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Title: The Animal Parasites of Man
Author: Theobald, F. V., Stephens, J. W. W., Fantham, H. B.
Language: English
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  H. B. FANTHAM, M.A.Cantab., D.Sc.Lond.

  _Lecturer on Parasitology, Liverpool School of Tropical Medicine_;
  _Sectional Editor in Protozoology,
  “Tropical Diseases Bulletin,” London_, _etc._

  J. W. W. STEPHENS, M.D.Cantab., D.P.H.

  _Sir Alfred Jones Professor of Tropical Medicine, Liverpool
  University, etc._


  F. V. THEOBALD, M.A.Cantab., F.E.S., Hon. F.R.H.S.

  _Professor of Agricultural Zoology, London University_; _Vice-
  Principal and Zoologist of the South-eastern Agricultural College_;
  _Mary Kingsley Medallist_; _Grande Médaille Geoffroy St. Hilaire_,
  _Soc. Nat. d’Acclim. de France_, _etc._


  Dr. MAX BRAUN’S “Die Tierischen Parasiten des Menschen” (4th Edition,
  1908) and an Appendix by Dr. OTTO SEIFERT.



The English edition of Braun’s “Die Tierischen Parasiten des Menschen,”
produced in 1906, being out of print, the publishers decided to issue
another edition based on the translation of Braun’s fourth German
edition, which appeared in 1908, to which had been added an appendix,
by Dr. Otto Seifert on Treatment, etc.

When the work was considered with a view to a new edition, it was found
that a vast amount of new matter had to be incorporated, numerous
alterations essential for bringing it up to date were necessitated,
and many omissions were inevitable. The result is that parts of the
book have been rewritten, and, apart from early historical references,
the work of Braun has disappeared. This is more particularly the case
with the Protozoa section of the present work. The numerous additions,
due to the great output of scientific literature and other delays in
publication, have led to the book being somewhat less homogeneous
than we desired, and have necessitated the use of appendices to allow
of the presentation of new facts only recently ascertained. Many new
illustrations have been added or substituted for older, less detailed
ones. Some of these new figures were drawn specially for this book.

The first section, on the Protozoa, has been written by Dr.
Fantham, there being little of the original text left except parts
of the historical portions, and thus the section on Protozoa must
be considered as new. The second section, on Worms (except the
Acanthocephala, Gordiidæ and Hirudinea), has been remodelled by
Professor Stephens to such an extent that this, too, must not be looked
upon as a translation of Braun’s book. With regard to the Arthropoda,
much remains as in the last English edition, but some new matter added
by Braun in his fourth German edition is included, and much new matter
by Mr. Theobald has been incorporated. As regards the Appendix by Dr.
Seifert, the first section has been remodelled, but the sections on
the Helminthes and the Arthropoda are practically translations of the

The authors desire to express their thanks to Miss A. Porter, D.Sc.,
J. P. Sharples, Esq., B.A., M.R.C.S., and H. F. Carter, Esq., F.E.S.,
for valuable help. They also wish to thank the authors, editors,
and publishers of several manuals and journals for their courtesy
in allowing the reproduction of certain of their illustrations. In
this connection mention must be made more particularly of Professor
Castellani, Dr. Chalmers, Professor Doflein, Dr. Leiper, the late
Professor Minchin, Professor Nuttall, Dr. Wenyon, Mr. Edw. Arnold,
Messrs. Baillière, Tindall and Cox, Messrs. Black, Messrs. Cassell,
Dr. Gustav Fischer, Messrs. Heinemann, the Cambridge University Press,
the Editors of the _Annals of Tropical Medicine and Parasitology_, the
Editors of the _Journal of Experimental Medicine_, and the Editor of
the _Tropical Diseases Bulletin_.

  H. B. F.
  J. W. W. S.
  F. V. T.

_December, 1915._



  PREFACE                                                             iii

  ERRATA                                                            xxxii

  ON PARASITES IN GENERAL                                               1
    Occasional and Permanent Parasitism                                 1
    Entozoa, Endoparasites, Helminthes, Turbellaria                     2
    Hermaphroditism                                                     4
    Fertility of Parasites                                              5
    Transmigrations                                                     5
    Commensals, Mutualists                                              6
    Incidental and Pseudo-parasites                                     6
    The Influence of Parasites on the Host                              8
    Origin of Parasites                                                10
    Derivation of Parasites                                            19
    Change of Host                                                     20
    Literature                                                         22

  THE ANIMAL PARASITES OF MAN                                          25
  *A. Protozoa*                                                        25


      Class I. SARCODINA                                               27
        Order. _Amœbina_                                               27
               _Foraminifera_                                          27
               _Heliozoa_                                              27
               _Radiolaria_                                            28
      Class II. MASTIGOPHORA                                           28
           III. SPOROZOA                                               28
      Sub-class 1. TELOSPORIDIA                                        28
        Order. _Gregarinida_                                           28
               _Coccidiidea_                                           28
               _Hæmosporidia_                                          28
      Sub-class 2. NEOSPORIDIA                                         28
        Order. _Myxosporidia_                                          28
               _Microsporidia_                                         28
               _Sarcosporidia_                                         28
               _Haplosporidia_                                         29
      Class IV. INFUSORIA                                              29
             V. SUCTORIA                                               29

  Class I. SARCODINA, Bütschli, 1882                                   29
    Order. _Amœbina_, Ehrenberg                                        29
      A. Human Intestinal Amœbæ                                        29
          _Entamœba coli_, Lösch, 1875, emend. Schaudinn, 1903         32
          _Entamœba histolytica_, Schaudinn, 1903                      34
              _Entamœba tetragena_, Viereck, 1907                      38
          Noc’s Entamœba, 1909                                         41
          _Entamœba buccalis_, Prowazek, 1904                          43
          _Entamœba undulans_, Castellani, 1905                        43
          _Entamœba kartulisi_, Doflein, 1901                          44
          _Amœba gingivalis_, _A. buccalis_, _A. dentalis_             44
        Genus. _Paramœba_, Schaudinn, 1896                             44
          _Paramœba (Craigia) hominis_, Craig, 1906                    45
      B. Amœbæ from other Organs                                       45
          _Entamœba pulmonalis_, Artault, 1898                         45
          _Amœba urogenitalis_, Baelz, 1883                            45
          _Amœba miurai_, Ijima, 1898                                  46
      _Appendix_: “Rhizopods in Poliomyelitis Acuta”                   46
    Order. _Foraminifera_, d’Orbigny                                   47
    Sub-order. _Monothalamia_ (Testaceous Amœbæ)                       47
        Genus. _Chlamydophrys_, Cienkowski, 1876                       47
          _Chlamydophrys enchelys_, Ehrenberg                          47
          _Leydenia gemmipara_, Schaudinn, 1896                        49

  Class II. MASTIGOPHORA, Diesing                                      50
  Sub-class. FLAGELLATA, Cohn emend. Bütschli                          50
    Order. _Polymastigina_, Blochmann                                  52
        Genus. _Trichomonas_, Donné, 1837                              52
          _Trichomonas vaginalis_, Donné                               52
          _Trichomonas intestinalis_, R. Leuckart, 1879 =
              _Trichomonas hominis_, Davaine, 1854                     54
        Genus. _Tetramitus_, Perty, 1852                               57
          _Tetramitus mesnili_, Wenyon, 1910                           57
        Genus. _Lamblia_, R. Blanchard, 1888                           57
          _Lamblia intestinalis_, Lambl, 1859                          57
    Order. _Protomonadina_, Blochmann                                  60
      Family. _Cercomonadidæ_, Kent emend. Bütschli                    61
        Genus. _Cercomonas_, Dujardin emend. Bütschli                  61
          _Cercomonas hominis_, Davaine, 1854                          61
          _Monas pyophila_, R. Blanchard, 1895                         62
      Family. _Bodonidæ_, Bütschli                                     63
        Genus. _Prowazekia_, Hartmann and Chagas, 1910                 63
          _Prowazekia urinaria_, Hassall, 1859                         63
          _Prowazekia asiatica_, Castellani and Chalmers, 1910         65
          _Prowazekia javanensis_, Flu, 1912                           66
          _Prowazekia cruzi_, Hartmann and Chagas, 1910                66
          _Prowazekia weinbergi_, Mathis and Léger, 1910               66
          _Prowazekia parva_, Nägler, 1910                             66
      Family. _Trypanosomidæ_, Doflein                                 66
        Genus. _Trypanosoma_, Gruby, 1843                              67
            Historical                                                 67
            General                                                    69
            Morphology                                                 70
          _Trypanosoma gambiense_, Dutton, 1902                        72
          _Trypanosoma nigeriense_, Macfie, 1913                       76
          _Trypanosoma rhodesiense_, Stephens and Fantham, 1910        76
            General Note on Trypanosomes with Posterior Nuclei         83
          _Trypanosoma cruzi_, Chagas, 1909                            83
          _Trypanosoma lewisi_, Kent, 1881                             88
          _Trypanosoma brucei_, Plimmer and Bradford, 1899             93
          _Trypanosoma evansi_, Steel, 1885                            95
          _Trypanosoma equinum_, Voges, 1901                           96
          _Trypanosoma equiperdum_, Doflein, 1901                      97
          _Trypanosoma theileri_, Bruce, 1902                          98
          _Trypanosoma hippicum_, Darling, 1910                        98
          _Endotrypanum schaudinni_, Mesnil and Brimont, 1908          99
          _Trypanosoma boylei_, Lafont, 1912                           99
        Monomorphic Trypanosomes                                       99
          _Trypanosoma vivax_, Ziemann, 1905                           99
          _Trypanosoma capræ_, Kleine, 1910                           100
          _Trypanosoma congolense_, Broden, 1904                      100
          _Trypanosoma simiæ_, Bruce, 1912                            100
          _Trypanosoma uniforme_, Bruce, 1910                         101
            General Note on Development of Trypanosomes in Glossina   101
            Adaptation of Trypanosomes                                101
        Genus. _Herpetomonas_, Saville Kent, 1881                     102
        Genus. _Crithidia_, Léger, 1902, emend. Patton, 1908          104
        Genus. _Leishmania_, Ross, 1903                               104
          _Leishmania donovani_, Laveran and Mesnil, 1903             105
          _Leishmania tropica_, Wright, 1903                          107
          _Leishmania infantum_, Nicolle, 1908                        109
        Genus. _Histoplasma_, Darling, 1906                           112
        Genus. _Toxoplasma_, Nicolle and Manceaux, 1908               112

    THE SPIROCHÆTES                                                   114
        The Spirochætes of the Blood                                  116
          _Spirochæta duttoni_, Novy and Knapp, 1906                  116
          _Spirochæta gallinarum_, Stephens and Christophers, 1905
              (= _Spirochæta marchouxi_, Nuttall, 1905)               119
          _Spirochæta recurrentis_, Lebert, 1874                      120
          _Spirochæta rossii_, Nuttall, 1908                          122
          _Spirochæta novyi_, Schellack, 1907                         122
          _Spirochæta carteri_, Mackie and Manson, 1907               122
          _Spirochæta berbera_, Sergent and Foley, 1910               122
        Other Human Spirochætes                                       122
        Some Animal Spirochætes                                       122

    TREPONEMATA                                                       124
          _Treponema pallidum_, Schaudinn, 1905                       124
          _Treponema pertenue_, Castellani, 1905                      127

  Class III. SPOROZOA, Leuckart, 1879                                 128
  Sub-class. TELOSPORIDIA, Schaudinn                                  129
    Order. _Gregarinida_, Aimé Schneider emend. Doflein               129
    Order. _Coccidiidea_                                              135
        Genus. _Eimeria_, Aimé Schneider, 1875                        142
          _Eimeria avium_, Silvestrini and Rivolta                    142
          _Eimeria stiedæ_, Lindemann, 1865                           145
            (_a_) Human Hepatic Coccidiosis                           148
            (_b_) Human Intestinal Coccidiosis                        148
            (_c_) Doubtful Cases                                      149
        Genus. _Isospora_, Aimé Schneider, 1881                       149
          _Isospora bigemina_, Stiles, 1891                           149
        Doubtful Species                                              150
    Order. _Hæmosporidia_, Danilewsky emend. Schaudinn                151
            The Malarial Parasites of Man                             155
            Development of the Malarial Parasites of Man              159
        The Species of the Malarial Parasites of Man                  164
          _Plasmodium vivax_, Grassi and Feletti, 1890                164
          _Plasmodium malariæ_, Laveran                               166
          _Laverania malariæ_, Grassi and Feletti, 1890
              (= _Plasmodium falciparum_, Welch, 1897)                167
          _Plasmodium relictum_, Sergent, 1907 (in birds)             170
            Cultivation of Malarial Parasites                         170
            Differential Characters of the Human Malarial Parasites   171
      Family. _Piroplasmidæ_, França, 1909                            172
        Genus. _Babesia_, Starcovici, 1893                            174
        Genus. _Theileria_, Bettencourt, França and Borges, 1907      178
          _Theileria parva_, Theiler, 1903                            178
          _Theileria mutans_, Theiler, 1907                           180
        Genus. _Anaplasma_, Theiler, 1910                             180
        Genus. _Paraplasm_a, Seidelin, 1911                           180
  Sub-class. NEOSPORIDIA, Schaudinn                                   181
    Order. _Myxosporidia_, Bütschli                                   181
    Order. _Microsporidia_, Balbiani                                  184
    Order. _Actinomyxidia_, Stolč.                                    187
    Order. _Sarcosporidia_, Balbiani                                  187
             _Sarcosporidia_ observed in Man                          193
    Order. _Haplosporidi_a, Caullery and Mesnil, 1899                 194
             _Rhinosporidium kinealyi_, Minchin and Fantham, 1905     195

  Class IV. INFUSORIA, Ledermüller, 1763                              198
        Genus. _Balantidium_, Claparède et Lachmann                   200
          _Balantidium coli_, Malmsten, 1857                          200
          _Balantidium minutum_, Schaudinn, 1899                      204
        Genus. _Nyctotherus_, Leidy, 1849                             204
          _Nyctotherus faba_, Schaudinn, 1899                         205
          _Nyctotherus giganteus_, P. Krause, 1906                    205
          _[Nyctotherus] africanus_, Castellani, 1905                 206
    THE CHLAMYDOZOA                                                   207
    PROTOZOA INCERTÆ SEDIS                                            210
          _Sergentella hominis_, Brumpt, 1910                         210

  *B. Platyhelminthes (or Flat Worms)*                                211


      Class I. TURBELLARIA (or Eddy Worms)                            212
        Order 1. _Rhabdocœlida_                                       212
            2. _Tricladida_                                           212
            3. _Polycladida_                                          212
      Class II. TREMATODA (Sucking Worms)                             212
           III. CESTODA (Tapeworms)                                   212

  Class II. TREMATODA, Rud.                                           212
      Development of the Trematodes                                   222
      Biology                                                         229


    Order. _Digenea_, v. Beneden, 1858                                230
    Sub-order. _Prostomata_, Odhner, 1905                             230
      Group. _Amphistomata_, Rudolphi, 1801, ep., Nitzsch, 1819       230
        Family. _Paramphistomidæ_, Fischoeder, 1901                   231
        Sub-family. _Paramphistominæ_, Fischoeder, 1901               231
                _Cladorchiinæ_, Fischoeder, 1901                      231
        Family. _Gastrodisciidæ_, Stiles and Goldberger, 1910         231
      Group. _Distomata_, Retzius, 1782                               231
        Family. _Fasciolidæ_, Railliet, 1895                          231
        Sub-family. _Fasciolinæ_, Odhner, 1910                        231
                _Fasciolopsinæ_, Odhner, 1910                         231
        Family. _Opisthorchiidæ_, Braun, 1901, emend, auctor.         232
        Sub-family. _Opisthorchiinæ_, Looss, 1899, emend, auctor.     232
                _Metorchiinæ_, Lühe, 1909                             232
        Family. _Dicrocœliidæ_, Odhner, 1910                          232
                _Heterophyiidæ_, Odhner, 1914                         232
                _Troglotremidæ_, Odhner, 1914                         232
                _Echinostomidæ_, Looss, 1902                          233
        Sub-family. _Echinostominæ_, Looss, 1899                      233
                _Himasthlinæ_, Odhner, 1910                           233
        Family. _Schistosomidæ_, Looss, 1899                          233

    THE TREMATODES OBSERVED IN MAN                                    234

        Family. _Paramphistomidæ_, Stiles and Goldberger,
                    emend. 1910                                       234
        Sub-family. _Cladorchiinæ_, Fischoeder, 1901                  234
          Genus. _Watsonius_, Stiles and Goldberger, 1910             234
                _Watsonius watsoni_, Stiles and Goldberger, 1910      234
        Family. _Gastrodisciidæ_                                      236
          Genus. _Gastrodiscus_, Lkt., 1877                           236
                _Gastrodiscus hominis_, Lewis and McConnell, 1876     236
        Family. _Fasciolidæ_, Railliet, 1895                          237
        Sub-family. _Fasciolinæ_, Odhner, 1910                        237
          Genus. _Fasciola_, L., 1758                                 237
                _Fasciola hepatica_, L., 1758                         237
                  Halzoun                                             242
                _Fasciola gigantica_, Cobbold, 1856                   244
        Sub-family. _Fasciolopsinæ_, Odhner, 1910                     245
          Genus. _Fasciolopsis_, Looss, 1898                          245
                _Fasciolopsis buski_, Lank., 1857                     245
                _Fasciolopsis rathouisi_, Ward, 1903                  246
                _Fasciolopsis goddardi_, Ward, 1910                   247
                _Fasciolopsis fülleborni_, Rodenwaldt, 1909           247
        Family. _Troglotremidæ_, Odhner, 1914                         249
          Genus. _Paragonimus_, Braun, 1899                           249
                _Paragonimus ringeri_, Cobb., 1880                    249
        Family. _Opisthorchiidæ_, Braun, 1901                         252
        Sub-family. _Opisthorchiinæ_, Looss, 1899                     252
          Genus. _Opisthorchis_, R. Blanch., 1845                     252
                _Opisthorchis felineus_, Riv., 1885                   252
          Genus. _Paropisthorchis_, Stephens, 1912                    255
                _Paropisthorchis caninus_, Barker, 1912               255
          Genus. _Amphimerus_, Barker, 1912 (?)                       257
                _Amphimerus noverca_, Barker, 1912 (?)                258
          Genus. _Clonorchis_, Looss, 1907                            258
                _Clonorchis sinensis_, Cobbold, 1875                  258
                _Clonorchis endemicus_, Baelz, 1883                   259
        Sub-family. _Metorchiinæ_, Lühe, 1909                         261
          Genus. _Metorchis_, Looss, 1899, emend. auctor.             261
                _Metorchis truncatus_, Rud., 1819                     261
        Family. _Heterophyiidæ_, Odhner, 1914                         262
          Genus. _Heterophyes_, Cobbold, 1866                         262
                _Heterophyes heterophyes_, v. Sieb., 1852             262
                _Metagonimus_, Katsurada, 1913; Yokogawa,
                    Leiper, 1913                                      264
                _Metagonimus yokogawai_, Katsurada, 1913              264
        Family. _Dicrocœliidæ_, Odhner, 1910                          265
          Genus. _Dicrocœlium_, Dujardin                              265
                _Dicrocœlium dendriticum_, Rud., 1819                 266
        Family. _Echinostomidæ_, Looss, 1902                          267
        Sub-family. _Echinostominæ_, Looss, 1899                      267
          Genus. _Echinostoma_, Rud., 1809; Dietz, 1910               267
                _Echinostoma ilocanum_, Garrison, 1908                267
                _Echinostoma malayanum_, Leiper, 1911                 268
        Sub-family. _Himasthlinæ_, Odhner, 1910                       269
          Genus. _Artyfechinostomum_, Clayton-Lane, 1915              269
                _Artyfechinostomum sufrartyfex_, Clayton-Lane, 1915   269
        Family. _Schistosomidæ_, Looss, 1899                          269
          Genus. _Schistosoma_, Weinl., 1858                          269
                _Schistosoma hæmatobium_, Bilharz, 1852               270
                _Schistosoma mansoni_, Sambon, 1907                   277
                _Schistosoma japonicum_, Katsurada, 1904              277

  Class III. CESTODA, Rud., 1808                                      282
      Anatomy of the Cestoda                                          284
      Development of the Tapeworms                                    297
      Biology                                                         306


    Order. _Pseudophyllidea_, Carus, 1863                             308
        Family. _Dibothriocephalidæ_, Lühe, 1902                      308
        Sub-family. _Dibothriocephalinæ_, Lühe, 1899                  308
    Order. _Cyclophyllidea_, v. Beneden                               308
        Family. _Dipylidiidæ_, Lühe, 1910                             309
                _Hymenolepididæ_, Railliet and Henry, 1909            309
                _Davaineidæ_, Fuhrmann, 1907                          309
        Sub-family. _Davaineinæ_, Braun, 1900                         309
        Family. _Tæniidæ_, Ludwig, 1886                               309

    THE CESTODES OF MAN                                               309
        Family. _Dibothriocephalidæ_                                  309
        Sub-family. _Dibothriocephalinæ_                              309
          Genus. _Dibothriocephalus_, Lühe, 1899                      309
            _Dibothriocephalus latus_, L., 1748                       310
            _Dibothriocephalus cordatus_, R. Lkt., 1863               315
            _Dibothriocephalus parvus_, Stephens, 1908                316
          Genus. _Diplogonoporus_, Lönnbrg., 1892                     316
            _Diplogonoporus grandis_, R. Blanch., 1894                316
            _Sparganum_, Diesing, 1854                                317
            _Sparganum mansoni_, Cobb., 1883                          317
            _Sparganum proliferum_, Ijima, 1905                       318
        Family. _Dipylidiidæ_, Lühe, 1910                             320
          Genus. _Dipylidium_, R. Lkt., 1863                          320
            _Dipylidium caninum_, L. 1758                             320
        Family. _Hymenolepididæ_, Railliet and Henry, 1909            323
          Genus. _Hymenolepis_, Weinland, 1858                        323
            _Hymenolepis nana_, v. Sieb., 1852                        323
            _Hymenolepis diminuta_, Rud., 1819                        326
            _Hymenolepis lanceolata_, Bloch, 1782                     328
        Family. _Davaineidæ_, Fuhrmann, 1907                          329
        Sub-family. _Davaineinæ_, Braun, 1900                         329
          Genus. _Davainea_, R. Blanch., 1891                         329
            _Davainea madagascariensis_, Davaine, 1869                329
            _Davainea_ (?) _asiatica_, v. Linst., 1901                330
        Family. _Tæniidæ_, Ludwig, 1886                               331
          Genus. _Tænia_, L., 1758                                    331
            _Tænia solium_, L., _p. p._, 1767                         331
            _Cysticercus acanthotrias_, Weinland, 1858                336
            _Tænia bremneri_, Stephens, 1908                          337
            _Tænia marginata_, Batsch., 1786                          338
            _Tænia serrata_, Goeze, 1782                              338
            _Tænia crassicollis_, Rud., 1810                          338
            _Tænia saginata_, Goeze, 1782                             338
            _Tænia africana_, v. Linst., 1900                         342
            _Tænia confusa_, Ward, 1896                               343
            _Tænia echinococcus_, v. Sieb., 1853                      344
              Structure and Development of Echinococcus(Hydatid)      347
            _Echinococcus multilocularis_ (Alveolar Colloid)          356
              Serum Diagnosis of Echinococcus                         359

  *C. Nemathelminthes*                                                360
  Class. NEMATODA                                                     360
      Anatomy of the Nematodes                                        360
      Development of the Nematodes                                    371


      Family. _Anguillulidæ_, Gervais and van Beneden, 1859           374
          _Angiostomidæ_, Braun, 1895                                 374
          _Gnathostomidæ_                                             374
          _Dracunculidæ_, Leiper, 1912                                374
          _Filariidæ_, Claus, 1885                                    374
          _Trichinellidæ_, Stiles and Crane, 1910                     375
          _Dioctophymidæ_                                             375
          _Strongylidæ_, Cobbold, 1864                                375
          _Physalopteridæ_                                            375
          _Ascaridæ_, Cobbold, 1864                                   375
          _Oxyuridæ_                                                  375

    THE NEMATODES OBSERVED IN MAN                                     376
        Family. _Anguillulidæ_                                        377
          Genus. _Rhabditis_, Dujardin, 1845                          377
            _Rhabditis pellio_, Schneider, 1866                       377
            _Rhabditis niellyi_, Blanchard, 1885                      378
            _Rhabditis_, sp.                                          378
          Genus. _Anguillula_, Ehrenberg, 1826                        379
            _Anguillula aceti_, Müller, 1783                          379
          Genus. _Anguillulina_, Gervais and Beneden, 1859            379
            _Anguillulina putrefaciens_, Kühn, 1879                   379
        Family. _Angiostomidæ_, Braun, 1895                           379
          Genus. _Strongyloides_, Grassi, 1879                        379
            _Strongyloides stercoralis_, Bavay, 1877                  380
        Family. _Gnathostomidæ_                                       384
          Genus. _Gnathostoma_, Owen, 1836                            384
            _Gnathostoma siamense_, Levinson, 1889                    384
            _Gnathostoma spinigerum_, Owen, 1836                      385
        Family. _Dracunculidæ_, Leiper, 1912                          385
          Genus. _Dracunculus_, Kniphoff, 1759                        385
            _Dracunculus medinensis_, Velsch, 1674                    386
          Genus (of _Crustacea_). _Cyclops_, Müller, 1776             390
        Family. _Filariidæ_                                           390
        Sub-family. _Filariinæ_                                       390
          Genus. _Filaria_, O. Fr. Müller, 1787                       390
            _Filaria bancrofti_, Cobbold, 1877                        390
            _Filaria demarquayi_, Manson, 1895                        403
            _Filaria taniguchi_, Penel, 1905                          404
            _Filaria_ (?) _conjunctivæ_, Addario, 1885                404
      Group. _Agamofilaria_, Stiles, 1906                             406
            _Agamofilaria georgiana_                                  406
            _Agamofilaria palpebralis_, Pace, 1867
                (_nec_ Wilson, 1844)                                  406
            _Agamofilaria oculi humani_, v. Nordmann, 1832            406
            _Agamofilaria labialis_, Pane, 1864                       407
            _Filaria (?) romanorum-orientalis_, Sarcani, 1888         407
            _Filaria (?) kilimaræ_, Kolb, 1898                        407
            _Filaria_ (?) sp. ?                                       407
          Genus. _Setaria_, Viborg, 1795                              407
            _Setaria equina_, Abildg., 1789                           408
          Genus. _Loa_, Stiles, 1905                                  409
            _Loa loa_, Guyot, 1778                                    409
          Genus. _Acanthocheilonema_, Cobbold, 1870                   414
            _Acanthocheilonema perstans_, Manson, 1891                414
          Genus. _Dirofilaria_, Railliet and Henry, 1911              416
            _Dirofilaria magalhãesi_, R. Blanchard, 1895              417
        Sub-family. _Onchocercinæ_, Leiper, 1911                      417
          Genus. _Onchocerca_, Diesing, 1841                          417
            _Onchocerca volvulus_, R. Leuckart, 1893                  417
        Family. _Trichinellidæ_, Stiles and Crane, 1910               419
        Sub-family. _Trichurinæ_, Ransom, 1911                        419
          Genus. _Trichuris_, Röderer and Wagler, 1761                419
            _Trichuris trichiura_, Linnæus, 1761                      419
        Sub-family. _Trichinellinæ_, Ransom, 1911                     421
          Genus. _Trichinella_, Railliet, 1895                        421
            _Trichinella spiralis_, Owen, 1835                        421
              History of the Development of _Trichinella spiralis_    423
        Family. _Dioctophymidæ_                                       431
          Genus. _Dioctophyme_, Collet-Megret, 1802                   431
            _Dioctophyme gigas_, Rudolphi, 1802                       431
        Family. _Strongylidæ_                                         432
        Sub-family. _Metastrongylinæ_, Leiper, 1908                   432
          Genus. _Metastrongylus_, Molin, 1861                        432
            _Metastrongylus apri_, Gmelin, 1789                       432
        Sub-family. _Trichostrongylinæ_, Leiper, 1908                 433
          Genus. _Trichostrongylus_, Looss, 1905                      434
            _Trichostrongylus instabilis_, Railliet, 1893             434
            _Trichostrongylus probolurus_, Railliet, 1896             435
            _Trichostrongylus vitrinus_, _Looss_, 1905                435
          Genus. _Hæmonchus_, Cobb., 1898                             436
            _Hæmonchus contortus_, Rudolphi, 1803; Cobb., 1898        436
          Genus. _Nematodirus_, Ransom, 1907, emend. Railliet, 1912   438
          Sub-genus. _Mecistocirrus_, Railliet, 1912                  438
            _Mecistocirrus fordi_, Daniels, 1908                      438
        Sub-family. _Ancylostominæ_, Railliet, 1909                   438
      Group. _Œsophagostomeæ_, Railliet and Henry, 1909               439
          Genus. _Ternidens_, Railliet, 1909                          439
            _Ternidens deminutus_, Railliet and Henry, 1905           440
          Genus. _Œsophagostomum_, Molin, 1861                        441
            _Œsophagostomum brumpti_, Railliet and Henry, 1905        441
            _Œsophagostomum stephanostomum_ var. _thomasi_,
                 Railliet and Henry, 1909                             443
            _Œsophagostomum apiostomum_, Willach, 1891                444
      Group. _Ancylostomeæ_, Railliet and Henry, 1909                 445
          Genus. _Ancylostoma_, Dubini, 1843, emend. Looss, 1905      445
            _Ancylostoma duodenale_, Dubini, 1843                     445
            _Ancylostoma ceylanicum_, Looss, 1911                     456
            _Ancylostoma braziliense_, Gomez de Faria, 1910           456
      Group. _Bunostomeæ_, Railliet and Henry, 1909                   456
          Genus. _Necator,_ Stiles, 1903                              457
            _Necator americanus_, Stiles, 1902                        457
            _Necator exilidens_, Cummins, 1912                        459
              Ancylostomiasis                                         459
      Group. _Syngameæ_, Railliet and Henry, 1909                     459
          Genus. _Syngamus,_ von Siebold, 1836                        459
            _Syngamus kingi_, Leiper, 1913                            459
        Family. _Physalopteridæ_                                      460
          Genus. _Physaloptera_, Rudolphi, 1819                       460
            _Physaloptera caucasica_, v. Linstow, 1902                461
            _Physaloptera mordens_, Leiper, 1907                      461
        Family. _Ascaridæ_, Cobbold, 1864                             461
        Sub-family. _Ascarinæ_                                        461
          Genus. _Ascaris_, L., 1758                                  461
            _Ascaris lumbricoides_, L., 1758                          463
            _Ascaris_ sp.                                             465
            _Ascaris texana_, Smith et Goeth, 1914                    465
            _Ascaris maritima_, Leuckart, 1876                        465
          Genus. _Toxascaris_, Leiper, 1907                           465
            _Toxascaris limbata_, Railliet and Henry, 1911            466
          Genus. _Belascaris_, Leiper, 1907                           466
            _Belascaris cati_, Schrank, 1788                          466
            _Belascaris marginata_, Rudolphi, 1802                    466
          Genus. _Lagocheilascaris_, Leiper, 1909                     466
            _Lagocheilascaris minor_, Leiper, 1909                    467
        Family. _Oxyuridæ_                                            467
          Genus. _Oxyuris_, Rudolphi, 1803                            467
            _Oxyuris vermicularis_, Linnæus, 1767                     467
        Family. _Mermithidæ_                                          469
          Genus. _Mermis_, Dujardin, 1845                             469
            _Mermis hominis oris_, Leidy, 1850                        469
            _Agamomermis_, Stiles, 1903                               470
            _Agamomermis restiformis_, Leidy, 1880                    470
    TECHNIQUE                                                         471

  *D. Acanthocephala*, Rud                                            475
            _Echinorhynchus gigas_, Goeze, 1782                       477
            _Echinorhynchus hominis_, Lambl, 1859                     478
            _Echinorhynchus moniliformis_, Bremser, 1819              478

  *E. Gordiidæ*                                                       479

  *F. Hirudinea s. Discophora* (Leech)                                480
        Family. _Gnathobdellidæ_ (Leeches with Jaws)                  481
          Genus. _Hirudo_, L., 1758                                   481
            _Hirudo medicinalis_, L., 1758                            481
            _Hirudo troctina,_ Johnston, 1816                         482
          Genus. _Limnatis_, Moq.-Tandon, 1826                        482
            _Limnatis nilotica_, Savigny, 1820                        482
          Genus. _Hæmadipsa_, Tennent, 1861                           482
        Family. _Rhynchobdellidæ_ (Leeches with Rostrum)              482
          Genus. _Hæmentaria_, de Filippi, 1849                       482
            _Hæmentaria officinalis_, de Filippi                      482
          Genus. _Placobdella_, R. Blanchard                          482
            _Placobdella catenigera_, Moq.-Tandon                     482

  *G. Arthropoda* (Jointed-limbed Animals)                            483
    _A._ ARACHNOIDEA (Spiders, Mites, etc.)                           483
      Order. _Acarina_ (Mites)                                        484
        Family. _Trombidiidæ_ (Running Mites)                         485
          Genus. _Trombidium_, Latreille (and Leptus)                 485
            _Leptus autumnalis,_ Shaw, 1790                           485
            _Trombidium tlalsahuate_, Lemaire, 1867                   486
            _Akamushi_ or _Kedani_                                    487
        Family. _Tetranychidæ_ (Spinning Mites)                       488
          Genus. _Tetranychus_, Dufour                                488
            _Tetranychus molestissimus_, Weyenbergh, 1886             488
            _Tetranychus telarius_, L., 1758, var. russeolus, Koch    488
        Family. _Tarsonemidæ_                                         488
          Genus. _Pediculoides_                                       489
            _Pediculoides ventricosus_, Newport, 1850                 489
          Genus. _Nephrophages_                                       490
            _Nephrophages sanguinarius_, Miyake and Scriba, 1893      490
        Family. _Eupodidæ_                                            491
          Genus. _Tydeus,_ Koch                                       491
            _Tydeus molestus_, Moniez, 1889                           491
        Family. _Gamasidæ_ (Coleopterous or Insect Mites)             491
          Genus. _Dermanyssus_, Dugès                                 492
            _Dermanyssus gallinæ_, de Geer, 1778                      492
            _Dermanyssus hirundinis_, Hermann, 1804                   492
          Genus. _Holothyrus_                                         493
            _Holothyrus coccinella_, Gervais, 1842                    493
        Family. _Ixodidæ_ (Ticks)                                     493
        Classification of _Ixodidæ_                                   496
        Synopsis of Genera                                            496
          Genus. _Ixodes_, Latreille                                  497
            _Ixodes reduvius,_ L., 1758                               497
            _Ixodes holocyclus_, Neumann, 1899                        499
            _Ixodes hexagonus_, Leach, 1815                           500
          Genus. _Amblyomma_, Koch                                    500
            _Amblyomma cayennense_, Koch, 1844                        500
            _Amblyomma americana_, Linnæus                            501
            _Amblyomma maculatum_, Koch                               501
          Genus. _Hyalomma_, Koch                                     501
            _Hyalomma ægyptium_, L., 1758                             501
          Genus. _Hæmaphysalis_, Koch                                 502
            _Hæmaphysalis punctata_, Canestrini and Fanzago,
                1877–1878                                             502
          Genus. _Dermacentor_, Koch                                  502
            _Dermacentor reticulatus_, Fabricius, 1794                502
            _Dermacentor venustus_, Banks                             503
            _Dermacentor occidentalis_, Neumann                       504
            _Dermacentor variabilis_, Say                             505
          Genus. _Margaropus_, Karsch                                 505
            _Margaropus annulatus australis_, Fuller                  505
            _Margaropus microplus_, Canestrini                        505
          Genus. _Rhipicephalus_, Koch                                505
            _Rhipicephalus sanguineus_, Latreille, 1804               505
        Neumann’s Table of Species of _Argas_                         505
          Genus. _Argas_, Latreille                                   506
            _Argas reflexus_, Fabricius, 1794                         506
            _Argas persicus_, Fischer de Waldheim, 1824               506
            _Argas brumpti_, Neumann                                  507
            _Argas chinche_, Gervais, 1844                            508
          Genus. _Ornithodorus_, Koch                                 508
            _Ornithodorus moubata_, Murray, 1877                      508
            _Ornithodorus savignyi_, Audouin, 1827                    509
            _Ornithodorus coriaceus_, Koch                            509
            _Ornithodorus talaje_, Guerin, 1849                       509
            _Ornithodorus turicata_, Dugès, 1876                      509
            _Ornithodorus tholozani_, Laboulbène and Mégnin, 1882     510
            _Ornithodorus mégnini, Dugès_, 1883                       510
        Family. _Tyroglyphidæ_                                        511
        Sub-family. _Tyroglyphinæ_                                    511
          Genus. _Aleurobius_, Canestrini                             511
            _Aleurobius (Tyroglyphus) farinæ_, de Geer (part), Koch   511
          Genus. _Tyroglyphus_, Latreille                             511
            _Tyroglyphus siro_, L., 1756                              511
            _Tyroglyphus longior_, Gervais, 1844                      512
            _Tyroglyphus minor_ var. _castellani_, Hirst              513
          Genus. _Glyciphagus_, Hering, 1838                          513
            _Glyciphagus prunorum_, Hering, and
                _G. domesticus_, de Geer                              513
            _Glyciphagus cursor_, Gervais                             513
            _Glyciphagus buski_, Murray                               513
          Genus. _Rhizoglyphus_, Claparède, 1869                      514
            _Rhizoglyphus parasiticus_, Dalgetty, 1901                514
          Genus. _Histiogaster_, Berlese, 1883                        515
            _Histiogaster_ (_entomophagus_ ?)
                _spermaticus_, Trouessart, 1900                       515
          Genus. _Cheyletus_                                          516
            _Cheyletus mericourti_, Lab.                              516
        Family. _Sarcoptidæ_ (Itch Mites)                             516
        Sub-family. _Sarcoptinæ_                                      518
          Genus. _Sarcoptes_, Latreille                               518
            _Sarcoptes scabiei_, de Geer, 1778                        518
            _Sarcoptes minor_, Fürstenberg, 1861                      520
        Family. _Demodicidæ_ (Mites of the Hair-follicles)            522
          Genus. _Demodex_, Owen                                      522
            _Demodex folliculorum_, Simon, 1842                       522
      Order. _Pentastomida_                                           523
        Family. _Linguatulidæ_                                        523
          Genus. _Linguatula_, Fröhlich_                              524
            _Linguatula rhinaria_, Pilger, 1802                       524
          Genus. _Porocephalus_                                       526
            _Porocephalus constrictus_, v. Siebold, 1852              526

    _B._ INSECTA (_Hexapoda_)                                         529


      (1) _Aptera_                                                    531
      (2) _Neuroptera_                                                531
      (3) _Orthoptera_                                                531
      (4) _Thysanoptera_                                              531
      (5) _Hemiptera_                                                 531
      (6) _Diptera_                                                   532
      (7) _Lepidoptera_                                               532
      (8) _Hymenoptera_                                               532
      (9) _Coleoptera_                                                532
      Order. _Rhyncota_                                               532
      (_a_) _Rhyncota aptera parasitica_                              532
        Family. _Pediculidæ_ (Lice)                                   532
          Genus. _Pediculus_, Linnæus                                 532
            _Pediculus capitis_, de Geer, 1778                        532
            _Pediculus vestimenti_, Nitzsch, 1818                     533
          Genus. _Phthirius_, Leach                                   534
            _Phthirius inguinalis_, Redi, 1668                        534
      (_b_) _Rhyncota hemiptera_                                      534
        Family. _Acanthiadæ_                                          534
          Genus. _Cimex_ , Linnæus                                    534
            _Cimex lectularius_ , Linnæus                             534
            _Cimex rotundatus_, Signoret, 1852                        536
            _Cimex columbarius_, Jenyns                               536
            _Cimex ciliatus_, Eversmann, 1841                         537
        Family. _Reduviidæ_                                           537
          Genus. _Conorhinus_, Lap.                                   537
            _Conorhinus megistus_, Burm.                              537
            _Conorhinus sanguisuga_, Lec. (Blood-sucking Cone-nose)   537
            _Conorhinus, sp. novum_ (Monster Bug)                     538
            _Conorhinus rubrofasciatus_, de Geer (Malay Bug)          538
            _Conorhinus renggeri_, Herr-Schäff (Great Black Bug
                of Pampas)                                            539
            _Conorhinus variegatus_ (Variegated Cone-nose)            539
            _Conorhinus nigrovarius_                                  539
            _Conorhinus protractus_                                   539
          Genus. _Reduvius_, etc.                                     539
            _Reduvius personatus_, Linné                              539
            _Coriscus subcoleoptratus_, Kirby, 1837                   540
            _Rasahus biguttatus_, Say, 1831                           540
            _Melanolestes morio_, Erichson, 1848 (non-Walker)         540
            _Melanolestes abdominalis_, Herrich-Schäffer, 1848        540
            _Phonergates bicoloripes_                                 541
        Family. _Aradidæ_                                             541
            _Dysodius lunatus_, Fabr. (Pito Bug)                      541
                The Ochindundu                                        541
        Family. _Lygæidæ_                                             541
            _Lyctocoris campestris_, Fabricius                        541
            _Rhodinus prolixus_, Stål, 1859                           541
      Order. _Orthoptera_                                             542
      Locusts Injurious to Man                                        542
      Order. _Coleoptera_                                             542
            _Silvanus surinamensis_, Linnæus (Saw-toothed
                Grain Beetle)                                         542
      Order. _Diptera_                                                543
      _Aphaniptera_ or _Siphonaptera_ (Fleas)                         543
        Family. _Sarcopsyllidæ_ (Jiggers)                             543
          Genus. _Dermatophilus_, Guérin                              544
            _Dermatophilus cæcata_, Enderl.                           544
            _Dermatophilus penetrans_, L., 1758 (Jigger, Chigoe)      544
          Genus. _Echidnophaga_, Olliff                               544
            _Echidnophaga gallinacea_, Westwood (Chigoe of Fowls)     544
        Family. _Pulicidæ_ (True Fleas)                               545
          Genus. _Pulex_, Linn.                                       545
            _Pulex irritans_, L., 1758                                545
          Genus. _Xenopsylla_, Glink                                  546
            _Xenopsylla cheopis_, Rothschild                          546
            _Xenopsylla brasiliensis_, Baker                          547
          Genus. _Ctenocephalus_, Kolenati                            547
          Genus. _Hoplopsyllus_, Baker                                547
            _Hoplopsyllus anomalus_, Baker                            547
          Genus. _Ceratophyllus_, Centis                              547
            _Ceratophyllus fasciatus_, Bosc                           547
          Genus. _Ctenopsylla_, Kolenati                              548
          Genus. _Hystrichopsylla_, Taschenberg                       548
            _Pulex pallipes_                                          548
    CULICIDÆ OR MOSQUITOES                                            555
    _The Classification of Culicidæ_                                  561
    _Notes on the Different Genera_                                   566
        Sub-family.   _Anophelina_                                    566
          Genus. _Anopheles_, Meigen                                  566
          Genus. _Myzomyia_, Blanchard; _Grassia_, Theobald           567
          Genus. _Neomyzomyia_, Theobald                              567
          Genus. _Cycloleppteron_, Theobald                           567
          Genus. _Feltinella_, Theobald                               567
          Genus. _Stethomyia_, Theobald                               567
          Genus. _Pyretophorus_, Blanchard; _Howardia_,
                     Theobald                                         567
          Genus. _Myzorhynchella_, Theobald                           568
          Genus. _Manguinhosia_, Cruz (in Peryassu)                   568
          Genus. _Chrystya_, Theobald                                 568
          Genus. _Lophoscelomyia_, Theobald                           568
          Genus. _Arribalzagia_, Theobald                             568
          Genus. _Myzorhynchus_, Blanchard; _Rossia_, Theobald        568
          Genus. _Nyssorhynchus_, Blanchard; _Laverania_, Theobald    569
          Genus. _Cellia_, Theobald                                   569
          Genus. _Neocellia_, Theobald                                569
          Genus. _Kertészia_, Theobald                                569
          Genus. _Manguinhosia_, Cruz                                 569
          Genus. _Chagasia_, Cruz                                     570
          Genus. _Calvertina_, Ludlow                                 570
          Genus. _Birónella_, Theobald                                570
        Sub-family. _Megarhininæ_                                     570
          Genus. _Megarhinus_, Robineau Desvoidy                      570
          Genus. _Toxorhynchites_, Theobald                           570
        Sub-family. _Culicinæ_                                        571
          Genus. _Mucidus_, Theobald                                  571
          Genus. _Psorophora_, Robineau Desvoidy                      571
          Genus. _Janthinosoma_, Arribalzaga                          571
          Genus. _Stegomyia_, Theobald                                571
            _Stegomyia fasciata_, Fabricius (Yellow Fever Mosquito)   574
            _Stegomyia scutellaris_, Walker                           575
          Genus. _Theobaldia_, Neveu-Lemaire                          575
            _Theobaldinella_, Blanchard                               575
            _Theobaldia annulata_, Meigen                             575
          Genus. _Culex_, Linnæus                                     575
          Genus. _Melanoconion_, Theobald                             576
          Genus. _Grabhamia_, Theobald                                576
          Genus. _Pseudotæniorhynchus_, Theobald; _Tæniorhynchus_,
                     Theobald, non-Arribalzaga                        576
          Genus. _Tæniorhynchus_, Arribalzaga; _Mansonia_,
                     Blanchard; _Panoplites_, Theobald                577
          Genus. _Chrysoconops_, Goeldi                               577
    _Other Nematocera_                                                577
        Family. _Simulidæ_                                            577
        Family. _Chironomidæ_ (Midges)                                579
        Sub-family. _Ceratopogoninæ_                                  580
        Family. _Psychodidæ_ (Owl Midges)                             581
    _Brachycera_ (Flies)                                              582
        Family. _Phoridæ_                                             582
            _Aphiochæta ferruginea_, Brun                             583
            _Phora rufipes_, Meig.                                    583
        Family. _Sepsidæ_                                             583
            _Piophila casei_, L.                                      583
        Family. _Syrphidæ_ (Hover and Drone Flies)                    583
        Family. _Drosophilidæ_                                        584
            _Drosophila melanogaster_, Br.                            584
        Family. _Muscidæ_                                             584
            _Teichomyza fusca_, Macq.                                 584
            _Homalomyia canicularis_, L., etc.                        584
            _Homalomyia scalaris_, Fabr.                              585
            _Anthomyra desjardensii_, Macq.                           585
            _Hydrotæa meteorica_, L.                                  585
            _Cyrtoneura stabulans_                                    585
            _Musca domestica_, Linn. (Common House-fly)               585
          Genus. _Chrysomyia_, Rob. Desv.                             587
            _Chrysomyia_ (_Compsomyia_) _macellaria_, Fabr.; _Lucilia
              macellaria_, Fabr.                                      587
            _Chrysomyia viridula_, Rob. Desv.                         588
          Genus. _Lucilia_, Rob. Desv.                                588
            _Lucilia nobilis_, Meig.                                  588
          Genus. _Pycnosoma_, Brauer and v. Bergenstamm               588
          Genus. _Sarcophaga_, Mg.                                    589
            _Sarcophaga carnaria_, L., 1758                           589
            _Sarcophaga magnifica_, Schiner, 1862                     589
            _Sarcophaga chrysotoma_, Wied                             590
            _Sarcophaga plinthopyga_, Wied                            590
            _Ochromyia anthropophaga_, E. Blanch.; _Cordylobia
               arthrophaga_,Grünberg                                  590
            _Auchmeromyia_ (_Bengalia_) _depressa_ (Walker)           591
          Genus. _Cordylobia_, Grünberg, 1903                         591
            _Cordylobia grünbergi_, Dönitz                            591
            _Cordylobia anthropophaga_, Grünberg                      592
            _Lund’s Larva_                                            593
            _Auchmeromyia luteola_, Fabricius                         593
        Family. _Oestridæ_                                            594
      _Cutaneous Oestridæ_                                            595
          Genus. _Hypoderma_, Latreille                               595
            _Hypoderma bovis_, de Geer                                595
            _Hypoderma lineata_, de Villers                           596
            _Hypoderma diana_, Brauer                                 596
          Genus. _Dermatobia_, Brauer                                 596
            _Dermatobia cyaniventris_, Macq.                          596
      _Cavicolous Oestridæ_                                           598
          Genus. _Oestrus_, Linnæus                                   598
            _Oestrus_ (_Cephalomyia_) _ovis_, L.                      598
      _Gastricolous Oestridæ_                                         599
          Genus. _Gastrophilus_, Leach                                599
      _Biting-mouthed and other Noxious Diptera which may be
          Disease Carriers_                                           600
        Family. _Tabanidæ_ (Gad Flies)                                600
        Family. _Asilidæ_ (Wolf Flies)                                602
        Family. _Leptidæ_                                             603
      _Blood-sucking Muscidæ_                                         603
          Genus. _Glossina_, Westwood                                 603
            _Glossina palpalis_, Rob. Desv.                           607
            _Glossina morsitans_, Westwood                            608
          Genus. _Stomoxys_, Geoffroy                                 609
          Genus. _Lyperosia_, Rondani                                 610
      _Pupipara_ or _Eproboscidæ_                                     611
      _Insects and Epidemic Poliomyelitis_                            612

  ADDENDA                                                             613
    Akamushi or Kedani Sickness                                       613
    Ticks.--African Tick Fever                                        613
    Tick Paralysis                                                    613
    _Diptera._--_Psychodidæ_                                          613
    _Pulicidæ._--_Dermatophilus_ (_Sarcopsylla_) _penetrans_,
        or the “Jigger”                                               613
    _Brachycera._--_Leptidæ_                                          613
    Myiasis                                                           615
    Auricular Myiasis                                                 615
    Body, Head, and Clothes Lice                                      615

    *Protozoa*                                                        617
    Introduction                                                      617
      I.--AMŒBIC DYSENTERY                                            618
      II.--TRYPANOSOMIASES                                            620
        African Sleeping Sickness                                     620
        South American Trypanosomiasis                                623
      III.--FLAGELLATE DIARRHŒA AND DYSENTERY                         623
      IV.--LEISHMANIASES                                              626
        A. Kala-azar                                                  626
          Indian                                                      626
          Infantile                                                   627
        B. Oriental Sore, due to _Leishmania tropica_                 627
          Naso-oral (Espundia)                                        628
      V.--SPIROCHÆTOSES                                               629
        A. Relapsing Fevers                                           629
        B. Yaws or Frambœsia tropica                                  632
        C. Syphilis                                                   632
        D. Bronchial Spirochætosis                                    632
      VI.--MALARIA                                                    633
      VII.--BALANTIDIAN DYSENTERY                                     637
    *Plathelminthes* (Flat Worms)                                     638
      FASCIOLIASIS                                                    638
        _Fasciola hepatica_                                           638
        _Fasciolopsis buski_                                          638
      PARAGONIMIASIS                                                  639
        _Paragonimus ringeri_                                         639
        _Clonorchis sinensis_                                         640
      BILHARZIASIS                                                    641
        _Schistosoma hæmatobium_                                      641
      CESTODES                                                        644
        General                                                       644
        _Dibothriocephalus latus_                                     658
        _Sparganum mansoni_                                           659
        _Dipylidium caninum_ (_Tænia cucumerina_)                     659
        _Hymenolepis nana_                                            661
        _Tænia solium_                                                662
        _Tænia saginata_                                              667
      NEMATODES                                                       674
        _Strongyloides stercoralis_                                   674
        _Dracunculus medinensis_ (Dracontiasis)                       675
        _Filaria bancrofti_                                           676
        _Loa loa_                                                     678
        _Trichuris trichiura_                                         678
        _Trichinella spiralis_                                        680
        _Eustrongylus gigas_                                          681
        _Ancylostoma duodenale_ (Ancylostomiasis)                     682
        _Ascaris lumbricoides_ (Ascariasis)                           687
        _Oxyuris vermicularis_ (Oxyuriasis)                           694
    *Hirudinea* (Leeches)                                             699
    *Arthropoda*                                                      702
      ARACHNOIDEA                                                     702
        _Leptus autumnalis_ (Grass, Harvest, or Gooseberry Mite)      702
        _Kedani, Akaneesch_ (The Japanese River or Inundation
            Disease)                                                  703
        _Dermanyssus gallinæ_ (_avium_)                               703
        _Ixodes reduvius_ (_ricinus_ )                                704
        _Sarcoptes scabiei_ (Scabies)                                 704
        _Demodex folliculorum_                                        708
        _Demodex folliculorum canis_                                  709
      INSECTA                                                         709
        _Pediculus capitis_ (Head Louse)                              709
        _Pediculus vestimenti_ (Clothes Louse)                        710
        _Phthirius inguinalis_ (_Pediculus pubis_) (Crab Louse)       711
        _Cimex_ (_Acanthia_) _lectularia_ (_Cimex lectularius_)
            (Bed Bug)                                                 713
        _Pulex irritans_ (Human Flea)                                 714
        _Dermatophilus_ (_Sarcopsylla_) _penetrans_ (Sand Flea)       714
        _Myiasis_                                                     715
        _Myiasis externa_                                             715
        _Gastricolous Oestridæ_ (Creeping Disease)                    729

