health= is favorable to the development of the malady. The presence of
=worms in the bowels= is a familiar example. Any debilitating disease
like =strangles=, =influenza=, =contagious pneumonia=, =indigestion=,
etc., and overwork or insufficient or indigestible food act in the same
manner.

Again, =local irritants= may rouse the latent tendency. Street or stable
dust, sand, hay seeds, chaff, blows on the eye with whip or other
object, wounds, irritant gases, smoke, fierce light, cold draughts,
storms, and whatever determines inflammation of the eye may be the
occasion of an outbreak of recurrent ophthalmia.

=Microbiology.= It will be recognized that none of these causes fully
account for the specific and recurrent nature of this affection, and it
is felt that something more is wanted to furnish a full and satisfactory
explanation of the malady. This explanation is sought in a direct
_infection_, but in spite of extended investigations by many observers
no specific microbe has been demonstrated as uniformly present in all
cases.

Potapenke found in the blood of the affected horses a plasmodium like
that of ague. This agrees with the damp regions in which the malady
prevails and no less with its intermittent or periodic character.

Vigezzi found in the aqueous and tissues a micrococcus
(ophthalmo-coccus) which, cultivated on gelatin agar and inoculated in
the anterior chamber or under the conjunctiva, produced an affection
which he recognized as recurrent ophthalmia.

Trinchera found in the aqueous of the affected animals a bacillus and
cocci. Drawing this aqueous into a sterilized syringe and injecting it
into the anterior chamber of sound horses produced in 12 to 48 hours
characteristic periodic ophthalmia. This was repeated by Schütz and
Schwartznecker.

Robert Koch found in the affected aqueous, cocci, singly or in chains
and bacilli with rounded ends. Injection of the latter into a sound
horse’s eye led to characteristic inflammation and loss of vision. In
the cornea of the rabbit it had no effect.

Richter found in the eyes of a foal born with recurrent ophthalmia, of
sound parents, diplococci and triplococci.

These observations do not demonstrate the constant presence of one
definite microbe, nor that the disease is invariably due to any one
particular organism, yet they may be held as strongly suggestive that
any one of a variety of microörganisms may prove an exciting etiological
factor in a susceptible system, or that, along with the organisms
heretofore demonstrated, there exists an essential microbian cause which
has up to the present eluded detection.

Other points which give circumstantial support to the microbian theory
may be shortly stated:

1. The recrudescence of the disease after its various intermissions, and
its preference for low, damp, cloudy localities seem to ally it to the
malarial diseases of man.

2. Its appearance in certain predisposed systems, whenever an injury or
debility of the eye seems to open the way for the admission of the
hypothetical microbe.

3. The increased susceptibility to the malady when the system has been
debilitated by disease, overwork, heating food, bad hygiene, or
parasitisms, which have undermined the native power of resistance.

4. The prevalence of the affection in given localities has been supposed
to imply the preservation and perhaps the multiplication of the germ in
such places.

5. The increasing number of victims, year by year, when the same
regiment or stud has been kept for a number of years in the same place.
The theory is that with the presence of infected horses the hypothetical
microbes become increasingly prevalent in the locality and above all in
the stables, until even the more resistent subjects tend to succumb
under the repeated infections. Thus Zundel says that in 1878, 700 army
horses were stationed in Saarsburg, in 1879, 6 were attacked with
recurrent ophthalmia, and in 1880, 84, Hofgeismar mentions that a
dragoon regiment in Frankfort had 5 horses attacked in 1876, 12 in 1877,
11 in 1878, 14 in 1879, and 42 in 1880. We have, however, no assurance
that the excessive rainfall, spoiled food or other unhygienic condition,
may not have been a potent factor in the increase.

6. The obvious connection of certain cases of recurrent ophthalmia with
a rheumatic condition suggests the probable operation of the same
microbian cause.

Up to the present the microbian causation of this malady cannot be taken
as proved, yet as a hypothesis it explains satisfactorily many of the
observed morbid phenomena. That there is no such rapidly spreading
infection, as would warrant us in listing this with animal plagues, is
conceded, and that constitutional conditions have a potent influence is
allowed, but that, in addition to these, microbian invasion is often a
means of precipitating the malady is altogether probable. It may not be
necessary that the microbe should in every case be of the same kind, yet
the addition of a germ as the last item in the chain of causes is
presumptively true.

=Parasitism.= Willach claims that many cases are directly due to
parasites in the eye. In 19 affected eyes he found one young filaria, a
number of rhabditis (?), 1 cysticercus, and a number of distomata.
Leider also found round worms in such eyes. Mayer and Dexler examined a
number of cases, using the centrifuge on the liquids of the eye, without
in any case finding such parasites. It may be assumed that the presence
of embryo worms may rouse a latent predisposition into activity, but
they cannot be adduced as active causes in the vast majority of cases.

_Symptoms._ These vary with the severity of the attack. In some cases
there is high fever while in others this may be absent, yet a lack of
vigor and energy bespeaks a general constitutional disturbance. The
attack is sudden with marked local irritation, photophobia and
lachrymation. The eyelids are closed some times so firmly as to suggest
blepharospasm, and if opened the pupil is seen to be contracted. The
affected eye is retracted and appears smaller, the conjunctiva is the
seat of diffuse redness and swelling, and there is a bright red
peri-corneal injection, occupying the anterior portion of the sclera.
The outer zone of the cornea is already the seat of a bluish white
opacity, the surface appearing dull and as it were smeared with oil. The
centre of the cornea may be opalescent but not so obscure as to prevent
examination of the interior of the eye. In a few days the outer margin
of the cornea may show vascularity, and the aqueous humor a certain
degree of turbidity. The iris if still visible is seen to be swollen and
rigid, and to have parted with some of its lustre, assuming a grayish or
lighter color owing to congestion and exudation. The pupil is usually
contracted and dilates only sluggishly and imperfectly in darkness or
under the action of atropia. The iris arches forward more than is normal
and may even approximate and adhere to the back of the cornea. Bayer
noticed that in a partial albino (watch eye) the iris becomes sulphur
yellow. The anterior chamber of the aqueous humor usually shows a
grayish yellow sediment which in severe cases may fill one-third or even
one-half of its depth. This may be grayish white flocculi of lymph only,
or it may be colored with blood or in suppurative cases by pus. In the
first day of its appearance this may be diffused through the humor, but
from the fifth to the seventh day it precipitates and leaves the iris
and pupil open to inspection. The pupil if not already open, may be
partially dilated with atropia and then discloses the interior of the
eye of a dark green, or sometimes with much exudate on the choroid, of a
more yellowish green. This greenish discoloration appears to depend on
opacity of the vitreous, on an exudate between the choroid and retina or
on some opacity of the cornea and aqueous. At the same time under a good
light some opacity of the lens or its capsule may be detected, or, with
direct illumination, of the vitreous as well.

The tension and hardness of the bulb is materially increased in some
cases but not at all perceptibly in others.

From the seventh to the tenth day the acute inflammation subsides, the
lids and pupils dilate, and the deposit in the anterior chamber is
rapidly reabsorbed. It may first assume a dull brownish green or
brownish tint. Meanwhile the opacity of the cornea commences to clear
up, and any redness or congestion of its margin to diminish or
disappear.

With this disappearance of opacities in the cornea, lens and humors, all
the symptoms of congestion subside and by the tenth or fifteenth day
from the commencement of the attack the eye may have become approximated
to its normal condition.

The characteristic of the disease, however, is its tendency to return
again and again until the eye is destroyed. From five to seven attacks
usually result in blindness, and then the second eye is likely to have a
similar experience until both are useless. In some instances the eye
which is first attacked may recover and remain well, while the second to
suffer is rapidly ruined by a succession of severe attacks. The
intervals between the attacks may be thirty, forty or sixty days and
upward according to the state of the health, the condition, the food,
the regimen, the exposure, and perhaps of other accessory causes.

Reynal claims that some eyes which have retained their normal function
after one or two attacks will sometimes gradually lose the power of
vision without any new appearance of inflammation. In other cases an eye
which has been clear and transparent becomes suddenly filled up with an
inflammatory exudation in the anterior chamber which obscures the iris
and lens and in a few days vision is permanently lost, yet without
conjunctivitis or apparent suffering.

=Condition of the eye between attacks.= After one, two or more attacks
the eye is not restored to its former condition in the intervals, but
continues to exhibit morbid phenomena which betray the previous
existence of the disease. The recognition of such persisting lesions is
all the more easy that one eye only is usually attacked at first and a
comparison between this and the sound eye renders the modifications all
the more patent. Even after a first attack there is usually a hazy
bluish white zone round the outer margin of the cornea and this becomes
more distinct after each successive attack. The faulty eye is distinctly
smaller in appearance, at first because it is retracted in its sheath
and later in certain cases because of actual atrophy. In proportion to
the retraction of the bulb, is the protrusion of the membrana nictitans
which covers a greater part of that eye than of its fellow. The upper
eyelid in place of forming a continuous and regular arch shows a
distinct abrupt bend between its inner and middle thirds caused by the
contraction of the levator muscle. The front of the iris has lost
something of its normal lustre, and the posterior chamber is liable to
show an abnormally light reflection, greenish yellow or yellowish blue.
Under direct illumination, lines of opacity may be detected in the
aqueous humor, or in the lens, or dark filaments in the vitreous. After
several attacks the lens is very distinctly obscure and this increases
with each relapse to a white or yellowish white complete opacity. After
the first or second attack the pupil may be distinctly contracted, while
later in the disease, with advanced cataract it is usually widely
dilated. Another feature is the erect, attentive carriage of the ear, to
compensate for the waning vision.

_Lesions._ These are not often seen, as animals do not often die of this
disease. Beside the superficial lesions of the conjunctiva and cornea
which may be seen during life, exudates have been found on the posterior
surface of the cornea, in some cases binding that to the iris. In
advanced cases the greatly contracted anterior chamber may contain a
little mucilaginous liquid strongly pigmented with debris from the iris,
the whole mixed with shreds of exudation. The iris is thickened by
congestion and by exudation on its surface and in its substance, and is
displaced forward so as to diminish the size of the anterior chamber,
and it may have contracted adhesions with the cornea (anterior synechia)
or with the lens (posterior synechia). This leads to unevenness in the
pupillary margin, where the iris is often torn into shreds. The
crystalline lens is usually opaque, and may have undergone various
changes, fibrous, calcareous, or atrophic. The anterior surface of its
capsule has often adherent masses of black pigment derived from the urea
in previous adhesions.

The vitreous humor and hyaloid membrane are sometimes clear, but usually
yellowish or blackish and reduced to one-half their normal bulk by
accumulations under the retina. A dense exudate often exists on the
lamina cribrosa. The choroid is very uneven showing irregular rounded
elevations, and like the iris is the seat of active congestion,
exudation and thickening. The exudate on its surface raises and detaches
the retina and, as shown by Eversbusch, this may increase so that the
retina from the two sides may come together in the centre of the eye,
the vitreous having been absorbed and removed. Reynal records instances
in which the exudate had become cretified, or as he claimed transformed
into true bony tissue. Finally the optic nerve is atrophied, often in
advanced cases to half its natural thickness.

_Prevention._ As treatment is somewhat unsatisfactory there is the
greater reason to give attention to measures of prevention.

In view of the great evil of low, damp, overflowed lands, it is
important to drain and improve such lands whenever possible, and when
this cannot be done, to abandon the breeding of horses upon them, and to
buy the animals necessary for agricultural purposes from high, dry,
healthy localities and introduce them only after they have passed the
age of five years at least.

The improvement of wet lands by liming, so as to lessen the amount of
decomposing organic matter, and improve the character of the vegetation
has proved very beneficial in different parts of England. The
substitution for the products of marshy meadows and wet lands, of those
of dry cultivated meadows and lands is important.

Misty cloudy regions in the vicinity of sheets of water, or cold
mountain ranges cannot be made wholesome, but they can be abandoned for
horse breeding, and devoted to more remunerative uses. Something may
also be done by stabling the working horses at night.

An insufficient or debilitating diet, for example, in winter, should be
carefully avoided, the more so if it is to be followed by a sudden
access to rich grass in the spring.

All forms of spoiled food, damp, musty, or fermented fodders should be
withheld, especially in the case of young and growing horses.

Indian corn, wheat and buckwheat should be carefully excluded from the
grain ration or if used should be combined with 1 oz. sulphate of soda
for each animal daily.

Damp, close, filthy and underground (basement) stables should be
avoided, the building on the other hand should be placed on high, porous
and well drained ground, and should be clean, moderately well lighted
and well ventilated but without draughts. While such special stable
hygiene is demanded for all it is doubly demanded for young horses under
six years of age.

As every debilitating condition renders the already predisposed animal
more open to attack, all causes of ill health should be guarded against,
and especially for the young, and in the case of such as are inevitable,
every effort should be made to curtail and lessen the evil influence.
Food or water which contains the eggs and embryos of intestinal worms,
must be avoided and parasites which have already invaded the system must
be got rid of as far as possible. Care must be taken to exclude the
various infectious diseases, and in case of their introduction, to adopt
every measure to mitigate their violence and to prevent debility and
weakness. Overwork and irregular feeding and watering must be guarded
against.

At the same time moderate work or exercise daily which will develop the
highest tone of the muscles, nervous system, digestion, assimilation and
other functions is a measure that can never be neglected. Idleness with
resulting fatness, softness and weakness of muscle, and lowering of the
power of endurance is always an invitation to renewed attacks. Regular
invigorating work is essential; exhausting work is injurious.

Change of locality to a drier soil, clearer, drier atmosphere, and more
abundant sunshine, when it can be availed of, is a most important
preventive measure. Reynal who made an extended official inquiry into
this matter found conclusive evidence of its truth. Young horses removed
from the low affected regions of Cantal, Poitou, Brittany and Anjou
rarely suffered another attack when taken to the high land of Catalonia,
and those moved from the damp lands of Franche Compté, Bresse, Dauphiny,
Provence, Languedoc, Bassigny and Belgium to the dry, calcareous
portions of Champaigne also escaped further trouble. In many such cases
the eyes already slightly affected would materially and permanently
improve.

Finally the influence of heredity is never to be over looked. The ideal
system would be to have all stallions professionally examined, and
licenses granted to such only as are free from this affection, and to
place the owners of such horses under obligation to serve only, mares
the eyes of which are sound. This might be enforced as a state or county
ordinance. Serious difficulties it is true stand in the way of such a
measure. The horse which has an extraordinary record on the track, and
to the development of the ophthalmia of which, overwork has doubtless
contributed, will be run after by breeders who seek speed at any cost,
and it may be questioned whether the State has any right to interfere
with the prospective profit which may be expected from the reproduction
of the strain of blood. But aside from such fancy products as racers and
trotters, this objection has much less force. For carriage, riding and
road horses and for the draught and agricultural animal the advantage of
sound eyes so greatly over balances all consideration of special values
with imperfect eyes, that a statute which will prevent the propagation
of such unsoundness is more than justified in every case. The importance
of this will be admitted when it is considered that in the great
majority of cases, the young animal is attacked after it leaves the
hands of the breeder, and therefore a high price is secured for a
subject which is almost certainly doomed to become blind in given
surroundings. Such a law would work well in every locality. In the low,
damp region where the disease prevails habitually, the unprofitable
breeding would practically cease, unless a race could be secured which
was proof against the infection. The value of such a race could hardly
be over-estimated. On the high, dry lands, on the other hand, the
natural tendency to immunity would be still further enhanced, as the
most susceptible animals which contracted the disease, in even such a
healthful district, could be in no sense fit for reproduction, and
should therefore be doubly condemned.

In the case of the mare the proprietor is under strong temptation to
ignore the sanitary measure under consideration. When her eyes fail, her
value in the public market is greatly depreciated, yet she can yearly
produce a foal, which is finely developed and will bring a high price if
sold young, before it has been attacked by the disease. Hence the great
importance, at least in the case of all horses which are not intended
for exclusive use on the race course, that a law shall be strictly
enforced which will put an absolute limit to the breeding from horses
that have been affected with recurrent ophthalmia.

Blows, dust, sand, smoke, irritant gases, fierce light, and all sources
of irritation must be avoided as in other eye diseases.

_Treatment._ Radical treatment for the disease is far from generally
satisfactory. Too often the affected animal is still in the environment
which has tended strongly to its development, and it is impossible to
secure a satisfactory change. As far as possible, however, every
available sanitary measure mentioned under the head of prevention should
be enjoined, and largely in proportion to the thoroughness of such
measures, and the slightness and recentness of the attack will be the
hope of a successful treatment.

In some instances in which there appears to be a rheumatic complication,
the employment of anti-rheumatic agents have proved of essential value.
Powdered colchicum corms may be given twice a day in doses of 1 scruple,
combined with salicylate of soda, salicylic acid, or salicin in 2 drachm
doses. To these may be added bicarbonate of soda or of potash in drachm
doses.

In cases attended with marked fever, hyperthermia and anorexia,
antiphlogistic treatment may be desirable, but with the primary
consideration that it must not be materially depleting, nor calculated
to induce debility or atony. A laxative dose of aloes will sometimes
benefit, but should be avoided in the absence of manifest fever. Two or
three ounces of Glauber salts, twice a day, will effect the same purpose
with less danger. Or saltpeter or other cooling diuretic may be given
daily. In most cases bitters may be added with advantage.

In severe cases, rest is essential until the violence of the
inflammation shall have abated, and a dark stall or a cloth to obscure
the light is equally important.

Trasbot advises bleeding from the jugular, but such a depleting measure
finds little support in England or America. =Local bleeding= from the
angular vein of the eye or by leeching or cupping is not open to the
same objection.

=Counter-irritants= are, however, more suitable. A stout silk thread may
be inserted above the lower end of the zygomatic ridge and bathed and
moved daily to prevent the lodgment of pus. Or a blister of cantharides
or biniodide of mercury may be rubbed in on an area as large as a silver
dollar in the same situation.

In all cases a strong solution of =atropia sulphate= (2 per cent.) may
be instilled into the eye once or twice daily. Or a mixture of atropia
and cocaine (1 per cent. of each) will give even greater relief. If to
these is added 1 per cent. of pyoktannin we get a collyrium which is at
once anæsthetic, midriatic and antiseptic. This is often of material
value. Vigezzi advises a mercuric chloride lotion (1 ∶ 1000) as a
collyrium, and for injection in the submucosa.

If the local inflammation runs high an astringent lotion may be applied
externally on a soft rag hung over the eye and kept constantly wet.
Sugar of lead or acetate of zinc may form the basis of such lotion with
a little atropia or morphia added.

=Puncture of the cornea= and =iridectomy= have been strongly advocated
on the ground that the disease is identical with glaucoma, but the
burden of evidence is decidedly against their use as a regular method of
treatment. In case of increased intraocular tension, however, the
puncture of the cornea can be very profitably employed, but it should be
reserved for such special cases. Theoretically, iridectomy should be
advantageous in preventing a relapse, but experience has not fully
sustained this. When employed, the most careful disinfection should be
secured. Under rational treatment the attack subsides in ten days and
the eye may appear to be restored to the normal condition in two weeks.
This natural tendency to a temporary recovery has served to give a wide
acceptance to the most irrational methods of treatment, which have not
in any sense hastened the recovery.

As soon as active inflammation and hyperthermia subside, every attention
should be given to prevent a relapse, and to this end all the measures
mentioned under prevention and which can be applied to the individual
case should be adopted. Among these, moderate exercise or regular work
must never be omitted.

A course of tonics embracing preparations of iron and bitters, is
equally essential, and may be begun as soon as fever and active
inflammation subside.

Special lesions, like corneal opacities and ulcers, must be treated as
in other affections.

=Jurisprudence.= The question of the right to return upon the seller a
horse attacked with recurrent ophthalmia has been beset with difficulty,
mainly because of the intermissions during which, to the ordinary
observer, the eyes may appear sound. In France a period of thirty days
is allowed in which to return such a horse after purchase. This is,
however, too narrow a margin as the second attack may not appear until
after two, four or six months. It does, however, provide for the return
of the worst cases in which the recurrence is likely to take place at an
early date. Another provision is that a suspected horse may be put in
pound under veterinary observation for thirty days, in anticipation of a
second attack, and if such fails to appear the purchaser is debarred
from returning him.

In many cases the symptoms during an attack and between attacks are such
as to identify the recurrent inflammation, and the expert can pronounce
positively as to the nature of the malady. In other cases there is a
degree of uncertainty, and the animal must either be returned on the
general plea of diseased eyes, if they can be shown to have been faulty
at the time of sale, or otherwise the horse must be put in the hands of
a veterinarian and the seller notified of the action, until it can be
shown whether it is the recurrent disease or not. If it can be shown
that the disease is the recurrent affection the seller is responsible at
common law for selling a diseased animal for a sound one. If on the
other hand, it is a non-specific ophthalmia, it must be shown that it
existed prior to sale, and that a warranty of soundness was given, in
order to hold the seller responsible.

PANOPHTHALMITIS.

General suppurative inflammation of eye. Experimental cases. From
traumas. Diagnosis; foul wound, violent eye inflammation, yellow
purulent appearance, high fever, involves second eye. Treatment:
antiseptic, enucleation.

This term has been applied to a general purulent inflammation of the eye
resulting from infection with pus germs entering from without through
traumatic injuries, or by reason of inflamed tissues, or on the other
hand, reaching the eye as a general infection through the blood. It may
begin therefore, as conjunctivitis, scleritis, or keratitis, and
gradually extend to active infection of the iris, choroid, and ciliary
body.

Möller produced an experimental case in a foal by the injection of the
staphylococcus pyogenes aureus into the anterior chamber. In 24 hours
there was violent inflammation: the eyelids were closed, the conjunctiva
dark red, and a mass of glairy pus under the eyelid. The cornea was
cloudy throughout, though still dimly transparent so that the
accumulating pus in the anterior chamber could be seen. The iris was
strongly dilated and the eyeball abnormally tense. The second day the
bulb was visibly enlarged, the eyelids greatly swollen, the conjunctiva
infiltrated so as to cause chemosis, and the cornea completely opaque.
The infiltration of the orbit caused the eyeball to protrude from its
sheath. A high fever set in and on the fifth day the foal died.

Cases in the lower animals are usually the result of direct infection
through some traumatic lesion of the eye.

The special feature of the disease is the rapid and abundant production
in all parts of the eye of pus cells until the whole organ has become a
bag of pus.

The chief diagnostic symptoms are the presence of a foul wound, the
rapid advance of the phlegmonous inflammation of the conjunctiva and
lids, the yellowish opacity of the cornea, and, if visible, of the
aqueous humor, the prominence of the entire eyeball, the high attendant
fever and the early destruction of the eye. In the domestic animals the
sympathetic irritation of the second eye has not been observed so
commonly as in man. If the patient survives, the pus makes its way
slowly to the surface, and escapes, and the cavity granulates and heals
with contraction of the eye into a small nodular mass.

The _treatment_ of the condition is essentially antiseptic and should be
made preventive if possible, as there is little hope of saving the eye
if the suppurative inflammation has been already established. The wound
should be treated at the earliest moment with antiseptic lotions,
sublimate solution (1 ∶ 5000) or potassium permanganate solution (1 ∶
100) or pyoktannin (1 ∶ 1000), or creolin (1 ∶ 100). When inflammation
has actually set in, these should be used still more assiduously by
frequent injection under the lids, or by inserting antiseptic cotton
between these and the bulb.

=Enucleation.= When the eye has become a virtual abscess the quickest
and most perfect relief is secured by the complete extirpation of the
eyeball. The patient is narcotized by ether or chloroform, and a thread
or hook being passed through the cornea, the globe is quickly dissected
out by curved scissors. Bleeding may be checked by pressure with cotton
wool steeped in tincture of the muriate of iron, and later the wound may
be dressed with stupes wet with a mixture in equal parts of standard
solution of sulphurous acid, glycerine and water.

GLAUCOMA.

Sea green pupil. Causes: intraocular pressure from serous choroiditis,
deranged fifth nerve, increased blood pressure, inflammatory
obstruction of sclero-corneal canal, irritation of the ciliary
ganglion. Symptoms: excessive tension and firmness of the globe,
anterior chamber shallow, iris contracted, sluggish, pupil grayish or
yellowish green, cupping of optic disc, pulsations of retinal
arteries. Acute inflammatory form, simple form, secondary form.
Convexity of pupil with synechia. Traumas. Luxations. Atheromas.
Lesions: inflammation of the iris, choroid, ciliary body or cornea,
round cell infiltration, cupped optic disc, atrophy of optic nerve,
hydrophthalmos. Treatment: massage, puncture of aqueous, iridectomy,
eserine, cocaine, antiseptic bandage.

This has been so named from the sea green color of the pupil. The nature
of the disease has been much debated and up to the present time
ophthalmologists are far from being agreed as to its true pathology. All
are agreed as to the essential feature of the malady, namely, increased
tension of the eye ball, but every case of increased tension of the bulb
is not recognized as glaucoma, and the true cause of the persistent and
progressive increase of pressure in cases recognized as glaucoma is not
absolutely settled.

_Causes._ The immediate cause of the condition is the increased
intraocular pressure, on this all are agreed, but as to the cause of
this pressure there is difference of opinion. Gräfe attributed it to a
serous choroiditis: Donders to deranged innervation of the 5th cranial
nerve which controls secretion; others to increased blood pressure;
others to inflammatory contraction at the sclero-corneal border where
the principal drainage canal of the aqueous humor lies. The increased
blood pressure theory appears to be contradicted by the fact that
exalted blood pressure, as in fever, does not tend to glaucoma. The
arrest-of-drainage-of-the-aqueous theory seems to be contradicted by the
reduction of the anterior chamber while the theory would demand its
increase. Priestly-Smith injected the sheep’s eye with a pressure of
water of 30 centimetres high, but while he caused an increased outflow
he failed to induce distinct glaucoma. Möller tied the ophthalmic vein
of the horse, but he also failed to produce glaucoma. “By artificial
stimulation of the ciliary ganglion in dogs, the internal tension of the
eye can be noticeably and permanently increased, and we may therefore
assume that when this ganglion is stimulated, the secretion of fluid is
increased, and that glaucoma depends upon an analogous process” (Fick).
It would seem that necessity demands at the same time an obstruction of
the normal drainage through nervous influence or otherwise. Schœn
ascribes glaucoma to overexercise of the accommodation, a cause which
would hardly be expected to operate in dogs. As bearing on the nervous
causation Fick mentions that in man glaucoma is often preceeded and
accompanied by trigeminal neuralgia. Again the symptoms of glaucoma
often appear in the course of recurrent ophthalmia in the horse.

While it seems impossible to ascribe the disease to any single definite
cause there appears to be good reason to accept as factors in different
cases, a derangement of trigeminal innervation, an irritation of the
ciliary ganglion, and an inflammation affecting the region of the
ciliary circle and the sclero-corneal line.

_Symptoms._ The tension of the eye ball is excessive as ascertained by
pressure of the finger, or by the spring tonometer. If the increase of
tension has come on suddenly, the cornea is somewhat cloudy, and less
sensitive to the touch. If one eye only is attacked the contrast between
the two is very marked and diagnostic. The anterior chamber is
diminished in size by the projection forward of the iris and lens. The
iris is usually contracted so as to show a dilated pupil reflecting a
smoky, grayish green or yellowish green hue. The iris is either
irresponsive to light or responds very slowly and imperfectly. With the
ophthalmoscope the most marked features are the “cupping” or depression
of the optic disc by pressure, and the pulsations in the retinal
arteries. These pulsations are especially easily seen at the margin of
the depression which represents the seat of the lamina cribrosa and the
point of entrance of the optic nerve. They are rendered even more
manifest by pressure on the eye. They are due to the prompt emptying of
the blood vessels by the intraocular pressure, so that these are only
momentarily filled at each cardiac systole.

Ophthalmologists recognize three varieties of glaucoma: =acute
inflammatory glaucoma=, =simple glaucoma= without apparent inflammation,
and =secondary glaucoma=, the result of another disease.

=Acute inflammatory glaucoma= is the one condition in which, in the
absence of a midriatic, inflammation is associated with dilated pupil.
It is liable to occur in a series of attacks, which increase in
severity, hence its supposed identity with recurrent ophthalmia in the
horse. The entire group of symptoms have, however, been rarely or never
seen in the horse. They are distinctly more common in dogs.

=Simple glaucoma= comes on more slowly, becomes chronic and is to be
recognized by the physical symptoms in the absence of inflammation,
notably by tension of the bulb, diminution of the anterior chamber and
cupping of the optic disc.

=Secondary glaucoma= is the direct result of some other disease of the
eye:

Complete posterior synechia acts by confining the liquid which is
secreted, to the posterior chamber whence it finds no ready outlet
through the pupil, and causes a marked bulging forward of the iris and
tension of the eyeball.

Slighter anterior synechia in the form of cicatricial adhesions between
iris and cornea in the sclero-corneal margin, acts by blocking the
principal drainage canal of the aqueous humor, which lies in this angle.

Traumatic injuries implicating the capsule of the lens and admitting the
aqueous humor freely to the lens substance determines softening,
swelling and so much irritation as to increase the secretion largely and
determine intraocular tension.

The same may result from luxation of the lens and irritation of the
ciliary circle by dragging.

Other causes are disease (atheroma) of the retinal vessels and the
growth of tumors in the interior of the eye.

_Lesions._ These are very varied. Inflammation of the iris, ciliary body
and choroid and even of the cornea is not uncommon. The iris and ciliary
body show round cell infiltration, as may also the choroid. In the
ciliary body this is likely to be especially abundant along the drainage
canal (canal of Schlemm) thereby reducing its calibre. Leber and Fuchs
found drops of liquid in the epithelium and cornea. One of the most
significant lesions in man is the cupping or depression of the lamina
cribrosa of a depth in ratio with the force of the intraocular pressure,
and inflammation or atrophy of the optic nerve, back of the eye. Möller,
however, has never been able to find actual cupping of the optic papilla
in animals, but instead thereof a general distension of the outer coats
of the eye, a hydrophthalmos. In view of the fact that these coats have
the same structure and nearly the same relative thickness as in man,
this throws considerable doubt on the supposed identity of glaucoma in
man and cases which have been considered such in the lower animals. The
comparative absence of pulsations in the retinal arteries in animals
adds to the uncertainty.

_Treatment._ Although such cases lack some of the diagnostic symptoms of
glaucoma in man, yet they agree with that in the increase of the
intraocular pressure, and demand similar measures for relief. Some
reduction of the tension can be secured by careful massage over the
eyeball so as to favor the progress of the lymph out of the bulb. A
prompt but rather transient relief can be obtained from evacuation of
the aqueous humor by puncture with a lancet close to and parallel with
the margin of the cornea. The most effective treatment is, however, by
iridectomy. On account of the great power of the muscles in the lower
animals it is usually desirable to anæsthetize the patient and then
fixing the eyeball with a pair of rat-tooth forceps, an incision is made
close in front of the upper border of the cornea, and the lancet slowly
withdrawn. A pair of iridectomy forceps are then introduced and the iris
seized and drawn out through the wound, and a portion snipped off with a
pair of fine scissors. The iris is then pushed back into the anterior
chamber, and a drop of eserin solution placed in the eye. The parts and
instruments must be rendered thoroughly aseptic before the operation,
and the eye cocainized both before and after. The eye should be kept
covered for some time with a cloth wet with a solution of mercuric
chloride (1 ∶ 5000) or other antiseptic.

Appropriate treatment may be employed in case of coexistent
inflammation, or to improve the general health.

EXOPHTHALMOS.

This consists in an increase of the media of the eye so as to cause an
excessive increase in size, and an unsightly bulging outward from the
orbit and between the lids. It may be said to be a more exaggerated
enlargement of the eye ball, than has been already noticed under
glaucoma.

It has been seen in nearly all classes of domestic animals. Everhardt
and Möller reports it in horses, Hausmann, Pradal, etc., in cattle,
LaNotte, in lambs, Cöster, Trasbot, etc., in dogs, and Trasbot, in birds
(chickens and parrots). It has been found congenitally in lambs and at a
few days old in foals, especially when weak and puny; in older animals
it appears to be most frequent in the anæmic or starved animal, in the
lymphatic, or, as in man, in the goitrous.

The manifest projection outward of the eye may occur as a nervous
phenomenon, without intraocular pressure, and without abscess, neoplasm,
or inflammation in the depth of the orbit. In a case of tuberculosis in
a three year old cow, I have found this condition, with normal tension
of the eyeball, but with acute tubercular meningitis of the pia,
surrounding the pons and crura cerebri, a grayish exudate with lighter
miliary centres, and a considerable clot of extravasated blood.

_Symptoms._ Mostly without any febrile reaction, there is a manifest
enlargement and bulging of the globe of the eye, so that it stands out
between the lids which can no longer cover it. The cornea, aqueous,
lens, and vitreous are not usually opaque, but show only a pale, blue,
opalescent tint. The pupil is often widely dilated so as to show clearly
the interior of the eye. Vertiginous symptoms have been observed in the
cow (Pradal), the supposed result of intraocular pressure.

_Treatment_ has had little effect when it stops short of puncture of the
cornea or iridectomy.

HYDROPHTHALMOS OR BUPHTHALMUS CONGENITUS.

This has been applied to a congenital enlargement of the eyes from
internal distension in children. The cases in lambs and foals quoted in
the last article were evidently of this nature. They are charged on
intraocular pressure acting on the delicate tissues of the embryo or
unborn animal. There is not necessarily cupping of the optic disc so
that persistent tension after birth cannot be insisted on.

Cases occurring in older animals, may be forms of secondary glaucoma
though classed under hydrophthalmos by Mayer and others.

_Treatment_ when demanded is along the same lines as in glaucoma.

CATARACT. OPACITY OF THE LENS OR ITS CAPSULE.

Definition. Forms: lenticular, capsular, cortical, nuclear, polar,
black, diabetic, traumatic, immature, mature, senile. Causes: impaired
nutrition of lens, inflammation of iris, choroid, ciliary body,
retina; recurrent ophthalmia. Proliferation of cells. Increased
density, chemical changes, degenerations. Sugar, sodium chloride,
naphthalin. Rachitis. Senile. Blood pigment. Symptoms: shrunken bulb,
opalescent zone around cornea, angle on upper lid, shying, extra ear
activity, high stepping, better sight in twilight, homatropia,
examination facing the light, Purkinje’s images, ophthalmoscopic
examination. Prognosis hopeless. Treatment: phosphureted oil, massage,
operation in horses, discission, under antiseptic precautions,
extraction under careful antisepsis, suction.

_Definition._ Any pathological change in the lens or its capsule
diminishing its transparency.

_Varieties._ The opacity may be situated either in the lens
(=lenticular=) or in its capsule (=capsular=). Again, it may be in the
outer part (=cortical=) or in the central part (=nuclear=) of the lens.
If the opacity is on the capsule in front of the lens it is =anterior
capsular=; if on the portion behind the lens it is =posterior capsular=.
If the opacity is caused by black iris pigment adherent to the capsule
it has been called =black cataract=. If the lenticular cataract is small
and round, it is =polar=, and it may be =anterior= or =posterior polar=
according as it is situated near the front or back of the lens.
=Diabetic cataract= is one associated with mellituria. A =traumatic
cataract= is one resulting from a wound of the lens which admits the
aqueous humor and causes softening, swelling and finally solution of the
substance of the lens. The =immature= or =unripe cataract= is one in
which the lens is not yet wholly involved and indurated; the =mature= or
=ripe=, when such consolidation has extended throughout. =Senile
Cataract= is seen in old horses, dogs, cats, birds and very
exceptionally in cows. This usually attacks both eyes at once. A
degeneration takes place in the fibres of the lens, which are invaded by
sclerosis beginning at the centre of the organ.

_Causes._ In domestic animals cataracts are commonly the result of
impairment of the nutrition of the lens in connection with inflammation
of the iris, choroid, ciliary body, retina, or hyaloid membrane, and
above all, in solipeds, in recurrent ophthalmia. It may be assumed that
a transparent tissue composed of cells can only maintain its
translucency so long as the most perfect equilibrium is maintained as
regards the mutual relation of the cells, the pressure of its
interstitial plasma, and the chemical composition of both plasma and
cell structures. The slightest deviation in any direction will impair or
abolish the transparency of the tissue. In inflammation this occurs in
various ways, through the increased cell multiplication and the change
in the nature of the cells, through the increased exudation and the
alteration of the solid parts as regards compression and relative
position, and through chemical changes in the exudate which contains
more salts, fibrinogenous material, etc., than the normal plasma. The
same is true of all the post inflammatory degenerative processes that
take place in the lens.

The formation of cataract from chemical alteration in the fluids is
familiar in diabetic subjects,—man or beast (Altenhof). It can be
produced experimentally in frogs by injecting sugar, common salt or any
other readily diffusible saline solution under the skin (Kunde). Rabbits
that are fed naphthalin develop cataract which radiates in lines and
streaks from the pole towards the periphery and in the cortical portion
of the lens. Perhaps the lamellar cataract of rachitic patients is also
to be attributed to the lack of earthy salts in the plasma of the lens.

_Senile cataract_ may be hypothetically attributed to impaired
nutrition, degeneration in the lens or its capsule, or less commonly to
disease of the blood vessels of the eye, or gradual changes in the
plasma. It occurs in horse, ox or dog at ten years old and upward.

=Anterior Capsular Cataract= sometimes results from the deposition of
=blood pigment on the capsule= in cases of extravasation into the
anterior chamber. This is closely allied to the black or spurious
cataract which consists in the adhesion of the uveal pigment to the
capsule, and its detachment from the iris.

Kunde who caused cataract in frogs by injection, subcutem or ingestion
of concentrated solutions of sugar or salt, attributes the result to the
sudden abstraction of water from the crystalline lens. Even the cell
multiplication in inflammatory cases, he holds to favor this, since the
new cells having little vitality are especially subject to granular and
other deposits and degenerations, with loss of water or of transparency.

_Symptoms and diagnosis._ The examiner should apprehend cataract after
internal ophthalmia. Much more so, if there is apparent diminution of
the bulb, an opalescent zone around the outer border of the cornea, or a
marked angle in the curvature of the upper eyelid, as usually occurs in
recurrent ophthalmia. When a horse suddenly acquires a habit of shying,
of starting back or to one side when approached, when confronted with
strange or unexpected objects, or with deep shadows like those from
electric lights, he is to be suspected. When he carries his ears in an
unusually alert manner, turning one forward and the other back, when he
steps higher than before to avoid unseen objects, suspicion should
attach to him. If he sees better in twilight than in the full sunlight,
central cataract may be feared, while the periphery which is exposed by
the dilatation of the pupil in semi-darkness is still clear. In all
examinations for soundness, the greatest care should be taken to exclude
the possibility of overlooking an existing cataract.

In the very early stages, while internal inflammation and photophobia
are still present, the pupil may be contracted so that lesion can easily
escape notice. Any contraction of the pupil therefore disproportionately
to the light, should demand a careful examination with the pupil dilated
in darkness or by the action of atropia or homatropin. In the more
advanced cases with no persistent inflammation and an advanced opacity
of the lens, sensitiveness to light is greatly lessened, the pupil is
dilated and the cataract is easily detected.

In cases approximating to the condition last named it is usually only
necessary to place the animal in a sombre or dark building, with his
head facing the light at an open door, or window and best with full
sunlight. Let this fall full upon the eye, and let the observer view the
pupil diagonally from each side when any opacity may be detected.

When the pupil is too narrow, several drops of a one per cent. solution
of atropia sulphate may be dropped within the lower lid and left for ten
minutes until the pupil is widely dilated. Then the examination may be
made as above, or still better the animal may be taken into a dark
chamber and examined by one of the following methods:

A light, preferably a candle, is placed in front of the eye and moved
from side to side, upward and downward, so as to bring its images over
all parts of the cornea and lens. In the normal eye there are reflected
three images of the light, one large, clear, and upright from the
anterior surface of the cornea, one, much smaller but still upright,
from the anterior capsule of the lens, and one, small and inverted, from
the posterior surface of the lens and capsule. Any opacity in the lens
or on its posterior capsule, will cause the posterior (inverted) image
to become indistinct, and as it were a diffuse white blur, as it passes
over that spot. The other small (erect) image may be even clearer than
normal in passing over the opaque area because of the mirror-like
reflecting action of the white cloud behind it. The movement of the
light so as to pass its image over all parts of its surface in
succession will certainly reveal the existence and seat of the cataract,
by the blurring of the inverted image of the flame.

Another method is by oblique illumination, the patient’s head being
turned away from the light and the interior of the eye being lighted up
by reflection from a mirror. If the pupil has been sufficiently dilated
all parts of the lens can be scrutinized in this way and the slightest
opacity detected by the grayish or whitish haze.

If there is still doubt as to the nature of such appearances, it may be
set at rest by illuminating the depth of the eye with the ophthalmoscope
when the opacities will appear as dark areas in the general red ground.
(See Systematic Examination of the Eye.)

The _prognosis_ of cataract is almost invariably hopeless. I have seen
newly formed opacities of the capsule clear up in a day or two, and such
recovery in very slight traumatic injury and superficial exudation is
recognized as possible, but a slowly forming cataract is usually there
to stay. Those that clear are presumably only exudates on the capsule
and not true cataracts.

_Treatment._ While exudates on the capsule may disappear under a course
of purgatives and diuretics, practically nothing is to be expected from
medical treatment in true cataract. The instillation of phosphorated oil
(1–2 per cent.) daily into the conjunctival sac as formerly recommended,
may be helpful in some of the superficially opaque membranes, but for
formed cataract it has proved useless. Massage with, or without
ointments can temporarily lessen ocular tension and reduce the liquids
in the zonula of Zinn, and canal of Schlemm, but it is only in very
exceptional recent cases, in which it has given permanent benefit, and
even these were probably spurious cataracts.

The question then is essentially whether we should operate or not. In
the =horse= the objections to operation are almost conclusive in all
cases. The eye in which the lens has been depressed or extracted can
never see objects clearly without the aid of biconvex glasses, and it is
impossible to fit these to the animal. The horse that is blind can go to
pasture or be driven in harness with safety, but the one that sees all
objects distorted or blurred is liable to become a shyer endangering the
life of his rider or driver. The greater number of cataracts in horses
come from recurrent ophthalmia and are associated with opacity of the
vitreous, detachment of the retina, exudates in the choroid,
degeneration of the optic nerve, or other lesion which of itself would
destroy vision. Almost the only object of removal of the lens in such
cases would be to make an unsound horse pass for a sound one. Even this
is usually unattainable because the thickened capsule remains as a dense
white cloud or the opacity of the vitreous shines through the pupil. In
dogs the cataract is usually associated with fewer complications, and
the resulting imperfect vision is not a source of danger to man.
Extraction of the opaque lens may in this case appeal so strongly to the
sense of comfort of the owner that the operation may become permissible
or desirable.

In man the operation may have to be delayed for a considerable time
because of the unripeness of the cataract. The center of the lens may be
firm and opaque while the outer layers are so soft that they would be
likely to be retained in the capsule and would not only produce
persistent opacity, but would be a continual threat of destruction of
the eye by active inflammation. The ripeness is ascertained by careful
scrutiny of the shadow of the iris during illumination of the interior
of the eye. If ripe, the dark shadow of the iris approximates closely to
the margin of the iris itself, whereas if the outer portion is unripe
there is a clear zone of greater or less depth between the margin of the
iris and the shadow reflected by the opaque portion of the lens.

In the lower animals the question is less important as we do not aim at
securing perfect vision, and the danger of inflammation is therefore the
main consideration. Escaping this, the aqueous humor may be expected to
dissolve and remove the greater part of the still adherent lens
substance, and the unsightliness of the dense white cataract is largely
done away with.

=Discission.= Tearing of the capsule so as to admit the aqueous humor to
the lens may be admissible in the =young= with =soft cataract=. The
liquid causes gradual swelling up, solution and absorption of the lens
so that in the course of a week or two the whole may be removed. It is
not, however, unattended by danger, as the rapid swelling of the lens
will sometimes determine an inflammation which will lead to complete
destruction of the eye. The eye is first thoroughly washed with aseptic
cotton and a sublimate solution (1 ∶ 1000), and is then rendered
anæsthetic by cocaine (5 to 10 per cent. solution) or in the large
animals general anæsthesia is produced by ether or chloroform. The
eyelids are held apart by the lid speculum, the nictitans held if
necessary by forceps, and the bulb steadied by seizing it with hooked
forceps. A cataract needle is passed through the cornea close to its
border, and carried through the pupil, previously dilated with atropia,
so as to tear an opening in the anterior capsule about two-thirds the
diameter of the lens. If the toughness of the capsule threatens to
endanger the ciliary body by dragging upon it, two needles or fine hooks
may be introduced through opposite borders of the cornea (inner and
outer) and the capsule may be torn without throwing any strain on
surrounding parts. The pupil must thereafter be kept dilated by atropia
to obviate adhesion of the iris to the wound and the eye must be kept in
comparative darkness and aseptic. If active inflammation sets in, cold,
astringent or iced dressings may be called for, while if the swelling of
the lens is threatening it should be at once extracted. If the eye
becomes unduly tense, puncture of the cornea is indicated, and the
relief of tension will sometimes start a tardy solution into renewed
activity.

=Linear extraction of the lens.= The animal and the eye having been
prepared anæsthetically antiseptically, and midriatically as for
discission, the lids are fixed with a speculum, the nictitans and the
bulb with forceps, a Gräfe cataract knife is introduced through the
inner side of the cornea, close to its margin and with its point
parallel to the front of the iris. The handle is then raised and the
cornea detached from the sclera by a series of gentle sawing motions
until it has reached a point parallel to the outer margin of the cornea.
If the pupil is insufficiently dilated, the iris should now be seized by
forceps drawn out through the corneal wound and snipped off by scissors
curved on the flat. Then the cystotome (hooked knife) is introduced with
its back turned downward and carried to the further side of the capsule
and close to the iris, its cutting point is turned backward and inserted
in the capsule, and drawn across from side to side to make an orifice
large enough for the escape of the lens. It is then given a quarter
revolution so as to turn the point of the knife downward and is
withdrawn from the wound back first. The lower part of the sclera and
cornea is now gently pressed with a lens spoon so as to dislodge the
lens from the capsule and deliver it through the corneal wound. Counter
pressure may be made on the sclera at the upper part of the eye ball.
The cornea is now gently stroked with cotton dipped in sublimate
solution to pass all blood from the anterior chamber, and render the
parts antiseptic. The iris is carefully replaced inside the cornea and
any obstinately protruding parts must be excised. The eye is now covered
with cotton steeped in a sublimate solution (1 ∶ 1000) and bandaged
without undue pressure, and the animal tied to two sides of the stall so
that it is impossible to rub the eye.

It is well to dress the eye on the second day, and if adhesion of the
wound is complete it may be left without bandage at the end of a week or
a fortnight.