  APPENDIX ON PROTOZOOLOGY                                            733
    I.--NOTES ON RECENT RESEARCHES                                    733
      Differences between _Entamœba histolytica_ and _E. coli_        733
      Phagedænic Amœbæ                                                733
      _Endamœba gingivalis_                                           733
      _Entamœba kartulisi_                                            734
      _Craigia_ and Craigiasis                                        734
      Human Trichomoniasis                                            734
      _Chilomastix_ (_Tetramitus_) _mesnili_                          735
      _Giardia_ (_Lamblia_) _intestinalis_                            736
      _Cercomonas hominis_                                            736
      Transmissive Phase of Trypanosomes in Vertebrates               737
      _Trypanosoma lewisi_                                            737
      Blepharoplastless Trypanosomes                                  737
      The Experimental Introduction of certain Insect Flagellates
          into various Vertebrates, and its bearing on the
          Evolution of Leishmaniasis                                  737
      The Transmission of _Spirochæta duttoni_                        739
      _Spirochæta bronchialis_                                        739
      The Spirochætes of the Human Mouth                              740
      Coccidia in Cattle                                              741
      The Hæmosporidia                                                742
      The Leucocytozoa of Birds                                       742

    II.--FORMULÆ OF SOME CULTURE MEDIA                                742
      Culture Media for growing Amœbæ                                 742
      Culture Media for the growth of Protozoa parasitic
          in the Blood                                                744

      Fresh Material                                                  745
      Stained Material                                                747
      Fixatives                                                       748
      Stains                                                          749

  APPENDIX ON TREMATODA AND NEMATODA                                  753
    TREMATODA                                                         753
      _Artyfechinostomum sufrartyfex_                                 753
      _Metagonimus_ (_Yokogawa_) _yokogawai_                          753
      _Opisthorchis sp._                                              753
      _Schistosome cercariæ_                                          753
      _Distomata cercariæ_                                            753
      Group. _Ferrocercous cercariæ_                                  753
      Family. _Schistosomidæ_                                         753
      _Cercaria bilharzia_, Leiper, 1915                              754
      _Cercaria bilharziella_, Leiper, 1915                           754
      _Schistosoma mansoni_, Sambon, 1907                             754
    NEMATODA                                                          754
      Ancylostomiasis                                                 754
      Ground Itch                                                     754
      _Ascaris lumbricoides_                                          754
      Filariasis                                                      755
      _Onchocerca volvulus_                                           755
      _Strongyloides stercoralis_                                     755

  BIBLIOGRAPHY                                                        756
  INDEX                                                               836


  FIG.                                                               PAGE

  1  _Amœba coli._ (After Loesch)                                      29
  2  Encysted intestinal amœbæ. (After Grassi)                         31
  3  _Entamœba coli_, life-cycle. (After Castellani and Chalmers)      32
  4  _Entamœba coli_, so-called autogamy. (From Minchin)               34
  5  _Entamœba histolytica_ (_tetragena_ form). (After Hartmann)       35
  6  _Entamœba histolytica_, ingestion of red blood corpuscles.
         (After Hartmann)                                              35
  7  _Entamœba histolytica_, section through infected intestinal
         ulcer. (After Harris)                                         36
  8  _Entamœba histolytica_ (_tetragena_), trophozoite and nuclei.
         (After Hartmann)                                              38
  9  _Entamœba histolytica_ (_tetragena_), cysts. (After Hartmann)     39
  10  _Entamœba buccalis._ (After Leyden and Löwenthal)                43
  11  _Entamœba kartulisi._ (After Kartulis)                           44
  12  _Amœba miurai._ (After Ijima)                                    46
  13  _Chlamydophrys enchelys._ (After Cienkowski)                     48
  14  _Chlamydophrys enchelys_, encysted. (After Cienkowski)           49
  15  _Leydenia gemmipara_, Schaudinn                                  50
  16  _Trichomonas vaginalis._ (After Künstler)                        53
  17  _Trichomonas intestinalis._ (After Grassi)                       54
  18  _Trichomonas intestinalis._ (Original, Fantham)                  55
  19  _Lamblia intestinalis._ (After Wenyon, from Minchin)             58
  20  _Lamblia intestinalis._ (After Grassi and Schewiakoff)           59
  21  _Cercomonas hominis._ (After Davaine)                            61
  22  _Cercomonas hominis_, from an echinococcus cyst. (After Lambl)   61
  23  _Monas pyophila._ (After Grimm)                                  62
  24  _Prowazekia urinaria._ (After Sinton)                            64
  25  _Prowazekia urinaria_, excystation. (After Sinton)               65
  26  _Trypanosoma brucei_ in division. (After Laveran and Mesnil)     70
  27  _Trypanosoma lewisi_, rosettes. (After Laveran and Mesnil)       71
  28  _Trypanosoma gambiense._ (After Dutton)                          73
  29  _Trypanosoma gambiense_, development in vertebrate host.
          (Original, Fantham)                                          73
  30  _Trypanosoma gambiense_, development in _Glossina palpalis_.
          (After Robertson)                                            75
  31  _Trypanosoma rhodesiense._ (After Stephens and Fantham)          77
  32  Chart showing daily counts of number of Trypanosomes per cubic
          millimetre of peripheral blood from a case of Rhodesian
          sleeping sickness. (After Ross and Thomson)                  79
  33  _Trypanosoma cruzi_, schizogony. (After Chagas, from Castellani
          and Chalmers)                                                84
  34  _Trypanosoma cruzi_ in muscle. (After Vianna, from Castellani
          and Chalmers)                                                85
  35  _Trypanosoma cruzi_, development in _Triatoma megista_.
          (After Chagas, from Castellani and Chalmers)                 86
  36  _Trypanosoma cruzi_, forms found in salivary glands of
          _Triatoma_. (After Chagas, from Castellani and Chalmers)     87
  37  _Trypanosoma lewisi_, from rat’s blood. (After Minchin)          89
  38  _Trypanosoma lewisi_, from stomach of rat-flea. (After Minchin)  91
  39  _Trypanosoma lewisi_, from rectum of rat-flea. (After Minchin)   92
  40  _Trypanosoma brucei._ (After Laveran and Mesnil)                 94
  41  _Trypanosoma evansi._ (Original, Fantham)                        96
  42  _Trypanosoma equinum._ (After Laveran and Mesnil)                96
  43  _Trypanosoma equiperdum._ (Original, Fantham)                    97
  44  _Trypanosoma theileri._ (After Laveran and Mesnil)               98
  45  _Trypanosoma vivax._ (Original, Fantham)                        100
  46  _Trypanosoma congolense._ (Original, Fantham)                   100
  47  _Trypanosoma uniforme._ (Original, Fantham)                     100
  48  _Trypanosoma rotatorium._ (After Laveran and Mesnil)            101
  49  _Herpetomonas_, _Crithidia_, _Trypanosoma_. (After Porter)      103
  50  _Leishmania donovani._ (After Christophers, Patton, Leishman;
          from Castellani and Chalmers)                               106
  51  _Toxoplasma gondii._ (After Laveran and Marullaz, from
          _Trop. Dis. Bulletin_)                                      113
  52  _Toxoplasma pyrogenes._ (After Castellani, from _Trop.
          Dis. Bulletin_)                                             113
  53  _Spirochæta balbianii._ (After Fantham and Porter)              114
  54  _Spirochæta duttoni._ (After Fantham)                           117
  55  _Spirochæta duttoni_ and its coccoid bodies in the tick.
          (After Fantham)                                             118
  56  _Treponema pallidum._ (After Bell, from Castellani and
          Chalmers)                                                   124
  57  _Treponema pallidum_, apparatus for cultivation of.
          (After Noguchi)                                             125
  58  _Treponema pertenue._ (After Castellani and Chalmers)           127
  59  _Monocystis agilis._ (After Stein)                              130
  60  _Gregarina longa_, stages of growth of trophozoite              130
  61  _Xyphorhynchus firmus._ (After Léger)                           131
  62  _Gregarina munieri._ (After Schewiakoff)                        131
  63  _Monocystis agilis_, spores. (After Bütschli)                   132
  64  Gregarines, conjugation and spore formation. (After Calkins
          and Siedlecki, modified)                                    133
  65  _Stylorhynchus oblongatus_, cyst and gametes. (After Léger)     133
  66  Gregarines, various spores. (After Léger)                       134
  67  _Eimeria_ (_Coccidium_) _schubergi_, life-cycle diagram of.
          (After Schaudinn)                                           139
  68  _Eimeria avium_ in gut epithelium of grouse chick.
          (After Fantham)                                             143
  69  _Eimeria avium_, life-cycle, diagram of. (After Fantham)        144
  70  _Eimeria stiedæ_ in section of rabbit’s intestine               145
  71  _Eimeria stiedæ_, oöcysts from rabbit’s liver. (After Leuckart) 146
  72  _Eimeria stiedæ_, spores. (After Balbiani)                      146
  73  _Eimeria stiedæ_, schizogony. (After R. Pfeiffer)               146
  74  _Eimeria stiedæ_, section through infected nodule of liver      147
  75  _Isospora bigemina._ (After Stiles)                             150
  76  _Hæmoproteus_ (_Halteridium_) _columbæ_, life-cycle.
          (After Aragão, from Castellani and Chalmers)                152
  77  _Leucocytozoön lovati._ (After Fantham)                         153
  78  Hæmogregarines from lizards. (After França)                     154
  79  _Leucocytogregarina canis_, life-cycle. (After Christophers,
          from Castellani and Chalmers)                               155
  80  _Plasmodium vivax_, life-cycle. (After Schaudinn and Grassi)    160
  81  Malignant tertian malarial parasite in intestine of
          _Anopheles_. (After Grassi)                                 162
  82  Oökinete of malignant tertian malaria  in stomach of
          _Anopheles_. (After Grassi)                                 162
  83  Section of stomach of _Anopheles_ with malarial oöcysts.
          (After Grassi)                                              163
  84  Sporulation of malarial parasites in _Anopheles_.
          (After Grassi)                                              163
  85  Tertian malarial parasite in human red blood corpuscles.
          (After Mannaberg)                                           165
  86  Quartan malarial parasite in human red corpuscles.
          (After Manson)                                              166
  87  Malignant malarial parasite in human red corpuscles.
          (After Manson)                                              168
  88  Malarial crescents. (After Mannaberg)                           168
  89  Section through tubule of salivary gland of _Anopheles_
          infected with malarial sporozoites. (After Grassi)          169
  90  _Nuttallia equi_, life-cycle in red blood corpuscles.
          (After Nuttall and Strickland)                              173
  91  _Babesia_ (_Piroplasma_) _canis_, life-cycle in blood of dog.
          (After Nuttall and Graham-Smith)                            175
  92  _Theileria parva._ (After Nuttall and Fantham)                  179
  93  Myxosporidian spores and infected gill of fish.
          (After J. Müller)                                           181
  94  _Myxobolus mülleri_, spore. (After Bütschli)                    181
  95  _Myxobolus_, schema of spore. (After Doflein)                   182
  96  _Chloromyxum leydigi._ (After Thélohan)                         182
  97  _Myxobolus pfeifferi_, spore formation. (After Keysselitz,
          from Minchin)                                               183
  98  _Nosema apis._ (After Fantham and Porter)                       185
  99  _Nosema bombycis_ from silkworm. (After Balbiani)               186
  100  _Nosema bombycis_, spores. (After Thélohan)                    186
  101  _Hexactinomyxon psammoryctis_, spore. (After Stolč)            187
  103} _Sarcocystis miescheriana_ in muscle of pig. (After Kühn)      188
  104  _Sarcocystis miescheriana_, mature trophozoite                 189
  105  _Sarcocystis tenella_ in section, as seen in œsophagus
           of sheep                                                   190
  106  _Sarcocystis tenella_, young trophozoite. (After Bertram)      190
  107  _Sarcocystis miescheriana_, end portion of trophozoite.
           (After Bertram)                                            190
  108  _Sarcocystis blanchardi_ from ox. (From Wasielewski,
           after van Eecke)                                           190
  109  _Sarcocystis tenella._ (After Laveran and Mesnil)              191
  110  _Haplosporidium heterocirri._ (After Caullery and Mesnil)      195
  111  Haplosporidian spores. (After Caullery and Mesnil)             195
  112  _Rhinosporidium kinealyi_, portion of ripe cyst.
           (After Minchin and Fantham)                                197
  113  _Balantidium coli._ (After Leuckart)                           200
  114  _Balantidium coli_, free and encysted. (After Casagrandi
           and Barbagallo)                                            200
  115  _Balantidium minutum._ (After Schaudinn)                       204
  116  _Nyctotherus faba._ (After Schaudinn)                          205
  117  _Nyctotherus giganteus._ (After Krause)                        206
  118  _Nyctotherus africanus._ (After Castellani)                    206
  119  Trachoma bodies in conjunctival cells. (Original, Fantham)     209
  120  Half of a transverse section through _Fasciola hepatica_, L.   214
  121  _Harmostomum leptostomum_, Olss.                               215
  122  Median section through the anterior part of _Fasciola
           hepatica_                                                  217
  123  _Polystomum integerrimum._ (After Zeller)                      218
  124  _Allocreadium isoporum_, Looss. (After Looss)                  218
  125  Terminal flame cell of the excretory system. (Stephens)        219
  126  Diagram of female genitalia. (Stephens)                        220
  127  Diagram of male and part of female genitalia. (Stephens)       220
  128  Ovum of _Fasciola hepatica_, L.                                223
  129  Miracidium of _Fasciola hepatica_. (After Leuckart)            223
  130  A group of cercariæ of _Echinostoma_ sp.                       225
  131  Development of _Fasciola hepatica_, L. (After Leuckart)        226
  132  Young redia of _Fasciola hepatica_. (From Leuckart)            227
  133  Older redia of _Distoma echinatum_                             227
  134  Cercaria of _Fasciola hepatica_. (After Leuckart)              228
  135  Encysted cercaria of _Fasciola hepatica_. (After Leuckart)     228
  136  _Watsonius watsoni._ (After Shipley)                           234
  137  _Watsonius watsoni_: ventral projection composed from a
           series of transverse sections. (After Stiles and
           Goldberger)                                                235
  138  _Gastrodiscus hominis._ (After Leuckart)                       236
  139  _Fasciola hepatica_, L.                                        238
  140  _Fasciola hepatica_, showing the gut and its branches          239
  141  _Fasciola hepatica_, L. (After Claus)                          239
  142  _Fasciola hepatica_: egg from liver of sheep. (After Thomas)   240
  143  _Limnæus truncatulus_, Müll. (From Leuckart)                   240
  144  Young _Fasciola hepatica_. (From Leuckart)                     242
  145  _Fasciola gigantica._ (After Looss)                            243
  146  _Fasciolopsis buski_, Lank. (After Odhner)                     245
  147  _Fasciolopsis rathouisi_, Poir. (After Claus)                  246
  148  _Fasciolopsis fülleborni._ (After Fülleborn)                   248
  149  _Paragonimus ringeri_, Cobb. (After Katsurada)                 250
  150  _Paragonimus ringeri_, Cobb. (After Kubo)                      250
  150A _Paragonimus westermanii_, Kerb. (After Leuckart)              250
  151  Egg of _Paragonimus ringeri_, Cobb. (After Katsurada)          251
  152  Egg of _Opisthorchis felineus_                                 253
  153  _Opisthorchis felineus._ (After Stiles and Hassall)            253
  154  _Opisthorchis pseudofelineus._ (After Stiles)                  254
  155  _Parapisthorchis caninus._ (After Stephens)                    256
  156  _Amphimerus noverca_, Braun. (After McConnell)                 257
  157  _Metorchis conjunctus._ (After Cobbold)                        258
  158  _Clonorchis sinensis._ (After Looss)                           259
  159  Ova of _Clonorchis sinensis_. (After Looss)                    259
  160  _Clonorchis endemicus._ (After Looss)                          260
  161  _Clonorchis endemicus_: eggs. (After Looss)                    260
  162  _Metorchis truncatus_                                          262
  163  _Heterophyes heterophyes._ (After Looss)                       263
  164  _Metagonimus yokogawai._ (After Leiper)                        264
  165  _Dicrocœlium dendriticum_                                      265
  166  Eggs of _Dicrocœlium dendriticum_                              266
  167  Miracidia of _Dicrocœlium dendriticum_. (After Leuckart)       266
  168  _Echinostoma ilocanum._ (After Brumpt)                         268
  169  _Echinostoma ilocanum._ (After Leiper)                         268
  170  _Echinostoma malayanum_, Leiper. (After Leiper)                269
  171  _Schistosoma hæmatobium._ (After Looss)                        270
  172  Transverse section through a pair of _Schistosoma
           hæmatobium_ in copulâ. (After Leuckart)                    271
  173  Anterior end of the male _Schistosoma hæmatobium_.
           (After Looss)                                              271
  174  _Schistosoma hæmatobium._ (After Leuckart)                     276
  175  _Schistosoma hæmatobium_, ovum of. (After Looss)               277
  176  _Schistosoma japonicum._ (After Katsurada)                     278
  177  _Schistosoma japonicum._ (After Katsurada)                     279
  178  _Schistosoma japonicum._ (After Looss)                         279
  180} _Schistosoma japonicum_ from dog. (After Katsurada)            280
  182  _Schistosoma japonicum._ (After Catto)                         281
  183  _Schistosoma japonicum._ (After Katsurada)                     282
  184  Schematic representation of a small part of a transverse
           section of _Ligula_ sp. (After Blochmann)                  287
  185  Half of a transverse section through a proglottis of _Tænia
           crassicollis_                                              288
  186  _Dipylidium caninum._ (After Benham)                           289
  187  Longitudinal section of the head and neck of _Tænia
           crassicollis_                                              290
  188  _Tænia cœnurus._ (After Niemisec)                              291
  189  Young _Acanthobothrium coronatum_. (After Pintner)             292
  190  Scolex of a cysticercoid from _Arion_ sp. (After Pintner)      292
  191  Proglottis of _Tænia saginata_, Goeze, showing genitalia       293
  192  _Dibothriocephalus latus._ (After Benham and Sommer
           and Landois)                                               294
  193  Diagram of genitalia of a Cestode. (Stephens)                  295
  194  Part of a transverse section through a proglottis of
           _Dibothriocephalus latus_                                  296
  195  Egg of _Diplogonoporus grandis_. (After Kurimoto)              298
  196  Uterine egg of _Tænia saginata_. (After Leuckart)              298
  197  Oncosphere of _Tænia africana_ (after v. Linstow) and
           oncosphere of _Dipylidium caninum_. (After Grassi
           and Rovelli)                                               299
  198  Diagram of a cysticercoid. (Stephens)                          301
  199  Diagram of a cysticercus. (Stephens)                           301
  200  Diagram of development of a cysticercus. (Stephens)            303
  201  Section through a piece of a _Cœnurus cerebralis_              304
  202  Median section through a cysticercus. (After Leuckart)         304
  203  _Cysticercus pisiformis_ in an evaginated condition            304
  204  Various chains of segments of _Dibothriocephalus latus_        311
  205  Transverse section of the head of _Dibothriocephalus latus_    311
  206  Fairly mature proglottis of _Dibothriocephalus latus_          311
  207  _Dibothriocephalus latus._ (After Benham and Schauinsland)     312
  208  Plerocercoid of _Dibothriocephalus latus_                      313
  209  A piece of the body wall of the Burbot, _Lota vulgaris_        313
  210  Cephalic end of _Dibothriocephalus cordatus_. (After Leuckart) 315
  211  _Diplogonoporus grandis_, Lühe, 1899. (After Ijima and
           Kurimoto)                                                  317
  212  _Diplogonoporus grandis._ (After Ijima and Kurimoto)           317
  213  Cephalic end of _Sparganum mansoni_, Cobb. (After Leuckart)    318
  214  _Sparganum mansoni._ (After Ijima and Murata)                  318
  215  _Sparganum prolifer._ (After Ijima)                            319
  216  _Sparganum proliferum._ (After Stiles)                         319
  217  _Dipylidium caninum._ (After Diamare)                          320
  218  _Dipylidium caninum._ (After Benham and Moniez)                320
  219  _Dipylidium caninum_: central portion of a proglottis.
           (After Neumann and Railliet)                               321
  220  _Dipylidium caninum_: development of embryo. (After Benham,
           Grassi, and Rovelli)                                       321
  221  Larva (cysticercoid) of _Dipylidium caninum_. (After Grassi
           and Rovelli)                                               322
  222  _Hymenolepis nana_, v. Sieb. (After Leuckart)                  324
  223  _Hymenolepis nana_: head. (After Mertens)                      324
  224  _Hymenolepis nana_: an egg. (After Grassi)                     324
  225  Longitudinal section through the intestinal villus of a rat.
           (After Grassi and Rovelli)                                 324
  226  _Hymenolepis nana_ (_murina_): cross-section of proglottis
           from a rat. (After v. Linstow)                             325
  227  _Hymenolepis nana_: longitudinal section of an embryo.
           (After Grassi and Rovelli)                                 325
  228  _Hymenolepis diminuta._ (After Zschokke)                       326
  229  _Hymenolepis diminuta._ (After Grassi)                         326
  230  _Hymenolepis diminuta._ (After Bizzozero)                      326
  231  _Hymenolepis diminuta._ (Stephens, after Nicoll and Minchin)   327
  232  _Hymenolepis lanceolata._ (After Krabbe)                       328
  233  _Hymenolepis lanceolata._ (After Wolffhügel)                   328
  234  Scolex of _Davainea madagascariensis_. (After Blanchard)       330
  235  Two fairly mature proglottids of _Tænia solium_                332
  236  Head of _Tænia solium_      332
  237  Large and small hooks of _Tænia solium_. (After Leuckart)      333
  238  _Tænia solium._ (After Leuckart)                               333
  239  Two mature proglottids of _Tænia solium_                       333
  240  Large and small hooklets of _Tænia marginata_. (After
           Leuckart)                                                  338
  241  Mature segment of _Tænia saginata_                             339
  242  Cephalic end of _Tænia saginata_                               339
  243  _Tænia saginata._ (After Leuckart)                             339
  244  A piece of the muscle of the ox, with three specimens of
           _Cysticercus bovis_. (After Ostertag)                      340
  245  Mature segment of _Tænia africana_. (After v. Linstow)         342
  246  Proglottis of _Tænia africana_. (After v. Linstow)             343
  247  Head of _Tænia africana_. (After v. Linstow)                   343
  248  _Tania confusa._ (After Guyer)                                 344
  249  _Tania confusa._ (After Ward)                                  344
  250  _Tania echinococcus_                                           345
  251  _Echinococcus veterinorum._ (After Leuckart)                   347
  252 }
  252A} Diagrams of mode of formation of brood capsule and
           scolices (Stephens)                                        348
  253  Section through an invaginated echinococcus scolex.
           (After Dévé)                                               350
  254  A piece of the wall of an _Echinococcus veterinorum_
           stretched out and seen from the internal surface           350
  255  _Echinococcus hominis_ in the liver. (After Ostertag,
           from Thomas)                                               351
  256  Section through an echinococcus scolex in process of
           vesicular metamorphosis. (After Dévé)                      351
  257 }
  257A} Diagram of transformation of a scolex into a daughter
           cyst. (Stephens)                                           352
  258  Hooklets of echinococcus. (After Leuckart)                     355
  259  _Echinococcus multilocularis_ in the liver of the ox.
           (After Ostertag)                                           357
  260  Diagram of a transverse section of _Ascaris lumbricoides_.
           (After Brandes)                                            362
  261  Anterior end of an _Ascaris megalocephala_. (After Nassonow)   362
  262  Transverse section through _Ascaris lumbricoides_ at the
           level of the œsophagus behind the nerve ring.
           (After Goldschmidt)                                        364
  263  Schematic representation of the nervous system of a male
           _Ascaris megalocephala_. (After Brandes)                   365
  264  Diagram of female genitalia                                    368
  264A Diagram of male genitalia of a strongylid                      368
  265  Transverse section through the ovarian tube of _Belascaris
           cati_ of the cat                                           369
  266  Male of the rhabditic form of _Angiostomum nigrovenosum_       370
  267  Transverse section through the posterior extremity of the
           body of _Ascaris lumbricoides_ (male)                      370
  268  Hind end of a male _Ascaris lumbricoides_ cut across at the
           level of the dilator cells of the gut. (After Goldschmidt) 371
  269  A piece of the trunk muscle of the pig with encapsuled
           embryonic Trichinæ                                         373
  270  _Strongyloides stercoralis_, female. (After Looss)             380
  271  _Strongyloides stercoralis_, male. (After Looss)               380
  272  _Strongyloides stercoralis_, female. (After Looss)             382
  273  _Strongyloides stercoralis._ (After Looss)                     382
  274  _Strongyloides stercoralis._ (After Looss)                     383
  275  _Gnathostoma siamense._ (After Levinsen)                       385
  276  Guinea worm (_Dracunculus medinensis_). (After Leuckart)       387
  277  Anterior extremity of Guinea worm. (After Leuckart)            387
  278  _Dracunculus medinensis._ (After Claus)                        387
  279  Transverse section of female Guinea worm. (After Leuckart)     388
  280  _Cyclops virescens_, female                                    389
  281  _Filaria bancrofti._ (After Leiper)                            391
  282  _Mf. bancrofti_ in thick film, dried and stained with
           hæmatoxylin. (After Fülleborn)                             397
  283  Schematic drawings of the anatomy of _Ml. loa_ and _Mf.
           bancrofti_. (After Fülleborn)                              399
  284  _F. demarquayi._ (After Leiper)                                403
  285  _Mf. demarquayi_ in thick film, dried and stained with
           hæmatoxylin. (After Fülleborn)                             404
  286  _Filaria_ (?) _conjunctivæ_. (After Addario)                   405
  287  _Filaria_ (?) _conjunctivæ_. (After Grassi)                    405
  288  _Setaria equina._ (After Railliet)                             408
  289  _Setaria equina_: anterior end. (After Railliet)               408
  290  _Loa loa_: the anterior end of the male. (After R. Blanchard)  410
  291  _Loa loa_: anterior portion of the female. (After Looss)       410
  292  _Loa loa_ in situ. (After Fülleborn and Rodenwaldt)            410
  293  _Loa loa_: male and female. (After Looss)                      410
  294  _Loa loa_: the hind end of a male and of a female.
           (After Looss)                                              411
  295  _Loa loa_: lateral view of tail of male showing papillæ.
           (After Lane and Leiper)                                    411
  296  _Loa loa._ (After Leiper)                                      411
  297  _Mf. loa_: in thick film, dried and stained with hæmatoxylin.
           (After Fülleborn)                                          413
  298  _Acanthocheilonema perstans._ (After Leiper)                   414
  299  _Mf. perstans._ (After Fülleborn)                              415
  300  _Dirofilaria magalhãesi._ (After v. Linstow)                   417
  301  _Trichuris trichiura_                                          420
  302  _Trichinella spiralis._ (After Claus)                          422
  303  Isolated muscular fibre of a rat, invaded by Trichinella.
           (After Hertwig-Graham)                                     425
  304  Calcified Trichinella in the muscular system of a pig.
           (After Ostertag)                                           426
  305  Various phases of the calcification of Trichinella of
           the muscles                                                426
  306  _Dioctophyme gigas._ (After Railliet)                          432
  307  Eggs of _Dioctophyme gigas_. (After Railliet)                  432
  308  _Metastrongylus apri._ (Stephens)                              433
  310} _Trichostrongylus instabilis._ (After Looss)                   434
  312} _Trichostrongylus probolurus._ (After Looss)                   435
  314} _Trichostrongylus vitrinus._ (After Looss)                     436
  316} _Hæmonchus contortus._ (After Ransom)                          437
  317  _Mecistocirrus fordi._ (After Stephens)                        439
  318  _Ternidens deminutus._ (After Railliet and Henry)              440
  320} _Œsophagostomum stephanostomum_ var. _thomasi_.
           (After Thomas)                                             442
  322} _Œsophagostomum stephanostomum_ var. _thomasi_.
           (After Thomas)                                             444
  324} _Ancylostoma duodenale_, male and female. (After Looss)        446
  325  _Ancylostoma duodenale_, showing ventral teeth. (After Looss)  447
  326  _Ancylostoma duodenale_: diagrammatic representation of
           excretory system. (After a drawing by Looss)               448
  327  _Ancylostoma duodenale._ (After Railliet)                      449
  328  _Ancylostoma duodenale_: bursa of male. (After Looss)          450
  329  _Ancylostoma duodenale_: eggs in different stages of
           development. (After Looss)                                 451
  330  _Ancylostoma duodenale_: larva. (After Leichtenstern)          452
  331  _Ancylostoma duodenale._ (After Looss)                         453
  332  _Ancylostoma ceylanicum._ (After Looss)                        456
  333  _Ancylostoma braziliense._ (After Gomez de Faria)              456
  334  _Necator americanus._ (After Looss)                            457
  335  _Necator americanus_: lateral view. (After Looss)              458
  336  _Necator americanus_: bursa of male. (After Looss)             458
  337  _Syngamus kingi_: anterior end of male. (After Leiper)         460
  338  _Syngamus kingi_: anterior end of female. (After Leiper)       460
  339  Bursa of _Syngamus trachealis_. (Stephens)                     461
  340  _Physaloptera mordens_, Leiper, 1907. (After Leiper)           462
  341  _Ascaris lumbricoides._ (From Claus)                           463
  342  Ovum of _Ascaris lumbricoides_                                 463
  343  Ovum of _Toxascaris limbata_                                   466
  344  Transverse section through the head part of _Belascaris
           cati_ from the cat. (After Leuckart)                       466
  346} Male female of _Oxyuris vermicularis_                          468
  347  _Oxyuris vermicularis_: egg freshly deposited                  468
  348  _Oxyuris vermicularis_: egg twelve hours after deposition      468
  348A The male of _Echinorhynchus augustatus_                        476
  348B Anterior portion of the female apparatus of _Echinorhynchus
           acus_. (After Wagener)                                     476
  348C Egg of _Echinorhynchus gigas_. (After Leuckart)                477
  348D The internal organs of the leech. (After Kennel)               480
  348E _Hirudo medicinalis._ (After Claus)                            481
  349  _Leptus autumnalis._ (After Gudden)                            485
  350  _Leptus autumnalis._ (After Trouessart)                        485
  351  The kedani mite. (After Tanaka)                                487
  352  _Tetranychus telarius_ var. _russeolus_, Koch.
           (After Artault)                                            488
  353  _Pediculoides ventricosus._ (After Laboulbène and Mégnin)      489
  354  _Nephrophages sanguinarius_: male, ventral surface.
           (After Miyake and Scriba)                                  490
  355  _Nephrophages sanguinarius_: female, dorsal aspect.
           (After Miyake and Scriba)                                  490
  356  _Tydeus molestus._ (After Moniez)                              491
  357  _Dermanyssus gallinæ._ (After Berlese)                         492
  358  _Dermanyssus hirundinis._ (After Delafond)                     492
  359  _Ixodes ricinus_, male. (After Pagenstecher)                   498
  360  Female of _Ixodes ricinus_. (After Pagenstecher)               498
  361  _Argas reflexus._ (After Pagenstecher)                         506
  362  _Argas persicus._ (After Mégnin)                               507
  363  _Tyroglyphus farinæ_: male. (After Berlese)                    512
  364  _Tyroglyphus longior_, Gerv. (After Fum. and Robin)            512
  365  _Rhizoglyphus parasiticus_: male and female. (After Dalgetty)  514
  366  _Histiogaster_ (_entomophagus_ ?) _spermaticus_.
           (After E. Trouessart)                                      515
  367  _Sarcoptes scabiei._ (After Fürstenberg)                       518
  368  _Sarcoptes scabiei_: male, ventral aspect.
           (After Fürstenberg)                                        519
  369  _Sarcoptes minor_ var. _cati_. (After Railliet)                521
  370  _Demodex folliculorum_ of the dog. (After Mégnin)              522
  371  _Linguatula rhinaria_: female                                  524
  372  Larva of _Linguatula rhinaria_ (_Pentastoma denticulatum_).
           (After Leuckart)                                           524
  373  _Linguatula rhinaria._ (After M. Koch)                         525
  374  Mouth-parts of _Pediculus vestimenti_. (After Denny)           533
  375  Ovum of the head louse                                         533
  376  Head louse, male                                               533
  377  _Pediculus vestimenti_, Burm.: adult female                    533
  378  _Phthirius inguinalis_, Leach                                  534
  379  Head of the bed bug from the ventral surface                   535
  380  _Dermatophilus penetrans_: young female. (After Moniez)        544
  381  _Dermatophilus penetrans_: older female. (After Moniez)        544
  382  _Pulex irritans_                                               546
  383  Larva of flea. (After Railliet)                                546
  384  _Pulex serraticeps_                                            546
  385  Head of a male and of a female Anopheles. (After Giles)        549
  386  Head of a male and of a female Culex. (After Giles)            549
  387  Mouth-parts of _Anopheles claviger_. (After Grassi)            550
  388  _Anopheles maculipennis._ (After Nuttall and Shipley)          550
  389  Longitudinal section of an Anopheles, showing alimentary
           canal. (After Grassi)                                      551
  390  _Anopheles maculipennis_, Meigen. (After Grassi)               552
  391  Larva of _Anopheles maculipennis_, Fabr. (After Grassi)        553
  392  Larva of Culex. (After Grassi)                                 553
  393  Pupa of _Anopheles maculipennis_, Meig. (After Grassi)         554
  394  Heads of Culex and Anopheles. (After Daniels)                  556
  395  Eggs of Culex, of Anopheles, of Stegomyia, of Tæniorhynchus,
           and of Psorophora                                          557
  396  Diagram showing the structure of a typical mosquito.
           (Theobald)                                                 558
  397  Types of scales, head and scutellar ornamentation, forms of
           clypeus. (Theobald, etc., etc.)                            559
  398  Neuration of wing. Explanation of wing veins and cells.
           (Theobald)                                                 560
  399  Wing of _Anopheles maculipennis_, Meigen                       566
  400  Wing of a Culex                                                575
  401  Wing of Simulium                                               579
  402  Wing of Chironomus                                             579
  403  A Ceratopogon, or midge                                        580
  404  An owl midge, _Phlebotomus_ sp. (From Giles’s “Gnats or
           Mosquitoes”)                                               581
  405  Larva of _Homalomyia canicularis_                              585
  406  Larvæ of _Calliphora vomitoria_                                585
  407  Larva of _Chrysomyia macellaria_. (After Conil)                585
  408  The screw-worm fly (_Chrysomyia macellaria_)                   587
  409  Ochromyia larva on the skin of man, South Africa.
           (After Blanchard)                                          590
  410  Head end of “larva of Natal.” (After Gedoelst)                 591
  411  Lund’s larva. (After Gedoelst)                                 593
  412  _Dermatobia noxialis_, Goudot                                  597
  413  Larva of _Dermatobia cyaniventris_. (After Blanchard)          597
  414  Larva of _Dermatobia cyaniventris_. (After Blanchard)          597
  415  The ox gad fly (_Tabanus bovinus_, Linn.)                      601
  416  The brimp (_Hæmatopota pluvialis_, Linn.)                      602
  417  Head of _Glossina longipalpis_. (After Grünberg)               604
  418  Antenna of _Glossina pallidipes_, male. (After Austen)         604
  419  _Glossina palpalis_ and puparium. (After Brumpt)               607
  420  The tsetse-fly (_Glossina morsitans_, Westwood)                608
  421  The stinging fly (_Stomoxys calcitrans_, Linn.)                609
  422  _Trichomonas_ from cæcum and gut of rat. (Original, Fantham)   735
  423  _Chilomastix_ (_Tetramitus_) _mesnili._ (Original, Fantham)    736

  |We regret to have taken without permission from the “Transactions of|
  |The Society of Tropical Medicine and Hygiene,” London, the following|
  |diagrams:--                                                         |
  |                                                                    |
  |     Pages     Figures                                              |
  |     268      No. 169                                               |
  |     269       "  170                                               |
  |     391       "  281                                               |
  |     411       "  295 and 296                                       |
  |     414       "  298                                               |
  |     460       "  337 and 338                                       |
  |                                                                    |
  |and tender our regret to the Society in question for having done so.|


  P. 31, line 6 from bottom: _delete_ “human,” as Leidy really worked
      with _Endamœba blattæ_, parasitic in the gut of the cockroach.
  P. 43, line 12 from bottom: _for_ “John’s” _read_ “Johns.”
  P. 44, line 13 from bottom: _for_ “_Amœba buccalis_, Sternberg,” _read_
      “_Amœba buccalis_, Steinberg.”
  P. 46, line 13 from top: _for_ “breath” _read_ “breadth.”
  P. 53, In footnote ^1, line 6 from bottom: _insert_ “see” before _Arch.
      f. Protistenk_.
  P. 75: To paragraph regarding development of the parasite in the fly’s
      salivary glands, _add_ that the crithidial phase takes two to five
  P. 111, line 8 from top: the date of Sangiorgi should be 1911.
  P. 142, line 7 from top: _insert_ “Genus.” before *Eimeria*.
  P. 252, _Insert_ heading “Family. *Opisthorchiidæ*, Braun, 1901,”
      _above_ “Sub-family. *Opisthorchiinæ*, Looss, 1899.”
  P. 351, description of fig. 255, line 3: _for_ “Thoma” _read_ “Thomas.”
  P. 471, line 15 from bottom: _for_ “alcohol 100 parts” _read_ “alcohol
      100 c.c.”
  P. 472, line 11 from bottom: _for_ “Or (2) 10 _per cent. formalin_,”
      _read_ “Or (2) _fix in hot_ 10 _per cent. formalin_.”
  P. 493, line 21 from top: _for_ “Conoy” _read_ “Couvy.”
  P. 589, line 2 from top: _for_ “*carnosa*” _read_ “*carnaria*.”
  P. 620, line 15 from top: _for_ “fo” _read_ “of.”
  P. 622, line 12 from bottom: _delete_ comma after quantity.
  P. 626, line 6 from bottom: _delete_ comma after Mackie (1915).
  P. 638: _insert_ title “*TREMATODES*” above that of “Fascioliasis.”
  P. 709, line 9 from bottom: _omit_ second Pediculus capitis.
  P. 748, line 8 from top: _for_ “cytologica” _read_ “cytological.”
  P. 753, line 4 from bottom: _for_ “*Fercocercous*” _read_
  P. 755 line 7: _for_ “*Oncocerca*” _read_ “*Onchocerca*.”


By the term PARASITES is understood living organisms which, for
the purpose of procuring food, take up their abode, temporarily or
permanently, on or within other living organisms. There are both plants
and animals (Phytoparasites and Zoöparasites) which lead a parasitic
life in or upon other plants and other animals.

Phytoparasites are not included in the following descriptions of the
forms of parasitism, but a very large number of animal parasites
(zoöparasites) are described. The number of the latter, as a rule, is
very much underrated. How great a number of animal parasites exists
may be gathered from the fact that all classes of animals are subject
to them. Some of the larger groups, such as _Sporozoa_, _Cestoda_,
_Trematoda_ and _Acanthocephala_, consist entirely of parasitic
species, and parasitism even occurs among the vertebrates (_Myxine_).
It therefore follows that the characteristics of parasites lie, not in
their structure, but in the manner of their existence.

Parasitism itself occurs in various ways and degrees. According to
R. Leuckart, we should distinguish between OCCASIONAL (temporary)
and PERMANENT (stationary) PARASITISM. Occasional parasites, such as
the flea (_Pulex irritans_), the bed-bug (_Cimex lectularius_), the
leech (_Hirudo medicinalis_), and others, only seek their “host” to
obtain nourishment and find shelter while thus occupied. Without being
bound to the host, they usually abandon the latter soon after the
attainment of their object (_Cimex, Hirudo_), or they may remain on
the body of their host throughout their entire development from the
hatching of the egg (_Pediculus_). It follows from this mode of living
that the occasional parasites become sometimes distinguishable from
their free-living relatives, though only to a slight extent. It is,
therefore, seldom difficult to determine the systematic position of
temporary parasites from their structure.

In consequence of their mode of life, all these temporary parasites
live on the external surface of the body of their host, though more
rarely they take up their abode in cavities easily accessible from
the exterior, such as the mouth, nose and gills. They are therefore
frequently called EPIZOA or ECTOPARASITES; but these designations do
not cover only the temporary parasites, because numerous epizoa (as for
instance the louse) are parasitic during their entire life.

In contradistinction to these temporary parasites, the permanent
parasites obtain shelter as well as food from their host for a long
period, sometimes during the entire course of their life. They do not
seek their host only when requiring nourishment, but always remain with
it, thus acquiring substantial protection. The permanent parasites,
as a rule, live within the internal organs, preferably in those which
are easily accessible from the exterior, such as the intestine, with
its appendages. Nevertheless, permanent parasites are also found in
separate organs and systems, such as the muscular and vascular systems,
hollow bones and brain, while some live on the outer skin. Here again,
the terms ENTOZOA and ENDOPARASITES do not include all stationary
parasites; to the latter, for instance, the lice belong, which pass
all their life on the surface of the body of their host, where they
find shelter and food and go through their entire development. The
ectoparasitic trematodes, numerous insects, crustacea, and other
animals live in the same manner.

All “HELMINTHES,” however, belong to the group of permanent parasites.
This term is now applied to designate certain lowly worms which lead
a parasitic life (intestinal worms); but they are not all so termed.
For instance, the few parasitic TURBELLARIA are never classed with
the helminthes, although closely related to them. The turbellarians,
in fact, belong to a group of animals of which only a few members are
parasitic, whereas the helminthes comprise those groups of worms of
which all species (_Cestoda_, _Trematoda_, _Acanthocephala_), or at
least the majority of species (_Nematoda_), are parasitic. Formerly the
Linguatulidæ (_Pentastoma_) were classed with the helminthes because
their existence is also endoparasitic, and because the shape of their
body exhibits a great similarity to that of the true helminthes. Since
the study of the development of the Linguatulidæ (P. J. van Beneden,
1848, and R. Leuckart, 1858) has demonstrated that they are really
degenerate arachnoids, they have been separated from the helminthes.

It is hardly necessary to emphasize the fact that the helminthes or
intestinal worms do not represent a systematic group of animals, but
only a biological one, and that the helminthes can only be discussed
in the same sense as land and water animals are mentioned, _i.e._,
without conveying the idea of a classification in such a grouping. It
is true that formerly this was universally done, but very soon the
error of such a classification was recognized. Still, until the middle
of last century, the helminthes were regarded as a systematic group,
although C. E. v. Baer (1827) and F. S. Leuckart (1827) strenuously
opposed this view. Under the active leadership of J. A. E. Goeze,
J. G. H. Zeder, J. G. Bremser, K. A. Rudolphi and F. Dujardin, the
knowledge of the helminthes (helminthology) developed into a special
study, but unfortunately it lost all connection with zoology. It
required the intervention of Carl Vogt to disestablish the helminthes
as one class of animals, by uniting the various groups with those of
the free-living animals most closely related to them (_Platyhelminthes,

PERMANENT PARASITISM in the course of time has caused animals adopting
this mode of life to undergo considerable, sometimes even striking,
bodily changes, permanent ectoparasites having as yet undergone least
alteration. The latter sometimes bear so unmistakably the likeness to
the group to which they belong, that even a superficial knowledge of
their structure and appearance often suffices for the recognition of
their systematic position. For instance, though the louse, like many
decidedly temporary parasites, has lost its wings--a characteristic of
insects--in consequence of parasitism, yet nobody would deny its insect
nature; such also occurs in other temporary parasites (_Cimex, Pulex_).
On the other hand, the changes in a number of permanent ectoparasites
(such as parasitic Crustacea) are far more considerable, and correspond
with those that have occurred in permanent endoparasites.

These alterations depend partly on retrogression and partly on the
acquisition of new peculiarities. In the former case, the change
consists in the loss of those organs which have become useless in a
permanent parasitic condition of existence, such as wings in the louse,
and the articulated extremities seen in the larval stage of parasitic
Crustacea. The loss of these organs goes hand in hand with the cohesion
of segments of the body that were originally separate, and alterations
in the muscular and nervous systems. In the same manner another means
of locomotion is lost--the ciliated coat--which is possessed by many
permanent parasites during their larval period. To all appearances,
this character is not secondary and recently acquired, but represents
a primary character inherited from free-living progenitors, and still
transmitted to the altered descendants, because of its use during
the larval stage (_e.g._, the larvæ of a great many Trematodes, the
oncospheres of some Cestodes). Amongst the retrogressions, the loss of
the organs of sense may be mentioned, particularly the eyes, which are
still present, not only in the nearest free-living forms but also in
the free-living larvæ of true parasites. It is only quite exceptionally
that the eyes are subsequently retained, as a rule they are lost.
Lastly, in a great many cases the digestive system also disappears,
as in parasitic Crustacea, in a few nematodes and trematodes, in all
cestodes and Acanthocephala. There remain at most the rudiments of the
muscles of the fore-gut, but these are adapted to entirely different

The new characters which permanent parasites may acquire are, first
of all, the remarkably manifold CLASPING and CLINGING ORGANS, which
are seldom (as in parasitic Crustacea) directly joined on to already
existing structures. In those instances in which organs for the
conveyance of food are retained, these likewise frequently undergo
transformation, in consequence of the altered food and manner of
feeding. Such alterations consist, for instance, in the transformation
of a masticating mouth apparatus into the piercing and sucking organs
of parasitic insects.

HERMAPHRODITISM (as in Trematodes, Cestodes, and a few Nematodes)
is a further peculiarity of many permanent parasites; moreover, the
association in couples that occurs, especially in trematodes, may
lead to complete cohesion and, exceptionally, also to re-separation
of the sexes. In many cases the females only are parasitic, while the
males live a free life, or there may be in addition the so-called
complementary males. Occasionally the male alone is parasitic, and in
that case lives within the female of the same species, which may live
free, like certain Gephyrea (_Bonellia_); or the female also may be
parasitic, as _Trichosoma crassicaudum_, which lives in the bladder of
the sewer rat (_Mus decumanus_).

We have numerous proofs that demonstrate how considerably the original
features of many parasites have become changed. We need only draw
attention to the aforementioned Linguatulidæ, also to many of the
parasitic Crustacea belonging to various orders. In all of these a
knowledge of the larval stages--in which there is no alteration, or
at most only a slight degree of change--serves to determine their
systematic position, _i.e._, the nearest conditions of relationship.

The most remarkable changes are observed in those groups that contain
only a few parasitic members, the majority leading a free life. A
striking instance is afforded by a snail, the well-known _Entoconcha
mirabilis_, Müller. This mollusc consists merely of an elongated sac
living in a Holothurian (_Synapta digitata_). It possesses none of
the characteristics of either the Gastropoda or any molluscs, and
in its interior there is nothing to be observed but the organs of
generation and the embryos. Nevertheless, the _Entoconcha_ is decidedly
a parasitic snail, as is clearly proved by its larvæ, but it is a snail
which, in consequence of parasitism, has lost all the characteristics
of molluscs in its mature condition, but still exhibits them in the
early stages of development.

Certain nematodes show very clearly to what devious courses parasitism
may lead. The _Atractonema gibbosum_, the life-history of which has
been described by R. Leuckart, and which lives in the larvæ and pupæ of
a dipterous insect (_Cecidomyia_), exhibits, in its early stage, the
ordinary characteristics of other threadworms. A few weeks later--the
males having died off immediately after copulation--the females are
transformed into spindle-shaped bodies, the mouth and anus of which are
closed. They carry with them an irregularly shaped appendage, in which
the segmenting ova are situated, and in which the further conditions of
life of the _Atractonema_ are accomplished. A minute examination has
demonstrated that this appendage is the prolapsed and enlarged vagina
of the animal which has become merely a supplementary attachment. The
conditions present in the _Sphærularia_, the nematoid nature of which
was long undiscovered, are still more remarkable. It was only when
Siebold proved that typical nematodes were hatched from their eggs that
their nature was recognized. The nematodes thus produced have not the
slightest resemblance to the parent.

The researches of Lubbock, A. Schneider, and more particularly of R.
Leuckart, have shown that what we call _Sphærularia bombi_ is not
an animal but merely an organ--the vagina--of a nematode worm. This
vagina at first grows, sac-like, from the body of the tiny nematode; it
gradually assumes enormous dimensions (2 cm. in length); it contains
the sexual organs and parts of the intestine. The remaining portion of
the actual animal then becomes small and shrivelled; it may be easily
overlooked, being but an appendage to the vagina with its independent
existence, and it finally disappears altogether.

The GREAT FERTILITY of parasites is another of their peculiarities,
though this may be also the case to a certain degree with some of the
free-living animals, the progeny of which are likewise exposed to
enormous destruction.

More remarkable, however, is the fact that the young of the
endoparasites only very exceptionally grow to maturity by the side
of their parents. Sooner or later they leave the organ inhabited by
the parents, frequently reach the open, and after a shorter or longer
period of free existence seek new hosts. During their free period,
moreover, a considerable growth may be attained, or metamorphosis
may take place, or even multiplication. In the exceptional cases in
which the young remain within the same host, they nevertheless usually
quit the organ inhabited by the parents. They likewise rarely attain
maturity within the host inhabited by the parents, but only, as in
other cases, after having gained access to fresh hosts.

These transmigrations play a very important _rôle_ in the natural
history of the internal parasites, but they frequently conceal the
cycle of development, for sometimes there are INTERMEDIATE GENERATIONS,
which themselves invade intermediate hosts. Even when there are
no intermediate generations, THE SYSTEM OF INTERMEDIATE HOSTS is
frequently maintained by the endoparasites.

According to the kind of food ingested by parasites, it has recently
become usual to separate the true parasites from those animals that
feed on the superfluity of the food of the host, or on products which
are no longer necessary to him, and to call the latter MESSMATES or
COMMENSALS. As examples, the Ricinidæ are thus designated, because,
like actual lice, they dwell among the fur of mammals or the plumage
of birds. They do not, however, suck blood, for which their mouth
apparatus is unsuited, but subsist on useless epidermic scales.
These epizoa, according to J. P. van Beneden, are, to a certain
extent, useful to their hosts by removing deciduous materials which
under certain circumstances might become harmful to them.[1] This
investigator, who has contributed so greatly to our knowledge of
parasites, assigns the Ricines to the MUTUALISTS, under which term
he comprises animals of various species which live in common, and
confer certain benefits on one another. The mutualists are usually
intimately connected in a mutually advantageous association known as

[1] According to Sambon, the Ricinidæ are by no means advantageous to
their hosts. These Hemipterous parasites give rise to an intolerable
itching which may cause loss of rest, emaciation, and sometimes even
death. Birds suffering from phthiriasis of the Ricines are usually in
bad health.

[2] For further information on these conditions, see “Die Schmarotzer
des Thierreichs,” by P. J. van Beneden, Leipzig, 1876; and “Die
Symbiose,” by O. Hertwig.

_Incidental and Pseudo Parasites._--In many cases the parasites
are confined to certain hosts, and may therefore be designated as
_specific_ to such hosts. Thus, hitherto, _Tænia solium_ and _Tænia
saginata_ in their adult condition have only been found in man; _Tænia
crassicollis_ only in the cat; _Brandesia_ (_Distoma_) _turgida_ and
_Halipegus_ (_Distoma_) _ovocaudatas_ only in _Rana esculenta_, and so
forth. In many other cases, however, certain species of parasites are
common to several, and sometimes many, species of hosts; _Dipylidium
caninum_ is found in the domestic cat as well as in the dog; _Fasciola
hepatica_ is found in a large number of herbivorous mammals (nineteen
species), _Diplodiscus_ (_Amphistomum_) _subclavatus_ in numerous
urodele and ecaudate amphibia, _Holostomum variabile_ in about
twenty-four species of birds, and so on. In these cases the hosts
are almost invariably closely related, belonging, as a rule, to the
same family or order, or at any rate to the same class. _Trichinella
spiralis_, which is found in man, and in the pig, bear, rat, mouse,
cat, fox, badger, polecat and marten, and is capable of being
artificially cultivated in the dog, rabbit, sheep, horse, in other
mammals, and even in birds, is one of the most striking exceptions.

Some parasites are so strictly confined to one species of host that,
even when artificially introduced into animals very closely related
to their normal host, they do not thrive, but sooner or later, often
very quickly, die off, and very rarely establish themselves. For
example, repeated attempts have been made to rear the adult _Tænia
solium_ in the dog, or to rear _Cysticercus cellulosæ_ in the ox,
or the _Cysticercus_ of _Tænia saginata_ in the pig, but they have
always proved unsuccessful. Only exceptionally has it been possible
to transfer _Cœnurus cerebralis_, the larval stage of a tapeworm
(_Tænia cœnurus_) of the dog from the brain of the sheep to that of
the domestic goat. On the other hand, in the case of the Trichinellæ
transference to a different host is easily accomplished.

Under natural conditions, it is not uncommon for certain kinds of
specific parasites to occur occasionally in unusual hosts. Their
relationship to the latter is that of INCIDENTAL PARASITES. Thus
_Echinorhynchus gigas_, a specific parasite of the pig, is only an
incidental parasite of man; _Fasciola hepatica_ and _Dicrocœlium
lanceatum_ are specific to numerous kinds of mammals, but may be found
incidentally in man. On the other hand, _Dibothriocephalus latus_, a
specific parasite of man, may occasionally take up its abode in the
dog, cat and fox. As a rule, all those parasites of man that are only
rarely met with, notwithstanding that human beings are constantly being
observed and examined by medical men, are termed INCIDENTAL PARASITES
OF MAN. In many cases we are acquainted with the normal or specific
host of these parasites. Thus we know the specific host of _Balantidium
coli_, _Eimeria stiedæ_, _Fasciola hepatica_, _Dipylidium caninum_,
etc.; in others the host is as yet unknown. In the latter case the
question partly relates to such forms as have been so deficiently
described that their recognition is impossible, partly to parasites
of man in various regions of the earth, the Helminthes and parasites
of which are totally unknown or only slightly known, or finally to
early developmental stages that are difficult to identify. Animals
that usually live free, and exceptionally become parasitic, may
likewise be called incidental parasites. In this category are included
a few _Anguillulidæ_ that have been observed in man; also _Leptodera
appendiculata_, which usually lives free, but may occasionally become
parasitic in black slugs (_Arion empiricorum_): when parasitic it
attains a larger size, and produces far more eggs than when living a
free life. In order to avoid errors, the term “incidental parasites”
should be confined to true parasites which, besides living in their
normal host, may also live in other hosts. Leuckart speaks of
FACULTATIVE PARASITISM in such forms as _Leptodera_. L. Oerley[3]
succeeded in artificially causing _Leptodera_ (_Rhabditis_) _pellio_
to assume facultative parasitism by introducing these worms into the
vagina of mice, where the parasites remained alive and multiplied.
_Leptodera pellio_ dies in the intestines of mammals and man; it
remains alive in frogs, but always escapes into the open with the fæces.

[3] Oerley, L., “Der Rhabditiden und ihre medizinische Bedeutung,”
Berlin, 1886, p. 65.

Recently the incidental parasites of man have also been called
“PSEUDO-PARASITES” or “PSEUDO-HELMINTHES.” Formerly, however, these
terms were applied not only to living organisms that do not and cannot
live parasitically, and that only exceptionally and incidentally get
into man, but also to any foreign bodies, portions of animals and
plants, or even pathological formations that left the human system
through the natural channels, and the true nature of which was
misunderstood. Frequently these bodies were described as living or
dead parasites and labelled with scientific names, as if they were
true parasites. A study of these errors, which formerly occurred very
frequently, would be as interesting as it would be instructive. It
is better not to use the expression pseudo-parasites for incidental
parasites, but to keep to the original meaning, for it is not at all
certain that pseudo-parasites are not described, even nowadays.

_The Influence of Parasites on the Host._--In a great many cases, we
are not in a position to state anything regarding any marked influence
exercised by the parasite on the organism, and on the conditions of
life, of the host. Most animals and many persons exhibit few signs of
such influence, an exception being infestation with helminthes and
certain other parasites which produce eosinophilia in the blood. As a
general rule, the parasite, which is always smaller and weaker than
its host, does not attempt to endanger the life of the latter, as
simultaneously its own existence would be threatened. The parasite,
of course, robs its host, but usually in a scanty and sparing manner,
and the injuries it inflicts can hardly be taken into account. There
are, however, numerous cases[4] in which the situation of the parasites
or the nature of their food, added to their number and movements, may
cause more or less injury, and even threaten the life of the host.
It stands to reason that a _Cysticercus cellulosæ_ situated in the
skin is of but slight importance, whereas one that has penetrated the
eye or the brain must give rise to serious disorders. A cuticular or
intestinal parasite is, as a rule, less harmful than a blood parasite.
A helminth, such as an _Ascaris lumbricoides_ or a tapeworm, that feeds
on the residues of foodstuffs within the intestine, will hardly affect
its host by depriving it of this material. The case is different when
the parasites are very numerous, especially when the heavily infested
host happens to be a young individual needing all it ingests for its
own requirements, and therefore unable to sustain the drain of numerous
intruders in the intestine. Disturbances also set in more rapidly when
the intestinal helminthes are blood-suckers, the injury to the host
resulting from the kind of food taken by the parasite.

[4] Lühe, M., “Ueber d. Fix. d. Helm. a. d. Darmwand ihrer Wirthe u.
die dadurch verursachten path-anat. Veränderungen d. Wirthsdarmes,”
_Trans. of IVth Intern. Zool. Cong._, Berlin, 1901; Mingazzini, P.,
“Ric. sul var. modo di fiss. delle tenie alla par. int. e sul loro
assorbimento,” _Ric. Lab. Anat. Roma e altri Lab. biol._, vol. x,
1904; Shipley, A. E., and E. G. Fearnsides, “The Effects of Metazoan
Parasites on their Hosts,” _Journ. Econ. Biol._, 1906, i, 2.

Generally, the disorders caused by loss of chyle are insignificant
when compared with those induced by the GROWTH and agglomeration of
the helminthes. The latter may cause chiefly obstructions of small
vessels or symptoms of pressure in affected or contiguous organs, with
all those complications which may arise secondarily, or they may even
lead to the complete obliteration of the organ invaded. Of course the
symptoms will vary according to the nature of the organ attacked.

In consequence also of the MOVEMENTS of the parasites, disorders are
set up that may tend to serious pathological changes of the affected
organs. The collective migrations, undertaken chiefly by the embryos
of certain parasites (as in trichinosis, acute cestode tuberculosis),
are still more harmful, as are also the unusual migrations of other
parasites, which, incidentally, may lead to the formation of so-called
worm abscesses or to abnormal communications (fistulæ) between organs
that are contiguous but possess no direct connection.

Recently, several authors have called attention to the fact that the
helminthes produce substances that are TOXIC to their host; and the
effects of such poisons explain the pathology of helminthiasis far more
satisfactorily than the theory of reflex action.

In a number of cases these toxic materials (leucomaines) have been
isolated and their effects on living organisms demonstrated by actual
experiments. It also appears that the absorption of materials formed by
the decomposition of dead helminthes may likewise cause toxic effects.
However, our knowledge of these conditions is as yet in its initial

[5] Moursson et Schlagdenhauffen, “Nouv. rech. clin. et phys. sur
quelq. liquides organ.,” _C. R. Acad. Sci._, Paris, 1882, p. 791;
Debove, “De l’intox. hydat.,” _Bull. et Mém. Soc. méd. des Hôpit._,
1888; Linstow, v., “Ueb. d. Giftgehalt d. helm.,”_Internat. Monatsschr.
f. Anat. u. Phys._, xiii, 1896; Peiper, “Z. Symptomatol. der thier.
Paras.,” _Deutsche med. Wochenschr._, 1897, No. 40; Mingazzini, P.,
“Ric. sul veleno d. elm. int.,” _Rass. intern. d. med. modern. Ann._,
1901, ii, No. 6; Vaullegeard, A., “Etud. exp. et crit. sur l’action d.
helm.,” _Bull. Soc. Linn. de Normandie_, 1901, 5, Ser. T, vii, p. 84,
and others.

Nearly all the symptoms caused directly or indirectly by parasites are
of such a nature that the presence of the parasites cannot be diagnosed
with any certainty, or only very rarely. The most that can be done is
to deduce the presence of parasites by the exclusion of other causes.
Fortunately, however, there are sufficient means by which we may
confirm the diagnosis in a great many cases. Such means consist not
only in a minute examination of the patient by palpation, percussion
and local inspection, but also in the microscopical examination of
the natural secretions and excretions of the body, such as sputum,
nasal mucus, urine and fæces. Though such examinations may entail
loss of time, they are necessary in the interest of the patient. It
appears, moreover, that quackery, which has gained considerable ground
even in the treatment of the helminthic diseases of man, can thus be
considerably limited.

_Origin of Parasites._[6]--In former times, when the only correct views
that existed related to the origin of the higher animals, the mode
of multiplication of parasites as well as of other lowly animals was
ascribed to SPONTANEOUS GENERATION (_generatio æquivoca_), and this
opinion prevailed throughout the middle ages. The writers on natural
science merely devoted their time to the interpretation of the views
of the old authors, and perpetuated the opinions of the ancients
on questions, which, even in those days, could have been correctly
explained merely by observation.

[6] Die Geschichte der “Klinisch wichtigen Parasiten,” behandelt H.
Vierordt im “Handb. d. Gesch. d. Med. hrsg.” v. M. Neuburger u. J.
Pagel, Bd. ii, 1903.

It was only when observations were again recommenced, and the
microscope was invented, that the idea of spontaneous generation became
limited. Not only did the microscope reveal the organs of generation
or their products (eggs) in numerous animals, but Redi succeeded in
proving that the so-called _Helcophagi_ (flesh maggots) are only
the progeny of flies, and never appear in the flesh of slaughtered
animals when fully developed flies are prevented from approaching and
depositing their eggs on it. Swammerdam likewise knew that the “worms”
living in the caterpillars of butterflies were the larvæ of other
insects (ichneumon flies) which had laid their eggs in their bodies;
he also discovered the ova of lice. The two authors mentioned were,
however, unwilling to see that the experience they had gained regarding
insects applied to the helminthes. Leeuwenhoek also vehemently opposed
the theory of a spontaneous generation, maintaining that, on a basis
of common-sense, eggs, or at all events germs, must exist, even though
they could not be seen.

The use of the microscope also revealed a large number of very small
organisms in the water and moist soil, some of which undoubtedly
resembled helminthes. Considering the wide dissemination of these
minute organisms, it was natural to conjecture that after their almost
unavoidable introduction into the human system they should grow into
helminthes (Boerhave, Hoffmann). Linnæus went even further, for he
traced the descent of the liver-fluke of sheep from a free-living
planaria (_Dendrocœlum lacteum_), the _Oxyuris vermicularis_ from
free-living nematodes, and the _Tænia lata_ (_i.e._, _Dibothriocephalus
latus_) from a tapeworm (_Schistocephalus solidus_) found free in
the water. Linnæus’ statements met with general approval. However,
we must bear in mind that at that time the number of helminthes
known was very small, and many of the forms that we have long ago
learned to differentiate as specific were then regarded as belonging
to one species. Linnæus’ statements were partly supported by similar
discoveries by other investigators, such as Unzer, and partly also
by the discovery of eggs in many helminthes. It was believed that
the eggs hatched in the outside world gave rise to free-living
creatures, and that these, after their introduction into the
intestine, were transformed into helminthes. By means of these eggs
the old investigators tried to explain the HEREDITARY TRANSMISSION
of the intestinal worms, which was universally believed until the
commencement of the last century. Some authors went so far as to regard
the intestinal worms as congenital or inherited; they maintained the
possibility of direct transmission, as in suckling, and denied that
the eggs reaching the external world had anything to do with the
propagation of the parasites.

The more minute comparison between the supposed free-living stages of
the helminthes and their adult forms, and the impossibility of finding
corresponding free forms for the ever-increasing number of parasitic
species, revealed the improbability of Linnæus’ statements (O. Fr.
Müller). It was the latter author also who recognized the origin of the
tapeworms (_Schistocephalus, Ligula_) found free in the water. They
originate from fishes which they quit spontaneously.

However, in spite of the fact that van Doeveren and Pallas correctly
recognized the significance of the eggs in the transmission of
intestinal worms, these statements remained disregarded, as did
Abildgaard’s observation, experimentally confirmed, that the (immature)
cestodes from the abdominal cavity of sticklebacks became mature in the
intestines of aquatic birds. Moreover, at the end of the eighteenth and
the commencement of the nineteenth centuries, after helminthology had
been raised to a special branch of study by the successful results of
the investigations of numerous authors (Goeze, Bloch, Pallas, Müller,
Batsch, Rudolphi, Bremser), many of whom experienced a “divine joy”
in searching the intestines of animals for helminthes, some authors
reverted to _generatio æquivoca_, without, however, entirely denying
the existence of organs of generation and eggs. The fact that a few
nematodes bore living progeny--a fact of which Goeze was already
aware--had no influence on the erroneous opinion, as in such cases
it was considered that the young continued to develop beside the old
forms. There were also many helminthes known that never developed
sexual organs and never produced eggs, and which therefore were
referred to _generatio æquivoca_. People were convinced that the
intestinal mucous membrane or an intestinal villus could transform
itself into a worm, either in a general morbid condition of the body,
or in pathological changes of a more local character. The appearance of
helminthes was even regarded as useful and as a means for the expulsion
of injurious matter.

These views, firmly rooted and supported by such eminent authorities
as Rudolphi and Bremser, could not easily be overthrown. First, a
change took place in the knowledge of the trematodes. In 1773, O. Fr.
Müller discovered _Cercariæ_ living free in water. He regarded them as
independent creatures and gave them the name that is still used at the
present time. Nitzsch, who also minutely studied these organisms and
who recognized the resemblance of the anterior part of their bodies
to a _Fasciola_, did not, however, arrive at a correct conclusion.
He regarded the combination rather as that of a _Fasciola_ with a
_Vibrio_, for which he mistook the characteristic tail of the cercaria.
He also noticed the encystment (transformation into the “pupa”) on
foreign bodies of many species of these animals, but was of opinion
that this process signified only the termination of life.

Considerable attention was attracted to the matter when Bojanus first
published a paper entitled “A Short Note on Cercaria and their Place
of Origin.” He pointed out that the cercariæ creep out of the “royal
yellow worms,” which occur in freshwater snails (_Limnæa, Paludina_),
and are probably generated in these worms.

Oken, in whose journal, _Isis_ (1818, p. 729), Bojanus published his
discovery, remarks in an annotation, “One might lay a wager that these
Cercariæ are the embryos of Distomes.” Soon after (1827), C. E. v.
Baer was able to confirm Bojanus’ hypothesis that the cercariæ as a
“heterogeneous brood” originated from spores in parasitic tubes in
snails (germinating tubes). Moreover, Mehlis (_Isis_, 1831, p. 190)
not only discovered the opercula of the ova of _Distoma_, but likewise
saw the infusorian-like embryo emerge from the eggs of _Typhlocœlum_
(_Monostomum_) _flavum_ and _Cathæmasia_ (_Distoma_) _hians_. A few
years later (1835) v. Siebold observed the embryos (miracidia) of
the _Cyclocœlum_ (_Monostomum_) _mutabile_, and discovered in their
interior a cylindrical body that behaved like an independent being
(“necessary parasite”), and was so similar in appearance to the “royal
yellow worms” (Bojanus) that Siebold considered the origin of the
latter from the embryos of trematodes as, at all events, possible.
Meanwhile, v. Nordmann of Helsingfors had in 1832 seen the miracidia
of flukes provided with eyes swimming in water; v. Siebold (1835)
had observed the embryos, or oncospheres, of tapeworms furnished
with six hooklets in the so-called eggs of the Tænia; while Creplin
(1837) had discovered the “infusorial” young of the _Diphyllobothrium_
(_Bothriocephalus_) _ditremum_, and conjectured that similar embryos
were to be found in other cestodes with operculated eggs. At all
events, the fact was established that the progeny of the helminthes
appeared in various forms and was partly free living. The researches
of Eschricht (1841) were likewise of influence, as they elucidated
the structure of the Bothriocephali, and proved that the encysted and
sexless helminthes were merely immature stages.

J. I. Steenstrup (1842) was, however, the first to furnish explanations
for the numerous isolated and uncomprehended discoveries. Commencing
with the remarkable development of the Cœlenterata, he established the
fact that the Helminthes, especially the endoparasitic trematodes,
multiply by means of alternating and differently formed generations.
Just as the polyp originating from the egg of a medusa represents a
generation of medusæ, so does the germinal tube (“royal yellow worm”)
originating from the ciliated embryo of a Distoma, etc., represent
the cercaria. These were consequently regarded as the progeny of
trematodes, and Steenstrup, guided by his observations, conjectured
that the cercaria, whose entrance into the snails he had observed
accompanied by the simultaneous loss of the propelling tail, finally
penetrated into other animals, in which they became flukes.

Part of this hypothetical cycle of development was erroneous, and
in other particulars positive observation was lacking, but the path
pursued was in the right direction. Immediately after the appearance of
Steenstrup’s celebrated work, v. Siebold expressed his opinion that the
encapsuled flukes certainly had to travel, _i.e._, to be transmitted
with their bearers into other hosts, before becoming mature. This view
was experimentally confirmed by de Filippi, La Valette St. George
(1855), as well as by Pagenstecher (1857), while the metamorphosis of
the ciliated embryo of Distoma into a germinal tube was first seen by
G. Wagener (1857) in _Gorgodera_ (_Distoma_) _cygnoides_ of frogs.
All that we have subsequently learned from the works of numerous
investigators about the development of endoparasitic trematodes has
certainly increased our knowledge in various directions, and, apart
from the deviating development of the _Holostomidæ_ has, as a whole,
confirmed the briefly sketched cycle of development.

Steenstrup’s work on the cestodes did not attract the same attention
as his work on trematodes. Steenstrup always insisted on the “nurse”
nature of the cysticerci and other bladder-worms. Abildgaard (1790), as
well as Creplin (1829 and 1839), had already furnished the information
that certain sexless cestodes (_Schistocephalus_ and _Ligula_) from
the abdomen of fishes only become mature after their transference
to the intestine of aquatic birds. These passive migrations were
confirmed in an entire series of other cestodes, particularly by v.
Siebold (1844, 1848, 1850) and E. J. van Beneden (1849), not by actual
experiment, but by undoubted observation.

It was correctly believed that the ova or oncospheres penetrate into
certain intermediate hosts, in which they develop into unsegmented
larvæ. Here they remain until, with their host, they are swallowed by
some predacious animal. They then reach the intestine, being freed from
the surrounding membranes through the process of digestion, and settle
themselves there to form the adult chain of proglottides. Though some
few scientists, such as P. J. van Beneden and Em. Blanchard, deduced
from these observations that the bladder-worms (Cysticerci), which had
hitherto been regarded as a separate class of helminthes, were only
larval Tæniæ, this correct view was not at first universally accepted.
The foundation was too slight, and van Beneden was of opinion that the
Cysticerci were not necessary, but only appeared incidentally.

v. Siebold was a strenuous opponent to this theory, notwithstanding
his experiences on the change of hosts of the Tetrarhynchus. Together
with Dujardin (1850) he conjectured that the Tæniæ underwent a
deviating cycle of development. He was of opinion that the six-hooked
oncospheres left the intestine, in which the older generation lived,
and were scattered about with the fæces, and finally re-entered _per
os_ (_i.e._, with water and food) a host similar to the one they
had left, in the intestine of which they were directly transformed
into tapeworms. A change of host such as occurred in other cestodes
was not supposed to take place (the history of the cestodes was
at this time not entirely established). As the oncospheres of the
Tænia are enveloped in one calcareous or several softer coverings
which they cannot leave actively, and as, in consequence of this
condition, innumerable oncospheres cannot penetrate into an animal,
and others cannot reach the proper animal, v. Siebold conceded, at
least for the latter, the possibility of a further development. But
this was only supposed to occur because they had either invaded wrong
hosts, or, having reached the right hosts, had penetrated organs
unsuitable to their development, and had thus gone astray in their
travels, and had become hydropically degenerated tæniæ. This was v.
Siebold’s explanation of bladder-worms. Naturally, v. Siebold himself
conjectured that a recovery of the diseased tapeworm might occur, in a
few exceptional cases, after transmission into the correct host, as,
for instance, in the _Cysticercus fasciolaris_ of mice, the host of
which is the domestic cat, and in which there is a seemingly normally
developed piece of tapeworm situated between the caudal vesicle and the
cysticercus head.

Guided by correct views, F. Küchenmeister undertook in Zittau the
task of confirming the metamorphosis of _Cysticercus pisiformis_ of
hares and rabbits, into tapeworms in the intestine of the dog by means
of feeding experiments. The first reports on the subject, published
in 1851, were not likely to meet with universal approval, because
Küchenmeister first diagnosed the actual tapeworm he had been rearing
as _Tænia crassiceps_, afterwards as _Tænia serrata_, and finally as
_Tænia pisiformis_ n. sp. However, in any case, Küchenmeister, by means
of the reintroduction of experimental investigation, rendered a great
service to helminthology.

The publication of Küchenmeister’s works induced v. Siebold to
undertake similar experiments (1852 and 1853), which were partly
published by his pupil Lewald in 1852. But the positive results
obtained hardly changed Siebold’s opinion, for although he no longer
considered the bladder-worms as hydropically degenerated tapeworms, he
still regarded them as tæniæ that had strayed. The change of opinion
was partly due to an important work of the Prague zoologist, v. Stein
(1853). He was able to examine the development of a small bladder-worm
in the larvæ of the well-known meal-worm (_Tenebrio molitor_) and
to demonstrate that, as Goeze had already proved in the case of
_Cysticercus fasciolaris_ of mice, first the caudal vesicle is formed
and then the scolex, whereas Siebold believed that in bladder-worms the
posterior end of the scolex was formed first, and that this posterior
end underwent a secondary hydropic degeneration.

In opposition to v. Siebold, Küchenmeister successfully proved the
necessity of the bladder-worm stage by rearing tapeworms in dogs
from the _Cysticercus tenuicollis_ of domestic mammals and from the
_Cœnurus cerebralis_ of sheep. He, and simultaneously several other
investigators independently, succeeded, with material provided by
Küchenmeister, in rearing the _Cœnurus cerebralis_ in sheep from the
oncospheres of the _Tænia cœnurus_ of the dog (1854). R. Leuckart
obtained similar results in mice by feeding them with the mature
proglottides of the _Tænia crassicollis_ of cats (1854).

Küchenmeister also repeatedly reared the _Tænia solium_ of man from
the _Cysticercus cellulosæ_ of pigs (1855), and from the embryos
of this parasite P. J. van Beneden succeeded in obtaining the same
_Cysticercus_ in the pig (1854). As Küchenmeister distinguished the
_Tænia mediocanellata_, known to Goeze as _Tænia saginata_, amongst
the large tæniæ of man (1851), so it was not long before R. Leuckart
(1862) succeeded in rearing the cysticercus of the hookless tapeworm
in the ox. It is particularly to this last-named investigator that
helminthology is indebted more than to any other author. He followed
the gradual metamorphosis from oncospheres to cystic worms in all its

In view of all the researches that were made, and which are too
numerous to mention individually, the idea that bladder-worms are
abnormal or only incidental forms had to be abandoned. Everything
pointed to the fact that in all cestodes the development is divided
between two kinds of animals; in one--the host, the adult tapeworm is
found; while in the other, the intermediate host, we find some form or
other of an intermediate stage (cysticercus in the broadest sense). The
practical application of this knowledge is self-evident. If no infected
pork or beef is ingested, no tapeworm can be acquired, and also the
rearing of cysticerci in the human body is prevented by avoiding the
introduction of the eggs of tapeworms.

Though these results were definitely proved by numerous researches,
yet they have been repeatedly challenged, notably by J. Knoch (1862)
in Petrograd, who, on the basis of experiments, sought to confirm a
direct development without an intermediate host and ciliated stage,
at all events as regards _Dibothriocephalus latus_. However, the
repeated communications of this author met with but little favour from
competent persons, partly because the experiments were conducted very
carelessly, and partly because their repetition on dog and man (R.
Leuckart) had no results (1863). It was only in 1883 that Braun was
able to prove that the developmental cycle of _Dibothriocephalus latus_
is similar to that of other Cestodes. The results obtained in other
places by Parona, Grassi, Ijima and Zschokke render any discussion of
Küchenmeister’s conclusions unnecessary.[7] Long after Knoch, a French
author, P. Mégnin, also pleaded for the direct development of some
cestodes, and especially some tæniæ. He (1879) also sought to prove a
genetic connection between the hookless and armed tapeworms of mammals,
but the arguments he adduced, so far as they rest on observations,
can be easily refuted or attributed to misinterpretation. Only one of
these arguments is correct, namely, that the number of the species
of tæniæ with which we are acquainted is far larger than that of the
corresponding cystic forms; but this disparity alone cannot be taken as
a proof of direct development. It can only be said that our knowledge
in this respect is deficient. As a matter of fact, we have during
recent years become acquainted with a large number of cystic forms,
hitherto unknown, belonging to tæniæ which have long been familiar. It
must also be borne in mind that no man in his lifetime can complete
an examination for bladder-worms of the large number of insects, for
instance, which may destroy an entire generation of an insectivorous
species of bird within a small district.

[7] Refer to the collected literature under _Dibothriocephalus latus_,
and the reply to Küchenmeister by Braun (“Ueber den Zwischenwirt des
breit. Bandw.” Würzb.: Stuber, 1886).

Naturally it does not follow that direct development in the cestodes
is altogether lacking. The researches of Grassi (1889) have furnished
an example in _Hymenolepis_ (_Tænia_) _murina_, which shows that
development may sometimes take place without an intermediate host,
notwithstanding the retention of the cystic stage. It was found that
the oncospheres of this species, introduced into rats of a certain age,
after a time grow into tapeworms without leaving the intestine, but not
directly, for they bore into the intestinal wall, where they pass the
cystic stage, the cysts afterwards falling into the intestinal lumen,
where they develop into tapeworms. The recent experiments of Nicoll
(1911) show that the larval stages of _Hymenolepis murina_ also occur
in the rat-flea, _Ceratophyllus fasciatus_.

Important observations were soon made on the remaining groups of
helminthes. The discussion on the origin of parasites soon became
confined to the helminthes. Amongst the Nematoda, it had long been
known that encapsuled forms existed that had at first been regarded as
independent species, but very soon they were pronounced to be immature
forms, in consequence of their lack of sexual organs. Though Dujardin
and also v. Siebold regarded them as “strayed” animals, v. Stein (1853)
very promptly demonstrated that the progeny of the nematodes were
destined to travel by discovering a perforating organ in the larval
nematodes of the mealworm. This was first experimentally confirmed
(1860) by R. Leuckart, R. Virchow and Zenker, all of whom succeeded not
only in bringing to maturity the muscle Trichinæ (known since 1830) in
the intestine of the animals experimented upon, but were likewise able
to follow the migrations of the progeny. Of course, the encapsulating
brood remained in the same organism, and in this respect deviated
from the broods of other helminthes which escape into the outer world
and find their way into other animals, but the encapsuled nematodes
could no longer be regarded as the result of straying. Subsequently,
R. Leuckart worked out, more or less completely, the history of the
development of numerous nematodes, or pointed out the way in which
further investigations should be made. It has been found that in
nematodes far more frequently than in other helminthes, the typical
course of development is subject partly to curtailment and partly to
complications, which sometimes considerably increase the difficulties
of investigation and have hitherto prevented the attainment of a
definite conclusion, though the way to it is now clear.

In a similar manner the works of R. Leuckart have cleared up the
development of the _Acanthocephala_ and _Linguatulida_. Of course,
much still remains to be done. So far, we do not even know all the
helminthes of man and of the domestic animals in all their phases
of life, and still less is known of those of other animals. We are
indebted to the discoveries of the last fifty years for the knowledge
arrived at, though comparatively few names are connected with it. The
gross framework is revealed, but the gaps have only been filled up here
and there. However, we may trustfully leave the completion of the whole
to the future, without fear that any essential alterations will take

The deductions to be drawn are as follows: That the helminthes like
the ectoparasites multiply by sexual processes, that the entire course
of development of the helminthes is rarely or never gone through in
the same host as is the case with several ectoparasites, that the
progeny at an earlier or later stage of development, as eggs, embryos,
or larvæ, quit the host inhabited by the older generation, and
almost always attain the outer world: only in _Trichinella_ does the
development take place directly in the definite host. Where the eggs
have not yet developed they go through the embryonic evolution in the
outer world. The young larvæ are transmitted, either still enclosed
within the egg or embryonic covering, to the intermediate host or
more rarely they are transferred straight to the final host. In other
cases they may hatch out from their envelopes, and after a longer or
shorter period of free life, during which they may partake of food
and grow, they, as before, penetrate, usually in an active way, into
an intermediate host, or at once invade the final host. Exceptionally
(_e.g._, _Rhabdonema_), during the free life there may be a propagation
of the parasitic generation, and in this case only the succeeding
generation again becomes parasitic, and then at once reaches its final
host. The young forms which have invaded the final host become mature
in the latter, or after a longer or shorter period of parasitism again
wander forth (as the Œstridæ, Ichneumonidæ, etc.), and reach the adult
stage in the outer world. The young stages, during which the parasites
undergo metamorphoses or are even capable of producing one or several
intermediate generations, are passed in the intermediate hosts until,
as a rule, they are passively carried into the final host and there
complete their cycle of development by the formation of the organs
of generation. This mode of development, the spending of life in two
different kinds of animals (intermediate and final host), is typical of
the helminthes. This is manifested in the Acanthocephala, the Cestoda,
the majority of the endoparasitic Trematoda, a number of the Nematoda,
and the Linguatulidæ. There are now and then exceptions, however,
in which, for instance, the host and intermediate host change order
(_Trichinella_, _Hymenolepis murina_).

Parasites are hardly ever inherited amongst animals.[8] According to a
few statements, however, _Trichinella_ and _Cœnurus_ are supposed to
be transmissible from the infected mother to the fœtus. Otherwise most
animals acquire their parasites, especially the Entozoa, from without,
the parasites penetrating either actively, as in animals living in the
water, or passively with food and drink. A particular predisposition to
worms is not more likely than a spontaneous origin of parasites.

[8] However, in the Protozoa there are examples of hereditary
transmission of parasites, _e.g._, in the case of _Babesia_
(_Piroplasma_) _bovis_ and _Babesia canis_ in their invertebrate hosts
(ticks); in _Crithidia melophagia_ and _Crithidia hyalommæ_; and in the
case of _Spirochæta duttoni_ in its invertebrate host (a tick).

_Derivation of Parasites._--Doubt now no longer exists as to the
derivation of the temporary and of many of the stationary ectoparasites
from free-living forms. This conclusion is founded on the circumstance
that not only are there numerous intermediate degrees in the manner of
living and feeding between predacious and parasitic animals, but that
there is more or less uniformity in their structure. The differences
that exist are easily explained as consequences of altered conditions
of life. The case is more difficult in regard to groups that are
exclusively parasitic (_Cestoda_, _Trematoda_, _Acanthocephala_,
_Linguatulidæ_, and _Sporozoa_), or groups that are chiefly parasitic
(_Nematoda_), because in these cases the gulf that divides these
forms from free-living animals is wider. It is true that we know
that the nearest relatives of the _Linguatulidæ_ are found amongst
the _Arachnoidea_, and indeed in the _Acarina_; that, moreover,
the structure and development of the _Sporozoa_ refers them to the
_Protozoa_, and allows some of them to be regarded as the descendants
of the lowest _Rhizopoda_. We know that the _Trematoda_, and through
these the _Cestoda_, are closely related to the _Turbellaria_,
from which they may be traced. The _Nematoda_, and still more the
_Acanthocephala_, stand apart. This is less evident, however, in the
Nematoda, for there are numerous free-living members of these from
which it is possible that the parasitic species may be descended.
Indeed, this seems more than probable if such examples as _Leptodera_,
_Rhabdonema_ and _Strongyloides_ are taken into consideration, as well
as the conditions of life of free-living nematodes. These mostly, if
not exclusively, spend their lives in places where decomposing organic
substances are present in quantities; some species attain maturity
only in such localities, and there propagate very rapidly. Should the
favourable conditions for feeding be changed, the animals seek out
other localities, or they remain in the larval form for some time until
more favourable conditions set in. It is comprehensible that such forms
are very likely to adopt a parasitic manner of life which at first is
facultative (_Leptodera_, _Anguillula_), but may be regarded as the
transition to true parasitism. The great advantages attached to a
parasitic life consist not only in protection, but also in the supply
of suitable food, and consequently in the easier and greater production
of eggs, and thus fully account for the gradual passage of facultative
parasitism into true parasitism. In many forms the young stages live
free for some time (_Strongylidæ_), in others, as is the case in
_Rhabdonema_, parasitic and free-living generations alternate; in
others, again, the free period is limited to the egg stage or entirely

Though it is possible thus to connect the parasitic with the
free-living nematodes, by taking their manner of life into account,
this matter presents greater difficulties in regard to other
helminthes. It is true that the segmented Cestoda may be connected with
and traced from the less known and interesting single-jointed Cestoda
(_Amphilina_, _Archigetes_, _Caryophyllæus_, _Gyrocotyle_). Trematodes
are all parasites, with the exception of one group, _Temnocephalidæ_,
several genera and species of which live on the surface of the bodies
of Crustacea and turtles of tropical and sub-tropical freshwaters.
_Temnocephalidæ_ are, nevertheless, predacious. They feed on Infusoria,
the larvæ of small insects and Crustacea. So far as is known they do
not nourish themselves on part of the host. They belong to the group
of commensals, or more correctly, to that of the SPACE PARASITES,
which simply dwell with their host and do not even take a portion of
the superfluity of its food. However, space parasitism may still be
regarded as the first stage of commensalism, which is again to be
regarded as a sort of transition to true parasitism.

It is possible that parasitism came about in this way in the
trematodes, in which connection we must first consider the
turbellaria-like ancestors of the trematodes. Much can be said
in favour of such a genetic relationship between turbellaria and
trematodes, and hardly anything against it. It should also be
remembered that amongst the few parasitic turbellaria there are some
that possess clinging discs or suctorial pores, and these are only
differentiated from ectoparasitic trematodes by the possession of a
ciliated integument, which is found only in the larval stages of the

The Acanthocephala occupy an isolated position. Most authors certainly
regard them as related to the nematodes; in any case, the connection
is not a close one, and the far-reaching alterations which must have
occurred prevent a clear view. Perhaps the free original forms of
Acanthocephala are no longer in existence, but that such must have
existed is a foregone conclusion.

An explanation of the CHANGE OF HOST so frequent in parasites is more
difficult than that of their descent. R. Leuckart is of opinion that
the present intermediate hosts, which belong principally to the lower
animals, were the original hosts of the parasites, and fostered both
their larval and adult stages. It was only in course of time that the
original hosts sank to the position of intermediate hosts, the cause
for this alteration being that the development of parasites, especially
of the helminthes, through further development and differentiation
extended over a larger number of stages. The earlier stages remained
in their original hosts, but the later stages sought out other hosts
(higher animals). To prove this, Leuckart points out that the mature
stages of the helminthes, with but few exceptions, occur only in the
vertebrates which appeared later in the development of the animal
kingdom, while the great majority of intestinal worms of the lower
animals only represent young stages, which require transmission
into a vertebrate animal before they can become mature. The few
helminthes that attain maturity in the lower animals (_Aspidogaster_,
_Archigetes_) are therefore regarded by Leuckart as primitive forms,
and he compares them with the developmental stages of helminthes,
_Aspidogaster_ with rediæ, _Archigetes_ with cysticercoids. He
classes the nematodes that become mature in the invertebrates with
_Anguillulidæ_, _i.e._, with saprophagous nematodes from which the
parasitic species descend.

Leuckart therefore regards the change of hosts as secondary, so does
Sabatier. The latter, however, adduces other reasons for this (lack of
clinging organs and the necessity to develop them in an intermediary
stage); but in this connection he only considers the Cestoda. In
opposition to Leuckart, R. Moniez, however, is convinced that the
migrations of the helminthes, as well as the system of intermediate
hosts, represent the original order of things. Moniez traces all
Entozoa from saprophytes, but only a few of these were able to settle
directly in the intestine and there continue their development. These
are forms that at the present day still lack an intermediate host,
such as _Trichocephalus_, _Ascaris_, and _Oxyuris_. In most other
cases the embryos, however, consisted of such saprophytes as were, in
other respects, suitable to become parasites, but were incapable of
resisting the mechanical and chemical influences of the intestinal
contents. They were therefore obliged to leave the intestine at once,
and accomplished this by penetrating the intestinal walls and burrowing
in the tissues of their carriers. In this position, assisted by the
favourable conditions of nutrition, they could attain a relatively high
degree of development. Mechanical reasons prevented a return to the
intestines, where the eggs could be deposited. Most of them doubtless
died off as parasites, as also their young stages do at present when
they penetrate wrong hosts. Some of them, nevertheless, passively
reached the intestine of beasts of prey. Many were destroyed in the
process of mastication; for a small part, however, there was the
chance of reaching the intestine of a beast of prey undamaged, and
there, having become larger and more capable of resistance, maturity
was attained. By means of this incidental coincidence of various
favourable circumstances, these processes, according to Moniez, have
been established by heredity and have become normal.

This is not the place to express an opinion either for or against the
various hypotheses advanced, but the existence of these diametrically
opposed views alone will show the great difficulty of the question.
Independently, however, it appears more natural to come to the
conclusion that parasitism, as well as change of hosts, were gradual

As a conclusion to this introductory chapter, a list of some of the
most important works on the parasitology of man and animals is appended.


  GOEZE, J. A. E. Versuch einer Naturgeschichte der Eingeweidewürmer
  thierischer Körper. Blankenburg, 1782. 4to, 471 pp., with 44 plates.

  ZEDER, J. G. H. Erster Nachtrag zur Naturgeschichte der
  Eingeweidewürmer. von J. A. E. Goeze. Leipzig, 1800. 4to, with 6

  RUDOLPHI, C. A. Entozoorum sive vermium intestinalium historia
  naturalis. I, Amstelod., 1808; ii, 1809. 8vo, with 18 plates.

  RUDOLPHI, C. A. Entozoorum synopsis. Berol., 1819. 8vo, with 3 plates.

  BREMSER, J. G. Ueber lebende Würmer im lebenden Menschen. Wien, 1819.
  8vo, with 4 plates.

  BREMSER, J. G. Icones helminthum, systema Rudolphii entozoologicum
  illustrantes. Viennae, 1824. Fol. (Paris, 1837).

  DUJARDIN, F. Histoire naturelle des helminthes ou vers intestinaux.
  Paris, 1845. 8vo, with 12 plates.

  DIESING, C. M. Systema helminthum. 2 vols. Vindobonnae, 1850, 1851.
  8vo. Supplements by the same author: Revision der Myzhelminthen
  (Report of the Session of the Imp. Acad. of Science. Wien,
  xxxii, 1858); with addendum (ibid., xxxv, 1859); Revision der
  Cephalocotyleen (ibid., xlix, 1864, and xlviii, 1864); Revision der
  Nematoden (ibid., xlii, 1861); Supplements (ibid., xliii, 1862).

  BENEDEN, P. J. VAN. Mémoire sur les Vers intestinaux. Paris, 1858.
  4to, with 12 plates.

  KÜCHENMEISTER, F. Die in und an dem Körper des lebenden Menschen
  vorkommenden Parasiten. Leipzig, 1855. 8vo, with 14 plates.

  LEUCKART, R. Die menschlichen Parasiten und die von ihnen
  herrührenden Krankheiten. I, Leipzig, 1863; II, Leipzig, 1876. 8vo.

  COBBOLD, T. Sp. Entozoa; an Introduction to the Study of
  Helminthology. London, 1864. 8vo. Supplement, London, 1869.

  DAVAINE, C. Traité des entozoaires et des maladies vermineuses de
  l’homme et des animaux domestiques. 2nd edit. Paris, 1877. 8vo.

  LINSTOW, O. V. Compendium der Helminthologie, ein Verzeichniss der
  bekannten Helminthen, die frei oder in thierischen Körpern leben,
  geordnet nach ihren Wohnthieren, unter Angabe der Organe, in denen
  sie gefunden sind, und mit Beifügung der Litteraturquellen. Hanov.,
  1878. 8vo. Supplement, including the years 1878–1888, Hanov., 1888.

  COBBOLD, T. Sp. Parasites; a Treatise on the Entozoa of Man and
  Animals, including some Account of the Entozoa. London, 1879. 8vo.

  LEUCKART, R. Die Parasiten des Menschen und die von ihnen
  herrührenden Krankheiten. 2nd edit. Leipzig, 1879–1886. The Protozoa,
  Cestodes, Trematodes and Hirudinea have hitherto appeared (continued
  by Brandes).

  BÜTSCHLI, O. Protozoa in Bronn’s Klass. u. Ordn. d. Thierreichs.
  Vol. i, Leipzig, 1880–1889. 8vo, with 79 plates.

  BRAUN, M. Trematodes in Bronn’s Klass. u. Ordn. d. Thierreichs.
  Vol. iv, 1, Leipzig, 1879–1893. 8vo, with 33 tables. (The first
  thirteen sheets, comprising the history of the worms up to 1830, were
  compiled by H. Pagenstecher.)

  ZÜRN, F. A. Die thierischen Parasiten auf und in dem Körper unserer
  Haussäugethiere, sowie die durch erstere veranlassten Krankheiten,
  deren Behandlung und Verhütung. 2nd edit. Weimar, 1882. 8vo, with 4

  COBBOLD, T. Sp. Human Parasites; a Manual of Reference to all the
  Known Species of Entozoa and Ectozoa. London, 1882. 8vo.

  KÜCHENMEISTER, F., and F. A. ZÜRN. Die Parasiten des Menschen. 2nd
  edit. Leipzig, 1888., 8vo, with 15 plates.

  BLANCHARD, R. Traité de zoologie médicale. I, Paris, 1889; II, 1890.

  NEUMANN, L. G. Traité des maladies parasitaires non microbiennes
  des animaux domestiques. 2nd edit. Paris, 1892. 8vo. English edit.,
  translated by G. Fleming. 2nd edit., revised by J. Macqueen. 1905.
  London: Baillière, Tindall and Cox.

  LOOSS, A. Schmarotzerthum in der Thierwelt. Leipzig, 1892. 8vo.

  RAILLIET, A. Traité de zoologie médicale et agricole. 2nd edit. I,
  Paris, 1895. 8vo.

  PARONA, C. L’elmintologia italiana da’ suoi primi tempi all’ anno
  1890. Genova, 1894. 8vo.

  BRAUN, M. Cestoda in Bronn’s Klass. u. Ordn. d. Thierreichs. Vol. iv,
  2, Leipzig, 1894–1900. 8vo, with 24 plates.

  MOSLER, F., and E. PEIPER. Thier Parasit. (Spec. Path. u. Ther. v. H.
  Nothnagel. Vol. vi.) Wien, 1894. 8vo, with 124 illustrations.

  LAVERAN, A., et R. BLANCHARD. Les hématozoaires de l’homme et des
  anim. Paris, 1895. 12mo, with 30 figs.

  SLUITER, C. R. De dierl. paras. v. d. mensch en van onze huisdier.
  Haag, 1895. 8vo.

  BLANCHARD, R. Malad. parasit., paras. animaux, paras. végét. à
  l’exclus. des bacter. (Traité de pathol. gén. de Ch. Bouchard,
  vol. ii.) Paris, 1895. 8vo, with 70 figs.

  HUBER, J. CH. Bibliographie der klin. Helminthol. München, 1895.
  8vo. With Supplement, 1898, and continued as Bibl. d. klin. Entomol.
  München, 1899–1900.

  MONIEZ, R. Traité de parasitol. anim. et veget. appl. à la médecine.
  Paris, 1896. 8vo, with 116 figs.

  WEICHSELBAUM. Parasitologie (Weil’s Handb. d. Hyg.). Jena, 1898. 8vo,
  with 78 illustrations.

  KRAEMER, A. Die thierischen Schmarotzer des Auges (Gräfe and
  Sämische’s Handb. d. ges Augenheilk.). Leipzig, 1899. 8vo, with 16

  CHOLODKOWSKY, N. A. Icones helm. hominis. St. Petersburg, 1898–99.
  Fol. (atlas with 15 plates).

  PERRONCITO, E. I parassiti dell’ uomo e degli animali utili e le più
  comuni malattie da essi prodotti. II_{a} ed. Milano 1902. 8^o. con
  276 fig. e 25 tav.

  STILES, Ch. W. and A. HASSALL. Index Catalogue of Medicine and
  Veterinary Zoology. Washington, 1902 (U.S. Dept. of Agric., Bur. of
  Anim. Ind., Bull. No. 39).

  NEVEU-LEMAIRE, M. Précis de parasitologie humaine, parasites végétaux
  et animaux. 4^e édit. Paris, 1911.

  HOFER, B. Handbuch der Fischkrankheiten. München, 1904. 8^o. 18 Taf.
  222 Abb.

  GUIART, J., and L. GRIMBERT. Précis de Diagnostic chimique,
  microscopique et parasitologique. Paris, 1906. With 500 figs.

  OSTERTAG, R. Handbuch der Fleischbeschau. V. Aufl. mit 265 Abb.
  Stuttgart, 1904.

  STILES, Ch. W. The International Code of Zoological Nomenclature as
  applied to Medicine (Hygienic Lab., Bull. No. 24, Washington, 1905).

  STILES, C. W., and HASSALL, A. Trematoda and Trematode Diseases.
  (Index Catalogue of Med. and Vet. Zoology.) Hygienic Lab., Bull. No.
  37, Washington, 1908.

  STILES, C. W., and HASSALL, A. Cestoda and Cestodaria. Hygienic Lab.,
  Bull. No. 85, Washington, 1912.

  LALOY, L. Parasitisme et mutualisme dans la nature. Paris, 1906. 8vo,
  284 pp., 82 figs.

  THEOBALD, F. V. A Monograph of the Culicidæ of the World. 5 vols. and
  plates. 1901–1910. London: Brit. Museum, Nat. Hist.

  JAMES, S. P., and LISTON, W. G. The Anopheline Mosquitoes of India.
  2nd edit. 1911. Calcutta: Thacker, Spink and Co.

  HOWARD, L. O., DYAR, H. G., and KNAB, F. The Mosquitoes of North
  and Central America and the West Indies. 2 vols. 1912. Washington:
  Carnegie Institution.

  AUSTEN, E. E. African Blood-sucking Flies. 1909. London: Brit.
  Museum, Nat. History.

  AUSTEN, E. E. A Handbook of Tsetse-flies. 1911. London: Brit. Museum,
  Nat. History.

  CASTELLANI, A., and CHALMERS, A. J. Manual of Tropical Medicine. 2nd
  edit. 1,747 pp. 1913. London: Baillière, Tindall and Cox.

  KOLLE and WASSERMANN. Handbuch der pathogenen mikroorganismen. Jena:
  Gustav Fischer.

  MINCHIN, E. A. An Introduction to the Study of the Protozoa. 1912.
  London: Arnold.

  LAVERAN, A., et MESNIL, F. Trypanosomes et Trypanosomiases. 2nd edit.
  1912. Paris: Masson and Co.

  DOFLEIN, F. Lehrbuch der Protozoenkunde. 3rd edit. 1911. Jena: Gustav

  Ticks--a Monograph of the Ixodoidea. Pt. I (1908). Pt. II. (1911).
  University Press, Cambridge, England.

  BRUMPT, E. Précis de Parasitologie. 2nd edit. 1913. Paris: Masson and

  PATTON, W. S., and CRAGG, F. W. A Text-book of Medical Entomology.
  1913. Christian Literature Society of India: London, Madras, and


For current researches the following, among others, should be

  _Annals of Tropical Medicine and Parasitology_, Liverpool.
  _Annales de l’Institut Pasteur_, Paris.
  _Archives de Parasitologie_, Paris.
  _Archives de Zoologie Expérimentale et Générale_, Paris.
  _Archiv für Protistenkunde_, Jena.
  _Archiv für Schiffs- und Tropen-Hygiene_, Leipzig.
  _Bulletin of Entomological Research_, London.
  _Bulletin de l’Institut Pasteur_, Paris.
  _Bulletin de la Société de Pathologie Exotique_, Paris.
  _Bulletins of the Bureau of Animal Industry_, Washington.
  _Centralblatt für Bakteriologie und Parasitenkunde_, Jena.
  _Compt. Rend. Acad. Sci._, Paris.
  _Compt. Rend. Soc. Biol._, Paris.
  _Indian Journal of Medical Research_, Calcutta.
  _Journal of Experimental Medicine_, New York.
  _Journal of Medical Research_, Boston.
  _Memorias do Instituto Oswaldo Cruz_, Rio de Janeiro.
  _Parasitology_, Cambridge.
  _Proceedings of the Royal Society_, London.
  _Quarterly Journal of Microscopical Science_, London.
  _Review of Applied Entomology_, London.
  _Tropical Diseases Bulletin_ (London: Tropical Diseases Bureau).
  _Zeitschrift für Infektionskrankheiten_, Berlin.


  Man is one of those organisms in on on which a whole host of
  parasites find conditions suitable for their existence: Protozoa,
  Platyhelminthes, Nematoda, Acanthocephala, Hirudinea, and a large
  number of Arthropoda (Arachnida as well as Insects) all include
  members which are parasites of man. These animals either live on
  the external surface of the body or within the intestine and its
  appendages. Other organs and systems are not quite free from foreign
  organisms--we are acquainted with parasites in the skeletal system,
  in the circulatory system, in the brain, in the muscles, in the
  excretory and genital organs, and even in the organs of sense.

  It is possible, and perhaps might be advantageous, to arrange and
  describe the parasites of man according to the situations in which
  they are found (parasites of the skin, intestinal parasites, etc.).
  Their description in the various stages of development would,
  however, be disturbed when, as is generally the case, the different
  stages are passed in different organs, and a work which treats more
  fully of the natural history of the parasites than of the local
  disorders to which they give rise would suffer thereby. It is,
  therefore, preferable to describe the parasites of man in their
  systematic order, and to mention their different situations in man in
  describing each species.



H. B. FANTHAM, M.A., D.Sc.

  All those animal organisms which throughout their entire life never
  rise above the unicellular stage, or merely form simple, loose
  colonies of similar unicellular animals, are grouped under the term
  _Protozoa_ (Goldfuss, 1820), as the simplest types of animal life.
  All the vital functions of these, the lowest forms of animals, are
  carried out by their body substance, the protoplasm (sarcode). Often
  particular parts possess special functions, but the limits of a cell
  are never over-stepped thereby. These special parts of the cell are
  called “cell-organs”; recently they have been termed “organellæ.”

  The living protoplasm has the appearance of a finely granular, viscid
  substance which, as a rule, when not surrounded by dense investing
  membranes or skeletons, exhibits a distinct kind of movement, which
  has been termed amœboid. According to the species, processes of
  different forms and varying numbers called pseudopodia are protruded
  and withdrawn, and with their assistance these tiny organisms glide
  along--it might almost be said flow along--over the surface. In most
  Protozoa two layers of cytoplasm may be recognised, and distinguished
  by their appearance and structure, namely, the superficially
  situated, viscid, and quite hyaline ectosarc or ectoplasm, and the
  more fluid and always granular endosarc or endoplasm, which is
  entirely enveloped by the ectoplasm. The two layers have different
  functions; the movements originate from the ectoplasm, which also
  undoubtedly fulfils the functions of breathing, introduction of food
  and excretion. The endoplasm, which in some forms (Radiolaria) is
  separated from the ectoplasm by a membrane, undertakes the digestion
  of the food. To this distribution of functions between the various
  layers of cytoplasm is due the development of particular cellular
  organs, such as the appearance of cilia, flagella, suctorial tubules
  (in the Suctoria) and the myophan striations, which are contractile
  parts of the ectoplasm in Infusoria and Gregarines. In many cases
  (Flagellata, Ciliata), an area is differentiated for the ingestion of
  food (oral part, cytostome) to which there is often added a straight
  or curved opening (cytopharynx), through which the food reaches the
  endoplasm. The indigestible residue is either cast off through the
  oral part or excreted by a special anal part (cytopyge). In rare
  cases, structures sensitive to light, the so-called pigment or eye
  spots are developed, _e.g._, _Euglena_. In the case of Infusoria
  the endoplasm circulates slowly, and agglomerations of fluids (food
  vacuoles) sometimes appear around each bolus of food; in these
  vacuoles the food is digested under the action of certain materials
  (ferments). Even in the lowliest Protozoa fluids to be excreted are,
  as a rule, gathered into one, or, more rarely, several contractile
  vacuoles, which regularly discharge their contents. This action,
  however, is to a certain extent governed by the temperature of the
  surrounding medium. In some Infusoria a tube-like channel in the
  cytoplasm is joined to the contractile vacuole which usually occupies
  a certain position; this forms a sort of excretory duct, and there
  are also supply-canals leading to these organellæ.

  Very frequently various substances are deposited in the endoplasm,
  such as fatty granules, drops of oil, pigment granules, bubbles of
  gas or crystals. More solid skeletal substances are secreted in or
  on the ectoplasm. To the latter belong the cuticle of the Sporozoa
  and Infusoria, the chalky shells containing one or several chambers
  of the Foraminifera, the siliceous and very ornamental framework
  of the Radiolaria, and the chitinous coat of many Flagellata,
  Infusoria, etc. Some forms make use of foreign bodies found in their
  surroundings, such as grains of sand, to construct their protective

  The food often consists of small animal or vegetable organisms and of
  organic waste; it is usually introduced _in toto_ into the endoplasm.
  On the other hand, the Suctoria extract nourishment from their prey
  by means of their tentacles. Many parasitic species also ingest solid
  food, others feed by endosmosis.

  In all cases one nucleus at least is present. It is true that the
  existence of non-nucleated Protozoa, the so-called _Monera_, is
  still insisted upon, but some of these have already proved to be
  nucleated, and the presence of nuclei in the others will no doubt be
  established. Very often the number of nuclei increases considerably,
  but these multinucleate stages are always preceded by uninucleate
  stages. In the Infusoria, in addition to the larger or principal
  nucleus (macronucleus) there is usually a smaller reproductive
  nucleus (micronucleus). This dualism of the nuclear apparatus is
  considered by some to be general, and usually to appear first at the
  onset of reproduction.

  The form and structure of the nucleus vary greatly in different
  species. There are elongate, kidney-shaped, or even branched nuclei
  as well as spherical or oval ones. In addition to vesicular nuclei
  with a distinct karyosome and incidentally also with a nuclear
  membrane, homogeneous and more solid formations are frequently
  encountered. The nuclei are always differentiated from the protoplasm
  by their reactions, particularly in regard to certain stains.

  In many Protozoa an extra-nuclear mass, sometimes compact, sometimes
  diffuse, arises from or near the nucleus. This mass, whose staining
  reactions resemble those of the nucleus, is termed the chromidial
  apparatus. On the dualistic hypothesis, two varieties of chromidia
  occur, one originating from the vegetative nucleus (macronucleus),
  being chromidia in the restricted sense, the other derived from the
  reproductive or micronucleus being termed sporetia. Chromidia consist
  of altered (? katabolic) nuclear material.

  The nucleus plays the same part in the life of the single celled
  organisms as it does in the cells of the Metazoa and Metaphyta. It
  appears to influence in a certain manner all, or at least most,
  of the processes of life, such as motility, regeneration, growth,
  and generally also digestion. Its principal influence, however, is
  exercised in the propagation of the cells, as this is always brought
  about by the nucleus.