Success depends mainly on the avoidance of infection. Therefore every
indication of local or general infection should forbid the operation.
Any existing infectious disease or any local eczema, conjunctivitis or
disease of the lachrymal apparatus should be cured and the region
thoroughly disinfected before proceeding. The head should have a good
soapy wash, followed by a sponging with sublimate solution (1 ∶ 1000),
the conjunctiva carefully washed out with the same and a bandage damp
with it applied over the eye. This bandage is only removed on the
operating table. Cloths dampened with the solution are laid on the face
around the eye, the eye is cocainized with a 5 per cent. solution
applied at intervals of one minute and when quite insensible the
operation is commenced. The greatest care must be taken to render the
hands of operator and assistants and all instruments thoroughly aseptic.
The instruments are taken from a 4 per cent. solution of carbolic acid
and placed in water (which has just been boiled) until needed, and to
wipe the eye or make any application, sterilized cotton only is used and
never touched to the eye more than once. A sublimate bandage is placed
over the eye and worn for ten days or a fortnight. Then if the corneal
incision is healed and pale it may be left off. The pupil should be kept
dilated by a few drops of atropia daily for this length of time.

Any occurrence of iritis or choroiditis usually indicates infection and
must be treated on general principles, but with especial reference to
disinfection, and if this cannot be secured the eye will be almost
inevitably lost.

In case of renewed opacity through thickening of the capsule an aperture
must be torn in that membrane by the same method as in discission. This
is commonly known as needling. It must be conducted under the same
antiseptic precautions as in extraction.

_Suction._ This is only applicable to a lens which has become fluid as
well as opaque. It consists in withdrawing the liquid lens through a
hollow needle.

DISLOCATION OF THE LENS.

Congenital; acquired; traumatic, softening of suspensory ligament:
hinge motion, lens drops behind iris, protrudes through pupil,
cataract. Apparent increased depth of anterior chamber, tremulous
iris, projecting edge of lens like black ring. Treatment: extraction.

Dislocation of the lens may be congenital, or acquired. In the latter
case it is explained by a traumatism or a liquefaction of the vitreous
and coincident softening of the suspensory ligament. In either case, if
the ligament is torn through in more than one-half its circumference,
the lens will hang by the remainder and move on it as on a hinge so as
to change its location in the different positions of the head. This is
especially so where the vitreous has become abnormally fluid as there is
then no resistance to the free backward movement of the lens. The writer
has seen the eye of a cow affected in this way, so that the cataractous
lens advances to the pupil and recedes from it as the eye is moved. In
other cases the dislocated lens, being attached below only, drops down
and virtually disappears behind the lower part of the iris. In still
other cases it becomes wedged into the pupil, or protrudes into the
anterior chamber and lies in front of the pupil and iris. The
semi-detached lens sooner or later becomes opaque. A cataract with
contraction of the newly formed tissue on the capsule and undue tension
on the suspensory ligament may, however, precede the dislocation which
is then precipitated by some shock, as a blow, fall, sneeze, cough or
emesis.

The condition leads to an apparent increase in the depth of the anterior
chamber, and tremulous movement of the iris, and if illuminated the
impacted condition of the lens or its changes of position can be
detected. If its edge is exposed it appears as a black ring.

_Treatment_ is useless, unless it be extraction of the lens, or
iridectomy in suitable cases.

PERSISTENT ARTERIA HYALOIDEA.

In the embryo this artery occupies the central canal of the vitreous and
extends from the optic papilla to the posterior pole of the lens. At
times it persists after birth and even to mature life and is then
detected as a gray or dark thread on ophthalmoscopic examination. Berlin
records a case in an old horse and others in young cats, and Möller
other cases in dogs. Treatment is manifestly hopeless.

OPACITY OF THE VITREOUS.

From inflammation of the ciliary body, choroid or retina. Pupil
copperas green with white points, lines or patches, move in opposite
direction from the eye, liquefied vitreous, crystals of cholesterine,
scintillance, opacity. Treatment.

Opacities visible with the ophthalmoscope usually come from effusion of
blood into the vitreous, or inflammation of the retina, choroid, or
ciliary body. Blood thrown into the vitreous will usually leave some
permanent turbidity. In choroiditis or retinitis the ophthalmoscope may
reveal the changes in these structures. A turbidity appearing in the
anterior portion of the vitreous, without any apparent cause, is
probably due to cyclitis which cannot be seen with the ophthalmoscope,
but may cause special tenderness around the sclero-corneal zone. It is
common in recurrent ophthalmia of the horse and in irido-choroiditis in
animals generally, and may be a distinct feature of glaucoma. The
general reflection of the pupil is copperas green, but gray or white
points, lines, bars or patches may often be recognized. These being back
of the lens and axis of the eye, move in the opposite direction from the
line of vision, thus if the eye looks upward they descend, if it looks
downward they ascend, if it turns to the right, they turn to the left
and vice versa. Tested by a burning candle the three reflections remain
clear and distinct unless lens or cornea are affected.

Not infrequently the vitreous is found abnormally fluid, and among its
solid particles in affected horses have been found crystals of
cholesterin (Jacobi) and tyrosin (Möller). In the illuminated vitreous
such crystals may be seen to reflect the light like a shower of sparks
(synchysis scintillans). Opacity of the vitreous has been seen in cases
of amaurosis in horses (Hertwig) and glaucoma in lambs (Prinz).

_Treatment_ is rarely satisfactory, though in some recent cases, and in
the absence of any other irremovable lesion, reabsorption of a slight
exudate may take place, in connection with the use of mild saline
laxatives and diuretics.

RETINITIS.

With choroiditis and cyclitis, albuminuria, nephritis, mellituria,
leukæmia, petechial fever, contagious pneumonia. Photophobia,
contracted pupil, redness around optic disc, enlarged retinal vessels,
white and gray spots and radiating lines, exudates, clots, fatty
degeneration. Treatment: correct primary disease.

Retinitis is usually an accompaniment of choroiditis and cyclitis, but
it also occurs as a complication in a number of constitutional maladies,
such as albuminuria, nephritis, mellituria, leukæmia, petechial fever,
contagious pneumonia, etc. Fröhner records a case in a leukæmic horse,
Peters in one suffering from petechial fever, Schindelka in cases of
contagious pneumonia in the horse, and Eversbusch in recurrent
ophthalmia of the horse, and under other conditions in dogs.

The attack is accompanied at the outset with much photophobia and
contraction of the pupil. When this is dilated and the fundus of the eye
examined with the ophthalmoscope, the retina is seen to be reddened for
some distance around the optic disc and the blood-vessels are materially
enlarged. Later, white or gray spots and lines are seen in and around
the disc, tending to assume a radiating direction, and the retina at
large, on careful examination may have a distinctly striped appearance.
Brownish, reddish or light colored exudates and hæmorrhages may be made
out in certain cases between retina and hyaloid, or between the retina
and choroid. Fatty degeneration of the fibrous tissue is common.

_Treatment_ must be first that for the primary disease of which the
retinitis is a complication, and the result will depend on how amenable
that affection is to therapeutic measures. In advanced albuminuria or
mellituria, the retinitis, which is usually double, is hopeless, while
in contagious pneumonia, petechial fever, leukæmia and other less fatal
affections, retinitis in its initial stages may recover. In cases of
advanced disease with serious structural changes in the retina, recovery
cannot be looked for.

DETACHMENT OF THE RETINA.

This may occur in any case of retinitis or choroiditis. It is especially
common in recurrent ophthalmia in horses. It may also occur through the
dragging by contracting inflammatory products in organization.
Spontaneous recoveries have taken place through reabsorption, and
attempts have been made by the injection of iodide lotion to hasten
this, or more safely by rest and diaphoresis. Puncture and aspiration
have also been tried with most varied results. As a rule in the lower
animals the treatment of the inflammation, with rest, a pressure
bandage, and pilocarpin will be indicated.

RETINAL HEMORRHAGE.

This occurs in inflammations of the retina or choroid, also in
degenerations of the vascular walls and as a result of traumas, or
poisons. Schindelka quotes a case in a dog from ptomaines, Eversbusch,
one from scurvy in the dog, Appenroth, one in a calf from a blow with a
cow’s horn, and others in cats and horses from traumas. It is present to
a slight extent in all inflammations of the retina. With the
ophthalmoscope the recent lesion appears as a bluish red blotch on a
bright red ground, and the older lesion of a brownish red. Rest and a
pressure bandage may be employed after subsidence of the inflammation.

TUMORS OF THE RETINA.

Eversbusch found subretinal cysts in a 24 year old horse, Merkel and
others have found similar bodies in old dogs and cattle. Sarcomata and
melanosarcoma are found on the surface of the choroid in gray horses,
implicating the retina. The only remedy is enucleation of the bulb.

INFLAMMATION OF THE OPTIC NERVE. PAPILLITIS.

Choked disc. Neuro-retinitis. Papillo-retinitis. Nerve swelling blocks
veins. Causes: lead, tumors in brain bilateral, in orbit unilateral,
influenza, petechial fever. Symptoms: redness of optic disc, retinal
arteries contracted, veins gorged, papilla swollen (woolly), vitreous
opacity. Treatment.

This is also known as _choked disc_ from the obstruction of the return
of blood by the veins of the retina which pass out at the cribriform
lamina. The swelling of the nerve ending and papilla compress the veins,
causing stagnation and venous congestion in the retina. When the retina
is thus involved the term neuro-retinitis or papillo-retinitis is often
applied.

_Causes._ The condition has been traced to lead poisoning, brain or
orbital tumors, and various infectious diseases. Except in orbital tumor
the disease is usually bilateral. In horses Schindelka has seen the
condition in influenza and Peters in petechial fever, heart failure and
dyspnœa. In a necropsy on a horse the writer found complete cataract,
atrophy of the bulb to less than two-thirds the size of its fellow,
thickening and furrowing of the sclera, the presence of an extensive old
blood clot in the seat of the vitreous, cupping of the disc,
retro-ocular neuritis with exudate inside the sheath, and a considerable
reddish brown tumor of the choroid plexus on the same side. The trouble
was attributed to the blow of a rope on the eye a considerable time
before. The blood in the vitreous retained its dark hue and showed no
evidence of microbian invasion.

_Symptoms._ To the phenomena of retinitis there is added violent
injection of the capillary plexus of the papilla. The arteries of the
retina are contracted while the veins are dilated and tortuous. The
papilla is swollen and is said to have a woolly appearance. The vitreous
may be opaque by reason of exudation or blood extravasation into its
substance. Retro-ocular neuritis is usually present, and brain tumor in
certain cases. Möller calls attention to the fact that with atrophy of
the bulb the elliptical outline of the papilla gradually lessens and it
becomes more nearly round. In dogs, too, the form of the papilla is also
changed and the same author has found it distinctly triangular. The
pupil may be at first strongly contracted and later freely dilated.

_Treatment_ is usually of little avail and does not differ materially
from that adopted in retinitis. In tumor of the orbit pressing on the
optic nerve it may sometimes be reached through the temporal fossa, but
usually in all such cases enucleation of the eyeball is demanded.

RETRO-BULBAR OPTIC NEURITIS.

Definition. Neurites descendens and ascendens. Extension to bulb,
other eye, or brain. Causes: traumas, meningitis, infectious diseases,
toxins, lead, tobacco, etc. Symptoms: partial blindness: congestion of
papilla, exudates in adjacent retina. Treatment: eliminate poisons,
lead, toxins, correct precedent disease, saline laxatives, diuretics,
potassium iodide, cupping, local bleeding, counter-irritants. Hygiene.

This is inflammation of the optic nerve commencing behind the eyeball
and only involving the papilla secondarily. Extension to the papilla has
been called _neuritis descendens_ in contradistinction to _neuritis
ascendens_ in which the inflammation extends along the nerve toward the
brain. There is always a tendency to extension, it may be to the papilla
and retina, it may be to the chiasma and opposite eye, and it may be
inward toward the ganglia and choroid plexus.

_Causes._ Apart from traumatic causes, retro-bulbar neuritis in the
domestic animals has been mainly seen in connection with constitutional
or infectious diseases; in the horse with petechial fever (Peters),
contagious pneumonia (Schindelka), meningitis (Peters, Straub) and
parotitis (Möller). It has also followed meningitis in cattle (Nebelen).
In man it has been traced to lead, tobacco, alcohol and other poisons.

_Symptoms._ At first the patient may seem partially blind without
apparent cause. Later ophthalmoscopic examination reveals congestion and
swelling of the papilla, and congestion (especially venous and
capillary) of the retinal vessels. The discolorations in streaks and
spots, from exudates and degenerations follow as noticed under
papillitis. It is difficult to distinguish between this and papillitis
during life.

_Treatment_ should be first directed toward the elimination of any
poisons, such as lead or tobacco, which may act as a causative factor.
Saline laxatives and in chronic cases potassium iodide would be
indicated. Every attention should be given to the maintenance of good
general health, and in acute attacks, local bleeding and
counter-irritation may be resorted to.

ATROPHY. PARALYSIS OF THE OPTIC NERVE. AMBLYOPIA. AMAUROSIS.

Definition. Horses, dogs, cattle, sheep. Amblyopia, Amaurosis. Causes:
retinal paresis from brilliant light, of cerebral ganglia, snow
blindness, poisons, lead, opium, atropine, lolium, tobacco, carbon
bisulphide, cryptogams, mushrooms, “loco” plants, carbon monoxide,
illuminating gas, quinine, heat apoplexy, cerebral concussion, brain
parasites, exudates, pressure, degeneration, gastric or intestinal
disorder, hæmorrhage, anæmia, diarrhœa, diuresis, excessive milk
secretion, gestation, embolism. Symptoms: constant excessive
dilatation of pupil, no response to light, brilliant reflection from
retina and choroid, blue or yellow, (glass eyes); bilateral, cerebral,
tract or chiasma; unilateral, bulbar or nervous; face without
expression, ears alert, head to one side, nose elevated, nostrils
dilated, ox and dog smell ground, slow pace, high stepping, does not
dodge a feint to strike. Lesions: inflammatory exudate and retinal
atrophy, congested, “woolly” papilla, retro-bulbar congestion or
atrophy of nerve, thickening of neurilemma, tumors of orbit or foramen
optica, cœnurus, cysts, abscesses, cholesteatomata, psammomata,
hydrocephalus, meningitis, pineal hypertrophy, cranial fractures or
tumors, embolisms or aneurisms, hypertrophy of dura, apoplexy.
Treatment: remove causes, laxatives, diuretics, for lead, sulphuric
acid and potassium iodide, darkness, extract cœnurus, elevate
depressed fractures, ice, cold snow, to head, blisters, setons,
electricity, strychnia, remove tumors.

Blindness without adequate, corresponding, visible changes in the
structure of the eye, has long been recognized in the lower animals,
having been observed in horses, dogs, cattle and sheep. When partial it
is known as amblyopia, and when complete as amaurosis or blindness. The
term amaurosis is, however, being gradually eliminated from
ophthalmological nomenclature in favor of that of atrophy.

_Causes._ These may be factors which act directly on the retina, as the
intense light of the sun, of an electric, lime or magnesium light, of
the reflection from snow, ice, water, sand, or white dust. These exhaust
the power of vision by over-stimulating it, but whether the blindness is
due to fatigue of the retina or of the cerebral ganglia which preside
over sight, it is difficult to decide. This form is much more likely to
occur in horses which spend most of their time in darkness, as in
unlighted stables or mines, when they are suddenly brought into the
sunlight. Snow blindness, however, from prolonged exposure, is common in
animals as in man, and the case of the staghound reported by Johan, is
by no means an isolated one.

Much more common are factors which act primarily on the nerve centres.
Poisoning with lead, poppy, belladonna (sheep and goats, Gerlach),
lolium temulentum (Klüver), tobacco, carbon bisulphide, cryptogams
(musty fodder), mushrooms, astragalus mollissimus, etc., abolishes
vision more or less perfectly. Common illuminating gas and carbon
monoxide have shown this effect on dogs and chickens. Quinia subcutem
has induced the condition in dogs (Becker and Eversbusch). More or less
complete amaurosis is noticed in connection with heat apoplexy in horses
and fat cattle.

Cerebral concussion from blows on the head, knocking the head against a
post or wall, or from violent falls induce blindness which is to be
attributed rather to lesion of the brain. The same remark applies to
cases that appear during the progress of brain disease, parasitic or
otherwise, to those that occur in connection with overloading of the
stomach or intestines, and from gestation (Riss).

In cases appearing after severe depletion, like profuse hæmorrhage,
diarrhœa, or diuresis, or excessive secretion of milk (bitch), the
anæmia of both eye and brain may be taken into account.

When amaurosis develops during some inflammatory or infectious disease,
as in parturition fever in cows, the immediate cause may sometimes be
found in embolism of the retinal, or cerebral arteries.

_Symptoms._ The most striking feature of amaurosis is the constant
excessive dilatation of the pupil. This is the same in light and
darkness, and in fully developed cases the animal may be taken from
perfect darkness to the full glare of sunlight or electric light without
the slightest contraction of the pupil. The pupillary reflex to light is
entirely lost. In the slighter cases (amblyopia) there remains some
slight response of the iris to light but always far short of the normal.
The widely dilated pupil admits a flood of light, and in the absence of
cataract, lights up the chamber of the vitreous to an unusual degree.
The blue or yellowish reflection of the tapetum is very striking, and
led to the obsolete names of gutta serena and glass eyes. Sometimes the
disease is unilateral and at others bilateral. In case it is unilateral
there is a strong presumption that the causative lesion is in the
affected eye or in the optic nerve in front of the chiasma. In the
bilateral cases it is more likely to depend on disease of the brain or
some more distant organ.

Certain important indications are to be drawn from the expression of the
face, the position of the head and ears and the mode of locomotion. In
all blind animals the face is without expression. The dilated pupils
give no suggestion of mind looking through them, they have on the
contrary an uniform stony stare. There is no sense of fire or life, but
the face is like a dull sculptured mass. The immobile face finds a sharp
contrast in the alertness of the ears, which may be carried one forward
and another back, but fixed and yet ready to turn to catch every sound.
In the horse the head is usually carried a little to one side for the
same reason, and with the nose elevated (_star-gazer_) and nostrils
dilated. The ox inclines to carry the head low, while the dog keeps his
nose near the ground to guide himself by the sense of smell. All blind
animals are disposed to move slowly and carefully, and the horse
acquires a habit of _high stepping_ to avoid stumbling.

A common and important test where both eyes are equally affected and
cannot be contrasted with each other, is to strike the lower part of the
face with the hand and immediately threaten to repeat the blow. If the
animal can see, it will seek to jerk the head out of the way as soon as
the hand is raised for the second blow, while if blind there will be no
such movement provided the motion of the hand has not been such as to
induce a current of air on the face.

_Lesions._ Blindness, or the general symptoms of amblyopia or amaurosis,
may attend on the atrophy of the retinal fibres in connection with
inflammatory exudation or blood extravasation on, in, or beneath, the
retina. In other cases the lesion is in the papilla which is inflamed
and swollen with the woolly aspect characteristic of choked disc. In
others there is congestion of the optic nerve behind the bulb, with
exudation into its substance or beneath its sheath, or the nerve has
already undergone extensive atrophy with thickening of its neurilemma.
In other cases there is atrophy of the arteria centralis retinæ, or
tumors of the orbit or optic foramen pressing upon the nerve. Cases of
this kind are reported in the larger animals by Leblanc and Tscheulin,
and in dogs and ducks by Hilbert.

Much more frequently the determining lesions are situated in the brain
or its meninges. In sheep it is very common from the development of
cœnurus cerebralis over the optic lobes. Kühnert found a cyst with
delicate walls in the brain of a horse affected in this way. Amaurosis
is occasionally seen in connection with the cerebral abscesses which
form in complicated cases of strangles or in pyæmia, also in cases of
cholesteatoma of the choroid plexus. Other conditions of its occurrence
are hydrocephalus, meningitis, hypertrophy of the pineal gland, fracture
of the cranium, tumors of the cranium or dura mater, embolism or
aneurism of the cerebral arteries, hypertrophy and induration of the
dura mater (ox, Leblanc), or sanguineous apoplexy. In a certain number
of cases there may be no lesion of brain or eye, or only a congestion of
the former in connection with lead poisoning, rye grass poisoning or
other gastric disorder, or of gestation.

_Treatment._ Success will depend on the sympathetic nature of the
condition or on the transient and removable character of its causative
factor. When the condition is but a symptom of overloaded stomach or a
transient poisoning by vegetable or mineral agents a direct recovery may
be expected to follow their disuse and elimination from the system. This
may be hastened by the exhibition of laxatives and diuretics, and in the
case of lead by sulphuric acid followed by iodide of potassium. In cases
of snow blindness it is only necessary as a rule to place the animal in
the shade until the over-stimulation shall have subsided. In all these
cases the attack has come on abruptly and without any local symptom of
ocular hyperæmia and this with the preservation of the general senses
can always be looked on as a favorable indication.

In cases that come on slowly and which are accompanied by symptoms of
vascular disturbance or structural changes in the eye, or brain,
treatment is likely to be less successful. Nevertheless cœnurus may be
removed by surgical means, depressed fractures may be elevated, and
acute cerebral and meningeal congestions may be met by appropriate
measures. If the cerebral congestion is acute, free bleeding from the
jugular with a strong purgative and the application of ice or cold water
to the head may prove useful. Apparent benefit has also followed the use
of blisters on the face or back of the ear, of setons, and later of a
weak electric current and strychnia. Tumors also may be advantageously
removed.

But in cases marked by destruction of the retina or papilla, by
congestion or atrophy of the optic nerve, by destructive disease of the
optic foramen, or of the brain or its meninges, treatment is futile.

ANOPHTHALMOS. ATROPHY OF THE EYEBALL. PHTHISIS BULBI. MICROPHTHALMOS.

In some cases the eye is congenitally absent (_Anophthalmos_). In others
it is abnormally small. One such case came under the notice of the
author in which the eyeball was represented by a small black sphere
about half an inch in diameter moved by the ocular muscles. The dam of
the filly, born with this defect, had, during the pregnancy, a burdock
entangled in the forelock and causing a violent ophthalmia which was
supposed to have lasted for months. In other cases there is a fistula
opening from the vitreous behind.

Cases of wasting and atrophy of the eye follow on exudates into the
vitreous and their subsequent contraction, or on suppuration and
granulation as noted under _internal ophthalmia_, _recurrent
ophthalmia_, and _panophthalmia_. The condition may also result from
atrophy or degeneration of the optic nerve or of its cerebral ganglia
(thalamus, corpora quadrigemini, geniculata, etc.). These conditions are
irremediable.

LUXATIO BULBI. DISLOCATION OF THE GLOBE OF THE EYE.

Definition. Dog, anatomical factors. Symptoms: protrusion of bulb
through palpebral orifice, orbicular spasm, vessel, muscle, nerve
stretching or tearing. Sphacelus. Panophthalmia. Fracture of orbit.
Treatment: early reduction, antisepsis, astringents, scarify sclera,
cold, astringents, puncture aqueous with hypodermic needle, enlarge
palpebral opening, suture and compress, remove foreign bodies and
injurious fragments of tissues, enucleation.

_Definition._ Displacement of the globe of the eye out of the orbit and
through the eyelids.

_Causes._ Among domestic animals the condition is most frequently seen
in the dog, which is predisposed by reason of the normal prominence of
its eye, the width of the aperture between the lids and the absence of
the orbital process of the frontal bone. Blows upon the region and the
insertion of pointed bodies, (teeth, horns, etc.), which can act as
levers using the margin of the orbit as a fulcrum are especially liable
to cause the lesion. Dog fights are the most common occasions. Other
animals may also suffer but not at all frequently.

_Symptoms and lesions._ In the simplest form the bulb is displaced
forward out of the orbit and through the palpebræ which latter contract
spasmodically behind it and effectually prevent a spontaneous reduction.
The optic nerve, muscles, and vessels are unduly stretched and the
circulation in the bulb is seriously impaired, so that even in the least
complicated cases any undue delay in reducing the dislocation will lead
to serious and destructive changes in the eye. Sphacelus of the globe is
not uncommon under such conditions.

In the more complicated cases, the conjunctiva, palpebræ, nictitans,
muscles, nerves, etc., maybe more or less lacerated and the globe itself
may be seriously damaged either by internal lesion or by an external
trauma. In all these cases there is most imminent danger of general
infective inflammation of the eye, of panophthalmia, and even of
secondary general infection of the system. Fracture of the bones of the
orbit may also be looked for.

_Treatment._ When dislocation is uncomplicated and recent, say of a few
hours standing only, it may be reduced and a favorable issue secured.
The bulb should be first washed with water which has been sterilized by
boiling or rendered antiseptic with sublimate (1 ∶ 5000), and can
usually be pressed back by steady uniform pressure. The insertion under
one lid of a small spatula bent at the end or the one limb of a lid
speculum may assist in difficult cases. When replaced the parts may be
again washed with antiseptic solution and covered by a bandage wet with
an astringent collyria.

When the condition has been neglected for a day or more the bulb is
congested and swollen so that its return is rendered much more
difficult, and its subsequent retention may require much care and
ingenuity. The reduction of the turgid globe may be assisted by opening
the veins and arteries on the sclera, by astringent applications, by
massage, and in obstinate cases by evacuation of a portion of the
aqueous humor, by the aid of a fine aseptic needle. Finally the
palpebral opening may be enlarged by incising the outer canthus with a
probe pointed bistuory. When the eye has been replaced in its socket
this must be closed by suture. For the retention of the eye in such
cases a bandage may suffice, or this failing, the lids may be held
together by strips of adhesive plaster, or by collodion. In very
difficult cases Lafosse and Trasbot recommend sutures through the skin
1½ to 2 inches from the palpebral borders and the whole covered with a
bandage impregnated with an antiseptic and astringent collyrium.

It is not requisite to keep the bandage in position for over four or
five days as the swelling of the eyelids and other adjacent structures
effectually prevents any tendency to repetition of the luxation, and the
eye may be treated like an ordinary traumatic lesion.

At the outset, and later if need be, any foreign body in the orbit
should be removed and any detached pieces of bone which cannot be
retained firmly in position, and which are liable to prevent healing or
to determine infection of the wound.

In the worst cases and in those that have been neglected until gangrene
or panophthalmitis threatens, the removal of the eyeball may be the only
resort. The animal may be anæsthetized by chloroform or ether, or
locally by cocaine. The conjunctiva covering the sclera is then pinched
up with forceps and cut through with scissors, this is continued all
around the globe. Then the recti muscles, the superior and inferior
oblique muscles, the retractor and finally the optic nerve are cut
through with a pair of scissors curved on the flat. The divided ends of
the muscles are now sutured together around the nerve which has been cut
shorter, and the cavity irrigated by a cold antiseptic solution.
Bleeding vessels may be twisted through with forceps if the flow is not
readily checked by cold irrigation. Or a pledget of cotton dipped in
tincture of muriate of iron may be loosely inserted (firm pressure would
be unnecessarily painful). As a subsequent dressing, standard sulphurous
acid solution, glycerine and water in equal proportions, or other
antiseptic dressings may be applied.

ARTIFICIAL EYE.

These are largely in use in the human being, and have been employed in
the lower animals in different cases, especially in the horse, with
excellent effect. The advantages may be summed up in this, that they do
away with the unsightly appearance of an empty orbit with the edges of
the lids turned into the dark aperture, enhance the value by restoring
the face to nearly the natural appearance, and prevent the lodgment of
dust and insects in the cavity.

The artificial eye may be made to appear more natural if made of glass,
yet when made of horn or still better of hard rubber, colored like the
normal iris and pupil, it has the advantage of greater lightness. It
must be perfectly smooth so as to cause no discomfort, and should never
be introduced so long as there is any irritation in the stump or
conjunctiva. It may be slipped in like a button, first beneath the
deeper upper lid, and then beneath the lower, and should be worn only
while at work and so long as it causes no irritation nor purulent
discharge. On the return of the animal to the stable, the artificial eye
is taken out, washed and placed in clean pure water. The orbit should be
sponged out with a weak collyrium (boric acid 1 ∶ 100).

In man, excentration is sometimes substituted for enucleation, the
cornea is removed together with the lens, vitreous, choroid and retina,
leaving only the sclera which contracts into a dense scar tissue with
the muscles attached. Or an artificial vitreous of glass or unoxidizable
metal is introduced around which the sclera is allowed to heal. This
introduces an additional element of danger over the formation of a
simple sclerotic stump, but, when successful, it affords a better
support to the artificial eye, turning it freely in harmony with its
fellow and giving it a more natural aspect.

STRABISMUS. SQUINTING. LACK OF MUSCULAR BALANCE.

Causes: paralysis of eye muscles, bulb rolls from affected muscle,
spasm of eye muscles, bulb rolls toward affected muscle, convergent
squint most common. Hold head still and move object in front of eyes,
imperfect movement toward paretic muscle or away from the spastic one.
Ptosis. Overfatigue. Debility. Nerve or brain lesion. Dislocation of
bulb. Treatment: treat any transient etiological factor, cerebral
congestion, parasitisms, debility, anæmia. Tenotomy of rectus: advance
of paretic rectus.

Strabismus may be due to a variety of causes, among others to the
following:

=Paralysis= of one of the ocular muscles. When the eyes are turned in
the direction away from the affected muscle the muscle is deficient in
power. It may be the external rectus (abducent nerve) producing
convergent squint. It may be of the superior oblique muscle (4th or
pathetic nerve) causing a faulty movement of the eye downward and inward
or a slightly convergent squint. Divergent squint commonly indicates
paralysis of upper, lower and inner recti, and the inferior oblique (3d
or oculo motor nerve): this is usually associated with ptosis or
drooping of the upper lid, the levator of which is supplied by the same
nerve. The existence of squint is usually so marked that no special
method of examination is required. If otherwise, however, the animal’s
head may be held still and some object which will attract his attention
is moved before the eyes, outward and inward, when the affected eye
moving in the direction of the paralytic muscle will lag visibly behind
its fellow. These conditions are usually due to lesions in the
respective nerves or their cerebral ganglia.

=Spasmodic or Spastic Squint= is the exact antithesis of the above, the
eye turning toward the muscle which is the seat of spasm. It may be seen
in certain cases of rabies and is always due to disorder of the central
nervous ganglia.

In some cases squinting is associated with over-fatigue, or debility,
and then usually partakes of the paralytic character.

In the lower animals convergent strabismus has been most frequently
observed. Brouwer records a case in the horse and Koch a congenital one
in the cow. Zschokke reports a case in the cow connected with an angioma
at the base of the brain. Other forms are noted by Peters, Barrier,
Bayer and others. Stockfleth quotes a case in the dog following
prolapsus bulbi and doubtless connected with injury to ocular muscles or
nerves, sustained in the accident.

_Treatment_ will vary with the ascertained cause. As a rule cases that
depend on structural changes in the brain are hopeless. Those that
depend on temporary congestion or other transient disorder of that organ
may recover when that has been overcome. In cases in which debility is a
prominent feature, tonics, moderate exercise in the open air and general
hygienic care are demanded. The final resort in bad cases is tenotomy of
the rectus on the side toward which the eye turns. In man when this is
found to be insufficient the opposing weak or paretic muscle is also
advanced. The tendon close to its sclerotic attachment is laid bare by
incision, and a silk or catgut thread is passed through each border,
upper and lower. The tendon is now cut through with scissors on the
corneal side of the sutures and, by means of their needles, the latter
are passed through the conjunctiva and capsule of Tenon, from within
outward and close to the margin of the cornea. The sutures are now tied
somewhat tighter than is absolutely necessary to properly balance the
eye so as to allow some room for relaxation in healing. We are not aware
that this measure of advancement has been employed in the domestic
animals.

NYSTAGMUS. OSCILLATORY MOVEMENT OF THE EYE.

This consists in spasmodic involuntary oscillation of the eyeball in a
horizontal, lateral, oblique or rotary direction. In animals it has been
seen in connection with poisoning and brain diseases. Johné has observed
it in horses in cerebro-spinal meningitis, Wenderhold in epilepsy, and
Möller in chloroform anæsthesia. Möller has further seen it in puppies
with congenital microphthalmos, and Siedamgrotzky in swine which had
been poisoned by herring brine.

Slight cases of functional disturbance may improve under good hygiene,
open air life and tonics, cases due to poisons may recover spontaneously
when such poisons have been eliminated, but those which depend on
structural disorder of the brain are beyond remedy.

DISEASES OF THE SKIN.

Ultimate skin lesions in man and animals similar. Masked by thick
cuticle, pigment, hair, fur, feathers. White, hairless skin. Lesions
and deranged functions: Maculæ, erythema, papules, nodules, blisters,
blebs, pustules, boils, carbuncles, scales, crusts, sitfasts, horny
growths, erosions, abrasions, chaps, fissures, ulcers, excrescences,
cicatrices, neuroses, morbid secretions, changes in glands, hairs, in
derma. Scleroderma. Elephantiasis. Vegetable and animal parasites.

In cutaneous diseases in man and animals the actual lesions are largely
of the same nature, yet in the animal covered with hair, fur or
feathers, and with the cuticle deeply pigmented, the diagnosis of the
different affections becomes much more difficult. On white-skinned
animals and on parts with little or no hair, the identification of the
different forms is usually possible. The following list may serve to
indicate the nature of the different lesions, but these must not be
accepted as indicating distinct diseases, as two or more of these forms
often coexist or succeed each other in the same affection:—

1st. =Maculæ: Spots: Discolorations.= Examples: Black, melanotic spots
in skins of white horses: white spots in dourine, after pustules, etc.:
ecchymosis after contusions, stings, insect bites, etc.: petechial spots
in anthrax, rouget, hog cholera, rinderpest, canine distemper, swine
plague, scurvy, etc.

2d. =Erythema: Rash: Flush.= Congestive redness usually disappearing
under pressure. _Physiological_ in blush or glow of exercise,
_pathological_ from insolation, friction, deranged innervation, etc.

3d. =Papulæ: Papules: Pimples.= Small, red, hard, conical elevations,
not forming blister nor pustule. Due to exudation and the accumulation
of leucocytes at given points, having a local or general cause,
(psoriasis, intertrigo, etc.).

4th. =Tuberculæ: Nodules.= Larger but still circumscribed thickening of
the entire skin from exudation and cell growth, from ½ inch to 2 or more
inches in diameter and sometimes becoming confluent. Examples: Urticaria
(surfeit) in solipeds, and cattle; petechial fever, farcy, etc.
Sometimes chronic.

5th. =Vesiculæ: Blisters.= Rounded or conical elevations the size of a
millet seed to a pea, and having a small liquid exudation under the
cuticle in the centre. In inflammations of the papillary layer, of a
sufficiently acute type the tendency is to the formation of vesicles.
These lesions are, therefore, often present in very different forms of
skin disease from those due to simple thermic irritation, to
constitutional diseases like eczema, or contagious ones like sheep pox.
May merge into pustules or other advanced lesions.

6th. =Phlyctenæ: Bullæ: Blebs.= In these the individual lesion is larger
than in vesicles. They are of any size from a pea upward. The most
striking example is in cantharides, blisters, scalds and burns, but in
other cases it depends on a constitutional condition or a specially
exudative dermatitis.

7th. =Pustulæ: Pustules.= These differ from vesicles in that the central
exudate becomes the seat of suppuration and a limited collection of pus,
at first central, though later involving, it may be the whole area of
the exudate. It is often merely an advanced stage of the papule or
vesicle. We find examples in the different forms of variola, in lesions
caused by tartar emetic or croton oil, and in several forms of
dermatitis. It is essentially microbian.

8th. =Furunculus: Furuncle: Boil.= Inflammatory nodosity of the derma,
resulting in a necrotic central core and suppuration. Is bacteridian and
common on the coronet and lower parts of the limbs in solipeds.

9th. =Carbunculus: Carbuncle.= An inflammatory nodosity or cluster of
nodes of much greater extent, tending to necrotic change and sloughing
over a much more extending area. Microbian.

10th. =Squama: Scales: Dandruff.= Exudation products and cells dessicate
and exfoliate as branlike scales or thicker coherent laminæ. Examples
are found in psoriasis, pityriasis, eczema, variola, rinderpest, etc.

11th. =Crustæ: Crusts: Scabs.= Hard, solidified masses of epidermis,
blood, pus and serous exudate.

12th. =Callositas: Callosity.= Abnormal thickening of the epidermis, as
a physiological protective cell growth. Examples: pads on the knees of
camels, cows and even horses from kneeling on a hard, uneven surface.

13th. =Sitfasts: Necrotic Callosities.= Combination of dried up exudate
of horny consistency, and a thickened, fibroid and partially necrotic
portion of the subjacent derma with little or no disposition to
spontaneous detachment.

14th. =Cornu Cutaneum: Keracele: Horny Growth.= Abnormal horny growth
from keratogenous tissue, or from the derma in its vicinity or at some
other point of the skin.

15th. =Erosions: Abrasions.= Lesions of the cuticle exposing the true
skin, and the result of itching, scratching, friction, biting or other
mechanical or thermic injury.

16th. =Rimæ: Cracks: Chaps.= These are linear breaches often confined to
the epidermis in the bends of joints, under congestion and suppression
of sebaceous secretion, in elephantiasis, dropsy, petechial fever, etc.
Unless they have ulcerated they may heal without cicatrix.

17th. =Crevasses: Fissures.= These are chaps, which extend into the
derma, giving rise to destruction of tissue and leaving a cicatrix on
healing. Examples are found in the hollow of the pastern, behind the
knee (Mallenders), in front of the hock (Sallanders), in the swellings
of petechial fever, malignant catarrh, stocked legs, grease, etc.

18th. =Ulcus: Ulcer.= A sore that extends by the continual molecular
breaking down of the forming granulations and of the adjacent and
subjacent diseased tissue.

19th. =Excrescences: Hyperplasiæ: Phymata: Dermatomata.= These may
include over luxuriant granulations which rise above the level of the
skin and become organized into projecting fibro-cellular, raw or scabby
masses: tumors of all kinds—warty, papillomatous, horny, epidermic,
cancerous, sarcomatous, pigmentary, angeiomatous, tuberculosis, etc.

20th. =Cicatrices: Scars.= These are puckered, raised or sometimes
depressed, lines or areas of condensed connective tissue with a covering
of epidermis, taking the place of the normal dermis and epidermis and
their appendages, which have been destroyed. They result from traumatic,
ulcerous, or atrophic destruction of the skin.

21st. =Neurosis.= These may be exemplified by the intense itching of the
skin without appreciable structural change. So in cutaneous anæsthesia
and hyperæthesia.

22d. =Modified Secretions.= These include absence of
perspiration—anidrosis, excessive perspiration—hyperidrosis,
suppressed sebaceous secretion—asteatosis, excessive sebaceous
secretion—steatorrhea or seborrhea, fœtid sweat—bromidrosis, colored
sweat—chromidrosis, _urinous sweat_—uridrosis.

23d. =Structural alterations in glands and ducts.= Cystic
ducts—hydrocystoma, blocked ducts—acne, inflamed glands—hidrosadenitis.

24th. =Abnormal conditions of the hair.= This embraces baldness,
hypotrichosis, alopecia, excessive growth of hair, hypertrichosis, white
patches, canities, nodular hairs, piedra, brittle hair, fragilitas
crinium, felted hair, plica, trichoma.

25th. =Scleroderma.= Hard, leathery, thickened skin. Examples in old
boars on shoulders, and in other animals.

26th. =Elephantiasis Pachydermia.= Enormous hypertrophy of the skin,
with usually distention of the lymph plexuses and vessels
(lymphangiectasis: see Vol. I).

26th. =Vegetable parasites.= Trichophyton, achorion, microsporon,
actinomyces, etc. (See parasites).

27th. =Animal parasites.= Lice, fleas, diptera, trombidium, Acari,
ixodes, cimex, filaria, coccidia, etc. (See parasites).

GENERAL CAUSES OF SKIN DISEASES.

External. Internal. Traumas, abrasions, excoriations, lacerations,
contusions, compression, radiating heat, scalding, incandescent
objects, solar heat, chemical caustics, cold, freezing, kicks, bites,
tusk horn or claw wounds, stings, venoms, envenomed bites, road dust,
sweat, excretions, sebum, mineral and vegetable poisons, essential
oils, fungi. Hyperæmia, exudation, depilation, sudation, moulting,
climatic changes, unwholesome or irritating foods, ptomaines,
alimentary fermentations, hepatic, renal or blood disorders, altered
innervation, youth, age, temperament, heredity. Experimental nervous
cases.

These may be =external= or =internal= or both.

=External Causes.= Some affections of the skin are due to external
causes exclusively, while in others the local cause of irritation is
accessory but no less important in maintaining the trouble. Among the
more prominent external factors may be named: traumatisms, abrasions,
excoriations, lacerations, contusions, compression, radiating heat,
boiling water, hot or incandescent solids or liquids, solar heat,
chemical caustics and irritants, cold, freezing, injuries by harness,
kicks, lacerations with teeth, tusks, horns or claws, stings, bites,
(leeches, snakes, etc.), venoms, (snake, toad, etc.), road dust and
sweat, liquid fæces or urine, excess of sebum in sheath or vulva,
mineral poisons (mercurial, iodides, bromides, arseniates, caustic
alkalies, caustic salts, etc.), vegetable poisons (croton, bryonia alba
and dioica, heracleum or cow parsnip, polygala or milk wort, cyclamen or
sow bread, polygonum hydropiper, mustard, œnanthe, cicuta, hypericum
perforatum and androsaemum, rhus toxicodendron, radicans and venenata,
capsicum, pepper, radish, Indian syringa, anemone nemorosa and patens,
ranunculus acris, scelerata, flammula, mericatus and bulbosus, cytisus,
euphorbium and the essential oils of turpentine, origanum, lavender,
etc.), fungi of musty food, ergot, etc.

=Internal Causes.= Among these are all conditions that induce stasis in
the capillaries or lymph vessels, active hyperæmia, exudation,
depilation, profuse perspiration, shedding the coat, exposure to cold,
chill, etc., sudden access of warm weather, poor and insufficient or
rich, stimulating food, cotton seed meal, indian corn, buckwheat, purple
clover, animal food (in dogs), spiced food, food spoilt by wet and
cryptogams, indigestions, gastric and intestinal fermentations, hepatic
disorders, renal disorders with imperfect elimination, blood disorders,
and nervous disorders which entail vaso-motor changes. Early age
predisposes to some affections (variola, warts); old age to others
(eczema). A nervous temperament in horses favors the drier eruptions
(pityriasis), a lymphatic temperament the exudative (grease, canker,
moist eczema). A hot, moist season favors most skin affections (eczema,
acariasis, etc.), dry insolation others (erythema) and cold still others
(chillblains, frost bite, chaps, etc.). Some eruptions are at first
summer troubles, disappearing on the advent of cold weather, yet in time
the predisposition increases, or the inflamed skin becomes less
resistant and the disease becomes permanent. A marked predisposition in
certain animals, appears to inhere in the constitution and proves
hereditary in the family (Blain, Lafosse, Cadeac). Nervous causes have
not been satisfactorily traced in the lower animals, yet the dermatitis
of the face and neck caused by the experimental lesion of the cervical
sympathetic or its connecting ganglia shows clearly enough how any
portion must be affected by disorder of its trophic or vaso-motor
nerves. Charcot found that experimental lesions causing inflammation of
the spinal cord, led to trophic changes and finally gangrene of a
corresponding part of the skin. Babesiu and Israï injected oil of
mustard in one side of the cord, in three dogs, and found in several
days a vesicular eruption and atrophy of the skin on the same side, a
result they supposed of the myelitis.

DIAGNOSIS OF SKIN DISEASES.

Diagnosis. Clip or shave skin. Examine in warmth: skin and mucosæ,
where uninjured by rubbing, moisture, dryness, color, odor, discharge.
Soapy wash. Exudation into skin: pliancy: rigidity: eruption:
tenderness, itching, history, association, feeding, watering,
exposure, housing, harnessing, driving. Coincident disease. Prognosis.
Microbian dermatosis, parasitic dermatosis, external irritants,
ingested irritants, toxic systemic products, constitution, renal
disease, movement of joints, harness.

The thick hairy covering of animals, and the vicious energy with which
they often rub, scratch and bite themselves, thus turning simple into
extensive and severe lesions, interfere seriously with a satisfactory
diagnosis. The following precautions are usually demanded:

1st. Clip the animal close to the skin to allow of careful examination.
In some affections, this may be dispensed with, but as a rule it should
be followed. What appears to be a circumscribed eruption may be shown to
be general, or at least extensively diffused over different regions. Or
what was shown only by scurf or scab may be seen in its earlier and more
characteristic stage as erythema, papule or vesicle. It may even be
desirable to shave the affected part, care being taken, not to slice off
the characteristic papules, etc.

2d. Make the examination in a clear day in full sunshine if possible. In
dark, cloudy weather, and in dimly lighted stables it is impossible to
identify the different lesions. Artificial light is very unsatisfactory.
Warmth, as in sunshine, or in a warm day or room, increases any itching
and the cutaneous circulation and congestion, and renders more lively
and active the animal parasites that may be present. These may be found
in the surface scrapings taken in warmth, and not at all if taken in
cold. A hand lens will assist in the discovery of the larger parasites,
while for the smaller ones the microscope must be employed.

3d. Examine carefully all parts of the skin and even the visible mucosæ,
estimating whether any lesions of the latter indicate extension from the
skin, by proximity, or a general constitutional affection. Scrutinize
particularly such parts as have not been abraded by mechanical
injury—those which show the primary character of the lesion. Is the
affected portion of the skin dry or moist? Some eruptions like impetigo
or grease are always moist, others like pityriasis or dry eczema are
habitually dry apart from mechanical injuries. Ascertain the color, odor
and consistency of any discharge. It may be a limpid or reddish serum in
grease, honey like in impetigo, oily in farcy, greasy in swine plague.
The odor is fœtid in grease, canker and thrush of the frog, cheesy in
variola, and mousy in favus.

4th. To learn the true nature of the eruption a warm, soapy wash may be
essential to remove scurf, scab, and other encrustations.

5th. Note the depth and extent of the skin lesions, the thickening of
the skin, its pliancy or rigidity, its adhesions to subjacent parts or
free movement upon them, whether it is contracted into folds or ridges,
the degree of congestion, the nature of the eruption, uniform congestive
redness, papule, vesicle, pustule, squama, sore, ulcer, nodule, slough,
etc. Are the individual lesions isolated or confluent?

6th. The presence of itching and its degree are important data. Pruritus
is always excessive in ordinary acariasis, marked in eczema,
phthiriasis, and some neuroses, and very slight in a number of skin
affections (pityriasis, ringworm, grease, thrush, contagious acne). The
abrasions and sores caused by rubbing, scratching, etc., will usually
give a key to the degree of pruritus, and handling the part will render
the condition evident.

7th. The history of the case is always important. Is it chronic or
acute? Continuous or intermittent? Associated with any special
conditions of proximity to other diseased animals, to special feeding,
watering, exposure, housing, harnessing, driving, which might account
for it? Did there coincide with its eruption any indigestion, gastric or
intestinal, or any hepatic, urinary or nervous disorder on which it
might be dependent?