  The PROPAGATION of the Protozoa is effected either by division or by
  means of direct budding. In division, which is preceded by direct
  or indirect (mitotic) division of the nucleus, the body separates
  into two, several, or even a great many segments. In this process
  the entire substance of the body is involved, or a small residual
  fragment may be left, which does not undergo further division
  and finally perishes. In the budding method of multiplication a
  large number of buds are formed, either on the surface or in the
  interior of the organism. Where divisions or buddings follow one
  another rapidly, without the segments separating immediately after
  their production, numerous forms develop, which are often unlike
  the parental forms, and these are termed swarm spores or spores.
  Divisions imperfectly accomplished lead to the formation of protozoal

  Sometimes encystment[9] takes place previous to division.
  Frequently, also, sexual processes appear, such as the union of
  two similar (isogamous) or dissimilar (anisogamous) individuals.
  In the latter case sexual dimorphism occurs, with the formation of
  males (microgametes) and of females (macrogametes). The union may
  be permanent (copulation), the process being comparable with the
  fertilisation of the ovum by a spermatozoon. On the other hand,
  attachment may be transient (conjugation) when, after the exchange
  of portions of the nucleus, the couple separate, to multiply
  independently of each other. Sometimes there is an ALTERNATION OF
  GENERATIONS, as there may be several methods of propagation combined
  in the same species, either direct multiplication, conjugation, or
  copulation being practised; the different generations may thus, in
  certain cases, be unlike morphologically.

[9] Independently of propagation, many protozoa protect themselves from
death by encystment when the water in which they are living dries up;
in this condition the wind may carry them over wide tracts of land.

  Protozoa inhabit salt water as well as fresh water; they are also
  found on land in very damp places, and invade animals as parasites.


  _Class I._--*Sarcodina* (_Rhizopoda_). Protozoa, the body substance
  of which forms pseudopodia; many of them are capable of developing
  chitinous, chalky, or siliceous coverings or skeletal structures,
  which, however, permit the protrusion of the pseudopodia either over
  the entire periphery or at certain points. They possess one nucleus
  or several.

      _Order 1._--_Amœbina_ (Lobosa) naked or with a simple shell,
      sometimes formed of a foreign substance; the pseudopodia may be
      lobose or finger-shaped; there may be a contractile vacuole;
      generally only one nucleus. They live in fresh or salt water, in
      the soil, and also parasitically.

      _Order 2._--_Foraminifera_ (Reticularia). Mostly provided with
      a calcareous shell, usually consisting of several chambers,
      and allowing the protrusion of the pseudopodia either at the
      periphery or only at the opening. The pseudopodia are filamentous
      and frequently anastomosed; there is no contractile vacuole;
      there are usually several nuclei. Mostly marine.

      _Order 3._--_Heliozoa._ Naked, or with a chitinous or simple
      radial siliceous skeleton; the pseudopodia are filamentous,
      and are frequently supported by firmer axes, which exhibit no
      tendency to anastomosis; there is a contractile vacuole; one or
      several nuclei. Live in fresh water.

      _Order 4._--_Radiolaria_. The body has radially-disposed
      filamentous pseudopodia, and the nucleus is hidden in the central
      capsule; there is almost always a siliceous framework, consisting
      of pieces arranged radially, tangentially, or lattice-like; there
      is no contractile vacuole, but fluid-containing hydrostatic
      vacuoles are present in the peripheral protoplasm. Marine.

  _Class II._--*Mastigophora* (_Flagellata_). Protozoa with one or
  several long flagella used for locomotion and for acquiring food; in
  stationary forms their only function is to take in food. Cytostome and
  contractile vacuole may be present. May be either naked or provided
  with protective coverings; one or more nuclei. They live either in
  fresh or salt water, or may be parasitic.

  This class is again divided into several sub-classes and orders, of
  which only the Euflagellata, with the Protomonadina and Polymastigoda
  are of interest here.

  _Class III._--*Sporozoa.* Protozoa that only live parasitically in the
  cells, tissues, or organs of other animals. They ingest liquid food
  by osmosis; the surface of the body is covered with an ectoplasmic
  layer, or cuticle; they have no cilia in the adult state, but may
  form pseudopodia. Flagella occur, but only on the male propagating
  individuals. There may be one or numerous nuclei, but no contractile
  vacuole. Propagation by means of spores, mostly provided with
  sporocysts, is characteristic.

    _Sub-class_ 1.--*Telosporidia.* These are usually of constant form,
    rarely amœboid; they are uninucleate in the mature state; they live
    within host cells in the first stage. Spore-formation occurs at the
    end of the life-cycle.

      _Order 1._--_Gregarinida._ Body of a constant, usually elongate
      form, surrounded by a cuticle. In the early stage they lead an
      intracellular existence; in the mature stage they live within the
      intestine or body cavity of invertebrate animals, especially the
      Arthropoda, and, like intestinal parasites, are provided with
      clinging organs. Copulation usually isogamous; the spores have
      coats (chlamydospores) and usually contain several minute germs

      _Order 2._--_Coccidiidea._ Body of uniform spherical or oval
      shape: they lead an intracellular life, but are not freely motile
      in cavities of the body. Fertilization is anisogamous; the spores
      have coats or shells (sporocysts), and usually contain several
      sporozoites. Exhibit alternation of generations.

      _Order 3._--_Hæmosporidia._ Parasites of the blood corpuscles of
      vertebrate animals; they exhibit amœboid movement; fertilization
      is anisogamous; many present alternation of generations and hosts;
      spores naked.

    _Sub-class 2._--*Neosporidia.* They are multinucleate when adult,
    and the form of the body varies exceedingly (often amœboid);
    spore-formation commences before the completion of growth.

      _Order 1._--_Myxosporidia._ The spores have valvular coats,
      with or without caudal appendages, with two, rarely four, polar
      capsules. They live free in such organs as the gall or urinary
      bladder, but are chiefly found in connective tissue. They occur
      especially in fishes.

      _Order 2._--_Microsporidia._ Spores with coats or sporocysts; no
      caudal appendage, with one polar capsule. They usually live in
      the tissues of Arthropoda.

      _Order 3._--_Sarcosporidia._ Elongate parasites of the muscular
      fibres of amniotic vertebrates, on rare occasions they occur
      also in the connective tissue; the spores, which are kidney or
      sickle-shaped, are naked and apparently have no obvious polar

      _Order 4._--_Haplosporidia._ Simple organisms, forming simple
      spores; they occur in Rotifers, Polychætes, Fish and Man.

  _Class IV._--*Infusoria* (_Ciliata_). The body is generally uniform
  in shape, with cilia and contractile vacuole, frequently also with
  cytostome; usually has macro- and micro-nucleus; live free in water
  and also parasitically.

  The orders _Holotricha_, _Heterotricha_, _Oligotricha_, _Hypotricha_
  and _Peritricha_ are classified according to the arrangement of the

  _Class V._--*Suctoria.* Bodies with suctorial tubes, contractile
  vacuoles, macro- and micro-nucleus, no cytostome. They generally
  invade aquatic animals as cavity parasites, yet also attack plants;
  early stage ciliated. Live sometimes as parasites on Infusoria. [The
  Suctoria are frequently regarded as a sub-class of the Infusoria.]

  The Protozoa and Protophyta are sometimes united under the term
  _Protista_ (Haeckel, 1866). The Spirochætes are Protists (see
  pp. 114–128).

Class I. *SARCODINA*, Bütschli, 1882.

Order. *Amœbina*, Ehrenberg.

A. *Human Intestinal Amœbæ.*

  The first record of the occurrence of amœba-like organisms in the
  human intestine, that is, in intestinal evacuations, was that of
  Lambl (1859); nevertheless, the case was not quite conclusive,
  as the occurrence of testaceous amœbæ of fresh water (_Arcella_,
  _Difflugia_) was also reported. In 1870 Lewis found amœbæ associated
  with disorders of the large intestine in patients in Calcutta. A year
  later Cunningham reported from the same locality that he had observed
  on eighteen occasions, in one hundred examinations of dejecta from
  cholera patients, colourless bodies with amœboid movements, which
  became encysted and multiplied by fission. The daughter forms were
  said to be capable of dividing again, but they might also remain
  in contact. Contractile vacuoles were not noticed. The same bodies
  were observed also in simple diarrhœa (twenty-eight cases out of one

[Illustration: FIG. 1.--_Amœba coli_, Lösch, in the intestinal mucus.
(After Lösch.)]

  The case reported by Lösch in 1875 attracted more attention. It was
  that of a peasant, aged 24, who came from the province of Archangel.
  He was admitted into Eichwald’s clinic at Petrograd with symptoms
  of dysentery. In the discharges containing blood and pus, Lösch
  found amœbæ in large numbers. When at rest these amœbæ measured from
  20 µ to 35 µ; in a state of movement their length might extend up
  to 60 µ (fig. 1). The pseudopodia appeared only singly, and, since
  they were hyaline (ectoplasmic), were thus distinguished from the
  markedly granular endoplasm that enclosed a spherical nucleus of from
  5 µ to 7 µ in diameter. One or more non-contractile vacuoles were
  present. Quinine enemata had the effect of making the amœbæ disappear
  from the fæces and thus causing the diarrhœa to abate. Four months
  after admission the patient died from the results of intercurrent
  pneumonia. At the autopsy ulceration of the large intestine was
  found, especially in the lower parts. Lösch connected the amœbæ with
  the ulcerations by experiments made on four dogs by injecting them
  with recently passed stools (_per os et anum_). Eight days after the
  last injection numerous amœbæ were found in the fæces of one of these
  dogs; eighteen days after the injection the animal was killed. The
  mucosa of the rectum was inflamed, covered with blood-stained mucus
  and ulcerated in three places. Numbers of amœbæ were found both in
  the pus of the ulcers and in the mucus. The three other dogs remained
  healthy. From these observations Lösch concluded that the species of
  amœba described by him as _Amœba coli_ could not be regarded as the
  primary cause of the disease, but that it was certainly capable of
  increasing a lesion of the large intestine already present, or at
  least of preventing its healing.

  B. Grassi (1879) found in the stools of healthy as well as in those
  of diarrhœic patients from various localities in Northern Italy,
  amœbæ similar to those discovered by Lösch. As this was of frequent
  occurrence, the pathogenicity could not be definitely established.
  Normand, formerly naval surgeon at Hong-Kong, observed numerous amœbæ
  in the dejecta of two patients suffering from colitis.

  Many further investigations, which cannot be quoted in detail, showed
  not only that intestinal amœbæ were widely distributed in man, but
  indicated with greater certainty their rôle as agents of dysentery.
  The Commission sent out by the German Government in the year 1883
  to investigate cholera in India and Egypt--whose members discovered
  the cholera bacillus--also collected information with regard to
  dysentery. In five cases of dysentery examined _post mortem_ at
  Alexandria, with the exception of one case in which ulceration of the
  colon had already cicatrized or was approaching cicatrization, R.
  Koch found amœbæ as well as bacteria in sections from the base of the
  ulcers, although such had previously escaped notice in examination of
  the dejecta. Encouraged by these results, Kartulis (1885), who had
  discovered amœba-like bodies in the stools of patients suffering from
  intestinal complaints at Alexandria, continued his investigations.
  The results, obtained from more than 500 cases, gave rise to the
  theory that typical dysentery was caused by amœbæ as were also the
  liver-abscesses that often accompany it. Kartulis supported his
  theory not only by the regular occurrence of amœbæ in the stools
  of dysenteric patients and their absence in other diseases, and by
  the occurrence of the parasites in ulcers of the large intestine
  and in the pus from liver-abscesses, but also by experiments which
  he performed on cats. These were infected by injection _per anum_
  of stool material rich in amœbæ from subjects of dysentery. The
  infection took place also when amœba-containing, but bacteria-free,
  pus from liver-abscesses was used. It has been objected that the
  infection of man with _Amœba coli_, as the dysenteric amœbæ were then
  generally designated, does not take place _per anum_ but _per os_.
  This difficulty, however, diminished in proportion as the encysted
  states of amœbæ (fig. 2), long known in the case of other Protozoa,
  became understood. The infection of man (Calandruccio, 1890) and of
  cats (Quincke and Roos) succeeded solely when material containing
  such stages was used. Amœbæ introduced into the intestine multiply
  there by fission (Harris, 1894). However, this theory, to which
  various other authors gave support on the grounds of their own
  observations, encountered opposition. Thus it was established that
  amœbæ were not found in patients in every place where dysentery was
  endemic, or else they were much rarer than was expected. Further,
  amœbæ were present in the most varied kinds of intestinal diseases,
  both of infective and non-infective characters. Also they were
  present in quite healthy persons.

  Moreover, for various reasons, infection experiments on animals
  failed to supply proof, and finally a bacterium was discovered
  (Shiga, 1898) to be the excitant of one form of dysentery.
  Agglutination attested the specific part played by this organism,
  as it was produced by the blood serum of a person suffering from
  or recovered from dysentery, but not by the serum of one who was
  uninfected. Bacillary dysentery consequently was a distinct entity.
  The final step to be taken was to decide whether there was a specific
  amœbic enteritis (amœbic dysentery or amœbiasis, according to

[Illustration: FIG. 2.--Encysted intestinal amœbæ showing nuclear
multiplication. (After B. Grassi.)]

  This question should decidedly be regarded from the positive point
  of view. It is intimately connected with another, namely, whether
  there are not several species of intestinal amœbæ. The possibility
  of this had already been recognized. In addition to the _Amœba coli_
  Lösch, R. Blanchard distinguished yet another, _Amœba intestinalis_,
  and designated thereby the large amœbæ described in the first
  communication made by Kartulis; later on he stated the distinction
  between the species. Councilman and Lafleur[10] (1891) considered
  the amœba of dysentery to be _Amœba coli_ Lösch and so re-named the
  species _Amœba dysenteriæ_. Kruse and Pasquale (1893) employed the
  same nomenclature, but retained the old name _Amœba coli_ Lösch for
  the non-infectious species. Quincke and Roos (1893) set forth three
  species: a smaller species (25 µ) finely granular, pathogenic for
  men and cats (_Amœba coli_ Lösch); a larger species (40 µ) coarsely
  granular, pathogenic for men but not for cats (_A. coli mitis_); and
  a similar species non-pathogenic either for man or cat (_A. intestini
  vulgaris_). Celli and Fiocca (1894–6) went still further, they

  (1) _Amœba lobosa_ variety _guttula_ (= _A. guttula_ Duj), variety
  _oblonga_ (= _A. oblonga_ Schm.) and variety _coli_ (= _A. coli_

  (2) _Amœba spinosa_ n. sp. occurring in the vagina as well as in the
  intestine of human patients suffering from diarrhœa and dysentery.

  (3) _Amœba diaphana_ n. sp. found in the human intestine in cases of

  (4) _Amœba vermicularis_ Weisse, present in the vagina and in
  dysentery; and

  (5) _Amœba reticularis_ n. sp. in dysentery.

[10] “Amœbic Dysentery,” _Johns Hopkins Hosp. Repts._, ii, pp. 395–548,
7 plates.

  Shiga distinguished two species; a larger pathogenic species with
  a somewhat active movement, and a small harmless species with a
  somewhat sluggish movement. Bowman mentions two varieties, Strong
  and Musgrave (1900) two species--the pathogenic _Amœba dysenteriæ_
  and the non-pathogenic _Amœba coli_; Jäger (1902) and Jürgens (1902)
  mention at least two species. In the following year (1903) a work
  by Schaudinn was published which marked a real advance. This, in
  conjunction with the establishing of a special genus (_Endamœba_ or
  _Entamœba_) for human intestinal amœbæ first by Leidy[11] and then by
  Casagrandi and Barbagallo,[12] for the time cleared up the confused
  nomenclature, the old name _Amœba coli_ being retained for the
  harmless intestinal amœbæ of man, whereas the pathogenic species was
  designated _Entamœba histolytica_. The history of more recent work is
  incorporated in the accounts of the entamœbæ given below.

[11] “On _Amœba blattae_,” _Proc. Acad. Nat. Sci._, Philadelphia
(1879), xxxi, p. 204.

[12] “_Entamœba hominis_ s. _Amœba coli_ (Lösch).” _Annali d’Igiene
speriment._ (1897), vii, p. 103. See also further remarks on p. 34.

*Entamœba coli*, Lösch, 1875, emend. Schaudinn, 1903.

Syn.: _Amœba coli_, Lösch, 1875. _Entamœba hominis_, Casagr. et Barbag.

The amœboid trophozoite, according to Lösch, measures 26 µ to 30 µ and
upwards; according to Grassi 8 µ to 22 µ; according to Schuberg 12 µ to
26 µ. A separation of the body substance into ectoplasm and endoplasm
is only perceived during movement. The pseudopodia, which are generally
only protruded singly, are broad and rounded at the end (lobopodia) and
are hyaline, while the remainder of the body is granular. The ectoplasm
is less refractile than the rest of the cytoplasm; it also stains less
intensely (fig. 1), and is best seen on protrusion of a pseudopodium.
Red blood corpuscles are rarely, if ever, found ingested in the

[Illustration: FIG. 3.--_Entamœba coli_: life-cycle, _a_-_e_, stages
in binary fission; _A_-_D_, schizogony, with formation of eight
merozoites; 2–10, cyst formation or sporogony, with formation of eight
nucleate cysts. (After Castellani and Chalmers)]

The nucleus is vesicular, and is spherical when inactive, measuring
5 µ to 7 µ, with a thick nuclear membrane. In the centre of the
nucleus is a chromatinic body or karyosome or sometimes several small
nuclear bodies formed of plastin and chromatin; the remaining chromatin
is arranged on the achromatic network in the form of fine granules,
especially thickly deposited on the nuclear membrane.

_Entamœba coli_ lives as a commensal in the upper portion of the
large intestine, where the fæces still possess a pulpy consistency.
With their concentration and change in reaction lower in the bowel,
the parasites either die or else if they are at a suitable stage of
development form resistant cysts. These cysts (fig. 2) can be found
in great abundance in normal fæces, as Grassi first observed. Slight
laxantia or intestinal diseases of any kind producing increased
peristalsis, however, show amœbæ even in the unencysted condition,
provided that the person harbours intestinal amœbæ generally. The
intensity of infection varies according to the locality; thus Schaudinn
found that 50 per cent. of the persons examined were infected with
harmless amœbæ in East Prussia, 20 per cent. in Berlin and about 66 per
cent. on the Austrian littoral.

The life-history (fig. 3) of the parasite exhibits two phases: (_a_)
asexual multiplication in the intestine, either by binary fission or
by schizogony with formation of eight merozoites, and (_b_) sporogony
leading to the production of eight-nucleate cysts. Infection results
from ingestion of cysts. Only cysts with eight nuclei are infective.
The diameter of such cysts is about 15 µ to 20 µ.

  There are varying accounts of the details of the life-cycle of
  _Entamœba coli_ in its different stages. Thus, regarding schizogony
  or multiple fission it was formerly stated that the nucleus of the
  parent amœba divided into eight portions, which after dissolution
  of the nuclear membrane, passed outwards into the cytoplasm, which
  segregated around each. Eight merozoites were thus produced. More
  recently the process of schizogony has been considered to consist
  in the repeated division of the nucleus into two, four, and finally
  eight nuclei (fig. 3, A-D), and the formation of eight merozoites or

  The process of encystment is initiated by the extrusion of all liquid
  and foreign bodies from the protoplasm, which assumes a spherical
  form (fig. 4, A). The rounded uninucleate amœba then secretes a soft
  gelatinous coat, which finally differentiates into a double contoured
  cyst wall in older cysts. According to Casagrandi and Barbagallo,
  the size of the cyst varies from 8 µ to 30 µ, and averages about
  15 µ. According to Schaudinn (1903) the cytological changes during
  cyst formation are as follows. The nucleus of a rounded uninucleate
  form divides into two (fig. 4, B). Each of these nuclei fragments
  into chromidia (fig. 4, C), some of which are absorbed, while
  others reunite so that the cell becomes binucleate again. Each of
  these nuclei, by a twice repeated division, produces three nuclei
  (fig. 4, D), the smaller two of which degenerate and were regarded as
  reduction nuclei. There is a clear zone or vacuole in the middle of
  the cyst during these maturation processes, dividing the cyst into
  two halves. After the nuclear reduction the clear space disappears,
  and each nucleus (termed by some a gamete nucleus) divides into
  two pronuclei (fig. 4, E). The pronuclei of the pairs were said by
  Schaudinn to differ slightly. Copulation occurs between pairs of
  unlike pronuclei, and is an example of autogamy (fig. 4, F). When
  complete, each of the fusion nuclei (synkarya) divides twice, giving
  rise first to four and finally to eight nuclei. Eight amœbulæ are
  thus formed within the cyst.

  According to Hartmann and Whitmore (1911)[13], however, autogamy
  does not occur within the cysts of _E. coli._ They consider that
  eight small amœbulæ are formed (fig. 3, _2_-_10_) which escape from
  the cyst and then conjugate in pairs (fig. 3, _10_-_12_), afterwards
  growing into a new generation of trophozoites.

[13] _Archiv f. Protistenkunde_, xxiv, p. 182.

  Only some 10 to 20 per cent. of the cysts evacuated with the
  fæces undergo the full course of development, the majority perish
  previously. In old dry fæces, only cysts with eight nuclei are found,
  and it is these alone that cause the infection.

  _Entamœba williamsi_, _E. bütschlii_, _E. hartmanni_ and _E. poleki_
  (Prowazek) are probably only varieties of _E. coli_.

[Illustration: FIG. 4.--So-called autogamy of _Entamœba coli_. A,
rounded amœba; B, nucleus dividing; C, the two daughter-nuclei giving
off chromidia; D, each nucleus has formed two reduction nuclei; E,
cyst membrane formed, and gamete nuclei are dividing; F, cyst with two

The principal feature distinguishing _Entamœba coli_ from _E.
histolytica_ is the formation of eight-nucleate cysts by the former as
contrasted with the tetra-nucleate cysts of the latter. The cyst-wall
of _E. coli_ is thicker than that of _E. histolytica_ (_tetragena_).
Further, _E. coli_ does not usually ingest red blood corpuscles, nor
are “chromidial blocks” present inside its cyst (see p. 40).

According to Chatton and Lalung-Bonnaire[14] (1912) the entamœbæ of
vertebrates should be placed in a separate genus _Löschia_, as they
differ in their life-history from _E. blattæ_, the type species of
_Entamœba_. Leidy (1879), however, named the genus _Endamœba_, but
further researches are necessary on biological variation among these

[14] _Bull. Soc. Path. Exotique_, v, p. 135.

*Entamœba histolytica*, Schaudinn, 1903.

  Syn.: _Amœba coli_, autt. p. p. _Amœba dysenteriæ_, autt. p. p.

The average size of the amœboid trophozoite is 25 µ to 30 µ. In fæces
diluted with salt solution the amœbæ swell to 40 µ and more. There is
sometimes separation of the body substance into a strongly refractile
vitreous ectoplasm and a corneous endoplasm, pronounced even in
repose, although the former is not equally thick at all parts of the
periphery. In the endoplasm generally there are numerous foreign bodies
(bacteria, epithelial cells, colourless and red blood corpuscles
(fig. 6), and occasionally living flagellates of the intestine). The
nucleus is 4 µ to 6 µ in diameter, and may be difficult to recognize
because it is sometimes weakly refractile and poor in chromatin. Its
shape is slightly variable; it is usually excentric, sometimes wholly
peripheral at the limit of the two parts of the body. Vacuoles are not
present in quite fresh specimens, but appear later. In the study of
_E. histolytica_, the morphological characters of the trophozoite or
vegetative stage of the organism formerly separated as _E. tetragena_
(figs. 5, 6, 8_a_) must be considered (see p. 38).

[Illustration: FIG. 5.--_Entamœba histolytica_ (_tetragena_ form),
showing three successive changes of form due to movement. × 1100.
(After Hartmann.)]

  The history of the development of these species, which give rise
  to amœbic enteritis as distinguished from bacillary dysentery,
  was formerly not so well known as that of _E. coli_. Upon being
  introduced into cats (_per anum_) dysenteric amœbæ provoke symptoms
  similar to those in man. In the latter, besides metastatic liver
  abscesses, abscesses of the lungs, and, according to Kartulis,
  cerebral abscesses are occasionally produced. Marchoux (1899) states
  that when the disease has lasted for some time liver abscesses are
  produced in cats also.

  [Illustration: FIG. 6.--_Entamœba histolytica_ which has ingested
  many red blood corpuscles. × 1100. (After Hartmann.)]

  [Illustration: FIG. 7.--Section through wall of large intestine (of a
  man) close under an ulcer caused by _Entamœba histolytica_. A, amœbæ
  that have penetrated partly in blood-vessels (Bv), partly in tissue
  of submucosa to the muscularis. Magnified. (After Harris.)]

  In the large intestine of infected cats the amœbæ creep over the
  epithelium, and here and there they force the epithelial cells
  apart, as well as removing them or pushing them in front of them;
  the amœbæ thus insert themselves into the narrowest fissures. They
  penetrate also into the glands through the epithelium, and thence
  into the connective tissue of the mucosa. Intestinal and glandular
  epithelia perish under the influence of these parasites: the cells
  are pushed aside, fall to pieces or are absorbed by the amœbæ. In the
  connective tissue of the mucosa the amœbæ migrate further, and often
  accumulate above the muscles. Finally they rupture this and force
  their way into the submucosa. In cats, apparently, the penetration
  is not so great as in men, according to Kruse and Pasquale. During
  their migration the parasites also gain access to the lymph-follicles
  of the wall of the intestine, which become swollen and commence
  to suppurate; follicular abscesses arise and after their rupture
  follicular ulcers. The diseased patches in the mucosa are markedly
  hyperæmic and numerous hæmorrhages are set up. Roos and Harris state
  that the amœbæ also penetrate into the blood-vessels (fig. 7) and
  this explains the occurrence of metastatic abscesses.[15] The whole
  submucosa is severely swollen at the diseased spot and undergoes
  small-celled infiltration in the neighbourhood of the colonies of
  amœbæ. From these findings Jürgens (1902) draws the conclusion[16]
  which is followed here, that the amœbæ are causative agents of the
  enteritis of cats, which disease is well defined, both pathologically
  and anatomically. Subsequent researches confirm the experience of
  earlier authors; great precautions were taken to exclude errors,
  hence, as with Gross and Harris, no exception can be taken to their
  results. The inoculation material was derived from soldiers who
  suffered from amœbic enteritis in China and who were admitted into
  the garrison hospital at Berlin. In order to be independent of the
  patients themselves, transmission experiments from cat to cat were
  performed, after the first experiments on cats yielded positive
  results. This was also effected by rectal feeding as employed by
  earlier workers. Such appeared necessary in order to prevent the
  evacuation of the inoculation material _per anum_, as well as to
  avoid the employment of morphia and ether narcosis. Forty-six cats
  were used for the experiments. Ten cats received tested stools
  containing motile amœbæ from soldiers suffering from amœbic enteritis
  contracted in China. Sixteen other cats received stools from cats
  infected by inoculation. All the animals sickened and suffered from
  the disease. Five cats received dejecta from human amœbic enteritis
  in which, however, no _motile_ amœbæ were present. Thirteen cats
  received stools from soldiers who suffered from bacillary dysentery.
  None of the latter cats took the complaint and none showed changes
  in the large intestine upon sectioning. The injection of various
  bacteria, obtained from a stool of amœbic enteritis pathogenic
  to cats, remained without result in both the cats employed for
  this experiment. Lastly, two cats, which had been kept with those
  artificially infected, were taken ill spontaneously and suffered from
  the disease. In the opinion of Harris, who ascertained the harmless
  nature of bacteria derived from the intestinal flora containing
  dysenteric amœbæ, young dogs are capable of being infected.

[15] Lung abscesses generally arise by the bursting of a liver abscess
through the diaphragm into the right lower lobe of the lung, sometimes
also through conveyance of amœbæ by means of the blood-stream (Banting).

[16] These findings were confirmed by Schaudinn by means of
investigations on cats and men. _Cf._ also Alfred Gross, Marchoux,
P. G. Woolley, W. E. Musgrave, H. F. Harris and others.

  Within the large intestine an active increase of _Entamœba
  histolytica_ must occur. Nevertheless, Jürgens did not definitely
  find changes that might be interpreted in this sense. Schaudinn
  (1903) observed division and gemmation _in vivo_. Both processes, in
  which the nucleus divides by amitosis, can only be distinguished by
  the fact that the daughter individuals are similar in binary fission
  but dissimilar in gemmation, whether they make their appearance
  singly or in greater numbers. Schizogony, resulting in the formation
  of eight individuals, which is so characteristic for _Entamœba coli_,
  was not observed. (But schizogony, into four merozoites, is now known
  to occur. Gemmation processes are apparently degenerative.)

  Resistant stages, which serve for transmission to other hosts, are
  according to Schaudinn[17] first formed when the diseased portions
  commence to heal, or more accurately, the recovery commences when
  the vegetative increase of the amœbæ in the intestine discontinues.
  The so-called spores of _E. histolytica_ were distinguished very
  definitely from those of _E. coli_; they were said to consist of
  spheres of only 3 to 7 µ in diameter, which were surrounded by a
  double membrane, at first colourless, but becoming a light brownish
  yellow colour after a few hours, and possessing a protoplasmic
  content containing chromidia. They were said to arise by fragments
  of chromatin passing outwards from the nucleus of the amœba into
  the surrounding cytoplasm (fig. 9, _a_) and undergoing so marked
  an increase that finally the whole cytoplasm became filled with
  chromidia. The remainder of the nucleus underwent degeneration and
  became extruded. On the surface of the cytoplasm there then arose
  small protuberances containing chromidia. These processes had
  been observed in the living organisms. They gradually divided and
  separated from membranes which later became yellow. The remainder of
  the amœba perished. Craig[18] had also seen phases of this process
  of development. It must be remarked that, according to recent
  researches, these processes of exogenous sporulation are degenerative
  in character (see p. 41). The small spores may be fungi. The
  “sporulation” processes are only mentioned here as a warning. They
  are now only of historic interest. By means of an experiment made on
  a cat, Schaudinn ascertained that ingestion of permanent cysts, which
  resist desiccation, is the cause of the infection. The animal took
  food containing dry fæces with amœba cysts; these fæces came from a
  patient suffering from amœbic enteritis in China. On the evening
  of the third day the cat evacuated blood-stained mucous fæces which
  contained large numbers of typical _Entamœba histolytica_. On the
  fourth day after the infection the animal experimented upon died, and
  the large intestine showed the changes previously stated.

[17] _Arb. a. d. kaiserl. Gesundheitsamte_, xix, pp, 547–576.

[18] “Life cycle of _Amœba coli_ in Human Body,” _American Medicine_,
1904, vii, p. 299; viii, p. 185.

  _E. histolytica_ also is found in the large intestine. This was
  originally shown to be the case by Kartulis, and the fact has
  recently been confirmed from many quarters. It is also present in
  the metastatic abscesses of which it is the cause (_cf._ among other
  authors, Rogers, _Brit. Med. Journ._, 1902, ii, No. 2,177, p. 844;
  and 1903, i, No. 2,214, p. 1315).

  It should lastly be pointed out in this connection that mixed
  infections also take place. For instance, in addition to _E.
  histolytica_, _E. coli_, and, under certain circumstances,
  flagellates may be found together. In the same way _E. coli_ may
  come under observation even in bacillary dysentery. On the other
  hand, Schaudinn stated that in cases of dysentery endemic in Istria,
  _Entamœba coli_, if it had hitherto been present, disappeared, to
  return again after recovery from the illness.

[Illustration: FIG. 8.--_Entamœba histolytica_. _a_, trophozoite
(_tetragena_ type) containing red blood corpuscles, × 1,300; _b_ and
_c_, two isolated nuclei showing different appearances of karyosome,
centriole and nuclear membrane, × 2,600. (After Hartmann.)]

(_Entamœba tetragena_, Viereck, 1907.)

This amœba must now be considered to be a part of the lifecycle of
_Entamœba histolytica_, in fact a very important part of that cycle,
especially in its tetranucleate cystic stages.

This organism, the so-called _Entamœba tetragena_, may occur in the
human intestine in cases of amœbic dysentery, especially in mild
or chronic cases. It was discovered by Viereck in 1907 in patients
suffering from dysentery contracted in Africa. Soon afterwards an
independent description was published by Hartmann, who called the amœba
_E. africana_. It was also studied by Bensen and Werner. Recently
(1912–13) much work has been published on this amœba by Darling and
others; in this way its relationship to Schaudinn’s _E. histolytica_
has been made known.

In general morphology it somewhat resembles _Entamœba coli_, and its
discoverer at first mistook it for a variety of that species. According
to Hartmann, a distinct ectoplasm is only clearly visible when a
pseudopodium is protruded (fig. 5). The granular endoplasm may contain
ingested red blood corpuscles (fig. 6). The large, round nucleus is
visible in the fresh state (fig. 8, _a_). So-called chromidial masses
(? crystalloidal substances) may occur in the cytoplasm.

[Illustration: FIG. 9.--_Entamœba histolytica_ (_tetragena_ form).
_a_, emission of chromatin from nucleus; _b_, nuclear division; _c_,
degenerating form with two nuclei; _d_, _e_, _f_, cysts containing
one, two and four nuclei respectively, and showing chromidial blocks.
× 2,000. (After Hartmann.)]

Some investigators, as Hartmann,[19] lay stress on the internal
structure of the nucleus (fig. 8, _b_, _c_), best seen in preparations
fixed wet and stained with iron-hæmatoxylin. The nucleus is limited
by a well-marked nuclear membrane, on the inside of which granules
or nodules of chromatin may occur. There is a karyosome, which, in
successfully stained specimens, shows, at times, a central dot called
a centriole. (The nucleus of _Entamœba coli_ does not contain such a
centriole.) However, the structure of the nucleus varies at different
periods during the life-cycle.

[19] _Arch. f. Protistenkunde_ (1911), xxiv, p. 163.

The diameter of the trophozoites or vegetative forms (fig. 8, _a_) is
variously given as from 20 µ to 40 µ. Multiplication proceeds by binary
fission and also by schizogony into four merozoites.[20]

[20] _See_ Darling, 1913, _Arch. Intern. Med._, vol. ii, pl. i, fig. 3.

Reproduction takes place by endogenous encystment (fig. 9, _d_-_f_),
which is preceded by nuclear division into two, reduction and then
autogamy. The interpretation of the latter phenomenon as autogamy is
disputed by some authors. The round cysts, which may measure 12 µ to
15 µ in diameter, contain four nuclei, together with darkly staining
masses of various shapes, the so-called “chromidial blocks” (fig. 9,
_f_). The cyst-wall of _E. histolytica_ (_tetragena_) is thinner than
that of _E. coli_, and the diameter of the cyst is rather less. _E.
histolytica_ has not yet been cultivated.

Infection in man occurs by way of the mouth by the ingestion of
cysts. A patient showing acute symptoms of dysentery is not usually
infective, for he is merely harbouring the large trophozoites, which,
by experiment, have been shown not to be infective to animals (kittens)
when administered by the mouth. The stools of recovered patients
may still contain cysts, and they may thus act as cyst-carriers or
reservoirs of disease by infecting water and soil. The stools of
such cyst-carriers are often solid, and so cysts of _E. histolytica_
(_tetragena_) are easily overlooked. Mathis (1913)[21] points out that
healthy carriers of _E. histolytica_ may be found; 8 per cent. of the
natives of Tonkin examined by him were healthy carriers of cysts.

[21] _Bull. Soc. Med. et Chirurg. Indo-Chine_, iv, p. 474.

In return cases, or prolonged untreated cases of entamœbic dysentery, a
generation of smaller trophozoites is associated with, or replaces the
larger ones. In stools they are frequently refractile and consequently
stain slowly _intra vitam_. These trophozoites are the “smaller,
senile, or pre-cyst generation” of Darling. This pre-cyst generation is
characterized by the presence of blocks of crystalloidal substance in
the cytoplasm, and by the possession of a prominent, densely stainable
karyosome. Darling believes this generation to be the same as that
described by Elmassian as _Entamœba minuta_.[22]

[22] _Centralbl. f. Bakter._, Orig., lii, p. 335.

Walker,[23] Darling,[24] Wenyon[25] and others believe that _Entamœba
histolytica_, which was only seen by Schaudinn in a single case, that
of a Chinaman, is really _E. tetragena_. Darling states that if the
published illustrations of _E. histolytica_ and of _E. tetragena_ are
collected from the literature and compared, it will be seen that the
writers have been calling _E. histolytica_ the large trophozoites seen
in dysenteric stools. These large trophozoites frequently display no
karyosome, but they can be demonstrated as _E. tetragena_ by animal
inoculation, or by the history of the case. On the other hand, the
illustrations of _E. tetragena_ show that the authors have been
dealing with the small generation or reduced forms (“_E. minuta_”),
which are the direct descendants of the large trophozoites. If kittens
are inoculated rectally with dysenteric material containing large
trophozoites, the strain may be carried in successive kittens for
four to six transfers. If, on the other hand, kittens are inoculated
rectally with small trophozoites of the pre-cyst generation, the
transmission cannot be carried through more than one or two kittens.
Wenyon has succeeded in maintaining _E. tetragena_ in kittens for
several generations.

[23] _Philip. Journ. Sc._ (1911), B, vi, p. 259.

[24] _Annals Trop. Med. and Parasitol._ (1913), vii, p. 321.

[25] _Brit. Med. Journ._, Nov. 15, 1913, p. 1287, and _Journ. Lond.
School Trop. Med._, ii, p. 27.

In some of the preparations from the last remove, pathological forms
of the trophozoites may be seen. These show abnormal forms of budding,
especially peripherally, such as have been described by Schaudinn and
by Craig as characteristic of _E. histolytica_. Schaudinn’s small
peripheral, exogenous buds and cysts are thus explained. Craig has
latterly changed his views.

Further, Darling states that _tetragena_ cysts fed by the mouth
to kittens produce bowel lesions in which trophozoites having the
characters of _E. tetragena_, _E. histolytica_ and _E. nipponica_
(Koidzumi) occur.

In view of the work of recent observers, the peculiar exogenous
encystment which Schaudinn made characteristic of _Entamœba
histolytica_ has been shown to be due to degenerative changes in senile
races of the amœba. _E. histolytica_ and _E. tetragena_ are one and the
same species, and its trophozoite is subject to variation. According
to some observers the _histolytica_ type of nucleus--described by
Schaudinn as being poor in chromatin and not easily seen in the
fresh state--occurs frequently in patients with severe symptoms of
dysentery; on the other hand, the _tetragena_ type of nucleus--round
and easily seen in the fresh state--may occur in cases presenting
slight dysenteric symptoms. Intermediate types of nuclei are seen. The
name of this species, the principal pathogenic amœba of man, must then
be _E. histolytica_ by priority. The cystic stages of _E. histolytica_
are those first recorded by Viereck and formerly described as _E.
tetragena_. The geographical distribution of _E. histolytica_ is wide.

*Noc’s Entamœba* (1909).

A species of Entamœba was cultivated by Noc[26] in 1909 from cysts
derived from liver abscesses, from dysenteric stools and from the
water supply of Saigon, Cochin China. He cultivated it in association
with bacteria. It is pathogenic. It has been considered allied to
_E. histolytica_, and shows internal segmentation or schizogony. It
exhibits polymorphism. This amœba has been found by Greig and Wells
(1911) in cases of dysentery in India. It is an important organism and
requires further investigation.

[26] Noc, F. (1909), _Ann. Inst. Pasteur_, xxiii, p. 177.

Certain other Entamœbæ[27] have been described at various times from
the intestinal tract of man. Probably most, if not all, of these are
not good species and in some cases much more information is needed.

[27] See Fantham, H. B. (1911), _Annals Trop. Med. and Parasitol._, v,
p. 111.

_Entamœba tropicalis_ (Lesage, 1908). This parasite is said to be
non-pathogenic, and to occur in the intestine of man in the tropics. It
has a general resemblance to _E. coli_, but forms small cysts (6 µ to
10 µ in diameter). The nucleus of the cyst is said to break up into a
variable number of daughter nuclei, from three to thirteen having been
noted. Lesage states that it is culturable in symbiosis with bacteria.
It is probably a variety of _E. coli_, if not a cultural amœba.

_Entamœba hominis_ (Walker, 1908) has a diameter of 6 µ to 15 µ. A
contractile vacuole is present. Encystment is total, and small cysts
are formed. It is culturable. The original strain, now lost, was
obtained from an autopsy in Boston Hospital. This organism is probably
a cultural amœba.

_Entamœba phagocytoides_ (Gauducheau, 1908). This parasite was
discovered in a case of dysentery at Hanoi, Indo-China. The amœba is
small, 2 µ to 15 µ in diameter. It is active. It ingests bacteria and
red blood corpuscles, while peculiar spirilla-like bodies are found in
its cytoplasm. It multiplies by binary and multiple fission. It can be
cultivated. More recently (1912) the author appears to consider the
amœba to be a stage of a _Trichomonas_, but abandons the view later
(1914). Further researches on this organism are needed.

_Entamœba minuta_ (Elmassian, 1909)[28] was found, in association with
_E. coli_, in a case of chronic dysentery in Paraguay. It resembles
_E. tetragena_ but is smaller, rarely exceeding 14 µ in diameter.
Schizogony occurs, four merozoites being produced. The encystment is
total and endogenous, giving rise to cysts containing four nuclei.
This amœba is considered by Darling and others to be the pre-cyst
trophozoite stage of _E. histolytica_ (_tetragena_).

[28] _Centralbl. f. Bakter._, Orig., lii, p. 335.

_Entamœba nipponica_ (Koidzumi, 1909) was found in the motions of
Japanese suffering from dysentery or from diarrhœa, in the former case
in company with _Entamœba histolytica_. Its diameter is 15 µ to 30 µ.
The endoplasm is phagocytic for red blood corpuscles. The nucleus is
well defined, resembling that of _E. coli_ and of _E. tetragena_.
Multiplication occurs by binary fission and by schizogony. Encystment
is total, but has not been completely followed. Darling and others
consider that this is an abnormal form of _E. histolytica_, while
Akashi (1913) doubts if it is an amœba at all, but rather is to be
regarded as shed epithelial cells.

GENERAL REMARK.--It is now considered by some workers that true
Entamœbæ cannot be cultivated on artificial media. Quite recently
Williams and Calkins (1913)[29] have somewhat doubted this opinion, and
state that certain cultural amœbæ, originally obtained from Musgrave in
Manila, exhibit the various morphological variations associated with
true entamœbæ of the human digestive tract.

[29] _Journ. of Med. Research_, xxix, p. 43.

*Entamœba buccalis*, Prowazek, 1904.

The size varies from 6 µ to 32 µ. Ectoplasm is always present; the
endoplasm contains numerous food-vacuoles. The nucleus is vesicular,
with a greenish tinted membrane which is poor in chromatin. The size
of the nucleus is from 1·5 µ to 4·5 µ. A contractile vacuole is not
visible. The pseudopodium is broad. It was discovered in the mouths of
persons with dental caries at Rovigno and also at Trieste, being most
easily found in dense masses of leucocytes, also among leptothrix and
spirochæte clusters. It can be easily distinguished from leucocytes
by more intense staining with neutral red. Multiplication proceeds by
fission. Transmission may take place through the small spherical cysts.
This species (fig. 10) has since been observed in Berlin, and is also
occasionally found in carcinoma of various regions of the oral cavity.
(Leyden and Löwenthal, 1905).

[Illustration: FIG. 10.--_Entamœba buccalis_, Prow. _a_-_d_, the same
specimen observed during five minutes. × 1,000. _e_, amœba fixed and
stained with iron-hæmatoxylin. × 1,500. (After Leyden and Löwenthal.)]

_Entamœba buccalis_, Prow., is said to be allied to a protozoön which
A. Tietze has found either encysted or free in the lumen of the
orifice of the parotid gland of an infant aged 4 months. The gland had
undergone pathological change, and had therefore been extirpated. The
organisms, which were roundish and three to four times the size of
the normal epithelial cells of the gland, were without a membrane and
possessed a nucleus in which the chromatic substance appeared to be
contained in a karyosome. Bass and John’s[30] (Feb. 1915) and Smith,
Middleton and Barrett (1914) state that _E. buccalis_ is the cause of
pyorrhœa alveolaris.

[30] _Journ. Amer. Med. Assoc._, lxiv, p. 553.

  _Entamœba undulans_, Aldo Castellani, 1905.

  Under this name a protozoön is described which A. Castellani found in
  addition to _Entamœba histolytica_ and _Trichomonas intestinalis_ in
  the fæces of an European planter living in Ceylon, who had suffered
  from amœbic enteritis and liver abscess. The shape of the body was
  roundish or oval, 25 µ to 30 µ in the greatest diameter. It was
  without a flagellum, but with an undulating membrane, and capable
  of protruding a long pseudopodium from different parts of its body
  at short intervals. The nucleus could not always be recognized in
  life; it was, however, always demonstrable by staining. One or
  two contractile vacuoles were present. The protoplasm was finely
  granular, showing no differentiation into ecto- and endo-plasm.
  According to Braun, in spite of the author declaring himself
  expressly against the flagellate nature of the parasite, such
  a nature may be assumed to be tolerably certain in view of the
  description and illustration.

  It is now considered that _Entamœba undulans_ is a portion of a
  flagellate, namely, _Trichomonas_.

*Entamœba kartulisi*, Doflein, 1901.

Doflein gave this name to amœbæ, from 30 µ to 38 µ in diameter, which
Kartulis (1893) found on examining the pus of an abscess in the right
lower jaw of an Arab, aged 43, and in a portion of bone that had been
extracted. The movements of the amœbæ (fig. 11) were more active
than those of “dysenteric amœbæ.” Their coarsely granular cytoplasm
contained blood and pus corpuscles, and a nucleus was generally only
recognizable after staining. Vacuoles were not seen with certainty.
Flexner reported upon a similar case, and Kartulis published five
additional cases. As in these cases dental caries was present the
infection is likely to have proceeded from the oral cavity as a result
of the carious teeth. Craig[31] (1911) considers that this parasite is
probably identical with _Entamœba histolytica_.

[31] “The Parasitic Amœbæ of Man,” Lippincott, Philadelphia.

[Illustration: FIG. 11.--_Entamœba kartulisi_, Dofl., from the pus of
an abscess in the lower jaw, showing different stages of movement.
(After Kartulis.)]

In the literature the following species have been reported as occurring
in the oral cavity of man:--

_Amœba gingivalis_, Gros, 1849. [? identical with _Entamœba buccalis_.]
_Amœba buccalis_, Sternberg, 1862. _Amœba dentalis_, Grassi, 1879.

  Far too little, however, is known concerning these to regard them
  as definite species, that is, independent organisms; Grassi thinks
  it even possible there may have been a confusion in their case with
  salivary corpuscles. If they really are amœbæ they are all of them
  probably identical with _Entamœba buccalis_.

  Genus *Paramœba*, Schaudinn, 1896.

  Schaudinn established the genus _Paramœba_ for a marine rhizopod
  which multiplied by division, became encysted at the end of its
  vegetative life and then segmented into swarm bodies with two
  flagella. These multiplied by longitudinal fission, and finally
  passed into the condition of Amœbæ. Whether the human parasite
  described by C. F. Craig (1906) as *Paramœba hominis.* belonged to
  this genus was for a time uncertain. It is now placed in a new genus
  Craigia, Calkins, 1912, since it possesses only one flagellum.[32]

[32] See Craig (1913), _Amer. Journ. Trop. Dis. and Prevent. Med._, i,
p. 351.

  In the amœbic stage it is 15 µ to 25 µ in diameter; ecto- and
  endo-plasm during rest are indistinguishable. The body substance
  is granular, with a spherical, sharply contoured nucleus and an
  accessory nuclear body. No vacuoles are present, but occasionally the
  endoplasm contains red blood corpuscles. The pseudopodia are hyaline,
  finger- or lobe-shaped, and are protruded either singly or in twos.
  Multiplication is by binary fission and by the formation of spherical
  cysts (15 µ to 20 µ in diameter) in which occurs successive division
  of the nuclei, ultimately forming ten to twelve roundish bodies
  each of which soon develops a flagellum. The flagellate stages have
  similarly a spherical shape and attain a diameter of 10 µ to 15 µ.
  They also occasionally contain red blood corpuscles and pass either
  directly or after longitudinal division into the amœboid phase.

  Craig found these Amœbæ and the flagellate stage belonging to them in
  six patients in the military hospital at Manila (Philippine Islands),
  five of whom were suffering from simple diarrhœa whilst the sixth
  exhibited an amœbic enteritis and contained also _Paramœba hominis_,
  with _Entamœba histolytica_, Schaudinn. In one of the other cases,
  _Trichomonas intestinalis_ was present.

B. *Amœbæ from other Organs.*

*Entamœba pulmonalis*, Artault, 1898.

Artault[33] discovered a few amœboid forms with nucleus and vacuole
in the contents of a lung cavity. In the fresh condition they were
distinguishable from leucocytes by their remarkable capacity of light
refraction. They were also much slower than the latter in staining
with methylene blue or fuchsine. Their movements became more lively
in a strong light. Water and other reagents killed them, and then,
even when stained, they could not be distinguished from leucocytes.
They have also been seen by Brumpt. R. Blanchard found amœbæ which may
belong here in the lungs of sheep. _A. pulmonalis_ is perhaps the same
as _Entamœba buccalis_. Smith and Weidman[34] (1910, 1914) described
an entamœba, _E. mortinatalium_, from the lungs and other organs of
infants in America.

[33] _Arch. de Parasitologie_, i, p. 275.

[34] _Amer. Journ. Trop. Dis. and Prevent. Med._, ii, p. 256.

*Amœba urogenitalis*, Baelz, 1883.

This species was found in masses in the sanguineous urine as well
as in the vagina of a patient in Japan, aged 23. Shortly before the
death of the patient, which was caused by pulmonary tuberculosis,
hæmaturia with severe tenesmus of the bladder had set in. The amœba,
which showed great motility, and had a diameter of about 50 µ when
quiescent, exhibited a granular cytoplasm and a vesicular nucleus.
Baelz is of opinion that these parasites were introduced into the vulva
with the water used for washing the parts, and thence had penetrated
into the bladder and vagina. Doflein places the organism in the genus
_Entamœba_, and it is perhaps identical with _E. histolytica_.

  Similar cases are also reported (1892–3) by other authors: Jürgens,
  Kartulis, Posner, and Wijnhoff. Jürgens found small mucous cysts,
  filled with amœboid bodies, in the bladder of an old woman suffering
  from chronic cystitis; they were also found in the vagina. The
  amœba observed by Kartulis in the sanguineous urine of a woman,
  aged 58, suffering from a tumour of the bladder, measured 12 µ to
  20 µ, and exhibited slow movements by protruding short pseudopodia.
  The vacuoles and nucleus became visible only after staining with
  methylene blue.

  Posner’s case related to a man, aged 37, who had hitherto been quite
  healthy and had never been out of Berlin. Suddenly, after a rigor,
  he passed urine tinged with blood. This contained, besides red and
  white blood corpuscles and hyaline and granular casts, large granular
  bodies (about 50 µ in length and 28 µ in breadth), which slowly
  altered their shape, and contained red blood corpuscles in addition
  to other foreign matter. These bodies exhibited one or several nuclei
  and some vacuoles. From the course of the disease, which extended
  over a year, and during which similar attacks recurred, Posner came
  to the conclusion that the amœbæ which had originally invaded the
  bladder had penetrated into the pelvis of the kidney, where they
  probably had settled in a cyst, and thence induced the repeated

  Wijnhoff observed four cases of amœburia in Utrecht.

*Amœba miurai*, Ijima, 1898.

[Illustration: FIG. 12.--_Amœba miurai_, Ij. × 500. _a_, fresh; _b_,
after treatment with dilute acetic acid. (After Ijima.)]

  Under this term the author describes protoplasmic bodies which Miura,
  in Tokyo, found in the serous fluid of a woman, aged 26, who had died
  from pleuritis and peritonitis endotheliomatosa. Two days before
  death these same forms had also appeared in the hæmorrhagic fæces
  of the patient. The bodies were usually spherical or ellipsoidal,
  and at one pole carried a small protuberance (fig. 12) beset with
  filamentous short “pseudopodia” (really a pseudopodium covered with
  cilia). Their size varied between 15 µ and 38 µ. The cytoplasm was
  finely granular, and no difference was observable in the ecto- and
  endo-plasm, only the villous appendage was clearer. The cytoplasm
  contained vacuoles more or less numerous, none of which was
  contractile. After the addition of acetic acid one to three nuclei
  could be distinguished, 8 µ to 15 µ in size. Actual movements were
  not observed. Taking everything into consideration, the independent
  nature of these bodies is, to say the least, doubtful, although it
  cannot be denied that they possess a certain similarity to the marine
  _Amœba fluida_, Grüber or Greeff, and to a few other species. (It
  is likely that cells present in serous exudation were mistaken for


“_Rhizopods in Poliomyelitis acuta._”

  In three cases of poliomyelitis acuta which were investigated
  by Ellermann, the spinal fluid obtained by puncture of the cord
  contained bodies, from 10 µ to 15 µ in size, which had amœboid
  movements and exhibited variously shaped pseudopodia in large
  numbers. After staining, a usually excentric nucleus, about 1·5 µ in
  size, was demonstrated in them.

Order. *Foraminifera*, d’Orbigny.

  The order is divided by Max Schultze into Monothalamia and
  Polythalamia. Only a few of the former can be considered here.

Sub-Order. *Monothalamia.* (Testaceous Amœbæ).

These forms occur frequently in fresh water, rarely in sea water.
They possess a shell which is either pseudo-chitinous in character,
or consists of foreign particles, or in a few cases is composed of
siliceous lamellæ. There is usually an orifice for the protrusion of
pseudopodia. The only representative of the order of interest here is:--

Genus. *Chlamydophrys*, Cienkowski, 1876.

  The genus is based on a form which A. Schneider carefully
  investigated and considered to be the _Difflugia enchelys_ of
  Ehrenberg. L. Cienkowski rediscovered this same form and created
  for it the genus _Chlamydophrys_. We agree with this view, but not
  with the renaming of the organism (so common at the time). If the
  parasite in dung, _Chlamydophrys stercorea_ Cienk. is identical with
  _Difflugia enchelys_ of Ehrenberg, the old specific name should be

The genus is characterized by the possession of a hyaline,
structureless, slightly flexible shell which is ovoid or reniform.
At the more pointed pole there is an orifice situated terminally
or somewhat laterally, serving for the emergence of the filiform
pseudopodia (fig. 13, _a_). The protoplasm does not entirely fill the
interior of the shell. An equatorial zone bearing excretory granules
divides the shell internally into two almost equal portions. The
anterior portion is rich in vacuoles and serves for the reception
of nutriment and for digestion. The posterior part is vitreous, and
contains the nucleus. One to three contractile vacuoles are situated in
the equatorial zone.

*Chlamydophrys enchelys*, Ehrbg.

  Syn.: _Chlamydophrys stercorea_, L. Cienkowski.

This species (fig. 13) is found in the fæces of various animals
(cattle, rabbits, mice, and lizards), and also in quite fresh human
fæces. According to Schaudinn, the parasite occurs so frequently in
the human fæces that it must be considered of wide distribution. The
species must traverse the intestine of man and animals during one stage
of its life cycle, as Schaudinn showed by experiments on himself and
on mice. He infected himself with cysts (fig. 14) by swallowing them,
and evacuated the first _Chlamydophrys_ as early as the following day.
After the evacuation of numerous specimens on one of the following days
the infection ceased.

The nucleus of a living specimen is surrounded by a hyaline, strongly
refractile chromidial mass, arranged in the form of a ring. Chromatin
stains colour it darkly.

_Asexual multiplication_ (fig. 13, _b_), which takes place in fæces,
follows a similar course to that of allied forms (_e.g._, _Euglypha_,
_Centropyxis_). It commences by the cytoplasm issuing from the
orifice of the shell and assuming the shape characteristic of the
mother organism, but in a reverse position. The nucleus then divides
by mitosis, when the daughter nuclei move apart from one another.
The chromidial ring also divides into two portions by a process of
dumb-bell like constriction. The one daughter nucleus remains in the
mother organism, the other moves towards the daughter individual, which
then separates from the parent.

[Illustration: FIG. 13.--_Chlamydophrys enchelys._ _a_, free, motile
form, showing nucleus, equatorial granules, vacuoles and pseudopodia;
_b_, dividing organism. × 760. (After Cienkowski.)]

  In this species plasmogamic union of two or more individuals (up
  to twenty) is frequently observed. Such colonies may similarly
  divide, and in this way monstrosities frequently arise. When drying
  of the fæces, or deficiency of food occurs, encystment takes place
  apparently spontaneously. The whole body, as stated by Cienkowski,
  issues from the shell, assumes a spherical shape (probably with
  discharge of water) and becomes surrounded with a thick membrane
  (fig. 14). After the addition of water and the escape of the encysted
  _Chlamydophrys_, a new shell must be formed. Schaudinn, who has not
  given a more detailed description of the process of encystment in
  this species, but refers to Cienkowski and to similar observations
  made on _Centropyxis_, states of the latter that the encystment takes
  place within the shell.

The _sexual multiplication_ is accompanied by shedding of all the
foreign bodies and of the degenerating nucleus. The protoplasm, now
contracting into a sphere, remains behind in the shell with the
chromidial mass. From the latter several new nuclei arise (sexual
nuclei) often eight in number. The cytoplasmic sphere then segregates
into as many spherical portions as there are nuclei present. When
they have assumed an oval form, two flagella develop at one pole
and the flagellispores swarm out of the shell.[35] The biflagellate
swarm-spores, or gametes, copulate in pairs and apparently the
individuals of the pairs of gametes arise from different mother
organisms. The zygote secretes a thick covering which soon becomes
brown and rough. These zygote cysts or resistant spores must now pass
from the intestine of an animal in order to complete their development.
The escape of the cyst contents does not always take place in the
intestine; often it does not occur until after defæcation. These
shell-less individuals (amœbulæ) soon become invested with a shell. But
in the alkaline intestinal contents, shell formation may proceed even
while the organism is in the intestine, and multiplication may take

[35] Schaudinn (1903), _Arb. a. d. Kaiserl. Gesundh._, xix, p. 547.

[Illustration: FIG. 14.--_Chlamydophrys enchelys_, encysted; on the
left the old capsule. × 760. (After Cienkowski.)]

Schaudinn’s further communication was of special interest; it was to
the effect that _Chlamydophrys_ was related to

*Leydenia gemmipara*, Schaudinn, 1896.

In the fluid removed by puncture from two patients suffering from
ascites in the first medical clinic in Berlin, cellular bodies with
spontaneous movement were found, which Leyden and Schaudinn regard as
distinct organisms. They remained alive without the use of the warm
stage for four or five hours, the external temperature being 24° to
25° C. In a quiescent condition they were of a spherical or irregular
polygonal form. Their surface was rarely smooth, being beset with
protuberances and excrescences (fig. 15). The substance of the body
was thickly permeated with light refractile granules with a yellowish
shimmer. The hyaline ectoplasm was rarely seen distinctly. All sizes
from 3 µ to 36 µ in diameter were observed. The movements were rather
sluggish, the ectoplasm in the meantime appearing in the form of one
or several lamellæ, in which also strings of the granular endoplasm
occurred, and frequently protruded over the border of the hyaline
pseudopodia. The tendency for the joining of several individuals by
means of their pseudopodia was so marked that associations ensued
similar to those known in free-living Rhizopoda.

The cytoplasm enclosed blood corpuscles as well as numerous vacuoles,
one of which pulsated slowly about every quarter of an hour. A
vesicular nucleus the diameter of which was about equal to one-fifth of
the body was present.

Multiplication took place by means of division and budding (fig. 15,
_c_), after previous direct division of the nucleus. The buds were
supposed to divide repeatedly soon after their appearance, thus giving
rise to minute forms of 3 µ.

There was a suspicion in both cases that the ascites was associated
with malignant neoplasms in the abdomen, and autopsy confirmed this
view in one case.

[Illustration: FIG. 15.--_Leydenia gemmipara_, Schaud. _a_, in a
quiescent condition, × 1000; _b_, in the act of moving, × 1000; _c_,
from a fixed preparation, showing a bud, × 1500.]

The parasite, which has seldom been observed, has been variously
interpreted; for example, it has been regarded merely as altered tissue
cells. It is now known, from Schaudinn’s researches, that _Leydenia
gemmipara_ is connected with abnormal conditions of _Chlamydophrys_,
occasionally occurring as a commensal in the ascitic fluid. The form is
produced when pathological conditions of the large intestine create an
alkaline reaction of its whole contents. The formation of shells then
often ceases, and these naked _Chlamydophrys_ are enabled to multiply
atypically by division and gemmation. Such stages, which are no longer
capable of a normal development, are the _Leydenia_, as Schaudinn has

Class II. *MASTIGOPHORA*, Diesing.

Sub-Class. FLAGELLATA, Cohn emend. Bütschli.

  During the motile part of their life the Flagellata possess one
  or more flagella which serve for locomotion, and in many cases
  also for the capture of food. A few groups (_Euglenoidinæ_,
  _Choanoflagellata_) have only one flagellum, others two or several
  of about equal length (_Isomastigoda_), or of various lengths
  (_Monadina_, _Heteromastigoda_, _Dinoflagellata_). The long flagellum
  is the principal one; the smaller ones on the same organism are
  accessory flagella. The flagella directed backwards, which occur in
  the Heteromastigoda and are used for clinging, are termed trailing
  flagella or tractella. At the base of the flagellum, which is
  almost always at the anterior end, a Choanoflagellate possesses a
  cytoplasmic funnel-shaped neck or collar. In the parasitic forms an
  undulating membrane is often present.

  The body of the Flagellata is usually small, generally elongate and
  of unchangeable form. It is frequently covered by a distinct cuticle,
  and, in certain groups, by a hard envelope, or it may be more or
  less loosely enveloped by a gelatinous or membranous covering. An
  ectoplasmic layer is thin and not always obvious. The granular
  cytoplasm contains a varying number of vacuoles, one of which may be
  contractile, and is generally situated near the area from which the
  flagella arise, that is, at the anterior extremity. The cytoplasm,
  moreover, contains the nucleus, which is nearly always single; and in
  many species there are also yellow, brown, or green chromatophores
  of various shapes, such as occur in plants. Some species feed after
  the manner of green plants (holophytic), or of plants devoid of
  chlorophyll (saprophytic); others, again, ingest solid food, and
  for this purpose usually possess a cytostome; the latter, however,
  in a few forms is not used for its original function, but is
  connected with the contractile vacuole. Many parasitic forms feed
  by endosmosis. A few species possess eye-spots with or without
  light-refracting bodies.

  Variation in the form of the nuclear apparatus occurs. One nucleus
  only, which may be compact or vesicular, is known in many species.
  This nucleus is situated either centrally or sometimes near the
  flagellar end of the body, but its position is subject to variation.
  The flagella may arise near the nucleus. Other structures, such as
  an axial filament and a rhizoplast, may be present. Some flagellates
  are binucleate, the two nuclei--which often differ in size and
  shape--being separated from each other. One of these nuclei is the
  principal, vegetative or trophic nucleus; the other is an accessory
  nucleus, frequently termed the blepharoplast, flagellar or kinetic
  nucleus. One or more small basal granules are often present at or
  very near the origin of the flagella.

  Multiplication is by fission, usually longitudinal, which may occur
  in either the free or encysted forms. Division is initiated by that
  of the nucleus or nuclei (especially the kinetic nucleus). The
  basal granule divides also. Collars and chromatophores, if present,
  likewise separate into two. Variation in the method of doubling the
  original number of flagella occurs. In most organisms, especially
  uniflagellate forms, the flagellum splits lengthwise, after division
  of the basal granule, blepharoplast and nucleus. The daughter
  flagella may be of the same or different lengths and thicknesses.
  Other flagellates at division are said to produce new flagella in the
  neighbourhood of the original ones. The daughter organisms in such
  cases are provided with one or more parental flagella in addition
  to newly formed ones. It has been stated that in certain cases the
  parent flagellate retains all its flagella, while new ones arise _ab
  initio_ in the cytoplasm of the daughter forms.

  Multiplication by longitudinal fission may be interrupted sooner or
  later by the production of gametes, which form zygotes, from which
  new generations of individuals arise. In many flagellates gamete
  formation and sporogony are unknown, and asexual reproduction by
  fission alone prevails.

  Incomplete division results in the formation of colonies of
  individuals. These colonies must not be confused with the aggregation
  rosettes of flagellates found among the parasitic Mastigophora.
  The individuals of aggregation rosettes are capable of immediate
  separation from the rosette at will.

  A number of parasitic Flagellata produce non-flagellate stages which
  are very resistant to external conditions, the assumption of which
  forms serves to protect the organisms during their transference
  from one host to another. Such non-flagellate forms possess one
  or more nuclei, are usually of an oval or rounded contour, and
  are capable of developing into the full flagellate on the return
  of more favourable conditions. These forms are often known as the
  post-flagellate stage of the organism. When ingested by a new host,
  the post-flagellate coat becomes more flexible, and the phase of the
  organism which now recommences growth is known as the pre-flagellate
  stage; it gradually develops into the typical flagellate organism.

  Many Flagellata live free in fresh and salt water. They prefer
  stagnant water, rich in organic products of decomposition, such as
  puddles, swamps and pools. Those forms developing shells and colonies
  are, as a rule, adherent. A number of species are parasitic in man
  and animals, living mostly within the intestine or in the blood.

  It is usual to classify the Flagellata in four orders:
  _Euflagellata_, _Dinoflagellata_, _Choanoflagellata_, and
  _Cystoflagellata_, of which only the _Euflagellata_ are of interest
  to us. This is a group comprising numerous species, for the further
  classification of which the number and position of the flagella are

  The Euflagellata observed in man belong to the Protomonadina as well
  as to the Polymastigina. The former possess either only one or two
  similar flagella, or one principal and one or two accessory flagella.
  The Polymastigina possess at least three flagella of equal size,
  or four to eight of unequal size, inserted at different points. An
  undulating membrane may be present in members of both groups.

  It must also be pointed out that unicellular organisms with one or
  several flagella are not always classified with flagellates, for such
  forms occur in Rhizopods as well as temporarily in the lower plants.
  In addition, the examination of the flagellates, especially the
  parasitic species, is very difficult on account of their diminutive
  size and great activity; thus it happens that certain forms cannot
  with certainty be included in the group because their description is

Order. *Polymastigina*, Blochmann.

The Polymastigina contains flagellates with three to eight flagella.
Some of the Flagellata parasitic in man belong to the Polymastigina,
and to two or three genera that are easily distinguishable.

Genus. *Trichomonas*, Donné, 1837.

  The body is generally pyriform, the anterior part usually rounded,
  the posterior part pointed. There are at the anterior extremity three
  (? four) equally long flagella that are sometimes matted together.
  A blepharoplast (kinetic nucleus) and basal granule are present,
  together with a supporting structure known as an axial filament or
  axostyle. In addition there is an undulating membrane, bordered by
  a trailing flagellum, that commences at the anterior extremity and
  proceeds obliquely backwards. The nucleus, which is vesicular, is
  situated near the anterior extremity, and behind it are one or more
  vacuoles, none of which seems to be contractile. These flagellates
  are parasitic in vertebrate animals, and live chiefly in the

*Trichomonas vaginalis*, Donné.

The form of the body is very variable, and is elongate, fusiform or
pear-shaped, also amœboid. The length varies between 15 µ and 25 µ,
and the breadth between 7 µ and 12 µ. The posterior extremity is drawn
out to a point and is about half the length of the remainder of the
body. The cuticle is very thin and the body substance finely granular.
At the anterior extremity there are three--some say four[36]--flagella
of equal length which are frequently united together, at least at the
base, and are easily detached.

[36] To explain this discrepancy it is stated that the border of the
undulating membrane can be detached in the form of an independent
flagellum. But Parisi (1910) places such quadriflagellate forms in the
sub-genus _Tetratrichomonas_, _Arch. f. Protistenk._, xix, p. 232.

There is an undulating membrane (fig. 16) which runs spirally across
the body, arising from the place of insertion of the flagella, and
terminating at the base of the caudal process. A cytostome seldom is
recognizable in fresh specimens, but is apparently present. The nucleus
is vesicular, elliptical and situated near the anterior extremity.[37]

[37] According to Marchand, the nucleus is connected with a line,
which becomes visible on addition of acetic acid, terminates at the
posterior extremity, and does not correspond to the line of insertion
of the undulating membrane. This formation probably is the same as the
axostyle in _Trichomonas batrachorum_, Perty. Blochmann (1884) also
mentions two longitudinal rows of granules, which commence at the same
place as the nucleus and converge posteriorly.

Multiplication takes place by division (Marchand). Encysted forms are
almost unknown.

  _Trichomonas vaginalis_ lives in the vaginal mucus of women of
  various ages, not in normal mucus, but in mucus of acid reaction.
  It is found in menstruating females as well as in females who
  have passed the menopause. It occurs in pregnant and non-pregnant
  women, even in very young girls, provided always that they have a
  vaginal catarrh with acid reaction of the secretion. Should the acid
  reaction change, as, for instance, during menstruation, the parasites
  disappear, as they do likewise on injection of any alkaline fluid
  into the vagina. A low temperature (below +15° C.) is also fatal to
  the parasites. These flagellates can pass from the vagina through the
  urethra into the bladder, and produce severe catarrh, and are not
  easily removed.

[Illustration: FIG. 16.--_Trichomonas vaginalis_, Donné. × 2,000
approx. (After Künstler.) Four flagella are represented, but usually
only three are present.]

_T. vaginalis_ appeared to be a parasite specific to the female organs
and not transmissible to man. However, several observations have since
been made that confirm the occurrence of this species in the urethra
of the male. The infection apparently takes place through coitus when
changes are present in the urethral mucous membrane. At any rate, three
cases observed point to this circumstance.

Attempts at experimental transmission to rabbits, guinea-pigs and dogs
failed (Blochmann, Dock). So far, the manner in which women become
infected is unknown.

*Trichomonas intestinalis*, R. Leuckart, 1879 = *Trichomonas hominis*,
Davaine, 1854.

Some authors believe that a second trichomonad inhabiting man,
_Trichomonas intestinalis_, R. Lkt., is identical with _Trichomonas
vaginalis_, Donné. Leuckart’s species was based on the discoveries
of Marchand (1875) and Zunker (1878), who stated that according to
all appearances, and in their opinion, it was the same as _Cercomonas
intestinalis_, Lambl, 1875 (_nec_ 1859), which they found in the fæces
of patients suffering from intestinal disorders. The organism is
described by them as being pear-shaped and 10 µ to 15 µ in length and
3 µ to 4 µ in breadth. The posterior extremity terminated in a point
(fig. 17).

[Illustration: FIG. 17.--_Trichomonas intestinalis_, Lkt. (After

  A row of twelve or more cilia was said to commence at the anterior
  end and extend over the body. Leuckart stated that this parasite,
  placed by the two authors in the genus _Cercomonas_, was a
  _Trichomonas_, and that they mistook the undulating membrane for
  cilia, and overlooked the flagella. Notwithstanding its striking
  similarity with _T. vaginalis_, it was said to be distinguishable
  from that species by differences in the undulating membrane. Lambl’s
  _C. intestinalis_[38] (of 1875) which corresponds with _C. hominis_,
  Davaine[39] (1854), is regarded by Leuckart as a true Cercomonad
  (characterized by a flagellum and the absence of an undulating
  membrane, see p. 61), and is thus generically distinct from

[38] Under the term _Cercomonas intestinalis_, Lambl in different
years has described two entirely distinct Flagellata, namely, in 1859
(“Mikr. Unters. d. Darm- Excrete,” _Prag. Vierteljahrsschr. f. prakt.
Hlkde._, lxi, p. 51; and Lambl, _A. d. Franz-Josephs-Kinderspitale in
Prag_, Prag, 1860, i, p. 360), a form that at the present day is termed
_Lamblia intestinalis_; and in 1875 (in the _Russian Medical Report_,
No. 33), a species identical with _Cercomonas hominis_, Dav.

[39] Davaine, C., “Sur les anim. infus. trouv. dans les selles d.
malad. atteints du cholera et d’autr. malad.,” _C. R. Soc. Biol._,
1854, ii, p. 129.

  The correctness of Leuckart’s judgment in regard to Marchand-Zunker’s
  flagellate was demonstrated by Grassi’s researches, accounts of which
  were published soon after. In about 100 cases of bowel complaints
  in North Italy and Sicily, Grassi found Flagellata in the stools,
  which he first named _Monocercomonas_ and _Cimænomonas_, but later
  termed _Trichomonas_. However, in opposition to Leuckart, Grassi
  has also classified Davaine’s _C. hominis_ (= _C. intestinalis_,
  Lambl, 1875) as _Trichomonas_, and most authors have followed his
  example. Hence arose the use of the name _Trichomonas hominis_. It
  was through Janowski (1896) that the former view was again taken
  up. After a review of the literature, the occurrence of Cercomonads
  in the intestine of human beings in addition to Trichomonads was
  considered by the author to have been proved, and he added a
  description of the Trichomonads. According to this, all morphological
  distinction between _T. vaginalis_, Donné, and _T. intestinalis_,
  Leuckart, disappeared. On the other hand, it is worthy of note
  that the smaller size, the more pear-shaped form, and the longer
  flagella differentiate _T. intestinalis_ (= _T. hominis_) from _T.

[40] For the present the following should be regarded as synonymous:
_Protoryxomyces coprinarius_, Cunningham (_Quart. Journ. Micr. Sci._
(2) 1880, xxi, p. 234), (_Zeitschr. f. Biol._, 1882, viii, p. 251).
_Monocercomonas hominis_, Grassi, 1882. _Cimænomonas hominis_,
Grassi, 1882. _Trichomonas hominis_, Grassi, 1888. _Cercomonas coli
hominis_, May (_Deutsches Archiv. f. klin. med._, 1891, xlix, p. 51).
_Monocercomonas hominis_, Epstein (_Prag. med. Wochenschr._ 1893,
Nos. 38–40). _Trichomonas confusa_, Stiles (_Zool. Anz._, 1902, xxv,
p. 689). _Trichomonas elongata_, _Trichomonas elliptica_, Cohnheim
(_Deutsche med. Wochenschr._, 1903, xxix, Nos. 12–14). _Trichomonas
elongata_, _Trichomonas caudata_, _Trichomonas flagellata_, Steinberg
(_Kiewer Zeitschr. f. neuere Medicin_, 1862). _Trichomonas pulmonalis_,
A. Schmidt, (_Münch. med. Wochenschr._, 1895, No. 51), and St. Artault
(_Arch. de parasit._ 1898, i, p. 279).

The easily deformed pear-shaped body has three free flagella
anteriorly, and an undulating membrane with its flagellar border
terminating in a short free flagellum posteriorly (figs. 17, 18).
The undulating membrane may coil itself spirally round the body. A
supporting rod or axostyle projects as a posterior spine. It appears
to begin near the nucleus and blepharoplast, which are situated near
the more rounded, anterior end of the body. There may be a chromatoid
basal supporting line along the body for the undulating membrane. Rows
of chromatoid granules are sometimes situated along one side of the
axostyle. A cytostome may sometimes be seen. In mice, Wenyon (1907)
found these parasites to vary in length from 3 µ to 20 µ. They occur
in the cæcum and intestine of mice, where their internal structure
seems more obvious than in man. The flagellates divide by longitudinal

[Illustration: FIG. 18.--_Trichomonas intestinalis_ from man, showing
anterior flagella, cytostomic depression anteriorly, undulating
membrane, nuclei, and axostyle. ×2,500. Original.]

_T. intestinalis_, R. Leuckart, appears to be capable of settling
in all parts of the human intestine in which the contents have an
alkaline reaction. Trichomonads have been cited as occurring in the
oral cavity by Steinberg, Zunker, Rappin and Prowazek; in the œsophagus
by Cohnheim, and in the stomach by Strube, Cohnheim, Zabel, Hensen
and Rosenfeld. The normal situation seems to be the small intestine.
The parasites then appear in the dejecta, especially in various
intestinal diseases the course of which is connected with an increased
peristalsis. They are also found in healthy persons, from whom they are
obtained after the administration of laxatives. They have been regarded
by some workers as commensals, which, however, have the power of
accelerating the onset of intestinal complaints, or at least of adding
to them. They have been found in cases of carcinoma of the stomach, and
in other diseases of that organ in which the acid reaction ceased.

  Naturally, whether all the reports relate to the same species of
  Trichomonas must remain undecided. Certain authors (Steinberg,
  Cohnheim, van Emden) accept several species. Prowazek speaks of a
  variety of _T. intestinalis_ inhabiting the oral cavity. This was
  distinguished by a posterior process exceeding the length of the
  body fourfold, and by a somewhat unusual course of the undulating
  membrane. The food of this form, which was found in the whitish
  deposit present, especially in the cavities of carious teeth,
  consisted almost exclusively of micrococci. Schmidt and St. Artault
  named the Trichomonads found in pathological products (_e.g._,
  gangrene, putrid bronchitis, phthisis) of the lungs of man, as
  _Trichomonas pulmonalis_. Trichomonads have also been found by
  Wieting in lobular pneumonia in the lungs of pigs.

  It is still uncertain in what way the infection takes place.
  Experiments in the transmission of free trichomonads to mammals (_per
  os_), in which the same or allied species occur (guinea-pigs, rats,
  apes), have been without result. Probably encystment is necessary.
  Such conditions are mentioned by May, Künstler, Roos, Schurmayer, van
  Emden, Prowazek, Galli-Valerio and Schaudinn. According to Prowazek,
  intestinal trichomonads of rats become encysted for conjugation. In
  the cyst an accumulation of reserve food material occurs, causing
  distension. The nuclei of the conjugants each give off a reduction
  body and, after fusion, produce the nuclei for the daughter
  individuals. According to Schaudinn the intestinal trichomonads lose
  their flagella before conjugation, become amœboid and encyst in
  twos, the formation of a large agglomeration of reserve substance
  accompanying this. Galli-Valerio found double-contoured cysts in
  the fæces of trichomonad-infected guinea-pigs, after the fæces had
  been kept for a month in a damp chamber. When exposed to heat small
  flagellates escaped from them. Administration of such material
  containing cysts resulted in severe infection with trichomonads,
  and death of the experimental guinea-pigs followed. The cyst wall
  is clearly a protection against the deleterious acid reaction of
  the stomach contents. Alexeieff (1911) and Brumpt (1912) think that
  the trichomonad cysts of man are really fungi, while other workers
  also doubt encystment among trichomonads. Wenyon (1907) states that
  _T. intestinalis_ in mice produces spherical contracted forms which
  escape from the body in the fæces.

  Air, water, and under certain circumstances even food may be regarded
  as vectors for the trichomonads. The occurrence of the organisms in
  the oral cavity, and still more so in the lungs, is in favour of the
  air being the transmitting agent. An observation made by Epstein
  supports the idea of water transmission. Multiplication of the
  trichomonads, once they have gained access to the body, is effected
  by longitudinal division commencing at the anterior end (Künstler).
  “Cercomonads” with several flagella and an undulating membrane, as
  well as trichomonads, have been observed by Ross in some cases of
  cutaneous ulcers.

Mello-Leitao (1913)[41] has described flagellate dysentery in children
in Rio de Janeiro. He states that it is due to _T. intestinalis_ and
_Lamblia intestinalis_ either separately or together. Flagellate
dysentery, he thinks, is benign and is the most frequent form of
dysentery in infants. The flagellates are pathogenic to infants under
three years of age. Escomel (1913)[42] found 152 cases of dysentery in
Peru due solely to Trichomonas. Such cases are probably widespread.

[41] _Brit. Journ. Children’s Diseases_, x, p. 60.

[42] _Bull. Soc. Path. Exot._, vi, p. 120.

Genus. *Tetramitus*, Perty, 1852.

  *Tetramitus mesnili*, Wenyon, 1910.

  Syn.: _Macrostoma mesnili_, _Chilomastix mesnili_, _Fanapapea

The genus _Tetramitus_ differs from _Trichomonas_ in possessing an
undulating membrane inserted in a deep groove or cytostome. There are
three anterior flagella. The pear-shaped organism measures 14 µ by 7 µ,
but smaller examples occur. _T. mesnili_ occurs in the human intestine,
having been described by Wenyon[43] (1910) from a man from the Bahamas
in the Seamen’s Hospital, London. Its occurrence is widespread.
Alexeieff considers that _Macrostoma_ and _Tetramitus_ are synonymous.
The parasite is the same as _Fanapapea intestinalis_, Prowazek, 1911,
from Samoa. Brumpt (1912) found _T. mesnili_ to be the causal agent of
colitis in a Frenchwoman. Nattan-Larrier (1912) considers it of little
pathological importance.

[43] _Parasitology_, iii, p. 210.

Gäbel[44] (1914) described an interesting case of seasonal diarrhœa
acquired in Tunis, in which a new Tetramitid was the causal agent. The
organism was pear-shaped, without an undulating membrane, and measured
6·5 µ to 8 µ by 5 µ to 6 µ. The cytostome was large, and there was
no skeletal support. Encystment occurred. Gäbel named the organism
_Difämus tunensis_ and considered that it was pathogenic.

[44] _Arch. f. Protistenk._, xxxiv, p. 1.

Genus. *Lamblia*, R. Blanchard, 1888.

  Syn., _Dimorphus_, Grassi, 1879, _nec_ Haller, 1878; _Megastoma_,
  Grassi, 1881, _nec_ de Blainville.

  The body is pear-shaped, with a hollow on the under surface
  anteriorly. It has four pairs of flagella directed backwards, of
  which three pairs lie on the borders of the hollow disc, and the
  fourth arises from the pointed posterior extremity.

*Lamblia intestinalis*, Lambl, 1859.

  Syn.: _Cercomonas intestinalis_, Lambl, 1859 (_nec_ 1875); _Hexamitus
  duodenalis_, Davaine, 1875; _Dimorphus muris_, Grassi, 1879;
  _Megastoma entericum_, Grassi, 1881; _Megastoma intestinale_, R.
  Blanch., 1886; _Lamblia duodenalis_, Stiles, 1902.

The organism is pear-shaped and bilaterally symmetrical. It is from
10 µ to 21 µ long and 5 µ to 12 µ broad and possesses a thin cuticle.
Anteriorly an oblique depression is present, which functions as a
sucking disc (fig. 19, _s_). Its edges are raised above the general
surface and are contractile. It corresponds to a peristome and acts as
an adhesive organ (fig. 20, _b_, _c_). No true cytostome is present.
A double longitudinal ridge, representing axostyles, extends from the
sucking disc to the tapering posterior extremity, which is prolonged as
two flagella from 9 µ to 14 µ long.

_Lamblia intestinalis_ possesses eight flagella (fig. 19). The first
pair of flagella, which cross one another, arise in a groove formed by
the anterior edge of the sucking disc. Two pairs of flagella (lateral
and median) are inserted on the posterior edge of the disc, while the
posterior flagella occur at the tapering posterior extremity of the
body. Basal granules are found at the bases of the flagella. The median
flagella are most active in movement, the anterior and lateral flagella
being less motile, as they are partially united to the body for part of
their length.

The nuclear apparatus is situated in the thin, anterior, hollowed
part of the body. It is at first dumb-bell shaped, the “handle” of
the dumb-bell being formed by a very slight connecting strand, which
eventually separates, so that the flagellate becomes binucleate, and
thus completes the general bisymmetry of the organism.

There is a karyosome in each nucleus. Other bodies of unknown function,
and possibly composed of chromatin, occur on or near the axostyles.

[Illustration: FIG. 19.--_Lamblia intestinalis_. A, ventral view; B,
side view; N, one of the two nuclei; _ax._, axostyles; _fl_^1, _fl_^2,
_fl_^3, _fl_^4, the four pairs of flagella; _s_, sucker-like depressed
area on the ventral surface; _x_, bodies of unknown function. (After

Division has not been observed in the flagellate stages of the Lamblia,
but it occurs within the cysts. The resistant cysts (fig. 20, _e_) are
oval and are surrounded by a fairly thick, hyaline cyst wall. They
measure 10 µ to 15 µ by 7 µ to 9 µ, and may be tetranucleate. According
to Schaudinn, the cysts arise from the conjugation of two individuals,
and nuclear rearrangement occurs.

_L. intestinalis_ occurs in its flagellate stage in the duodenum and
jejunum, and rarely as such in the other parts of the intestine.
Normally it is found in the large intestine as cysts, which are voided
with the fæces. The hosts of Lamblia include _Mus musculus_, _M.
rattus_, _M. decumanus_, _M. silvestris_, _Arvicola arvensis_ and _A.
amphibius_, the dog and cat, rabbit, sheep and man. Cysts voided with
the fæces of infected animals reach plants or drinking water, and
thence are transferred to man.

The flagellate in these different hosts exhibits some variation in
size and in the problematic chromatic bodies. Bensen has suggested the
species _L. intestinalis_ from man, _L. muris_ from the mouse and _L.
cuniculi_ from the rabbit. It is not certain whether these different
species are necessary, as the variation may be due to differences of

[Illustration: FIG. 20.--_Lamblia intestinalis._ _a_, from the surface;
_b_, from the side; _c_, on intestinal epithelium cells; _d_, dead and
_e_, encysted. (After Grassi and Schewiakoff.)]

Like Trichomonas, Lamblia can multiply under inflammatory conditions
of the alimentary tract. Thus they are found in cases of diarrhœa,
carcinoma of the stomach, etc. The parasites attach themselves by
their sucking discs to the epithelial cells of the gut (fig. 20, _c_),
and though their numbers may be very great, their direct pathological
significance is not fully known. Their occurrence in cases of diarrhœa
has been explained as being due to the increased peristalsis, which
has detached the parasites from the epithelium. Free flagellate forms
perish in stools if kept, more especially if the temperature falls
below 0° C. or rises above 40° C. Lamblia has often been found in
dysenteric diseases, especially in the East, and is said to be the
causal agent of certain diarrhœas in India. Mathis (1914)[45] found
Lamblia in cases of diarrhœa with dysenteriform stools in Tonkin. He
also discovered healthy carriers of Lamblia cysts.

[45] _Bull. Soc. Med. Chirurg. Indo-Chine_, v, p. 55.

  The parasite under discussion was first observed by Lambl (1859) in
  the mucous evacuations of children. He regarded the parasite as a
  Cercomonad and termed it _Cercomonas intestinalis_, which name as a
  rule is applied to _Cercomonas hominis_, Davaine, although Stein had
  already pointed out the difference between the two species. Grassi
  (1879) observed this species first in mice (calling it _Dimorphus
  muris_), and subsequently in human beings in Upper Italy and named
  it _Megastoma entericum_. Bütschli and Blanchard then laid stress on
  the identity of this species with Lambl’s _C. intestinalis_ (1859),
  and consequently called it _Megastoma intestinale_. Later, Blanchard
  drew attention to the circumstance that the generic name _Megastoma_
  chosen by Grassi had already been used four times for various kinds
  of animals, and established the genus _Lamblia_. Accordingly, _L.
  intestinalis_ is the valid name, and should be generally adopted.

  In Upper Italy the parasite in the encysted condition has also
  been seen by Perroncito in man. At the same time, Grassi and
  Schewiakoff began a new investigation of specimens from mice and
  rats. In Germany, _L. intestinalis_ was found by Moritz and Hölzl,
  Roos, Schuberg and Salomon. Moritz and Hölzl confirmed the relative
  frequency of the species. In Königsberg, Prussia, a student found
  encysted _Lamblia_ in his fæces. One case was reported from Finland
  by Sievers, another case from Scandinavia by Müller. Frshezjesski and
  Ucke reported cases from Russia. Jaksch announced the occurrence of
  the parasite in Austria; Piccardi mentioned their presence again in
  Italy. They were reported from Egypt by Kruse and Pasquale, and from
  North America (Baltimore) by Stiles. Noc stated that 50 per cent. of
  the population of Tonkin harboured _Lamblia_. Finally, the structure
  of _L. intestinalis_ has been described by Metzner (1901), and by
  Wenyon[46] (1907) in mice.

[46] _Arch. f. Protistenkunde_, Suppl. i, p. 169.

In all these cases _L. intestinalis_ has been observed in the small
intestine, or in the evacuations of patients with intestinal diseases.
It has also been found in the intestine of healthy subjects. Just
as _Trichomonas intestinalis_ may be found inhabiting the stomach
in diseases of that organ, in which an alkaline reaction is present
(carcinoma), so has _L. intestinalis_ been found to occur under
similar circumstances (Cohnheim, Zabel). However, in Schmidt’s case,
1 per cent. hydrochloric acid was certainly stated to be present.
Infection takes place by the ingestion of cysts (fig. 20, _e_), as was
established by Grassi, experimentally on himself. Cereal food-stuffs,
contaminated with Lamblia cysts from vermin of the locality, such as
rats and mice, serve to convey the infection to man. Such cysts may
probably be found in street-dust, etc. Stiles induced infection in
guinea-pigs, and Perroncito in mice and rabbits, by means of cysts of
Lamblia from human beings. Stiles suspected that flies could transport
Lamblia cysts. Mathis (1914) found that _L. intestinalis_ was not
amenable to emetine, at any rate in its cystic stage.

Order. *Protomonadina*, Blochmann.

The smallness of the Protomonadines and their less superficial
situation than the Polymastigines, may be the cause that so far as
the species occurring in man are concerned, they were formerly less
well known. As regards parasitic species, this group may be divided
as follows, according to the number of flagella and the presence or
absence of an undulating membrane:--

(1) _Cercomonadidæ_, with one flagellum at the anterior extremity,
without an undulating membrane.

(2) _Bodonidæ_, with two flagella, without an undulating membrane,
except in Trypanoplasma.

(3) _Trypanosomidæ_, with one flagellum, and an undulating membrane
along the length of the body in some genera.

Family. *Cercomonadidæ*, Kent emend. Bütschli.

Small uniflagellate forms, without cytostome.

Genus. *Cercomonas*, Dujardin emend. Bütschli.

Oval or rounded organisms, with the aflagellar end often drawn out into
a tail-like process.

*Cercomonas hominis*, Davaine, 1854.

Davaine found flagellates in the dejecta of cholera patients. They
had pear-shaped bodies, lengthening to a point posteriorly. Their
length was from 10 µ to 12 µ, and a flagellum about twice as long as
the body projected from one extremity (fig. 21). A nucleus was hardly
recognizable. Occasionally a somewhat long structure (cytostome?)
appeared at the anterior extremity. The animals moved with remarkable
activity. They also attached themselves by means of their posterior
extremities and swung about around the point of attachment. Davaine
found a smaller variety, only about 8 µ long, in the dejecta of a
typhoid patient (fig. 21, _b_).

[Illustration: FIG. 21.--_Cercomonas hominis_, Dav. _a_, larger,
_b_, smaller variety. Enlarged. (After Davaine.)]

[Illustration: FIG. 22.--_Cercomonas hominis_, Dav. From an
Echinococcus cyst. (After Lambl.)]

  The Flagellata observed by Ekeckrantz (1869) in the intestine of
  man belong to this form--at least to the larger variety--and Tham
  (1870) reported fresh cases soon after. Lambl’s publication of 1875,
  which was written in Russian, and became known through Leuckart’s
  work on parasites, also alludes to apparently typical Cercomonads,
  which, however, were discovered, not in the intestine, but in an
  _Echinococcus_ cyst in the liver (fig. 22). The elliptical, fusiform,
  rarely pear-shaped or cylindrical bodies of the parasites measured
  5 µ to 14 µ in length, and were provided with a flagellum at one end,
  while the other extremity usually terminated in a long point. An oral
  aperture occurred at the base of the flagellum, and there were one or
  two vacuoles near the posterior extremity. Longitudinal division was
  also observed (fig. 22).

As already mentioned, this form, which Lambl termed _Cercomonas
intestinalis_, differs considerably from the form found by the same
author in 1859, which received the same designation (_cf. Lamblia
intestinalis_, p. 60), but it corresponds with _Cercomonas hominis_,
Davaine. The latter, as well as _C. intestinalis_, Lambl, 1875, is
usually classed with the Trichomonads, but, as has already been
remarked (_cf._ _Trichomonas intestinalis_, p. 54), this cannot be
considered correct, as only _one_ flagellum is present.

_Cercomonas vaginalis_ (Castellani and Chalmers, 1909) was found in the
vagina of native women in Ceylon.

Other species of _Cercomonas_ have, at various times, been recorded
from man. However, the parasitic species of the genus _Cercomonas_
require further investigation.

  According to Janowski (1896–7), typical Cercomonads have also been
  observed in the intestine of man by Escherich, also by Cahen,
  Massiutin, Fenoglio, Councilman and Lafleur, Dock, Kruse and
  Pasquale, Zunker, Quincke and Roos, and others. However, it is an
  open question whether the Flagellata observed by Roos in one of his
  cases belonged to Davaine’s species, the size showing some deviation
  (14 µ to 16 µ). In his, as in many other cases, doubts have been
  raised as to whether the flagellates found in the stools had actually
  lived in the intestine, or had subsequently appeared in the fæces:
  for this a surprisingly short time only is necessary. Salomon also
  appears to have observed Cercomonads (_Berl. klin. Wochenschr._,
  1899, No. 46).

  As with _T. intestinalis_ so with _C. hominis_, it appears that
  the parasite settles not only in the intestine but also in the
  air-passages. This is demonstrated by the statements of Kannenberg
  and Streng of the occurrence of Monads and Cercomonads in the
  sputum and putrid expectoration in gangrene of the lungs, which no
  doubt apply to _C. hominis_ (_cf._ also Artault). Possibly also the
  Flagellata observed in the pleural exudation by Litten and Roos may
  be included here; this is the more probable in Roos’s case as the
  process ensued in the pleura after the breaking through of a vomica.

  Perroncito and Piccardi have described encysted stages of Cercomonads.

*Monas pyophila*, R. Blanch., 1895.

[Illustration: FIG. 23.--_Monas pyophila_, R. Blanch. (After Grimm.)]

  R. Blanchard thus designates a Flagellate that Grimm found in the
  sputum, as well as in the pus of a pulmonary and hepatic abscess,
  in the case of a Japanese woman living in Sapporo. The parasites
  resemble large spermatozoa (fig. 23). The body, 30 µ to 60 µ, has
  the shape of a heart or a myrtle leaf, and is surrounded by a thick
  cuticle which is supposed to extend into the interior of the body,
  dividing it into three parts. A long appendix at the rounded pole
  is covered for the greater part of its length by the cuticle; the
  extremity, however, is free and resembles a flagellum. The parasites
  were very active, frequently changed their shape, and were able to
  retract the long appendix within the body, which then assumed a round

  [This organism requires further investigation.]

Family. *Bodonidæ*, Bütschli.

_Protomonadina_ which are either free-living or parasitic, with two
dissimilar flagella, while the possession of an undulating membrane and
of a kinetic nucleus or blepharoplast is variable.

There are three genera:--

  1. _Bodo_, Stein, 1878, without a kinetic nucleus and undulating

  2. _Prowazekia_, Hartmann and Chagas, 1910, with a kinetic
  nucleus and without an undulating membrane.

  3. _Trypanoplasma_, Laveran and Mesnil, 1901, with a kinetic
  nucleus and undulating membrane.

Of these genera _Prowazekia_ must be discussed. _Bodo_ does not occur
in man. Species of _Trypanoplasma_ occur in the blood and in the gut
of various fishes, in the seminal receptacle of certain snails, in
the gut and genitalia of a flatworm (_Dendrocœlum lacteum_) and in
the vagina of a leech. Closely allied to _Trypanoplasma_ is the genus
_Trypanophis_, parasitic in the cœlenteric cavity of Siphonophores.

Genus. *Prowazekia*, Hartmann and Chagas, 1910.

The genus was founded for a flagellate parasite, _Prowazekia cruzi_,
discovered in a culture of human fæces in Brazil. Various other species
have been referred thereto. The genus is separated from _Bodo_ by
the possession of a second nucleus, the so-called kinetonucleus or
blepharoplast. It differs from _Trypanoplasma_ in the absence of an
undulating membrane. It is heteromastigote, that is, it possesses two
dissimilar flagella, one anteriorly directed and the other lateral and

The principal species are:

*Prowazekia urinaria*, Hassall, 1859.

  Syn.: _Bodo urinarius_, Hassall, 1859; _Trichomonas irregularis_,
  Salisbury, 1868; _Cystomonas urinaria_, Blanchard, 1885; _Plagiomonas
  urinaria_, Braun, 1895.

Hassall[47] in 1859 first found Bodo-like flagellates in human urine.
He examined fifty samples of urine from patients suffering from
albuminuria and from cholera. The reaction of the urine was alkaline
or sometimes only feebly acid. The flagellates were only seen after
the urine had been standing for several days. Hassall named the
organism _Bodo urinarius_, and gave a very good description of it
with illustrations. The flagellate, which was round or oval, measured
14 µ by 8 µ. The organism had “one, usually two, and sometimes three
lashes or cilia.” In 1868 Salisbury described a similar flagellate in
the urine under the name _Trichomonas irregularis_. Künstler in 1883
described the latter parasite under the name _B. urinarius_. In 1885
Blanchard, considering Künstler’s organism a different parasite from
Hassall’s, called it _Cystomonas urinaria_. Braun, in 1895, gave the
name _Plagiomonas urinaria_. Barrois (1894) considered Künstler’s and
Hassall’s organisms to be identical and not to be true parasites of
man. Sinton,[48] in 1912, found the flagellate in the deposit, after
centrifuging, of a 24-hour old specimen of alkaline urine from a
Mexican sailor in the Royal Southern Hospital, Liverpool. Sinton found
a kinetic nucleus or blepharoplast in the organism, and therefore
placed it in the genus _Prowazekia_.

[47] _Lancet_, 1859, ii, p. 503.

[48] _Annals Trop. Med. and Parasitology_, vi, p. 245.

[Illustration: FIG. 24.--Types of _Prowazekia urinaria_. (_a_)
sausage-shaped; (_b_) round; (_c_) carrot-shaped form. (After Sinton.)]

The flagellate stage (fig. 24) of the organism is polymorphic, and
may be either (_a_) sausage-shaped, 10 µ to 25 µ in length by 2·5 µ
to 6 µ in breadth; (_b_) round or oval, varying from 4 µ in diameter
to oval forms 15 µ by 10 µ; (_c_) a carrot-shaped form, of varying
size up to 25 µ by 4 µ. The kinetic nucleus is large and pear-shaped.
Near it are basal granules, closely applied to one another, from which
the flagella arise. There is a small cytostome near the roots of the
flagella. There is a well-marked karyosome in the nucleus. The movement
is jerky. The shorter, anterior flagellum may be used in food-capture.
In life, bacteria have been seen to be ingested. Food-vacuoles tend to
accumulate at the posterior (aflagellar) end. A contractile vacuole
may be present, near the base of the cytostome, and may really be the
dilated fundus of the latter. Division occurs by binary fission. The
organism can encyst (fig. 25, _a_), when the flagella are lost, and
round or oval cysts are found, 5 µ to 7 µ in diameter. After a time
flagella are formed inside the cyst, and the organism emerges therefrom
in its typical flagellate form (fig. 25, _b_-_f_).

Sinton’s case is interesting. He obtained the flagellate only twice
from the same patient, a Mexican then in hospital in Liverpool. The
flagellate was not found in the patient’s fæces, nor was it found in
the urine on later occasions when taken aseptically.

[Illustration: FIG. 25.--_Prowazekia urinaria_. Flagellate emerging
from cyst. (After Sinton.)]

In cultures _Prowazekia urinaria_ was always found in association with
bacteria. The cultures died at a temperature of 37° C., but grew well
at 20° C. Various media were useful at the lower temperature, such as
urine, salt agar, nutrient agar, serum agar, blood agar, peptone salt
solution, and diluted blood serum. The flagellate was, then, considered
to be an accidental contamination and not a true parasite of human

*Prowazekia asiatica*, Castellani and Chalmers, 1910.

The flagellate was found by the discoverers in the stools of patients
suffering from ankylostomiasis and diarrhœa in Ceylon. It was referred
by them to the genus _Bodo_, but in 1911 Whitmore[49] further studied
it and placed it in the genus _Prowazekia_. In the stools the
flagellate is found either as a long, slender form measuring 10 µ to
16 µ by 5 µ to 8 µ or as a rounded form 8 µ to 10 µ in diameter. Its
cytoplasm is alveolar. A rhizoplast connects the basal granules to the
kinetic nucleus. There is multiplication and cyst formation as before.
The organism is easily cultivated, especially in the condensation water
of nutrose agar and maltose agar. The pathogenicity is stated to be nil.

[49] _Arch. f. Protistenk._ xxii, p. 370.

*Prowazekia javanensis*, Flu, 1912.

Found in agar cultures from the motions of patients at Weltevreden,
Dutch East Indies.[50] The flagellates are 12 µ long and 5 µ broad. The
lateral flagellum is stated to be attached to the cell body for a short
distance. Regarding the karyosome in the nucleus, the author states
that the smaller the karyosome the more chromatin is deposited on the
nuclear membrane. Flu mentions that the specific name _javanensis_ is a
temporary one, as in the course of time it may be shown that there is
only one species of _Prowazekia_.

[50] _Geneesk. Tijdschr. v. Nederl. Ind._, lii, p. 659; _Med. v. d.
Burg. Geneesk. d. Nederl. Ind._, iii, p. 1.

*Prowazekia cruzi*, Hartmann and Chagas, 1910.

Found in a culture from human fæces on an agar plate in Brazil, and
considered to be a free-living form.[51] The organism is oval or
pear-shaped, 8 µ to 12 µ long and 5 µ to 6 µ broad. In human stools
at Tsingtau, China, a _Prowazekia_ has been found by Martini which he
thinks is the same as _Prowazekia cruzi_. He considers it to be a cause
of human diarrhœa and intestinal catarrh.

[51] _Mem. Inst. Osw. Cruz._, ii, p. 64.

*Prowazekia weinbergi*, Mathis and Léger, 1910.

This species was found in the fæces of men, both healthy and diarrhœic,
in Tonkin.[52] It is pear-shaped, 8 µ to 15 µ long by 4 µ to 6·5 µ
broad. The flagella occur at the broad end.

[52] _Bull. Soc. Med. Chir. Indo-Chine_, i, p. 471.

The discoverers think that _Prowazekia weinbergi_ is an intestinal
inhabitant, but non-pathogenic, since it was found to occur in the
fæces even when obtained with aseptic precautions.

*Prowazekia parva*, Nägler, 1910.

A free-living form found in the slime on the stones at the biological
station at Lunz. Another _Prowazekia_ was found in 1914 in tap-water in

Family. *Trypanosomidæ*, Doflein.

The Trypanosomidæ, broadly considered, are uniflagellate organisms,
the flagellum being at the anterior end. The flagellum arises near the
blepharoplast (kinetic nucleus), which lies anterior, near or posterior
to the nucleus.

The following genera will be considered:--

  _Trypanosoma_--with an undulating membrane along the length
  of the body.

  _Crithidia_--with a less well-developed undulating membrane
  anteriorly (see fig. 49).

  _Herpetomonas_--including the so-called _Leptomonas_, with anterior
  free flagellum only, and no undulating membrane.

  _Leishmania_--non-flagellate forms in mammalian blood, flagellate
  herpetomonad stages in culture, probably occurring
  naturally in Arthropods.

Genus. *Trypanosoma*, Gruby, 1843.

The members of the genus possess a single flagellum, which arises
posteriorly, adjacent to a blepharoplast or kinetic nucleus. The
flagellum forms a margin to an undulating membrane, and may or may not
be continued beyond the body as a free flagellum. Many species are
parasitic in vertebrate blood and in the digestive tracts of insects.


  The history of blood flagellates goes back to the year 1841, in which
  Valentin discovered in the blood of a brook-trout (_Salmo fario_ L.)
  minute bodies, from 7 µ to 13 µ in length, with active movements and
  presenting marked changes in form. Valentin considered the parasite
  a new species of the old genus _Proteus_ or _Amœba_, Ehrbg. This
  announcement led Gluge (1842) to publish a similar discovery he had
  made in frog’s blood. The latter forms were called by Mayer (1843)
  _Amœba rotatoria_, _Paramœcium loricatum_ and _P. costatum_, while
  Gruby (1843) called them _Trypanosoma sanguinis_.[53] Later it was
  discovered that similar organisms occurred also in the blood of birds
  (Wedl (1850), Danilewsky) and of mammals. Gros (1845) found them in
  the mouse and mole, Chaussat (1850) in the house rat, Lewis (1879) in
  the Indian rat, Wittich (1881) in the hamster. Danilewsky (1886–89)
  and Chalachnikow (1888) investigated the structure and division of

[53] Gruby’s generic name is generally accepted. Still others have
been used, _e.g._, _Undulina_, Ray _Lankester_, _Globularia_ Wedl,
_Paramecioides_ Grassi, _Trypanomonas_ Danilewsky, _Hæmatomonas_

  In the case of all these forms, there was no discussion as to a
  pathogenic influence on the host. Opinion, however, as to the action
  of trypanosomes changed when, in 1880, Evans found flagellates in
  the blood of horses in India that suffered from a disease endemic
  there called “surra,” and associated the parasites with the disease.
  Steel and Evans were successful in transmitting the parasites--first
  known as _Spirochæta evansi_, Steel, then as _Trichomonas evansi_,
  Crookshank, and finally as _Trypanosoma evansi_--to dogs, mules and
  horses. They recognized that the above mentioned flagellates in the
  blood of the experimental animals were the causal agents of the

  From that time there was a considerable increase in the literature,
  the contents of which have been summarized by Laveran and Blanchard.
  In 1894 Rouget discovered trypanosomes in the blood of African horses
  that suffer from “stallion’s disease” (dourine). In 1894 Bruce
  found similar forms (_T. brucei_) in the blood of South African
  mammals suffering from “nagana,” and in consequence attention was
  drawn to the part which the much dreaded tsetse-fly played in the
  transmission of “nagana.” In 1901 Elmassian discovered trypanosomes
  in the blood of horses that were stricken with “mal de caderas,”
  which is very common in the Argentine. The disease in cattle named
  “galziekte” (gall-sickness), occurring in the Transvaal, was also at
  one time attributed to a trypanosome remarkable for its great size,
  and like some other species, bearing the name of its discoverer (_T.

  The study of the species hitherto known has been carried on partly
  by the above mentioned authors and in part by others, _e.g._,
  Rabinowitsch and Kempner, Laveran and Mesnil, Wasiliewski, Senn.
  It was greatly advanced by the method of double staining (with
  alkaline methylene blue and eosin) introduced by Romanowsky (1891)
  and elaborated by Ziemann, Leishman, Giemsa and others. By this means
  the presence of a terminal flagellum and of an undulating membrane
  at the side of the flattened and extended body was demonstrated.
  Laveran and Mesnil (1901) discovered allied flagellates in the blood
  of the fish, _Scardinius erythrophthalmus_. These flagellates, now
  placed in the genus _Trypanoplasma_, had a second free flagellum in
  addition to the one bordering the undulating membrane. Trypanoplasms
  have since been found in both freshwater and marine fishes. The
  transmission of trypanoplasms of freshwater fishes is effected by
  leeches. _Trypanoplasma varium_ from _Cobitis_ is transmitted by
  _Hemiclepsis marginata_ according to Léger, while the Trypanoplasmata
  of _Cyprinus carpio_ and _Abramis brama_ reach new hosts by the
  agency of _Piscicola_ according to Keysselitz.