_Prognosis._ This is subordinate to the nature, causes, course, duration
and complications of the disease.

=Microbian dermatosis= (variola, aphthous fever, rouget) usually follows
a rapid course and recovery is perfect with some measure of immunity.

=Parasitic dermatosis= (acariasis, phthiriasis) is liable to have
serious secondary results (infection to man or animals, loss of wool,
tender skin), and to run a chronic course.

=Maladies from external irritants= (chafing, caustics, traumas,
vegetable, or animal irritants), do not tend to chronicity and are often
promptly curable.

=Maladies due to ingested irritants= (urticaria, distillery waste
eruptions), also tend to recovery when the source of irritation is cut
off.

=Maladies due to toxic products of the system= will be obstinate or
incurable, in ratio with the incurability of the causative factor. Those
due to the absorbed products of a simple indigestion, will tend to
terminate with the removal of the cause, while those dependent on
chronic and perhaps irremediable disease of the digestive organs, liver,
or kidneys will be correspondingly inveterate or incurable.

=Maladies due to a constitutional vice=, in sanguification, nutrition,
innervation, etc., are likely to be irremovable or only temporarily
curable.

=Burns and some other skin diseases= are liable to become complicated by
renal embolisms, albuminuria, indigestions, etc., which may render the
skin affection inveterate or incurable.

=Dermatitis= on the folds of articulations or on the seats of harness,
are sustained by the local irritation, and may necessitate long rest, or
abstention from work requiring the use of such harness.

All dermatites are liable to show special features of inveteracy, or
amenability to treatment according to surrounding conditions—hygienic or
otherwise.

GENERAL PRINCIPLES OF TREATMENT OF SKIN DISEASES.

General and local. Diet: wholesome diet following laxative:
restricted, generous, vegetable. Rest, avoiding congestion,
perspiration, friction, stretching, pressure. Cleanliness. Diuretics.
Purgatives. Tonics. Alteratives. Sulphur. Antimony. Phosphorus.
Calcium sulphide. Pilocarpin. Baths, tepid, warm, soapy, alterative.
Emollients, simple, medicated. Drying powders. Protective films.
Stimulating and antiseptic applications. Parasiticides. Caustics.
Counter-irritants. Bandages.

These must be general and local, and the first hygienic, dietetic and
medicinal.

The =diet= is especially important in eruptions due to poisons such as
green food, distillery refuse, silage, roots, ergoted or smutty food,
musty fodder, irritant plants in hay or grain feed, buckwheat, etc. In
many cases a change to sound fodder and a laxative to clear the
alimentary canal of the irritant, may be all that is required. In cases
where the feeding has been parsimonious, a judiciously gradual change to
a generous diet may be required. Again when the feed has been unduly
rich, or spiced as in the patent food for stock or the table leavings
for dogs, a plainer, simpler and less exciting diet will be called for.
Indigestions, urinary and hepatic disorders due to diet may be often
corrected by a more judicious ration.

=Rest= is a most important element in horses and hunting dogs. When
pressure of the harness keeps up the irritation, or when active movement
reopens cracks in the tense rigid congested skin of the heel, carpus or
tarsus of the horse, the parts must be kept quiescent. When on the other
hand chaps and fissures are caused and maintained by _stocking_, the
patient may do much better with exercise. In skin congestions which are
aggravated by work and increased cutaneous circulation, rest is
imperative.

=Cleanliness= is no less imperative. Many cases are started and
maintained by filth on the skin and in the air of the stable and hence
sponging, currying, brushing, rubbing, are directly therapeutic. Yet
care must be taken to avoid irritation where the skin is tender. In the
sensitive heels of the horse congestion, chaps, and _stocking_ are often
determined by washing in ice cold water and leaving to dry uncovered, in
a draught of air, or by washing with common laundry soap having alkali
in excess. Even tar soap will sometimes keep up the trouble in a
specially sensitive skin. Apart from such exceptional conditions,
thorough grooming is commendable, not only in cleaning the skin, but in
improving its circulation and nutrition.

=Diuretics= are often beneficial in eliminating from the system the
irritant products generated from disorders in sanguification, digestion,
urinary secretion and hepatic function, as well as those that are
derived from the cutaneous disorder. They tend further to reduce any
existing fever, and to cool and relieve the burning integument. The
alkaline diuretics are often very useful.

=Purgatives= act in a similar way and are especially indicated in cases
due to ingested irritants, and in such as depend on morbid products of
gastro-intestinal or hepatic disorder. In many acute attacks these may
be said to be almost specific in their action as in urticaria, and in
the eruptions due to distillery products or green food.

=Tonics= are often called for to correct dyspepsias, to improve the
general health and vigor, the sanguification and nutrition in weak and
debilitated conditions. Iron, cod liver oil, bitters, quinia, quassia,
calumba, gentian, nux, are often of value in such cases.

=Alteratives.= =Arsenic= may be said to act as a tonic with a special
tendency toward the skin where it affects the epidermis and epidermic
products and is applicable to many subacute and chronic disorders, as
psoriasis, acne, dry eczema, and pemphigus. It has been further supposed
to be most useful in superficial lesions, and in those due to a neurotic
origin, from the known operation of arsenic on the nerves. It is little
suited to acute skin diseases, and though often valuable is not to be
trusted as universally applicable.

=Sulphur= is often useful as a laxative, but also as a stimulant to the
cutaneous secretions when these are impaired.

=Antimony= is similarly a cutaneous stimulant and is sometimes useful in
chronic inactive conditions.

=Phosphorus= has been found useful in obstinate cases and probably acts
on the nerve centres in improving nutrition of the integument.

=Calcium sulphide= is sometimes useful with free secretion from the
diseased surface, but its action is somewhat uncertain.

=Pilocarpin= operates by securing free secretion from the skin as well
as from the various mucosæ, and seems to benefit by elimination, as well
as by modifying the cutaneous functions and nutrition.

=Local Applications.= =Baths= may be placed foremost among these.
Cleanliness is a prime necessity in treating skin disease. Tepid or warm
water is especially required in acute disease in sensitive skins. In
chronic cases with accumulation of scabs a soap wash following a 24
hours inunction with oil or lard may be demanded, but as a rule castile
or other non-caustic soap should be used. In certain cases the baths may
be advantageously medicated, as with calcium sulphide, potassium
sulphide, salt, alum, tannic acid, tar, creolin, lysol, cresol,
chloro-naphtholeum, arsenic, mercury, etc. The water alone is, however,
of great value in soothing and moderating inflammation, softening and
dissolving scabs and epidermis, and relieving the dryness and rigidity.

=Emollients= are used for the same end as calmatives, and relaxing and
protective agents. Fatty bodies occupy a front rank, the bland vegetable
and animal oils being not only soothing but nutritive (cod, lard, olive,
cotton, almond, linseed, rape, pea nut, lanolin, neats foot and goose
oil). Care should be taken that these are pure and in no sense rancid.
Vaseline or petrolatum are free from the risk of rancidity, yet it
should be free from contamination unless a stimulating action is wanted.
Glycerine often used as an emollient has the disadvantage of drawing
water from the surface and of actually irritating some sensitive skins.
Glycerol made with glycerine and starch is more soothing. Glycogelatine
made with glycerine 5, gelatine 3, and water 9, is very emollient and
protective. This can be made the basis of astringent, sedative and
antiseptic preparations by adding zinc oxide, lead acetate, chrysarobin,
salicyclic acid, tannin, sulphur, oil of birch or of tar, etc. An
excellent emollient paste is compounded of zinc oxide and vaseline
one-half ounce of each, salicylic acid, ten grains. Oleate of lead is an
excellent sedative application in irritation or pruritus.

=Drying powders= are found in starch, talc, magnesia, zinc oxide,
lycopodium, bismuth oxide, boric acid, iodoform, aristol, salicylic
acid, tannin, and, above all, magnesia carbonate. A slight addition of
morphia sulphate will render them analgesic. Tar in zinc oxide or
bismuth will secure antiseptic and stimulating qualities.

=Protective films= for irritable surfaces may be had from collodion, or
from a solution of gutta percha in chloroform 1 ∶ 10 (traumaticin).

=Stimulating and antiseptic applications= are found in tar or oil of tar
in suitable excipient and of a strength suited to the case, oil of white
birch, oil of lavender, oil of cade, oil of cashew nut, oil of juniper,
oil of hemlock, Canada balsam, balsam of Tolu or Peru, creolin, lysol,
cresyl, creosote, carbolic acid, chloro-naphtholeum, etc. Ichthyol, of
great value in chronic affections, may be used in oil or vaseline (5 ∶
100), or in the form of Nuna’s varnish: Ichthyol 40, starch 40,
concentrated albumen solution 1 to 1½, and water 20. Add the water to
the starch, then rub in the ichthyol and finally the albumen. Resorcin
is a useful stimulant, alterative, and antipruritic (1 ∶ 30 alcohol and
oil).

As =antiseptics= and =parasiticides=, in addition to the above, are
alpha- and beta-naphthol, iodized phenol, chloral camphor (rub together
till they form a clear fluid), phenol camphor (add camphor gradually to
the melted phenol crystals), mercuric chloride, cupric sulphate and
silver nitrate. Potash (green) soap, medicated or not with tar or other
agent, is of great use in many chronic affections. The phenol
combinations are all more or less anæsthetic, and therefore sedatives
and antipruritic. Quassia, Stavesacre, tobacco, etc., are of great use
in parasitisms though not antiseptic. Sulphur fills both indications,
and is a bland generally applicable agent.

=Caustics= (silver nitrate, antimony chloride, electric or
thermocautery) are useful in luxuriant granulations, hyperplasias, and
often in excessive secretion, or on infected surfaces.

=Counter-irritation= over the vaso-motor centres, is often of value,
when the distribution of the eruption coincides with that of particular
nerves, and indicates a nervous element in the causation.

=Bandages= of various kinds may be demanded to afford support in
threatened dropsical effusion or excessive granulation or hyperplasia,
to protect the surface against outside infection, to confine volatile
applications to the affected part, and to prevent injury from biting,
licking, scratching, or rubbing.

For the same reason it may be desirable to employ a muzzle, beads on the
neck, tying to two opposite rings by short halters, hobbles, or other
means of restraint.

ERYTHEMA. ERYTHEMATOUS DERMATITIS.

Definition, congestion, heat, redness, tenderness without eruption.
Sheep: swine: dogs: white horses and cattle. Causes: slight irritants.
Symptoms: congestion momentarily effaced by pressure, may go on to a
distinct irruption.

_Definition._ Congestion of the papillary and adjacent layers of the
skin with heat, redness, and tenderness, or a diffuse superficial
inflammation with some superadded swelling.

_Genera susceptible._ The affection is seen in sheep, swine, dogs, and
in white horses and cattle or on white parts of the skin. It is not
readily recognized on pigmented parts.

_Causes._ The action of any slight irritant: pressure, friction,
brushing, currying, blows, vesicants, rubefacients, stings, parasitism,
radiant heat, intense sunshine, cold (reaction), storm, plunging in cold
streams when heated, feeding on stimulating agents, notably buckwheat.

_Symptoms._ On white skins there is a uniformly diffused redness,
without papule or other eruption, and the color may be momentarily
effaced leaving a perfectly white spot, made by the pressure of the
finger. The affected part is warm, tender, and it may be, itchy. It may
be but the first step of a distinct eruption of another kind, such as
variola, vesicles, papules, pustules, but then the affection takes a
different name. It has been named according to its seat, cause and
nature as follows:

INTERTRIGO. INTERTRIGO OF CHAFING.

Causes: friction, inside thighs, side of scrotum or mammæ, inner side
of elbow, between digits on clipped heels, under harness. Dried sebum,
sweat, dust, clay. Pricks with stubble. Symptoms: lameness on
starting, abduction, straddling, knuckling, steps on toe. Treatment:
abate cause, cleanse, rest, dusting powders, zinc, lycopodium,
magnesia, starch, bismuth, alum, lead, morphia, surgeon’s cotton.
Carron oil, vaseline, antiseptics.

This occurs where the folds of skin come in contact and rub on each
other as between the thighs or beside the scrotum, sheath or mammæ in
fat horses and other animals, on inner side of the elbow, between the
digits in ruminants, on clipped heels in horses, and under harness.
Irritant perspiration and sebaceous matter dried on, and mixed with more
or less gritty or septic road dust contribute to it. Drying of clay and
mud in the cleft of the frog, or in the interdigital space of ruminants
is a common cause, also pricking with stubble.

_Symptoms._ These are most marked when the animal has been standing with
the raw surfaces partially dried and adherent. After moving for some
time, and when the surface has been moistened by the exudate there may
be little lameness. Until then he moves hesitatingly and stiffly, with
the legs abducted or in case of the hind ones straddling. With
intertrigo of the pastern or frog, the horse stands on the toe or with
the fetlock knuckled forward, and avoids as far as possible a full
extension. The same is true of cattle with interdigital intertrigo.

The affected part is hot, perhaps swollen, red, damp and exceedingly
tender. Under renewed work, lameness disappears, but becomes worse on
standing, and an extensive exudation may occur subcutaneously. If this
becomes infected it may result in severe and even destructive lesions,
but it usually remains simple and proves readily responsive to soothing
and protective treatment. It is most amenable to treatment in dogs and
meat producing animals of which no work is required. On the contrary the
latter when travelled long distances on foot may suffer severely.

_Treatment._ First abate the cause. With castile soap wash from the
affected part the dried accumulations of sweat, sebum, dust and other
matters, remove clay from frog, interdigital space or heels. Rest until
the congestion and tenderness subside. Drying applications in the form
of dusting powders are usually best: zinc oxide, lycopodium, magnesia
oxide, may be dusted in freely after the affected part has been
thoroughly exposed and dried. In the absence of these use gloss starch,
corn starch, farina or white bismuth. To one or other of these may be
added a little alum, lead acetate or morphia. The addition of a layer of
surgeons’ cotton is useful, if in a place where it will be retained. Of
liquid applications the veterinarians white lotion (zinc sulphate and
lead acetate, of each 1 oz. water 1 qt.) is one of the best, being at
once sedative and astringent. It may be applied on cotton. Astringent
preparations with glycerine are useful but glycerine has the serious
drawback of attracting moisture and increasing the secretion when drying
is desirable. Carron oil (equal parts of lime water and linseed oil) is
most effective and free from this objection. Vaseline alone or medicated
with zinc oxide, lead acetate, alum or tannic acid may be resorted to
when dusting powders fail. Morphia and camphor have been added when
itching is violent.

In intertrigo of the frog or interdigital space the danger of infection
from the floor or road is so great that the demand for antisepsis must
overcome other considerations. Calomel freely applied to the surface,
previously cleansed and dried, is most successful. It may be bound in
place by a pledget of cotton and bandage. In other cases alum 5 parts,
copper sulphate 1 part, or carbolic acid and tar may be bound to the
part.

ERYTHEMA CALORICUM: SOLAR ERYTHEMA.
WHITE FACE AND FOOT DISEASE IN HORSES.

England to Africa, on white skins, especially of face. Symptoms: local
congestion, swelling, itching, desquamation, during extreme heat: in
worst cases fever, dullness, inappetence, costiveness, diarrhœa, head
constantly moving, rubbing, vesicles, pustules, excoriations, cracks,
fissures, septic ulcers in nose and mouth, submaxillary and pharyngeal
swellings, recovery with dermal thickening and tenderness. Diagnosed
from petechial fever by the itching, and the absence of petechiæ.
Prevention: breed solid dark colors, avoid white skinned in hot
climates or work in shade, away from hot winds; sunshade; avoid
friction and wetting in sunshine. Treatment: shade, astringents, cool
irrigation, vaseline, zinc ointment, lamp black, antiseptics. Tie so
as to prevent rubbing.

This has been observed in different latitudes from the cool climate of
Great Britain, to the burning suns of Africa, though it reaches its
highest intensity in the hotter regions. The parts to suffer are those
that are devoid of pigment, as the white star, snip or blaze on the
face, the white feet or legs, the white areas in the piebald, and the
whole surface in the albino. The white face, however, suffers more than
the white legs, apparently because of its more constant exposure, the
absence of shadow from the trunk, and the delicacy of the skin and
fineness and thinness of the hair.

_Symptoms._ In slight cases there may be no constitutional disorder,
only redness, itching, swelling and subsequent desquamation of epidermis
on the white portion of the skin, which may prove persistent so long as
hot weather lasts and recover on the advent of cold.

The more violent cases seen in warmer climes, may be heralded by febrile
reaction, dullness, prostration, inappetence, constipation and sometimes
diarrhœa. The head may be kept in constant movement, the itchy white
parts being rubbed on any object within reach, and the limbs are
stretched, the front ones forward and the hind backward, with a tendency
to rub them with the nose or foot. The skin at first red, becomes later
swollen, covered with vesicles which pass into pustules, burst and
discharge. Meanwhile the subcutaneous connective tissue is infiltrated
and gravitates toward the lowest parts, causing extensive submaxillary
swellings and stocking of the limbs. In its worst forms it may go on to
necrosis and sloughing, but more commonly the affected part becomes raw,
excoriated, cracked and fissured. Sometimes the pituita or even the
buccal membrane becomes involved, with muco-purulent discharge. In other
cases the absorption of septic products causes inflammation and swelling
of the submaxillary or pharyngeal lymph glands. Under favorable
conditions, the secretions dry, the sores heal and the exudate is in
great part absorbed, but there usually remains some thickening of the
affected parts and a diminished vitality of the skin, which renders it
morbidly sensitive to sources of irritation.

Severe cases might be mistaken for petechial fever, but there is much
more pruritus, and there is an absence of the petechiæ, on the mucosæ,
and of a tendency to the extension of the disease far beyond the patches
of white.

_Treatment. Prevention._ This malady should be warded off by breeding or
selecting for warm, sunny climes, animals of a solid color, and
discarding all with white patches. Animals bred in a cooler climate
should not be suddenly transferred to a hot one. When the animal with
white face or feet is found in the hot sunny climate, it should be
devoted as far as possible to work in the shade (indoors or in mines),
or its white patches should be protected against the full unmitigated
rays of the sun, and the hot winds. Sun shades are useful or in their
absence leafy branches fastened to the bridle so as to protect the face.
It is further important to avoid the friction of harness on the
susceptible parts, or wetting of them when in the full glare of
sunshine. Another obvious precaution is to keep the white patches well
covered with lamp black.

When attacked the animal must be placed under cover and eruption treated
with cooling astringents, constant irrigation with cool water, or
lotions with acetate of lead, tannic acid, alum or sulphate of zinc.
When the skin is dry and rigid it may be treated with vaseline, alone or
with zinc oxide, lamp black or any one of the astringents above named.
Open sores may be treated like ordinary wounds, tense engorgements may
be drained by punctures followed by antiseptic dressings, and abscesses
may be opened and evacuated.

During the treatment the patient should be tied short to two sides of
the stall, and other measures taken to prevent him from rubbing or
otherwise injuring the affected parts.

BUCKWHEAT ERYTHEMA: FAGOPYRISM. WHITE SKIN DISEASE.

Form of white face disease, with irritating ingesta, buckwheat, etc.,
occurs from dried products, no insects; growing potatoes; sunshine;
idiosyncrasy. Symptoms: as in white face disease: in winter itching
and rubbing: in summer may go on to nervous symptoms. Treatment: stop
feeding buckwheat. Give laxative and diuretics. Local treatment as in
white face disease.

This may be held to be but a form of the last named affection, in which,
however, certain irritating ingesta (buckwheat, maize, wheat), are
essential factors in addition to the white skin and strong sunshine. It
is seen only on white skins or the white portions of parti-colored
skins, while the blacks, browns and other colors usually escape. Black
breeds of hogs (Essex) escape under the same feeding and exposure, as do
solid colored horses of the darker shades. Of the different food
factors, buckwheat (Polygonum fagopyrum, persicare, etc.), is the most
to be feared, and the poison seems to be inherent in all the products
(green vegetable, dry seeds, bran and straw) and is not destroyed by
cooking. Buckwheat cakes sometime produce erythema in man. This excludes
the idea of the transfer of a living cryptogam to the skin, though not
the theory of pathogenic products of the fungi. The invoking of bee
stings and the bites of insects, which are strongly attracted to the
buckwheat, is untenable because the affection occurs from the dried
seeds, bran and straw, and has been known to break out weeks after the
buckwheat was withdrawn from the ration.

In addition to buckwheat, maize and even wheat when liberally fed have
been known to cause erythema. Hemminger records a similar outbreak in
horses working among growing potatoes.

In addition to the food, clear sunshine is essential and an individual
idiosyncrasy. All animals, though equally exposed are not equally
attacked.

_Symptoms._ These do not differ materially from those of the white face
and foot disease already described. There are intense redness and
tumefaction of the white skin or the white portions, showing prominently
in the delicate parts (ears, eyelids, lips), with violent itching,
rubbing and sometimes vesicles with yellowish contents, followed by
sores and scabs. In the winter season there may be itching and rubbing
only. In summer it may become erysipelatoid and extend to the mucosæ, of
the respiratory and digestive organs, with hyperthermia, nervous
excitement, vertigo, turning in a circle and even spasms and
convulsions.

_Treatment._ This is essentially the same as for the white face and foot
disease with this additional that the buckwheat or other offensive
ingredient must be withdrawn from the ration, and what remains in the
bowels must be expelled by saline or other laxative. Cooling diuretics
must follow to eliminate irritant matters that may have been absorbed.

ERYTHEMA FROM IRRITANTS.

Irritant agents of all kinds, even if caustic or pustulant in
concentrated forms, may be so diluted as to cause simple erythema. Among
chemical agents we have ammonia, lye, caustic acids and salts, iodine,
carbolic acid, the various tar products, kerosene, aniline, chloroform,
ether, formaline, etc. Of thermic irritants may be named solar heat,
fire heat, steam, hot water, hot air, and congelation (chillblains,
freezing) the latter being especially common in the digital region when
salt has been applied to snow or ice. Vegetable irritants include
mustard, capsicum, moulds, euphorbium, rhus, milkwort, the volatile
oils, etc. Among animal irritants must be named cantharides, mylabris,
potato beetle, insect stings, venom of the irritated toad, liquid
discharges from the kidneys or bowels, and discharges from open sores.
Even the escape of tears upon the face will cause erythema.

The _symptoms_ in all such cases will vary with the potency of the
factor and the susceptibility of the skin. Beside the common symptoms
the color and odor of the skin will often yield valuable diagnostic
indications. There is the white of muriatic acid, carbolic acid or zinc
chloride, the black of silver salts or sulphuric acid, the yellow of
iodine, chromium compounds and nitric acid, the well known odors of
ammonia, iodine, chlorine, carbolic acid, tar, essential oils,
chloroform, ether, formaline, kerosene, mustard, etc.

_Treatment_ is that of simple erythema after one has applied the
appropriate antidote to the particular irritant. For the alkalies and
carbolic acid use vinegar, for the acids oxide or carbonate of magnesia,
chalk or lime water, for iodine and chlorine weak alkaline solutions,
for rhus, ammonia or other alkali, or potassium permanganate, and for
insect stings and animal venoms, alkalies or permanganates. The caustic
salts may demand milk, white of egg, or some other albuminous solution.
When no chemical antidote is available, the first step is to wash off
the offending agent, and then treat the erythema.

DERMATITIS.

Under this head may be included a class of inflammations of the skin,
due mainly or entirely to external causes, not essentially parasitic,
and attended by distinct eruptions (papular, vesicular, pustular, etc.).
Many of these are but an advance beyond the simple erythematous
inflammation, and coincide with it, the one condition being present at
one part of the diseased area, and the more advanced and severe lesions
at another part. Bearing in mind the frequency of this connection, it
will be unnecessary to dwell at length on this class of affections.

=Dermatitis Traumatica. Dermatitis from Mechanical Injury.= Besides the
veritant factors already named as causing traumatic erythema, we must
here recognize contusions, over-reaching, treads, interfering, bruising
and chafing by harness, girths, circingles, hobbles, ropes, traces,
twists, and blows with whip, club, chain or rope. Here the source of
injury must be removed, by attention to shoeing, harness, etc., and the
lesions treated according to their gravity as simple wounds.

=Dermatitis Venenata: Dermatitis Calorica.= These, like the
corresponding erythema, come from contact with irritant plants or
animals or their products, from excessive heat or cold, and may show any
grade of eruption or even gangrene and sloughing. Apart from the washing
off of the irritant or venomous matter and the application of alkalies
or permanganates in the case of the latter, these must be treated like
ordinary sores. In burns, especial value attaches to solutions of sodium
bicarbonate, and preparations that will exclude the air. Vesicles may be
emptied by puncture and the part covered with cotton soaked in
carbolated sweet oil and lime water, or carron oil (linseed oil and lime
water) may be freely applied, or a resorcin solution (2:100 water), or a
thick varnish of linseed oil and litharge, equal parts, with 5 per cent.
of salicylic acid, melted and painted over the surface. A layer of
surgeon’s cotton covered by a rubber bandage where admissible, will
complete the dressing. In the process of healing, skin grafting may be
required. Thin slices of cuticle are placed in the center of the
granulating surface, or at intervals and carefully bound in place.

When a part has been frozen the usual method is to recover circulation
slowly by rubbing with cold water or snow. The parts are then treated by
astringent and antiseptic dressings. If the skin sloughs use antiseptics
until it separates, and then treat like an ordinary sore.

Chillblains may be treated with a mixture of sweet oil, 5 ozs., oil of
turpentine ½ oz., Aqua Ammonia ½ oz., oil of peppermint 1 dr., or
powdered camphor 10 grs., Peru balsam 20 drops, linseed oil 2 ozs.
Nourishing food and a course of iron should be given.

=Dermatitis Medicamentosa.= Medicines given by the mouth sometimes cause
inveterate skin eruptions. Among these are arsenic, belladonna,
bromides, iodides, mercurials, salicylates, tansy, turpentine, tar, and
the carminative seeds and oils. The latter are chargeable with many
eruptions in live stock fed on patent foods. In cattle treated with
iodides for actinomycosis, an universal eruption and desquamation is a
common condition. In all such cases the drug must be withheld, the
bowels cleared out by a purgative and the elimination of any remaining
irritant products favored by gentle diuretics.

ECZEMA. A BOILING OUT. A PUSTULE.

General method of eruption. Successive advancing lesions. Definition.
Causes: usual factors and special susceptibility.

This term, standing for what boils out, has long been applied to
vesicular eruptions on the skin, but inasmuch as the inflammation rarely
stops short with vesiculation, but usually in part at least goes on to
more advanced lesions, it must be held to include in many cases
erythema, papules, vesicles, pustules, crusts, desquamations and
erosions. All of these may coexist or succeed each other in the same
subject, so that considerable latitude must be allowed to the name to
cover all parts and stages of the same attack. Dermatologists have
defined eczema as a non-infectious inflammation of the skin with
multiform manifestations, but recent observations would indicate that it
may at times, at least, be contagious, and micrococci have been found in
the serum of the vesicles, while the very occurrence of pus must
virtually imply the existence of a bacterial infection. Doubtless
different diseases pass under this name in the different genera and
species, and even in the same variety of animals, yet until we learn to
discriminate sharply the one from the other, it is convenient to
consider the whole as a kindred clinical group, if not a pathological
entity.

_Definition._ An acute or more frequently, a chronic inflammation of the
skin and sometimes of the mucosæ, characterized by itching, erythema,
papules, vesicles, serous or sero-purulent exudation with squama or
crusts and loss of hair, and usually largely due to an internal cause.
The exudative condition has suggested a catarrh of the skin.

_Causes._ These are the usual causes of skin disease, local and general,
together with a special susceptibility, under which, what are ordinary
irritants produce this characteristic disease. Many local irritants can
produce eczema, but again it is often the case that these factors will
operate on a given susceptible subject while on another they are without
much effect. This susceptibility is called a “dartrous diathesis” by the
French writers, while most English and American writers are willing
rather to find the hidden cause or causes in the disorder of internal
organs (digestive, hepatic, urinary, generative, hæmatic, trophic,
infective, plethoric, atonic).

ACUTE ECZEMA IN SOLIPEDS. DORSAL ASPECT.

Head, neck, shoulder, back, under girths, breeching, crupper. Summer.
Moulting. Heavy coat. Thin skin. Youth. Symptoms: erect hair, papular
groups, hot, thick rigid skin, itching, abrasion, ulceration,
encrusting, pustules, white spot and hair. Treatment: laxative,
cooling diet, cleanliness, pure air, shade, rest, alkalies, locally
vaseline, astringents, dusting powder, anodynes, tar water, creolin,
etc.

This shows itself especially on the head, the sides of the neck, under
the collar, or saddle, the circingle or crupper, the breeching or
general surface. In these cases the profuse secretion of sweat, and the
friction of the harness is a marked local factor in its production. It
often shows a preference for the summer season, the period of shedding
the coat, the heavy coated animal, the animal with white, thin or
delicate skin. Youth also predisposes.

_Symptoms._ There is usually erection or roughness of the hair, and the
formation at such points of minute papules like small peas collected in
groups. The skin may feel hot, thickened, lacking in pliancy, not to be
pinched up in folds, the panniculus is contracted and manipulation shows
tenderness. Soon the papules flatten and desicate and more or less
violent itching sets in. The patient rubs or scratches himself, causing
deep red congestion of the surface or even abrasion, or ulceration.
Apart from abrasion the skin becomes covered with crusts or even scales
which agglutinate tufts of hairs and dry up and desquamate.

In other cases the eruption advances from the condition of papules to
that of vesicles and even of pustules, though finally drying up with the
same pruritus as in the papular form.

In either case the affected parts are more or less depilated, red if on
unpigmented skin, grayish and scabby or scurfy if on the darker. At
times, after recovery, the patch remains devoid of pigment and hairs
growing from it are white.

_Treatment._ It is usually desirable to clear out the prima viæ by aloes
or Glauber salts, to resort to a carefully regulated, non-heating diet,
to clean the skin of all concretions from sweat or otherwise, to give
pure air and shade and to protect the animal from active exertion,
profuse sweating and friction by harness or otherwise. In the early
stages benefit will often come from the use of alkalies, especially
sodium bicarbonate. Locally an inunction with vaseline to soften crusts,
and the subsequent removal of these with tepid water, may be followed by
some soothing or astringent application, always bearing in mind that
what is soothing to one skin is irritant to another. Dusting powders
(starch, lycopodion, magnesium carbonate, oxide of zinc, calamine,
bismuth) will often do good; soothing lotions or liniments (lead acetate
with laudanum, lime water and olive oil; sodium bicarbonate in well
boiled gruel of oatmeal or marsh mallow; zinc oxide or sulphate in water
or glycerine or as ointment in vaseline, etc, etc). In chronic stages
with much squama and pruritus tar water or ointment; a lotion of tar and
alcohol; creolin lotion; chloral lotion; or other stimulant application
may be used.

CHRONIC ECZEMA OF THE HEAD IN SOLIPEDS.[1]

Affects face, eyelids, cheeks. Symptoms: papules, vesicles, dry, rigid
skin, scurf, glistening, shedding hairs. Treatment: as in eczema;
antiseptics.

Footnote 1:

Acute eczema of the heels. See chapped heels and grease.

The cheeks and forehead are the most liable to suffer in this affection,
yet the eyelids and the parts below the inner canthus may participate in
connection with the escape of tears and the disease of the lachrymal sac
or ducts. It has been seen in the young when strangles had merged into
skin eruption, but also in the aged and independently of that affection.

_Symptoms._ Following strangles the papules or vesicular eruption may
have passed leaving the skin thick, rigid, dry and scurfy. The pigment
may be increased and the hairs are usually shed in connection with
atrophy of their follicles and rubbing of the itching surface, so that
the cuticle is smooth, glabrous and even glistening. In implication of
the lachrymal apparatus, there is shedding of hairs beneath the eye or
the wet matted condition of those that remain.

_Treatment._ In strangles use a lotion of silver nitrate or sodium
hyposulphite to destroy the local infection. In other cases treat as for
ordinary eczema.

CHRONIC MOIST ECZEMA (IMPETIGO) AT THE MANE AND TAIL.

Fleshy neck, thick mane and tail, lymphatic constitution, profuse
perspiration, lack of cleanliness, alkaline soaps, plethora, foul
stable, pus microbes. Symptoms: itching or tenderness, shedding hair,
thinning of mane and tail, skin thickened, ridges and folds,
tenderness, moisture, crusts raise hairs from follicles, fœtor, sores
and ulcers, matted hairs. Treatment: remove general and local causes,
cleanse, cool, pure stable, clip, reduce grain; cooling, laxative
food, soothing or stimulating applications, zinc oxide, talc, olive
oil and diachylon plaster, iodoform, silver nitrate, oil of cade, or
of white birch, sulphur iodide, Canada balsam and sulphur, green soap,
dusting powders, ointments.

This condition is especially common in horses with a profusion of long
hairs in the mane and tail, and in the heavy draught animal with a
thick, fleshy neck. In such the skin is very sensitive, and when profuse
perspiration soaks the skin, or concretes and decomposes about the roots
of the hairs, the local irritation necessary to the production of the
eruption is present. A lack of careful grooming is therefore a common
cause, yet soap left in washing the mane or tail may be no less
injurious. Plethora has its influence in many cases, and the ammoniacal
fumes from a wooden stable saturated with excretions are not to be
ignored. Finally in cases accompanied by pustular eruption, the pus
microbes must be recognized as factors.

_Symptoms._ There may be marked itching or extreme tenderness of the
part affected or in the absence of both there may occur a gradual
shedding of the long hairs, so that an increasing thinness of the mane
and tail (rat tail) becomes apparent. The skin covering the affected
parts is thickened, inflamed and thrown into ridges and folds, one
rubbing against another. The surface feels moist or is covered by crusts
formed by the condensation of the moist exudate, and embracing the hairs
and drawing them out of their follicles. Beneath the concretions the
skin is soaked in the tenacious fœtid liquid discharge. The hair
follicles become atrophied in connection with the evulsion of the hairs,
or under congestion the hairs stand rigidly erect, and bristly or curly.
As the freer secretion abates, the exudate become more purely scally or
encrusted, but the skin remains thickened and thrown into folds. Under
the inveterate rubbing or gnawing the skin is often extensively abraded
and large open sores are formed which are indolent and slow to heal.
That matting together of the hairs which has been known as _plica
Polonica_ is often the result of the disease of the hair follicles and
the accumulation of scabs which takes place in this disease, rather than
to a special infection like gregarina (coccidiosis).

_Treatment._ The first consideration must be to remove all general and
local causes of eczema, insure perfect cleanliness and good grooming in
any case in which these may been lacking, purify the air of the stable
if that has been foul, procure a cool environment when that has been too
hot, clip the patient if habitually soaked with perspiration by reason
of a heavy coat, suspend or moderate the work if that has been too
exacting, withhold a heating grain ration (corn, buckwheat, barley,
wheat, peas, beans), and furnish cooling, laxative, easily digested
food. In the cases before us the acute, irritable stage has usually
passed, so that the more stimulating applications may be safely used,
yet in many old standing cases a fresh eruption may have taken place,
which would demand for a time the most soothing applications only. Apart
from such cases the more stimulating dressings are applied at once.

The affected surface is exposed by clipping or shaving off the long
hairs, thus at once removing a source of heat and irritation and
allowing of the direct and thorough application of the dressing. Among
the astringent and stimulant applications oxide of zinc ointment and
benzoated oxide of zinc are among the simplest and least likely to
irritate, but the stronger applications can usually be borne. The Lassar
paste consists of two parts each of finely powdered talc and zinc oxide,
four parts of vaseline and three per cent. of salicylic acid. Oxide of
bismuth may substitute the zinc oxide. Three parts of olive oil and four
of diachylon plaster melted together and stirred until cool, makes
another mildly astringent and sedative application. Iodoform 1 dr. to an
ounce of vaseline is an excellent agent. A mixture of iodoform and
tannin is used as a dusting powder by Friedberger and Fröhner: or silver
nitrate solution (6:100) may be used. Tar ointment (1:8) with a little
subcarbonate of potassium added makes an excellent application. Oil of
cade and oil of white birch may be used in the same way, the latter
being the most desirable as a rule. Ammonia chloride of mercury as an
ointment (1:10), often acts well and the black wash, formed by the
decomposition of calomel with potash is often serviceable. Iodide of
sulphur and vaseline (1:10) is often an excellent resort. An ointment of
equal parts of Canada balsam and sulphur or iodide of sulphur in four
parts of vaseline is often effective. Other valuable preparations are
ointments (10%) of ichthyol, naphthol, chrysarobin or pyrogallol.
Hebra’s _last resort_ of green soap is never to be forgotten, the
affected skin being thickly smeared with the soap which is left to dry
on, and is repeated and rubbed in, for several days in succession. It
may seem at first to aggravate the disease by reason of the solution and
removal of the covering of the vesicles or pustules and the exposure of
a pink sensitive surface, but day by day this improves and the skin
becomes smooth and more natural. After a few days of this treatment, it
may, if necessary, be followed by astringent or stimulant dressings, or
the varied medicaments may be incorporated with the soap so as to form
one dressing to be applied from the first. When a healthy action has
been once established, all that is required further may be cleanliness,
with the use of bland dusting powders or ointments to establish the
cure.

CHRONIC ECZEMA OF THE CARPUS AND TARSUS; MALANDERS: SALLENDERS.

Eruption in bends of carpus and tarsus and downward: Causes: lymphatic
temperament, constitutional predisposition, deranged internal organs,
excessive secretions, modified, congested skin, friction between
dermal folds. Symptoms: stiffness, heat, thickening and redness,
vesicles or oozing, crusts, erect hairs, shedding hair, squamæ,
cracks, abrasions, fissures, subcutaneous engorgement,
lymphangiectasis. Treatment: Cleanse, get pure air, regular exercise,
non-stimulating food, avoid cold water, mud, slush, caustic soap,
lime, sharp sand, foul organic matter. Massage. Light bandages. Bland
ointments. Dusting powders. Rest. Iodoform. Starch. Zinc oxide. Boric
acid. Magnesia. Bismuth. Lycopodion. Lead. Tannin. Pyoktannin.
Stimulating ointments. Green soap. Arsenic.

The bends of the carpus and tarsus in heavy, lymphatic, coarse skinned
horses are especially subject to eczema followed by a dense scabby
eruption, which in the old farrier’s nomenclature was known as malanders
in the fore limb and sallenders in the hind. It is not always confined
to the joints but may extend down the limb, especially on the back,
where the hair is coarser and the skin thicker, as far as the fetlock or
even to the hoof.

In the matter of _causation_ much depends on the general constitutional
state which tends to eczema, and on the torpor or derangement of some of
the internal organs the functions of which are interdependent with those
of the skin. Something too must be attributed to the freer secretions of
these parts in coarse bred horses, to the accumulation of such
secretions and of extraneous irritants under the long hair, to the
sluggishness of the circulation in the limbs which has to overcome the
force of gravitation, and to friction between the thick folds of skin in
flexion, and stretching in extension. Swelling of the lower limbs is at
once a cause and an effect of the disease.

_Symptoms._ At the outset the animal may be seen to move rather stiffly,
and the skin is found to be hot, thickened and if white reddened. Soon a
close observation may detect the eruption of vesicles, or simply an
oozing of a yellowish or bloody serum which concretes around the hairs
forming an encrusted covering for the part, holding the hairs erect and
bristly, and even lifting them out of their follicles. Cracks also
appear in the depth of the fold, leading to a more abundant exudate, and
the disease may extend around the whole surface of the limb.

In the more acute cases this may be followed by more or less depilation,
dessication and recovery, but too often the condition becomes chronic,
the thickened, encrusted or squamous skin continues to exude, crack and
cover itself with crusts, under which the decomposing liquids macerate
and irritate the exposed cuticle, and engorgment of the whole limb with
hyperplasia of the connective tissue and lymphatic plexus and vessels is
the result. This hyperplasia of the skin and connective tissue
(elephantiasis) is also a common result of lymphangitis.

_Treatment._ As in other skin affections attention must first be given
to removal of the causes. Ensure cleanliness, pure air, regular
exercise, non-stimulating food, the avoidance of cold water, melting
snow, soapy washes and all other sources of irritation. Deep mud,
especially if charged with lime, sharp sand, decomposing organic matter
or other irritant, is particularly offensive.

Hand-rubbing (massage) of the limbs and evenly applied light bandages
are often of the greatest value in dispersing or obviating swelling.

The slighter attacks may be met at the outset by bland ointments or
dusting powders and rest from all but necessary exercise. Dressing with
iodoform may bring about a recovery in a few days. Starch and oxide of
zinc, boric acid, magnesia carbonate, bismuth or lycopodion may give
good service. Lotions of lead acetate, tannin, iron sulphate, alum,
potassium permanganate or pyoktannin may be used as in other forms of
eczema. In obstinate cases green soap followed by stimulating ointments
or liniments, tar, oil of white birch, Canada balsam, turpentine and
glycerine, oil of cade, etc., will often serve an excellent purpose. In
these advanced cases an alterative such as arsenic may be employed.

ECZEMA OF ALIMENTARY ORIGIN IN CATTLE.
STARVATION MANGE. STALK DISEASE. MALT ECZEMA. POTATO ECZEMA.

In low condition: erythema, hæmorrhagic extravasations, or vesicles on
tail, lips, fore legs, udder. Trombidium holosericeum. Malt or potato
eczema: marc eczema on legs and body. Causes: feeding on marc only,
skins, green potatoes, fermenting. Attack in ratio with marc eaten.
Worst on new stock, and feeding cattle. Calves have diarrhœa, children
eruption. Bean trefoil and milk sickness act similarly. Solanin.
Unaffected by boiling. Season. Field. Chlorophyl. Narcosis absent. Is
brain adaptable? Other ingredients inoperative. Eczema ceases with
change of food: is not inoculable. Symptoms: fever, costiveness,
inappetence, red mucosæ, weeping, stringy salivation, debility,
emaciation, black diarrhœa. May lie with extended head, grinding
teeth, tympany, lethargy, coma. Pig and dog vomit. Abortion. Redness,
swelling, stiffness on pasterns: may extend to whole body: exudations:
thick crusts: erect or shed hairs: rigid thickened, folded, cracked
skin, buccal mucosa may suffer: abscess, sloughs. Mortality slight and
up to 20 per cent. Lesions: congestions of small intestine, brain and
muscle. Treatment: stop or lessen the marc adding grain: turn to
pasture: locally bathe, cold or tepid: lead lotions: dusting powders:
tannin: blue stone: creolin: cresol: tar or birch oil: carbolic acid.

The skin of cattle seems to suffer more than that of other animals in
connection with the ingestion of poisons. In starved or very low
conditioned animals, eruptions are met with which may be in the form of
a simple erythema, a hæmorrhagic extravasation in spots, or an eruption
on the end of the tail in the form of epidermic concretions or pustules
(impetigo). Among the vineyards it is common to find an eruption with
papules and vesicles on the lips, fore legs and udder of cows which were
fed on the succulent young shoots and leaves of the grape vine. In cases
of this disease, Railliet and Moreau have found a great number of the
silky trombidium larvæ (harvest bug), and accordingly attribute the
affection exclusively to their attacks. The growth of the vine on the
warmest and sunniest exposures, the most favorable to the propagation of
this acarus, gives much support to this conclusion.

=Malt or Potato Eczema.= On the continent of Europe where potatoes are
largely used for distillation and the production of starch, herds of
cattle are fed often almost exclusively on the refuse or marc, and in
such herds an eczematous eruption of the legs and exceptionally of the
body is a familiar occurrence.

_Causes._ The disease has been definitely traced to an exclusive dietary
on potato marc, and still more so to the skins, to tubers rendered green
by exposure to the sun, and to the distillery potato refuse which has
undergone fermentation. Thus 80 litres of the pulp daily without dry
food will determine a violent attack in the animal consuming it, while
the animal consuming 40 litres has it much milder (Friedberger and
Fröhner). It attacks animals living in the best conditions of
cleanliness and pure air, and the essentially toxic quality of the cause
may be deduced from the fact that newly bought animals, which are not
yet habituated to it suffer the most, that fattening cattle are the
common victims, while work oxen which perspire more freely and milch
cows escape, yet calves fed upon their milk may suffer from diarrhœa and
infants from a cutaneous eruption (Johné). The poison it is to be
inferred is eliminated in the milk. Similar examples of the protecting
of the milch animal by elimination of the poison through the milk are
found in bean trefoil (cytisus) which poisons the milk while proving
harmless to the goat which yields it, and the poison of milk sickness
which is deadly to cattle which are not giving milk, and harmless to the
milch cow, yet deadly to those that consume her milk.

The exact nature of the poison is as yet uncertain, and as solanin is
the only toxic principle so far discovered in potato, this has been held
tentatively to be the essential cause. The amount of solanin in young
and germinated potatoes has been given by Cornevin as follows:

Germinated tubers Young tubers.
The entire tuber contains 0.21 0.16
The central fleshy part 0.16 0.12
The parings and pickings 0.24 0.18

The toxic strength of the marc is not impaired by boiling, cooking or
other culinary treatment, and the same is true of solanin. The toxicity
is greatest after the potato has been subjected to germination, or when
it has become green by exposure to the sun, and in these conditions the
solanin is increased. The toxicity of the marc is higher in certain
years, and in the product of certain fields, than in others, and this is
in keeping with the effect of environment in modifying the products of a
plant. The increased production of chlorophyl under the action of
sunlight is associated with a material increase of the amount of
solanin. Until therefore another toxic product can be shown to be the
essential cause of this affection the solanin must be charged with this
result. This conclusion would be more inviolable if the animals attacked
showed other symptoms of solanin poisoning such as narcotism, vertigo,
stupor and paralysis, and the absence of these may perhaps be due to the
gradual advance of the toxic action, and the progressive immunizing of
the animal system. The brain may be able to accommodate itself more
readily than the skin.

The other constituents of the potato or of the marc fail to produce the
eruption under other conditions: the alcohol in brewers and distillers’
grains, the acetic, lactic and butyric acids in the refuse of starch,
beet sugar and canning factories, the potash in turnips and other roots,
the yeast ferment in brewers’ grains. The acarus of foot mange
(symbiotis bovis) is rarely present in the affected animal though the
eruption in the same situation would strongly suggest its presence and
lead to a search for it. Moreover the eczema appears at once in a large
number of animals, affecting a large area without evidence of slow and
steady progression and disappears with equal rapidity in many cases when
the diet is changed. Finally the eczema has not been successfully
propagated by inoculation which conveys mange infallibly from animal to
animal.

_Symptoms._ The disease is associated with slight fever, costiveness,
impaired appetite, hyperæmia of the mucosæ, epiphora, viscous
salivation, muscular weakness, and finally emaciation and black
diarrhœa. The gravity of these symptoms varies, being greater when the
animals have eaten the leaves and stems, the raw potatoes in their
skins, the young shoots and parings, or green potatoes which have been
sunned. The animals may lie most of their time stretching themselves out
with head extended on the ground, they may grind the teeth, may have
pulse small and rapid, tympany, lethargy, coma and even paraplegia but
these severe symptoms are exceptional and almost altogether confined to
the cattle of distilleries which receive an exclusive diet of potato
marc. In the pig and dog vomiting has been noticed (Cornevin). Pregnant
animals may abort.