  Another ally of the Trypanosomidæ, _Trypanophis_, lives in the
  cœlenteric cavity of Siphonophores. It has also an extra terminal
  flagellum (Poche, Keysselitz). [_Trypanoplasma_ and _Trypanophis_
  belong to the _Bodonidæ_, see p. 63].

  Finally it was shown that Trypanosomes occurred in human beings.
  Although Nepveu’s early report of trypanosomes in the blood of
  malarial patients may be doubtful, subsequent researches by Forde
  and Dutton demonstrated trypanosomes (fig. 28) in the blood of a
  European, apparently suffering from malaria, living in the Gambia.
  Dutton (1902) called the human trypanosome, _T. gambiense_. The
  expedition despatched by the Liverpool School of Tropical Medicine
  (1902) to Senegambia found trypanosome infections in six cases among
  a thousand inhabitants examined.

  About the same time attention was devoted to the disease of West
  African negroes known for a century as “sleeping sickness.”
  Castellani (1903) was the first to succeed in demonstrating the
  presence of trypanosomes (at first called _T. ugandense_) in
  centrifugalized cerebro-spinal fluid obtained by puncture from cases
  of sleeping sickness in Uganda. Similar discoveries were made by
  Bruce, who also found trypanosomes in the blood of those attacked
  with sleeping sickness. Sambon regarded a species of _Glossina_ as
  the transmitter. From consideration of the geographical distribution
  of the disease Christy regarded _Glossina palpalis_ as the
  transmitter. Brumpt first thought it was _G. morsitans_, but, later,
  supported the view of _G. palpalis_. Bruce, Nabarro and Greig also
  named the same insect as the transmitter, not only for geographical
  reasons but also because healthy apes became infected by the bite
  of certain _G. palpalis_. The inoculation of cerebro-spinal fluid
  from subjects of sleeping sickness into the spinal canal of apes
  (_Macacus_) had the same result.

  Just as the discovery of the malarial parasites called forth a whole
  flood of research memoirs which were followed by a second series on
  the relation of the mosquitoes to malaria, so a similar outpouring
  occurred after the discovery of the pathogenic trypanosomes of
  mammals and men. In both cases the inquiry was not limited to the
  stages in man and other vertebrate hosts, but the fate of the
  parasites in the intermediate (invertebrate) hosts was investigated,
  and allied species were obtained from many different hosts.

  Novy and MacNeal (1903) were the first to cultivate trypanosomes in
  artificial media (blood-agar).

  In 1910 Stephens and Fantham recorded the presence of another human
  trypanosome, _T. rhodesiense_, from a case of sleeping sickness
  in Rhodesia, where _G. palpalis_ was absent. Kinghorn has since
  demonstrated that _T. rhodesiense_ is transmitted by _G. morsitans_.
  Kinghorn and Yorke believe that big game (_e.g._, antelope) is the
  reservoir of _T. rhodesiense_.

  The output of literature on trypanosomiasis in men and animals is
  enormous. To cope with it the Sleeping _Sickness Bureau Bulletin_
  was founded in 1908, and it is now (since November 1912) continued
  as a section of the _Tropical Diseases Bulletin_, wherein current
  literature is reviewed.


Trypanosomes occur in the blood of representatives of all the
vertebrate classes. Often the trypanosomes occur so scantily in
the blood that they are overlooked on examination. A useful aid in
detecting the flagellates in such cases consists in the use of cultures
of the blood of the host on artificial media. Stimulated by the
medium multiplication occurs, and hence the parasites are more easily
detected. [For the composition of such culture media see Appendix.]

There is a periodicity in the appearance of the trypanosomes in
the peripheral blood of the host, due to alternating phases of
multiplication and of rest on the part of the parasites. Such
periodicity has been established both by biological and enumerative
methods. Again, a seasonal variation has been observed in the
occurrence of certain trypanosomes in the peripheral circulation of the
hosts; for example, some trypanosomes (_e.g._, _T. noctuæ_ in birds)
are found only in the summer in the blood, while in the winter they
occur in the internal organs.

Recent cultural researches have established that trypanosomes, _e.g._,
_T. americanum_, may be present in very small numbers in hosts,
such as cattle, which are quite unharmed by them, and in which the
presence of these flagellates formerly was never suspected (“cryptic
trypanosomiasis.”) However, the majority of the trypanosomes occurring
in domestic animals are usually deleterious or even lethal to their
hosts. Many wild animals, such as various species of antelope, harbour
trypanosomes without being injured thereby. In such cases it is
probable that the vertebrate hosts have been so long parasitized in the
past, that they have become tolerant and immune to the effects of the
flagellates. Should such trypanosomes of wild animals be transmitted to
domesticated stock or man, they may re-acquire their initial virulence
and become pathogenic to the new host. As a general statement, the
newer a parasite is to its host the greater is its virulence. For
example, _T. gambiense_, _T. rhodesiense_ and _T. brucei_ are innocuous
to big game in Africa, but are pathogenic to man and domestic animals
respectively. Pathogenic trypanosomes appear to have a wider range
of hosts, that is, to be less limited to one specific host than
non-pathogenic forms. Thus, _T. rhodesiense_ is pathogenic to man and
all laboratory animals, while it is non-pathogenic to antelopes and
their kind.


[Illustration: FIG. 26.--_Trypanosoma brucei_ in division. _n_,
nucleus; _bl_, blepharoplast; _fl_, flagellum. × 2,000. (After Laveran
and Mesnil.)]

The general structure of the various trypanosomes shows much
uniformity, though variations in size and shape occur. Typically the
body is elongate and sinuous. The flagellar end tapers gradually to a
point, the aflagellar extremity usually being rounded or more blunt.
In some trypanosomes there is much diversity in size, the organisms
varying from long, slender forms to short, stumpy ones; in other
species relative constancy of size is maintained. The former are known
as polymorphic trypanosomes, the latter as monomorphic forms.

Two nuclei are present. The main or principal nucleus, sometimes termed
the trophic nucleus, is often situated towards the centre of the body;
it is frequently of the vesicular type, containing a karyosome. The
blepharoplast or kinetic nucleus is posterior to the nucleus, and
usually is rod-like. The flagellum arises close to the blepharoplast,
and forms an edge to the undulating membrane. It may or may not
extend beyond the limits of the undulating membrane. If it does so,
the unattached part is known as the free flagellum. Sometimes a small
granule is found at the origin of the flagellum. This is the basal
granule, and is considered by some to function as the centriole of the
kinetic nucleus.

The undulating membrane is a lateral extension of the ectoplasm or
periplast, and is the main agent in locomotion. It is edged by the
flagellum, which forms a deeply stainable border to it. Within the
membrane substance, often arranged parallel with its edge, are a number
of fine contractile elements, the myonemes. These contractile elements
may also occur on the body of the trypanosome. They are easily seen in
some large trypanosomes, but are difficult of demonstration in others,
owing to their great fineness.

[Illustration: FIG. 27.--_Trypanosoma lewisi_. Multiplication rosettes.
× 1,000. (After Laveran and Mesnil.)]

Multiplication of trypanosomes in the blood is brought about by binary
longitudinal fission (fig. 26). Division is initiated by that of the
blepharoplast and nucleus. The division may be equal or subequal,
whereby differences in size of individuals partly arise. Multiple
division by repeated binary fission, without complete separation of the
daughter forms, is known in some trypanosomes (_e.g._, _T. lewisi_),
and rosettes of parasites thereby are produced (fig. 27).

The classification of trypanosomes is very difficult. Laveran
(1911)[54] has suggested the examination of the relative length
of the flagellum as a diagnostic character, and so arranged these
flagellates in mammals in three groups. The first group included those
trypanosomes always having part of the flagellum free (_e.g._, _T.
evansi_, _T. vivax_); the second group comprised forms without a part
of the flagellum free (_e.g._, _T. congolense_), while the third group
included forms some members of which have free flagella, while others
have not (_e.g._, _T. gambiense_). Bruce[55] (1914) and Yorke and
Blacklock[56] (1914) have also devised classifications.

[54] _Ann. Inst. Pasteur_, xxv, p. 497.

[55] _Trans. Soc. Trop. Med. & Hyg._, viii, p. 1.

[56] _Annals Trop. Med. and Parasitol._, viii, p. 1.

Resting stages of some trypanosomes have been found in the internal
organs of their vertebrate hosts. The formation of these oval,
Leishmania-like bodies will be noted in individual cases later. Similar
small oval bodies form an important phase in the life-history of _T.
cruzi_, which multiplies normally by multiple fission or schizogony
into these oval, daughter elements, and not by binary longitudinal
fission in the circulating blood.

Polymorphism in trypanosomes (_e.g._, _T. gambiense_, _T. rhodesiense_)
is now interpreted as a phenomenon resulting from growth and
division.[57] Long, thin forms are those about to divide. Fully mature
forms are shorter and broader. Various intermediate types occur and
represent growth forms. Formerly, polymorphism was interpreted in terms
of sex, thin forms being regarded as males, broad forms as females,
while the intermediate types were termed indifferent. Conjugation
was not observed, and there is no evidence in support of the sexual

[57] Robertson (1912), _Proc. Roy. Soc._, B, lxxxv, p. 527.

The transmission of trypanosomes from one vertebrate host to another is
usually accomplished by the intermediation of some biting arthropod in
the case of terrestrial animals, while leeches are usually considered
to act as transmitters in the case of the trypanosomes occurring
in aquatic animals. Developmental phases of the life-histories of
trypanosomes occur in the invertebrate transmitters, and will be
considered in individual cases.

*Trypanosoma gambiense*, Dutton, 1902.

  Syn.: _Trypanosoma hominis_, Manson, 1903. _Trypanosoma nepveui_,
  Sambon, 1903. _Trypanosoma castellanii_, Kruse, 1903. _Trypanosoma
  ugandense_, Castellani, 1903. _Trypanosoma fordii_, Maxwell Adams.

In vertebrate blood _Trypanosoma gambiense_ is polymorphic, for long,
thin forms may be seen in contrast with short, stumpy forms, as well
as intermediate forms (fig. 29, _a_--_c_). This polymorphism has been
interpreted in terms of sex, especially by German investigators,
following Schaudinn (see above). However, there is no evidence of
conjugation, and the polymorphic forms are more easily interpreted in
terms of growth and division, for the long thin forms are potential
dividing organisms, and the stumpy or short parasites, with little or
no free flagellum, are the adult individuals.

_Morphology of T. gambiense in the Circulating Blood._

_T. gambiense_ varies from 13 µ to 36 µ in length, its average length
being 24·8 µ, as was determined in 1913 by exact biometrical methods
by Stephens and Fantham.[58] Three forms of parasite occur. According
to Miss Robertson,[59] the relatively short forms from 13 µ to 21 µ
long may be regarded as the mature or “adult” type of parasite in
the blood. They carry on the cycle in the vertebrate. From them
intermediate forms, which are longer than the “adult” but at first have
the same breadth, arise by growth. They possess a free flagellum. The
intermediate forms grow into long individuals, which are those about to
divide. The products of division give rise, directly or indirectly, to
the adult forms.

[58] _Annals Trop. Med. and Parasitol._, vii, p. 27.

[59] _Phil. Trans._, B (1913), cciii, pp. 161–184.

[Illustration: FIG. 28.--_Trypanosoma gambiense_. × 1,700. (After

[Illustration: FIG. 29.--_Trypanosoma gambiense_. Development in
vertebrate host. _a_, long, slender, _b_, intermediate and _c_, short,
stumpy forms, found in the blood; _d_, _e_, _f_, non-flagellate, latent
forms from internal organs. × 2,000. (Original. From preparations by

The organism has an elongate body with an anterior or flagellar end
and a blunter posterior or non-flagellar end. The protoplasm is finely
granular, large inclusions being rare. The central nucleus is oval
and large, often containing most of its chromatin concentrated as a
karyosome, with small granules only scattered near or on the fine
nuclear membrane. The blepharoplast is either rounded or rod-shaped.
The undulating membrane is thrown into folds and is bordered by the
flagellum. A small basal granule may be present near, or at the actual
origin of the flagellum.

_Multiplication_ in the vertebrate is brought about by longitudinal
division. According to the recent account of division by Miss
Robertson, the blepharoplast doubles, then the flagellum splits for
the greater part of its length, and the daughter flagella separate,
one being shorter than the parent flagellum. The nucleus often shows
two well marked dark granules on the membrane at opposite poles, and
these appear to act as centrosomes. Nuclear constriction occurs and
the halves gradually separate. Finally the two daughter organisms
become free, the aflagellar end splitting last. The products of
division may be equal or unequal. Repeated division goes on in the
general circulation until the blood swarms with parasites. Then the
trypanosomes gradually disappear, and a period occurs when it is
practically impossible to demonstrate the parasite in the blood.
At such a period, trypanosomes can be obtained by puncture of the
enlarged lymphatic glands or of the spinal canal, or can be found in
the internal organs, more particularly in the spleen, lungs, liver and
bone-marrow. In the latter organs, latent bodies are produced (fig. 29,
_d_--_f_) which are capable of again becoming flagellates and entering
the general circulation. Their formation was described by Fantham
(1911).[60] The parasite contracts, the blepharoplast migrates towards
the nucleus, a very thin coat differentiates around the two nuclei
and a certain amount of cytoplasm, and the parts exterior to the coat
disintegrate, leaving a small, oval body behind. Fuller details are
given in connection with _T. rhodesiense_. Laveran (1911)[61] considers
that latent bodies are “involution” forms, but acknowledges that they
can flagellate and become infective in fresh blood.

[60] _Proc. Roy. Soc._, B, lxxxiii, p. 212.

[61] _C. R. Acad. Sci._, 153, p. 649.

No multiplication of the trypanosomes within the cells of the lung,
liver or spleen of infected monkeys was found by Miss Robertson in her
recent researches.

There appear to be negative periods in infected monkeys, since,
although trypanosomes may occur in their blood at such times, they are
not infective to _Glossina_.

_Development in Glossina palpalis._--The principal accounts are
those by Sir D. Bruce and his colleagues (1911),[62] and by Miss
Robertson[63] (1912), whose results will be followed. According to the
latter investigator _T. gambiense_ never enters the body cells of the
fly (_G. palpalis_), nor does it penetrate the gut wall into the body
cavity. Practically no crithidial stage occurs in the fly’s main gut,
but a trypanosome facies is retained therein.

[62] _Proc. Roy. Soc._, B, lxxxiii, p. 513.

[63] _Proc. Roy. Soc._, B, lxxxvi, p. 66.

After the trypanosomes are ingested by the fly during a meal of
infected blood, sooner or later multiplication occurs. This development
usually begins in the middle or posterior part of the mid gut, and
trypanosomes of varying sizes are produced. After the tenth or twelfth
day, many long, slender trypanosomes (fig. 30, _a_) are found, which
gradually move forwards into the proventriculus. Such long, slender
forms represent the limit of development in the lumen of the main gut.
The proventricular type, developed about the eighth to the eighteenth
or twentieth day, is not infective; it may occur in the crop, but is
not to be found permanently there. Between the tenth and the fifteenth
days multinucleate forms of trypanosomes are found, and may be styled
multiple forms (fig. 30, _b_). Some of these latter may be degenerative.

[Illustration: FIG. 30.--_Trypanosoma gambiense_. Development in the
fly, _Glossina palpalis_. _a_, slender, proventricular form; _b_,
multinucleate form; _c_, _d_, crithidial forms; _e_, infective type of
trypanosome found in salivary gland. × 2,500. (After Robertson.)]

_Invasion of the Salivary Glands of the Fly._--Long, slender
trypanosomes from the proventriculus pass forward into the hypopharynx.
They then pass back along the salivary ducts, about sixteen to thirty
days after the fly’s feed. The trypanosomes reach the salivary glands
as long, slender forms. In the glands they become shorter and broader,
attach themselves to the surrounding structures, and assume the
crithidial facies (fig. 30, _c_, _d_). As crithidial forms they remain
attached to the wall and multiply in the glands. These crithidial
stages differentiate into the short, broad trypanosome forms, capable
of swimming freely (fig. 30, _e_).

Miss Robertson considers the development in the main gut to be
indifferent multiplication, and that salivary fluid seems necessary to
stimulate trypanosomes to the apparently essential reversion to the
crithidial type. The second development in the salivary gland is the
essential feature. The short, stumpy forms of trypanosomes (fig. 30,
_e_) finally produced in the salivary glands are alone infective. No
conjugation of trypanosomes occurs in the fly. Only about 5 per cent.
of captive tsetse flies fed on trypanosome-infected blood become
infective, but they probably remain infective for the rest of their

J. G. Thomson and Sinton (1912)[64] have obtained in cultures the
various trypanosome forms of _T. gambiense_ seen in the fly’s main gut.

[64] _Annals Trop. Med. and Parasitol._, vi, p. 331.

Duke (1912)[65] found _T. gambiense_ in a species of antelope, the
situtunga (_Tragelaphus spekei_), on Damba Island in Victoria Nyanza.
Wild _G. palpalis_ could be infected therefrom. The antelope may then
act as a sleeping sickness reservoir in that district, but men are
apparently the chief reservoir.

[65] _Proc. Roy. Soc._, B, lxxxv, pp. 156, 483.

*Trypanosoma nigeriense*, Macfie, 1913.[66]

Macfie has recently (August, 1913) described a human trypanosome
from the Eket district of Southern Nigeria. It is common in young
people. The disease produced does not seem to be of a virulent type
in Nigeria, and does not occur in epidemic form. In the early stages
the glands of the neck are enlarged. In the later stages--cases of
which are rarer--lethargy appears. The parasite is a polymorphic
trypanosome, morphologically almost indistinguishable from _T.
gambiense_, though it may be slightly shorter. Macfie recorded the
occurrence in his preparations of a few trypanosomes appearing to have
a flagellum free during their whole length. Some of the parasites,
as seen in a sub-inoculated guinea-pig, are very small (8 µ long).
Other trypanosomes have their nuclei displaced somewhat anteriorly.
This parasite may only be a variety of _T. gambiense_. The parasite is
perhaps spread by _Glossina tachinoides_.

[66] _Annals Trop. Med. and Parasitol._, vii, p. 339; viii, p. 379.

*Trypanosoma rhodesiense*, Stephens and Fantham, 1910.

The parasite was found in the blood of a young Englishman who had
contracted sleeping sickness in the Luangwa Valley, North-eastern
Rhodesia, in the autumn of 1909. The patient had never been in an area
infested with _Glossina palpalis_.

(1) _Morphology._--The morphology of the parasite in man and
sub-inoculated rats was studied by Stephens and Fantham in 1910.[67]
They pointed out a morphological peculiarity in the presence of certain
trypanosomes with posterior nuclei in sub-inoculated animals, that is,
parasites in which the nucleus (trophonucleus) was situated towards
the posterior or aflagellar end, close up to or even beyond the
blepharoplast or kinetic nucleus (fig. 31, _4_, _5_). When the nucleus
was beside the blepharoplast, the former was seen to be kidney-shaped
(fig. 31, _4_). The posterior nuclear forms were of the stout and
stumpy variety, and about 6 per cent. of the stumpy forms were found to
have their nuclei displaced from the centre. The anterior or flagellar
end of these trypanosomes often contained chromatoid granules. _T.
rhodesiense_ varies in length from 12 µ to 39 µ[68]; short stumpy forms
vary from 13 µ to 21 µ, intermediate forms from 21 µ to 24 µ, and long,
slender forms from 25 µ onwards. The average length is 24·1 µ.

[67] _Proc. Roy. Soc._, B, lxxxiii, p. 28.

[68] Stephens and Fantham (1912–13), _Proc. Roy. Soc._, B, lxxxv,
p. 223, and _Annals Trop. Med. and Parasitol._, vii, p. 27.

[Illustration: FIG. 31.--_Trypanosoma rhodesiense._ 1, Long narrow
form; 2–4, nucleus passing to posterior (aflagellar) end; 5, nucleus
quite posterior. × 1,800. (After Stephens and Fantham.)]

Certain regular periods occur in the course of the trypanosomiasis when
few or no flagellate trypanosomes are found in the peripheral blood
of the patient or of the sub-inoculated animal. These periods can be
explained in terms of morphology, for the trypanosomes are capable of
assuming a non-flagellate form in the internal organs of the host,
particularly in the lungs and in the spleen. Such forms are known as
“latent” or “resting” forms. The term “latent body” was first used
by Moore and Breinl in 1907[69] in connection with _T. gambiense_.
Fantham[70] (1911) has described the process of formation of latent
from motile forms and the reconversion of the latent bodies into
active flagellates. Fresh preparations of splenic blood or lung blood
containing trypanosomes were made. A trypanosome gradually withdrew or
cast off its flagellum, concentrated its cytoplasm, and became more or
less elongate oval. Nucleus and blepharoplast approached one another
and came to lie more or less side by side. Then an opaque line often
made its appearance around the nuclear area and differentiated as a
slight envelope or covering, the cytoplasm external to this merely
degenerating. The small, oval, refractile body (fig. 29, _d_--_f_) thus
formed was a non-flagellate latent body, 2 µ to 4 µ in diameter, like
_Leishmania_ or the non-flagellate, multiplicative forms of _T. cruzi_
(fig. 34), and remains temporarily inactive in the internal organs of
the host. After this period of inactivity, the non-flagellate body,
recuperated by its rest, begins to elongate again. The nuclei separate.
From a small vacuole-like portion the flagellum differentiates and
forces out the ectoplasm, which assumes the form of the undulating
membrane with its flagellar border. Subsequent growth results in
the production of the typical trypanosome form, which re-enters the
circulating blood and multiplies by longitudinal binary fission.
Division of the parasite prior to the formation of a latent body may
occur and division of the latent forms themselves is known, though
less common. Consequently latent bodies, like the flagellate forms
themselves, show diversity in size. The blepharoplast of the latent
bodies is sometimes less well marked than in _Leishmania_ (see fig. 29,
_d_-_f_). Laveran’s views on these bodies have already been given on
p. 74.

[69] _Annals Trop. Med. and Parasitol._, i, p. 441.

[70] _Proc. Roy. Soc._, B, lxxxiii, p. 212.

(2) _Animal Reactions._--The posterior nuclear trypanosomes were found
in all sub-inoculated animals, such as rats, guinea-pigs, dogs, mice,
Macacus, rabbits and horses, but were not seen in the human patient,
as few trypanosomes occurred in his peripheral blood. R. Ross and D.
Thomson[71] found a periodic, cyclical variation in the number of the
parasites in the patient’s blood from day to day, the cyclical period
being about a week (fig. 32). Fantham and J. G. Thomson[72] (1911)
found a similar periodic, cyclical variation in the trypanosomes
in the blood of sub-inoculated rats, guinea-pigs and rabbits. On
counting the parasites in the blood of similar animals inoculated
with _T. gambiense_, they established, by enumerative methods, that
_T. rhodesiense_ was more virulent than _T. gambiense_, while Yorke
also showed this marked virulence of _T. rhodesiense_ in practically
all laboratory animals. In other words the duration of infection in
the case of _T. rhodesiense_ was shorter. It was also found that _T.
rhodesiense_ was resistant to atoxyl. The patient, from whom the
original strain was obtained, died about nine months after the probable
date of infection. Some patients infected with _T. rhodesiense_ have
died in an even shorter period, such as four or five months.

[71] _Proc. Roy. Soc._, B, lxxxii, p. 411.

[72] _Annals Trop. Med. and Parasitol._, iv, p. 417.

In sheep and goats _T. rhodesiense_ causes an acute disease, marked by
high fever, œdema of the face, and keratitis, as shown by Bevan and
others, death resulting after a relatively short period. _T. gambiense_
gives rise, in these animals, to no symptoms except fever, which may be
overlooked. _T. rhodesiense_ produces keratitis in dogs.

[Illustration: FIG. 32.--Chart showing daily counts of number of
trypanosomes per cubic millimetre of peripheral blood from a case of
Rhodesian sleeping sickness. (After R. Ross and D. Thomson.)]

Stannus and Yorke (1911) observed _T. rhodesiense_ in animals
inoculated from a case of sleeping sickness in Nyasaland. Sir D. Bruce
and his colleagues[73] have shown (1912) that _T. rhodesiense_ is the
parasite usually found in man and in animals sub-inoculated from cases
of sleeping sickness in Nyasaland. It has since been found in German
East Africa and Portuguese East Africa, while Ellacombe has described a
case from North-western Rhodesia.

[73] _Proc. Roy. Soc._, B, lxxxv, p. 423.

(3) _Serum Reactions._--Interesting experiments on this subject were
performed during 1911 and 1912 by various French investigators.

(_a_) _Action of Immune Serum_ (Mesnil and Ringenbach)[74]: (1) A
goat was infected with _T. rhodesiense_. Twenty-two days later its
serum mixed with _T. rhodesiense_ was injected into a mouse. Result:
Protection. (2) The serum mixed with _T. gambiense_ was injected into a
mouse. Result: Infection.

[74] _C.R. Soc. Biol._, lxxii, p. 58.

(_b_) _Action of Baboon Serum._--Contrary to _T. gambiense_, _T.
rhodesiense_ is very susceptible to human and baboon sera. Mesnil and
Ringenbach[75] showed that a dose of 1 c.c. of baboon (_Papio anubis_)
serum cured mice infected with _T. rhodesiense_. In the same dose it
acted very feebly on _T. gambiense_.

[75] _C.R. Acad. Sci._, 153, p. 1,097.

(_c_) _Action of Human Serum._--_1 c.c._ of human serum cured _T.
rhodesiense_ mice in three out of four cases; on _T. gambiense_ mice
there was no appreciable effect.

Laveran and Nattan-Larrier[76] have shown the same, namely, that human
sera act on _T. rhodesiense_, but are quite without action on _T.

[76] _C.R. Acad. Sci._, 154, p. 18.

(_d_) _Trypanolytic Reactions._--Mesnil and Ringenbach[77] have also
shown that the sera of animals (man, monkey and guinea-pig) infected
with _T. gambiense_ are trypanolytic for the homologous trypanosome,
that is, _T. gambiense_, but have no action on the heterologous
trypanosome, that is, _T. rhodesiense_.

[77] _C.R. Soc. Biol._, lxxi, p. 609.

(4) _Cross Immunity Experiments._--(_a_) Mesnil and Ringenbach[78]
immunized a monkey (_Macacus rhesus_) against _T. gambiense_. It
was inoculated with _T. rhodesiense_ on June 7, 1911; on June 27
trypanosomes appeared, the infection being slight; on July 4 it died. A
control died in ten and a half days.

[78] _C.R. Soc. Biol._, lxxi, p. 271.

(_b_) Laveran[79] immunized a goat and mice against _T. gambiense_.
When they had acquired a solid immunity, they were inoculated with _T.
rhodesiense_. They became infected like the controls.

[79] _Bull. Soc. Path. Exot._, v, pp. 26, 241.

(_c_) Laveran and Nattan-Larrier[80] immunized a ram against _T.
brucei_, it subsequently became infected with _T. rhodesiense_.

[80] _C.R. Acad. Sci._, 154, p. 18.

(_d_) Laveran[81] immunized a ram and a sheep against different strains
of T_. brucei_. Inoculated with _T. rhodesiense_ they both acquired
acute infections and died. Conclusion: _T. rhodesiense_ is not _T.

[81] _Bull. Soc. Path. Exot._, v, p. 101.

When the converse set of experiments is tried, namely, immunizing
an animal against _T. rhodesiense_, and then inoculating with _T.
gambiense_, the difficulty immediately arises that it is impossible
to immunize an animal against _T. rhodesiense_, owing to its
virulence. But a partial and transitory immunity to _T. rhodesiense_
can be obtained by treating the infected animal with drugs, such as
arsenophenylglycin. The results, so far as they go, seem to show that
an animal immunized against _T. rhodesiense_ is immune not only to
_T. rhodesiense_, but also to _T. gambiense_, a fact which, according
to Mesnil and Léger, does not invalidate the specificity of _T.
rhodesiense_, but tends to show that the two trypanosomes are closely

(5) _Mode of Transmission and Reservoir._--Kinghorn has shown that
_T. rhodesiense_ is transmitted by _Glossina morsitans_ in which it
undergoes development. Kinghorn and Yorke[82] found that about 16 per
cent. of the wild game examined in Northern Rhodesia was naturally
infected with _T. rhodesiense_. The wild game examined included
waterbuck, hartebeest, mpala, bushbuck and warthogs. One native dog
near the Nyasaland border was found infected, but not domestic stock.
Taute doubts whether _T. rhodesiense_ really occurs in wild game.
Approximately 3·5 per cent. of the tsetse flies fed on infected animals
may become permanently infected with _T. rhodesiense_, and capable of
infecting clean animals. Furthermore, a tsetse fly when once infective
probably remains infective for the rest of its life.

[82] _Annals Trop. Med. and Parasitol._, vii, p. 183.

Kinghorn and Yorke, however, have shown that climatic conditions,
namely, those of temperature, also affect the infectivity of the tsetse
fly, as the ratio of flies capable of transmitting _T. rhodesiense_
to those incapable of transmitting the virus is 1 : 534 in hot valley
districts (_e.g._, Nawalia, Luangwa Valley, temperature 75° to 85° F.),
while on elevated plateaux (_e.g._, Ngoa, on the Congo-Zambesi
watershed, temperature 60° to 70° F.) the ratio falls to 1 : 1312.

Mechanical transmission by the tsetse fly does not occur, if a period
of twenty-four hours has elapsed since the infecting meal.

_Developmental Cycle in the Fly._--The period which elapses between the
infecting feed of the flies and the date on which they become infective
varies from eleven to twenty-five days in the Luangwa Valley, according
to Kinghorn and Yorke. Attempts carried out at laboratory temperature
on the Congo-Zambesi plateau, during the cold season, to transmit _T.
rhodesiense_ by means of _G. morsitans_ were always unsuccessful. The
developmental cycle of the trypanosome in the fly is influenced by
the temperature to which the flies are subjected (as stated above).
The first portion of the developmental cycle proceeds at the lower
temperatures (60° to 70° F.), but higher temperatures are necessary
for the completion of the development of the trypanosome. Kinghorn
and Yorke found that the trypanosomes may persist in the fly, at an
incomplete stage of their development, for at least sixty days when the
climatic conditions were unfavourable.

The first portion of the developmental cycle of the trypanosome takes
place in the gut of the fly. Invasion of the salivary glands of the
tsetse is secondary to that of the intestine, but is necessary for
the infectivity of the fly. A relatively high mean temperature, 75°
to 85° F., is essential for the passage of the trypanosomes into the
salivary glands and the completion of their development therein.

Kinghorn and Yorke[83] state that the predominant type of trypanosome
in the intestine of infected _G. morsitans_ was a large broad form,
quite different from that which is most common in the salivary glands.
The trypanosome in the glands resembles the short form seen in the
blood of the vertebrate host. The authors quoted state that both the
intestinal and salivary gland forms of infective _G. morsitans_ are
virulent when inoculated into healthy animals.

[83] _Annals Trop. Med. and Parasitol._, vii, p. 281.

Bruce and colleagues[84] have quite recently (June, 1914) published
an account of their investigations of _T. rhodesiense_ in _G.
morsitans_ in Nyasaland. (Incidentally it may be remarked that Bruce
considers _T. rhodesiense_ to be identical with a polymorphic strain
of _T. brucei_--see pp. 83, 94). The development of _T. rhodesiense_
takes place in the alimentary canal and salivary glands, not in the
proboscis, of the tsetse fly. In feeding experiments with laboratory
bred flies, as well as with a few wild flies, fed on infected dogs
or monkeys, only 8 per cent. of the flies were found to be infected
on dissection. Of such infected flies, however, only some allow of
the complete development of the trypanosomes within them, in other
words only about 1 per cent of the flies become _infective_. The
length of time which elapses before a fly becomes infective varies
from fourteen to thirty-one days, averaging twenty-three days, when
kept at 84° F. (29° C.). The dominant intestinal type of flagellate
in the fly is that seen in the proventriculus, which contains many
long, slender trypanosomes. These proventricular forms find their
way to the salivary glands, wherein crithidial and encysted forms
are seen. They change into “blood forms,” which are short, stumpy
trypanosomes and are infective. “The infective type of trypanosome in
the salivary glands--corresponding to the final stage of the cycle of
development--is similar to the short and stumpy form found in the blood
of the vertebrate host.” The cycle is thus very similar to that of _T.
gambiense_ in _G. palpalis_ (fig. 30).

[84] _Proc. Roy. Soc._, B, lxxxvii, p. 516.

CULTURE.--J. G. Thomson (1912),[85] and subsequently Thomson and
Sinton, succeeded in cultivating _T. rhodesiense_ in a modified
Novy-MacNeal medium. The development obtained resembled that of the
trypanosome in the intestine of _Glossina_.

[85] _Annals Trop. Med. and Parasitol._, vi, pp. 103, 331.


Posteriorly placed nuclei have been found to occur not only in _T.
rhodesiense_ by Stephens and Fantham (1910), but also in _T. pecaudi_
by Wenyon (1912), in _T. brucei_ by Blacklock (1912), and in _T.
equiperdum_ by Yorke and Blacklock (1912).

Recently Stephens and Blacklock (1913)[86] have shown that two
trypanosomes, different morphologically, have been confused under the
name _T. brucei_. One of these is polymorphic (_i.e._, it exhibits long
and slender as well as short and stumpy forms) and came from Uganda,
while the other is monomorphic and is the original Zululand strain
described by Bruce from cattle suffering from “nagana.” Bruce (1914)
considers that morphological change has occurred in _T. brucei_ in its
passage through laboratory animals, and thus explains the diversity of
views. The posterior nuclear forms described by Blacklock occurred in
the Uganda strain of _T. brucei_. (See p. 95.) Similarly, a posterior
nuclear form, _T. equi_, has been separated from _T. equiperdum_. (See
p. 98.)

[86] _Proc. Roy. Soc._, B, lxxxvi, p. 187.

Again, Bruce and his colleagues on the Royal Society Commission
investigating sleeping sickness in Nyasaland, have stated (April,
1913) that “evidence is accumulating that _T. rhodesiense_ and _T.
brucei_ (Plimmer and Bradford) are identical.” The exact identity of
trypanosomes showing posterior nuclei is, then, far from settled,
although Laveran by cross immunity tests has declared that _T. brucei_
is distinct from _T. rhodesiense_. No one has yet seen posterior nuclei
in _T. gambiense_.

*Trypanosoma cruzi*, Chagas, 1909.

  Syn.: _Schizotrypanum cruzi_, Chagas, 1909.

The trypanosome was discovered by Chagas[87] in the intestine of the
bug, _Triatoma_ (_Conorhinus_) _megista_, in Brazil, and then in the
blood of a small monkey bitten by the bug. A little later it was found
in the blood of a child, aged two years, suffering from irregular
fever, extreme anæmia and enlarged glands in the State of Minas Geraes,
Brazil. Chagas found that he was able to infect many of the usual
laboratory animals with the trypanosome, by allowing the bug to bite
them. He was also able to culture the parasite on blood agar.

[87] _Mem. Inst. Oswaldo Cruz._, i, p. 159.

Chagas found the Reduviid bug, _Triatoma megista_, in the houses of the
poorer inhabitants of the Brazilian mining State, and that it attacked
the people, more especially the children, at night, biting the face.
On this account the insect is called “barbeiro” by the inhabitants.
The bite is somewhat painful. The disease has since been found in other
parts of Brazil, _e.g._, Matta de São João in Bahia province, Goyaz,
Matto Grosso and São Paulo provinces, as well as in Minas Geraes.

_Morphology._--The trypanosome has a large blepharoplast or kinetic
nucleus. It is stated to occur both free and in the red blood
corpuscles in the peripheral blood. It is about 20 µ long, on an

Two forms of the parasite (fig. 33, _6_, _7_) are described in the
human blood. In one free form there is a large egg-shaped blepharoplast
and the posterior (aflagellar) end of the parasite is drawn out. The
blepharoplast (kinetic nucleus) may have a chromatin appendage. The
nucleus is oval or band-like, containing a karyosome. The flagellum,
starting close to the blepharoplast or its appendage, has a free
portion of variable length. The other free form in the blood has a more
or less round, terminal blepharoplast, smaller than in the first form,
without a chromatin appendage as a rule. The body of this second form
is decidedly broader than that of the first mentioned.

[Illustration: FIG. 33.--_Trypanosoma cruzi_. Schizogony. _1_,
merozoite in red blood corpuscle; _2_, parasite totally enclosed in
red cell, no flagellum or undulating membrane; _3_-_5_, parasites
partially enclosed in red cell; _6_, _7_, parasites in human blood;
_8_-_11_, parasites in lungs of the monkey, _Callithrix_; _12_, _13_,
initial forms of schizogony; _14_, _15_, schizogony in the lungs of
_Callithrix_. (After Chagas.)]

The dimorphism has been interpreted sexually, the first mentioned forms
being termed males, the second ones females. The correctness of this
interpretation is very doubtful.

No sign of longitudinal division was ever seen in the peripheral
blood or in the internal organs. The “endocorpuscular” forms may be
completely or partially enclosed in the red cell or only attached
thereto (fig. 33, _1_-_5_). At the beginning of infection the
endocorpuscular forms are the more numerous. Some authorities, however,
doubt these stages.

_Life-history in the Vertebrate Host._--Chagas found fluctuations in
the number of the parasites in the peripheral blood. He believes the
increase of the parasites to be periodic.

The investigations of Chagas and of Hartmann have revealed two types
of multiplication which take place in the internal organs of the
vertebrate host.

(_a_) The first type--which possibly belongs to another organism,
_Pneumocystis carinii_, see p. 90--occurs in the capillaries of the
lungs. The flagellate parasite entering the lung capillaries loses
its flagellum and undulating membrane. Its body becomes curved, and
the two ends fuse, and so an oval mass is formed (fig. 33, _8_-_11_).
In some cases the blepharoplast disappears, in other cases it blends
or fuses with the nucleus. The nucleus of the rounded parasite then
divides into eight by successive divisions (fig. 33, _12_-_15_). Next
the body, which is surrounded by its own periplast, also divides,
giving rise to eight tiny daughter individuals or merozoites (fig. 33,
_15_). The merozoites lie inside the periplast, which acts as a sort of
“cyst wall.” The merozoites are said to exhibit dimorphism, and Chagas
has interpreted the dimorphism in terms of sex. The daughter forms,
produced by the parent trypanosomes which kept their blepharoplasts,
themselves have blepharoplasts as well as nuclei, and have been
termed “males” or “microgametes.” The merozoites, arising from parent
trypanosomes which lost their blepharoplasts, have themselves only
nuclei, and have been called “females” or “macrogametes.” In the case
of the so-called “female” forms the single nucleus divides into two
unequal parts, of which the smaller becomes the blepharoplast, and
a flagellum is formed later. The so-called “males” possess early a
rudiment of a flagellum. Both kinds of merozoites escape from the
parent periplast wall, and enter red blood corpuscles. They grow into
flagellates within the corpuscles, and then become free as adult
trypanosomes in the blood-stream.

[Illustration: FIG. 34.--_Trypanosoma cruzi_. Transverse section of a
striated muscle containing rounded forms of the parasite in the central
portion. × 1,000 approx. (After Vianna.)]

(_b_) The second mode of multiplication is one of asexual reproduction
(schizogony or agamogony). It was first described by Hartmann from
hypertrophied endothelial cells of the lungs. It has since been found
in the cardiac muscle, in the neuroglia of the central nervous system,
and in striped muscle (fig. 34). In laboratory animals it has also
been found in the testicle and suprarenal capsules. In these tissues
the parasite is intracellular, appearing as a small rounded body with
nucleus and blepharoplast, without flagellum or undulating membrane. In
other words the parasite is _Leishmania_-like in the body tissues, and
recalls the organism of kala-azar.

Chagas considers this second mode of multiplication to be strictly
asexual. By this means the number of parasites in the vertebrate host
is increased, and symptoms are produced. On the other hand the first
mode of multiplication, seen in the lung capillaries, is considered
by Chagas to be a process of gametogony, in which sexual forms are
differentiated. He finds that (1) the adult trypanosomes exhibit
a dimorphism in human blood rarely seen in artificially infected
guinea-pigs. In these guinea-pigs (infected from guinea-pigs) the
so-called gametogony in the lungs is seldom seen. (2) The intermediate
host, _Triatoma_ (_Conorhinus_), becomes infective if fed directly on
infected human blood, but very rarely so if fed on guinea-pigs. Chagas
is led to believe that the occurrence of sexual forms constantly in
the blood of man implies a greater resistance to infection on the part
of man than on the part of guinea-pigs or other animals, assuming the
general hypothesis that the formation of gametes represents a reaction
of the Protozoön to unfavourable conditions. In human infection the
number of parasites is always less than in laboratory animals, and
their presence in the blood is transitory, lasting from fifteen to
thirty days in acute cases. In many cases examination of the tissues
at death has shown the presence of parasites in patients who did not
exhibit them in the general circulation.

[Illustration: FIG. 35.--_Trypanosoma cruzi_. Development in _Triatoma
megista_. _1_-_6_, forms found in the mid gut of _Triatoma_; _7_
flagellate forms found in the posterior part of the gut of _Triatoma_.
(After Chagas.)]

_Life History in the Invertebrate Host._--About six hours after the
ingestion of infected blood by the bug (_Triatoma megista_), the
kinetic nucleus of the trypanosome moves towards the nucleus, and the
flagellum is usually lost (fig. 35, _1_-_5_). The parasite becomes
rounded and _Leishmania_-like (fig. 35, _3_-_5_), and multiplies
rapidly by division. After a time, multiplication having ceased,
the rounded forms become pear-shaped and develop a flagellum at the
more pointed end. Crithidial forms (fig. 35, 7) are thus produced
and pass into the intestine, where they multiply and may be seen in
about twenty-five hours after the ingestion of blood. The crithidial
forms may also be found in the rectum and fæces. The last stage in the
invertebrate is a small, trypanosome-like type, long and thin with a
band-like nucleus and conspicuous kinetic nucleus. These parasites
are found in the hind gut and in the body cavity. They find their
way into the salivary glands, and are the forms (fig. 36) which are
transmissible to a new vertebrate host. The development in the bug
takes about eight days altogether, after which time the bugs are

There are thus three principal phases in the development of _T. cruzi_
in _Triatoma megista_: (1) A multiplicative phase (_Leishmania_-like)
in the stomach of the bug, (2) a crithidial phase, which is also
multiplicative, in the hind-gut, and (3) a trypanosome phase, which is
“propagative,” and apparently passes through the wall of the alimentary
canal into the body cavity and so into the salivary glands.

[Illustration: FIG. 36.--_Trypanosoma cruzi_. Forms found in the
salivary glands of _Triatoma megista_. (After Chagas.)]

Brumpt found that _T. cruzi_ could live in _Cimex lectularius_,
_C. boueti_, and _Ornithodorus moubata_. The _Cimex_ fæces may be
infective. Blacklock found multiplication of the parasite in _C.

_Culture._--The trypanosome can be cultivated on Novy-MacNeal’s blood
agar, and the cultural forms resemble those described in the bug.

_Possible Reservoir._--Chagas thinks that probably the armadillo or
“tatu” (_Dasypus novemcinctus_) may be the reservoir of _T. cruzi_.
He also thinks that _Triatoma geniculata_ is a transmitter; it lives
in the burrows of the armadillo. Other carriers may be _Triatoma
infestans_ and _T. sordida_.

_Clinical Features._--The trypanosomiasis of Brazil, produced by _T.
cruzi_ and spread by _Triatoma_ spp. has received various names, such
as oppilação, canguary, parasitic thyroiditis, and coreotrypanosis. It
is also known as the human trypanosomiasis of Brazil, South American
trypanosomiasis, and Chagas’ disease.

Chagas[88] reports two principal forms--acute and chronic. The _acute
infection_ is rare, and is characterized by increase in the volume
of the thyroid gland, pyrexia, a sensation of crackling in the skin,
enlarged lymphatic glands in the neck, axilla, etc., while the liver
and spleen are increased in volume. Sclerosis of the thyroid gland is
found at autopsy and fatty degeneration of the liver. During an attack
of fever, trypanosomes are found in the blood. The acute form was only
observed in children.

[88] _Brazil Medico_, Nov. 15, 1910. Longer account in _Mem. Inst.
Oswaldo Cruz_, iii, pp. 219–275. See _Sleep. Sick. Bull._, Nos. 35 and

_In the chronic form_ Chagas reports several varieties: (_a_) A
pseudo-myxœdematous form, occurring in most cases, especially up to
the age of 15. There is hypertrophy of the thyroid gland or at least
signs of hypothyroidism, general hypertrophy of glands, disturbance
of heart rhythm, and nervous symptoms. (_b_) The myxœdematous form
is characterized by similar symptoms, especially by considerable
swelling of the thyroid body, and myxœdema of the subcutaneous cellular
tissue; sometimes there is a true pachydermic cachexia. (_c_) In the
nervous form there are motor disturbances, aphasia, disturbances of
intelligence or signs of infantilism, athetosis of the extremities
and idiocy. There are also paralytic symptoms of bulbar origin,
disturbances of mastication, phonation and deglutition, and in some
cases convulsive attacks. (_d_) The cardiac form, characterized by
disturbance of the heart rhythm. In all these forms the parasite is
found at autopsy in the nervous substance, brain, bulb and heart.

Vianna (1911)[89] has studied the histopathology of the disease.
Some of the chief points are: in the heart muscle destruction of the
sarcoplasm, followed by interstitial myocarditis; in the central
nervous system invasion of the neuroglia cells and inflammatory
reaction; in the suprarenal capsule invasion of medulla or cortex;
inflammatory reaction can also be seen in the kidneys, the hypophysis
and thyroid gland.

[89] _Mem. Inst. Oswaldo Cruz_, iii, p. 276.

Recently Chagas states[90] that “schizotrypanosomiasis” has been found
in a child 15 to 20 days old, and that _Trypanosoma cruzi_ has also
been found in a fœtus--the mother being infected with the trypanosome.
The trypanosomiasis can, then, be transmitted hereditarily.

[90] _Rev. Med. S. Paulo_ (1912), xv, p. 337.

*Trypanosoma lewisi*, Kent, 1881.

The trypanosome has a nucleus somewhat displaced anteriorly, about
one-third of the way from the anterior (flagellar) end of the body, a
relatively straight edge to the undulating membrane, and a rod-shaped
blepharoplast (fig. 37, A). It averages about 25 µ long and 1·5 µ broad.

Much attention has been devoted in recent years to the elucidation
of the life history of the rat parasite, _Trypanosoma lewisi_. It
is usually non-pathogenic to its host. It has been shown that the
trypanosome can be transmitted from rat to rat by the rat-flea,
_Ceratophyllus fasciatus_, and by _Ctenocephalus canis_ (the so-called
dog-flea). (See also p. 92). The flagellate may also persist, but
doubtfully develop, in the rat-louse, _Hæmatopinus spinulosus_. These
researches may now be summarized.

[Illustration: FIG. 37.--_Trypanosoma lewisi_, from rat’s blood. A,
ordinary form; B, small form; C, D, stages in equal binary fission; E,
elongate form (_longocaudense_ type), resulting from division as seen
in D; F, unequal binary fission; G, H, multiple fission into four and
eight; I, small form; J, binary fission of small form; K, division
rosette. × 2,000. (After Minchin and Thomson.)]

_Life Cycle in the Vertebrate Host._--After infection of a rat, the
trypanosomes usually appear in the animal’s blood in five to seven
days. This incubation period applies either to a natural or an
artificial infection. The trypanosomes first observed in the rat’s
blood are diverse in form (fig. 37), being small, medium and large
in size. This diversity is explained by the rapid multiplication
taking place. A trypanosome may divide by equal longitudinal fission
(fig. 37, C, D), but more commonly multiple fission occurs (fig. 37,
G, H), and is unequal. Rosette forms are produced, in which the parent
form can be recognized by its long flagellum (fig. 37, H) and attached
to it are daughter individuals, smaller in size, from which flagella
are growing. Minchin and J. D. Thomson (1912) find that the daughter
forms may be set free sometimes with a crithidia-like facies (fig. 37,
I), the blepharoplast being anterior but near to the nucleus. The
daughter forms, when set free, may themselves divide by binary or
multiple fission, in the latter case forming rosettes (fig. 37, K).
Rosette forms were described by Moore, Breinl and Hindle in 1908.

Lingard, some years ago, described as a distinct species, _T.
longocaudense_, certain forms with markedly elongate posterior ends
(fig. 37, E). According to Minchin, “these forms appear to arise
by binary fission” (fig. 37, D). These long drawn-out forms “are
of constant occurrence and very numerous at a certain stage of the
multiplication period.” It is about the eighth or tenth day after
infection that the multiplication of _T. lewisi_ is at its maximum in
the rat’s blood. About the twelfth or thirteenth day the trypanosomes
seen in the blood appear uniform. According to Minchin (1912)[91] the
rat “gets rid of its infection entirely sooner or later, without having
suffered, apparently, any marked inconvenience from it, and is then
immune against a fresh infection with this species of trypanosome.”
There is, then, a cycle of development in the vertebrate host. Minchin
notes that the records of the pathogenicity of _T. lewisi_ in rats,
causing their death, need further investigation.

[91] “Protozoa,” p. 294.

_T. lewisi_ inoculated into dormice (_Myoxus nitela_) and jerboas may
become pathogenic thereto.

Carini found cysts in the lungs of rats infected with _T. lewisi_.
He thought the cysts were schizogonic stages of the trypanosome,
comparable with those found in the lungs of animals sub-inoculated
with _T. cruzi_. Delanoë (1912)[92] has found, however, that such
cysts, containing eight vermicules, occurred in rats uninfected with
_T. lewisi_. Delanoë concludes that the pneumocysts are independent of
_T. lewisi_, and represent a new parasite, _Pneumocystis carinii_. The
pneumocysts may be allied to the Coccidia, and must be considered when
investigating the life-cycle of a trypanosome in a vertebrate host.
Some of the stages of _T. cruzi_ may possibly be of this nature.

[92] _C. R. Acad. Sci._, clv, p. 658.

_Life-cycle in the Invertebrate Host._--This occurs in fleas, and has
been investigated in considerable detail by Minchin and Thomson in
_Ceratophyllus fasciatus_, and by Nöller in _Ctenocephalus canis_ and
_Ctenopsylla musculi_.

When infected rat’s blood is taken up by the flea, the parasites pass
with the ingested blood direct to the mid-gut of the Siphonapteran.
In the flea’s stomach they multiply in a somewhat remarkable manner,
namely, by penetration of the cells of the lining epithelium, and
division inside the epithelial cells. Inside these lining cells the
trypanosomes first grow to a large size and then form large spherical
bodies, within which nuclear multiplication occurs (fig. 38, A-F).
Any one of these large spherical bodies contains at first a number of
nuclei, blepharoplasts and developing flagella, the original flagellum
still remaining attached for a time. The cytoplasm then divides into
daughter trypanosomes which are contained within an envelope, formed
by the periplast of the parent parasite. Inside the periplast envelope
are a number of daughter trypanosomes “wriggling very actively; the
envelope becomes more and more tense, and finally bursts with explosive
suddenness, setting free the flagellates, usually about eight in
number, within the host-cell” (fig. 38, F). The daughter forms escaping
from the host cell into the stomach lumen of the flea are fully formed,
long trypanosomes.

[Illustration: FIG. 38.--_Trypanosoma lewisi_. Developmental stages
from stomach of rat flea. O, ordinary blood type; A-F, stages occurring
in gut-epithelium of flea, when the trypanosome becomes rounded and
undergoes multiplication, forming in F eight daughter trypanosomes; G,
type of trypanosome resulting from such division which passes back to
the rectum. × 2,000. (After Minchin.)]

The trypanosomes (fig. 38, G) pass into the flea’s rectum. The next
phase is a crithidial one. The parasites become pear-shaped, in which
the blepharoplast (kinetic nucleus) has travelled anteriorly past the
nucleus towards the flagellum (fig. 39). The crithidial forms attach
themselves to the wall of the rectum, and multiply by binary fission
(fig. 39, D). A stock of parasites is thus formed which, according to
Minchin and Thomson, “persist for a long time in the flea--probably
under favourable conditions, for the whole life of the insect”
(fig. 39, A-I).

From the crithidial forms of the rectum, according to Minchin,
small infective trypanosomes arise by modification morphologically
(fig. 39, J--M). The flagellum grows longer and draws out more the
anterior part of the body, the blepharoplast migrates posteriorly,
behind the nucleus, and carries with it the flagellar origin. These
trypanosomes are small, but broad and stumpy (fig. 39, N), and can
infect a rat. Minchin and Thomson formerly considered that the small,
stumpy, infective trypanosomes pass forwards from the rectum into the
stomach, and “appear to be regurgitated into the rat’s blood when the
flea feeds.” However, the small infective trypanosomes were previously
described by Swellengrebel and Strickland.[93] They may be found in the
flea’s fæces. Nöller (1912)[94] has found that the development of _T.
lewisi_ proceeds quite well in the dog flea (_Ctenocephalus canis_) in
Germany. Wenyon confirms this, and states that the human flea, _Pulex
irritans_, and the Indian rat-flea, _Xenopsylla cheopis_, are also able
to serve as true hosts for _T. lewisi_.

[93] _Parasitology_, iii, p. 360.

[94] _Arch. f. Protistenkunde_, xxv, p. 386.

[Illustration: FIG. 39.--_Trypanosoma lewisi_. Developmental stages
from rectum of rat-flea. A, early rectal form; C, D, division of
crithidial form; E, group of crithidial forms; F--I, crithidial forms
without free flagella, some becoming rounded; J--M, transitional forms
to trypanosome type seen in N, which represents the final form in the
flea. × 2,000. (After Minchin.)]

Nöller stated that rats were not infected with _T. lewisi_ by infective
fleas biting them, but by the rats licking up the fæces passed by
the fleas while feeding. This is not in agreement with Minchin and
Thomson’s earlier views of regurgitation, which, apparently, they have
now abandoned.[95] Wenyon (1912) confirms Nöller’s experiments. He took
a dog flea, containing infective trypanosomes in its fæces, and allowed
it to feed on a clean rat. The fæces of the flea, passed while feeding,
were carefully “collected on a cover glass and taken up in culture
fluid with a fine glass pipette.” The contents of the pipette were
discharged into the mouth of a second clean rat. Injury to the rat’s
mouth was carefully avoided. The first rat, on which the infective flea
was fed, did not become infected, while the second rat, in whose mouth
infective flea fæces were placed, became infected in six days.

[95] Report to Advis. Comm. Trop. Dis. Research Fund for 1913, p. 74.

When infective forms of _T. lewisi_ have been developed within the gut
of a rat flea, they may enter and infect the vertebrate host by[96]
(_a_) being crushed and eaten by the rodent; (_b_) the rat may lick
its fur on which an infected flea has just passed infective excrement;
or (_c_) the rat may lick, and infect with flea excrement, the wound
produced by the bite of the flea.

[96] Nuttall, _Parasitology_, v, p. 275.

The time taken for the full development of _T. lewisi_ in the flea is
about six days. The intracellular phase is at its height about the end
of the first day; the crithidial phase, in the flea’s rectum, begins
during the second day; the stumpy, infective trypanosomes are developed
in the rectum about the end of the fifth day.

Wenyon[97] writes that, “the fleas, when once infected with _T.
lewisi_, remain infected for long periods, for though many small
infective trypanosomes are washed out of the gut at each feed, those
that remain behind multiply to re-establish the infection of the hind
gut. Further, the infection is still maintained even if the flea is
nourished on a human being, so that fresh human blood does not appear
to be destructive to the infective forms in the flea.”

[97] Report to Advis. Comm. Trop. Dis. Research Fund, October, 1912,
p. 91. See also _Journ. Lond. Sch. Trop. Med._, ii, p. 119.

The best method of controlling fleas during experiments is that due to
Nöller. He adopted the method of showmen who exhibit performing fleas,
and secure them on very fine silver wire.

Of fleas fed on an infected rat only about 20 per cent. become
infective. About 80 per cent. are immune. If fleas are examined
twenty-four hours after feeding, trypanosomes will be found in all, so
that many of the parasites are destined to degenerate.

It may be of interest to note that Gonder[98] (1911) has shown
that a strain of _T. lewisi_ resistant to arsenophenylglycin loses
its resistance after passage through the rat-louse, _Hæmatopinus
spinulosus_. These experiments suggest that physiological “acquired
characters” may be lost by passage through an invertebrate host.

[98] _Centralbl. f. Bakt._, Orig., lxi, p. 102.

*Trypanosoma brucei*, Plimmer and Bradford, 1899.

_Trypanosoma brucei_ was discovered by Sir D. Bruce in 1894 in cattle
in Zululand and was named _T. brucei_ by Plimmer and Bradford in 1899
in honour of its discoverer. This trypanosome is of considerable
economic importance, as it is responsible for the fatal tsetse fly
disease, or “nagana,” in cattle, horses and dogs. The disease is widely
distributed in Africa and is transmitted from host to host by the
tsetse, _Glossina morsitans_, and other species of _Glossina_. The
virus is maintained in nature in certain big game, such as wildebeest,
bushbuck and koodoo, which thus act as living reservoirs of disease
from which the tsetse may become infected. These reservoir hosts are
not injured, apparently, by the presence of the parasites.

_T. brucei_ is rapidly fatal to the small laboratory animals, such as
rats and mice. Horses, asses and dogs practically always succumb to its
attacks, while a very small number of cattle recover from “nagana.” The
disease is characterized by fever, destruction of red blood corpuscles,
severe emaciation and by an infiltration of coagulated lymph in the
subcutaneous tissue of the neck, abdomen and extremities giving a
swollen appearance thereto. The natural reservoirs in which _T.
brucei_ has been long acclimatized are unaffected by the trypanosomes,
while the newer hosts, such as imported cattle in Africa, are rapidly
destroyed by their action.

[Illustration: FIG. 40.--_Trypanosoma brucei._ × 2,000. (After Laveran
and Mesnil.)]

The general morphology and life history in the vertebrate host is that
of a typical trypanosome (fig. 40). Its length is from 12 µ to 35 µ,
its breadth from 1·5 µ to 4 µ. Multiplication by longitudinal division
proceeds in the peripheral blood (fig. 26), while latent, leishmaniform
bodies are produced in the internal organs.

Bruce and colleagues[99] have quite recently (June, 1914) described
the development of a Zululand strain of _T. brucei_ in _G. morsitans_.
The tsetse flies were bred out in Nyasaland. In vertebrate blood
the _brucei_ strain was polymorphic. The development was like that
found for _T. gambiense_ in _G. palpalis_ (fig. 30), and by Bruce
and colleagues for _T. rhodesiense_ in _G. morsitans_ in Nyasaland.
Long trypanosomes were found in the proventriculus of the tsetse.
Crithidial, rounded or encysted, and immature “blood forms” occurred in
the salivary glands; and finally infective, stumpy, “blood forms” were
differentiated in the salivary glands. The period of development of _T.
brucei_ in _G. morsitans_ takes about three weeks, and then the fly
becomes infective. Bruce believes that _T. rhodesiense_ of Nyasaland
and _T. brucei_ of Zululand are the same, their cycles of development
in _G. morsitans_ being “marvellously alike.” (But see Laveran, p. 80.)

[99] _Proc. Roy. Soc._, B, lxxxvii, p. 526.

_T. brucei_ has been cultivated with difficulty by Novy and MacNeal,
using blood agar. The best treatment for nagana is arsenic in some form.

It is probable that more than one trypanosome has been confused under
the name _T. brucei_, more especially as the occurrence of many species
of trypanosomes in various animals in Africa was not suspected
until comparatively recent times. It has been shown by Stephens and
Blacklock (1913) that the original Zululand strain of _T. brucei_
was monomorphic, while the organism sent from Uganda, and at the
time believed by Bruce to be the same as the Zululand trypanosome,
has been found to be polymorphic, with morphological resemblances
to _T. rhodesiense_. Stephens and Blacklock[100] have suggested the
name _T. ugandæ_ for the polymorphic trypanosome, which, however, has
marked resemblances with *Trypanosoma pecaudi*, and they are, perhaps,
identical. _T. pecaudi_ was the name given by Laveran[101] in 1907 to
the causal agent of “baleri” in equines and sheep in the French Sudan.
_T. pecaudi_, which is dimorphic, is widely distributed in Africa.
An extremely small number of both _T. pecaudi_ and _T. ugandæ_ have
been shown to possess posterior nuclei. _T. pecaudi_ is transmitted by
various species of _Glossina_, and is said to develop in the gut and
proboscis of the fly.

[100] _Proc. Roy. Soc._, B, lxxxvi, p. 187.

[101] _C.R. Acad. Sci._, cxliv, p. 243.

On the other hand, Bruce and colleagues (1914), examining a strain sent
from Zululand in 1913, state that _T. brucei_ is polymorphic. Bruce
(1914) suggests that passage through laboratory hosts has influenced
and altered the morphology of the parasite.

*Trypanosoma evansi*, Steel, 1885.

  Syn.: _Spirochæta evansi_, Steel, 1885; _Hæmatomonas evansi_,
  Crookshank, 1886; _Trichomonas evansi_, Crookshank, 1886.

_Trypanosoma evansi_, first found by Evans in 1880, in India, is the
causal agent of the disease known as “surra.” The malady affects more
particularly horses, mules, camels and cattle in India and neighbouring
countries, such as Burma and Indo-China. It occurs also in Java, the
Philippines, Mauritius and North Africa. Elephants may be affected.
A serious outbreak among cattle in Mauritius occurred in 1902, the
disease being imported into the island. The symptoms are fever,
emaciation, œdema, great muscular weakness and paralysis culminating in

_T. evansi_ varies from 18 µ to 34 µ in length and 1·5 µ to 2 µ in
breadth. It has a pointed posterior extremity, and, anteriorly,
there is a free portion to the flagellum (fig. 41). It is possibly
monomorphic, but a few broad forms occur. The trypanosome multiplies by
longitudinal fission in the blood. Rounded leishmaniform stages occur
in the spleen of the vertebrate host, which stages Walker[102] (1912)
considers to be phases of schizogony.

[102] _Philippine Journ. Sc._ (Sect. B), vii, p. 53.

The parasite is transmitted in nature by various species of _Tabanus_
and _Stomoxys_, though at present little is known of the life-history
within these invertebrate hosts.

Dogs are said to contract the disease by feeding on animals dead of

A variety of _T. evansi_ is the cause of “mbori” in dromedaries in
Africa (Sahara and Sudan). Another possible variety, or closely allied
form, is _T. soudanense_, the causal agent of “el debab” in camels and
horses in North Africa, especially Algeria and Egypt.

[Illustration: FIG. 41.--_Trypanosoma evansi_. × 2,000. (Original. From
preparation by Fantham.)]

An extraordinary example of the possible infection of a human being
with an animal trypanosome is recorded in the case of Professor
Lanfranchi, of the Veterinary School, Parma. The Professor became
infected with trypanosomes, although only nagana and surra were
maintained in his laboratory, and he himself had never visited the
tropics. He suffered from irregular attacks of fever and was œdematous,
but his mind remained clear. The identification of the trypanosome
from Lanfranchi’s blood has been a matter of great difficulty.
Apparently Mesnil and Blanchard (1914)[103] consider the strain found
in the patient is almost indistinguishable in its reactions from _T.
gambiense_, though the parasite is monomorphic. Lanfranchi considers
that he was infected with _T. evansi_.

[103] _Bull. Soc. Path. Exot._, vii, p. 196.

*Trypanosoma equinum*, Voges, 1901.

  Syn.: _Trypanosoma elmassiani_, Lignières.

_Trypanosoma equinum_ was found by Elmassian to be the cause of the
fatal disease, “mal de caderas,” of horses and dogs, in South America
(Paraguay, Argentine, Bolivia). The name refers to the fact that in
the disease, as in other trypanosomiases, the hind quarters become
paralysed. Cattle are refractory to inoculation.

[Illustration: FIG. 42.--_Trypanosoma equinum_. × 2,000. (After Laveran
and Mesnil.)]

_T. equinum_ is about 22 µ to 24 µ long and about 1·5 µ broad
(fig. 42). Although this trypanosome is very active, yet it is
characterized by the blepharoplast (kinetic nucleus) being very minute
or even absent, as the granule sometimes seen may be the basal granule
of the flagellum.

The mode of transmission of _T. equinum_ is not known with absolute
certainty. Migone has shown that the parasite causes a fatal disease
in the large South American rodent, the capybara (_Hydrochœrus
capybara_). This animal appears to be a reservoir of the parasite. Dogs
may become infected by eating diseased capybaras, and it is suggested
that the infection is spread from the dogs to horses by the agency of
fleas. Some authorities consider that _T. equinum_ may be spread by
various _Tabanidæ_ and by _Stomoxys_. Neiva (1913)[104] doubts all
these modes of transmission in Brazil, and suggests _Chrysops_ or
_Triatoma_ as vectors.

[104] _Brazil Medico_, xxvii, p. 366.

*Trypanosoma equiperdum*, Doflein, 1901.

  Syn.: _Trypanosoma rougeti_, Laveran and Mesnil.

The malady of horses known as “dourine” or “mal du coït” is due
to a trypanosome, _T. equiperdum_, discovered by Rouget in 1894.
“Dourine”--also known as “stallion disease” or “covering disease”--is
found among horses and asses in Europe, India, North Africa and North
America. The trypanosome is transmitted by coitus, and so far as is
known not by insect agency.

[Illustration: FIG. 43.--_Trypanosoma equiperdum._ × 2000
approximately. (Original. From preparation by Fantham.)]

The progress of the disease may be considered under three periods. The
_period of œdema_, when signs of œdema of the genitalia are seen. The
œdema is generally painless and non-inflammatory. This period lasts
about a month. It is succeeded by the _period of eruption_, which
sets in about two months after infection. Circular œdematous areas
(“plaques”), often about the size of a two-shilling piece, appear
under the skin of the sides and hind quarters, and also, at times,
under the skin of the neck, thighs and shoulders. The eruption is
variable, but usually lasts about a week and leaves the animal in an
enfeebled condition. Gland enlargement and swelling of the joints and
synovia also may occur. The third period of the disease is described
as that _of anæmia and paralysis_. The animal becomes very anæmic,
emaciation is marked, superficial non-healing abscesses often form, and
conjunctivitis and ulcerative keratitis can occur. Paralysis ensues,
and in from two to eighteen months the animal dies. In the acute form
of the disease the animal may die after the first period from acute

It is difficult to find the trypanosomes in naturally infected animals,
and they are best obtained from the plaques of the eruption. Apparently
the parasite occurs more in the lymph than in the blood.

Ruminants are said to be refractory to this trypanosome.

_T. equiperdum_ is about 25 µ to 28 µ in length on an average, but
varies from 16 µ to 35 µ. Its cytoplasm is relatively clear, and does
not show chromatic granules (fig. 43). It is stated to be monomorphic.

It has been shown recently by Blacklock and Yorke (1913)[105] that
there is another trypanosome giving rise to dourine in horses. This
trypanosome is dimorphic (resembling _T. pecaudi_ and _T. ugandæ_), and
is named _T. equi_. Previously _T. equiperdum_ and _T. equi_ had been

[105] _Proc. Roy. Soc._, B, lxxxvii, p. 89.

Uhlenhuth, Hübner and Worthe have demonstrated the presence of
endotoxins in _T. equiperdum_. These endotoxins may be set free by

*Trypanosoma theileri*, Bruce, 1902.

This parasite, 60 µ to 70 µ long, and 4 µ to 5 µ broad, is
distinguished for its large size, though it is not so large as _T.
ingens_ from Uganda oxen, whose length may be 72 µ to 122 µ, and
breadth 7 µ to 10 µ. The posterior end of _T. theileri_ is drawn out.
Small forms of the flagellate are known, 25 µ to 53 µ in length.
Probably other forms of the parasite have the nucleus posterior, and
these flagellates were formerly separated as _T. transvaaliense_
(Laveran, 1902). Myoneme fibrils may be seen on its body. The
pathogenicity of this organism is doubtful, it was formerly thought
to be the causal agent of “gall-sickness” in cattle in South Africa.
_T. theileri_ also occurs in Togoland, German East Africa, and
Transcaucasia. Allied or identical parasites occur in cattle in India.

[Illustration: FIG. 44.--_Trypanosoma theileri._ × 2,000. (After
Laveran and Mesnil.)]

_Trypanosoma theileri_, specific to cattle, is perhaps transmitted by
the fly _Hippobosca rufipes_ in South Africa.

*Trypanosoma hippicum*, Darling, 1910.

_Trypanosoma hippicum_ causes the disease of mules known as
“murrina.”[106] It was found in mules imported to Panama from the
United States. It can live in other equines. The parasite varies
from 18 µ to 28 µ in length, and is from 1·5 µ to 3 µ broad. Its
undulating membrane is little folded. The trypanosome has a noticeable
blepharoplast. It can penetrate mucous membranes, and it is thought
that the trypanosome may be transmitted during coitus. It may also
be spread mechanically by species of _Musca_, _Sarcophaga_ and
_Compsomyia_, sucking the wounds of infected animals and carrying over
the trypanosomes to wounds on healthy ones.

[106] _Bull. Soc. Path. Exot._, iii, p. 381.

*Endotrypanum schaudinni*, Mesnil and Brimont, 1908.

This organism was discovered in the blood of a sloth (_Cholœpus
didactylus_), in South America (French Guiana).[107] It possesses
special interest, in that the best known form of the organism is
endoglobular, inhabiting the erythrocytes of the sloth. A free
trypanosome in the same animal was considered to be different from the
endoglobular form, which was somewhat like a peg-top, and possessed a
short flagellum. Darling[108] (November, 1914) has seen the organism in
Panama. He describes free crithidial forms in shed blood, but not in
the blood-stream of the sloth.

[107] _C. R. Soc. Biol._, lxv, p. 581.

[108] _Journ. Med. Research_, xxxi, p. 195.

*Trypanosoma boylei*, Lafont, 1912.

This is a parasite of the Reduviid bug, _Conorhinus rubrofasciatus_.
The insect attacks man in Mauritius, Réunion and other places.
Lafont infected rats and mice by intraperitoneal injection with the
gut-contents of infected bugs. Trypanosomes appeared in the mice. Other
flagellate types were assumed by the parasites in the bug.


A number of trypanosomes, characterized by relative uniformity in
size and structure, may be considered under this heading. They occur
in cattle, sheep, goats and horses in Africa, especially West Africa.
Morphologically, they are characterized by the posterior (aflagellar)
part of the body being swollen, while the anterior part narrows. The
nucleus is central and situated at the commencement of the narrowing of
the body. The blepharoplast is almost terminal, the undulating membrane
is narrow and not markedly folded, so that the flagellar border lies
close to or along the body. The flagellum may or may not possess a free

Some recent workers have considered that _T. brucei_ (Zululand strain)
and _T. evansi_ are also monomorphic, but they do not exhibit the
general characteristics outlined above. _T. brucei_ and _T. evansi_
have already been considered separately.

The monomorphic trypanosomes, as defined above, include:--

*Trypanosoma vivax*, Ziemann, 1905.

This trypanosome[109] occurs in cattle, sheep and goats, and was
first found in the Cameroons. It is fatal to cattle. Equines are also
affected. Antelopes are the possible reservoirs of the trypanosome. It
is probably transmitted by _Glossina palpalis_ and other tsetse flies.
Its movement is very active. It possesses a free flagellum (fig. 45)
and it averages 23 µ to 24 µ in length. _T. cazalboui_ (Laveran,
1906)--the causal agent of “souma” in bovines and equines in the French
Sudan--is probably synonymous with _T. vivax_.

[109] See Bruce and colleagues (1910), _Proc. Roy. Soc._, B, lxxxiii,
p. 15.

[Illustration: FIG. 45.--_Trypanosoma vivax_. × 2,000. (Original. From
preparation by Fantham.)]

*Trypanosoma capræ* (Kleine, 1910) is allied, but is somewhat broader
and more massive. It was found in goats in Tanganyika.

*Trypanosoma congolense*, Broden, 1904.

  Probable synonyms.--_Trypanosoma dimorphon_, Laveran and Mesnil,
  1904; _Trypanosoma nanum_, Laveran, 1905; _Trypanosoma pecorum_,
  Bruce, 1910; _Trypanosoma confusum_, Montgomery, 1909.

This trypanosome causes disease among horses (_e.g._, Gambia horse
sickness), cattle, sheep, goats, pigs, and dogs. It is widely
distributed in Central Africa (_e.g._, Gambia, Congo, Uganda,
Nyasaland), the strain probably being maintained naturally in big game.
It is transmitted by various _Glossinæ_, and perhaps by _Tabanus_
and _Stomoxys_. It is said to develop in the gut and proboscis of
_Glossina palpalis_ and _G. morsitans_. The trypanosome averages 13 µ
to 14 µ in length and has no free flagellum (fig. 46). It is about 2 µ
broad. Formerly _T. nanum_ and _T. pecorum_ were said to differ in
their pathogenicity, the former being said not to infect the smaller
laboratory animals. Yorke and Blacklock (1913), however, consider that
the virulence varies and that these trypanosomes are probably the same.

[Illustration: FIG. 46.--_Trypanosoma congolense_. × 2,000. (Original.
From preparation by Fantham.)]

[Illustration: FIG. 47.--_Trypanosoma uniforme_. × 2,000. (Original.
From preparation by Fantham.)]

The _T. dimorphon_ originally obtained by Dutton and Todd (1903) in
Gambian horse sickness has been shown to be a mixture of _T. vivax_ and
_T. congolense_.

*Trypanosoma simiae* (_T. ignotum_) is like _T. congolense_. It
averages 17·5 µ long. It is virulent to monkeys and pigs.

*Trypanosoma uniforme*, Bruce, 1910.

This trypanosome was found in oxen in Uganda.[110] It can be inoculated
to oxen, goats and sheep, but is refractory to dogs, rats and
guinea-pigs. It has been found in antelopes. It resembles _T. vivax_,
but is smaller (fig. 47), averaging 16 µ in length. A free flagellum is
present. It is transmitted by _Glossinæ_.

[110] _Proc. Roy. Soc._, B, lxxxiii, p. 176.

[Illustration: FIG. 48.--_Trypanosoma rotatorium_, from blood of a
frog. × 1,400. (After Laveran and Mesnil.)]

Many other trypanosomes occur in mammals, while birds, reptiles,
amphibia (fig. 48) and fish also harbour them. The discussion of these
forms does not come within the scope of the present work. They are
dealt with in Laveran and Mesnil’s “Trypanosomes et Trypanosomiases,”
2nd edit., 1912.


Before concluding the account of trypanosomes, it may be of interest to
remark that several African trypanosomes develop in various species of
_Glossina_, and are found in different parts of the alimentary tract
and in the proboscis. Thus (_a_) _T. vivax_, _T. uniforme_ and _T.
capræ_ develop in the fly’s proboscis (labial cavity and hypopharynx)
only; (_b_) _T. congolense_, _T. simiæ_ and _T. pecaudi_ develop first
in the gut of the fly and then pass forward to its proboscis; and (_c_)
_T. gambiense_ and _T. rhodesiense_ develop first in the gut and later
invade the salivary glands of the tsetse. The proboscis or the salivary
glands in such cases are termed by Duke[111] the _anterior station_ of
the trypanosome, wherein it completes its development.

[111] _Repts. Sleeping Sickness Commission Roy. Soc._ (1913), xiii,
p. 82.


These flagellates may exhibit power of adaptation to changes of
environment, such as those due to the administration of drugs,
change of host, etc. A few examples of such mutations may be briefly

(1) _Blepharoplastless Trypanosomes_.--_T. brucei_ may become resistant
to pyronin and oxazine. Accompanying this drug resistance is a change
in morphology, namely, the loss of the blepharoplast (Werbitzki).[112]
A race or strain of blepharoplastless trypanosomes may be thus produced
which retains its characteristic feature after as many as 130 passages
(Laveran).[113] Oxazine is the more powerful drug, and it acts directly
on the blepharoplast. (Compare the natural blepharoplastless character
of _T. equinum_.)

[112] _Centralbl. f. Bakt._ (1910), Orig., liii, p. 303.

[113] _Bull. Soc. Path. Exot._, iv, p. 233.

(2) Reference has been made on p. 93 to the experiments of Gonder,
who showed that a strain of _T. lewisi_ rendered resistant to
arsenophenylglycin lost its resistance after passage through the rat
louse. This is in marked contrast with the retention of drug resistance
during passage by inoculation from rat to rat.

(3) _T. lewisi_ from the blood of a rat when transferred to a snake
seems largely to disappear, as very few flagellates are seen. When
blood from the snake is inoculated into a clean rat, then trypanosomes
reappear in the rat, but they are not all like those originally
inoculated. It seems certain that, in such a case, changes in form and
virulence of the trypanosome have occurred. Similar experiments were
made with _T. brucei_ from rats to adders and other animals and back to
rats. Changes in the form and virulence of _T. brucei_ occurred.

These interesting experiments were performed by Wendelstadt and

[114] _Zeitschr. f. Immunitatsforschung_, iv, p. 422 (1909), and v,
p. 337 (1910).

Genus. *Herpetomonas*, Saville Kent, 1881.

_Herpetomonas_ is a generic name for certain flagellates possessing a
vermiform or snake-like body, a nucleus placed approximately centrally,
and a blepharoplast (kinetic nucleus) near the flagellar end. There
is no undulating membrane (fig. 49, _a_). The organisms included
in this genus certainly possess one flagellum, while according to
Prowazek (1904) _Herpetomonas muscæ-domesticæ_, the type species,
possesses two flagella united by a membrane. Patton,[115] Porter[116]
and others affirm, however, that the biflagellate character of _H.
muscæ-domesticæ_ (from the gut of the house-fly) is merely due to
precocious division. The matter is further complicated by the generic
name _Leptomonas_, given by Kent in 1881, to an uniflagellate organism
found by Bütschli in the intestine of the Nematode worm, _Trilobus
gracilis_. This parasite, _Leptomonas bütschlii_, has not yet been
completely studied. Until these controversial points relating to
the identity or separation of _Herpetomonas_ and _Leptomonas_ have
been satisfactorily settled, we may retain the better known name
_Herpetomonas_ for such uniflagellate, vermiform organisms. However,
the name _Leptomonas_, having been used by Kent two pages earlier
in his book (“Manual of the Infusoria”) than _Herpetomonas_, would
have priority if the two generic names were ultimately shown to be

[115] _Arch. f. Protist._, xiii, p. 1.

[116] _Parasitology_, ii, p. 367.

A full discussion of these interesting and important flagellates hardly
comes within the purview of the present work; brief mention can only be
given here to certain species.

The Herpetomonads occur principally in the digestive tracts of insects,
such as Diptera and Hemiptera. They are also known in the guts of
fleas and lice, but are not confined to blood-sucking insects. One
example, _H. ctenocephali_ (Fantham, 1912)[117] occurs in the digestive
tracts of dog fleas, _Ctenocephalus canis_, in England, France,
Germany, Italy, India, Tunis, etc. It is a natural flagellate of the
flea, and might easily be confused with stages of blood parasites in
the gut of the dog flea. Dog fleas are stated by Basile to transmit
canine kala-azar, which is believed to be the same as human infantile
kala-azar. Confusion is further likely to arise since herpetomonads
pass through pre-flagellate, flagellate and post-flagellate or
encysted stages; pre- and post-flagellate stages being oval or rounded
and _Leishmania_-like. The post-flagellate stages are shed in the
fæces, and are the cross-infective stages by means of which new hosts
are infected by the mouth. The possible presence of such natural
flagellates must always be considered when experimenting with fleas,
lice, mosquitoes, etc., as possible vectors of pathogenic flagellates
like _Leishmania_ and _Trypanosoma_. _H. pediculi_ (Fantham, 1912)
occurs in human body lice.[118] See further remarks on pp. 107, 112.

[117] _Bull. Path. Exot._, vi, p. 254.

[118] _Proc. Roy. Soc._, B, lxxxiv, p. 505.

[Illustration: FIG. 49.--_a_, _Herpetomonas_; _b_, _Crithidia_; _c_,
_Trypanosoma_. (After Porter.)]

Laveran and Franchini (1913–14)[119] have recently succeeded in
inoculating _Herpetomonas ctenocephali_, from the gut of the dog flea,
intraperitoneally into white mice, and producing an experimental
leishmaniasis in the mice. A dog was also infected. They have also
succeeded in infecting mice with _H. pattoni_--a natural flagellate of
the rat flea--by mixing infected rat fleas with the food of the mice,
and by causing them to ingest infected fæces of rat fleas. Further,
they have shown that infection with the herpetomonas occurs naturally
by this method, that is, by the rodents eating the fleas and not by the
insects inoculating the flagellates into the vertebrates when sucking
blood. These experiments shed an interesting light on the probable
origin of _Leishmania_ and its cultural herpetomonad stage, which were
very probably once parasitic flagellates in the gut of an insect.

[119] _C. R. Acad. Sci._, clvii, pp. 423, 744. _Ibid._, clviii,
pp. 450, 770. _Bull. Soc. Path. Exot._, vii, 605.

Fantham and Porter[120] (1914–15) have shown that young mice may be
inoculated or fed with _Herpetomonas jaculum_, from the gut of the
Hemipteran, _Nepa cinerea_ (the so-called “water-scorpion”), with fatal
results. The pathogenic effects are like those of kala-azar. They also
showed that the post-flagellate stages of the herpetomonads seemed most
capable of developing in the vertebrate.

[120] _Proc. Camb. Philosoph. Soc._, xviii, p. 39.

  A herpetomonad, _H. davidi_, has been found in the latex of species
  of the plant-genus _Euphorbia_ in Mauritius, India, Portugal, etc. It
  is apparently transmitted to the plants by _Hemiptera_. The plants
  sometimes suffer from “flagellosis.”

Franchini (1913)[121] has described a new parasite, _Hæmocystozoon
brasiliense_, from the blood of a man who had lived in Brazil for many
years. It possesses flagellate and rounded stages, and is closely
allied to the herpetomonads.

[121] _Bull. Soc. Path. Exot._, vi, pp. 156, 333, 377.

Genus. *Crithidia*, Léger, 1902, emend. Patton, 1908.

_Crithidia_ is the generic name of vermiform flagellates with a central
nucleus, a blepharoplast or kinetic nucleus in the neighbourhood of the
principal nucleus, and a rudimentary undulating membrane bordered by a
flagellum arising from a basal granule, which is the centrosome of the
kinetic nucleus (fig. 49_b_). The anterior or flagellar end of the body
is attenuated and fades off as the undulating membrane.

_Crithidia fasciculata_, the type species, was found by Léger in the
alimentary canal of _Anopheles maculipennis_. Crithidia occur in
bugs, flies, fleas,[122] and ticks. Some of them are found in the
body-fluid of the invertebrate host as well as in the gut. Others
may be restricted to the body cavity or intestine respectively. _C.
melophagia_ from the sheep-ked, _Melophagus ovinus_, and _C. hyalommæ_
from the hæmocœlic fluid of the tick, _Hyalomma ægyptium_, pass into
the ovaries and eggs of their hosts, and the young keds or ticks are
born infected.

[122] See Porter, _Parasitology_, iv, p. 237.

_C. fasciculata_ has been shown by Laveran and Franchini to be
inoculable into white mice, producing a sort of experimental
leishmaniasis therein. In one case cutaneous lesions were produced like
those of Oriental sore.

Crithidia are natural flagellates of Arthropoda, with their own
pre-flagellate, flagellate and post-flagellate stages, and must not be
confused with transitory crithidial stages of trypanosomes.

Genus. *Leishmania*, Ross, 1903.

With an oval body containing nucleus and blepharoplast (kinetic
nucleus) but no flagellum. An intracellular parasite in the vertebrate

Included in the genus _Leishmania_ are three species, namely:--

  (1) _Leishmania donovani_, Laveran and Mesnil, 1903, the parasite
      of Indian kala-azar, a generalized systemic disease, usually
      fatal, occurring in subjects of all ages.
  (2) _Leishmania tropica_, Wright, 1903, the parasite of Delhi boil,
      Oriental sore, Aleppo button--a localized, cutaneous disease,
      usually benign.
  (3) _Leishmania infantum_, Nicolle, 1908, the parasite of infantile
      kala-azar, occurring in children (and a few adults) around
      the shores of the Mediterranean. The disease is perhaps a
      form of Indian kala-azar, and the parasite is probably identical
      with _L. donovani_.

These diseases may be termed collectively leishmaniases. The morphology
of the various species is practically identical.

*Leishmania donovani*, Laveran and Mesnil, 1903.

  Syn.: _Piroplasma donovani_, Laveran and Mesnil.

The parasite of Indian kala-azar was demonstrated in 1900 by Leishman
from a _post-mortem_ examination of a case of “Dum-Dum fever,” but
details were not published till May, 1903. In July, 1903, Donovan found
similar bodies from cases in Madras. Rogers succeeded in cultivating
the parasite in July, 1904.[123] The original centre of the disease was
probably Assam; it occurs also in Madras, Ceylon, Burma, Indo-China,
China and Syria. A variety of this leishmaniasis is found in the Sudan.
The patient becomes emaciated, with a greatly enlarged spleen. There is
anæmia and leucopenia.

[123] The literature up to 1912, on kala-azar and other leishmaniases
is reviewed in the _Kala-azar Bulletin_. Afterwards in the _Tropical
Diseases Bulletin_.

The parasite, commonly known as the Leishman-Donovan body, is
intracellular (fig. 50, 2, 3). It is found in the endothelial cells
of the capillaries of the liver, spleen, bone-marrow, lymphatic
glands and intestinal mucosa, and in the macrophages of the spleen
and bone-marrow. Some host cells may contain many parasites. It is
rather rare in the circulating blood, but may be found in the blood
from the femoral, portal and hepatic veins. It does not occur in
the red blood corpuscles as was formerly thought. The parasites
liberated from the endothelial cells are taken up by the mononuclear
and polymorphonuclear leucocytes. The Leishman-Donovan body is the
resting stage of a flagellate. As found in man it is a small, oval
organism, about 2·5 µ to 3·5 µ in length by 2 µ in breadth, and
containing two chromatinic bodies, corresponding to the nucleus and
kinetic nucleus (blepharoplast) of a flagellate. The latter element
is the smaller and more deeply staining, and is usually placed at the
periphery, transversely to the longer axis of the oval organism.
There is sometimes a very short, slightly curved filament to be seen,
which may be a rhizoplast. Multiplication takes place by binary or
multiple fission. The presence of the parasite used to be demonstrated
by splenic or hepatic puncture; nowadays it can be demonstrated in
peripheral blood, _e.g._, of the finger, or by culture of infected

[Illustration: FIG. 50.--_Leishmania donovani_. _1_, Free forms,
each with nucleus and rod-shaped blepharoplast (after Christophers);
_2_, endothelial cell and leucocytes containing parasites (after
Christophers); _3_, capillary in the liver showing endothelial cells
containing parasites (after Christophers); _4_, two parasites escaping
from a leucocyte in the alimentary canal of the bug (after Patton);
_5_, further development in bug (after Patton); _6_, young flagellate
forms in bug (after Patton); _7_-_11_, culture forms (after Leishman);
_7_, _8_, _9_, show development of flagellum.]

_L. donovani_ can be cultivated in citrated splenic blood, under
aerobic conditions, at 22° to 25° C. This was first accomplished by
Rogers (1904). It is not so easily culturable as _L. infantum_ on the
Novy-MacNeal-Nicolle medium.[124] _L. donovani_ is inoculable with
some difficulty into experimental animals--in India, white rats, white
mice, dogs and monkeys (_Macacus spp._), have been inoculated. The
Sudan variety, somewhat less virulent, is inoculable to monkeys. Row
also produced a local lesion in _Macacus sinicus_ by subcutaneous
inoculation of _L. donovani_. Parasites taken from such a local lesion
were found to be capable of producing a generalised infection in
_Macacus sinicus_ and white mice.

[124] For the composition of this medium, see Appendix.

In cultures the various species of _Leishmania_ all grow into
herpetomonad, uniflagellate organisms (fig. 50, 10), about 12 µ to
20 µ in body length. On this account Rogers[125] and Patton place the
Leishman-Donovan body within the genus _Herpetomonas_. The method of
culture may be used in diagnosing leishmaniases.

[125] _Proc. Roy. Soc._, B, lxxvii, p. 284.

Kala-azar is very probably an insect-borne disease. Patton[126]
suspects the bed-bug to be the transmitter and finds (fig. 50, _4_-_6_)
that the Leishman-Donovan body can develop into the flagellate stage
in the digestive tract of the bed-bug. Feeding experiments are
unsatisfactory, since there are very few cases in which the parasites
occur in sufficient numbers in the peripheral blood to make the
infection of the insect possible, or at any rate easy. In examining
the alimentary tracts of insects for possible flagellate stages of
_Leishmania_, it must be remembered that in many insects natural
flagellate parasites, belonging to the genus _Herpetomonas_, may occur
therein; such natural insect flagellates may be harmless, and have no
connection with the life-cycle of _L. donovani_. Natural herpetomonads
are known to occur in the alimentary tracts of flies, mosquitoes,
sand-flies, fleas and lice, but not in bed-bugs. Further, if such
flagellates are able to be inoculated into and live within vertebrate
hosts, producing symptoms like those of leishmaniasis, the origin of
kala-azar is indicated (see pp. 104, 112).

[126] _Sci. Mem. Govt. India_, Nos. 27, 31 (1907–08).

*Leishmania tropica*, Wright, 1903.

  Syn.: _Helcosoma tropicum_, Wright, 1903; _L. wrighti_, Nicolle,
  1908; _Ovoplasma orientale_, Marzinowsky and Bogrow.

  It is believed by some that the parasite was first described by
  Cunningham in 1885, and studied by Firth in 1891, being called by
  him _Sporozoon furunculosum_. If these earlier studies were of the
  parasite, then its correct name is _L. furunculosa_, Firth, 1891.

The benign disease produced by this parasite has received many names,
among the best known being Oriental sore, Tropical sore, Delhi boil and
Aleppo button. These names, however, are not happy ones, as cutaneous
leishmaniasis (_e.g._, on the ear) is now known to occur in the New
World, for example in Mexico, Venezuela, Brazil and neighbouring
States. However, it may be necessary to subdivide cutaneous
leishmaniases later.

In the Old World the disease occurs in India, Persia, Arabia and
Transcaucasia. It is also known in Algeria, Northern Nigeria, Egypt,
Sudan, Crete, Calabria, Sicily and Greece.

The boils often occur on the face, and before ulceration the parasites
may be found in the cells at the margin and floor of the “button.” In
searching for parasites the scab should be removed and scrapings made
from the floor and edges. Where lesions occur atrophy of the epidermis
takes place, and infiltration of mononuclear cells (_e.g._, plasma
cells, lymphoid and endothelial cells) follows. The parasites are
intracellular, being found inside mononuclear cells. In non-ulcerating
sores, Cardamitis found some free parasites. Non-ulcerating forms
are said to occur in the Sudan. In the Old World the sores are often
limited to exposed surfaces of the body. Infection of mucous membranes
(such as the lip, palate, buccal and nasal membranes) may occur,
especially in South America, and are often known there as “Espundia.”
Christopherson (1914) has recorded a case in Khartoum.

_Leishmania tropica_ is equally well cultivated on Novy-MacNeal-Nicolle
medium or on citrated blood. The usual temperature for cultivation
is 22° to 28° C., though Marzinowski claims to have cultivated the
parasite at 37° C. _L. tropica_ can be inoculated into monkeys and
dogs, with the production of local lesions. Material from a human sore
or flagellates from a culture may be thus successfully inoculated. Also
infected material may be rubbed directly into a scarified surface. The
incubation period is long, extending over several months. The duration
of the disease may be from twelve to eighteen months. Recovery from
one attack of tropical sore confers immunity, and the Jews in Bagdad
inoculate their children with the disease on a part of the body which
will be covered, and so secure immunity in adult life.

The mode of transmission of _L. tropica_ is unknown. Wenyon (1911)[127]
has found that the parasite develops into the flagellate stage in the
digestive tract of _Stegomyia fasciata_ in Bagdad. Patton (1912)[128]
has found similar development in the bed-bug in Cambay. The house-fly,
_Phlebotomus_ and _Simulium_ have been suspected as transmitters in
different parts of the world.

[127] _Parasitology_, iv, p. 387.

[128] _Sci. Mem. Govt. India_, No. 50.

An interesting announcement has been made recently (May, 1913), that
Neligan has found that _L. tropica_ occurs in dogs in Teheran, Persia,
producing ulcers on the dogs’ faces (_cf._ natural occurrence of _L.
infantum_ in dogs--see p. 110). Yakimoff and Schokhor (1914),[129] have
found the disease in dogs in Tashkent.

[129] _Bull. Soc. Path. Exot._, vii, p. 186.

Gonder[130] (1913) has performed some interesting experiments showing
the relation of infantile kala-azar to Oriental sore. Gonder infected
mice with _L. infantum_ and with _L. tropica_. He used culture material
and injected intraperitoneally or intravenously. In each a general
infection resulted, with enlargement of the liver and spleen. Later,
however, mice injected with Oriental sore (North African variety)
developed peripheral lesions on the feet, tail and head, and the
lesions contained _Leishmania_. No such peripheral lesions developed
in the case of the mice infected with the kala-azar virus. Gonder
suggested that Oriental sore, like kala-azar, is really a general
infection overlooked in its earlier stages, and that it is in the
later stages that peripheral lesions on the skin are developed. Row
(1914)[131] also obtained a general infection in a mouse by the
injection of cultures of _L. tropica_ from Oriental sore of Cambay.

[130] _Arch. f. Schiffs- u. Trop. Hyg._, xvii, p. 397.

[131] _Bull. Soc. Path. Exot._, vii, p. 272.

*Leishmania infantum*, Nicolle, 1908.[132]

Infantile splenic anæmia has been long known in Italy. It also
occurs in Algeria, Tunis, Tripoli, Syria, Greece, Turkey, Crete,
Sicily, Malta,[133] Spain and Portugal. This leishmaniasis is, then,
distributed along the Mediterranean littoral; also in Russia. Cathoire
(1904) in Tunis and Pianese (1905) in Italy were among the first to see
the parasite. Nicolle then found the parasite in patients in Tunis, and
further found spontaneous infection in dogs. The patients are usually
children between the ages of 2 and 5 years. There are a few cases known
in which the infantile type of leishmaniasis occurred in youths and
adults of the ages of 17 to 19, while one patient in Calabria was 38
years old. The symptoms are like those of Indian kala-azar. Several
Italian investigators and others consider that _L. infantum_ is the
same as _L. donovani_, and that the latter name should be used for the
parasite of Mediterranean leishmaniasis. This view, as to the identity
of _L. donovani_ and _L. infantum_, seems coming into general favour.

[132] _Arch. Inst. Pasteur Tunis_, i, p. 26.

[133] _See_ Wenyon (1914), _Trans. Soc. Trop. Med. and Hyg._, vii,
p. 97; also Critien (1911), _Annals Trop. Med. and Parasitol._, v,
p. 37.

There are, however, differences between the Indian and infantile
kala-azars, in addition to the ages of the patients affected,
thus: (_a_) As regards cultures, it is found that _L. infantum_ is
readily grown on the Novy-MacNeal-Nicolle (“N.N.N.”) medium (saline
blood-agar), and that sub-cultures are easily obtained; in citrated
blood _L. infantum_ grows with difficulty. The reverse is the case with
regard to culture media for _L. donovani_, which grows with difficulty
on the N.N.N. medium, but relatively easily in citrated splenic blood.
(_b_) Considering inoculability into experimental animals, it is found
that _L. donovani_ is inoculated generally with some difficulty into
white rats, white mice and monkeys, and with greater difficulty into
dogs, while _L. infantum_ can be inoculated into several experimental
animals, especially into dogs and monkeys, with ease. (_c_) At present
_L. donovani_ is not known to occur spontaneously in animals, but _L.
infantum_ is found naturally in dogs in the Mediterranean region, and
the disease in dogs is often referred to as canine kala-azar. Kittens
have occasionally been found infected. However, these differences must
not be emphasized too much.

The material for cultivation is obtained from punctures of spleen,
liver or bone-marrow of cases infected with _L. infantum_. It is
not always easy, however, to infect from cultures, as the cultural
flagellates inoculated into the body are often phagocytosed.

Similarly, the material for animal inoculation is obtained from
emulsions of infected spleen, liver or bone-marrow. Dogs and monkeys
are easily inoculated with such material; Nicolle inoculates into the
liver or the peritoneal cavity. Mice, white rats, guinea-pigs and
rabbits only show slight infections after such inoculations.

Dogs infected experimentally with infantile leishmaniasis may show
either acute or chronic symptoms. The acute course occurs more often in
young dogs, and is usually fatal in three to five months. The chronic
course is found more commonly in older dogs, and may last seventeen to
eighteen months. In acute forms there is irregular fever, progressive
wasting, diarrhœa occasionally, motor disturbances involving the hind
quarters, and the animal dies in a comatose condition. In the chronic
form the animal may appear well, except for loss of weight. The
parasites may be found in the internal organs of these experimental
dogs, but are not numerous in the peripheral blood except at times of
high fever. Experimental monkeys live about three months.

It may be interesting to record the number of dogs found to be infected
naturally with leishmaniasis in various countries. In Tunis, Nicolle
and Yakimoff found about 2 per cent. infected out of about 500 dogs
examined. Sergent in Algiers found 9 infected out of 125 dogs examined.
In Italy and Sicily, Basile found about 40 per cent. of the dogs to be
infected out of 93 examined at Rome and Bordonaro. Cardamitis found
15 infected out of 184 examined in Athens. In Malta, Critien found 3
infected out of 30 dogs examined. Alvares found 1 infected dog out of
19 examined in Lisbon. Pringault has recently (December, 1913) found
an infected dog in Marseilles.[134] Yakimoff and Schokhor found 24 per
cent. infected out of 647 dogs examined in Turkestan.

[134] _Bull. Soc. Path. Exot._, vii, p. 41.

The distribution of the parasites in the body of the human patient is
much the same as in the case of Indian kala-azar. Critien records
the finding of parasites in the mucous flakes of the stools of a
three-year-old Maltese child.[135] Intestinal lesions rarely occur in
infantile leishmaniasis.

[135] Quoted by Leishman (1911) in his interesting review of
Leishmaniasis, _Journ. Roy. Army Med. Corps_, xvii, p. 567, xviii,
pp. 1, 125. Also _Quart. Journ. Med._ v, pp. 109–152.

_Ætiology._--Infantile leishmaniasis is stated to be transmitted
by fleas, especially dog fleas, _Ctenocephalus canis_ (= _Pulex
serraticeps_), and by _Pulex irritans_. Children living in contact with
infected dogs may be bitten by infected dog fleas, and so contract
the disease. Basile (1910–11) and Sangiorgi (1910) state that they
found _L. infantum_ parasites in the digestive tract of the dog flea.
After searching they found infected dog fleas on the beds, mattresses,
and pillows used by children suffering from the disease. Franchini
(1912) thinks that _Anopheles maculipennis_ may be concerned in the

Basile[136] tried a number of experiments to show that infantile
leishmaniasis is transmitted by fleas, thus:--

[136] Numerous papers in _Rendiconti R. Accad. dei Lincei_ (Rome), xix,
xx (1910–11).

(1) Fleas were taken from a healthy dog. They were placed in vessels
containing infected spleen-pulp and allowed to feed thereon. The fleas
were then killed and dissected, and portions of the gut-contents
examined for parasites. The remainder of the gut was emulsified
and injected into a young puppy, whose bone-marrow had been shown
previously to be uninfected. Basile states that the puppy became
infected. The parasites are said to increase in number in the flea’s

(2) Two healthy pups, each a month old, and born in the laboratory,
were placed in a disinfected, flea-proof cage. A few days after, an
infected dog was placed in the cage, so that fleas from the infected
dog could pass on to the puppies. A month later the two pups became
infected, parasites being found in them after liver puncture. A number
of control puppies from the same litter remained uninfected and in good

(3) Basile next used other laboratory-born puppies, a month old. Four
of the litter were placed in a disinfected, flea-proof gauze cage in
Rome. The cage was isolated from other dogs. Fleas obtained from an
infected area in Sicily were placed in the cage. The puppies were
examined by hepatic puncture, but were found to be negative for two
months. Then two of the puppies showed infection, and six days later
the remaining two puppies were found to be infected, and all four died.
They showed irregular temperatures, and were getting thin. Control
puppies remained healthy.

From these experiments Basile concludes that fleas transmit
leishmaniasis. However, Basile did not exclude the possible occurrence
of natural herpetomonads in the gut of the fleas.[137] _Herpetomonas
ctenocephali_ is known to occur in the gut of _Ctenocephalus canis_. A
natural _Herpetomonas_ is also known in the gut of _Pulex irritans_,
as well as a _Crithidia_ (_C. pulicis_, Porter). These natural
flagellates of the fleas pass through non-flagellate stages, like the
Leishman-Donovan body. In consequence Wenyon and Patton, among others,
have criticized Basile’s results. Further, other investigators, such as
Wenyon and Da Silva (1913), have repeated Basile’s flea experiments and
been unable to confirm them.

[137] See Fantham, _Brit. Med. Journ._, 1912, ii, p. 1196.

In feeding and inoculation experiments the incubation period of the
parasite may be long, and so it is necessary to wait a long time to see
whether the parasite will develop.

_Immunity._--Nicolle has tried some experiments with _L. infantum_ and
_L. tropica_. He finds that in animals recovery from an attack of the
former confers immunity against infection by the latter and vice-versâ.

Laveran[138] records that a monkey having an immunity against _L.
infantum_ was also immune to _L. donovani_.

[138] _Annales Inst. Pasteur_ (1914–15), xxviii, pp. 823, 885; xxix,
pp. 1, 71.

As mentioned on p. 103, Laveran and Franchini (1913), working in Paris,
have succeeded in inoculating _Herpetomonas ctenocephali_, a natural
flagellate in the gut of the flea, _Ctenocephalus canis_, into white
mice. Leishmaniform stages of the flea flagellate were recovered
from the peritoneal exudate, blood and organs of the mice some weeks
after inoculation. The parasites may also be conveyed by way of the
digestive tract of the vertebrate. Similar experiments have succeeded
with _H. pattoni_. These experiments go to show, together with those
of Fantham and Porter with _H. jaculum_ (see p. 104), that, in the
words of the latter authors, “it may be expected that the various
leishmaniases, occurring in different parts of the world, will prove to
be insect-borne herpetomoniases.”

Genus. *Histoplasma*, Darling, 1906.

Under the name _Histoplasma capsulatum_,[139] Darling described
small round or oval parasites, enclosed in a refractile capsule, and
each containing a single nucleus. The bodies were found in cases of
splenomegaly in Panama. They occurred in the endothelial cells of
the small blood-vessels of the liver, spleen, lungs, intestine and
lymphatic glands, and also within the leucocytes. A few flagellates
were stated to occur in the lungs. The parasite has usually been
placed near _Leishmania_, but recently Rocha-Lima has stated that
_Histoplasma_ is a yeast.

[139] _Journ. Amer. Med. Assoc._, xlvi, p. 1283: _Journ. Exptl. Med._
(1909), xi, p. 515.

Genus. *Toxoplasma*, Nicolle and Manceaux, 1908.

  The genus was created for crescentic, oval or reniform parasites,
  2·5 µ to 6 µ by 2 µ to 3 µ, possessing a single nucleus and
  multiplying by binary fission. They occur in mononuclear and
  polymorphonuclear cells in the blood, spleen, liver, peritoneum etc.
  (fig. 51). The parasites have been found in the gondi, dog, rabbit,
  mole, mouse, pigeon and other birds. Although various species names
  have been given to the parasites in these hosts, it seems probable,
  from cross infection experiments, that there is but one species with
  several physiological races. Splendore[140] (1913) has described a
  flagellate stage.

[140] _Bull. Soc. Path. Exot._, vi, p. 318.

[Illustration: FIG. 51.--_Toxoplasma gondii_, endocellular or free in
the peritoneal exudate of infected mice. 1, 2, mononuclear leucocytes
containing toxoplasms. 3, polynuclear, containing parasites. 4, 5,
6, endothelial cells containing toxoplasms, agglomerated in 6. 7,
agglomeration forms. 8–11, free forms. 12–13, division stages. × 1,600.
(After Laveran and Marullaz.)]

[Illustration: FIG. 52.--_Toxoplasma pyrogenes._ 1, body found in
blood. 2–7, bodies found] in spleen. [1 is about the size of a red
blood corpuscle, as drawn in the figures]. Magnification not stated.
(After Castellani.)]

Castellani (1913–14)[141] has described similar parasites from a case
of splenomegaly, with fever of long standing, in a Sinhalese boy. The
bodies were found in the spleen and more rarely in the blood (fig. 52).
Castellani has named them _Toxoplasma pyrogenes_. Further researches
are needed.

[141] _Journ. Trop. Med. and Hyg._, xvii, p. 113.


The Spirochætes are long, narrow, wavy, thread-like organisms, with
a firm yet flexible outer covering or periplast. There is a diffuse
nucleus internally in the form of bars or rodlets of chromatin
distributed along the body. In some forms there is a membrane or crista
present (fig. 53), which in the past was compared with the undulating
membrane of a trypanosome, but the membrane of a spirochæte does not
undulate. Progression is very rapid, corkscrew-like and undulatory
movements occurring simultaneously.

The genus _Spirochæta_ was founded by Ehrenberg in 1833 for an organism
which he discovered in stagnant water in Berlin. Ehrenberg named
the organism _Spirochæta plicatilis_. According to Zuelzer (1912)
_S. plicatilis_ does not possess a membrane or crista, but an axial
filament. _S. gigantea_ has been described by Warming from sea-water.

Spirochætes occur in the crystalline style and digestive tract of many
bivalve molluscs. The first molluscan spirochæte to be studied was
that of the oyster, named by Certes (1882) “_Trypanosoma_” _balbianii_
(fig. 53). Similar spirochætes, probably belonging to the same species,
occur in various species of _Tapes_ and in _Pecten_ (the scallop).
_S. balbianii_ has rounded ends (fig. 53). Other spirochætes occur
in freshwater mussels (_Anodonta_ spp). _S. anodontæ_, studied by
Keysselitz (1906) and by Fantham (1907), has pointed ends. Gross (1911)
suggested the generic name _Cristispira_ for molluscan spirochætes,
because they possess a well-marked membrane or “crista,” which appears
to be absent from _S. plicatilis_, according to Zuelzer’s researches.