The local symptoms begin with redness and swelling of the skin around
the pasterns, especially of the hind limbs, stiffness and a disposition
to lie most of the time; then small flattened vesicles appear, isolated
or confluent, which bursting, form extended, raw patches the abundant
exudations of which concrete into thick crusts. The hairs stand erect
and are abnormally thick at their roots. The eruption may extend to the
whole limb, the scrotum, mamma, tail and body at large, so that in
severe cases it is practically universal. The skin becomes thick, rigid,
hide bound, wrinkled and folded with intervening cracks. As a rule,
however, the eruption is confined to the limbs, scrotum, mammæ and tail.
In some extensive and persistent cases the buccal mucosa suffers,
particularly on the pad on the upper jaw, which shows extensive and
irregular ulcers with purulent centre and swollen, congested margin.
Abscesses may develop in the skin and subcutem and sloughing of the
integument is not unknown.

_Mortality_ is slight as a change of food is usually made and a recovery
ensues in a few weeks. Yet Baranski noted 20 per cent. of deaths in
Galicia, mostly in old, worn out animals which had been stabled for a
length of time.

_Lesions._ On examination, _post mortem_, there are found hyperæmia and
inflammation of the small intestine, some congestion of the cerebral
meninges, and a red, bloody condition of the muscular system.

_Treatment._ The toxic provender must be stopped, or reduced to 20 or 30
litres of pulp daily, supplemented by sound wholesome dry fodder. Marker
claims that 70 quarts daily of the potato marc may be given if combined
with a fair ration of Indian corn. Turning out doors to pastures usually
effects a speedy cure.

Local treatment is rarely demanded but when the irritation is great it
may be soothed by bathing with cold or tepid water, lead lotion,
glycerine and lead lotion, or by the application of ointments of lead,
tar, oil of cade or birch, or carbolic acid. Dusting powders of zinc
oxide, starch, lycopodium, boric and tannic acids may also be employed.
Decoction of oak bark or solution of blue stone is often used, also
creolin or cresol one part, to alcohol five parts.

It is rarely necessary to use other than the cooling and astringent
lotions, yet the persistence of irritable sores, ulcers and crusts must
be treated as in other chronic skin affections.

MOIST ECZEMA OF THE PASTERNS IN THE OX.

Causes: hot season, foul stables, streptococcus. Symptoms: sudden
attack, red, swollen, warm, tender pastern, vesicles, crusts, scabs,
lameness, foot rested on toe, cracks, fissures, interdigital foot rot,
shedding hoof, scaly chronic form. Treatment: clean stables and yards,
cleanse feet, lead lotion or zinc, phenol, iron or copper. Tar water,
tar, creolin, creosote, iodol.

This affection is comparable to the simpler forms of grease or digital
eczema in horses.

_Causes._ It occurs especially in the hot midsummer season in cattle
kept in filthy stables, where the feet and pasterns are kept filthy and
the air charged with irritant ammoniacal fumes. A streptococcus is
usually met with and may be found in pure cultures in resulting
abscesses.

_Symptoms._ The attack is sudden, the skin around the pastern becoming
red, warm, swollen and tender, with the formation of vesicles, isolated
or confluent, which rupture and discharge a serous exudate that dries up
into crusts and scabs. Lameness is a marked symptom and in bad cases the
swelling and pain are such that the foot may be habitually raised from
the ground and rested only on the toe. The swollen skin is thrown into
folds which rub on each other, and breaks open into cracks from which
exudes a serous fluid that macerates and irritates the skin, the heel
pad and the interdigital space, so as to determine interdigital foot
rot. This may lead to inflammation inside the hoof with shedding of the
horny mass, or it may subside into a chronic form with an abundant
squamous product.

_Treatment_ should be mainly prophylactic in the direction of
cleanliness and abundant litter in the stables, and the avoidance of
pools of liquid manure and of septic mud puddles in the yards and roads.

In the early stages of the affection the pasterns and interdigital
spaces should be thoroughly cleansed and covered with a bandage with a
weak solution of acetate of lead, or of sulphate of zinc, or carbolic
acid, or sulphate of iron or copper. In the more advanced stages tar
water or crude tar will serve a good purpose, or watery or alcoholic
solutions of creolin, creosote, oil of tar, carbolic acid or iodol. When
the horn has been separated from the quick, it is usually best to pare
away all such, to bevel the edges so as to make them less rigid and more
pliant and to dress with tar water and later to cover with undiluted tar
and bandage.

MOIST ECZEMA OF THE TAIL, NECK, CHINE AND DEWLAP OF CATTLE.

Definition. Causes: in work oxen, winter, foul stables; dairy cows on
spoiled fodder or maize, wheat, buckwheat, cotton seed, etc.
Contagion. Symptoms: skin hot, thick, tender, exuding, matted hair,
vesicles, itching, excoriation, ulceration, bleeding, sloughing.
Treatment: Soothing. Cleanliness. Pure air. Tepid sponging. Dusting
powder. Clip or shave. Calomel with care. Phenol. Creolin. Silver or
copper salts. Tannic or boric acid.

This is an acute eczematous eruption of cattle beginning as a congestion
and swelling of the skin and advancing to an exudation or secretion
which bedews the surface with a sticky discharge, and concretes into
scabs and crusts.

_Causes._ The disease has been mainly seen in work oxen during winter,
when kept in close, foul stables and not properly groomed. It is also
seen in dairy cows and may be attributed to the indigestion and gastric
disorders which come from the ingestion of spoiled fodders, or from a
too stimulating diet, such as Indian corn, wheat, buckwheat, barley,
cotton seed, and the seeds of the leguminosæ. Lafosse looked upon it as
contagious, but Cadeac denies both this and its alimentary origin.

_Symptoms._ The attack is severe, the skin becoming swollen, hot and
tender, especially at the base of the tail, on the neck, chine and
forehead. Soon the turgid, congested skin exudes a somewhat glutinous
serous product, which mats the hairs into tufts and exposes the
intervening red, excoriated skin, with here and there vesicles singly or
in groups. Itching is usually intense and the animal licks, rubs and
scratches the affected surface unmercifully. The resulting excoriations
and sores add greatly to the severity of the troubles, including
ulceration, bleeding and even sloughing.

_Treatment._ Prophylaxis should be the first consideration, and in the
acute stages of the disease, its arrest by soothing applications.
Cleanliness, pure air, and tepid sponging, to be followed by a dusting
powder of boric or salicylic acid, or a lotion of acetate of lead or
sulphate of zinc may serve a good purpose. If the case proves obstinate,
the hair may be clipped or shaved to allow of the more direct and
thorough application of the dressings. Cadeac especially recommends an
ointment of calomel (1 ∶ 10) but this must not be applied over an
extended surface, nor must it be recklessly repeated owing to the
dangerous susceptibility of the bovine race to mercurialism.

Lotions and ointments of carbolic acid are of great value in moderating
the intense pruritus, and a combination of this with lead acetate will
often prove quite effective. Lotions, liniments or ointments of tar, oil
of cade, creosote, or creolin. When ulcers are present they may be
treated by solutions of silver nitrate (2 ∶ 100) or cupric sulphate (2 ∶
100) or powdered iodoform. When the exudate is excessive, astringent
dusting powders often serve a good purpose; tannic acid and boric acid,
with starch or lycopodion.

CHRONIC ECZEMA IN CATTLE.

Summer disease. Depilation. Scaly. Itchy at first. Lesions of bones,
red zones representing successive attacks. Alterative tonics
indicated.

Megnin records the case of an ox which on three successive springs had a
miliary vesicular eruption on the loins and upper walls of the abdomen,
which persisted until the advent of cold weather in the fall. The
vesicles were followed by an exudate which concreted in solid crusts,
enveloping the roots of the hairs which were lifted from the follicles
and failed to be renewed, so that the animal entered on the winter with
an appearance of alopecia. The denuded surface was red, shining and
covered with a dense covering of lamelliform epidermic scales. In the
early stage of the eruption there was moderate pruritus, but when the
scaly stage was reached it was neither tender nor itchy to any marked
degree. Tar ointments had no effect in stimulating the growth of the
hair, and the skin remained bald until the next attack. The second and
third years the eruption extended farther, invading not only the trunk,
but the legs, and passing through the same successive stages.

The animal was butchered and the shafts of the bones were found to be
abnormally red, and showed three concentric rings of deeper brown,
manifestly representing the three acute attacks and resembling the
concentric rings formed in growing bones when the young animals are fed
on madder.

The manifest disorder of nutrition in this chronic skin disease, is an
argument for the _treatment_ by alterative tonics, such as arsenic, as
well as for the employment of tonics and corroborants in general. In
such cases the presumption is that local treatment would be useless or
nearly so until the general disorder could be repaired.

ECZEMA IN SHEEP.

In anæmias squamous eruptions. In cold rainy weather moist eczema.
Salving. Thin wooled. Congestion, swelling, papules, vesicles, scabs,
depilation. Recovery with dry weather. Prevention: fold in rainy
weather, covers. Pruriginous eczema. Fagopyrism.

The skin of the sheep is so densely covered by wool and so lubricated
with its own secretion, that it is little liable to non-parasitic
dermatitis, or such as exist are to a large extent overlooked. In
internal parasitisms (distomatosis, strongyliasis, etc.), the wool
becomes flattened (“clapped”) and the skin the seat of a dry (squamous)
eczema with scaly accumulations around the roots of the wool.

MOIST ECZEMA, the “_rain rot_” of the Germans is seen in low conditioned
sheep which have been left out in the heavy cold rains, and is
attributed to the direct entrance of the rain by the dorsal shed of the
wool. In salving sheep it is a great point with the shepherds to avoid
opening the way for such entrance, by shedding only at a short distance
on each side of the spine, and never directly in the center. Thin wooled
sheep are also specially liable to the disease. When the rain enters so
as to soak the skin and deeper layers of the wool, it softens and
macerates the skin, introduces microbes and favors decomposition and in
various ways incites to dermatitis. The skin becomes red and swollen
with an eruption of papules and vesicles, and an exudation which
concretes in scabs around the wool, which under the constant accretions
from below lifts the wool from its follicles, leaving bare scurfy, or
vesicular patches. This appears in different parts of the body beginning
in the region of the vertebræ (back, loins, croup), and extending on the
shoulders, neck, sides of the chest and abdomen. The disease is rarely
inveterate and generally subsides spontaneously on the return of the dry
weather. Still it may cause considerable loss of wool and hence it may
be desirable to fold the flocks during cold rainy seasons, or, if they
must be run at pasture, to cover the back of each with a piece of
sacking.

OTHER CUTANEOUS ERUPTIONS IN SHEEP.

A _dry_ and a _moist eczema_ have been noticed in the sheep,
(_pruriginous eczema: impetiginous eczema_) and a moist eczema of the
pastern comparable to grease in the horse. _Fagopyrism_ also occurs.

ECZEMA IN SWINE.

Secondary skin lesions, maculæ, vesicles, seborrhœa, crusts. Impetigo
of young: cold weather: exposure: filth: spoiled or improper food.
Symptoms: eyelids, etc., show itchy, red, swelling, pustules, scabs,
erosions, may affect nose or mouth. Duration 20 days. Hot weather
aggravates. Treatment: cleanse: soapy washes: emollient ointments,
astringent lotions, saline laxative, diuretics.

Disease of the skin is by no means uncommon in swine, but it occurs
mostly as a manifestation of an acute general malady. Thus in the
different specific diseases, caused by microbes, maculæ in the form of
blood extravasations, punctiform or in extended patches are constant
phenomena. In some cases this is complicated by a vesicular eruption, or
by a seborrhœa and by a dense accumulation of black crust on the
surface.

=Impetigo of Pigs.= Benion and Cadeac describe this as a sporadic
affection of young pigs especially, which has been attributed to cold
stormy weather, lack of shelter, filthy pens, spoiled food and
insufficient nourishment.

_Symptoms._ The skin of the eyelids and other parts of the body presents
itchy, red, hot and swollen patches, which gradually pass into a
pustular eruption. The pustules no larger than a millet seed, burst in
forty-eight hours, and discharge a yellowish or purulent liquid which
concretes around the eyelashes or bristles, and glue the eyelids
together. The crusts may increase so as to cover the affected part of
the skin by a dense scabby covering which is firmly adherent and when
detached leaves a bleeding surface. It may extend to the different
mucosæ of the eye, nose or mouth. The disease runs a course of twenty
days or less being retarded by the extremes of temperature. During the
heats of summer the attendant pruritus is very great and annoying.
During convalescence the scabs and crusts gradually detach themselves
and drop off leaving the healthy skin covered at first by a somewhat
delicate epidermis.

_Treatment_ is confined to cleanliness, soapy washes, emollient
ointments and astringent lotions (lead acetate, sulphuric or
hydrochloric acid) but no premature detachment of scabs is permissible.
Saline laxatives and diuretics are often called for.

VESICULAR IRRUPTION IN PIGS. PITCHY AFFECTION. SEBORRHŒA.

This also affects the young and is characterized by the successive
appearance of vesicles, pustules and scabs or crusts. Friedberger and
Fröhner associate it with debility from youth, disease or neglect, from
articular rheumatism, rachitism, hog cholera, etc., but also as a result
of lying on manure, and the accumulation of sebaceous matter and filth
of all kinds on the skin.

_Symptoms._ Among the symptoms of general disorder are dullness,
inappetence, prostration and slight fever. There is red eruption with
vesicles and even pustules on the early rupture of which the discharge
concretes into a black pitchy layer. It may be at first most marked on
the ventral aspect of the body, but usually extends to the whole
integument.

_Treatment._ Where it is not dependent on some grave internal disorder,
this commonly yields to soapy washes, generous food and a clean pen.

GRANULAR ERUPTION IN SWINE.

Zschokke describes a disease of this kind affecting the ears, back and
croup, and caused by a micrococcus in the epidermis and papillary layer
of the derma. It appears in the form of patches, often of the size of
the palm, showing bluish gray papules which dry up without forming
pustules. It runs a chronic course and produces little or no itching.

_Treatment_ would consist in absolute cleanliness, soapy or alkaline
washes, and the free use of solutions of the hyposulphites, sulphites,
or other antiseptics which are neither irritant nor poisonous.

URTICARIA is met with in swine as already noticed.

SCLERODERMA occurs in boars especially in the region of the shoulders
and back.

ACUTE ECZEMA OF THE DOG.

Prevalence and forms. Red Mange. Causes: constitutional, hereditary,
races most susceptible, short-haired, delicate skins, 1st and 2d
years, flesh fed, overfed, spiced food, secondary to internal
disorders, heat, cold, dust, irritants. Symptoms: blush inside elbow,
thigh, belly, heat, tenderness, itchiness, scratching, vesicles,
abrasions, sores, skin thickens, wrinkles, moistens. Diagnosis: from
demodex, distemper, mange. Treatment: change diet, restrict in
quantity, from flesh, or stimulating food, one meal daily, laxative,
bitters; locally, cleanse skin, antipruritic non-poisonous dusting
powders or lotions, starch, magnesia, bismuth; with muzzle, phenol,
lead, thymol, thiol, later creolin, oil of cade, lysol, etc. Acute
general eczema. Causes as in red mange. Symptoms: Common on head,
ears, back, rump, eyelids, lips, scrotum, arms, digits, crusts and
depilation, large vesicles, bleeding digits. Treatment.

In none of our domestic animals is this condition so common as in the
dog, and of all skin affections of this animal this is the most
frequent. As in other animals it may show itself in all forms or grades
from simple erythema, through the papular, vesicular, pustular and
scurfy or scabby, and all of them may often be seen at the same time in
one animal. Yet special names have been given to different forms and
localizations and it seems convenient to retain some of these for every
day use.

=Eczema Rubrum. Red Mange.= This form is familiar to dog fanciers as one
of the acute types of this disease.

_Causes._ Among these are recognized a constitutional predisposition, so
that the disease appears in successive generations in the same family,
without apparent reason for charging the trouble on any particular
feeding or management. While not confined to any race or group of races
it has been noticed especially in greyhounds, setters, pointers, fox
hounds, harriers, bulldogs, St. Germains and braque hounds. It is
especially common in dogs in their first and second years, and those
that are nervous and lively, with a delicate and naturally dry skin.
Again, the dog fed largely on flesh, and above all the house dog fed
thrice a day or oftener on highly spiced animal food from the table, or
on cakes, rich in fat, is a frequent victim. There is besides that
tendency to irritation of the skin which comes from hereditary
peculiarities and idiosyncrasy, from diseases of the stomach,
intestines, liver or kidneys, from faults in sanguification, nutrition
and secretion, agencies that disturb the circulation in the skin, like
excessive heat or cold, irritant dust, dessicated perspiration or sebum,
overheating and subsequent plunging in cold water. These acting locally
may serve to precipitate that which was otherwise imminent from a
generally acting cause.

_Symptoms._ There is first erythema, usually on the inner side of the
elbow, or thigh, with redness, heat and tenderness, which soon extend to
the belly, breast and intermaxillary region, but it confines itself as a
rule to the ventral aspect of the body where the hair is sparse and
delicate, and the skin thin and sensitive. The symptoms are more marked
in white haired dogs. The tender skin is more or less (usually
intensely) itchy, causing violent scratching with the development of
minute vesicles and even open sores. The skin may become moist,
thickened and wrinkled, but is rarely encrusted to any degree.
Spontaneous recovery may take place under a change of diet (restricted
or vegetable), or an outdoor life in summer with liberal exercise, or
the disease may last indefinitely so long as the etiological conditions
are unchanged.

_Diagnosis._ The affection is easily distinguished from demodectic
acariasis which attacks a different part of the body, namely, the head,
the eyelids, the feet, and the back, whereas, this form of eczema
confines itself to the ventral aspect of the trunk. From the eruption of
distemper it is diagnosed by the absence of the hyperthermia and
catarrhal symptoms of that disease, and by the very small size of the
vesicles; those of distemper are broad, flattened and often have dark
colored contents. From acariasis it is differentiated by its confinement
to the ventral aspect, in place of attacking the head, ears, neck and
back, by the less severe and incessant itching, and above all by the
absence of the acarus, and the element of contagion.

_Treatment._ A change of diet is a prime consideration. It may be in the
direction of simple restriction, but usually also in the avoidance of
meats that are highly peppered or spiced. A change to vegetable
food,—biscuit or mush and milk, is of great importance, but in some
animals a little fresh plainly cooked steak or raw lean meat may be
essential. In other cases a little beef juice or gravy well skimmed of
fat may tempt the patient to eat mush. In the same way it may be
necessary to temporize in the matter of meals. Some dogs can be safely
put on one meal a day, while for others accustomed to frequent feeding
it may be needful to give two and restrict the amount. For the overfed
or dyspeptic animal a laxative, at the outset, serves to remove
irritating and fermenting ingesta, and to place the stomach and liver,
and indirectly, the skin in a better condition for recovery. Any
persistent indigestion should be treated in the ordinary way.

Locally it may be requisite to first clean the surface by sponging with
tepid water, to be followed by soothing and antipruritic agents, due
care being taken to avoid such as when licked will poison the patient.
Starch powder, magnesium carbonate, and bismuth oxide may be used
without apprehension. The same is true of limewater and to some extent
of zinc oxide. When we advance to others we must take the precaution to
use a close wire muzzle, to prevent the ingestion of the agent. Carbolic
acid lotion (1–2 ∶ 100) acts as a local anæsthetic, and often materially
lessens both licking and scratching. Lead acetate or thymol or both (1 ∶
100) have a similar action. Thiol 20, glycerine 50, water 50, often acts
as well. When the acute symptoms have subsided the more stimulating
agents may be employed: Creoline (2 ∶ 100); oil of cade 1, vaseline 5;
Canada balsam 1, vaseline 5; zinc ointment, or lead acetate ointment.

OTHER ACUTE ECZEMAS IN DOGS.

Apart from eczema rubrum, the acute forms have been designated according
to their seat and the nature of the attendant eruption.

=Acute General Eczema.= This may be often traced to various causes of
irritation local or general: overfeeding, over-stimulating or spiced
food, digestive, hepatic, or urinary disorders, irritant dust or
inspissated secretions on the skin, hot seasons, over exertion, cold
baths when heated, skin parasites and scratching.

_Symptoms._ The whole skin, or a portion thereof is the seat of
pruritus, causing active scratching and on separating the hairs on the
affected parts there is found redness, congestion, and swelling with the
formation of papules or vesicles, abraded, or moist surfaces, and scales
or crusts. These patches are common on the _back_, the _head_, _ears_,
_rump_, (=Caudal eczema=), the _palpabræ_, the _lips_ (_eczema
labialis_), the _interdigital space_ (=interdigital eczema=), the
_scrotum_, or the _anus_.

Sometimes the formation of crusts and the loss of hairs is to be noted,
sometimes the eruption of large vesicles which burst and discharge a
honey like fluid (=impetiginous eczema=), sometimes blood escapes from
the irritated surface and concretes in dark crusts. The vesication and
moist exudation is especially common about the head, ears, eyelids, and
rump, while bleeding is especially seen around the claws and in the
interdigital spaces in connection with running on rough ground, snow or
stubble. The impetiginous form often bears a strong resemblance to
vesicles caused by a burn with hot water. The treatment of these
different forms does not differ materially from that of eczema rubrum,
being first dietetic and hygienic, then soothing, and finally
stimulating.

CHRONIC ECZEMA IN THE DOG.

Follows acute. Same general causes. Symptoms: skin thickens with
papules, vesicles or pustules, scurf, crusts, depilation, surface
glossy, abraded, scratched, raw, rough, fœtid, itching, emaciation,
exhaustion. Chronic eczema of the back. Fat, old, gluttons. Symptoms:
circumscribed patches on back, loins, quarters, tail, intense itching,
skin thickened, cracked, raw, encrusted, black, folded, rigid, fœtid,
hair broken, erect, shedding. Very inveterate. Chronic eczema of elbow
and hock. Causes: friction on summits of prominent bones, filth,
infection, predisposition. Symptoms: red, thickened, bare, indurated,
calloused skin, cracks, sores, discharge. Inveterate. Chronic dry
eczema of head, ears, neck and limbs. Circumscribed area, slow
progress, thick, rigid, folded skin, hairless, dry, scaly, moderate
itching. Treatment: Fresh eruption like acute form. For old chronic
form, stimulating astringents, silver, mercury, copper, boric acid,
tannic acid, iodoform: for dry and scaly, ointments of oil of cade,
tar, green soap, zinc, cresol, lysol, chloro-naphtholeum, sulphur,
sulphur iodide, ichthyol, salicylic acid, chrysarobin, naphthalin,
naphthol, resorcin.

While acute eczema may recover permanently under hygienic measures
alone, yet any case is subject to relapse and the new eruptions may
succeed each other so persistently that the affection becomes
essentially chronic. Like the acute, chronic eczema may be general or
local and be named accordingly.

The same general _causes_ as produce acute eczema are operative in
maintaining the disease indefinitely. Faults in diet, overfeeding,
unhealthy kennels, foul air and surroundings, hot weather, licking and
scratching are among the common causes.

_Symptoms._ Under the continued inflammation the skin becomes thick (on
the back it may be double or treble its normal thickness), it has a
general angry congested appearance, papules, vesicles and pustules
coexist or succeed each other and as these dry up, scales and crusts
accumulate. The hair drops off over extensive patches, leaving a
somewhat shining skin. What hair remains is largely twisted or broken by
rubbing and scratching. Hypertrophy of the papillary layer is not
uncommon giving a rough uneven aspect and feeling to the skin. A common
feature is an offensive odor from the affected skin, and which may
betray the persistence of the disease when it has been supposed that all
eruption has been overcome. While not prepared to follow Cadeac in
making this a diagnostic symptom from other skin diseases, yet as an
evidence that an eczema is not yet entirely healed it serves a very
useful purpose. In oldstanding cases the continued irritation, the
unintermitting itching, the absorption or circulation of morbid
products, and the constant nervous excitement may lead to emaciation,
exhaustion and death.

=Chronic Eczema of the Back in Dogs.= =Rodent Eczema= is a disease of
fat, old, voracious dogs. It appears in circumscribed spots and patches
on the back, loins, croup or tail and is marked by inveterate itching,
congestion and thickening of the skin, cracking of its surface,
bristling, breaking and shedding of the hair, exudation from the surface
and its dessication in the form of crusts. These crusts may be black
from contamination with dust or blood, and the affected surface is more
or less fœtid. The skin may be puckered into irregular folds, thick and
inelastic. Not infrequently the malady may remain dormant for some time,
only to break out again and again with renewed energy. It is very
obstinate and intractable.

=Chronic Eczema of the Elbow and Hock in Dogs.= This attacks the summit
of the olecranon or calcis and is manifestly connected with compression
and friction on these parts when lying down, and perhaps with foul and
irritating matters on the ground. This need not be looked on as the sole
cause but only as the occasion for the localization of a predisposition
which was already present in the general system. The skin becomes red,
thickened and indurated, the epidermis undergoing hypertrophy to form a
callus, in which a few cracks and sores may form, giving rise to a
discharge which encrusts the surface and adds to the thickness and
induration. The affection is very inveterate.

=Chronic Dry Eczema of Head, Ears, Neck and Limbs in Dogs.= The dry
eczema of the head, neck and limbs is characterized by its slow progress
and its restriction in the majority of cases to one or more of these
parts. The small affected patches, have some thickening and folding of
the skin, which is usually dry, scaly and largely divested of hair.
Itching is moderate only, and the hairs are shed less rapidly than in
the encrusted forms.

_Treatment._ When there has been a fresh irruption it may be requisite
to treat chronic eczema, for a time, after the manner of the acute, so
as to avoid any tendency to aggravation of the already existing
irritation. A careful regulation of the diet is as essential in the
chronic forms as in the acute and in the inveterate types, especially
those of a squamous character, alteratives like arsenic are often of
value. In the acute stage or during a recrudescence the mild dusting
powders (starch, zinc oxide, lycopodium, magnesia bicarbonate, bismuth
oxide, thiol) may be applied, or bland unguents (zinc, benzoated zinc,
lead, vaseline, glycerine, spermaceti and almond oil, paraffin, wax), or
sedative lotions (lead, opiate, thymol, thiol, carbolic acid).

In the more advanced and moist forms astringents and stimulants may be
adopted: silver nitrate (2 ∶ 100), applied with soft cotton, mercuric
chloride (1 ∶ 1000), or black wash (calomel 1 : lime water 60) care
being taken to use a close wire muzzle to prevent licking. Copper
sulphate (1 ∶ 100) is at times useful, and boric acid, and tannin may be
tried. Iodoform 1 part and tannic acid 5 has a good effect in many
cases.

For the dry and scaly forms, and indeed for many of the others, as well,
the more stimulating ointments and liniments are called for. Cadeac
recommends oil of cade, tinctures of cantharides, or a tar liniment made
with alcohol, as a supersedent to produce an active inflammation and
displace the unhealthy eczematous one. The agent is rubbed upon the skin
and the resulting scabs are left for a week when it is washed off with
tepid water and the skin is found healthy or greatly improved. As a rule
a second dressing of the tar is then applied. Müller strongly recommends
Hebra’s treatment with green soap and alcohol (2 ∶ 1) to be rubbed on
the affected surface and washed off the following day when all scales
and crusts will come off with little trouble. He follows with zinc oxide
or lotions of mercuric chloride or silver nitrate. Friedberger and
Fröhner use cresol 2 parts, green soap 2 parts, alcohol 1 part; also
creosote in alcohol (1:10) or in paraffin (1 ∶ 10). Zuill looks upon
sulphur iodide as virtually a specific: sulphur iodide 1 part, sublimed
sulphur 7 parts, cod liver oil 7 parts. This is applied once and
repeated at the end of ten days, if necessary. Application is made to
the whole skin healthy and diseased alike, and rarely requires to be
repeated.

Ichthyol is commended by Müller in cases which show great cutaneous
thickening with cracks and fissures. It may be made with water (1:5) or
in glycerine or lanolin of the same strength. Müller combines it with
lime water and olive oil and applies it daily.

Other agents in use are salicylic acid in olive oil (1:3): chrysarobin
in paraffin ointment (1:4): naphthalin or naphthol (1:10): resorcin in
water (2:100)

LICHEN. HEAT PAPULES. PRICKLY HEAT.

Horses, cattle, sheep and dogs suffer in hot season or hot stables.
Nervous temperament. Delicate skin. Over-driving. Heating foods. Cold
water when heated. Unwholesome food. Indigestion. Chronic affections
of stomach, liver, kidneys, etc. Symptoms: Clusters of small papules
on neck, back, croup, or thighs, crest, tail, exudate concretes, lifts
hairs from follicles, depilation in round spots, or patches,
abrasions, ulceration, corrugated skin. Diagnosis; sudden eruption,
its isolation, subsidence on the coming of cold weather, and
re-appearance with the hot, intense itching. Treatment: As in eczema.
Protect against friction, give shade, and spray with cold water.

Under this name has been described a papular eruption occurring in
horses, cattle, sheep and dogs in the hot season, but also occasionally,
in winter, in hot, confined stables.

It is seen especially on the neck, back, croup and thighs, is common in
fine bred horses with delicate skins, and nervous temperament, and is
pre-eminently a disease of hot weather. Over-driving, heating food, a
drink of cold water when heated or indigestion connected with unsuitable
food may be the occasion of its irruption or tend to perpetuate it. In
the same way different chronic affections of the stomach, liver, kidneys
or other organs may be causative factors.

_Symptoms._ The affection usually begins with a few minute papules,
isolated or in clusters, which dry up into scales or crusts. These are
mostly situated at the roots of the mane or tail or on the sides of the
neck, withers or trunk, and as a rule produce a pruritus, resembling
that of scabies in its intensity. When the exudate agglutinates a tuft
of hair, enclosing it in a dense crust, the hairs may be lifted from
their follicles and thus small, round spots of depilation appear. If
recovery ensues and new hair starts, it differs in color from the old
and gives a dappled appearance to the skin. In many cases, however, the
points of eruption and encrustation become confluent and an extensive
area of bareness, with more or less abrasion, and even ulceration may be
formed.

Megnin mentions two cases and the author can adduce another in which the
eruption appeared in vertical lines, so that the skin of the trunk was
raised in a series of elevated lines or ridges, running transversely to
the body, like the stripes of a zebra. In the author’s case the skin
seemed to be thrown into a series of folds to the production of which
the cutaneous muscle evidently took part. The itching was doubtless the
immediate cause.

_Diagnosis_ is based largely on the suddenness of the eruption; on its
limitation to a given area instead of spreading from the primary seat of
invasion as in acariasis; on the fact that it is usually confined to a
single animal and has not spread with the use of the same brush, comb
and rubber; and on the absence of acari and vegetable parasites from the
affected parts. The absence of chicken roosts or manure is another
valuable indication.

_Prognosis._ Appearing in spring or early summer, the disease is liable
to persist until the advent of cold weather in fall, and even after a
winter’s intermission there is a strong tendency to its re-appearance on
the following spring or summer. The intolerable itching interferes
seriously with docility and steadiness in harness, and the loss of hair
renders the subject very unsightly, and as a family or driving horse
practically useless.

_Treatment._ As in cases of eczema the general and special causes should
be corrected by hygienic and general medicinal measures, laxatives,
diuretics, antacids, tonics, and in the advanced stages, alteratives
coming in as important factors. (See under acute eczema). Great care
should be taken to prevent irritation by pressure of the harness, and
shade and daily cold spraying may be availed of.

PITYRIASIS: SQUAMOUS SKIN DISEASE: HORSE.

Dry, scaly, or powdery affection. Causes: Fine, thin, dry skin with
little hair, race, Arab, Barb, racer, trotter, nervous temperament,
age, dry summer heat, dry winter cold, foul skin, caustic soaps,
ingestion of salt, iodides, bromides, etc., derangement of internal
organs bacteria or cryptogams. Symptoms: scurfy patches, general or
circumscribed, where little hair is, where harness rubs, depilation of
ears, crest, tail, shoulder, back. Diagnosis, from eczema by lack of
pruritus, of rapid extension, of thickening of the skin, from
acariasis by absence of acarus. Treatment: correct disorder of
stomach, liver, or kidneys: green, succulent or nutritive food;
alkalies; arsenic; tonics; locally potash soaps, ointments of tar,
birch oil, creolin, creosote, naphthalin, lysol, mercury, iodine,
salicylic acid, zinc oxide.

This is a skin disease characterized by excessive production of
epidermic scales, and depilation without any attendant elevation of the
skin. The desquamation may be of fine scales like wheat bran, or of a
fine dust like flour.

_Causes._ The disease is especially characteristic of animals in which
the skin is naturally fine, thin and dry and covered sparsely with hair.
It is therefore more common in the Arabian, Barb, English racer,
American trotter and other breeds of a nervous organization than in the
heavier draught breeds. Old horses in which the skin is drier and the
hair thinner are more subject to it than the young. Again it has been
especially noticed in the heats of summer with thin coat and a withering
action of radiant heat on the skin, and less frequently in winter when
the blood is driven from the surface by cold. Much also depends at times
on the lack of grooming, on the accumulation of dust and dried up
secretions about the roots of the hair, and on washing with caustic
irritant soaps especially in long-haired regions. It has even been
claimed that the ingestion of salt, potassium iodide, or bromide, etc.,
contributes to the affection. There is undoubtedly a certain individual
predisposition to the disease, shown as already stated in certain
breeds, but also inherent in particular families and even animals, and
associated not only with the character of the skin, but also probably
with variations in the activities and products of various internal
organs. In man pityriasis versicolor is associated with a specific
fungus, and in the horse Megnin has described cases in which the surface
of the skin and especially the hair follicles show a mass of epidermic
cells mingled with mycelium and an abundance of spores.

_Symptoms._ The scurfy product and depilation may be found in patches
scattered indiscriminately over the body (generalized), or confined to
particular regions (circumscribed) as to the head, ear, crest, tail, or
the parts that receive the friction of the harness. It may commence as a
dry, rigid, state of the skin under the headstall with loss of hair and
the excess of dandruff. From this or from another point the extension
takes place slowly and with comparatively little irritation or itching.
The hair is pulled out with great ease, and from its spontaneous
evulsion, more or less baldness appears progressing slowly from the
original centres of the disease. It may leave the whole crest divested
of the mane, or the tail of its hairs (rat tail), or the ears may become
bare and scurfy. Again the parts subject to friction like the back of
the ears, the crest, in front of the shoulder, or the seat of the saddle
may be the main seats of depilation and baldness.

It is to be distinguished from dry eczema mainly by its tendency to
spread over a larger area in place of confining itself to circumscribed
patches, and more particularly by the absence of the marked thickness
and rigidity of the skin which characterize eczema. From acariasis it is
distinguished by the lack of the intense itching, of the tendency to
more or less moist exudation and above all by the absence of the acari.

_Treatment._ It is well to correct any disorder of any of the internal
organs, notably of the stomach, liver or kidneys, and to encourage a
free circulation in and secretion from the skin. To fill the latter
indication green food, ensilage, roots, sloppy mashes of bran, oilcake
and the like may be given. Also bicarbonates of soda or potash or other
alkaline diuretics, and in certain obstinate cases a course of arsenic.
The alkalies tend to eliminate offensive and irritant matters and to
lessen the irritation in the skin. A course of tonics is often valuable.

Locally Cadeac recommends potash soaps rubbed well into the affected
parts. If this should fail some of the stimulant ointments as of tar,
oil of tar, oil of white birch, oil of cade, creoline, creosote, lysol,
naphthalin, may be tried. Megnin strongly recommends a combination of
ointment of biniodide of mercury, 1 part, to mercurial ointment 3 parts.
Others advocate salicylic acid (10 to 20%) mixed with Lassar paste which
is compounded of 1 part each of zinc oxide and starch in 4 parts
vaseline.

PITYRIASIS IN CATTLE.

On neck and dewlap; Causes: anæmia, debility, spoiled food,
starvation, constitutional predisposition. Symptoms: shedding hair and
scales without skin thickening, or itching. Treatment: green soap,
tar, creolin, lysol, naphthalin, etc. Alkaline lotions: generally
nutritive, succulent food, bitters, iron, arsenic, etc.

This is noticed especially on the neck and dewlap in connection with
anæmia, low condition, unsuitable, innutritious and spoiled fodder and a
constitutional predisposition. It has the same general characters as in
the horse, an excessive production of dandruff or dry scales without any
marked change in the thickness of the skin or in its circulation.
Treatment consists in the application of green soap, pure or medicated,
with tar, creolin, lysol, or other empyreumatic product. Lotions of
carbonate or bicarbonate of potash are often effective. Any disorder of
digestion, or of the urinary or hepatic functions, or of general
nutrition should be corrected, and in most cases, a course of bitters,
with iron and arsenic is desirable. A good, indoor hygiene or a run on
succulent grass in the open air may be resorted to with benefit.

PITYRIASIS IN THE DOG AND CAT.

Head, neck and back of overfed, old house dogs. Symptoms: floury
dandruff, with little itching or redness, on limited areas; in cats
over the whole back, where stroking causes electric development, the
collecting of the hair in tufts, and insufferable irritation. Hair
constantly shedding without necessarily bare patches. Treatment:
simpler, restricted diet, correct internal disorders, laxatives,
arsenic, locally solutions of alkalies, borax, potassium sulphide,
sulphur iodide, baths.

In dogs this affection attacks especially the head, neck and back of pet
and house dogs gorged with dainties, and particularly in those that are
already becoming aged. The affected parts are covered with a floury or
branlike product lying upon a dry surface usually devoid of irritation
or congestion, though it may be distinctly congested and reddened, and
even the seat of pruritus. The affection is usually confined to limited
areas, more or less destitute of hair, and without showing a disposition
to active extension. In the cat, however, it may affect the whole dorsal
aspect of the body, being associated with extreme electrical
susceptibility, so that on being stroked the hair at once collects in
tufts, crackles, and in the darkness sparkles, and the animal at first
fawning on the hand, will fly at and scratch it after a few strokes. The
scaly product is excessive and drops off abundantly when handled,
without, however, leaving thin or bare patches.

_Treatment_ is mainly in the line of a simpler and more natural diet,
the avoidance of sugar and cake, the correction of disorders of the
digestion, or of the hepatic or urinary functions, the exhibition of an
occasional laxative, and of alteratives, especially Fowler’s solution.

Locally, alkaline lotions, carbonate or bicarbonate of soda or potash,
borax, sulphide of potassium and iodide of sulphur are often useful. A
moderately strong solution of common salt with glycerine in water is an
useful alternate, and a warm saline or bran bath may soften the skin and
modify its nutrition.

CONTAGIOUS PUSTULAR DERMATITIS IN THE HORSE. ACNE.

History. Cause: bacillus. Symptoms; incubation 6 to 15 days, skin
tenderness, heat, swelling like peas, hazel nuts, vesicles, pustules,
exudation, concretions among hairs, depilation, healing in 15 days.
Leaves white spots with lighter hair. Extension by grooming: general
eruption: subcutaneous swelling, sloughs, delayed healing.
Lymphangitis. Diagnosis: from chaps and bruises, from horse pox, from
impetiginous eczema, from urticaria, from farcy. Prevention,
quarantine new horses, separate diseased, disinfect skins of the
unaffected, disinfect stables and harness. Treatment: soapy wash:
germicide lotions.

This has been largely described as an imported disease thus on the
European continent it is the English variola, and in England the
Canadian contagious pustular affection. Yet the first authentic account
dates back to 1841–2 when Goux found it attacking an entire squadron of
the French army in a fortnight. Axe described it in England in imported
Canadian horses in 1877, and Weber observed it in the same year on the
continent, where it was attributed to imported English horses. In 1883
it was noted by Schindelka, in 1884 Siedamgrotzky inoculated it from the
horse on two rabbits and two Guinea pigs, and to horse and goat. The
rodents developed a “malignant œdema” at the point of inoculation and
died in six days. Grawitz and Dieckerhoff cultivated the bacillus on ox
or horse serum and found it 2μ in length, dividing by segmentation into
round or ovoid refractive spores, which may remain connected as
diplococci or short chains and which color deeply in fuchsin. It grows
most rapidly at a temperature of 37° C., growth ceases at 17° C., and it
is destroyed in half an hour at 80° to 90° C. Preserved, dry, it
remained virulent for four weeks and produced the characteristic
eruption when rubbed on the skin of the horse, ox, dog, sheep or rabbit.
It proved fatal to all rodents, including white mice. The microbe is
found abundantly in the pus and crusts and is easily shown when these
are treated with potash. It produces no putrid fermentation.

_Symptoms._ When inoculated it had an incubation of six to fifteen days
followed in mild cases by swelling heat and tenderness of the skin with
collection of the hair in erect tufts. Next day there are rounded
elevations like peas or hazel nuts, discrete or confluent on the swollen
patches. These nodules, at first firm and resistant soon become soft in
the center, forming vesicles and finally pustules, which burst in five
or six hours and exude an abundant liquid which concretes in a thick
amber colored mass. The hairs in the center of the resulting raw surface
are easily detached leaving bare spots the size of a dime, with often
times a slough attached in the center. When this is finally eliminated
the surface gradually cicatrices and recovery may be complete in fifteen
days. The skin remains long dappled from the partial discoloration of
the epidermis in the seat of the pustules. The malady is local and
hyperthermia is rarely seen. The submaxillary and pharyngeal lymph
glands are usually swollen and indurated, but this disappears speedily
after the subsidence of the eruption.

In certain cases the extent of the primary eruption is greater from the
first, or it extends through reinfection by combs, brushes and rubbers
used in grooming or by friction by the harness, the affected skin is
hot, painful, congested and thickened throughout its entire substance,
the pustules are much more numerous, often confluent, and may even
implicate the subcutaneous connective tissue. The crusts formed on the
sores may acquire a breadth of 1 inch to 1½ inch. Considerable abscesses
may be formed and the lymph glands communicating with the affected part
are hot and swollen. Even after the opening and discharge of the
abscess, the base of the sore remains indurated and indolent, and
centres of softening and caseation may appear so that healing is delayed
for one or two months or more. In such cases extensive cicatrices remain
after recovery. Lymphangitis is a common accompaniment with even abscess
of the lymphatic glands.

_Diagnosis._ From chafing and bruising by the harness, this is easily
recognized by its appearing also on other parts than those covered by
the harness, by the development of the characteristic pustules, by its
following a regular cycle of eruption and subsidence covering a definite
period of usually 15 days, and by the indisposition to maintain itself
indefinitely under the friction of the harness.

From _horsepox_ it is distinguished by the habitual avoidance of the
common seats of election of that disease (heels, lips, nostrils, buccal
and nasal mucosæ, lips of the vulva), by the absence of hyperthermia,
and by the comparative absence of the remarkable amber-like concretions
which characterize horsepox in the lower limb.

From _impetiginous eczema_ it is diagnosed by its contagious and
inoculable properties, by the absence of the early falling of the hair
from the circumscribed rounded nodules, and by the absence or moderate
character of the pruritus which is usually intense in the eczema.

The eruption of _urticaria_ appears much more suddenly, shows no
tendency to form vesicles nor pustules, is not inoculable, and subsides
often as suddenly as it appeared when the irritant food materials have
been expelled from the alimentary canal.

From acute _farcy_ it is distinguished by the moderate degree of the
implication of the lymph vessels and glands, by the white creamy nature
of the contents of the pustules, as compared with the glairy, oily
nature of the farcy discharge, by the absence of coincident nasal
ulcers, submaxillary nodular swellings or other lesions of glanders, by
its short course and tendency to spontaneous early recovery, and by the
absence of reaction under the mallein test.

In all cases the known prevalence of the contagious pustular dermatitis
in the locality, or the introduction of strange horses which exhibit
sequelæ of the lesions will assist greatly in the diagnosis.

_Prevention._ If animals are introduced from an infected or unknown
locality they should be kept apart from others for two weeks. In a
stable where it has already appeared the diseased and healthy should be
carefully separated and the skins of those as yet unaffected may be
washed with a solution of mercuric chloride (1 ∶ 1000) or creolin (1 ∶
100). The walls of the stable should be whitewashed, and all stable
utensils disinfected in boiling water or one of the above named
antiseptics. The harness demands particular attention.

_Treatment._ This is essentially germicide. After a soapy wash, any one
of the usual disinfectants may be used: aluminum acetate, (1 ∶ 15),
mercuric chloride (1 ∶ 1000), carbolic acid (1 ∶ 50), creolin (1 ∶ 50),
copper sulphate (1 ∶ 50), etc. Lead acetate 2 parts, alum 1 part and
water 50 parts, has been found to be effective.

PEMPHIGUS IN HORSE, OX, PIG AND DOG.

On rare occasions the horse or ox is attacked with a skin eruption,
attended with the formation of bullæ or blisters, from the size of a
hazel nut to a hen’s egg, or larger. It is sometimes shown sporadically
and at others appears at once in a large number of animals in the same
herd. The _causes_ are obscure, yet the enzootic appearance of the
affection is suggestive of a common factor entering probably by the
food. Loiset and Seaman have recorded enzootic outbreaks in cattle and
Dieckerhoff in the horse.

_Symptoms_ are cutaneous congestion with the formation of swellings like
a walnut, but exceptionally as large as the fist, on the head, neck and
thorax, which in 2 to 4 days form a large central vesicle, with
yellowish serous contents. Cases in the ox (Loiset, Seaman) had a
similar eruption on the loins, quarters and hind limbs, some of the
swellings attaining the size of a hen’s egg, and with similar contents.
Later these ruptured, crusted over and healed, with, for a time, a
smooth glistening surface. Winkler records cases in swine and
Schneidemühl in dogs, but the condition is rare in both animals.

_Treatment._ To a nutritious, non-stimulating and easily digestible
diet, may be added a course of arsenic and, in low condition, of
bitters. Locally dusting powders of zinc oxide, boric acid, starch and
lysol. Should the exudate form these into hard cakes, they may be
replaced by carbolized oil or, better, a 5 per cent. mixture of ichthyol
in vaseline.

CRACKED HEELS IN HORSES. SCRATCHES.

Special susceptibility and exposure of posterior pastern region.
Divisions. Causes: local irritants, decomposing manure, chill water,
slush, mud, pools of liquid manure, septic irritation, stones, sand,
lime in mud, salted snow or ice, washing heels, caustic soaps,
stubble, clipped or singed hair, stocking of limbs, lymphangitis,
sprains, arthritis, anæmia, cardiac, urinary or hepatic disease,
parasites, heavy bedding, constitutional predisposition. Symptoms:
redness, heat, tenderness, swollen, erect hairs, lameness, knuckling,
or exudate, crusts, scabs, abrasions, chaps, fissures, ulcers, loss of
pliancy, engorgment of limbs, fœtid secretion. Prognosis according to
cause. Treatment: remove causes, give rest, cleanse limb and stable,
astringent antiseptic lotions, sulphurous acid, carbolic acid,
creolin, lysol, pyoktannin, chrysophanic acid, moderate laxative food,
diuretics, arsenic, bandaging, hand rubbing, exercise.

The affections of the heel or posterior part of the pastern in horses
are largely modified by the anatomical character of the skin in this
region, and the special exposure to inimical agents, so that it is
convenient to consider them under special headings, even though the
eruption may be of the same kind with that seen in other parts. The
dermatitis of this region, which are not primarily contagious may be
conveniently divided into 1st, such as are unattended with free
secretion, and 2d, those that implicate the sebaceous glands and are
marked by an offensive discharge. Cracked heels belong to the former
category.

The _causes_ are extremely varied, consisting in the application of
irritants of many kinds, to the susceptible skin in a system too often
already predisposed to skin disease.

Standing on reeking dungheaps, or on heating manure in filthy stalls
subjects the heels, and especially the hind ones, to ammonia and other
irritating fumes, and when taken out to the cold air, chill water and
mud, the sensitive parts suffer. Again in the farm yard and even in
neglected stalls the hind feet are immersed in pools of liquid manure,
the ferments and toxic matters of which dry on the skin, attack the
surface and determine septic congestions and inflammations. On country
roads where there is no pretense of pavements, or macadam, the mud in
spring and fall is a source of great irritation on certain soils which
contain small flat stones, pebbles or sand, or in which lime or
decomposing manure is a prominent feature. Standing in snow or slush,
especially if chilled by salting, produces partial or complete
congelation with the result of chillblains or even more active and
destructive inflammation or sloughing. The habit of washing the heels
and allowing them to dry spontaneously in the stall is only less
injurious by the chill induced. This is still further aggravated by the
use of caustic soaps on the already tender skin. The lighter breeds of
horses, devoid of long hair on the pasterns, though less subject to the
_greasy_ secretion, are even more exposed to chills and direct injuries,
and suffer readily and often persistently from erythema and cracks. In
many cases trouble comes from the ends of stubble and other vegetables
acting on the skin. A common fault is the close clipping and even
singeing of the hair in the hollow of the heel. The stiff, bristly ends
of the hairs on one fold of the pastern continually prick the skin of
the adjacent fold when the animal is in motion and not only is this
irritating to the healthy skin, but it becomes incomparably more so when
that is congested and tender. Even in summer the deep dust on unpaved
roads, mixing with the normal secretions of the heel, rolls into
semi-solid masses between the folds and proves the more irritating, the
greater the admixture of sand or solid bodies. A common cause is the
stocking of the limbs, with the attendant congestion, distension and
debility of the skin. This may be due in its turn to a great variety of
proximate or remote causes, lymphangitis, sprains, arthritis, osteitis,
anæmia, cardiac, urinary or hepatic disorder, parasitisms, etc., so that
accessory causes must often be widely sought. Even an excess of straw
around the hind limbs will cause stocking in some animals which escape
on bare pavement. Finally we must take into account that constitutional
predisposition in some animals that makes them liable to inveterate skin
diseases under the slightest causes.

_Symptoms._ In the _milder forms_ there may appear a redness, with heat,
tenderness and swelling in the hollow of the pastern, the hairs stand
stiffly erect, and the surface may be perfectly dry. The affected limb
has the pastern more upright than the others and the fetlock starts
slightly forward. In a nervous, sensitive horse the skin is so tender
and rigid, that the animal can hardly be persuaded to use the limb, and
goes dead lame for a considerable distance until it has become more
pliant.

With some aggravation of the condition the skin is felt to be somewhat
rough and uneven by reason of the encrustations of epidermis, dried
secretions and dust over its surface, which may convey to the finger a
slightly oily sensation. In many cases these epidermic and exudation
products form scabby elevations, and a chronic condition of this kind
may persist indefinitely, constituting what is known in America as
_scratches_. This will vary by reason of the detachment of these
concretions with the formation of abrasions and sores of various sizes,
which may heal, or extend by coalescence, chapping, or ulceration.

In other cases, even at an early stage, the formation of chaps or cracks
is a marked feature. At times this may seem to be the result of over
distension in the inflamed superficial layers of the skin which have
lost their natural pliancy and cohesion. They will, sometimes, form
under slight exercise, but not when at rest. They may simply extend
through the epidermis, exposing the papillary layer, or in bad cases one
or more fissures may extend through the integument and expose the
tendons beneath. They may extend forward on the sides of the pastern or
upward over the back of the fetlock and metatarsus.

In all cases, when the local inflammation is acute, some swelling of the
limbs appears, and this keeps pace with the character and extent of the
trouble. With extensive chaps or fissures it becomes extreme, extending
up toward the hocks and attended by great pain and stiffness. The sores
become the seat of active suppuration, with it may be considerable
destruction of tissue. Even in the milder forms there may often be seen
a fœtid muco-purulent secretion in the depth of the folds of the
pastern, and in the worst cases this extends to the whole surface after
the manner of _grease_.

_Prognosis._ The milder uncomplicated cases recover readily and
perfectly under rest and judicious treatment; the more advanced cases
are liable to leave swelled legs with susceptibility to a relapse, and
in cases associated with a constitutional diathesis or chronic internal
disease, recovery may become problematical and uncertain.

_Treatment._ In all cases the cause must be done away with, whether
filthy stalls, reeking dunghills, septic pools, work in irritating road
mud, or melting snow, washing the heels with caustic soaps, drying them
in cold draughts, pricking with stubble or clipped hairs, and all the
causes of stocking of the limbs. If heels are washed, use pure tepid
water, and, if necessary, the best Castile soap, and rub them dry at
once. If this cannot be done bandage them rather than leave them in a
cold draught.

Give rest in a clean stall and thoroughly clean the affected heel, then
wrap in a bandage wet with an acetate of lead or sulphate of zinc lotion
(1 ∶ 50), or apply benzoated oxide of zinc, or cream of glycerine and
salicylic acid.

When chaps have formed they will often promptly heal under standard
solution of sulphurous acid 1, glycerine 1, and water 1. This is applied
on soft cotton and covered by a rubber bandage to confine the acid. The
sulphurous acid solution should be recently prepared, since it will
prove injurious if it has oxidized into sulphuric acid. To one or other
of these preparations the addition of a little carbolic acid, creolin,
pyoktannin, or lysol will often prove useful. When the cracks have
healed, zinc ointment, chrysarobin ointment, chrysophanic acid 1,
vaseline 15, or other soothing and antiseptic agent may be employed till
all inflammation has subsided, and the animal must not be returned to
work until the skin has been restored to its former healthy and elastic
condition.

It may be desirable to greatly restrict the grain during treatment and
even to giving cooling laxatives or diuretics. With a constitutional
diathesis arsenic or other alterative may be tried, and any internal
disease must be attended to. For stocking, use careful bandaging,
hand-rubbing and exercise.

With the formation of the deeper fissures the same antiseptic agents may
be employed, or salol, iodoform, glutol, aristol, or some tincture of
iodine, or iodide of starch may be used. A weak solution of copper
sulphate has often an excellent effect. The measures advised below for
_grease_ will usually apply in this condition.

SEBORRHŒA OF THE DIGITAL REGION: DIGITAL IMPETIGO, GREASE: STREPTOCOCCIC
DERMATITIS IN HORSES.

A sequel of erythema or cracked heels. Causes: constitutional
predisposition in lymphatic draught horses, rare in ass and mule,
anatomical conditions, wet damp regions, digestive disorder,
overfeeding and lack of exercise, diseases of liver or kidney, change
to stable life, cold water, slush, mud, salted snow, steaming manure,
urine in mares, infection, streptococcus pyogenes. Symptoms: swelling,
heat, and tenderness of pastern hollow, itching, hairs erect, unctuous
exudate, vesicles, excoriations, discharge opaque, grayish, sticky,
fœtid, chaps, knuckling, resting on toe, kicking: in severe cases
discharge purulent, more opaque, sloughs, excessive granulations,
“grapes,” extensions forward, upward, downward, canker, quittor, sand
crack, etc. Lesions: first, congestion of derma, hair follicles full,
hairs loose, connective tissue infiltrated, or thickened, ligaments:
and bones involved, grapes in superposed clusters pediculated.
Diagnosis: from horsepox. Treatment: remove causes, secure
cleanliness, laxative, diuretics, moderate grain ration, or tonic
regimen; locally, soothing antiphlogistic, antiseptic treatment, lead,
zinc, phenol, creolin, lysol; when advanced, antiseptic dusting
powders, calomel, salicylic acid, iodine, zinc oxide, salol, or
solutions, zinc chloride, tar. Value of changes. For “grapes” actual
cautery, excision, ligature.

This may develop as an advanced condition of the erythema or cracked
heels already described. Yet it is so distinctive in its habit of
profuse secretion, the eruption of vesicles or pustules and the
abundant, fœtid sebaceous discharge that it deserves a special
consideration.

_Causes._ Something depends on constitutional predisposition. This is
preëminently a disease of the heavy, lymphatic, draught horse, being
rare in racers and trotters, with fine sinewy limbs, no long hair on the
fetlock, delicate skins, and less abundant sebaceous glands. It is
almost, though not quite, unknown in the spare limbs of ass and mule,
and though claimed by Reynal as attacking cattle its occurrence is
equally rare in them. Much of this may be attributed to conformation.
The limb of the draught horse is so much thicker and coarser, with a
great excess of connective tissue and lymph plexus which become readily
gorged in idleness, inducing stocking, congestion and debility of the
whole limb. This same condition operates as a powerful predisposition to
lymphangitis. Again the great length and profusion of the long hairs,
entails the necessary compliment of an excessive development of the
sebaceous glands which become over-stimulated by congestion, and afford
a much more open and favorable infection atrium for the pus microbes.
These structural conditions are much more marked in the draught horses
of wet regions as in Ireland, the western counties of Great Britain,
Belgium, Holland, and the Atlantic provinces of France, and in these the
affection is remarkably prevalent. In our Eastern States and on the
Plains, where the progeny of imported draught horses lose their digital
hair, the malady is comparatively rare. A similar immunity has long been
noticed in the horses of Spain and Africa. Disturbances of the digestion
in heavily fed horses, subjected to transient confinement in the stall,
and diseases of the liver and kidneys, must be recognized as further
predisposing causes. The age of five and six when many horses change
hands, and are subjected to extreme changes of stabling, feed and work,
has furnished the greatest number of cases.

External causes we find in all those conditions already enumerated which
favor chapped heels. Wet, mud, gritty masses, irritant fumes of manure,
cold, heat, filth are potent factors. In connection with these are the
pus and septic microbes that are always present in stables, farm yards,
manure, street dust, etc. No one of these can be adduced as the constant
and exclusive cause, and it is inevitable that a complex infection
should be present, yet the propagation and persistence of the disease
may often be connected with the streptococcus pyogenes.

As emphasizing the importance of such external irritants and infections,
it should be noted that the disease bears an appreciable relation to the
filth and wet of the stable and farm yard, and to the absence of
cleanliness in dealing with the feet, and that the extension of good
pavement and protection from road mud have invariably lessened its
prevalence. The irritant action of the urine renders mares more
susceptible in the hind limbs than horses.

_Symptoms._ The disease may appear as a swelling, heat and tenderness of
the hollow back of the pastern, involving the fetlock and lower part of
the metatarsus or metacarpus, and this may last for one or two weeks,
the engorgement lessening or disappearing during exercise and
reappearing when at rest in the stall. The local tenderness is great as
manifested by the prompt and excessive lifting of the leg when the heel
is touched, as well as by the lameness when first moved, which subsides
with further exercise. Itching may be shown by kicking the floor, or by
a disposition to rub the pastern. The hairs of the affected part are
rigidly erect, and a slightly moist, soapy sensation is felt on the
skin. Close examination may detect the presence of small vesicles with
as yet limpid contents, but the greater part of the liquid product is
traceable to the openings of the hairs and gland ducts. This is followed
by small excoriations taking the place of the ruptured vesicles, and the
discharge becomes more profuse, opaque, white or grayish white, sticky,
and fœtid. It covers the entire affected surface, mats together the hair
in tufts and forms a thicker grayish border. The hairs are loosened in
their follicles and easily pulled out. The erosions become complicated
by chaps, and the swelling increases around the pastern and above the
fetlock. When at rest in the stall the foot may be rested on the toe
only, or held suspended and occasionally kicked backward as if to
dislodge the cause of irritation, yet if moved the patient may gradually
get over the greater part of the lameness, and the swelling partially
subside.

In severe, protracted cases the discharge becomes essentially purulent,
but often with a darker, greenish, reddish or blackish tinge, and
portions of the skin may slough, leaving deep intractable sores. Still
more commonly the raw surfaces become the seat of hypertrophied
granulations, which grow out to form raw, red fungous like, pediculated
neoplasms familiarly known as _grapes_. Between these the spaces are
filled with tufts of hairs and the condensed discharges, in process of
active septic change, and giving off a most repulsive odor. Like the
preceding eruption these _grapes_ may extend around the front and sides
of the pastern, and upward beyond the fetlock, but especially behind.

This advanced condition shows no tendency to spontaneous recovery and
the connective tissue and lymphatic plexus becoming involved, the leg
often swells to enormous dimensions, from six to twelve inches in
diameter at the fetlock. It may last indefinitely until the patient is
worn out, or it may extend to other organs by contiguity or embolism.
Canker of the frog and sole, fistula (quittor), sand crack and seedy toe
may be named as complications, also septicæmia or pyæmia with abscesses
in the lungs, liver, brain or bowels.

_Lesions._ In the first stage there is mainly the congestion of the skin
extending into the large and numerous hair follicles of the pastern. If
pressed, a transparent serum bedews the surface, and if sectioned the
follicles around the hair bulb are seen to be distended by a similar
product. The hairs are easily pulled out. The subcutaneous connective
tissue is filled with a yellowish serosity and at intervals may be seen
a red point of vascular stagnation or blocking. Later these products are
more abundant and those on the now swollen and excoriated surface are
distinctly fœtid. The infiltrated lymph plexuses in the connective
tissue are more distended, their walls thickened and consolidated, and
the rigid skin is thus firmly bound to the structures beneath. A careful
examination shows the presence of subepidermic vesicles of various
sizes. The congestion may extend deep enough to involve the periosteum
of the digital bones and the ligaments of the joints. The _grapes_ are
each attached by a pedicle from which branch out cauliflower-like, fine
papillary processes, that aggregate into a solid cluster. They are very
vascular and grow out cluster above cluster until they reach large
dimensions.

_Diagnosis from Horse Pox._ Since the days of Jenner the claim has been
constantly made that _grease_ and _horse pox_ were one and the same.
Horse pox is however to be distinguished by its transient course, its
inoculability, its incubation of three days, its abundant exudate
concreting on the hairs of the pastern as a yellow mass suggestive of
crystalline structure, by the red pit in the skin in which this mass is
imbedded, by the spontaneous recovery in about 15 days, and by the
immunity on a subsequent inoculation. It is communicable to cattle and
to man, producing the characteristic large umbilicated vesicle and scab.

_Treatment._ The first consideration is to remove the causes of local
irritation and infection, give a clean sweet stall, with dry floor, and
allow no contact with putrid liquids, mud, cold water, melting snow or
other irritant. If exercise is needful to obviate _stocking_ of the legs
give it on dry clean ground.

If inflammation runs high with fever and costiveness a laxative will be
valuable and it may be well to follow this in some cases with cooling
diuretics. When the animal has been on a heavy grain ration this should
be largely cut down in keeping with enforced idleness, or restricted
work. If on the other hand condition is low, and the discharge profuse a
more generous ration may be desirable.

Local treatment is essentially soothing and antiphlogistic, and in view
of the infection should be antiseptic. _White lotion_ (acetate of lead
and sulphate of zinc of each ½ oz., water 1 quart) has been long used
with fair success, for although lead sulphate is thrown down, it is in
part freed again through contact with the exudate. It will be materially
improved by the addition of 1 dr. carbolic acid, creolin, lysol or
chloro-naphtholeum or by some other antiseptic. Lead acetate alone with
an antiseptic is an excellent substitute. In mild cases the surface may
be wet with the lotion several times a day: while in severe ones the
lotion may be applied on a bandage kept constantly wet. When secretion
is well established it may be better to use dry applications, as
calomel; salicyclic acid 10 parts, with iodine 10 parts; calomel and
lamp black; carbolated oxide of zinc or burned alum, salol, etc. After
washing and drying the skin, dust this freely even into the deepest
wrinkles and cover with cotton and bandage. Dress twice daily. For very
fœtid cases, Robertson recommends zinc chloride 1 oz. in 1 qt. water
with the addition of glycerine and phenol, and again a saturated
solution of copper sulphate with carbolized glycerine. For profuse
secretion after the subsidence of active inflammation Renal highly
recommends wood tar with 5 to 10 drops of sulphuric acid to the ounce.
Under these circumstances a powder of gloss starch 5 ozs. with iodine ½
oz. may be employed twice daily. Or again, 1 oz. each of carbolic acid,
tincture of iodine and glycerine may be employed. When one agent seems
to be losing effect, it is well to change for another and never to
neglect the regular dressing, until full recovery has been secured.

In case of _grapes_ the actual cautery is the most efficient measure.
Heat a blacksmith’s fire shovel to a bright red and use this to cut
through the pedicles, a cool shovel being kept constantly beneath it and
in contact with the pedicles, so as to protect the adjacent skin from
injury by the radiated heat. The lower shovel must be dipped in cold
water at very frequent intervals to cool it and prevent cauterization of
the skin between the pedicles. This not only removes the diseased and
infected masses, but leaves the stumps of the pedicles aseptic. Another
method is to cut off the “grapes” and staunch the blood with the actual
cautery at a dull red heat. Still another is to tie the pedicle of each
excrescence separately so as to cut off circulation and secure
sloughing. This is, however, a long, tiresome process, and entails
prolonged contact with much infecting dead tissue. After either method
the parts must be dressed with antiseptics, and dealt with generally
like cases in which the excrescences had not formed.

CUTANEOUS HEMORRHAGE: BLOODY SWEAT: HÆMATIDROSIS. HÆMATOPEDESIS.

Forms of cutaneous hæmorrhage; in specific diseases; in parasitism; in
insect bites; in congestions of sweat glands; in deranged innervation;
in hæmophilia. Section of sympathetic. Salt on sciatic. Hysteria.
Sclerosis of cord. Inflammation. Symptoms: drops, crusts. Hæmorrhagic
nodules. Treatment: styptics, cold, ice, snow, tannin, matico, iron
chloride, alum, gelatine, atropine, ergot, lead acetate, quinia.
Gravitation.

The escape of the blood by the skin is seen in a variety of morbid
conditions, due it may be to profound changes in the blood and capillary
walls, as in petechial fever, anthrax, scorbutus, septicæmia, swine
erysipelas, etc., in which this is only a subsidiary phenomenon of a
general disorder:—to the presence of parasites (Filaria hæmorrhagica,)
in the skin:—to insect bites:—to violent congestions implicating the
sweat glands (bloody sweat):—or to deranged innervation of the part as
in cases of trauma of the sympathetic or sciatic nerve, or disease of
the nerve centres. It may further be a manifestation of hæmophilia in
which any slight lesion becomes the occasion of persistent hæmorrhage.

Cases that appear in the course of specific contagious diseases and
those dependent on filaria will be considered under these headings, and
we may confine our attention here to the forms of sweating and oozing of
blood from independent causes. German writers draw attention to its
frequency in eastern horses, attributing it to the great development of
the vascular system especially of the skin, but its comparative
infrequency in the English racer and American trotter would throw doubt
on this doctrine. It may be questioned whether the frequency of the
disease in Oriental horses is not to be ascribed rather to filariasis.
This idea is not contradicted by the especial prevalence of the bleeding
in summer when the filaria is most active, but when also the skin is the
most vascular and its tissues most relaxed.

Of nervous hæmorrhages we have the experimental examples of Bouchard and
Simon from section of the sympathetic nerve in animals, also those of
Glen and Mathieu from irritation of the sciatic in dogs with common
salt. In man the nervous causation has been seen in hysteria, under
profound nervous shock, in sclerosis of the cord, and even as the result
of auto-suggestion. This influence is constantly operative in violent
inflammations in which diapedesis and minute hæmorrhages into the
affected tissues are marked phenomena, and under such a cause the gland
ducts especially are the seat of transudation. When the skin is abraded,
cracked, or blistered it occurs also on the surface of the exposed
derma.

_Symptoms._ With active local congestion or inflammation the blood
usually oozes in drops from the surface, and drying concretes into dark
red crusts. In other instances, however, it drops from the surface, or
even flows, producing anæmia and even death. Into such cases hæmophilia
presumably enters. Hæmorrhagic swellings like wheat kernels or beans
also form in the skin.

_Treatment._ Apart from the contagious and parasitic diseases, and
scurvy, the general treatment will be styptic. Cold water, ice, snow, a
stream from a hose, solutions of tannin, matico, iron chloride or
sulphate, alum or gelatine may be employed. Internally the iron salts,
gelatine, atropine, ergot, lead acetate, or quinia may be given. In
hæmophilia the gelatine especially should be tried both locally and
generally. When it is possible, as in the case of the head, gravitation
should be availed of. Elsewhere a compress bandage may be used.

ULCERATION. GANGRENE. BED SORES.

Causes: inflammation, exudation, obstructed circulation, lesions in
trophic nerve centres, sclerosis, toxins, ergot, caustics, freezing,
gangrene, microbes, cryptogams, spoiled fodder, white skins,
buckwheat, insolation. Symptoms: inflammation, molecular
disintegration, dry sloughs. Treatment: camphorated spirit or
vaseline, antiseptics, phenol, salicylic acid, iodoform, iodine,
creolin, lysol, tar, detach sloughs.

In all cases in which the skin is violently inflamed, and particularly
when the seat of an abundant exudation or infiltration which blocks
circulation and retards nutrition, the tissues are especially liable to
death, molecular or by sloughing, and formation of bedsores. As a
general cause lesions of the trophic centres in the medulla and cord
must be accepted as a cause of the imperfect nutrition and lack of
vitality. This is seen in sclerosis of the cord, but may appear as the
result of poisoning of the myelon as well as the gangrenous tissues by
absorbed toxins. Again a common cause of circumscribed cutaneous
gangrene is the capillary contraction and obstruction of ergotism. This
usually involves all the tissues, soft and hard, at the distal end of a
member or organ, causing the separation of all at one common level, but
in less severe forms the skin only sloughs, in the form of round or
irregular masses, usually around the coronet, and the resulting sores
heal up under an appropriate diet. Cauterization and freezing may be a
further occasion of gangrene. Finally, the local operation of the
microbes of gangrene, determines both ulceration and sloughing.
Cryptogams on spoiled fodders (trefoil, lupins, vetches, rusty gramineæ)
are also charged with developing gangrene.

White skins or white patches on the skin are especially liable to suffer
as in cases of fagopyrism and “grease”. The action of the solar rays in
summer must therefore be accepted as a concurrent cause.

_Symptoms._ The first symptoms are usually those of cutaneous congestion
or inflammation. Redness, swelling, pitting on pressure, or tension, are
accompanied or followed by vesicles, chaps or erosions. The margins of
the sores become thick and irregular, often undermined, and they
gradually increase by breaking down of tissue in their depth or on their
margin. In other cases patches of skin dry or wither up, either in
superficial layer or throughout its entire thickness, and these dried
extra vascular sloughs are gradually detached by granulation beneath.
The surrounding tumefaction is always extensive and the sores may expose
the deep seated structures—tendons, ligaments, fascia, bones,
joints—causing widespread destruction.

_Treatment._ If the disease is due to capillary occlusion of nervous
origin, compresses with camphorated spirit, followed by camphorated
vaseline may be of advantage. If otherwise, antiseptics will be in
order: carbolated vaseline, salicylic acid cream, iodoformed vaseline, a
weak iodine ointment, creolin, or lysol in water, tar water. When the
dead tissues are partially separated the detachment may be hastened with
knife or scissors and the sores treated like a septic sore.

CUTANEOUS HYPERTROPHY. ELEPHANTIASIS. PACHYDERMIA.

Chronic thickening of skin and lymph plexuses, horse hind limb after
eczema, grease, glanders, ox neck and head, knees, shoulder.
Calcification. Treatment: laxatives, diuretics, exercise, elastic
bandage, friction, astringents, iodine.

Chronic thickening of the skin is most commonly seen in horses as a
sequel of lymphangitis in the hind limb, the engorgment of the lymph
plexus and thickening of its walls being associated with a general
productive inflammation and thickening of the derma until the fetlock
may be thirty inches or more in diameter. It may follow eczema, grease
or chronic glanders. In cattle a productive dermatitis in the region of
the head and neck, has led in the experience of the author to a similar
distention of the lymph vessels and morbid thickening of the skin. The
pads and calluses which form on the knees of the camel and on other
parts subject to friction, furnish examples of hypertrophy of another
kind. Again the thick dense cutaneous plates on the shoulders of the old
boar may serve to illustrate a physiological hypertrophy. The writer has
seen thickening of the skin in the seat of an incision made in spaying
the pig and the deposition of earthy salts so as to form a distinct
calcification.

_Treatment_ is very unsatisfactory, yet something may be done by
laxatives, diuretics, regular exercise, an evenly applied elastic
bandage when in the stable, massage and the use of astringent and dilute
iodine ointments. It is much more important to prevent the lesion by
cutting short the morbid condition on which it depends. When developed,
attention is usually given to prevent its advancement and to utilize the
animal at slow work.

ICHTHYOSIS. FISH-SKIN DISEASE.

This consists in a scaly formation of the epidermis which is also formed
in excess, and is supposed to be dependent on disordered trophic
innervation. In new born calves suffering in this way Van Stettin found
an excess of phosphate of lime in the epidermis. The calves usually die
in a few days.

FURUNCULUS. BOIL.

Definition: pustule with necrotic core. Digital region. Microbes.
Symptoms: Prevention: antisepsis. Treatment: phenol, iodine, alcohol,
boric or salicylic acid, iron, bitters, calcium sulphide, sulphur,
sodium sulphite.

A deep seated inflammation of the derma resulting in suppuration with
the formation of a central adherent necrotic slough or core.

Boils are not uncommon on the digital region of horses in winter; or
where the parts are exposed to street mud containing an abundance of
decomposing organic matter. They are unquestionably due to pyogenic
microbes, and have been largely associated with staphylococcus pyogenes
aureus. As they often come out in successive crops, it may be assumed
that the second focus is infected from the first, or that there is a
special susceptibility in the particular animal system, or that both
these factors contribute to the result. Debility, and traumas contribute
to bring about the infection.

_Symptoms._ A nodular, hot, and very painful swelling, implicating the
substance of the true skin, and surrounded by a hot, swollen zone,
progresses to suppuration in the centre, yet when it bursts, or is
opened, a core or small mass of necrotic, tough, fibrous tissue is found
to be firmly adherent in the center of the bottom of the sore.

_Prevention._ Must be sought in sustaining the general health and in
preserving the greatest cleanliness of stables and skin. Washing with a
weak antiseptic solution when returning from muddy streets may be of
use.

_Treatment._ When developing, the application of carbolic acid in
crystal or on the end of a glass rod may often relieve the pain and
destroy the microbes. Next day the part may be painted with tincture of
iodine. If already opened the phenol may still be applied and followed
after five minutes by alcohol to check the caustic action. Or boric or
salicylic acid may be applied. To counteract the constitutional
tendency, iron, bitters and other tonics and antiseptics, calcium
sulphide, sulphur and sodium sulphite may be given.

HYPERPLASIA OF THE SKIN.

Productive inflammations and tumors of the skin are common in domestic
animals but as they are essentially surgical lesions, they will be
better considered under that head. We may name papilloma, warts,
fibroma, melanoma, epithelioma, sarcoma, adenoma, carcinoma, dermoid
cysts. Parasitic and microbian diseases of the skin will be found under
their respective headings.

ALOPECIA CONGENITA. CONGENITAL BALDNESS.

Cases of this kind have been met with in foals and calves, which were
born entirely bald or with only a few thin delicate hairs scattered over
the surface. In a calf observed by the author, and which lived for
several months, the body was almost absolutely bald, and the mouth
remained edentulous, a coincidence which has been observed in other
cases. The teeth belong to the same class of embryonic tissues as the
epidermis, and a failure in the development of the one is likely to
entail a corresponding failure of the other. Schneidemühl observed that
the few hairs present in such cases were especially delicate and
brittle.

ALOPECIA. POST PARTEM. ALOPECIA AREATA.

Normal shedding. Shedding out of time; laminitis, dropsy, exudative
dermatitis, acariasis, ringworm, traumas, folliculitis. Debility,
excessive lactation, starvation, petechial fever, spoiled fodder.
Without apparent cause, alopecia areata, neurosis, micrococci, disease
of derma. Symptoms: general disorder has general shedding. Local
disorder extends from a centre. In horse with increased pigmentation.
Treatment: correct general causes, use hair stimulants, cantharides,
kerosene, tar, pilocarpin, mercuric chloride, cresol, iodine, balsam
of Peru, silver nitrate. Arsenic.

Acquired baldness is recorded in horse, cattle, sheep and dog.

_Causes._ The simple shedding of hair occurs physiologically in animals
with the change of season, and if anything interferes with the growth of
the new hair a transient baldness may ensue. If such shedding occurs
from any cause at the wrong season, before the new hair has started, the
baldness may be accentuated. Thus shedding may occur in some forms of
indigestion, in laminitis, in dropsical swelling of the limbs or ventral
aspect of the body, in dermatitis with an exudation which concretes
around the hairs and raises them out of their follicles, in mange, in
demodectic acariasis, in circinate ringworm, in traumas as on the elbows
of dogs, etc., from lying on them, and in inflammation of the hair
follicles from a variety of infections. It has been charged on general
debility in excessive lactation, in gestation, and in starvation, on
poisons in the blood as in petechial fever, and on musty or spoiled
fodders in bad seasons, or from low damp lands.

When in the absence of such appreciable causes it commences at one or
more points and gradually extends, and persists, it constitutes alopecia
areata. This has been attributed to a disorder of the cutaneous nerves
(tropho-neurosis), but the progressive advance of the disease, without
limitation to areas representing the distribution of given cutaneous
nerves, and the complete absence of other derangement of nerve function,
throw doubt on this conclusion. Another doctrine attributes it to a
microbe, but though micrococci and other organisms have been found, they
have not been proved to be constant nor to be absolutely causative of
the disease. Still another theory holds that it is a disease of the
derma and not of the hair at all, the evulsion of the hair following the
implication of the tissues around the follicles.

_Symptoms._ The baldness dependent on a general disorder occurs at once
over an extended area. That of ringworm, acariasis, and of the specific
alopecia areata, advances gradually and often slowly from a given point,
until it may include a large area. Röll has seen it extend from a few
points to nearly the whole body of the horse in a single year. In this,
as in other cases in horse and dog, the baldness was followed by a
considerable increase of the pigmentation of the skin.

_Treatment._ In cases that occur as the result of other diseases, the
rational treatment is to deal with these diseases, and then to stimulate
the growth of hair by some one or other of the known stimulants (dilute
tincture of cantharides, kerosene, tar water, solution of pilocarpin
hydrochlorate). In the more specific form, no treatment has been very
successful, yet the best results on the whole appear to have come from
local germicide applications. Mercuric chloride in alcohol and water (1
∶ 500); cresol 1, alcohol 20; tincture of iodine reduced to half its
strength by addition of alcohol; balsam of Peru 1, alcohol 5; nitrate of
silver 1, alcohol 15, serve as examples.

As general treatment arsenic has been employed, but with no very
encouraging results.

TRICHORRHEXIS NODOSA. NODULAR SWELLING AND SPLITTING OF HAIR.

Debility, ringworm, nodular hair. Hair bursts with brush like end.
Cases in horse like singed hair. Causes: infection probable, disturbed
innervation, dry air, impaired nutrition. Treatment: shave, oil,
vaseline, petroleum, cantharides, sulphur, tar, favor shedding coat.

In a variety of conditions the hairs split up and break, leading to
bristling or baldness. In debilitated conditions, when the hair is badly
nourished, in ringworm when it is invaded by a cryptogam, and in the
various nodular or ringed conditions of the hair this brittleness and
splitting appears. The term _Trichorrhexis_ (rexis a bursting forth) has
been applied to one of these affections, in which the hair swells and
bursts into a number of filaments giving it a broom-like termination.
Trofimo describes this as affecting two-thirds of the horses of an
artillery brigade, and showing upon the back, croup, mane and tail in
isolated patches. Megnin, Trasbot and Roy have observed similar cases.
The affected hair a short distance from the skin swells into a grayish
white nodule and breaks across, leaving a tuft of fine filaments. The
patches look to the naked eye as if singed, but when the hair is
magnified the difference is easily made out, as there may be several
nodular enlargements on the same hair, and the brushlike spread of
filaments at the broken end is entirely unlike the solid node on the end
of a singed hair.

The _causes_ of the affection have not been demonstrated, though
indications point to an infection which gradually extends from the first
point of attack. This extension is not limited to the area presided over
by particular nerves, and there is no other indication of disordered
innervation. Trasbot has seen the disease transmitted from horse to
horse by the use in common of combs, brushes and rubbers, and in other
cases experimentally by rubbing the scurf from a diseased animal on the
skin of a healthy one. From observations on the human subject Montgomery
looks on it as a result of extreme dryness and brittleness of the hair,
and charges dry climates and seasons, and an abuse of soap in washing as
conducive causes. Debility and impaired nutrition of the hair may
operate in the same way. No specific microbe has been constantly found
in these cases and until such factor can be proved, it may be held that
among the etiological agents impaired nutrition and dry air are
important.

In the way of _treatment_ shaving of the affected parts and oily or
vaseline applications may be tried, together with such slight cutaneous
stimulants as petroleum, weak tincture of cantharides, sulphur, tar
ointment, etc. Roy noticed that cases that had lasted all winter
recovered after shedding of the coat. It might be assumed that the
evulsion of the infected hair, and the vascular stimulus necessary to
the new growth contributed to the result.

CONSTITUTIONAL DISEASES.
RHEUMATISM.

Definition. Past views. Causes: heredity, age, cold, damp, cold
climates, seasons, exposure, buildings, cellars, night chills, weather
vicissitudes, valleys, wading, checked perspiration, lactic acid,
metabolic products, acid phosphate of soda, vegetable acids,
neuropathic causation, infection, microbes, injuries, overwork.
Lesions: in joints, synovia, serosa, articular cartilage,
fibro-cartilage, articular lamella, bone, eburnation, ligaments,
joints affected in horse and ox, blood changes, albumen, fibrine,
blood globules, pericardium, endocarditis, valvular disease,
myocarditis, embolisms in lungs, pleura, nervous lesions, digestive
system.

_Definition._ A constitutional, inflammatory affection, probably toxic,
tending to localization in the joints, muscles, tendons, fascia, skin,
heart and serous membranes and with a marked disposition to shift from
place to place.

The word is derived from _rhein_ (γειν) to flow, and was originally
employed to indicate that an acrid humor, generated in the brain or
elsewhere escaped mainly by the nose and eyes as a catarrh. The idea
naturally followed that the retention of this humor caused inflammation
in the joints, muscles, heart or elsewhere. The connection of these
various conditions with exposure to cold, led to the association of the
name with the various internal inflammations in which chilling appeared
to have been a factor, until it was difficult to limit it by any
definite line. Finally infectious diseases implicating the joints or
muscles (influenza, contagious pneumonia, omphalitis, gonorrhœal
rheumatism), and diseases of metabolism (gout and possibly rheumatoid
arthritis) have added to the general confusion.

GENERAL CAUSES. _Heredity._ This has been more definitely traced in man
than in the lower animals, the line of family descent being more easily
followed in man. Children of rheumatic parents are more obnoxious to the
disease in the ratio of 5 to 1. In the absence of data for animals, we
may say that it is probable that the influence of heredity will hold
good for live stock in this matter. Whether the disease results from
faulty metabolism or from microbian invasion or toxins, the hereditary
defensive powers of the animal cell are likely to be an important
factor.

_Age._ Genuine rheumatism is not common at a very early age, but in
animals as in man, attacks especially those in the prime of life,
accustomed to vigorous exercise, free perspiration and succeeding
chills. There is as yet no direct evidence of an exhaustion of the
susceptibility of early maturity and of any consequent immunity of the
old.

_Cold and damp._ The association of rheumatism with cold and damp has
always been so notorious that no argument is needed to enforce the
truth. It is pre-eminently the disease of cold climates and cold
situations exposed to the north and east in Europe, or to the north and
west in North America on the Atlantic slope. It is very little prevalent
in the tropics. Buildings and yards that lack sunshine and exposed
storm-swept hillsides show cases most numerously. Dogs kept in cold,
damp sunless cellars often suffer. Cold, damp or frosty nights start or
aggravate cases in animals left out in the field, while warm sunshine
usually brings immediate improvement. A sudden change of weather to cold
and wet is the signal for aggravation of the existing disease, though
this may have set in before the change of weather has been fully
developed. Late autumn and early spring with their sudden changes, their
sleet and rain are especially hurtful and particularly to chronic cases.
The cold, raw ocean winds on the Pacific coast contrasting with the warm
sunshine is a marked contributing cause. The currents of cold air that
draw up through shaded valleys, gullies and ravines expose their
denizens to attacks. Rheumatism is more rare among well housed and
carefully treated family horses, and less so in draught, dray and other
hard working horses that are made to cross streams and stand with feet
and legs in cold water while the body is drenched with perspiration.
Dogs suffer in the same way while hunting. Haycock attributes many
attacks to washing the legs with ice cold water when the animal has just
returned to the stable heated and perspiring. If then left undried and
unbandaged in a cold draught these conditions are still farther
aggravated. This was formerly attributed to the suppression of
perspiration, but it occurs in an animal which has just perspired freely
and is now in no special need of further elimination through the skin.
It appears to be due rather to the action of the cold on the nerve
endings, the susceptibility of which has been enhanced by the free
secretion and general relaxation.

But potent as cold is in precipitating or aggravating an attack, it
cannot be looked on as the sole or essential cause of rheumatism. The
great majority exposed to the cold escape. The animal which has stood in
the stall, or shed, is less likely to be attacked than the one at work
in which the heat production has been more active. Indeed an immunity
has been claimed for the Arctic regions, provided the subject is not
exerted so as to cause perspiration. One might readily conclude that
this apparent immunity, depended on the absence of an essential germ, as
is also claimed for catarrhs, yet Nansen after his prolonged bath in the
frigid waters seems to have had an attack of rheumatism. Cold appears to
be one of the most potent accessory causes, but evidently not in itself
the essential cause.

Cold undoubtedly affects profoundly the metabolism of the body and
especially when the vital powers have been reduced by severe exertion,
fatigue and perspiration. The same applies to many other affections
especially such as are associated with an infecting element, which takes
occasion of the debility caused by the cold to establish itself in the
tissues.

_Lactic acid and other metabolic products._ Prout long ago claimed that
rheumatism was caused by an excess of lactic acid in the system, and
this was supported by the fact that an exclusive diet of buttermilk
given in diabetes, is likely to produce acute articular rheumatism.
Again the production of rachitis in the young can be traced in certain
cases to excess of this acid. The strongly acid odor of the sweat in
certain rheumatic attacks is thought to support this theory. The excess
of lactic acid is variously explained by the overwork of the muscles of
which it is the normal product, and by the imperfect oxidation of the
muscular tissue and its product into lactic acid (C_{3}H_{4}O(OH)_{2}),
instead of carbonic acid (CO(OH)_{2}). But in spite of the perfect
theory, there is the fact that as a rule no special increase of lactic
acid can be found in blood or urine in acute rheumatism and the
improbability that an excess of this acid caused by sudden excessive
muscular waste could be kept up during a long attack of acute much less
of chronic rheumatism. Again the comparative immunity of sucklings in
which there is the greatest opportunity for the production of lactic
acid, would imply that that alone cannot be accepted, as the one
essential cause of the affection. That its excess in the system will
aggravate rheumatism, or even produce it under favorable circumstances
must be freely acknowledged; also that acidity of the saliva is a marked
feature of rheumatism.

The acid phosphate of soda may be assigned a somewhat similar rôle. In
strongly predisposed subjects the ingestion of citric or other organic
acid will sometimes precipitate rheumatic articular pains.

Still other products, the result of imperfect oxidation or metabolism
must be allowed a place as probable factors in rheumatism. The
occurrence of gout in connection with the excess of uric acid in the
system is strongly suggestive of this, and the frequency of muscular
rheumatism in pampered, overfed dogs with diseased livers and abnormal
hepatic products, seems to give further support. Even in man, the
subject of acute rheumatism, often leads a luxurious life and suffers
from inactive or disordered liver, while in man and animals alike, a low
grade of health and imperfect functional activity of important organs,
are often precursors and accompaniments of acute rheumatism.

_Neuropathic theory._ The doctrine of a neurotic cause originated by Dr.
Mitchell, of Philadelphia, has considerable basis in theory. The primary
chill tends to nervous derangement, which may readily affect the
overworked or already diseased and debilitated joints. Similar
peripheric disturbance of nutrition occurs in locomotor ataxia in which
the central nervous lesion is very evident. There is a strong
disposition in rheumatism to show a bilateral symmetry, which points
directly to a central nervous control. The frequent violence of the
pain, disproportionate to the moderate structural changes, points in the
same direction, and the free perspiration present in some severe
attacks, points alike to its origin in cutaneous chill and to
derangement of the centres presiding over perspiration. It may be added
that the development of rheumatic symptoms in the advanced stages of
infectious diseases, when the toxins are accumulating in the system,
suggests that they are the direct result of a toxic action on the nerve
centres. In man the influence of severe nervous shock in developing and
maintaining rheumatism is recognized.

_Theory of infection._ This has been advocated by Cornil and Babes and
Friedberger and Fröhner. The former quote the frequent presence of
microörganisms and above all of micrococci in the liquids of the
affected joints, serosæ and valvular exudates and ulcers, and even in
the blood, and the occurrence of rheumatism in the course of various
septic affections. The latter quote Auer and others as to the frequent
supervention of articular rheumatism on the retention of the afterbirth
in the cow. The weak point in these theories is the multiplicity and
variety of the microbes found in the exudates. Either we must accept the
rheumatic lesions as an occasional result of many microbes, which
habitually act differently on the system, or we must look upon them as
mere accessory causes or accidental complications. It might even be,
that the invasion of these microbes are made possible by the
inflammation and debility of the tissues, without being directly
chargeable with the rheumatic process. Even then there remains the
possibility that a specific microbe is present, which by reason of its
infinitesimal size, or other physical property, has as yet escaped
recognition. If such specific microbe is present, it manifestly requires
a very special predisposition, since it is not seen to advance from one
individual to another unless such favoring conditions are present. The
symptoms and lesions of rheumatism are not incompatible with the idea of
such an essential, specific germ, but as yet no such germ has been
satisfactorily demonstrated as present in all cases.

_Local injuries._ Rheumatism seems to attack by preference parts that
have already been debilitated by disease, a disposition which is also
true of distinctly microbian infections. A pre-existing sprain, blow,
bruise or an inflammation arising from any other cause seems to
practically invite the localization of the morbid process at that point,
and thus what was at first a purely traumatic lesion becomes the seat of
active and perhaps permanent rheumatism. Unusual overwork and fatigue of
given joints and muscles induce a similar predisposition, and habitual
overexertion, sprain, injury or inflammation affecting repeatedly the
rheumatic organ tends to fix the process in chronic form.

_Articular lesions._ These tend to concentrate as a form of inflammation
in the synovial membranes, but usually implicate all the constituent
structures of the joint, capsular and binding ligaments, cartilage and
fibro-cartilage, articular lamella and osseous tissue. The synovial
membrane may show only slight hyperæmia, or in severe cases it may be
congested, red, thickened or even extensively infiltrated with a
serogelatinoid liquid. These lesions are most marked around the line of
attachment on the articular surface and in the synovial fringes. The
synovia is usually in excess, distending the capsule and is whitish,
opaque, flocculent or more or less deeply colored with red. It contains
flakes of fibrine, leucocytes, albumen and it may be red blood globules.
Pus cells are usually absent unless in distinctly infective cases.
Coagula and false membranes floating from or adherent to the solid
tissues, may be present in considerable amount and if these become
organized they tend to lay the foundation for future stiffening and
rigidity. In and beneath the serosa, cell proliferation may go on
actively, especially in the synovial fringes. The synovia is usually
neutral or slightly alkaline, though in rare instances it has proved to
be acid.

The inflammation of the synovial membrane of the joint often extends to
those of the adjacent tendons, implicating at the same time the tendons
and their fibrous sheaths. Softening and rupture of the tendons have
been noted by different observers (perforans, Oger; gastrocnemii,
Trasbot; suspensory ligament, Olivier).

The articular cartilages and the fibro-cartilages may be the seat of
congestion, with ramified or uniform redness, and areas of swelling,
softening, absorption, erosion and ulceration, the ulcers varying in
size from a millet seed upward. The nuclei increase in size and the
cartilage cells multiply. In chronic forms calcification is not
uncommon.

The articular lamella and subjacent bone may show inflammation with
increased vascularity, softening and even ulceration. In the chronic
forms on the parts denuded of cartilage, the surface of the bone may
show the clear, polished condition known as eburnation.

The binding ligaments may show congestion, thickening, exudation,
softening, with increased rigidity, or in some cases relaxation.
Calcification is not uncommon in chronic cases. The soft parts around
the joints are often extensively infiltrated and swollen.

In _horses_ these lesions are specially common in the fetlock, but occur
also in the knee, elbow, shoulder, hips, stifle and hock. In _cattle_
they tend to attack the same parts with a preference perhaps for the
hocks and fetlocks.

_Changes in the blood._ The blood becomes profoundly altered, the
albumen reduced, the fibrinogenous elements increased (5 to 10 parts per
1000 instead of three), the red blood globules disappear (in man
2,850,000 per cubic millimeter instead of 4,500,000), the hæmoglobin and
oxidizing power of the blood are reduced by about 50 per cent., the
leucocytes are relatively increased, and coagulation takes place with
unusual firmness, a cupped surface and an excess of buffy coat. No
excess of urea, uric acid, nor lactic acid, has been found, nor has
acidity been found save in very rare cases. In rare and severe cases
petechiæ have appeared on the skin and mucosa.

_Lesions of the heart._ The implication of the fibrous structures of the
pericardium and heart and especially of the valvular structures is a
common lesion, and to be dreaded more than all others. In all animals
this tendency to cardiac lesion is well marked, but especially in
solipeds in which the great demands made on the heart during rapid
paces, heavy draught, jumping, etc., severely strain the cardiac
mechanism. In dogs there is not only the violent exertion and high blood
pressure, but also the great irritability of the nervous mechanism
presiding over the heart and the tendency to irregularity and
intermissions in the rhythm and palpitations even when the organ is
sound. There is every reason to conclude with Trasbot, Megnin, Heu and
Laurent that in many cases the heart is primarily attacked, and that
this heralds the articular rheumatism. In other cases undoubtedly the
cardiac affection is secondary, following the articular attack.

Endocarditis is the most frequent, being found in a large proportion of
fatal cases, and thickening of the valves, wart-like exudates and
coagula are especially common. The clots may fill nearly the entire
ventricular cavity, or at times the auricular, and show a preference for
the left side, probably because of the more vigorous systole and the
higher blood tension. The clots as a rule are firmly adherent to the
diseased valve. Ulceration of the valve is rare in rheumatism. Other
parts of the ventricular endocardium may be involved, becoming red,
congested, rough or thickened, with adherent blood clots.

Pericarditis is less common though it may exist on either or both the
cardiac and visceral folds. It is shown by vascularization, thickening,
fibrinous exudate, and serous effusion. Haycock found in a horse a quart
of reddish serous exudate with floating fibrous shreds and false
membranes. Pus has been found in exceptional cases manifestly indicating
a complex infection. Like endocarditis it may precede, follow, or
coincide with an articular attack (Leblanc, Cadeac).

Myocarditis is usually seen as a complication and extension of rheumatic
inflammation of the visceral pericardium, or of the ventricular
endocardium. The muscular tissue may appear parboiled and friable, and
shows granular or fatty degeneration.

_Pulmonic and pleuritic lesions._ Embolism of the lungs and pleura may
occur from the transference of clots from the right heart, yet the
sequence is much more commonly an articular rheumatism following
infective disease of the lungs. Cadeac suggests that the impaired
nutrition in pneumonic and pleuritic animals predisposes to the
rheumatic arthritis, and again that the microbes of the infectious chest
affection, colonizing the joints and other synovial sacs, determine the
rheumatism. This last theory has the weakness of identifying influenza
and contagious pneumonia with articular rheumatism, and is negatived by
the experience that these two pulmonary affections never develop _de
novo_ from simple rheumatism. The rheumatism which follows influenza and
contagious pneumonia therefore must either be considered as a
pseudo-rheumatism, or a rheumatism occurring only concurrently and
accidently with the pulmonary affection. Apart from this, pleurisy or
even pneumonia occurs as a simple extension from a rheumatic
pericarditis.

The occurrence of the rheumatoid affection as a complication of
influenza and contagious pneumonia in the horse, usually appears not
earlier than 15 days after the outset of the pulmonary affection and may
be delayed, according to Palat, for 102 days. Palat who had excellent
opportunities for observation in army horses found that about one in ten
was the ratio in which the rheumatic affection followed these pulmonary
diseases.

The pulmonary lesions in these affections are essentially those of
uncomplicated influenza, or contagious pneumonia.

_Cerebro-Spinal Lesions._ Nervous disorders are occasionally seen in
rheumatism in man (dullness, prostration, delirium, coma, spasms) and
traced in different cases to hyperthermia, congestion, exudation,
embolism and toxins. In a few cases in the horse, cerebral complications
have been observed. Olivier saw a horse with lachrymation, closed
eyelids and hot, tender forehead, which showed at the necropsy articular
inflammation, and sanguineous effusion in the cranium, encephalon,
frontal and maxillary sinuses and ethmoid cells. Jacob records two cases
(mare and horse) in which rheumatism was complicated by
meningo-encephalic congestion but without necropsy as both recovered.

_Digestive system._ In man rheumatism has been exceptionally preceded by
pharyngitis, dysphagia, and diarrhœa. In the horse Haycock has seen
concurrent congestion of the pharyngeal mucosa, Olivier congestion of
the stomach and intestine, and Jacob diarrhœa and abdominal pain,
Leblanc and Palat record cases of peritonitis accompanying articular
rheumatism in the horse.

SYMPTOMS OF ACUTE ARTICULAR RHEUMATISM IN THE HORSE.

Chill, hyperthermia, lameness in fetlock, hock, knee, shoulder,
stifle, hip, elbow, tendons, sheaths, bursæ, bilateral, shifting,
swelling, heat, tenderness, decubitus, joint semi-flexed, pain on
extension or flexion, signs of cardiac disease. Course: rapid to
recovery, improvements and relapses, metastasis, debility.

The attack is usually sudden and marked by a slight chill, shivering or
staring coat with hyperthermia and lameness. The temperature may vary
from normal to 107° or 108° F. in severe attacks. In many cases the
fever and lameness appear simultaneously, the former being in ratio with
the extent and severity of the latter, but not infrequently the
elevation of temperature precedes the articular symptoms, and then it is
to be considered as concurrent with the internal lesions—cardiac,
pericardial or otherwise. In other cases the articular lesions and
lameness precede by several days the appearance of the fever. So far as
we know the fever never antedates the occurrence of some local lesion,
external or internal.

The joints affected are very varied. The fetlock is the most frequently
attacked, but some of the other larger joints, the hock, knee, shoulder,
stifle, hip and elbow are often involved or exclusively affected. The
adjacent tendons and their synovial sheaths are very often implicated;
the attack is very prone to show a bilateral symmetry, the same joints
(right and left) on the corresponding fore or hind limbs, suffering at
once, or, as in the case of the fetlocks, all four are simultaneously
attacked. A joint that is weak by reason of previous injury or disease
is especially liable to suffer, and is then less likely than joints that
had been previously healthy to undergo speedy improvement. When the
symptoms wander from joint to joint or from joint to muscle, or fascia
or tendon, the disease in its earlier seat seeming to undergo almost
complete resolution, while it advances with great intensity in the newly
affected joint or part, the occurrence is highly significant. These
transitions often take place with great rapidity. Thus the centre of
suffering may shift from one joint to another in an hour, (Megnin,
Cadeac), or from a limb to the loins in a quarter of an hour (Lewis).
The fact that the inflammation remains fixed in one or several joints,
is not, however, proof of the absence of rheumatism. A joint with a
primary weakness or injury may remain the seat of disease through even a
chronic rheumatism.

The affected joint is usually swollen, hot and tender; the tenderness
being as a rule greatest where the capsular ligament is pressed upon.
These symptoms are very evident in joints that approach the surface, and
obscure in such as are thickly covered by muscle (shoulder, hip). The
swelling is soft, or tense and elastic (especially over the synovial
membrane), or œdematous and pitting on pressure. On white skins sparsely
covered by hair there is marked redness and congestion, the veins
standing out prominently and the arteries above the joint pulsating
strongly. When the tendinous sheaths are involved, they stand out as
elastic lines following the course of the tendons, and with more or less
pasty swelling adjacent.

In some cases, however, the swelling may be entirely absent, and the
trouble is to be located only by the local tenderness and pain during
motion.

Small, hard, pea like, subcutaneous nodosities were first noticed by
Floriep, in 1843, in rheumatism in man, and have been met with in
different cases in the horse. Rodet fils met with great numbers of these
nodules crepitating under pressure, in a horse that had suffered for
months from chronic rheumatism.

Acute pain on moving the affected joint or tendon is a most
characteristic symptom. The horse goes dead lame, walks on three legs,
or with great stiffness, and avoids as far as possible all flexion of
the joint. If left alone the animal stands stock still, never moving
from the place, or in the worst cases lies down and refuses to rise. If
compelled to walk his suffering is shown by hastened breathing, dilated
nostrils, anxious, pinched countenance and low plaintive neighing. The
affected joint is held semi-flexed, to relieve the tension, the pastern
is habitually more upright, and if the foot is lifted and the affected
joint bent or extended, the animal winces, or resists, and tries to draw
away the limb and groans. The movements of the affected joint in walking
or under manipulation, are often attended by cracking which may be both
felt and heard. It has been variously attributed to lack of synovial
lubrication (Cadeac), and ulceration of the articular cartilage
(Lafosse), yet it may occur from the constrained position assumed, as in
the case of a man attempting to walk noiselessly on tip toe, and in
other cases from the extension of false membranes, or of rigid or
contracted binding ligaments.

Rheumatism of the fetlock and sesamoid pulley, as the most common form
in solipeds, demands a special notice. The swelling of one fetlock, of
the two fore, of the two hind or of all four at once, extends beyond the
limits of both joint and sesamoid pulley and may form a general
engorgement or _stocking_ which serves to hide the synovial distension.
Pressure however shows that while all is tender, the extreme tenderness
is referable to the joint, the synovial sheath of the flexors, to the
flexors or suspensory ligaments. As the general swelling subsides the
rounded or ovoid synovial distensions become more patent. The swelling
and tenderness may extend to the knee in which case the synovial
membrane of the carpal arch is especially distended and tender from the
carpus down, or in the hind limb the synovial membrane of the tarsal
arch is distended showing in this case on the inner and outer sides in
front of the calcis, and not infrequently implicating the summit of that
bone as a capped hock.

In rheumatism of the shoulder the coraco-radial tendon and pulley may be
involved, causing a diffuse swelling on the point of the shoulder. If
the hip is the seat of disease the median gluteal may suffer, causing an
indefinite swelling over the joint. If the stifle is affected the
patellar capsule suffers and not infrequently the tendon and pulley of
the flexor metatarsi are involved.

The most important internal complications, pericarditis and
endocarditis, are manifested by their usual symptoms, sharp, variable,
irregular, unequal or intermittent pulse, blowing murmur usually with
the first heart sound, oppressed breathing, and it may be muffled heart
sounds, or dropsies.

_Course._ This is exceedingly uncertain. Some cases make a rapid
progress to complete convalescence; others make partial improvements
interrupted by relapses; others have the morbid process subside in great
measure in one joint or organ only to reappear in full force in another;
others leave complications on the part of the heart especially and are
rendered permanently useless. Even should the heart escape, the health
often suffers so much in connection with the destruction of the red
globules, the malnutrition, and the local disease, swellings and
distortions of the joints that a perfect recovery seems distant and
problematical.

SYMPTOMS OF CHRONIC ARTICULAR RHEUMATISM IN THE HORSE.

Larger joints, muscles, heart, false membranes, indurations,
thickenings, calcifications, remittent, weather changes, cold, damp
beds, winds, open windows or doors, draughts, cold sponging, clipping.
Diagnosis: lameness variable, shifting, electric and meteoric storms.

Chronic rheumatism may be a sequel of the acute, or it may occur from
the same causes acting with lessened force, or on a less susceptible
animal. It tends to attack the larger joints especially, though it may
implicate the muscles as well. Coincident affection of the heart is less
common than in the acute, and when it does arise seems to advance
slowly. It is liable to cause permanent distensions of the affected
joint capsules, as well as false membranes, articular abrasions,
degenerations and ulcerations and less frequently bony enlargements and
calcifications, the latter implicating the soft tissues in the vicinity.

The attendant lameness is liable to be remittent or intermittent,
subsiding in warm buildings and during genial, clear sunny weather, and
relapsing in connection with cold, raw nights and mornings, exposure in
the dew or rain, and before and during great changes of weather. Cold,
damp beds, chilling draughts between open doors or windows, washing with
iced water, sudden intense cooling of the body after perspiration,
clipping during cold weather, any cause of sudden rigor, when followed
by stiffness, lameness and articular swelling, serves to identify the
latter as rheumatic. Even the warmth induced by judicious exercise, may
cause improvement, so that a horse, starting out stiff or lame, may
drive out of it after going a mile or two. The formation of subcutaneous
nodules, though rare, appears to be more frequent than in acute
rheumatism.

_Diagnosis_ is to be based largely on the variability of the lameness at
different times, its propensity to shift from place to place, its
manifest association with exposure to cold, and with the immanence of
electric storms or change in the barometric pressure, and its
improvement under genial weather, warmth and comfort.

SYMPTOMS OF MUSCULAR RHEUMATISM IN HORSES.

Under usual causes, muscles tender, stiffness, groaning, loins,
quarter, shoulder, neck, chest.

Developed under conditions similar to those causing rheumatism of the
joints, rheumatism of the muscles tends to attack those of a particular
region, and to continue in these throughout the attack rather than
change to others. The affected muscles are very tender to the touch, but
usually show no swelling nor heat. The muscles are relaxed and tend to
atrophy, fever is little marked, there is comparatively little tendency
to the implication of the heart, and the suffering and stiffness vary
with the variation of the weather, or with electric or barometric
changes. When generalized, however, fever may supervene, and the joints
may be implicated (Thompson).

When the _loins_ are affected they become extremely tender to the touch,
and the horse shows great stiffness, and groans when made to walk and
above all when turned or backed. He does not, however, show the
unsteadiness in gait and tendency to stagger that is shown in sprain of
the loins, and there is no history of a slip, fall or injury, but an
unmistakable connection with cold, exposure, change of weather, or
overfeeding on grain.

When the _gluteal muscles_ are attacked there is intense lameness, and
dragging of the hind limb, with an acute sensitiveness of the skin of
the region, which characterizes neither disease of the hip nor of the
trochanterean bursa.

When the _scapulo-humeral muscles_ are the seat of disease, there is a
marked stiffness, shortness of step, drooping of the head, and great
tenderness of the skin and muscles to manipulation or the use of the
currycomb. Like the other cases named it occurs suddenly, without
evidence of accident, but bearing a relation to cold or other change of
the weather, and is better or worse as the weather is more or less
genial.

When the _cervical muscles_ are affected (torticolis), the same features
are noted, the absence of traumatic cause, the presence of a
meteorological one, or at least of cold or wet, the responsiveness of
the disease to the state of the weather, and to revulsive agents applied
to the part. The neck may be held rigidly in one position, to one side
or elevated so that there is great difficulty in getting the nose to the
ground.

The _costal muscles_ are less frequently attacked (pleurodynia), but the
same general principles guide in diagnosis.

Seidamgrotzky alleges the constant existence of acidity of the urine in
muscular rheumatism. This may be attributed to the active trophic
changes going on in the muscles.

SYMPTOMS OF ACUTE ARTICULAR RHEUMATISM IN CATTLE.

Sudden onset, hyperthermia, chill, fever, acid saliva, decubitus, does
not stretch on rising, lameness, joints involved, metastasis,
variability, morning and noon, suppuration, walking on toe, secondary
articular rheumatism. Course: muscular symptoms, cardiac, pleuritic,
digestive. Chronic. Muscular rheumatism: of back, loins, shoulder,
quarter, neck. Changes in blood and nutrition.

There is a sudden attack with constitutional disorder, chill, staring
coat, cold horns and ears, dry muzzle, impaired appetite and rumination,
acid saliva, constipation, thirst, hurried breathing, hard accelerated
pulse and more or less hyperthermia. Then there may come reaction with
surface heat and glow. The patient inclines to lie and when raised fails
to stretch the back or the hind limbs, stands with arched back, and
walks stiffly and with more or less lameness. The joints attacked may be
determined by local strain, compression on concussion, hence the
frequency of lesions of the knees and fetlocks. Yet any of the great
joints of the limbs may suffer,—hip, stifle, hock, shoulder or elbow—or
several may be affected at once. The disease may extend from one joint
to another, may improve in one or more, only to suffer a relapse, and
may oscillate better and worse according to the state of the weather or
the exposure to cold or warmth. Often almost helpless in the early
morning, the patient improves greatly in the heat of the sun.

The affected joint is swollen, distended with liquid, hot and tender
with considerable infiltration of the surrounding tissues, including the
tendons and their synovial sheaths. Suppuration is much more common than
in the same affection of the horse appearing to be due to a complex
infection with pus microbes. In walking in severe cases the foot of the
affected limb is planted with great care and caution mainly on the toe
and there appears to be exquisite suffering when weight is thrown on it,
so that the fetlock and knee may knuckle over and the patient comes to
the ground. Great infiltrations, fibroid, and other hyperplasias and
even calcifications are not uncommon.

Cadeac describes as secondary articular rheumatism, those infective
inflammations of the joints that follow on parturition, abortion,
omphalitis, enteritis, etc., but it is manifest that these are special
disorders due to the presence of the microbes of specific diseases or
their toxins and should be described with these rather than with
rheumatism.

The _course_ of acute rheumatism in the ox is very uncertain. Mild cases
may recover in a few days. In others the lesions become extensive, great
hyperplasia and induration occur around the joint and permanent
stiffness and even anchylosis may supervene. The occurrence of temporary
improvements and relapses is a common feature. The extension of the
disease to other joints, tendinous sheaths, muscles and even internal
organs is to be dreaded. Extreme tenderness of the back and loins when
handled or pinched, with groaning is a marked feature especially in cold
and damp times or in early morning. Cardiac complications show
themselves by shortness of breath, palpitations, hard intermittent,
irregular or unequal pulse, blowing murmur with the first heart sound,
and other signs of circulatory trouble. Pleuritic, pulmonic and
abdominal complications are also to be looked for. The costiveness by
which acute rheumatism is ushered in, becomes complicated by congestion
of stomach and intestine, and impaction of the first and third stomachs,
great dullness, anorexia and even nervous disorder. Colic and even
diarrhœa are occasional consequences.

Many cases subside into a _chronic form_ which shows a variable
condition, better and worse, according to the condition of the weather,
the exposure to cold and damp, and even the changes of diet. This may
last throughout life.

SYMPTOMS OF MUSCULAR RHEUMATISM IN CATTLE.

This may set in with the same abruptness as articular rheumatism, the
animal in the morning after a wet, dewy or frigid night showing general
stiffness and lameness with extreme sensitiveness of the skin and
muscles along the back and loins. The animal moves slowly and stiffly,
grunting perhaps at each step and shows inappetence, fever, dry muzzle
and costiveness. This is essentially _rachialgia_ or _lumbago._
Pandiculation on rising is entirely omitted.

Not infrequently the _muscles of the shoulder_ are mainly affected and
become exceedingly tender to manipulation. The patient seeks to remain
recumbent and when raised will get up on his hind parts and remain thus
for some time resting on the knees before he can be made to get up in
front.

When the _muscles of the croup_ are attacked the mode of getting up is
reversed, the animal rising first on its fore feet and remaining for a
time sitting on its haunches or resting on the hocks before it gets on
the hind.

If the _muscles of the neck_ are involved there is the same stiffness,
soreness, tenderness and twisting to one side or rigid elevation of the
neck as seen in the horse in similar circumstances.

In any case there is a tendency to extension or shifting from one part
to another, and notably to the implication of the tendons, synovial
sheaths and joints. This is especially the case in the acute type, while
chronic rheumatism may remain long confined to the groups of muscles
which are first attacked. In the acute forms too there is the greatest
liability to internal complications not only cardiac, but according to
Cruzel abdominal and thoracic as well.

A fatal result is rare, but the impairment of appetite and digestion,
the constant and often severe suffering, the destruction of the red
globules, and the malnutrition, and increased and perverted metabolism
as shown in the pallor of the visible mucous membranes, the steady loss
of condition and advancing emaciation, the rigid, dry, scurfy, hidebound
skin, tends to wear out the subject or render it unprofitable. In the
chronic form it may last for months.

SYMPTOMS OF RHEUMATISM IN SHEEP.

Articular rheumatism seems to be very rare in mature sheep, while it has
been recorded in lambs. Muscular rheumatism on the other hand has been
seen in connection with untimely shearing, exposure to cold storms and
cold, damp folds. The back and loins, are tender to the touch, or in
other cases the neck or hind quarter, the limbs are carried straight and
rigid, the animal moves slowly and stiffly, falls behind the flock, and
is found alone, unthrifty and emaciated. It usually terminates in
recovery though it may cause chronic disease and distortion of the
affected joints or it may even prove fatal. The usual tendency of the
morbid process to shift from joint to joint or to muscles, is here again
characteristic.

SYMPTOMS OF ARTICULAR RHEUMATISM IN SWINE.

Climatic influences. Rheumatoid. Joints attacked. Muscles. Decubitus.
Stiff, rigid, steps on toes, grunts, swelling, heat, tenderness,
chaps, cracks, suppurations, inappetence, emaciation, metastasis,
cardiac disorder. Duration; course. Chronic form. Muscular form.
Diagnosis from trichinosis. Connection with arthritis. Metastasis.
Remissions.

The pig which shows an extreme sensitiveness to climatic vicissitudes
and cold winds, fleeing instantly to his lair on their advent, is yet
protected by his subcutaneous fat, so that he is not a frequent victim
of simple rheumatism. Leblanc attributes it to unwholesome pens.
Chaussade to too rapid fattening (overfeeding). Rheumatoid attacks are
very common at the onset of hog cholera, swine plague and other
infectious diseases, when they are probably but local manifestations of
the general infection.

The lesions are mainly concentrated in the stifle, hock, knee and
fetlock. In some cases the dorsal and lumbar muscles suffer and there is
arching of the back with great tenderness on manipulation. In other
cases the muscles of the quarter or shoulder are involved as shown by
their stiffness and extreme sensibility to touch.

The pig is found down, indisposed to rise, and when up, stands drawn
together with limbs rigid and feet resting on the toes. He will often
point one toe to the ground repeatedly, before resting on the foot, or
shift the weight uneasily from foot to foot. If moved he grunts
plaintively and if handled squeals.

The affected joints may be surrounded by hot tender swellings or they
may be nearly normal in outline, but they are always very sensitive to
pressure and above all to flexion and extension, and the skin is usually
hyperæmic and red. There may be engorgements of the lymphatics on the
inner side of the limbs, and chaps and cracks in the flexures of the
joints. Suppurations may follow (Graignard) suggesting a complex
infection.

There is little appetite and though the disease becomes subacute or
chronic there is a steady loss of condition or at least a failure to
thrive.

Benion’s reference to a coincident or sequent inflammation of the
respiratory or digestive organs and Spinola’s similar reference to
pleurisy are strongly suggestive of swine plague and hog cholera. Any
manifest disposition to shift from one part to another and any
concurrent disorder of the heart, other than simple palpitation is
strongly confirmatory of rheumatism.

The disease tends to recovery in from four to twenty days, or to pass
into the _chronic form_. In this state the symptoms are materially
mitigated. Fever is absent, but the appetite, digestion and assimilation
are poor, the animal remains stunted, emaciated or unthrifty, there is a
disposition to lie most of the time under the litter, and when up it
moves stiffly with short steps, semi-flexed joints and upright digits.
Sometimes the joints are permanently swollen and rigid by reason of
thickening and shortening of the binding ligaments, by the organization
of false membranes or by anchylosis.

=Muscular Rheumatism in Swine.= This appears to be rarely seen as an
independent disease, but appears at times to coincide with the arthritic
form. In such cases the back is arched and very sore to the touch or to
pressure. It must be distinguished from the muscular soreness of
trichinosis which occurs in infested localities, after trichinous food
or water, is preceded by digestive disorder and diarrhœa, and by the
passage of the nearly microscopic worms in the stools, and is
independent of arthritis.

Muscular rheumatism leads to atrophy of the muscles, especially those of
the quarters, and this may resemble, somewhat, partial paraplegia from
disease of the spinal cord. Its connection with arthritis, its tendency
to shift from place to place, to undergo ameliorations and relapses, and
its exquisite tenderness, serve to distinguish it from paralysis.

SYMPTOMS OF ARTICULAR RHEUMATISM IN THE DOG.

Articular rheumatism rare. Femoro-tibial joints, bilateral,
remissions. Exudation, swelling of joint; muscular atrophy, weakness,
swaying, staggering, falling, paresis. Chronic, muscular rheumatism
common, back, loins, neck, general, stiff, painful movement,
decubitus, muscles tender, yelps, stiff neck, wry-neck. Masseteric.
Painful defecation and urination. Metastasis. Cardiac symptoms.
Pleurodynia. Digestive troubles. Emaciation, weakness, atony,
paraplegia. Diagnosis from strongylus, stephanurus, and cysticercus.

This affection seems to be rare in the dog. What is known as rheumatism
in this animal, consists in an inflammation with hyperplasia around the
articular ends of the long bones, the new material being partly fibrous
and partly calcified. It shows a special predilection for the
femoro-tibial and confines itself mainly to the inner side of the head
of the tibia. Here the swelling may reach the size of a walnut, The
whole head of the tibia and lower end of the femur are however often
involved, entailing a general enlargement of the joint. It follows the
general rule of rheumatism in usually attacking both stifle joints at
once, and also in alternate ameliorations and relapses. Less frequently
other joints are affected. In all such cases the joints become
overdistended and swollen, partly by synovia, and partly by surrounding
exudate, the muscles of the quarter and thigh become atonic, soft and
flaccid, and are steadily atrophied. The dog shows a lack of strength in
the hind parts, swaying, staggering or even falling, and advancing to a
marked paresis. The malady follows a chronic course, lasting for months,
a year, or more.

SYMPTOMS OF MUSCULAR RHEUMATISM IN THE DOG.

Muscular rheumatism is common in dogs. It is most common and most marked
in the back and loins, though the neck may suffer, or the disease may be
generalized. It is painful to move and the subject seeks to be as much
as possible undisturbed. He walks stiffly and slowly, carrying the limbs
with as little movement of the joints as possible, and in bad cases
yelps occasionally from sudden pain. He can no longer be tempted to go
up or down stairs or to make any special effort. When touched on the
back or loins he will wince, cry out, or even snap at the offender. In
some cases the pain is so acute that even a feint to touch the back will
draw out a yelp. If the neck is affected it may be held so stiffly that
the dog can barely reach the ground to find his food, or if unilateral
the head is turned to one side. Even the muscles of the jaws may be
affected, causing prehension and mastication to be difficult and
imperfect. Defecation and urination are also interfered with and the
straining may draw forth plaintive cries.

The rapid shifting of the morbid process from one group of muscles to
another is often very striking, and if one pronounces on the exact seat
of the disease, it is liable to be speedily rendered inexact by a sudden
change of place. There is further a great disposition to the implication
of the heart and especially the valves. This is shown by irregularity
and inequality of the pulse by intermissions and palpitations, by a
blowing murmur with the first heart sound and by oppressed breathing.

Short, shallow breathing is also caused when the intercostal muscles are
attacked (pleurodynia). Various digestive troubles are also common, to
which the difficult defecation and impacted rectum largely contribute.

Emaciation makes more or less progress, and the muscles of the hind
parts especially become weak and atonic until marked paresis or actual
paraplegia sets in, and the hind limbs are extended backward and dragged
helplessly. In fat, sluggish, overfed and pampered animals the lack of
control of the hind limbs may come on at an early stage. Stiffness due
to strongylus gigas in the kidney or stephanurus or cysticercus
cellulosa in the lumbar muscles must not be mistaken for rheumatism.

PREVENTION AND TREATMENT OF RHEUMATISM.

Prevention. Avoid known causes, untimely clipping, exposed buildings,
over-fatigue, chills, cold rains, dews and frosts, disorders of liver
and bowels, sweets, spiced food, overfeeding, constipation, torpid
liver, injuries to joints or tendons. Treatment: warm stall and
clothing, laxative food in moderation, purgatives, aloes, castor oil,
jalap, saline enemas, colchicum, alkalies, trimethylamine, acetate of
ammonia, salicylic acid, salicylates, salicine, oil of gaultheria,
salicine for debilitated. Large doses hourly or every two hours. Less
effective in chronic cases. Heart failure. Salol. Salophen. Phenocoll.
Antipyrin. Acetanilid. Pilocarpin. Tartar emetic. Dover’s powder.
Ammonium acetate. Chamomile. Boneset. Hot baths and packs, with cold
on head. Hand-rubbing. Hot drinks. Nauseants. Hot iron. Anodyne
liniments. Rubefacients. Blisters. Salicylate of methyl and other
salicylates. Quinine and potassium iodide. Tincture of muriate of
iron. In chronic cases, tonics, cod liver oil, arsenic, guaiacum,
potassium iodide. Essential oils. Electricity.

_Prevention._ This consists in the avoidance of all known causes of the
disease and must vary to some extent for different genera of animals.
The avoidance of cold and exposure, of clipping at unsuitable seasons,
of exposed sites for buildings (north and northwest exposures, narrow
valleys and ravines), of over-fatigue, of perspiration and subsequent
chilling, of cold rains, dews and frosts, of inactivity, or habitual
overloading of the liver and bowels, and of local injuries of joints or
tendons. House dogs especially should be protected from sweets, spiced
food, frequent feeding, constipation and torpid liver.

_Treatment._ One of the most important considerations is a warm stall or
building, or warm clothing including loose woolen bandages on the legs,
in the horse. Laxative food is called for.

In acute cases and especially in fat pampered dogs, and in all cases
associated with torpid or disordered liver, a preliminary laxative will
be of great service, and others should be given later as demanded. The
horse may have aloes or salines, and saline enemata may be given to all
animals when called for throughout the progress of the disease. Pigs may
take 1 or 2 drops croton oil, or like dogs they may be given castor oil
or jalap. Torpid liver and constipation must always be carefully guarded
against.

To cut short the attack much reliance was formerly placed on colchicum
which increases the elimination of solids in the urine, and on alkalies,
which beside the theoretic antagonism to acidity are at once chologogne
and diuretic. The action was somewhat slow but on the whole
satisfactory, usually abating the suffering very materially in the
course of a few days. To the horse or ox ½ dram doses of colchicum were
given daily in combination with 4 to 6 drams of bicarbonate of soda;
pigs of 100 lbs. may take 1 grain of the former to 10 grains of the
latter; a shepherd’s dog may take half the amount just named.
Trimethylamine proved even more effective than colchicum, and acetate or
citrate of ammonia, soda, or potassium was often substituted for the
carbonate.

But the modern treatment of rheumatism dates from 1876, when the
introduction of salicylic acid and later sodium salicylate, salicine and
ol. gaultheriæ gave to such treatment an efficacy previously unknown.
Salicylic acid acts very harshly on the gastric mucosa, and with
sensitive stomachs is advantageously replaced by sodium salicylate, into
which it is transformed in any case in the blood. Salicine which is held
to be transformed into salicylic acid in the system, is specially
recommended for its bitter and tonic action exercised in the stomach and
prior to such transformation. In debilitated subjects, therefore, and in
those that suffer from the characteristic rheumatic reduction of the red
blood globules it would be somewhat preferable. As a prompt and
effective anti-rheumatic agent however it appears to be somewhat less
reliable than sodium salicylate or ammonium salicylate. Ol. gaultheriæ
may be better borne by the stomach of the dog and pig than the
salicylates, the dose being 10 to 15 drops thrice a day.

The secret of success with all of these salicylate compounds, lies in
the speedy saturation of the system with the drug, rather than in its
moderate and continuous administration. The horse or ox may take ½ oz.
repeated every two hours for ten hours if relief is not obtained
earlier. The pig may take 20 grains, and the dog 5 to 10 grains at
similar intervals. It is not desirable, however, to continue this
indefinitely, and therefore when immediate relief has been secured it is
well to give the agent but twice or thrice a day, and resort in part to
the alkaline treatment. If the salicylates fail to relieve when pushed
energetically for ten hours, there is reason to fear that the case is
not one of genuine rheumatism.

The salicylates are less applicable to chronic cases and may be even
dangerous when the heart is affected, as they tend to render the heart’s
action slower and weaker, and thus add to the dangers of
hypo-hæmoglobin, and heart failure. A similar caution applies to an
excessive use of alkalies and especially of compounds of potassium which
depress the heart action.

As substitutes for the salicylates, salol, salophen, phenocoll,
antipyrin and acetanilid have been largely resorted to. The first is
safe and trustworthy and does not irritate the stomach nor interfere
with digestion. It may be given to horse or ox in a dose of 3 drams,
thrice a day, to the pig in 10 grain, and to the dog in 5 grain doses.

Hübner had good success with pilocarpine hydrochlorate hypodermically (4
grains for a 7 months colt,) but this was not equally successful in the
hands of Siedamgrotzky. Other sudorifics like tartar emetic, Dover’s
powder, ammonium acetate, hot or spiced drinks (chamomile, boneset,) hot
baths, hot air baths, and wet packs have been used successfully and may
still be employed in suitable cases. The opium is often very helpful in
relieving intense suffering, and beside or in place of the Dover’s
powder internally, morphia may be injected subcutem over the affected
region. The main objection to its use is its tendency to lock up the
liver and bowels. Liquor of the acetate of ammonia fills at once the
rôle of a potent diaphoretic, an antacid, and an eliminant.

In the use of baths and packs it is well to consider the condition of
the patient. If the surface is cold with little reaction, and if the
attack has supervened on exposure, or chill, persistent hot applications
are indicated. Dogs and other small animals should have full hot baths
lasting for 15 or 20 minutes, and while in full glow may be quickly
sponged with cold water and rubbed dry in blankets, great care being
taken to avoid exposure or chill when damp. Or for these and the larger
animals as well, a hot air or steam bath may be applied under similar
precautions. A cold wet wrapping on the cranium will tend to relieve
cerebral congestion during the administration of the hot bath. In horses
and cattle surface heat and sudation may be secured by active rubbing
with wisps of straw, of both body and limbs, or by covering the neck and
trunk with large bags containing a small amount of chaff, sand or grain
hot from an oven. Hot carminative or alcoholic drinks are excellent
adjuvants, and even sedatives or nauseants (opium, veratrum, aconite,
tobacco). Another resort is to pass a hot smoothing iron an indefinite
number of times over the affected region. The part may be finally
wrapped in cotton.

In cases where the temperature runs high, on the other hand, and when
the surface glows, this dread of chill and reaction may be dismissed.
For the small animal a bath starting at 70° F. may be gradually lowered
to 60° or 50° F. Or a full pack may be employed, a sheet wrung out of
cold water being closely wrapped around the body, and covered at all
points with two or more dry woolen blankets, care being taken to avoid
the entrance of air and the occurrence of evaporation from the inner,
damp layer. This cools the surface and the blood returning inwards, and
in fifteen or twenty minutes it should induce free perspiration. It may
be kept up twenty to thirty minutes and may be repeated as often as
there is a serious rise of temperature. A less energetic method is the
mere sponging of the surface with cold water. In all such cases friction
is a valuable accessory.

Anodynes and revulsives are often applied to the affected parts with
good results. In very acute cases (especially articular), lotions and
liniments of salicylic acid or salicylate of soda with laudanum,
aconite, or chloral hydrate may be used. In the less violent cases
camphorated spirit, soap liniment, or a combination of essential oils
(gaultherium, turpentine, cajeput, origanum, peppermint) with aqua
ammonia and sweet oil may secure great relief. Mustard or essential oil
of mustard in vaseline is an excellent alternate. Finally active
cantharidine blisters are usually most effective. These are applied over
the affected joints or muscles and if the inflammation shifts to other
parts it is followed up until it finally disappears. A concurrent
alkaline treatment, and more important still, absolute rest, will serve
to protect the heart to some extent, against a metastasis from the
exterior. It has been supposed that the beneficial action of the blister
is in ratio with the amount of exudate, and hence cantharides has been
highly esteemed in this connection. Friedberger and Fröhner have used
tincture of iodine and biniodide of mercury.

The local application of anti-rheumatic agents would embrace all the
salicylates, oil of wintergreen and guaiacol, the latter mixed with an
equal amount of glycerine. Methyl salicylate has been strongly
recommended for external use.

Stengel covers the surface with lint smeared with salicylate of methyl
ointment, and then applies a plaster bandage over all. This removes
muscular spasm, pain and swelling and is rarely required for longer than
a few days.

In cases in which salicylates fail, other agents have been resorted to
in man and to a lesser extent in the lower animals. Greenhow strongly
advocates a combination of quinine and potassium iodide internally,
while Russell Reynolds has successfully employed tincture of muriate of
iron in large doses repeated every three hours.

In _chronic_ cases these would especially commend themselves as
calculated to repair the general health and overcome the loss of
hæmoglobin. In _chronic rheumatism_ a course of tonics is often the best
resort, and in dogs especially cod liver oil has benefited when all else
had failed. Arsenic too (3 to 8 drops Fowler’s solution thrice daily)
has been beneficial in both dogs and pigs. In other cases iodide of iron
has been helpful. So also with gum guaiacum given in combination with
potassium iodide. In such cases too, treatment by alkalies and
salicylates may be called for, and close attention should always be
given to secure a free action of the liver, bowels and kidneys. The
local treatment recommended for acute rheumatism, (hot baths, frictions
with essential oils and above all blisters of mustard or cantharides) is
even more applicable to the chronic. A firm bandage over a covering of
cotton wool, and a systematic application of electricity will often
help. Warmth, a run at grass in a sheltered sunny paddock, moderate
exercise and a nutritious and easily digestible diet are important
conditions.

GOUT. PODAGRA. ARTHRITIS URICA.

Definition. Affects birds, dogs, perhaps pigs. Causes: excess of
nitrogenous food, imperfect oxidation, impaired metabolism and
elimination. Susceptibility of birds in confinement. Xanthin bases.
Nuclein. Hepatic torpor. Contracted kidney. Affects tissues of little
vascularity. Lesions: chalky deposits around joints, and in internal
organs. Solubility of biurate of soda in synovia, serum, etc.
Symptoms: arthritis, joint tenderness, resting on breast, hard or
fluctuating swellings, desquamation, ulceration, chalky urates.
Diagnosis: test for biurate. Treatment: less albuminoid diet,
eliminating salts, colchicum, piperazin, surgical and antiseptic
dressing.

_Definition._ An arthritis characterized by periodical exacerbations, by
the deposit of sodium biurate in and around the joints and at times in
other parts of the body, and by more or less constitutional febrile
disturbance during the paroxysms.

_Animals susceptible._ Among the lower animals the disease has been
noticed almost exclusively in birds, which even normally excrete so much
uric acid that the liquid may be semi-solid as found in the cloaca or in
the droppings. While this is a constitutional peculiarity in the bird
yet it is enhanced in connection with an abundant diet of rich
nitrogenous materials, as in forced feeding, and in old animals in which
the eliminating action of the kidneys is more or less impaired. Ebstein
has shown that gout can be produced in birds by tying the ureters. All
domesticated birds, chickens, turkeys, pigeons, ostriches, geese, ducks,
Guinea fowl, have been found to suffer. A case of gout has been reported
in a =dog=, and Pradal has described it as existing in swine, but the
symptoms given are more in accord with articular rheumatism.

_Causes._ The causes of gout are overfeeding especially on highly
concentrated nitrogenous food, acid sweets, and in turn sweet and acid
alcoholic drinks, an excess of uric acid in the blood and tissues,
imperfect oxidation of albuminoids, impaired metabolism, imperfect
elimination of uric acid, and impaired innervation. Probably no single
morbid condition is in itself sufficient to induce the disease but a
combination of several, unquestionably operate in many cases.

The uric acid theory is favored by the constant presence of this acid in
considerable amount in the blood of birds, and by Ebstein’s experiment
in tying the ureters, but it has to face the fact that young and active
birds living in the open air, and hunting for their food do not suffer,
that it is usually scanty in the blood of man just before an attack,
that Gilman Thompson failed to produce any symptoms of gout by injecting
into the blood of animals more uric acid than the amount which they
normally excrete in twenty-four hours, that the familiar symptoms of
uric acid poisoning are not at all those of gout, and that the excess of
uric acid in leucæmia, anæmia and pneumonia produces no such symptoms.
In addition to excess of uric acid some other factor is required.

_Xanthin bases_ (Xanthin, hypoxanthin, etc.) found in the blood by
various observers, are derived from albuminoids, especially nuclein and
nuclein bases, including in man caffein and theine, and being closely
allied to uric acid are believed to have a nearly similar action.

Various forms of abnormal metabolism are invoked as the cause of uric
acid and gout, and Haig and Vaughan hazard the theory that the breaking
down of the nuclein is an important factor. This and other metabolisms
are attributed to the local action of the uric acid and urates, and
again to a fault in innervation. The imperfect action of the liver where
the uric acid should be largely resolved into the more soluble urea, and
of the kidneys through which it should be promptly excreted must be
attributed to a nervous source. Levison incriminates the granular,
contracted, inactive kidneys.

Ebstein attaches great importance to impaired nutrition in the affected
tissues which undergo necrotic changes that pave the way for the
deposition of urates in their substance. This is somewhat sustained by
the occurrence of the local deposits in tissues in which circulation and
nutritive changes are slow, and in older animals in which not only are
the osseous tissues more calcic and less vascular, but the articular
lamella has been formed by cretefaction of the bone and cartilage. Haig
suggests that in the old, the joints are less vascular and less
alkaline, and more sensitive to cold. On the other hand those in the
greatest vigor of life are more ravenous, digest more actively and are
in this sense more subject to injury from excess of uric acid and allied
products. Birds at this age, confined and in process of fattening are
thereby exposed. Overfed, obese, lazy, old house dogs are under similar
causative conditions.

_Lesions._ The most prominent lesions in birds are chalky concretions of
urates on the articular ends of the bones and in the structures around
the joints including even the tendons, with more or less inflammatory
exudate and even necrosis, invading the bony tissue and articular
cartilage. Abscesses may be present usually outside the bursa. Birds
suffer especially in the tarsal, metatarsal and phlangeal joints, but
often also in the corresponding joints of the wing, and less frequently
in the joints of the trunk, and in the internal organs,—kidneys, liver,
lungs, serosæ,—and skin. In these last, miliary chalky concretions and
encrustations are found. In Brückmüller’s case in the dog the chalky
deposits of urates were found mainly on the epiphyses of the ribs, but
also on the joints of the limbs.

Uric acid is always abundant in the blood of birds, and Roberts has
shown that biurate of soda (the usual form of precipitate) is insoluble
in blood serum, synovia and other body fluids when in excess of
1:10,000.

_Symptoms._ In birds the febrile and constitutional symptoms have not
been carefully observed so that the objective symptoms in the affected
joints have been mainly relied on. There is extreme tenderness marked by
standing on one limb, or resting on the breast, and hence moping apart
from the flock. When made to rise, the affected limb may be used to
steady the body, or even to walk, with a limp, though in bad cases the
sound limb only may be used. The affected joints are swollen, soft, hot,
extremely tender, pitting on pressure, and later the seat of nodular
yellow masses, usually hard, but sometimes fluctuating and in size from
a pea to a hazel nut. The superimposed epidermis is thick, dry and
scaly, falling off in flakes. At a more advanced stage the concretions
may burst through the skin, discharging a buffy, granular, debris
containing crystals of urates of ammonium or calcium, or of uric acid.
Later still are ulcerous sores, involving the disintegrating urate
nodules and the necrotic bones and cartilages. The deposits deflect the
bones from their normal direction, causing not only nodular swellings on
the toes but much crookedness and distortion. As in man the disease is
essentially chronic and advances slowly, with anæmia, emaciation,
debility and at times diarrhœa.

_Diagnosis_ depends largely on the recognition of the excess of urates
in the deposits. These appear under the microscope as fine acicular
crystals, which in the harder portions have a concentric arrangement. A
portion of the concretion may be moistened with a few drops of nitric
acid and evaporated to dryness. To one part of the residue is added, by
means of a pipette, a drop of aqua ammonia, and to another caustic soda.
The ammonia develops a beautiful purple red color, and the soda a blue
or purplish blue ring (Murexide test). In tubercular joints, which are
common in birds, the caseated nodule is made up of cells and granular
debris, with tubercle bacilli, and though cretaceous particles may be
present they fail to give the microscopic and color appearances of uric
acid.

_Treatment._ This must be largely preventive. The rich albuminoid
feeding and close confinement must be modified especially in the older
birds, and eliminating agents must be given in the drinking water. The
Carlsbad combination (sodium sulphate 22; potassium sulphate 1; sodium
chloride 9; sodium bicarbonate 18) may be used. Powdered colchicum ¼ gr.
once or twice daily during an attack, or piperazin ½ gr. twice a day.
Locally, abscesses should be opened, and like any sores or ulcers,
treated with antiseptics (Salicylate of sodium 75 grs., glycerine 2
ozs.; or piperazin solution 2:100).

SCURVY: SCORBUTUS.

Definition. Susceptible animals: pigs, dogs. Causes: unwholesome salt
meat, lack of fresh food, vegetables, potassium, bad environment,
unvarying diet, lack of free range, putrescent food, foul water,
infection; non-recurrence. Lesions: blood black, diffluent, little
rigor mortis, excess of sodium, petechiæ and extravasations, red
marrow, softened, swollen, bleeding, ulcerating gums. Symptoms:
Anorexia, prostration, debility, tardy movements, petechiæ, loss of
bristles, ulcers, gum lesions, joint swellings, blood extravasations.
Diarrhœa. Prognosis unfavorable. Treatment: correct unwholesome
environment and food, wash, rich food partly green or animal, iron,
bitters, arsenic, mouth wash (potassium chlorate), for suckling milk.
Butcher.

_Definition._ Scurvy is a subacute or chronic trophic disorder
characterized by debility, inanition, anæmia, swelling and bleeding of
the gums, gingival ulceration, dropping of the teeth, and petechial or
more extensive hæmorrhages and exudations in the skin, serosa, and solid
tissues.

_Animals susceptible._ In past times _man_ has suffered extensively in
connection with unwholesome food and environment, on long sea voyages,
on uninhabited islands, in military campaigns, in besieged cities, in
famines, when restricted to one article of food, etc. Among the lower
animals, =pigs= especially suffer, when kept in close, foul quarters and
fed a monotonous and insufficient ration. =Dogs= suffer under similar
conditions, and probably other animals would if equally badly used.

_Causes._ Formerly it was attributed to an exclusive diet of salt meat
and bread; to excess of sodium, and deficiency of potassium salts; to
the absence of fresh vegetables; to tainted food, etc. A broader
generalization shows the Eskimo living on a pure meat diet, the
Mongolian on rice alone, the Congoese on plantains, and without scurvy.
Yet it cannot be denied that these various conditions undermine the
general health, and prepare the system for those faulty states of
nutrition which are seen in scurvy. In pigs the food and environment are
usually chiefly at fault, the subjects have been kept closely confined
in foul buildings, in a hot, moist atmosphere, and with an uniform diet
of maize or other unvarying and insufficient ration. It does not appear
when there is a free access to a spacious yard or open field, and when
the monotonous diet can be varied by a variety of slugs and other
invertebrates. Röll attaches great importance to a putrid condition of
the aliments (putrescent swill). Benion has found it mainly in obese
swine, the forced feeding and intestinal fermentations manifestly
operating as factors. Corrupt drinking water has proved a manifest
factor among men living in camps, and pigs above all other animals are
subjected to this cause. Benion says it occurs in the advanced stages of
measles (cysticercus cellulosa).

It is evident that unwholesome conditions of life such as the above,
contribute strongly to the affection, yet probably no one of these is by
itself an effective factor. Its rapid extension among men and animals,
that are huddled together in close, filthy quarters suggests an
epizootic or infective element, and Cornevin, Hess and others attribute
the disease in pigs to the germ of erysipelas. Stengel has produced
purpuric disease in animals by inoculation of the extravasated blood
from human scurvy patients. Müller and Babes found a slender bacillus
and streptococci in the tissues of scorbutic gums. The bacillus was
present in the mouth of non-scurvy persons. Boruträger found cocci in
the spleen. Berthensen alleges that after complete recovery the disease
does not attack the same person a second time, which, if confirmed, will
go far to establish a bacteridian origin. There is considerable
presumption of the existence of a microbian cause, the efficiency of
which is dependent on the unhygienic conditions above stated, while
these unwholesome conditions are equally nonpathogenic in the absence of
the microbe.

_Lesions._ The blood is black and incoagulable or clots loosely, rigor
mortis is slight, changes may be found in the number and character of
the white and red blood globules, but are not constant, there is usually
an excess of sodium salts and deficiency of potassium ones, and there is
marked petechiation of the skin, mucosæ and serosæ. The bone marrow may
be abnormally red and the bones fractured at the epiphyses, or carious.
The addition of the gum lesions makes the case characteristic. The gums
are softened, swollen, red and uneven, with hæmorrhagic discoloration,
erosions, necrotic areas and ulcers.

_Symptoms._ Anorexia or fastidious appetite, prostration, debility and
sluggish indifferent movements, are followed by the local lesions on the
skin and gums. On the skin appear petechiæ, and extravasations, which
often implicate the bristles, so that they may be shed or pulled out
with ease, the bulbs appearing dark and bloodstained (bristle rot).
These may be followed by necrotic sloughs, and deep ulcers that are slow
to heal. The gums are red and swollen, with hæmorrhagic spots, and bleed
on the slightest touch. Erosions, sores and ulcers are not uncommon, the
tongue is dry and furred, and the mouth exhales a fœtid odor. The teeth
may become loose in their sockets. Swelling of the joints, from
hæmorrhage or effusion, may be noticed, and lameness or stiffness from
muscular or intermuscular extravasation. Blood effusions into the
anterior or posterior chamber of the eye have been noticed and paralytic
or comatose symptoms from similar effusions on the brain. In the absence
of improvement the patient becomes more and more debilitated and
exhausted, and death may be preceded by profuse exhausting diarrhœa.

_Prognosis_ is unfavorable in advanced cases, and when the faulty
regimen cannot be corrected.

_Treatment._ The first consideration is to correct the unwholesome
conditions of life, purify the building and its surroundings, and allow
a free range on a pasture. Subject each patient to a thorough soapy
wash, and if possible allow clean running water in which a bath may be
taken at will. Access to green food and invertebrates (slugs, larvæ,
etc.) is important, or a varied diet of grain, middlings, bran, roots,
fruits, tubers, cabbage, silage, etc., must be furnished. Iron and
bitters (mix vomica, gentian,) are useful and sometimes small doses of
arsenite of soda solution, or cream of tartar are useful. Acorns or
horsechestnuts are recommended. For the mouth a wash of potassium
chlorate, soda biborate, or potassium permanganate may be resorted to.
Friedberger and Fröhner advise for the dog extract of meat in wine.

In the case of fat pigs it is more profitable to butcher at once, as
soon as early symptoms appear.

In pigs or puppies brought up by hand, as in babies, the true course, is
to discard milk substitutes and give sweet new milk, preferably of the
genus to which the patient belongs. The important elements of
cleanliness and outdoor life must not be forgotten.

GOITRE. BRONCHOCELE. ENLARGEMENT OF THE THYROID.

_Definition._ A non-inflammatory enlargement of the thyroid gland,
independent of known microbes or parasitism.

_Causes._ Goitre is an endemic disorder in man and beast, though it may
occur sporadically during or after a _debilitating disease_, or in
animals that are overworked or out of condition. As occurring
endemically all accessory factors that undermine the general health must
be admitted as potent factors, though insufficient of themselves to
develop the malady in the absence of the specific cause. Thus in Europe
women suffer more than man, being more _confined indoors_ and being less
muscular and vigorous. In New York the new born offspring of ewes, kept
in close confinement during winter, may be all goitrous, while those of
flocks, having a free run through the whole season, escape. Gurlt has
seen the same in goats. Apart from debilitating diseases New York horses
and cattle develop the greater number of cases in winter, the period of
confinement and idleness. House dogs suffer more than hounds.

_Poor diet_ has a similar effect. In Europe where the disease is very
prevalent in the underfed peasant population, it is rare among the
highly fed domestic animals. Bouley says it is excessively rare in
animals even in the localities in which it prevails in man, and though
mentioned by Lydtin, Johné, Haubner and others it is not as a common
affection. In New York and Pennsylvania on the other hand it is rare in
the well-fed human population, and very common in horses, mules, cattle,
sheep, swine and dogs. I have known congenital goitre to prove fatal to
a new born dromedary in Central Park, New York. The long, severe winter,
close confinement, and impure air, doubtless as much as the spare diet
contribute to this prevalence among the animals in New York.

_Intestinal worms_ and other parasitisms must be accepted as secondary
factors, the development of goitre often going on simultaneously with
the increase of the parasites.

_Heredity_ is claimed as a cause by Möller and others, and doubtless a
weak constitution transmitted from parent to offspring, is more
susceptible. Apart from this the exposure of both to a common specific
cause is the main factor in its production.

_Locality._ This must be accorded a first position in the causation of
goitre, so far at least as it occurs endemically and enzootically. In
England it has prevailed, in man, on the limestone hills of Derbyshire,
and Gloucester (Cotswold); in Europe it is common in the Alps, Pyrenees,
Savoy, Styria, Silesia, in the Black Forest and in the Rhone valley; in
Asia it prevails in the Himalayas, the Altai Mountains, the hills of
China, and in the Punjaub; in South America it is seen in the valley of
the Oronoco; in North America in Saskatchewan, Ontario, Michigan, Ohio,
Pennsylvania, New York, Vermont, Virginia and Alabama. A large number of
these localities lie on magnesian limestone or are supplied with water
that has percolated through this, so that at one time the excess of
magnesia and the lack of iodine were held to be the main causative
factors. This contention cannot be sustained in all cases, so that the
disposition is, at present, to attribute the disease to some unknown
poison. This unknown poison may be present in districts apart from the
magnesian limestone, yet the disease is so frequently seen upon this
formation that its presence must always be looked upon with suspicion as
a probable bearer of the poison, and waters bearing its products are
unsuited to the victims of goitre.

_Pathological Anatomy._ Sometimes the swelling of the gland which
appears during catarrh or pharyngitis will subside on recovery. In other
cases it remains as a distinct hypertrophy. This is usually an increase
of the parenchyma and dilatation of its follicles with an albuminous
fluid (_hypertrophic goitre_). This may affect one lateral lobe or both.
In other cases the fibrous tissue mainly increases and the gland becomes
hard and resistant (_fibrous goitre_). In other cases the individual
follicles become distended, and may even break into each other forming a
large cavity or several with liquid contents (_cystic goitre_). In other
cases there is a great increase of the vascular network of the gland so
that blood alone is obtained on puncture (_varicose goitre_). Tumors of
all kinds may be found in the gland, thus encysted adenoma, sarcoma and
melanoma in horses, carcinoma in old dogs.

_Symptoms._ In _horses_ there may be swelling of one lateral lobe of the
gland or of both, reaching individually the size of a hen’s egg or the
fist, or larger. Cadeac cites cases that weighed 4 lbs. In _dogs_,
_cattle_, _sheep_ and especially in _swine_, the two lobes are much more
closely connected, and the disease affecting both, together with the
commissure, the whole may be resolved into one uniform swelling, much
larger than in the horse relatively to the size of the animal, often
covering the whole front of the neck, and extending into the chest.
Cadeac mentions cases in the dog in which the mass weighed 4 lbs.

The smaller swellings appear in the solipeds on the two sides of the
larynx, and in other animals more in front. They are mobile, but rise
somewhat with the larynx in swallowing, and are usually covered by
loose, movable skin. The consistency of the swelling varies; some are
soft, elastic or pitting on pressure, others fluctuate and still others
are firm and resistant. Old cases that have become calcified may even
feel bony. In dogs it will sometimes pulsate like an aneurism.

Functional secondary troubles are rare in solipeds. In the other animals
the goitre may compress the pharynx or gullet causing dysphagia, or the
larynx, trachea or recurrent nerves causing more or less wheezing or
dyspnœa. Asphyxia is not uncommon in new born sheep, and goats, and
Johné and the present writer have seen cases in dromedaries. The soft
embryonic tracheal rings had been so compressed from side to side that
respiration became impossible. Honert records a case of asphyxia in an
adult horse. Cases of _roaring_ in adult horses and mules and of
asphyxia in adult dogs are also on record. Warz records the obliteration
of the jugular in a dog, and Cadeac œdema of the lips and face.

The _course_ of goitre is usually slow, extending over years, yet in
young dogs it may make a very rapid progress. It will often stand still
for a time, and later start a new growth under a fresh access of the
cause. Spontaneous disappearance is rare.

_Prevention._ This is especially important in localities in which goitre
is enzootic, and embraces careful attention to the general health, the
avoidance of overwork, exhaustion, indoor life, lack of exercise, impure
air, faulty feeding, starvation, and water from the goitrous soils. Rain
water is preferable.

_Treatment._ First remove the various causes, and secure the best
hygiene. If a change to a non-goitrous district can be had, avail of it.

Among medicinal agents iodine holds the foremost place. It may be given
internally as potassium iodide, alone, or along with tincture of iodine,
and applied locally as iodine ointment rubbed into the skin, or tincture
of iodine painted on the surface.

Of surgical measures the simplest and best is the injection of iodine
into the diseased thyroid. The nozzle of a hypodermic syringe is
inserted into the gland, preferably into the largest cyst or follicular
mass, and the liquid drawn off as fully as possible. It is then injected
with the following mixture: compound solution of iodine one part,
distilled water two parts. The amount may vary with the size of the
goitre. In cases of moderate size ½ dr. to 1 dr. is suitable. There is
usually some resulting inflammation, which may be met by a wet compress
around the throat. A second and third injection may be made if
necessary, when the effects of the preceding one have passed off. In
simple forms it is very successful. For dogs Möller recommends from 5 to
15 drops of undiluted tincture of iodine at an injection. In other cases
he used a watery solution of papain (1:10) to be left in for 48 hours.
The thyroid was then soft and, on incision, discharged its digested
parenchyma as a milky fluid, and favorable healing followed.

The removal of the diseased lobe has been successfully accomplished in
horses, the reservation of the other lobe, or even of the connecting
commissure, being sufficient to prevent the occurrence of tetany. From
the extreme vascularity of the organ it is important to ligature the
arteries before attempting the removal.

In the other domestic animals in which the commissure is practically
obliterated and the two lobes confluent in goitre, the excision of the
mass is liable to be followed by tetany, dropsy (myxoedema), stunted
development, anæmia or marasmus. If a portion of the gland is left these
results do not follow. Grafting of a portion of healthy gland may
correct the tetany. The hypertrophy of the gland may sometimes be
arrested by ligature of its nutrient arteries, and without the dangers
above named. This may be combined with the internal and external use of
iodine.

EXOPHTHALMIC GOITRE.

_Definition._ A complex disorder manifested by hypertrophy of the
thyroid, excessive bulging of the eye balls out of the orbits, cardiac
palpitations or tardy heart action and other nervous or trophic
disorders.

Cadiot records a case in a horse, in low condition, with painful
œdematous swelling of one fore foot, and swellings in other parts of the
body, great enlargement of the left lobe of the thyroid, tumultuous
heart action with beats 70 to 80 per minute, and strong visible
pulsations in the superficial arteries. There was no leukæmia and no
exophthalmia. The patient died on the third day.

Jeswejenko records that of a four year old English thoroughbred which
after a race showed anorexia, weakness, thirst, rapid pulse,
palpitations, conjunctivitis, enlarged thyroid and after fourteen days
exophthalmia with thyroid pulsations. It died in the fourth week, anæmic
and exhausted. A second case in a 7 year old bitch recovered in three
months under treatment with iodine.

Röder gives the case of a cow with palpitations, abnormally strong
pulsations, thyroid hypertrophy and double intense exophthalmia. This
persisted for four years.

RACHITIS. RICKETS.

Definition. Lesions and pathology; gastro-intestinal disorder,
hepatic, splenic and renal congestion and hypertrophy, lessened blood
salts, dilated arteries, hyperæmia of bone, deep red marrow, blue
articular cartilage, softening of epiphyseal cartilage and under the
periosteum, with hyperplasia, decrease of lime salts, bending of bone,
loose periosteum; sclerosis in repaired cases. Causes: appears as if
infection, lack of lime salts in food, inconstant, free phosphorus,
glycero-phosphoric acid, lactic acid, oxalic, acetic and formic acids,
heredity, bad air, crowding, damp soils, cold, confinement, darkness,
infection, toxic matters. Symptoms: unthrift, thin neck, arched or
hollow back, drooping pelvis, weariness, stiffness, recumbency, limbs
not plumb, tender, swollen puffed joints, enlarged epiphyses, bent
shafts, or spine, brittleness. Swine fed on potatoes or corn,
“snuffles”, breaking teeth, diarrhœa, bronchitis, skin eruptions,
arthritis. Cattle, epiphyseal swellings, bow legs, crooked back. Dogs,
bow legs. Goats. Birds, knotted thickening of bones, flexibility.
Fever, colics, indigestion. Lameness shifting, intermittent,
relapsing. Paraplegia. Treatment, hygienic, vigorous breeding animals,
nutritious rations, rich in earthy salts, well balanced, from sound
land, rich abundant milk without excess of fat, avoid spoiled food,
adapt cow’s milk to foal or puppy, fresh air, sunshine, damp soils,
antacids, lime water, laxatives, bitters, phosphates, bone dust,
phosphorus.

_Definition._ A constitutional disease of young animals, associated with
disorders of digestion, nutrition, assimilation, and sanguification, and
especially characterized by softening and distortion of the bones.

_Lesions and Pathology._ Apart from the bones there does not seem to be
an absolute constancy in the lesions. There is usually, however, a
period of ill-health and faulty nutrition before the lesions in the
bones can be recognized. Thus, there may be gastric or intestinal
congestion, or catarrh, indigestions, constipation alternating with
diarrhœa, enlargement of the liver, spleen and kidney with hyperæmia,
and according to V. Jaksch, a diminution of the salts of the blood.
Beneke found that the arteries are dilated throughout the entire body,
but the heart does not always participate in this distension. The
arterial dilatation is very marked in the pulmonary artery, yet the
lungs are relatively small. In the bones there is a well marked
hyperæmia, most prominent beneath the periosteum, in the cancellated
tissue, the line of junction of the epiphysis and diaphysis, and near
the articulating surface. The contents of the cancelli are of a deep
red, and the color shines through the articular cartilage giving it a
bluish tinge. The shaft of the bone does not escape, but like the
epiphysis and epiphyseal cartilage may be soft and yielding to pressure,
and cut readily with the knife.

At both points the process of growth is increased and its area extended,
but it is not completed by the full deposition of earthy salts, and the
softening is not confined to the new tissues, but extends into the
subjacent bone as well.

The chemical composition of the bone is profoundly altered, the organic
basis, at times amounting to 65 per cent., as compared to 33.30 per cent
in the normal bone. The softened bone, yielding under the weight of the
body, bends out of shape at the epiphyseal cartilage, or even elsewhere,
giving rise to bow legs, deviation of the joints inward, or other
distortion. The periosteum is red, thickened, the seat of exudate and
easily torn from the bone.

The bones are often thickened by new deposit under the periosteum and
especially at the junction with the epiphyses. Old cases of distortion,
the result of rickets, do not necessarily show a deficiency of earthy
salts, as these are restored in case of repair and they may even be
found in excess of the normal, increasing the hardness of the bone.

_Causes._ This disease does not seem to have been recognized in Great
Britain until the beginning of the 17th century, the period of England’s
early activity on the sea, and the beginning of extensive commerce and
manufactures. From that time it has been increasingly and extensively
prevalent. Yet it has not been shown to be propagated by any specific
germ, nor to have extended in line with the introduction and use of new
food products like the potato. It appears to be traceable rather to
unwholesome conditions of life and a reduction of the general tone and
nutritive vigor.

_A deficiency of earthy salts in the food_ has been a natural and
favorite explanation, and the ill-health that is thereby brought about
is often an important factor. Yet rachitis occurs independently of such
a condition.

In Roloff’s experiments, pigs fed on aliment deficient in lime salts,
suffered from bone softening, while the control animals on food rich in
lime salts remained well. The diseased animals further recovered on a
diet rich in lime. Voight, Chossat, Milne-Edwards, Lehmann,
Bousaingault, Heitzmann, etc., had similar experimental results, and the
effects were shown in goats, sheep and dogs, in curvature, shortening,
swelling of the costal cartilages and joints and contracted pelvis.
Growing pigs have often been found to suffer in this way when placed on
an exclusive diet of maize. The great improvement often secured in
feeding an excess of calcareous phosphates tends to corroborate the
hypothesis. Wagner found that food rich in lime salts, and the
administration of small doses of phosphorus, rendered the epiphyses of
the growing bones more compact. Kassowitz, on the other hand, found that
an excess of phosphorus caused absorption from the bone substance and an
irritable inflammation of the osseous tissue. Schneidemühl has seen the
disease in calves raised on milk, poor in lime, the product of emaciated
cows; in pigs getting only potatoes and swill, and in puppies that were
denied bones. It is common in pigs on an exclusive diet of maize. Yet it
is most destructive in many breeding studs where the alimentation is
rich and generous. It must be admitted that as a concurrent cause, the
paucity of lime salts and phosphates is a powerful factor, and that in
supplying the bone ash, and improving the nutrition, these often prove
of great value. Their privation is, however, not an essential condition
of rachitis.

_Free phosphorus._ Ziegler and Kassowitz emphasize the hyperæmia of the
cancellated tissue, and Wagner shows that this condition can be induced
by excess of phosphorus, but this excess of phosphorus has not been
found in the blood in ordinary cases, and is not likely to occur in a
great number of young, at the same place and time, irrespective of food,
as has been shown in breeding studs in New Jersey, in the South and
West. In particular cases excess of phosphorus may operate, but it
cannot be looked on as universal or essential.

The presence of _glycero-phosphoric acid_ is alleged by Trasbot, but
there is no proof of its constancy in rachitis, nor would its presence
explain the real cause of the disease.

_Lactic acid in the system._ Lactic acid, in vitro, dissolves the
calcareous salts of the bones. Trasbot alleges that it opposes the
precipitation of lime in the form of tribasic phosphate, as found in
bone. Siedamgrotzky and Hofmeister found that the salts of the bone were
lessened under the administration of lactic acid. Heitzmann and Baginsky
showed that by restricting the lime in food and giving lactic acid, by
the mouth or subcutem, the lime salts in the bone were lessened
relatively to the organic basis. It should be noted that an exclusive
diet of buttermilk is liable to cause an attack of arthritic rheumatism.
Lactic acid is undoubtedly a coöperative factor in certain cases, but
though often found in the diseased bone and urine of rachitic children
(Ragsky, Morehead, Simon, Lehmann), it is not shown to be constant.

_Oxalic acid. Acetic acid. Formic acid._ Beneke found oxalic acid in the
urine in many cases of rachitis and attributed to it the removal of the
lime salts. Others have made the same charges on acetic and formic acids
which are sometimes found in the diseased bone.

It is quite plain that the process of normal ossification is easily
disturbed, and that the same agent (lime, phosphorus) will assist or
hinder according as it is present in small or large amount, and that
certain chemical agents like organic acids may act injuriously even in
the presence of an abundance of bone salts.

_Heredity._ Rickety parents have often rickety offspring, the weak
somatic cells, failing in both cases to build healthy, strong tissues,
but as a rule also, both have been condemned to live in similar
unwholesome surroundings.

_Unhygienic Conditions._ Schneidemühl notes that in animals as in man,
bad ventilation, close impure air, crowding, damp impervious soils, and
cold, are found more or less in places where rachitis prevails. By
lowering the general health and tone, these debilitate the tissue cells
and impair nutrition and growth.

_Confinement_ has a manifest influence. Rickets prevails in children in
the great manufacturing cities, where the exclusion of sunlight and the
breathing of impure air rob the system of its vigor. The children of
soldiers in India kept in close barracks are largely rickety, while the
more poorly fed native children outside escape. Wild beasts in
confinement are often rachitic, unlike their fellows of the forest.
Colts in confined stables suffer while those in the fields and yards
remain healthy. Swine in Sweden in close pens and fed on potatoes alone
suffer (Stockfleth).

_Darkness_ usually coincides with confinement and it is noteworthy that
deep sea fishes, living in comparative darkness, have usually
cartilaginous skeletons.

_Infection._ Certain facts seem to point to a direct infection, as
coöperating with the debilitating conditions above named. The advent of
the disease in England about 1700: its frequency in English swine on the
European continent (Schneidemühl); and its enzootic prevalence in
different parts of America, give seeming support to the doctrine.

Dr. W. L. Williams has seen it appear on an Illinois farm twenty years
after reclamation from virgin prairie, prevail for ten years and then
disappear. There was a remarkable coincidence of recurrent ophthalmia,
and disease of the bones and joints (navicular disease, spavin, splints,
ring bones, etc.).

In most of these cases the trouble occurred on low, damp or impervious
soils, agreeing with rickets in children, which avoids the Alps or hilly
districts, and abounds in valleys or bottom lands.

_Symptoms._ The colts show a lack of thrift and though there may be no
lack of growth or size, they have a rough coat, a poor development of
the neck, arching of the back and drooping pelvis. The chest may seem to
sink between the scapulæ. They move stiffly with swaying of the limbs,
or even staggering and are easily wearied or lacking in endurance. They
lie a great portion of their time or even persistently, refusing to
rise. When up they do not hold the limbs plumb, but allow them to
deviate one way or another in an unsightly way. There is liable to be
swelling of important joints of the limb, (knee, hock, stifle, fetlock),
which are tender to pressure and kept partly flexed. The ends of the
ribs are often enlarged. Bending of the long bones (tibia or radius),
and deviations of the back or sternum from the straight line are
significant. Thickening of the ends of the bones, or in the region of
the epiphyseal cartilages are largely diagnostic. The bones are easily
fractured. In _swine_ fed on potatoes, corn, etc., besides the
affections of the limbs, the thickening of the bones and swelling of the
joints, especially the hock and pastern, there is enlargement of the
nasal and maxillary bones so as to seriously obstruct breathing
(“Snuffles”). The teeth suffer and break readily and in the general
break down diarrhœa, bronchitis or skin eruption appears and the subject
falls into marasmus and perishes. In the necropsy arthritis is commonly
found. In _cattle_ beside the epiphyseal swellings, the bow legs and
joint enlargements, the back becomes crooked, vertically or laterally.
The same general symptoms appear in _dogs_ in which bow legs are a very
prominent feature. Goats suffer badly and mostly remain recumbent.

_Birds_ suffer most, showing knotty thickening of the bones of the legs
and wings, and flexibility of the bones generally but above all of the
keel of the sternum, which is usually badly distorted from sitting on
the perch.

In all alike there are usually a few days of fever, followed by
indigestion, colics, anorexia, and a general air of illness. Then appear
the lameness, stiffness and swelling of bones and joints. Any joint may
suffer, shoulder, elbow, knee, hips, stifle, hock, or fetlock. The
lameness may shift as in rheumatism, it may intermit, occurring
periodically, or it may advance uninterruptedly to a fatal issue.
Paraplegia is common and appears to be due at times to pressure on the
spinal nerves by the diseased vertebræ. Before this becomes complete,
the animal may walk with the whole digits and metatarsi in contact with
the ground, and the softened crumbling calcis may project through the
skin forming an unsightly sore which soon becomes septic. The same
happens at times to the point of the elbow.

_Treatment._ The most important, are the hygienic considerations. Reject
weak or cachectic animals from breeding, and those that have been
rachitic to a marked degree, as their progeny are likely to show the
same weakness. Change the ration giving one that is well balanced and
rich in nutritive matters and earthy salts. Clover, alfalfa, and a
generous grain diet may serve as an example for herbivora, and a fair
allowance of meat and bones for dogs. Food from land that has apparently
contributed to the disease in other cases is best avoided. If the land
is poor, sandy, or destitute of earthy salts and phosphates, so much the
more is it to be suspected and set aside. In the case of sucking animals
it should be seen that the milk is rich and abundant, and that it is not
too rich in fat, nor otherwise calculated to disagree and induce
indigestion. Above all soured or otherwise fermented milk should be
withheld, and any buckets or troughs used in feeding should be regularly
washed, scalded and disinfected. In case colts, or dogs are being raised
on cow’s milk it may be requisite to dilute it with one-third its volume
of barley water, or solution of gum arabic, and to sweeten with sugar.
Lime water with each meal is valuable in counteracting acidity, and
fermentation, and in furnishing lime which may be absorbed in part.

In prevention and treatment alike, fresh air and sunshine must never be
neglected and in warm weather, an outdoor life, night and day is of the
greatest value. At the same time cold storms, damp beds, or any
condition which may induce chill must be excluded. Close stalls, pens,
or kennels must be absolutely forbidden.

Among medicinal agents antacids are often essential on account of the
acid condition of the ingesta, lime water will often suffice, but if
there is manifest constipation calcined magnesia three times a day on an
empty stomach so as to counteract costiveness will often serve a good
end. The atony of the bowel may be further met by small doses of
strychnia. Other bitters may be used if this has little effect. Small
doses of phosphate of soda, or bone dust have been long lauded in the
affection, and probably act beneficially as a tonic as well as a food
material. Phosphorus in minute doses tends to increase the deposit of
earthy salts and consolidate the bones. Large doses induce hyperæmia of
the epiphyseal ligament and even favor fracture. A grain of phosphorus
daily may be given in olive oil or better in cod liver oil which acts as
a valuable tonic. Dieckerhoff recommends the intratracheal injection of
the solution of phosphorus in olive oil.

BRAN DISEASE: SHORTS DISEASE: BRAN RACHITIS.

Miller’s horses. Bran and middlings as fodder. Torpid bowels,
impaction, indigestion, colic, early fatigue and perspiration,
stiffness, lameness, epiphyseal swelling, facial bones swell and
soften symmetrically, teeth drop, dyspnœa. Ash of bran. Treatment.

A curious form of rickets has been observed, especially in miller’s
horses as a result of an excessive consumption of bran or middlings. It
is characterized by torpor of the bowels, impaction, indigestions,
slight colics, early fatigue and profuse perspiration under slight
exertion followed by stiffness, lameness, enlargement of the bones in
the region of the epiphyseal cartilage (near knee or hock), or of the
bones of the face. The superior and inferior maxillary bones are
symmetrically enlarged, the teeth are shed, mastication becomes
difficult and there may be some dyspnœa and snuffling. This resembles
the “snuffles” in pigs on an exclusive diet of Indian corn or potato and
Friedberger and Fröhner seek to explain both, by the lack of lime and
phosphorus in the food. But wheat bran has 5.1 per cent. of ash, and
middlings 2.3 per cent. as compared with wheat flour 1.7 per cent. or
oats 2.7 per cent. Putz on the contrary attributes the disease to the
excess of phosphorus in the bran acting as the free phosphorus in
lucifer match factories in causing necrosis of the jaw. But the
phosphorus in bran occurs as phosphate of lime which has no such action
on the bone and one must infer that the phosphoric acid is set free by
some acid developed perhaps in the intestinal fermentations. This is,
however, as yet unproved.

The _treatment_ of this affection consists in the suspension of the bran
and the expulsion of offensive accumulations and products from the
bowels, followed by a course of tonics and the general treatment for
rickets.

OSTEO-MALACIA (MALAXOS SOFT): CACHEXIA OSSIFRAGA; FRAGILITAS OSSIUM:
“THE CRIPPLE:” “THE STIFFNESS.”

Definition. Disease of the mature. Decalcifying in cancelli and Canals
of Havers. Dairy cows. Heavy milkers. Perverted appetite. Limed soils,
sandy or limestone. Low, damp, soils rich in organic matter.
Cultivation. Watery food. Plethoric. Debilitated. Cold. Change of
locality improves. Microbes. Toxins. Lesions: vary with stage,
congestion of marrow, excess of cells and fat, osteoclasts, exudates,
friability of bone, distortions and fractures in pelvis and elsewhere.
Symptoms: low condition, projecting bones, rough coat, perverted
appetite, stiffness, decubitus, swaying limbs, inappetence, drying of
milk, fever, bed sores, sloughs, sepsis, pus infection, fractures.
Duration, 2 to 3 months and upward. Enzootic. Prognosis, varies with
enzootic, and stage; best in recent cases, occurring, sporadically.
Treatment: according to cause, rich, generous diet, grain, salt
bitters, cod liver oil, apomorphia, wholesome pasturage, intensive
culture change water, dry up milk, dry stables, pure air, sunshine.
Slaughter. Local derivatives.

_Definition._ A softening and fragility of the bones of adult animals,
in connection with solution and removal of the earthy salts.

This is essentially a disease of mature animals and is thus easily
distinguished from rachitis, in which the lesions are due to a faulty
development of young, growing bone. In osteo-malacia, too, the
decalcifying proceeds most actively in the walls of the Haversian canals
and cancelli, while in rachitis it progresses especially under the
periosteum and in and around the epiphyseal cartilage.

The disease is found most commonly in dairy cows, but softening of the
bones of mature animals has also been seen in horses and other animals.
Dieckerhoff, who quotes cases in mature horses, adduces similar
instances in colts under a year old, occurring enzootically, and without
the specific lesions of rachitis. Seven out of sixteen broke their
femurs in October, 1886, all kept on the same place, in good box stalls,
and well cared for. Landois found in bones an abnormal amount of fat,
ossein, water and lime salts. Grawitz found no material change in the
cancellated tissue. In one district in Jutland, Stockfleth found an
extraordinary number of broken legs as the result of castration of
colts, which had not shown the thickening or distortions of rachitis.

_Causes._ The disease is particularly common in cows which yield a calf
every year, and especially in heavy milkers, in which respect it agrees
with the osteo-malacia of woman. The heavy demands upon the system for
the nourishment of the fœtus and the supply of milk, undoubtedly lay the
system open to attack, if they do not directly cause the disease. An
early and usually a persistent feature of the malady is a _depraved
appetite_, the causes of which may be read up in Vol. II. The statements
there made, require some qualification, inasmuch as osteo-malacia is at
times found on limestone soils with hard, calcareous water, and on rich,
alluvial valley soils abounding in both clay and lime (Sarginson,
Leclainche), as well as on barren sands and granite soils deficient in
both lime and phosphorus. It may even appear on virgin or mucky soils
after liming, which had been free from the trouble up to that time
(Thorburn). The decomposition of the abundance of organic matter,
hastened by the quicklime, has evidently been a contributing cause.

The excess of organic matter in the soil seems to be a considerable
factor. Both Thorburn and Sarginson mention the “mossy” soils and
waters, and in Lanarkshire, Scotland, and Westmoreland, England, where
they practised, black muck and peats abound. This is corroborated by the
prevalence of the disorder in the damp lowlands of Belgium and Jutland,
in the Swiss valleys, on the damp lands of New Jersey and the Carolina
seaboard, and generally on damp pastures with rank, watery herbage.

When land has been better cultivated and enriched by manure, the disease
has in many cases disappeared. This has been observed in England
(Sarginson), Wurtenberg, Switzerland, etc. (Leclainche).

Succulent, watery food (potatoes, turnips), have been quoted as causes,
as also rank, watery grasses, deficient in nutritious solids, but such
food has invariably come from habitual osteo-malacia soils. On the rich,
cultivated soils of the Lothians, Scotland, cattle are fed in large
numbers on turnips alone, and osteo-malacia and pica are alike unknown.
It is often noticed that the fodder grown on particular (osteo-malacia)
soils will cause the disease when fed elsewhere, so that the inference
is that some agent derived from these soils, and which is destroyed or
rendered harmless by cultivation, is carried in the food. It cannot be a
mere defect of nutritive matter, as this could be counter-balanced by
the simple expedient of consuming a larger ration. Leclainche has seen
the disease in its worst form in herds which received a rich and varied
ration, while it spared adjacent herds that were kept on rather short
rations. Even young plethoric animals suffered badly, though having all
they would eat of natural fodders (hay) from districts where the disease
was unknown, and in addition grain, linseed cake, cooked legumes and
bread. In two neighboring stables, where the stock were kept in
identical conditions, receiving the same food, in equal quantity, one
was decimated by the malady, while the other was spared (Leclainche).

The affection often prevails on the higher lands, which, beside having
the poorer soils, are specially exposed to cold storms and frosts, so
that chill enters as an accessory condition. In Westmoreland, England,
the river Eden divides the affected from the sound lands; the victims
are found on the west bank which receives the cold, east winds, and not
at all on the east bank where the warm, soft, west winds prevail.
Thorburn noticed that the majority of cases start in spring, when the
animals, debilitated by the winter’s seclusion, are exposed to severe
vicissitudes of temperature and driving storms, to the strain of
parturition, a fresh, heavy milk yield, and moulting.

The presence of a contagion has been suggested, but if this exists it
must be habitually introduced in the food or water rather than
transmitted from victim to victim. The healthy will often stand beside
the diseased for an indefinite length of time without injury, and in
certain recent cases a change to an uncontaminated farm, or an abundant
ration drawn from such sound soil, will secure immediate improvement and
recovery in a few weeks. In view of such prompt recoveries it would be
quite as reasonable to suspect some ptomaine or toxin taken in with the
food. The question of a microbe or a microbian poison is as yet a mere
hypothesis.

Cows become more susceptible with advancing age, and Dengler alone
claims to have seen the disease in calves. This is unfavorable to the
idea of immunity, and rather favors that of debility or cachexia.

_Lesions._ These are confined to the bones. Decalcification in the
Haversian canals and cancelli, reduces the bony tissue to a thin soft
plate. Yet the condition is not constant. Grawitz found no special
dilatation of the canals or cancelli in colts. Nessler and others found
decrease of the lime salts, Bibra and Grouven detected no marked change,
and Hoffmann and Begemann found an actual excess of phosphates.
Doubtless the specimens selected and the stage of the disease, whether
in active progress or during convalescence, may somewhat explain
discrepancies. The fat cells increase in the cancelli, with more or less
hyperæmia, and even blood staining as the disease advances, the bone
cells become less branching, and there may be gelatinoid exudates. The
resistance of the bone is diminished, it may be indented with the
finger, or scraped off with the nail, or cut with a knife. It breaks
under a slight strain, and is easily crushed under the weight of the
animal so that fractures and distortions of all kinds are met with. In
breeding cows the earliest and most marked lesions are in the pelvic
bones, but fractures of the bones of the limbs are common.

_Symptoms._ Poor condition or even emaciation, with very visible
projection of the bones is common. The coat is rough, the skin tense,
inelastic and hide bound, appetite variable, sometimes impaired, and
nearly always perverted so that the patient will lick the manger
continually or pick up and chew all sorts of objects, bones, leather,
articles of clothing, pieces of wood or iron, stones, etc. The amount of
food consumed may, however, be up to the normal. The most marked feature
is the difficulty and stiffness of locomotion. The patient lies most of
the time, rises languidly and with difficulty and moves the limbs as if
each were a rigid post without joints. The hocks will knock together,
and the restricted movements of the joint are often attended by
cracking. Yet appetite, temperature and yield of milk may remain normal.

Later appetite and milk secretion fail, temperature rises a degree or
two, the animal refuses to rise, remaining down twelve to twenty-four
hours at a time, and rising first on the hind parts, and remaining on
the knees for a length of time, moaning and indisposed to exert herself
further. Many cases at this stage begin to improve and may get well in
five or six weeks. Some will remain down for several weeks and finally
get up and recover. With constant decubitus however, the animal falls
off greatly, becoming emaciated and weak, the appetite may fail
altogether, and the patient is worn out by the persistent fever, nervous
exhaustion and poisoning from the numerous bad sores. Abscesses, sloughs
and fistulæ are common over the bony prominences.

It is in these last conditions above all that fractures and distortions
of the pelvic bones and less frequently of the bones of the legs occur.
They occur earlier as well in connection with falls, blows, crowding by
their fellows and sudden active movements of various kinds.

The disease may advance for two or three months, and in case of pelvic
fractures and distortions, there may be permanent lameness, and
dangerous obstruction to parturition, even though the bones should
acquire their normal hardness through the deposition of lime salts.

It has been noted that the disease is usually confined to well defined
areas, and that even in these it has its periods of abatement and
recrudescence so that given years are osteo-malacia years. In the
department of l’Aube, France, Leclainche, particularly noted the
enzootics of 1865–6, 1870, 1875–6, and 1883–4.

_Prognosis._ The gravity of the affection varies greatly under different
conditions. Some outbreaks are mild while others are very severe, and
the prognosis must vary with this gravity. Again at the decline of an
enzootic the disease is more benign and less ruinous. A case in its very
earliest stage is much more hopeful, than one that is far advanced, with
bones extensively softened or even broken, digestion and assimilation
badly impaired, and infecting sores and sloughs on different parts of
the body. Isolated cases are usually much milder than when the affection
has gathered strength enough to determine an enzootic.

_Treatment._ This will vary with the predominance of the causes,
essential or accessory. In some cases the suspension of the injurious
food and a rich alimentation on well grown fodders from sound lands will
meet every need. Green clover, alfalfa, and other leguminous products,
ground oats, beans, peas, linseed cake, rape cake, cotton seed and
vetches may be especially named. Even animal food may be availed of, and
cases are recorded in which cows have themselves hunted for snails and
frogs and devoured them greedily. The free access to common salt, and a
liberal supply of bone meal are helpful. Iron and bitter tonics,
(gentian, quinine, salicine, nux, copperas, tincture of iron) and cod
liver oil, in pint doses daily, have been found advantageous. Apomorphia
has been found especially valuable in correcting the preverted appetite,
and stimulating digestion.

Where it is feasible to move the affected herd from the unwholesome
pasturage or locality to one in which the aliment is rich and the
disease unknown, success usually follows the change.

On poor, uncultivated lands where the disease appears yearly, or at
short intervals, intensive culture with heavy manuring, and the heavy
feeding of the herd on grain products, linseed cake, etc., will often
banish the trouble.

Care should be taken to change the water as well as the food.

Finally every drain upon the system should be lessened or stopped. The
milk may be dried up and the animal should not be bred. Sweet, dry
buildings, pure air, sunshine and grooming are important auxiliaries.

In severe outbreaks, in high conditioned animals, the owner often
consults his interest, in sending the victims to the butcher as soon as
the affection shows itself and before time has been allowed for the
inevitable emaciation and loss.

Some, on osteo-malacia lands, have profited by changing the entire herd
every two years, as they become rapidly worn out under successive
attacks.

As local derivatives, oil of turpentine, hot vinegar, tincture of iodine
and biniodide of mercury have been employed. Open sores are treated with
antiseptic lotions, creolin, lysol, carbolic acid, iodine lotions,
iodoform, etc.

RAREFYING OSTEITIS. OSTEOPOROSIS. OSTEO-MALACIA OF THE HORSE. BIG HEAD.

Definition. Distinction from rachitis. Process of rarefaction, cell
proliferation, congestion, solution of earthy salts and fibrous
matrix, osteoclasts, Howship’s lacunæ. Dried bone light, spongy,
friable, though enlarged in repaired cases, dense, heavy. Face
lesions. Dyspnœa. Dropping teeth. Causes: microbian hypothesis,
disturbance of bone nutrition, faulty food, lack of bone salts, cellar
stables, floor on ground, malaria, cold, damp soils, city life, early
life, breed, asses and mules, breeding. Nature. Symptoms: illness,
inappetence, lifelessness, early fatigue and perspiration, stiffness,
lameness, distortions, stumbling, knuckling, arthritis, tender puffed
joints, thickened softened bones, facial swellings, narrowing of
intermaxillary space, chisel teeth, difficult mastication, shedding
teeth, emaciation, marasmus. Phosphates in urine when disease is
active. Relation to exostosis. Prevention and treatment. Hygienic,
move from cellar stable, or ground floor, secure air space under
floor, ventilation, warmth, sunshine, grain feeding, pasture, change
food, rest, salicylates, salicin, salol, phenacetin, blisters,
phosphates, bone dust, phosphorus, bitters, iron, barium chloride.

_Definition._ A form of osteo-malacia occurring in the mature as well as
in the growing horse, characterized by the absorption of earthy salts
from the walls of the cancelli and Haversian canals with excessive
production of the organic basis and cell elements and enlargement,
softening, lightness and fragility of the bones.

It differs from rachitis essentially in this that while the latter
attacks the young growing bone at the chief seats of growth, under the
periosteum and in the epiphyseal ligament, and therefore especially on
the surface of the true bony tissue, osteoporosis attacks the formed and
often the mature bone in its interior, producing attenuation of the
walls of its vascular canals and cancellar cavities and increase of
their fibro-cellular contents. Both result in enlargement of the bone,
but in rachitis this is determined largely by deposition on the surface
while in osteoporosis it takes place by expansion from within. The
further distinction that rachitis appears enzootically and osteoporosis
sporadically applies only to localities in which the latter is not
common. At different points on Long Island, in New Jersey and on the
rich soils in the Mississippi valley and on the Atlantic and Gulf
coasts, osteoporosis often prevails enzootically and has its
recrudescences like rachitis.

The process of rarefaction and softening may be thus stated. In the
Haversian canals and narrow spaces there is an active proliferation of
cells and increase of vascularity, with a gradual solution and removal,
not only of the earthy salts, but also of the fibrous matrix in the
walls of these spaces. As in the normal changes in bone, the absorption
appears to be effected through the large cells or osteoclasts grouped
around the blood vessels. In the osseous tissue, which abuts on the
vascular tissue, are to be found excavations, simple or irregular,
(Howship’s lacunæ), containing granular cells and the larger
osteoclasts. In a similar manner bone is softened and absorbed in
connection with tubercle, or the pressure of tumors, aneurisms,
actinomycosis. In case of recovery, repair takes place by the
disposition of new bone, so that the enlarged and rarefied bone may in
the end become harder than before. This applies especially to the
cancellated bone. On the articular ends of the affected bones, the
granulation tissue makes its way into and through the cartilage of
incrustation with resulting active disease of the joint.

The condition of the bone is well illustrated in the dried or macerated
specimen. Taken from a bad case in the active stage of the disease, it
crumbles under pressure and weighs as light as a sponge, whilst from an
advanced or recovered case, it is hard and resistant, and weighs as much
more than the normal bone as it exceeds it in bulk. The morbid
rarefaction usually affects the whole skeleton more or less, yet in
perhaps the majority of cases; the change is greatest in the bones of
the face, and the resulting distortions are usually symmetrical on the
two sides. It may show mainly in the maxilla, which is thickened to
twice or even five times its normal thickness, it may show in rounded,
general swelling of the nasal and superior maxillary bones and those
around the orbit, or it may involve the turbinated bones, the vomer and
even the cartilaginous nasal septum. Loosening and evulsion of the molar
teeth is common and snuffling breathing may occur as in rachitis
affecting the nasal bones of dogs and swine.

_Causes._ We are still in the dark as to the essential cause of
rarefaction of bone. There is a growing tendency to suspect a microbian
origin, and many facts are held to point in that direction. It seems to
have been unknown in England in the early part of the 19th century, and
is not noticed by Blaine, Youatt, Percivall nor other of the early
writers. In Varnell’s cases the same man had two farms not far apart and
equal in soil, drainage and stabling, stocked with horses bred from the
same parents with the same kind and amount of feed and work, yet on one
farm six cases of osteoporosis occurred, and on the other not a single
case. McNeil, in charge of street car stables, found the disease
destructively prevalent in the best appointed stables and absent from
others in the worst hygienic condition. In a superior stable with 220
horses he had 47 cases in two years, and in a fine stable with 100
horses he had 26 cases in the same length of time. In the poorer
stables, the horses bred in the same way on all kinds of soils and with
no difference in feeding nor management escaped. It is the common
experience in Europe and America that a farm or district, which has been
previously free from the disease suddenly has an outbreak in enzootic
form, and this will last for a year or two, then remit only to appear
with its old force after an interval of some years. Even during the
active prevalence of the disease on one or on several adjacent farms,
others in the immediate vicinity, and differing in no appreciable way,
geologically, hydrostatically, in buildings, food, water, general
management nor work, completely escape. Berus, Hoskins and other city
veterinarians have noticed, that it was almost the rule, that a fresh
horse put in the stall of one that had suffered from osteoporosis soon
contracted the disease.

W. L. Williams noticed on two different farms in Central Illinois, on
which the disease suddenly appeared, that for years after the
comparative subsidence of the affection there was an unusual prevalence
of spavins, splints, ringbones and other diseases of the bones. Meyer
has noticed that cases sent from Cincinnati into the country, and that
have got well, will succumb to the affection if brought back into the
city stables in which they originally contracted it.

All of this points very strongly to one of two things; either a
pathogenic germ in the system of the affected animal; or the presence of
a pathogenic microbe in the stable, water, or other part of the
environment, the toxic products of which are taken into the animal
system.

But as yet no specific pathogenic microbe has been demonstrated so that
this doctrine must still be held as a mere plausible hypothesis.

Many veterinarians with long experience in such cases absolutely deny
contagion. The hypothetical contagion undoubtedly extends slowly, and
uncertainly from animal to animal, probably, like actinomycosis, taking
place mainly through the soil, or some outside medium, rather than by
direct contact; or a special susceptibility on the part of the
individual animal may be necessary to render it effectual.

_Accessory Causes_ can be spoken of more confidently but even of these
no one, nor small group, can be advanced as essential. The process of
bone nutrition is readily disturbed by a variety of conditions, and such
disturbances may easily become the occasion of weakening the resisting
power and mayhap of admitting the hypothetical microbe to get in its
pathogenic work.

_Faulty food_ has been a favorite explanation. A lack of lime in the
soil and fodder seems, at times, to have had a baneful effect, if only,
in lowering the general tone and impairing the nutrition. Yet we see
osteoporosis on limestone soils (New York, etc.), and in animals
generously fed on grain. The same remarks apply to phosphorus and
phosphates. Their deficiency apparently contributes to the production of
the disease, and yet under other conditions, their abundance is no
barrier to its development. The excess of free phosphorus produces
osteitis and it is held by some that an over-abundance of phosphates
acts in the same way. It has been sought to incriminate a too
nitrogenous diet in some cases, and in others one too rich in fat or
carbohydrates. The many cases in Philadelphia and Pennsylvania were
mostly in animals that had been well fed and were in good condition when
attacked (Marshall).

Special food may be the direct cause, bran diet has been already noted.
Hinebauch found an acute osteitis with bone softening and arthritis in
horses fed on millet, green, partially matured and ripe. Horses
elsewhere have fed on millet, without such results, but not perhaps, in
the same environment, nor in presence of the hypothetical microbe.
Millet is not the sole nor common cause of osteoporosis, but there is
reason to suspect that it is at times an important accessory cause.

Of all prejudicial conditions none is to be so dreaded as _unwholesome
stables_. Of 200 cases reported by Berus, in Brooklyn, almost all were
in cellar stables or those with floors laid on the soil. Meyer finds
that “most all cases can be traced to an unwholesome atmosphere, or
gases arising from vaults, sewers, cellars, filthy streams, or from a
hollow space under the floor.” Harbaugh says every case was stabled in
damp, ill-drained, unventilated and badly lighted buildings. The worst
outbreak was in a basement with a damp wall, on one side, and none
suffered except those that stood next to this wall. The horses standing
on the opposite side, which was on a level with the ground outside,
escaped. Removal from a cellar stable to the floor above, put a sudden
stop to the appearance of new cases. James, of St. Louis, found 20
successive cases in a stable on a dirt floor, and Jasme, of Charlestown,
finds nearly all his many cases on earth floors in malarial regions.

_Malaria_ has been blamed, especially by southern observers, accustomed
to see the disease on the warm alluvial seaboard and river bottoms. That
this environment predisposes to the disease, by undermining the health,
is doubtless the case, but in spite of occasional remissions in the
symptoms, malarial germs cannot be set down as the constant cause. One
of the worst cases I ever saw, with every bone in the body soft, spongy
and light, developed at Inglis Green laundry, Edinburgh, where malaria
is absolutely unknown, but where the brook received large quantities of
chlorine.

_Cold_ is an undoubted factor, though the disease is most prevalent in
our warm southern states. Many veterinarians have noticed its
coincidence with rheumatism, in which cold is so often the dominating
accessory cause. Some have even suspected that it is only a modified
type of the rheumatic condition. Hinebauch found his cases of _millet
disease_ in cold basement barns, or with leaking roofs, so that the
floor and bedding were constantly wet. He found that cold always
aggravated the disease, and bad air even more so, while salicylates
seemed to have a marked curative influence.

_Damp soils_ should be named in this connection. These not only chill
the air by evaporation, and condense the cold dews at night,
contributing to produce the extremes of hot noon day and cold night
temperature, with corresponding disturbances of the bodily health, but
they favor the preservation of the infinitesimal forms of life
(bacteria, protozoa) and therefore of the hypothetical microbe of the
disease.

_City life_ is a most potent cause. Berus tells us that hundreds of
horses die yearly in Brooklyn of osteoporosis, and that if sent early to
the country a large proportion recover. The same is true of New York
City and Philadelphia. Of Cincinnati, Meyer says that he has failed to
find a case more than five miles outside the city limits, and that cases
sent to the country make a partial or complete recovery. If returned to
their former city stables, nearly all contract the disease anew within a
year.

Many cases, however, are found in the country and often within a
circumscribed area. These indicate, as in the city cases, a localized
cause, bacteridian or otherwise.

_Early life_ predisposes, the majority of cases taking place before the
sixth or seventh year, yet the disease occurs at all ages up to twenty
years and over.

_Breed_ does not seem to make a material difference, and though Shetland
ponies have acquired a bad reputation, their propensity to become fat
and soft, their too often idle, pampered life, and the confined quarters
in which they are frequently kept, account for much of the mortality.

_Asses and mules_ habitually escape, even in the South, where the latter
animal is so numerous and often so poorly kept. In Hinbauch’s millet
disease, the mules suffered more than the horses.

_Breeding horses_, male and female, have often acute attacks and die
early. The drain on the system and confinement seem to act injuriously.

_Nature._ Until we know the essential cause or causes of osteoporosis,
we must be in doubt as to its pathology. We are even debarred from
pronouncing authoritatively upon the essential identity or difference of
the various forms of softening, or rarefaction of bone. In obedience to
the clinical manifestations and structural changes, rachitis, fragilitas
ossium and osteoporosis have been separately described, but we cannot
positively say that they are not all due to one essential cause,
manifesting itself differently according to the activity of trophic
processes in the bones of the victim. In the growing foal the active
developmental processes in the epiphyseal ligament and periosteum may
determine that the symptoms shall be pre-eminently those of rickets, yet
we often see these complicated by the facial and other lesions of
osteoporosis. Both may be the result of one etiological factor, or there
may be a complex disease resulting from the presence of two. Again in
the pregnant cow in which the relaxation of the ischio-pubic symphysis
and pelvic ligaments means a profound change in the bone nutrition at
this point, the presence of the hypothetic microbe, or other essential
factor, may determine a decalcifying and fragility of the pelvic bones
generally. Again in the mature male and non-breeding female, in the
absence of the disturbing conditions of nutrition just named, the
vascular elements in the Haversian canals and cancelli may determine the
simple rarefaction and expansion of the bone which characterizes
osteoporosis. When present in the bone in any of these conditions, acids
doubtless fulfill an important rôle in the decalcifying and softening
process, but behind these it may be surmised that there is an unknown
cause or causes, which it is for the bacteriologist, chemist or botanist
to discover.

_Symptoms._ These are largely the same as in brain disease. There may be
first a period of illness, with poor appetite, lack of spirit and
energy, early perspiration and fatigue, or if at large, leaving the
herd, soon followed by some stiffness of gait and lameness, which may be
intermittent, disappearing under exertion, or shifting from one joint or
limb to another after the manner of rheumatism. Sometimes it shows in
stiffness of the neck, so that the patient finds difficulty in lowering
the head to graze; in others the back and loins are stiff and arched so
that the animal has difficulty in rising and turns slowly and painfully;
in still other cases the dorsal and lumbar vertebræ are depressed so
that the back is hollow. Even before the manifestation of lameness, the
affected limb may stand forward at the fetlock or knee, the gait is
clumsy and awkward, and the patient may suddenly stumble and fall,
showing little or no power of prompt recovery of balance. A horse, and
especially a young horse, with this habit of stumbling is always to be
suspected. The long bones of the limbs tend to enlarge or thicken, and
this is likely to be more uniform than in rachitis, and not to be
confined so much to the epiphysis. The implication of the stifle, hock
or other joint, with marked synovial distention, and mobility or
dislocation of the patella, is common and may be the earliest
manifestation of illness. The bones of the face usually show early
changes. The superior maxillary and nasal bones, beneath the zygomatic
spine and infra-orbital foramen and along the line of the molar alveoli
become especially bulging and rounded, the other facial and cranial
bones suffering to a lesser degree. In the lower jaw, also, the disease
predominates along the region of the molar alveoli, and the loosening of
the molars permits them to deviate inward so that the grinding surfaces
come perceptibly nearer to the median line, and the outer half of the
tooth is rapidly worn while the inner edge projects as a sharp cutting
ridge (chisel teeth).

For the same reason, the softening branches of the lower jaw deviate
inward, tending to still further destroy the due approximation of the
upper with the lower molars, and to diminish the breadth of the
intermaxillary space. The great thickening of the rami of the maxilla
tends still further to reduce the intermaxillary furrow.

Fractures and detachment of tendons and ligaments are common results of
the rarefaction, a portion of the bone often remaining adherent to the
tendon.

Cary gives the following statistics of fifteen cases: lame in the fore
limbs 11 (mostly shoulder), in hind limbs 11 (mostly hip and stifle),
stiff in loins 8, unable to rise without aid 3, had indented ribs 4, had
shifting lameness 8, had chronic indigestion 6; mares 5; geldings 8;
mules 2; ages were—_one_ 3 years, _five_ 6 years, _three_ 7 years, _one_
8 years, _two_ 9 years and _three_ 10 years.

When the bones are enlarged their softness and friability may be shown
by pricking with a needle, which will often freely penetrate the
rarefied bony tissue. It should be first rendered antiseptic by dipping
in strong carbolic acid.

From the first the general health fails, there is difficulty in
mastication, digestion is more or less impaired, nutrition is imperfect
and muscular flabbiness, weakness and wasting advance more or less
rapidly. In advanced cases emaciation is often a marked feature.

Examination of the urine gives valuable indications, though the results
obtained have been supposed to be contradictory. While rarefaction of
the bone is advancing rapidly the urine is charged with an excess of
phosphates in ratio with the activity of the morbid process. When on the
other hand the disease has come to a standstill and the process of
repair in the rarefied bones has begun, the absence of phosphates is no
less characteristic. A patient therefore may show greatly enlarged and
softened bones with persistent lameness, and yet the urine may show
little or no phosphate. The phosphaturia may, therefore, be made the
basis of a reasonable prognosis. Excess of phosphates indicates an
active pathological process, with an uncertain outcome, while the
absence of phosphates indicates an arrest of rarefaction and holds out
good hope of recovery.

I have long observed the same in cases of obstinate and intractable
spavins, splints, ringbones and other bone diseases. Phosphaturia
bespeaks a faulty nutrition of the bone and explains the failure of
remedial measures, while lack of phosphates in the urine, or a reduction
to the normal amount is likely to become a guarantee of improvement
under local treatment. The treatment however, must be first
constitutional to correct the condition of malnutrition and then local
to correct the osteitis.

_Prevention and treatment._ As in rachitis hygienic measures give the
most uniformly good results. The change of stable is especially demanded
from a cellar or basement stable, one with joists laid on the ground or
one with an earth floor saturated with urinary and feculent products. In
different cases an enzootic has been arrested, coincidently with the
removal of the stock to the floor above, and in others with the removal
of the filth saturated earth beneath a ground floor, and the laying of a
new floor with ample space beneath for the free circulation of air. In
the same line would be thorough drainage of the site and to carry off
liquid manure to a well ventilated receptacle. Exposure to cold and wet
is to be sedulously avoided as greatly favoring the onset of the
disease, and hurrying the milder cases into a fatal activity. Free air
and sunshine are all important and it is the universal experience that
city cases taken early and sent to dry, sunny pastures, mostly recover,
or at least undergo marked amelioration. The fact that certain cases
originate during an open air life does not invalidate this position but
merely shows that other pathogenic conditions may be too potent to be
overcome by this hygienic one.

A liberal allowance of sound grain is essential to success, even in the
case of patients sent to pasture. Those that have recovered or improved
at pasture, should be retained in the country and on no account returned
to the same city stables in which they contracted the disease. Even in
the country a different stable should be secured if possible.

Any food that has manifestly contributed to the disease, should be
withheld (bran, millet, musty or fermented food or that drawn from
particular fields).

Overwork must be forbidden, and indeed any work at all during the active
stage of the disease. The victim should also be withdrawn from breeding,
at least until it has fully recovered the normal consistency of its
bone.

In cases aggravated by cold or wet, or which show the rheumatic
propensity to shift from place to place, sodium salicylate in ounce
doses several times a day may appear to benefit, and as a germicide this
may be tried on all cases. Salicin, salol, or phenacetin may be used as
substitutes. Where the disease has been largely localized, blisters have
appeared to be beneficial.

Phosphates and phosphorus have been lauded by German veterinarians, but
in other hands, and when the morbid process was active they have proved
useless, or even hurtful. Bone dust or phosphate of lime or soda may be
freely used at any time and appears to act as a general tonic, beside
supplying lime and phosphoric acid which may possibly be availed of for
bone nutrition. Phosphorus and phosphorated oil in excess always softens
the bone and much more so when this process is already excessive. In
small doses (gr. ⅙ to ½) and after the process of rarefaction has
ceased, it is valuable in hastening bone consolidation and fitting the
patient to return to work.

Bitters, iron and other tonics are valuable in improving the general
tone and indirectly the bone nutrition.

Cary had prompt improvement in connection with intravenous injection of
barium chloride once a week for four weeks, and ½ oz. doses of sodium
salicylate thrice a day. It remains to be seen whether or not this is
generally applicable.

OSTEO-MALACIA IN OTHER ANIMALS.

The internal softening and rarefaction of bones in mature animals has
been noted in dogs by Pillvax and Röll, in lambs by Haubner, in pigs by
Haubner and Anaker, and in goats by different observers. The genuineness
of these cases has been questioned by Cadiot and Leclainche, by Virchow
and by others, but in the present uncertainty as to the dividing lines
between rarefaction, rachitis and other diseases, they deserve notice in
this connection.

In _dogs_ the lesions are mostly in the young and are largely rachitic,
yet the enormous swelling of the facial bones, and especially of the
superior maxillary in the comparatively mature animal suggests
osteo-malacia. As in rachitis there are usually impaired digestion,
unthriftiness, slow, stiff movements and lack of life and vigor.

In _goats_ Virchow believes the disease to be neither rachitic nor
osteo-malacia, basing his opinion on the lesions in the bones: “On the
maxillary bones of goats there are often found peculiar formations in
which the parts that have already assumed osseous structure, have failed
to fix the earthy salts. The tumor, which forms a circumscribed swelling
on the upper or lower maxillary bone, is soft and easily cut with the
scalpel, with at certain points only, a hard resistant material. It is a
simple osteoid chondroma, though veterinarians for some reason associate
it with rheumatism.” Profuse salivation is present.

In _lambs_ it is according to Haubner an atrophy with destructive
ulceration of the bones of the face, complicated by purulent
infiltration of the medullary spaces. “The incisors, and later the
molars, fall one by one, because of the changes in the alveoli, the gums
swell, become violet, red, and ulcerate, the ulcers extending through
the hard palate into the nose, and causing a highly offensive discharge
from both nose and mouth.

In _pigs_ the disease has been mainly seen in connection with
insufficient or unwholesome food, and badly balanced rations, and
especially with fermented swill and an exclusive maize diet. The
symptoms are shown in the limbs and face, especially (“snuffles”), as
noted under rachitis.

_Prevention and treatment_ are to be sought in avoidance of the obvious
causes, and in applying the same line of tonic treatment as in the
larger animals.

INDEX.

Abnormal conditions of the hair, 456.

Abrasions, 455.

Abscess behind eye, 350.
of brain, 125.
of spine, 175.

Acariasis, 460.

Acetone in urine, 198.
test for, 198.

Acne, 343.
in horse, 504.

Acromegaly, 133.

Acute eczema in dogs, 492, 495.
in solipeds, 475.
keratitis, 378.
myelitis, 154.

Adenoma of the gland of Harder, 357.

Akinesis, 2.

Albinism, 399.

Albumen in urine, 199.
test for, 199.

Alcoholic intoxication, 147.

Alimentary origin, eczema of, in cattle, 482.

Allantoin, 199.

Alopecia areata, 524.
congenita, 524.
postpartum, 526.

Alterations in glands and ducts, structural, 456.

Amaurosis, 442.

Amblyopia, 442.

Amyloid kidney, 246.

Anæsthesia, 9.

Analgesia, 10.

Anal sphincter, 21.

Aniline poisoning, 148.

Animal parasites, 456.

Ankyloblepharon, 337.

Anophthalmos, 446.

Aperture in iris, congenital, 399.

Aphthous conjunctivitis, 371.
fever, 460.

Apoplexy, 84.
cerebral, 84.
of spinal cord, 170.

Arteria hyaloidea, persistent, 436.

Arthritis, rheumatic, in horse, 536.
urica, 554.

Articular rheumatism in cattle, 542.
in the dog, 547.
in horse, 536.
in sheep, 545.
in swine, 545.

Artificial eye, 449.

Astragalus Mollissimus, 135.

Ataxia, 5, 165.

Atheroma, 425.

Atresia of lachrymal puncta, 351.

Atrophy, 442.
degenerative, of nerves, 6.
of ovary, 280.
of the eyeball, 446.
of nerves, 189.

Bacillus diphtheriæ avium, 372.

Bacteria in encephalitis, 97.

Baldness, congenital, 524.

Balking, 26.
jurisprudence of, 28.
treatment of, 30.

Bed sores, 520.

Black cataract, 396.

Bladder, anomalies of, 261.
atony of, 258.
eversion of, 260.
hernia of, 261.
parasites, 259.
rupture of, 260.
spasm of neck of, 259.
tumors of, 259.

Big head, 579.

Bile in urine, 200.

Birds, gout in, 554.

Blebs, 454.

Blennorrhœa, 366.

Blepharadenitis, 343.

Blepharitis, 340.

Blepharophymosis, 339.

Blepharospasm, 337.

Blind staggers, 69.

Blisters, 454.

Bloody sweat, 518.

Boil, 454, 522.

Brain, abscess of, 125.
concussion of, 80.
congestion of, 90.
cortical lesions of, 13.
disease, 572.

Brain, pressure on, 13.
tumors of, 128.

Bright’s disease, acute, 220.

Bronchocele, 560.

Buckwheat erythema, 470.

Bulbar paralysis, 134.

Bullæ, 454.
in horse, ox, pig and dog, 507.

Buphthalmos congenitus, Hydrophthalmos or, 427.

Burns, 460.

Cachexia ossifraga, 573.

Calculus of prostate, 278.
renal, 247.

Callositas, 455.

Callosities, necrotic, 455.

Calorica, dermatitis, 473.

Caloricum, erythema, 468.

Calving fever, 299.

Cancer of prostate, 278.

Canker, 515.

Canthoplasty, 337.

Capsule of lens, opacity of, 428.

Carbon disulphide poisoning, 150.

Carbuncle, 454.

Carbunculus, 454.

Cardiac accelerating centre, 21.
inhibition, 15.

Carpus, chronic eczema of, 480.

Caruncle, lachyrmal, diseases of the, 356

Casts, composition of urinary, 201.
in urine. 201.

Catalepsy, 36.

Cataract, 393, 428.
anterior capsular, 428, 429.
anterior polar, 428.
black, 396, 428.
blood pigment on capsule, 429.
capsular, 428.
cortical, 428.
diabetic, 428.
discission, 433.
immature or unripe, 428.
lenticular, 428.
mature or ripe, 428.
nuclear, 428.
polar, 428.
posterior capsular, 428.
posterior polar, 428.
ripe, mature or, 428.
senile, 428, 429.
soft, in the young, 433.
suction of lens, 435.
traumatic, 428.
unripe, immature or, 428.

Catarrhal conjunctivitis, simple acute, 360.

Catarrh of the urethra, 262.

Catheterization, 264.
of bitch, 267.
of bull, 266.
of cow, 267.
of dog, 266.
of horse, 264.
of mare, 266.
of ram, 266.

Cattle, alimentary eczema of, 482.
chronic eczema in, 488.
moist eczema of the tail, neck, chine and dewlap, 487.

Central canal of the spinal cord, dilatation of, 178.

Centre for dilating pupil, 21.

Cerebellar disease, 133.

Cerebellum, 17.

Cerebral cortex, lesions of, 13.
hæmorrhage, 84.
hyperæmia, 90.

Cerebro-spinal lesions in rheumatism, 536.
meningitis, 118.

Cervical lateral columns, transverse section of, 21.

Cervix vesicæ, imperforate, 261.

Chafing, 460.
intertrigo of, 466.

Chalazion, 344.

Chapped heels in horse, 508.

Chaps, 455.

Chloroform, action on dog, 23.

Choked disc, 440.

Cholesteatomata, 129.

Cholesteatoma of spine, 175.

Chondroma of spine, 176.

Chorea, 63.

Choroid, detachment of the, 403.
rupture of the, 403.
tumor of, 403.

Choroiditis, 402.
suppurative form, 403.

Chronic eczema of the back in dog, 497.
keratitis, 382.

Cicatrices, 455.

Coloboma iridis, 399.
palpebrarum, 336.

Compression of spinal cord, 175.

Concussion of the brain, 80.

Congenital aperture in iris, 399.
hydrophthalmos or buphthalmos, 427.

Conical cornea, 388.

Conjunctiva, burns of, 360.
dermoid tumor of the, 375.
lipoma of, 375.

Conjunctiva, melanosis of, 375.
neoplasms of the, 375.
polypus of, 375.
wounds of, 359.

Conjunctival sac, foreign bodies in the, 358.

Conjunctivitis, aphthous, 371.
catarrhal, simple acute, 360.
chronic, 364.
diphtheritic, in birds, 371.
follicular, 374.
in herbivora, infectious, 368.
phlyctenular, 371.
purulent, 366.
variolous, 370.

Constitutional diseases, 528.
vice, maladies due to a, 460.

Contagious pustular dermatitis, 504.

Convulsions, 61.

Convulsive twitching, 66.

Cornea, conical, 388.

Corneæ, ectasia, 388.
xerosis (epithelialis), 376.

Cornea, foreign bodies in, 378.
inflammation of the, 378.
opacity of, 384.
pigment spots on, 384.
tumors of the, 388.
ulcer of, 385.
wounds of the, 377.

Corneal staphyloma, 387.

Cornu cutaneum, 455.

Corpora nigra, cysts of, 323.
quadrigemini, 16.

Corpus striatum, 17.

Cortical localization, 17.

Cotton seed, poisoning with, 381.

Cracks, 455.

Cracked heels in horse, 508.

Creatinin in urine, 198.
test for, 198.

Crevasses, 455.

Cripple, 573.

Crossed hemiplegia, 3.

Crura cerebra, 16.

Crustæ, 454.

Crusts, 454.

Cryptogams in encephalitis, 97.

Cutaneous eruptions in sheep, 490.
hæmorrhage, 518.
hypertrophy, 521.

Cutaneum, cornu, 455.

Cyanuric acid, 199.

Cyclitis, 393, 400.

Cystic ovary, 287.

Cystitis acute catarrhal, 253.
acute croupous, 255.
chronic catarrhal, 256.
Cystitis, in dog, 257.
in ox, 257.

Cysts of the iris and corpora nigra, 401.

Dacryo-adenitis, 351.

Dacryo-cystitis, 353.

Dandruff, 454.

Degeneration, Waller’s law of, 7.

Delirium, 30.

Dermatitis, 460, 472.
calorica, 473.
contagious pustular, 504.
erythematous, 465.from mechanical injury, 472.
medicamentosa, 473.
traumatica, 472.
Venenata, 473.

Dermatomata, 455.

Dermatosis, microbian, 460.
parasitic, 460.

Dermoid cysts of ovary, 291.
tumor of the conjunctiva, 375.

Detachment of the choroid, 403.
of the retina, 439.

Diagnosis of skin diseases, 458.

Diphtheritic conjunctivitis in birds, 371.

Diplococcus (streptococcus) pneumoniæ equina, 397.

Disc, choked, 440.

Diseases of the nervous system, 1.
of the skin, 453.
urinary organs, 190.
skin, diagnosis of, 458.
skin, general causes of, 456.

Disease, white skin, 470.

Dislocation of the globe of the eye, 447.
of the lens, 435.

Dog, acute eczema of the, 492.
chronic eczema in the, 496.
myelitis in, 161.

Dogs, acute eczemas in, 495.

Double pupil, 399.

Dropsy of cerebral ventricles, 110.
of eyelids, 341.

Dry keratitis, 376.

Ducts and glands, structural alterations of skin, 456.

Dyskinesis, 5.

Earthy phosphates, test for, 197.

Eclampsia, 61.
of nursing bitches, 62.

Ectasia (bulging) of the sclera, 389.
corneæ, 388.

Ectropion, 346.

Eczema, 474.
acute general, 495.
acute, in solipeds, 475.
acute, of the dog, 492.
caudal, 495.
chronic, in cattle, 488.
chronic, in the dog, 496.
chronic, of the carpus and tarsus, 480.
chronic, of the head in solipeds, 476.
impetiginous, 495.
interdigital, 495.
in sheep, 489.
in swine, 490.
of alimentary origin in cattle, 482.
of elbow and hock in dog, 497.
of head, ears, etc., 497.
of the back in dog, 497.
malt, 482.
moist, chronic, at the mane and tail, 477.
moist, of the pasterns in the ox, 486.
moist, of the tail, neck, chine and dewlap of cattle, 487.
potato, 482.
rubrum, 493.
acute, in dogs, 495.

Egg impaction in oviduct, 293.

Electric shock, 80.

Elephantiasis, 521.
pachydermia, 456.

Embolism of spinal cord, 168.

Emphysema of eyelids, 342.

Encanthis, 356.

Encephalic congestion, 90.
lesions, 13.

Encephalitis calorica, 98.
from bacterial products, 97.
from cryptogams, 97.
from exertion, 98.
from lead, 99.
from narcotics, 96.
from parasites, 99.
from poisons, 99.
from travel, 98.
from tumors, 99.
treatment of, 107.

Encephaloid of spine, 176.

Encephalon, pressure on, 13.

Endocarditis in rheumatism, 534.

Entropion, 345.

Epilepsy, 47.
jurisprudence of, 57.
partial, 48.
treatment of, 58.

Episcleritis, 389.

Epispadias, 262.

Epithelial xerosis, 376.

Erosions, 455.

Eruptions, cutaneous, in sheep, 490.
distillery waste, 460.
granular skin, in swine, 492.
of nervous origin, 7.

Erythema, 453, 465.
buckwheat, 470.
caloricum, 468.
from irritants, 471.
solar, 468.

Erythematous dermatitis, 465.

Essential oils, action on dog, 23.

Ewes, neurasthenia in pregnant, 179.

Excrescences, 455.

Exophthalmic goitre, 564.

Exophthalmos, 338, 426.

Extraction, linear, of the lens, 434.

Eye, artificial, 449.
defects, blemishes, etc., 318.
diseases of, 316.
desirable features of, 316.
dislocation of the globe of, 447.

Eyeball, atrophy of, 446.

Eyelash turned in, 344.

Eyelids adherent to bulb, 339.
deficiency of, 336.
dropsy of, 341.
emphysema of, 342.
inability to close, 338.
inflammation of, 340.
narrow opening between, 337.
organic union of, 337.
seborrhœa of, 343.
tumors of, 348.
wounds of, 333.

Eyelid, tubercle of, 344.
turned in, 345.
turned out, 346.

Eye, systematic inspection of, 320.

Face, convulsive twitching of, 66.

Fagopyrism, 470.

Falling sickness, 47.

Fallopian tubes, inflammation of, 292.

Fatty degeneration of the kidney, 244.

Female generative organs, diseases of, 279.

Filaria hæmorrhagica, 518.

Fish-skin disease, 522.

Fissures, 455.

Fistula of lachrymal sac, 352.
recto-vesical, 261.

Follicular conjunctivitis, 374.

Foreign bodies in the conjunctival sac, 358.
in the cornea, 378.
in the iris, 398.

Fracture of the orbit, 348.

Fragilitas ossium, 573.

Furuncle, 454.

Furunculus, 454, 522.

Gadfly, panic from, 24.

Gangrene, cutaneous, 520.

Generative organs, diseases of female, 279.

Genital centre, 21.

Giantism, 133.

Glands and ducts, structural alterations in skin, 456.

Glaucoma. 422.
acute inflammatory, 424.
secondary, 424.
simple, 424.

Glioma of spine, 176.

Globe of the eye, dislocation of, 447.

Glomerulitis, 225.

Glucose in parturition fever, 308.
in urine, 200.
test for, 200.

Glycogenic centre, spinal, 21.

Glycosuria, 200.

Goitre, 560.
congenital, 561.
cystic, 562.
exophthalmic, 564.
fibrous, 562.
hypertrophic, 562.
its distribution, 561.
varicose, 562.

Goll, column of, 21.

Gout, 554.

Granular skin eruption in swine, 492.

Grapes, 515.

Grease, 512.

Growth, horny, 455.

Hair, abnormal conditions of, 456.
nodular swelling of, 526.
splitting of, 526.

Hallucinations, 11, 22.

Harder, gland of, adenoma of the, 357.

Hare-eye, 338.

Hæmatidrosis, 518.

Hæmatopedesis, 518.

Hæmatorrachis, 170.

Hæmaturia, 200, 204.
prevention of, 208.
treatment of, 208.

Hæmoglobinuria, 200.

Hæmophilia, 518.

Hæmorrhage, cutaneous, 518.
into spinal cord, 170.
on ovary, 282.
retinal, 439.

Hippuric acid, 197.

Hippuric acid, test for, 198.

Head, convulsive movements of, 67.

Health, nervous control in, 1.

Heart lesions in rheumatism, 534.

Heat exhaustion, 39.
treatment of, 40.
papules, 499.

Hemianæsthesia, 3.

Hemiplegia, 3.

Hemispasm, 4.

Hernia of ovaries, 279.

Hordeolum, 343.

Horny growth, 455.

Horsepox, 515

Hyaloidea, persistent arteria, 436.

Hydrocephalus, chronic, 110.
jurisprudence of, 116.
treatment of, 116.

Hydro-metra, 296.

Hydronephrosis, 248.

Hydrophthalmos or buphthalmos congenitus, 427.

Hymen, imperforate, 298.

Hyperæsthesia, 8.
cutaneous, 8.
muscular, 8.
to cold, 8.
visceral, 9.

Hyperalgesia, 10.

Hyperkinesis, 4.

Hyperplasiæ, 455.

Hyperplasia of the skin, 523.

Hypertrophy, cutaneous, 521.
of the prostate, 274.

Hypospadias, 262.

Hypoxanthin, 199.

Ichthyosis, 522.

Immobility, 110.

Impetigo, 477.
digital, 512.
of pigs, 491.

Incoördination, 5.
in cerebellar disease, 133.

Indican in urine, 197.
test for, 197.

Infection in osteo-malacia, 575.
in osteoporosis, 581.

Inferior columns, transverse section of, 20.

Inflammation of the cornea, 378.
of the optic nerve, 440.
of the sclera, 389.

Inhibition, cardiac, 15.
respiratory, 15.

Insolation, 39.

Internal ophthalmia, 390.

Intertrigo, 466.
of chafing, 466.

Iridis, coloboma, 399.

Iris, congenital aperture in, 399.
cysts of the, 401.
foreign bodies in the, 398.
prolapse of the, 390.
tuberculosis of, 401.

Iritis, simple, 395.
symptomatic or metastatic, 397.

Irritants, animal, 460.
erythema from, 471.
external, maladies from, 460.
ingested, maladies due to, 460.
vegetable, 460.

Irruption, vesicular in pigs, 491.

Itching, 9.

Keracele, 455.

Keratitis, acute, 378.
chronic, 382.
dry, 376.

Keratoconus, 388.

Keratoglobus, 388.

Kidney, acute congestion of, in carnivora, 218.
in cattle, 214.
in horse, 209.
in sheep and goat, 216.
in swine, 217.
treatment, 213.
amyloid, 246.
atrophy of, 241.
fatty degeneration of, 244.
hypertrophy of, 240.
lardaceous, 246.
waxy, 246.

Lachrymal caruncle, disease of, 356.
tumors of, 356.
gland, disease of, 351.
puncta, obstruction of, 351.
sac, catarrh of, 353.
fistula of, 352.

Lachrymo-nasal duct, stenosis of, 355.

Lactic acid in rickets, 568.

Lagophthalmos, 338.

Limbs, disorderly movements of, 69.

Lead poisoning, 141.

Lens, dislocation of the, 435.
linear extraction of the, 434.
opacity of the, 428.

Leucin in urine, 199.
test for, 199.

Leucoma, 384.

Leucorrhœa, 298.

Lichen, 499.

Lightning stroke, 82.

Linear extraction of the lens, 434.

Lipoma of spine, 176.

Lips, flapping of, 68.

Localization in ass’s brain, 17.
in dog’s brain, 18.
of nervous lesions, 12.
of nervous troubles, 17.

“Loco” poisoning, 135.

Luxatio bulbi, 447.

Macula, 384.

Maculæ, 453.

Maladies, skin, due to a constitutional vice, 460.
due to ingested irritants, 460.
due to toxic products of the system, 460.
from external irritants, 460.

Malanders, 480

Mange, red, 493.

Medulla, disease of, 134.

Megrims, 69.

Meibomian glands, disease of, 343.

Melanoma of the brain, 130.
of spine, 175.

Mellituria, 200.

Membrana nictitans, hypertrophy of, 357.
lesions of, 357.
tumors of, 357.

Membrane, persistent pupillary, 400.

Meningitis, cerebro spinal, 118.
tubercular, 127.

Meningo-encephalic congestion, 90.

Meningo-encephalitis, 94.

Meningo-myelitis in the dog, 161.

Metastatic iritis, symptomatic or, 397.

Microbes in nervous disease, 2.
in parturition fever, 304.
in udder, 305.

Microbian dermatosis, 460.

Microphthalmos, 446.

Milk fever, 299.
poisonous in nervous disorder, 8.

Millet disease, 582.

Modified secretions of skin, 456.

Moist eczema, chronic at the mane and tail, 477.
of the pasterns in the ox, 486.

Monoplegia, 3.
cerebral, 4.

Monospasm, 4.

Moonblindness, 404.

Motor disorders, 2.
tracts in brain, 14.

Muscular balance, lack of, 450.
rheumatism in cattle, 544.
rheumatism in the dog, 548.
rheumatism in horse, 540.
sense tract, 21.

Musty fodder in encephalitis, 97.

Mydriatics, 331.

Myelitis, 154.
chronic, 165.
in the dog, 161.

Myosin coagulated under heat, 41.

Myxoma of the brain, 131.

Nebula, 384.

Necrotic callosities, 455.

Neoplasms of brain, 128.
of the conjunctiva, 375.

Nephritis, 219.
acute, 220.
chronic, 234.
interstitial, 225.
purulent, 228.
suppurative, 225.
treatment, 225.
tubular, 225.

Nerve, optic, inflammation of the, 440.
optic, paralysis of the, 442.

Nerves, atrophy of, 189.

Nerve trunk, pressure on, 9.

Nervous centres, respiratory, 14.
disease, diagnosis of, 2.
disease, microbes in, 2.
disease, symptoms of, 2.
disorders, diagnosis of, 12.
functional, 13.
structural, 12.
lesions, destructive, 12.
organs, irritation of, 12.
system, diseases of, 1.

Neuralgia, 184.
of ovary, 281.

Neurasthenia in pregnant ewes, 179.

Neuritis, 181.
ascendens, 441.
descendens, 441.
optic, retro-bulbar, 441.

Neurosis, 456.

Nictitans, membrana, lesions, 357.

Nigra, corpora, cysts of, 401.

Nitro-benzol poisoning, 149.

Nodules, 453.

Nose, rhythmic movements of, 68.

Nystagmus, 452.

Oblique focal illumination of the eye, 324.

Occluded pupil, 400.

Oöphoritis, 284.

Opacity of the cornea, 384.
of the lens or its capsule, 428.
of the vitreous, 437.

Ophthalmia, enzootic, 368.
internal, 390.
periodic, 404.
of solipeds, recurrent, 404.

Ophthalmoscope, 328.

Optic nerve, inflammation of the, 440.
paralysis of, 442.

Optic neuritis, retro-bulbar, 441.

Optic thalamus, 17.

Orbit, fracture of, 348.
periostitis of, 350.
tumors of, 350.
wounds of, 349.

Oscillatory movement of the eye, 452.

Osteomalacia, 573.
in pigs, dogs, goats and lambs, 489.
of the horse, 579.

Osteoporosis, 579.
treatment of, 587.

Ovarian cysts, 287.
tumors, 292.

Ovaries, absent, 280.
atrophy of, 280.
hernia of, 279.
supernumerary, 281.
undeveloped, 280.

Ovary and womb, malposition of, 279.
dermoid cysts of, 291.
hæmorrhage on, 282.
inflammation of, 284.
irritable, 281.

Oviduct, diseases of, 293.
egg impaction in, 293.
eversion of, 293.
imperforate, 293.
inflammation of, 295.
polypus of, 293.

Oxalic acid in rickets, 568.
in urine, 198.
test for, 198.

Ox, moist eczema of the pasterns, 486.

Oxytropis Lamberti, 135.

Pachydermia, 521.
elephantiasis, 456.

Pain, insensibility to, 10.

Palpebral fissure, widened, 338.

Panic, 23.
treatment, 24.

Panophthalmitis, 390, 403, 421.
enucleation, 422.

Papilloma of spine, 176.

Papulæ, papules, 453.

Paræsthesia, 9.

Paralysis, 2, 175.
local, 4.
of ocular muscles, 450.
of the optic nerve, 442.
sensory, 9.

Paraplegia, 3.

Parturient apoplexy, 299.

Parturition collapse, 299.
fever, 299.

Parturition fever, prevention, 311.
fever, treatment, 313.
paresis, 299.

Parasites, animal, 456.
of the bladder, 259.
of the kidney, 248.
vegetable, 456.

Parasitic dermatosis, 460.

Paresis, 2.

Pasterns, moist eczema of, in the ox, 486.

Pemphigus, 507.

Pericarditis in rheumatism, 535.

Perinephritis, 230.

Perineuritis, 181.

Periodic ophthalmia, 404.

Perioöphoritis, 284.

Periostitis of orbit, 350.

Persistent arteria hyaloidea, 436.
pupillary membrane, 400.

Perspiratory centre, 16.

Phenol in urine, 198.
test for, 198.

Phlyctenæ, 454.

Phlyctenular conjunctivitis, 371.

Phosphates in rickets, 568.
in urine, 196.
in urine in osteoporosis, 587.

Phosphorus in rickets, 567.

Phymata, 455.

Phthiriasis, 460.

Phthisis bulbi, 446.

Physical properties of urine, 192.

Pigs, impetigo of, 491.
vesicular irruption in, 490.

Pilous cysts of ovary, 291.

Pimples, 453.

Pinguecula, 375.

Pitchy affection, 491.

Pituitary body, hypertrophy of, 133.

Pityriasis in dog and cat, 503.
in cattle, 503.
in horse, 501.

Pleuritic lesions in rheumatism, 535.

Plumbism, 141.

Podagra, 544.

Poisoning by aniline, 148.
by carbon disulphide, 150.
with cotton seed or cotton seed meal, 381.
by lead, 141.
by “loco”, 135.
by nitro-benzol, 149.

Poliomyelitis, 154.

Polypi of oviduct, 293.

Polyuria, of nervous origin, 8.

Pons, 16.

Prickly heat, 499.

Prolapse of the iris, 390.

Prostate, abscess of, 269.
cancer of, 278.
cysts of, 278.
hyperæmia of, 267.
hypertrophy of, 274.
tuberculosis of, 277.

Prostatic calculus, 278.

Prostatitis, acute, 267.
chronic, 271.
follicular, 268.
interstitial, 269.

Pruritus, 9.

Psammomata of the brain, 131.

Pseudo-paralysis, 4.

Psychic peculiarities, 10.
symptoms, 10.

Pterygium, 376.

Ptosis, 337, 340.

Pupil dilatation, 21.
double, 399.
occluded, 400.

Pupillary membrane, persistent, 400.

Purkinje-Sanson images, 327.

Pus in urine, 201.

Pustulæ, pustules, 454, 474.

Pustular dermatitis, contagious, 504.

Pyelitis, 231.

Pyelonephritis, 231.

Pyometra, 296.

Quittor, 515.

Rachitis, 565.
from bran, 572.

Rain rot, 489.

Rarefaction of bone, 579.

Rarefying osteitis, 579.

Rash, 453.

Recto-vesical fistula, 261.

Recurrent ophthalmia, jurisprudence, 420.
microbiology, 410.
of solipeds, 404.

Red mange, 493.

Reflex action, 5.
increased, 6.
morbid, 5.
tonic spasm, 6.

Renal calculus, 247.
parasites, 248.
pelvis, inflammation of, 231.
tumors, 248.

Respiratory tract, 21.
inhibition, 15.
nerve centers, 14.

Restiveness, 26.

Retina, detachment of the, 439.

Retinal hemorrhage, 439.

Retina, tumors of, 439.

Retinitis, 438.

Retro-bulbar abscess, 350.
optic neuritis, 441.

Rheumatism, 528.
articular in cattle, 542.
in the dog, 547.
in horse, 536.
in sheep, 545.
in swine, 545.
blood changes in, 534.
cerebro-spinal lesions in, 536.
chronic articular, in horse, 540.
heart lesions in, 534.
infection, theory of, 532.
lactic acid, theory of, 530.
muscular, in cattle, 544.
muscular, in dog, 548.
muscular, in the horse, 541.
neuropathic theory of, 531.
nodosities in, 538.
prevention and treatment of, 549.
theory of chill, 529.

Rickets, 565.
basement, stables in, 569.
confinement in, 569.
damp soils in, 569.
food experiments, 567.
infection in, 569.
lactic acid in, 568.
on poor soils, 567.
treatment of, 570.

Rimæ, 455.

Rocking hind quarters, 69.

Rodent eczema, 497.

Rouget, 460.

Rubrum, eczema, 493.

Rupture of the choroid, 403.

Sallenders, 480.

Salpingitis, 292.

Sarcoma of spine, 176.

Scabs, 454.

Scales, 454.

Scars, 455.

Sclera, ectasia (bulging) of the, 389.
inflammation of the, 389.
wounds of the, 389.

Scleroderma, 456.

Sclerosis, 5.
of spinal cord, 165.

Scorbutus, 557.

Scratches, 508.

Scurvy, 557.

Seborrhœa, 491.
of digital region, 512.

Secretions, modifications of, 7.
modified, skin, 456.

Sensory and motor tracts in brain, 14.
symptoms, 8.

Sheep, cutaneous eruptions in, 490.
eczema in, 489.

Shorts disease, 572.

Simple iritis, 395.

Sitfasts, 455.

Skin, discolorations of, 453.
diseases, diagnosis of, 458.
external causes of, 456.
internal causes of, 457.
general causes of, 456.
diseases of the, 453.
treatment of, general principles of, 461.
disease, white, 470.
gangrene of, 520.
hyperplasia of, 523.
hypertrophy, 521.
spots of, 453.
ulceration of, 520.

Softening of the brain, 84.

Solar erythema, 468.

Spasm, 4.
centre, 15.
clonic, 4.
of eyeballs, 4.
of sphincter vesicæ, 259.
paraplegic, 4.
tetanic, 4.
tonic, 4.

Spasms, 61.
general, 4.
local, 4.

Sphincter ani, centre, 21.
vesicæ, centre, 21.

Spina bifida, 171.

Spinal arteritis, 168.
caries, 172.
cord, congestion of, 153.
cord, cross hemi-section, 20.
cord, inflammation of, 154.
cord, lesions and phenomena, 22.
cord, longitudinal vertical section, 20.
hæmorrhage, 170.
hemiplegia, 3.
hyperæmia, 153.
lesions, 14.
lesions, localizations in, 20.
meningitis, 118, 160.
sclerosis, 165.

Spine, slow compression of, 175.

Squama, 454.

Squamæ in horse, 501.

Squinting, 450.

Squint, spasmodic or spastic, 451.

Staggering, 5.

Staggers, 69.
cerebral, 94.

Stalk disease, 482.

Stampede, 23.

Staphyloma, corneal, 387.

Starvation mange, 482.

Static refraction, 330.

Steatosis of the kidney, 244.

Stenosis of lachrymo-nasal duct, 355.

Stiffness, 573.

Strabismus, 450.

Streptococcic dermatitis, 512.

Streptococcus pneumoniæ equina, 397.

Stricture of the urethra, 264.

Structural alterations in glands and ducts, 456.

St. Vitus dance, 63.

Stye, 343.

Sun-stroke, 39.

Superior columns, 21.
transverse section of, 20.

Swine, eczema in, 490.
granular eruption in, 492.

Symblepharon, 339.

Symptomatic or metastatic iritis, 397.

Synechia, anterior, 392.
posterior, 392.

Syringomyelia, 178.

Tarsus, chronic eczema of, 480.

Tenderness, 10.

Tetany, 151.

Thalamus, 17.

Thermic fever, 39.
treatment of, 46.

Thrombosis of spinal cord, 168.

Thyroid enlargement, 560.

Timidity, 23.

Titubation, 5.

Tongue, abnormal movements of, 68.

Tonic spasm, 4.

Torpor, 11.

Toxic products of the system, maladies due to, 460.

Toxins in nervous disease, 2.

Traumas, 460.

Traumatica, dermatitis, 472.

Trembling, 4.

Tremor, 4.

Trichiasis, 344.

Trichorrhexis nodosa, 526.

Trophic spinal tract, 21.
symptoms, 6.

Tubercle of eyelid, 344.
of prostate, 277.
of womb, 298.

Tuberculæ, 453.

Tubercular disease of spine, 172.
meningitis, 127.

Tuberculosis of the iris, 401.

Tumor, dermoid of the conjunctiva, 375.

Tumors of eyelids, 348.
of kidney, 248.
of orbit, 350.
of ovary, 292.
of the brain, 128.
of the cornea, 388.
of the lachrymal caruncle, 356.
of the retina, 439.
of the vagina, 299.

Tyrosin in the urine, 199.
test for, 199.

Ulcer, 455.
of the cornea, 385.

Ulceration of the skin, 520.

Ulcerations of nervous origin, 7.

Urachus, persistent, 261.

Urea, 197.
test for, 197.

Ureteritis, 252.

Urethral anomalies, 261.

Urethra, foreign bodies in, 264.
imperforate, 261.
injuries of, 249.
stricture of, 264.
wounds of, 262.

Urethritis, acute catarrhal, 262.

Uric acid, 197.
test for, 197.

Urinary calculus, 247.

Urinary disease, general symptoms of, 202.

Urinary organs, diseases of, 190.

Urinary secretion, 190.
nervous control of, 191.

Urine, acetone in, 198.
albumen in, 199.
bile in, 200.
blood in, 200.
casts in, 201.
chemical changes in morbid, 196.
chemical reaction of, 196.
color of morbid, 193.
consistency, 195.
creatinin in, 198.
epithelium in, 200.
glucose in, 200.
indican in, 197.
odor of morbid, 195.
opacity of morbid, 195.
oxalic acid in, 198.
pathological, 193.
phenol in, 198.
phosphates in, 196.
physical properties, 192.
purulent, 224.
pus in, 201.

Urine, sodium chloride in, 196.
specific gravity of, 195.
translucency, 194.
viscid, 195.

Urticaria, 460.

Uterine tubercle, 298.
tumors, 297.

Vagina, tumors of, 299.

Vaginitis, 298.

Variola, 460.

Variolous conjunctivitis, 370.

Vaso-motor nervous centre, 15.
spinal centre, 21.
tract, 21.

Vegetable parasites, 456.

Venenata, dermatitis, 473.

Vertigo, 69.
aural, 72.
cardiac, 71.
cerebral, 74.
embolic, 71.
essential, 75.
from venous obstruction, 71.
gastric, 71.
nasal, 75.
optic, 72.

Vertigo, pulmonary, 71.
toxic, 75.
treatment, 78.

Vesical parasites, 259.

Vesiculæ, 454.

Vesicular irruption in pigs, 491.

Vetch, action on dog, 23.

Vice, 11, 33.
constitutional, maladies due to a, 460.
jurisprudence of, 34.
treatment of, 35.

Violence, 11.

Vitreous, opacity of the, 437.

Watch eye, 399.

Weaving, 68.

White face and foot disease in horses, 468.

White skin disease, 470.

Womb, dropsy of, 296.
pus in, 296.
tumors in, 297.

Wounds of the cornea, 377.
of the sclera, 389.

Xanthin, 199.

Xerosis corneæ (epithelialis), 376.

------------------------------------------------------------------------

TRANSCRIBER’S NOTES

1. Added table of Contents.
2. Silently corrected obvious typographical errors and variations in
spelling.
3. Retained archaic, non-standard, and uncertain spellings as printed.
4. Re-indexed footnotes using numbers.
5. Enclosed italics font in _underscores_.
6. Enclosed bold or blackletter font in =equals=.
7. Denoted superscripts by a caret before a single superscript
character or a series of superscripted characters enclosed in
curly braces, e.g. M^r. or M^{ister}.
8. Denoted subscripts by an underscore before a series of subscripted
characters enclosed in curly braces, e.g. H_{2}O.

*** End of this LibraryBlog Digital Book "Text book of veterinary medicine, Volume 3 (of 5)" ***

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