[Illustration: FIG. 53.--_Spirochæta balbianii._ _a_, basal granule
or polar cap. _b_, chromatin rodlets. _c_, membrane (“crista”). _d_,
myonemes in membrane. (After Fantham and Porter.)]

Schaudinn in 1905 founded the genus _Treponema_ for the parasite of
syphilis (_T. pallidum_), discovered by him and by Hoffmann. According
to Schaudinn the Treponemata have no membrane or crista. The pathogenic
agent of yaws or frambœsia, discovered by Castellani, is also placed in
the genus _Treponema_, as _T. pertenue_.

There remain the blood spirochætes. It is somewhat disputed as to
whether these organisms possess a membrane. The present writer
considers that they have a slight membrane or crista. The name of
the genus in which to place the blood-inhabiting forms is somewhat
uncertain and disputed. Various generic names given to them are
_Spirochæta_, _Treponema_, _Spiroschaudinnia_ (Sambon) and _Borrelia_
(Swellengrebel). Included in this division are the causal agents
of relapsing or recurrent fever. These Protists will be named, for
description, Spirochætes without prejudice as to the ultimate correct
generic name.

It is sometimes made a matter of argument as to whether the spirochætes
are Protozoa or Bacteria. Such arguments are somewhat unprofitable.
Morphologically the spirochætes are like the Bacteria in possessing a
diffuse nucleus. They differ from _Spirillum_, an undoubted bacterial
genus, in being flexible and not possessing flagella. Molluscan
spirochætes, however, may appear to have flagella if their membrane
becomes frayed or ruptured, when the myonemes therein (fig. 53),
becoming separated, form apparent threads or flagella (Fantham,

[142] _Quart. Journ. Microsc. Sci._, lii, p. 1.

Again, the mode of division of spirochætes has been used as a criterion
of their bacterial or protozoal affinity. They have been stated to
divide transversely, longitudinally, and by “incurvation,” or bending
on themselves in the form of a *U*, “a form of transverse fission.”
The present writer believes that they divide both transversely and
longitudinally, and that there is a periodicity in their mode of
division at first longitudinal (when there are few spirochætes in, say,
the blood) and then transversely (when spirochætes are numerous in
the blood).[143] Some authors consider that longitudinal division is
explained by “incurvation.”

[143] _Proc. Roy. Soc._, B, lxxxi, p. 500.

The spirochætes of relapsing fever show a remarkable periodic increase
and decrease in numbers in the blood. They are transmitted by ticks
or by lice. They react to drugs (_e.g._, salvarsan or “606”) rather
like trypanosomes, and--like Protozoa, but unlike Bacteria--they
are cultivated with difficulty. These and other criteria have
been used to endeavour to determine whether they are Protozoa or
Bacteria. The present writer believes that they are intermediate in
character, showing morphological affinities with the Bacteria and
physiological and therapeutical affinities with the Protozoa. The group
Spirochætacea, as an appendix to the Protozoa, has been created for
them by the present writer (Jan., 1908). Others have placed them in the
Spirochætoidea of the Bacteria or with the Spirillacea. Doflein (1909)
called them Proflagellata. Further discussion is unnecessary, as they
are undoubtedly Protista (see p. 29).

There is no true conjugation, sex or encystment in spirochætes, but
morphological variation may occur.[144] They may agglomerate.

[144] Fantham, _Parasitology_, ii, p. 392.

The Spirochætes form an interesting chapter in the evolution of
parasites. There are free living forms, parasitic forms in the guts
of both vertebrates and invertebrates, and blood-inhabiting forms.
These probably represent the order of evolution of parasitism. The
blood-inhabiting forms are pathogenic to warm-blooded hosts.

We must now consider the blood Spirochætes and the Treponemata
(organisms of syphilis and of yaws).


There are at least two important human parasites included hereunder:--

(_a_) _Spirochæta recurrentis_ (=_S. obermeieri_), (_b_) _Spirochæta

More is known of the life-cycle of _Spirochæta duttoni_, and it will be
convenient to consider that first.

*Spirochæta duttoni*, Novy and Knapp, 1906.

  The specific name _duttoni_ was also given, independently, to this
  parasite in 1906 by Breinl and Kinghorn.

_S. duttoni_ is the pathogenic agent of African tick fever in man,
prevalent in the Congo State and other parts of Africa. The full-grown
organism is about 16 µ to 24 µ long, and has pointed ends. It is 0·25 µ
to 0·5 µ broad. P. H. Ross and Nabarro were among the earliest to see a
spirochæte in the blood of patients in Uganda. It is transmitted by the
tick, _Ornithodorus moubata_.

In the blood of the patient some of the spirochætes may show, after
staining, lighter and darker portions (chromatin dots) and evidence
of the possession of a very narrow membrane (fig. 54). The mode of
division has already been discussed. Periodicity in the direction
of division was first described by Fantham and Porter,[145] (1909).
Just before the crisis in African tick fever, Breinl has stated that
_S. duttoni_ becomes thinner in the spleen and bone-marrow and rolls
up into skein-like forms, which are surrounded by a thin “cyst” wall
(probably the periplast). Such occur in apyrexial periods. Inside
the cyst the spirochæte breaks up into granules. Balfour and Sambon
have described somewhat similar rolled up forms, breaking into
granules, inside the red blood cells of Sudanese fowls in the case
of _S. granulosa_ (possibly only a variety of _S. gallinarum_). The
intracorpuscular stage is not definitely established.

[145] _Proc. Roy. Soc._, B, lxxxi, p. 500.

The granule phase, however, is an essential one in the invertebrate
transmitter (fig. 54_c_). In 1905,[146] Dutton and Todd proved
experimentally that _O. moubata_ transmitted _S. duttoni_. They fed
ticks, obtained from Congo native huts in which infected persons
lived, on monkeys and the latter became infected. Dutton and Todd also
found the offspring of infected ticks to be capable of transmitting the
infection to experimental animals. They concluded that _O. moubata_ was
a true intermediate host.

[146] _Liverpool Sch. Trop. Med._, _Memoir_ xvii; _Lancet_, Nov. 30,
1907, p. 1523.

[Illustration: FIG. 54.--_Spirochæta duttoni_. _a_, blood form showing
slight membrane; _b_, granules or coccoid bodies clearly formed within
the organism; _c_, beginning of extrusion of coccoid bodies in the
tick. (After Fantham.)]

A little later in 1905, Koch stated that spirochætes from the gut of
the tick penetrated the gut wall and tissues and found their way into
the eggs in the ovary. Koch figured tangled masses of spirochætes as
occurring in the tick eggs. He found ticks infective to the third
generation. He thought that the infection was spread by the salivary
fluid of the tick, in the act of biting. (This is now known to be
incorrect.) Markham Carter (1907) corroborated Koch’s work on the
spirochætes in the tick eggs, and they have been seen since by Kleine
and Eckard (1913).

Sir William Leishman,[147] in 1909–10, found that at ordinary
temperatures the salivary glands of infected ticks (_O. moubata_) were
not themselves infective, and that the infection occurred by way of the
ticks’ excretion. The spirochætes (contained in the ticks’ excrement)
found their way into the vertebrate host through the wound made by
biting. While feeding, ticks pass large quantities of clear fluid from
the coxal glands; in this fluid an anticoagulin occurs. Some of the
ticks also pass thick, white Malpighian secretion, that is, excrement,
towards the end of the feed. Leishman, using experimental monkeys,
showed that if infected ticks were interrupted while feeding, then no
infection resulted in the monkeys. If, however, the ticks were allowed
to finish their feed, and the Malpighian secretions were passed, then
the experimental monkeys became infected. Fantham[148] and Hindle[149]
(1911), independently, have repeated the experiments with mice.

[147] _Journ. Roy. Army Med. Corps_, xii, p. 123; _Lancet_ (1910),
clxxviii, p. 11.

[148] _Annals Trop. Med. and Parasitol._, v, p. 479.

[149] _Parasitology_, iv, p. 133.

Leishman’s methods and results may be summarized thus: Saline emulsions
of the organs of infected ticks were made, after the organs had been
most carefully dissected out. The ticks were first kept for several
days at certain constant temperatures, such as 24° to 25° C. or blood
heat, 37° C. The saline emulsions of the organs were inoculated,
separately, into experimental animals, and the results recorded:--

                       At 24° C.     At 37° C.
  Salivary glands      Negative      Positive
  Malpighian tubules   Positive      Positive
  Gut and contents     Positive      Positive
  Excrement            Positive      Positive
  Genital organs       Positive      Positive

Coxal fluid is usually negative; thick, white excrement from Malpighian
tubes is positive.

When the ticks were incubated at 21° to 24° C. no spirochætes, as such,
were seen in the organs, except perhaps in the gut, where they often
disappeared in a few days. When the ticks were previously incubated at
35° to 37° C. for two to three days, spirochætes, as such, reappear in
the gut, organs and hæmocœlic fluid. The infection proceeds, not from
the salivary gland, but from the infective excrement, that is, from the
thick, white material voided by the tick while feeding, usually towards
the end of the meal. This Malpighian excrement passes into the wound
caused by the bite, being greatly aided by the clear and more limpid
coxa fluid, which bathes the under surface of the tick’s body, and
mixes with and carries the infective excrement into the wound. Ticks
remain infective for a long time.

[Illustration: FIG. 55.--_Spirochæta duttoni_ and its coccoid bodies
in the tick (_O. moubata_).--Mononuclear cells of the tick (_O.
moubata_) containing (_a_) Spirochæte breaking up into coccoid bodies;
(_b_) Similar tick-cell containing coccoid bodies or granules. Such
mononuclear cells occur in various organs of ticks and in developing
Malpighian tubules. (Original. From preparations by Fantham.)]

The spirochætes in the gut of infected ticks divide by a process
of multiple transverse fission into granules, which are composed
of chromatin (fig. 54). These granules--sometimes known as coccoid
bodies--are capable of multiplication. Leishman first found them in
clumps inside the cells of the Malpighian tubules (_cf._ fig. 55).

To summarize, when spirochætes are ingested by a tick, some of them
pass through the gut-wall into the hæmocœlic (body) fluid. They then
bore their way into the cells of various organs (fig. 55_a_) and break
up into coccoid bodies. In this manner the granules find their way
into the ovaries and ova, thus explaining how the young ticks are born
infected. Inoculation of these chromatinic granules usually produces
infection. Infective granules are also seen in the rudiments of the
Malpighian tubules of embryo ticks. Bosanquet and Fantham (1911),
independently, have shown that molluscan spirochætes also break up
into similar granules or coccoid bodies. Gross has also demonstrated
multiple transverse fission in molluscan forms. Marchoux and Couvy
(1913) and Wolbach (1914) consider the granules or coccoid bodies to be
degeneration products. This is unlikely (see below).

Schuberg and Manteufel have found that certain _O. moubata_, perhaps
30 per cent. of the specimens of a given neighbourhood, may acquire a
natural active immunity against infection with _S. duttoni_.

_S. duttoni_, or a closely allied form (by some termed _S. novyi_),
occurs in Colombia, and is spread by the tick _Ornithodorus turicata_.
In Panama a similar spirochæte is probably spread by _O. talaje_.

*Spirochæta gallinarum*, Stephens and Christophers, 1905 (= *Spirochæta
marchouxi*, Nuttall, 1905).

This Spirochæte, which occurs in fowls and is pathogenic, is
transmitted by the tick _Argas persicus_. It is about 10 µ to 20 µ
long. There is a pathogenic spirochæte known to occur in geese, named
by Sakharoff (1891) _S. anserina_, and found in Caucasia. This may be
the same as _S. gallinarum_, in which case the name _S. anserina_ will
have priority. These organisms cause fever, diarrhœa, anæmia and death.
The life history of the avian pathogenic spirochætes has been studied
by Balfour, by Hindle[150] and by Fantham.[151] It is essentially
similar to that of _S. duttoni_.

[150] _Parasitology_, iv, p. 463.

[151] _Annals Trop. Med. and Parasitol._ (1911), v, p. 479.

Marchoux and Couvy[152] (1913) consider that the “fragmentation of
the chromatin” in spirochætes is a process of degeneration. Working
with _A. persicus_ and _S. gallinarum_, they state that a large number
of the spirochætes ingested by the Argas almost immediately pass
through the wall of the alimentary canal and appear in the hæmocœlic
fluid. Marchoux and Couvy consider that Leishman’s granules may be
found in the Malpighian tubules of various Arachnids. They found
spirochætes in the cephalic glands of infected Argas. They consider
that spirochætes remain as wavy spirochætes within the tick, if they
are to be infective, though the spirochætes may become so thin as to
be invisible! The latter argument is obviously weak, and it was never
asserted that all granules in the Malpighian tubules of infected ticks
were derived from spirochætes. With dark-ground illumination small,
refractile spirochætal granules may be seen to grow into spirochætes.
The granule phase of spirochætes has recently been discussed by
Fantham[153] (1914).

[152] _Annales Inst. Pasteur_, xxvii, pp. 450, 620.

[153] _Annals Trop. Med. and Parasitol._, viii, p. 471.

*Spirochæta recurrentis*, Lebert, 1874.

  Syn.: _Spirochæta obermeieri_, Cohn, 1875.

This organism was discovered by Obermeier (1873) in cases of relapsing
fever in Berlin. Short forms 7 µ to 9 µ long, and longer (probably
adult) forms, 16 µ to 19 µ, are found in the blood. The width is
0·25 µ. Parasites 12 µ or 13 µ long are often observed.

The spirochæte is found in the blood during febrile attacks and
relapses, but not during intervening periods. It can be inoculated
into monkeys, rats and mice. It can live in the bed-bug, _Cimex
lectularius_, and Nuttall has succeeded in transmitting _S.
recurrentis_ from mouse to mouse by the bites of the same bug. The
French investigators Sergent and Foley (1908–9) in Algeria, and
Nicolle, Blaizot and Conseil (1912) in Tunis, have shown experimentally
that _S. recurrentis_ (var. _berbera_) is transmitted by lice. The
latter workers also demonstrated the method of infection that commonly
occurs, namely, by the scratching of the skin and crushing of lice
containing spirochætes on the excoriated surface of the body.

  Lice as transmitting agents for relapsing fever were indicated
  by Mackie[154] in 1907. An epidemic among Indian school children
  furnished the materials.[155] It was noted that out of 170 boys, 137
  were infected, and the boys were very verminous. Among the girls, 35
  out of 114 suffered, and few lice were found on them. Twenty-four
  per cent. of the lice taken from the boys contained spirochætes as
  compared with 3 per cent. of those from the girls. As the epidemic
  died out among the boys, the lice also became fewer, and an increase
  in the number of cases among the girls coincided with an increase in
  the number of lice. Spirochætes were found in the gut, Malpighian
  tubules and genital organs of the lice. Mackie thought that infection
  of the patients was brought about by the regurgitation of the
  spirochætes when the lice fed, but proof of this was lacking.

[154] _Brit. Med. Journ._, Dec. 14, 1907, p. 1706.

[155] See also Nuttall, Herter Lecture on Spirochætosis,
_Parasitology_, v, p. 269.

In 1912, Nicolle, Blaizot and Conseil,[156] working in Tunis and using
chiefly an Algerian strain of relapsing fever spirochætes (sometimes
called _S. berbera_), showed by direct experiments that infection by
means of the bites of _Pediculus vestimenti_ and _P. capitis_ was
untenable. As many as 4,707 infected lice were fed on one man, and
6,515 on another occasion were allowed to bite a man after they had
fed on a monkey heavily infected with spirochætes, yet no infection of
the man followed. Examination of the lice showed that the spirochætes
left the gut soon after they were ingested, and passed into the body
cavity, which swarmed with spirochætes. The contents of the alimentary
tract and the fæces of the lice alike were uninfective. The spirochætes
did not reappear in the gut till eight days after an infective feed,
but some persisted as late as the nineteenth day when kept at 28° C.

[156] _C.R. Acad. Sci._, cliv, p. 1636; clv, p. 481.

It was noted that the irritation due to the lice caused scratching,
and that thereby lice became crushed on to the skin. An emulsion was
made of two infected lice and rubbed on to the slightly excoriated
skin of one of the above workers. Infection followed five days later.
A drop of emulsion placed on the conjunctiva of the human eye produced
spirochætosis after an incubation of seven days. The body contents of
such lice, then, produce infection when they reach the blood by any
excoriated or penetrable surface. The stages leading up to infection
in nature briefly are: The irritation due to the louse bites causes
scratching, and the lice are crushed on to the skin. The slight
abrasion is quite sufficient to permit the entry of the parasite. The
louse bite alone is harmless. Infection by way of the eye is quite
probable in Africa, remembering the constant trouble due to sand, dust,
insects, etc., resulting in frequent touching of the eyes.

The spirochætes occur in the body fluid of the lice and can pass in
it to the adjacent organs. Thus they probably find their way into
the genital organs, and into the eggs of the lice. Eggs laid twenty
to thirty days after the parent became infected have retained the
infection, and the larvæ issuing from such eggs must have contained
some form of spirochætes, for an emulsion of either the eggs or the
larvæ produced spirochætosis when inoculated into monkeys. Further
details regarding the spirochætosis in the eggs of the lice and
in the larvæ are needed. Hereditary infection, however, has been
demonstrated, but is not very common. Sergent and Foley (1914) state
that the spirochæte possesses a very small and virulent form which it
assumes during apyrexial periods in man and during a period following
an infecting meal in the louse. Nicolle and Blanc (1914) find that
the organisms are infective in the louse just before they reappear
as spirochætes. Nicolle and Blaizot found that female lice were more
susceptible to spirochætes than males, four times as many females as
males being infected.

  Tictin (1897) found _S. recurrentis_ in bugs recently fed on
  patients, and infected a monkey with the fluids of crushed bugs.
  Karlinski (1902) found the spirochætes in bed-bugs in infected
  houses. There is some other evidence to show that bugs may transmit
  the spirochæte in Nature. Further researches are needed regarding the
  relationship of bed-bugs and human spirochætosis.

Multiplication of _S. recurrentis_ is by longitudinal and transverse
division (including so-called “incurvation”), and the organism forms
small, ovoid bodies (“coccoid” bodies) in the same way as _S. duttoni_.

_S. recurrentis_ is the cause of European relapsing fever, and a number
of possible varieties of it are associated with relapsing fevers in
other parts of the world. Such spirochætes only differ by biological
reactions, such as acquired immunity tests. They include:--

_S. rossii_, the agent of East African relapsing fever; _S. novyi_, the
agent of North American relapsing fever; _S. carteri_, the agent of
Indian relapsing fever; _S. berbera_, the agent of North African and
Egyptian relapsing fever.


_S. schaudinni._ This organism, according to Prowazek, is the agent of
ulcus tropicum. It varies in length from 10 µ to 20 µ.

_S. aboriginalis_ has been found in cases of granuloma inguinale in
British New Guinea and Western Australia. It also occurs in dogs, and
may not be truly parasitic.

_S. vincenti._ This spirochæte is 12 µ to 25 µ in length, tapers
at both ends and has few coils. It has been associated with angina
vincenti. It often occurs in company with fusiform bacilli.

_S. bronchialis_, found by Castellani in 1907 in cases of bronchitis in
Ceylon. The parasites are delicate, but show morphological variation.
This organism is important and has since been found in the West Indies,
India, Philippine Islands and various parts of Africa, such as the
Anglo-Egyptian Sudan, Uganda and West Africa. It has recently been the
subject of research by Chalmers and O’Farrell, Taylor, and Fantham.

_S. phagedenis_ was found by Noguchi in a ten days old ulcerated
swelling of the labium. The organism shows much variation in size,
being 4 µ to 30 µ in length.

_S. refringens_ (Schaudinn, 1905) occurs in association with _Treponema
pallidum_ in syphilitic lesions, but is non-pathogenic. It is 20 µ to
35 µ long and 0·5 µ to 0·75 µ broad, being larger than _T. pallidum_
and more easily stained.

Various spirochætes have also been notified in vomits, chiefly in
Australia; others from the human intestinal tract, _e.g._, _S.
eurygyrata_; _S. stenogyrata_ (Werner); _S. hachaizæ_ (Kowalski), in
cholera motions; _S. buccalis_ (Cohn, 1875) and _S. dentium_ occurring
in the human mouth and in carious teeth (_S. dentium_, Koch, 1877,
being the smaller); _S. acuminata_ and _S. obtusa_ found by Castellani
in open sores in cases of yaws.

Animal spirochætes of economic importance include:--

_S. anserina_, highly pathogenic to geese.

_S. gallinarum_ (= _S. marchouxi_) in fowls. (See p. 119.)

_S. theileri_ in cattle and _S. ovina_ in sheep also occur in Africa;
their pathogenicity is not clear.

_S. laverani_ (= _S. muris_), occurring in the blood of and pathogenic
to mice, is probably the smallest spirochæte from the blood, being only
3 µ to 6 µ long.

Numerous spirochætes have been recorded from the guts of various
mammals, birds, fishes, amphibia and insects.

CULTIVATION OF SPIROCHÆTES.--Cultures of spirochætes have been made
with little success or with great difficulty until comparatively
recently, when Noguchi (1912) devised a means whereby he has cultivated
most of the pathogenic spirochætes as well as some Treponemata.

Noguchi has now cultivated _S. duttoni_, _S. recurrentis_, _S. rossii_,
_S. novyi_ and _S. gallinarum_ from the blood; _S. phagedenis_[157]
from human phagedænic lesions; _S. refringens_[158] and spirochætes
from the teeth.

[157] _Journ. Exptl. Med._, xvi, p. 261.

[158] _Journ. Exptl. Med._, xv, p. 466.

His method is as follows:--

A piece of fresh, sterile tissue, usually rabbit kidney, is placed in
a sterile test-tube. A few drops of citrated blood from the heart of
an infected animal, _e.g._, rat or mouse, is added, and about 15 c.c.
of sterile ascitic or hydrocœle fluid is poured quickly into the tube.
Some of the tubes are covered with a layer of sterile paraffin oil,
others are left uncovered. The tubes are incubated at 37° C. The best
results are obtained if the blood is taken from an animal forty-eight
to seventy-two hours after it has been inoculated, that is, before
the spirochætes reach their maximum multiplicative period in the
blood. The presence of some oxygen seems indispensable for these blood
spirochætes, and they fail to develop _in vacuo_ or in an atmosphere of

For subcultures, 0·5 c.c. of a culture is added to the medium instead
of citrated blood, and it is useful to add a little fresh, normal
blood, either human or from an animal, such as a rat.

Noguchi found that the events in cultures were:--

_S. duttoni_,[159] maximum multiplication on the eighth to ninth day;
disintegration beginning on the tenth day, spirochætes disappeared
after about the fifteenth day. No diminution of virulence was found at
the ninth day.

[159] _Journ. Exptl. Med._, xvi, p. 202.

_S. rossii_ (= _S. kochi_).[160] Maximum development on the ninth day,
after which the virulence diminishes. The incubation period is also

[160] _Ibid._, p. 205.

_S. recurrentis_[161] (= _S. obermeieri_). Maximum growth on the
seventh day.

[161] _Ibid._, p. 205.

_S. novyi._[162]--Maximum development on the seventh day. It is more
difficult to grow than the preceding forms.

[162] _Ibid._, p. 208.

All the above spirochætes showed undoubted longitudinal division and
transverse division was observed in part.

_S. gallinarum_[163] can be cultivated as above, but transverse
division was usual here. Maximum growth occurred in the culture about
the fifth day.

[163] _Ibid._, p. 620.


The genus _Treponema_ (Schaudinn, 1905), includes minute, thread-like
organisms, with spirally coiled bodies, the spirals being preformed
or fixed. No membrane or crista is present, according to Schaudinn,
though a slight one is said by Blanchard to be present in the
organism of yaws. The ends of the organisms are tapering and pointed.
Multiplication is by longitudinal and transverse division. The most
important members of the genus are _T. pallidum_, the agent of
syphilis, and _T. pertenue_, which is responsible for frambœsia or yaws.

*Treponema pallidum*, Schaudinn, 1905.

  Syn.: _Spirochæta pallida_.

_Treponema pallidum_ was first described by Schaudinn and Hoffmann
in 1905 under the name of _Spirochæta pallida_. It has also been
described under the names of _Spironema pallida_, _Microspironema
pallida_ and _Trypanosoma luis_. Siegel in 1905 described an organism
which he called _Cytorhyctes luis_ and considered to be the agent
of syphilis. Schaudinn reinvestigated Siegel’s work and found _T.
pallidum_, which he considered to be the causal agent of the disease,
and pronounced against _Cytorhyctes luis_. It is probable now that
both workers were correct, for Balfour (1911) has seen the emission
of minute granules or “coccoid” bodies from _T. pallidum_ and these
granules probably correspond to the _C. luis_ of Siegel. Recently E. H.
Ross, having observed a spirochæte stage in the development of Kurloff
bodies, thinks that _T. pallidum_ is a stage in the life-history of a
Lymphocytozoon. MacDonagh has also described a complicated and somewhat
similar cycle, but these observations require further study and

[Illustration: FIG. 56.--_Treponema pallidum_. (After Bell, from
Castellani and Chalmers.)]

_T. pallidum_ varies from 4 µ to 10 µ in length, its average length
being 7 µ, while its width is usually about 0·25 µ. Longer individuals
of 16 µ to 20 µ have been recorded. The body has from eight to ten
spiral turns and forms a tapering process at each end (fig. 56). The
organism is most difficult to stain, and its internal structure is
little known. It is possibly like that of _Spirochæta duttoni_ or _S.
balbianii_, as the “granule shedding” observed by Balfour is strongly
suggestive of the formation of resistant bodies by those spirochætes.
Hoffmann (1912) has seen the formation of spores in _T. pallidum_.

The Treponemata occur in the primary and secondary sores, but are
difficult to find in the tertiary eruptions of syphilis. Noguchi and
Moore (1913) and Mott[164] (1913) have demonstrated _T. pallidum_
in the brain in cases of general paralysis of the insane. Marie and
Levaditi (1914), however, consider that the treponeme found in the
brain in such cases is different from _T. pallidum_.

[164] _Brit. Med. Journ._, Nov. 15, 1913. p. 1, 271.

CULTIVATION _of T. pallidum_.--This has been accomplished successfully
by Noguchi,[165] using a modification of his method for spirochæte
cultivation, for _T. pallidum_ is much more difficult to grow than
spirochætes, being a strict anaerobe.

[165] _Journ. Exptl. Med._, xv, p. 90; xvi, p. 211.

[Illustration: FIG. 57.--Diagram of apparatus for cultivation of
_Treponema pallidum_ by Noguchi’s method. (After Noguchi.)]

The apparatus consists of two glass tubes, the upper being connected to
the lower by a narrower tube passing through a rubber cork (fig. 57).
Both tubes are carefully sterilized.

A piece of fresh, sterile rabbit’s kidney is placed in the lower tube,
which is filled with ascitic fluid, or ascitic fluid and bouillon
mixture. The tube is inoculated with syphilitic material and corked
by inserting the upper tube. In the bottom of the upper tube a piece
of sterile rabbit’s kidney is placed and syphilitic material poured
over it. A mixture of one part ascitic fluid and two parts of slightly
alkaline agar is then poured over the tissue and allowed to solidify.
When solid, a layer of sterile paraffin oil is poured on top of it,
and the top plugged with cotton wool (fig. 57). The whole is then
incubated at 37° C. for two or three weeks. The tissue removes traces
of oxygen from the lower levels of the medium and also probably
provides a special form of nourishment. At first _T. pallidum_ grows in
the solid medium, and then when the cultural conditions in the lower
fluid portion become favourable, the organisms migrate thither and
multiply abundantly. At first the culture is impure, but after several
transferences a pure culture is obtained readily.

The syphilitic material for culture is prepared by cutting off pieces
of tissue from the lesions, washing in sterile salt solution containing
1 per cent. sodium citrate, and then emulsifying the tissue in a mortar
with sodium citrate.

Good cultures show rapid multiplication, which is invariably by
longitudinal division.

In his various cultivation experiments Noguchi[166] found morphological
and pathogenic variations in _T. pallidum_. Three forms of the organism
were found, namely, thicker, average and thinner types. The lesions
caused in the testicle of the rabbit differ according to the variety
inoculated, but more work is necessary on the subject.

[166] _Journ. Exptl. Med._, xv, p. 201.

Noguchi[167] has cultivated a separate organism, _T. calligyrum_, from
the surface of human genital or anal lesions, either syphilitic or
non-syphilitic. It is apparently non-pathogenic, and is 6 µ to 14 µ

[167] _Journ. Exptl. Med._, xvii, p. 89.

Hata (1913)[168] has modified the Noguchi technique for the cultivation
of spirochætes and treponemes, with a view to simplification and
convenience. Hata substitutes normal horse serum for ascitic fluid
and the “buffy coat” of the clot of horse blood in place of the small
pieces of rabbit’s kidney. It is unnecessary to place sterile paraffin
on the surface of the medium.

[168] _Centralbl. f. Bakt._, Orig., lxxii, p. 107.

The horse serum is mixed with twice its volume of physiological
saline solution. The mixture is placed in tubes which are heated on
a water-bath at 58° C., the temperature being raised gradually until
it reaches 70° or 71° C. in three hours. The tubes are then heated at
71° C. for half an hour. After cooling, the contents will consist of
an opaque semi-coagulated mass. This semi-coagulated serum and saline
mixture may be substituted for Noguchi’s ascitic fluid.

The buff coagulum is cut into small pieces, about 1 c.c. in volume.
They must be forced with a sterile glass rod to the bottom of the
semi-coagulated serum and saline mixture. The medium is inoculated with
a small quantity of infected blood and kept at 37° C. In the case of
_S. recurrentis_, growth of spirochætes is observed on the second day,
reaching a maximum in five to seven days. The growth of the organisms
proceeds rather more slowly, they live for a longer period and maintain
their virulence better than in Noguchi’s medium.

*Treponema pertenue*, Castellani, 1905.

  Syn.: _Spirochæta pertenuis_; _S. pallidula_, Castellani, 1905.

Castellani discovered the organism in 1905, in scrapings of yaws
pustules. He first described it under the name of _Spirochæta

[Illustration: FIG. 58.--_Treponema pertenue_. (After Castellani and

_Treponema pertenue_ (fig. 58), though delicate and slender, shows
great morphological variation both in length and thickness. It may be
short, _e.g._, 7 µ, but can attain 18 µ to 20 µ in length and may be
even larger. In cultures made by Noguchi, thick, medium and thin forms
were found, each giving rise to a different type of frambœsial lesion
when inoculated into the testicles of rabbits, thus suggesting the
possibility of the occurrence of varieties of _T. pertenue_.

The organism is difficult to stain, but occasionally deeper staining
granules are found along its body. They may represent a diffuse
nucleus. Granule formation similar to that of _T. pallidum_ has been
observed by Ranken, using dark-ground illumination.

Many experiments have been made with a view to establishing the
identity of the organism of yaws and also of differentiating between
the causative agents of yaws and syphilis. Both monkeys and the human
subject have been experimentally inoculated with yaws material and have
developed the disease.

In an early experiment, negroes were inoculated with the secretion
from lesions of yaws. All of them developed the disease, nodules
appearing, chiefly at the seat of inoculation, in from twelve to twenty
days, followed by the usual eruption. Similar results were obtained
with thirty-two Chinese prisoners, who were inoculated with yaws,
twenty-eight becoming infected.

A naturally infected yaws patient when inoculated with syphilis,
contracted that infection, thus showing that yaws does not confer
immunity to syphilis. This has also been observed naturally, when yaws
patients have contracted syphilis.

Experiments with monkeys have been successfully performed. The
incubation period varies from sixteen to ninety-two days. Lesions
appear first at the seat of inoculation, and in some monkeys the
eruption is localized to this spot, though the infection is general,
_T. pertenue_ occurring in the spleen, lymphatics, etc. Monkeys
inoculated with splenic blood of a yaws patient, and also sometimes
with blood from the general circulation, have become infected.

Castellani and others have shown that monkeys successfully inoculated
with syphilis do not become immune to yaws, and vice-versâ.

Craig and Ashburn, using the monkey _Cynomolgus philippinensis_, found
these animals susceptible to yaws but not to syphilis.

The ulcerated lesions of frambœsia are rapidly invaded by numerous
bacteria as well as by different spirochætes, of which Castellani has
described three distinct species. One is identical with _Spirochæta
refringens_, Schaudinn, the other two are thin and delicate. One, _S.
obtusa_, has blunt ends; the other _S. acuminata_, has pointed ends.
_T. pertenue_ is also present.

The reasons for considering _T. pertenue_ to be the specific cause of
frambœsia are:--

(1) _T. pertenue_ is the only organism present in non-ulcerated
papules, in the spleen and in the lymphatics of yaws patients, or of
monkeys artificially infected with the disease. By no method has any
other organism been obtained.

(2) Extract of frambœsia material, free from all organisms other than
_T. pertenue_, reproduces the disease if inoculated.

(3) Extract of frambœsia material deprived by filtration of _T.
pertenue_ is no longer infective on inoculation.

The method of infection is contaminative, by direct contact. Women
in Ceylon are frequently infected by their children. Any slight skin
abrasion is sufficient to admit the parasite. In some cases, insects
may carry the disease from person to person, and even in hospitals,
when dressings are removed, it has been noticed that flies greedily
suck the secretion from the ulcers. _T. pertenue_ has been recovered
from flies that have fed on yaws, and monkeys have contracted the
disease when flies were placed and retained on them for a short time,
after the insects had fed on yaws material.

CULTIVATION.--_T. pertenue_ has been cultivated by Noguchi, who finds
three types of parasites in his cultures, as before mentioned. Its
multiplication is by longitudinal division.

Noguchi[169] (1912), has cultivated species of Treponema from the human
mouth, e.g., _T. macrodentium_, _T. microdentium_ and _T. mucosum_, the
latter from pyorrhea alveolaris. These parasites in the past may have
been confused under the name _Spirochæta dentium_.

[169] _Journ. Exptl. Med._, xv, p. 81; xvi, p. 194.

Class III. *SPOROZOA*, Leuckart, 1879.

The third group of the Protozoa consists entirely of parasitic
organisms forming the class known as the Sporozoa or spore-producing
animals. The members of this class are characterized by possessing
very great powers of multiplication, coupled with a capacity for
producing forms that serve for the transference of the organisms
to other hosts. These reproductive bodies, whether for increase of
numbers within one host or for transmission to another host, are called
spores. But, strictly, the term spore should be used only in the latter
connection, when a protective or resistant coat known as a sporocyst
envelops the body of the spore.

The Sporozoa are widely distributed, occurring in various tissues and
organs of Annelids, Molluscs, Arthropods, and Vertebrates. Their food,
which is fluid, is absorbed osmotically. The life-cycle of a Sporozoön
may be completed within one host or may be distributed between two
different hosts.

The Sporozoa were divided by Schaudinn into two groups or sub-classes,
called (1) the *Telosporidia*, and (2) the *Neosporidia*.

The Telosporidia are Sporozoa in which the reproductive phase of the
parasites is distinct from the growing or trophic phase, and follows
after it. The Neosporidia include Sporozoa in which growth and
spore-formation go on simultaneously. This classification is not final,
for certain exceptions and difficulties are already known with regard
to it. It is possible that the class Sporozoa is not a natural entity,
but should be replaced by two classes of equal rank, corresponding in
most respects with the Telosporidia and Neosporidia.

The *Telosporidia* comprise the *Gregarinida*, the *Coccidiidea*, and
the *Hæmosporidia*. Doflein combines the two latter orders into one
known as the *Coccidiomorpha*.

The *Neosporidia* comprise the *Myxosporidia*, the *Microsporidia*, the
*Actinomyxidia*, the *Sarcosporidia*, and the *Haplosporidia*. Doflein
combines the first three orders into one, the *Cnidosporidia*.

Sub-Class. TELOSPORIDIA, Schaudinn.

Sporozoa in which the reproductive phases follow completion of growth.

Order. *Gregarinida*, Aimé Schneider emend. Doflein.

  Knowledge of the Gregarinida probably goes back as far as the year
  1684, when Redi observed gregarines in the crab, _Cancer pagurus_.
  Von Cavolini (1787) found them in _Cancer depressus_. The name
  _Gregarina_ was created by L. Dufour (1828), who observed masses
  of these organisms in the gut of insects of different orders.
  Hammerschmidt (1838) and von Siebold found rich infestations in
  insects, while Dujardin (1835) and Henle described various genera
  from segmented worms. Henle (1835) also observed cysts containing
  “navicellæ” in the sperm-sacs of segmented worms, and attention was
  drawn to his researches by the discovery by von Siebold (1839) of
  “pseudonavicellæ” in the gut of _Sciara nitidicollis_. Up to this
  time many workers considered the gregarines to be worms, but Kölliker
  (1845) investigated many of them and maintained their unicellular
  nature, while Stein’s work (1848) showed the interrelation of the
  pseudonavicellæ and the gregarines. The discovery of amœboid germs
  in the pseudonavicellæ by Lieberkühn (1855) and the demonstration of
  myonemes further aided in the elucidation of their true systematic
  position. The entire process of conjugation, of which Dufour had seen
  one phase, was followed by Giard under the microscope.

  From 1873 onwards Aimé Schneider made important additions to the
  knowledge of the morphology, life-history, and systematic position
  of numerous gregarines. Bütschli (1881) and L. Léger (1892) also
  contributed much work on the subject. The discoveries of Schaudinn
  with regard to the life-cycle of Coccidia gave a fresh stimulus to
  the study of the Gregarines, whereby the life-cycles of numerous
  forms and the phases thereof have been elucidated.

  Asexual multiplication is not common among the Gregarines, but is
  known to occur in the sub-order Schizogregarinea, formerly known as
  the Amœbosporidia.

  Although the Gregarinida are not known to be parasitic in man or
  other vertebrates, they are of great interest, inasmuch as they are
  among the earliest known Sporozoa, and therefore will be briefly
  described here.

[Illustration: FIG. 59.--_Monocystis agilis_ from seminal vesicles of
_Lumbricus_ × 250. (After Stein.)]

[Illustration: FIG. 60.--_Gregarina longa_ from larva of crane-fly
(_Tipula_). _a_, in epithelial cell of host; _b_, _c_, gradually
leaving host-cell; _d_, adhering to host-cell; _e_, fully developed
free trophozoite.]

The Gregarines are usually elongate, somewhat flattened organisms
(figs. 59, 60), whose bodies are enclosed in an elastic and often
thick cuticle. The enclosed living substance shows a separation into
ectoplasm and endoplasm, as is common among Protozoa. The cuticle is
sometimes regarded as the outer portion or epicyte of the ectoplasm.
A single, vesicular, spherical, or elliptical, large nucleus, with
its chromatin concentrated to form a spherical karyosome, is present.
The body of some gregarines may be divided by ingrowing ectoplasmic
partitions or septa, and are then said to be “septate” or “polycystid”
(fig. 61). Other gregarines remain simple and non-septate, and are
termed “monocystid” (fig. 59). The monocystid gregarines occur
especially in the body cavity of Chætopoda and Insecta, more rarely
in Echinodermata, in the parenchyma of Platyhelminthes, also in the
gut of Tunicata and Insecta (fig. 60) and in the seminal vesicles
of Annelida. In the polycystid gregarines a single septum only is
present as a rule, and thus the body presents two portions: (1) an
anterior portion termed the protomerite; (2) a posterior, larger
portion, known as the deutomerite, which generally contains the
nucleus. The protomerite is often modified anteriorly to form an organ
of attachment, termed the epimerite (fig. 61), which is developed
from the pointed rostrum of the sporozoite or primary infecting young
gregarine. The structure of the epimerite may be complicated, being
provided with hooks, spines, knobs, and other appendages. An extension
of the polycystid condition is seen in _Tæniocystis mira_ Léger (from
the dipteran larva, _Ceratopogon solstitialis_), whose body shows a
number of partitions, giving the organism a superficial resemblance to
a tapeworm.

[Illustration: FIG. 61.--_Xyphorhynchus firmus_ with epimerite in
intestinal epithelial cell of host. (After Léger.)]

The ectoplasm of a gregarine exhibits three layers: (1) An epicyte
(cuticle) externally of which the epimerite is composed; (2) a
sarcocyte which forms the septa if present; (3) the deeper myocyte
layer containing contractile elements in the form of fibrils or threads
termed myonemes (fig. 62).

[Illustration: FIG. 62.--_Gregarina munieri_ (from the beetle,
_Chrysomela hæmoptera_). Section through surface layers. _Cu_, cuticle;
_E_, ectoplasm proper; _G_, gelatinous layer; _My_, myonemes in myocyte
layer. × 1500. (After Schewiakoff.)]

The endoplasm is fluid and granular, containing many enclosures,
which are of the nature of reserve food materials. They consist of
fat droplets or of paraglycogen, and give the organisms an opaque
appearance. _Lithocystis_ contains crystals of calcium oxalate in its

Many gregarines are capable of active movements, though they do not
possess obvious locomotor organs. The movement is of a smooth, gliding
character and two suggestions have been put forward to explain it.
According to Schewiakoff, a gelatinous substance is secreted between
the layers of the ectoplasm. This is extruded posteriorly and thus the
animal is pushed forward. On the other hand, Crawley considers that
the movements are produced by contractions of the myonemes. These two
explanations are probably correct as far as each goes, and are to be
regarded as supplementary to one another.

[Illustration: FIG. 63.--_Monocystis agilis_. Spores from vesicula
seminalis of the Earthworm. _a_, Sporoblast with single nucleus,
enclosed in sporocyst; _b_, mature spore containing sporozoites; _c_,
diagrammatic cross-section of spore, showing eight sporozoites round
residual protoplasm. (After Bütschli.)]

Occasionally, temporary associations of gregarines are formed by
a number of individuals adhering to one another end to end. Such
temporary associations are examples of syzygy. Such syzygies must not
be confused with true associations which form an essential part of the

The life-cycle of a relatively simple gregarine, such as _Monocystis
agilis_ (fig. 59), parasitic in earthworms, may now be considered.
The gregarines, being members of the Sporozoa, produce spores at one
phase of the life-cycle. Each gregarine spore (fig. 63) develops
within itself a number of minute, sickle-shaped or vermicular bodies,
known as sporozoites or primary infecting germs. Eight sporozoites are
often formed within each spore. When absorbed by a new host, the spore
softens and the sporozoites issue from it. They are capable of active
movement and may or may not enter a cell, such as one of those of the
digestive tract, or, as in _Monocystis_, a cell lining the vesicula
seminalis which becomes a sperm-cell aggregate (sperm morula). When the
sporozoite has reached the place of its choice in the host it ceases
active movements and proceeds to feed passively on the fluid substances
around it, whether they be those of tissues or body fluids. This
passive, growing and feeding form is known as the trophozoite. After a
trophic existence of longer or shorter duration, the trophozoite ceases
to feed and prepares for reproduction. Two trophozoites associate
together, each of them first becoming somewhat rounded. The two
trophozoites, now known as sporonts or gametocytes, become invested
in a single common envelope or cyst (fig. 64, _a_). The nucleus of
each gametocyte then divides by a series of binary fissions (fig. 64,
_b_), and the daughter nuclei thus produced arrange themselves at the
periphery of the parent cells (fig. 64, _c_). Cytoplasm collects around
each of these nuclei, and thus a number of gametes are formed within
each gametocyte. The gametes for a time exhibit active movements, and
ultimately ripe gametes of different parentage fuse in pairs, that is,
conjugation occurs (fig. 64, _d_). In this way zygotes are produced,
the nucleus of each zygote being formed by the fusion of two gamete

[Illustration: FIG. 64.--Schematic figures of conjugation and spore
formation in Gregarines. For details see text. (After Calkins and
Siedlecki, modified.)]

[Illustration: FIG. 65.--_Stylorhynchus oblongatus_. _a_, cyst
containing two sporonts or gametocytes, each full of gametes, those in
the upper one being male. _b_, ripe male and female gametes. × 1,600.
(After L. Léger.)]

The zygote grows slightly and becomes oval or elongate, and at this
period is often called the sporoblast. It then secretes an external
membrane, the sporocyst. Nuclear division occurs inside the sporocyst
by a series of three binary fissions (fig. 64, _e_), so that each
sporocyst, now usually referred to as a spore, contains eight nuclei.
The cytoplasm collects around each nucleus and eight vermicular
sporozoites are produced within each spore (fig. 64, _f_), thus
completing the life-cycle.

It will be noticed that in the above life-cycle no asexual
multiplication occurs. These organisms, such as _Monocystis_, are known
as the Eugregarines, and include the majority of the gregarines. The
remainder, which have introduced schizogony into their life-cycle, are
known as the Schizogregarines.

[Illustration: FIG. 66.--Spores of various Gregarines. _a_,
_Xiphorhynchus_. _b_, _Ancyrophora_. _c_, _Gonospora_. _d_,
_Ceratospora_. (After Léger.)]

There are variations in the morphology and life-cycle of gregarines
besides those that have been mentioned. It is not within the scope of
this book to discuss them in detail, but the following may be noted:--

Morphological differentiation of gametes may occur as in _Stylorhynchus
oblongatus_ (fig. 65), which differentiation is probably of a sexual

The sporocyst really consists of two layers, an epispore and an
endospore. Externally the spores of different gregarines show great
variety in shape and markings, and spines, or long processes may be
present (fig. 66).

The resistant spores serve for the transmission of the gregarines
from host to host. The mode of infection is contaminative, the spores
expelled with the dejecta of one host being absorbed with the food of a
new host.

The Gregarinida may be classified as follows:--

Sub-order I.--*Eugregarinea*, without schizogony.

Tribe 1.--_Acephalina_.--Without an epimerite and non-septate; often
“cœlomic” (body-cavity) parasites. _E.g._: _Monocystis_, with several
species parasitic in the seminal vesicles of earthworms. Many other
genera parasitic in Echinodermata, Tunicata, Arthropoda, etc.

Tribe 2.--_Cephalina_.--With an epimerite, either temporarily
or permanently, in the trophic phase. Usually septate (except
_Doliocystidæ_). Many families, genera and species. Common in the
digestive tracts of insects. _E.g._: _Gregarina_, with several
species, _Gregarina ovata_ in the earwig, _Gregarina blattarum_ in the
cockroach, _Stylorhynchus_ in beetles, _Pterocephalus_ in centipedes,

Sub-order II.--*Schizogregarinea*, with schizogony.

Tribe 1.--_Endoschiza_.[170]--With schizogony occurring in the
intracellular phase, _e.g._, _Selenidium_ (from Annelida and Gephyrea),
_Merogregarina_ (from an Ascidian).

[170] See Fantham (1908), _Parasitology_, i, p. 369.

Tribe 2.--_Ectoschiza_.--In which the schizont is free, and schizogony
is extracellular, _e.g._, _Ophryocystis_ (from _Blaps_, a beetle), and
_Schizocystis_ (from _Ceratopogon_ larva).

  Order. *Coccidiidea*.

  Hake (1839) first saw the organisms now termed Coccidia during
  his investigations on the so-called coccidial nodules of rabbits.
  The opinions as to the nature of these peculiar formations were
  very diverse. The discoverer considered them to be a sort of pus
  corpuscle; Nasse (1843) took them for epithelial cells of the biliary
  passages, others for helminthes, especially the ova of trematodes
  (Dujardin, Küchenmeister, Gubler, etc). Remak (1845) was the first to
  draw attention to their relation to the Psorospermia (Myxosporidia),
  and this investigator found them also in the small intestine and
  vermiform appendix of rabbits. Lieberkühn (1854), who examined
  not only the coccidia of rabbits, but found similar forms in the
  kidneys of frogs, likewise called them definitely psorosperms. To
  differentiate Müller’s psorosperms, which are found in fishes, from
  those of rabbits, etc., the latter were called egg-shaped psorosperms
  (Eimer), until R. Leuckart (1879) named them _Coccidia_ and placed
  them in a group of the Sporozoa analogous to that of the Gregarinida,
  Myxosporidia, etc. Numerous works confirmed the occurrence of
  coccidia, not only in all classes of vertebrate animals, but also in
  invertebrates (Mollusca, Myriapoda, Annelida, etc.). A large number
  of genera and species have in the course of time been described
  which inhabit the epithelium of the intestine and its appendages for
  choice, but are also found in other organs (kidneys, spleen, ovaries,
  vas deferens, testicles). Some also live in the connective tissue of
  various organs, more particularly of the intestine.

  The knowledge of the development of the coccidia was of particular
  importance in determining their classification. By means of encysted
  coccidia from the liver of rabbits, Kauffmann (1847) first confirmed
  the fact that the cyst, which was partly or entirely filled with
  granular contents, divided into three or four pale bodies (fig. 71)
  after a long sojourn in water. Lieberkühn observed the same process
  in the host in the case of the coccidia of the kidney of the frog.
  Stieda (1865) studied more minutely the changes that occur within
  the encysted coccidia of the liver of rabbits after the death of
  the host. He discovered that the bodies now known as “spores” were
  oval formations pointed at one pole, and surrounded by a delicate
  membrane, which exhibited a certain thickness at the pointed
  extremity and enclosed a slightly bent rodlet, expanding at either
  end into a strongly light-refracting globule; a finely granular
  globule was present in the middle of the spore. Waldenburg (1862) saw
  the same phenomenon in coccidia from the epithelium of the villi and
  Lieberkühn’s glands of the intestine of the rabbit; but the process
  in this case took place in a much shorter time.

  According to the discovery of Kloss (1855), the spores of the
  coccidia of the urinary organ of the garden snail were formed in far
  greater numbers: the round spores also harboured several (five to
  six) rodlets, which after the bursting of the spore-envelope became
  free. Eimer’s researches (1870) afforded information regarding a
  Coccidium from the intestine of the mouse, which was transformed
  _in toto_ into a “spore,” containing small sickle-shaped bodies.
  The fact was, moreover, established that the little bodies left the
  delicate envelope when in the intestine, made movements of flexion
  and extension, and were finally transformed into amœboid organisms,
  which apparently penetrated the epithelial cells; at all events,
  similar bodies of various sizes were seen in these cells. Taking the
  immense number of these parasites into account and the lack of any
  other cause, Eimer attributed the sudden death of his mice to the
  _Gregarina falciformis_, as the parasite was then called, just in the
  same way as a few years previously Reincke ascribed the acute and
  fatal intestinal catarrh of rabbits to the invasion of intestinal

  All that had become known about coccidia up to 1879 was then
  compiled by Leuckart, and completed by his own observations on
  the coccidia of the liver of the rabbit. Experimental infections
  had already been conducted by Waldenburg (1862) with intestinal
  coccidia of rabbits, and by Rivolta (1869–73) with the coccidia of
  fowls, which experiments confirmed the importance of the spores,
  or bodies enclosed in them, in the transmission of the parasites
  to other animals. Accordingly, it was assumed that after the entry
  of the spores into the intestine the sporozoites were set free,
  actively penetrated into the intestinal cells, where they grew into
  coccidia, and finally became encysted. The further development,
  _i.e._, the formation of spores, took place outside the host’s body
  in these cases; in other cases (Kloss, Eimer) it took place within
  the host. Although much regarding the cycle of development was still
  hypothetical, the ideas coincided with the observations, and were
  therefore universally regarded as established. Further research
  confirmed this view in numerous new forms.

  L. Pfeiffer’s statements (1891) on the part that certain coccidia or
  their sporozoites played, or seemed to play, as causes of disease
  gave a renewed impetus to the investigation of the coccidia. The
  ingestion of even very numerous spores did not appear to account for
  the mass infection so frequently observed, even after Balbiani had
  confirmed the fact that there were two, and not one, sporozoites
  contained in every spore of the coccidia of rabbits (fig. 72). The
  hypothesis was therefore advanced that the sporozoites or young
  coccidia were able to divide once again by sporulating. The question
  was finally solved quite differently. R. Pfeiffer (1892) first
  confirmed the fact that in addition to the well-known method of
  sporulation in the coccidia of the rabbit that causes the infection
  of fresh hosts (“exogenous sporulation”), an enormous increase may
  follow in the already infected host in a manner that Eimer first
  observed in the coccidia of the intestine of the mouse (“endogenous
  sporulation”). It had hitherto been believed that some of the
  species of coccidia increased like the rabbit parasite, then known
  as _Coccidium oviforme_, and others like _Eimeria falciformis_, and
  this difference had been made the foundation of a classification. R.
  Pfeiffer was successful in observing the occurrence of both kinds
  of development in the same species, and expressed the opinion that
  endogenous sporulation (fig. 73), which takes place within the host,
  was the cause of the mass-infection that is mostly accompanied by
  serious consequences (fig. 74). L. Pfeiffer sought, especially, to
  demonstrate the correctness of this view as regards other species of
  coccidia and for this purpose he utilized the experiences already
  published. Coccidia were known to exist in a number of different
  hosts, and to propagate in some according to the _Coccidium_ type,
  in others according to the _Eimeria_ type. It therefore was reasoned
  that in this case it was not a question of two species belonging
  to different genera living side by side, with a different mode of
  development, but of one species, in the life of which both forms of
  development occurred alternately.

  This interpretation of facts was combated especially by A. Schneider
  (1892) and by Labbé, but has, nevertheless, proved true, apart from
  the circumstance that Schuberg succeeded in discovering the hitherto
  unknown _Coccidium_ form in the intestine of the mouse; and that,
  moreover, Léger confirmed the fact that there are no Arthropoda in
  which Eimeria are not found together with coccidia. The question
  was finally settled by experiments made by Léger with the coccidia
  of _Scolopendra cingulata_, by Schaudinn and Siedlecki with those
  of _Lithobius forficatus_, and by Simond with the coccidia of the
  rabbit. On Simond’s suggestion the sickle-shaped germs corresponding
  to the sporozoites, which are formed by endogenous sporulation, are
  generally termed merozoites; and in accordance with Schaudinn’s
  suggestion, those individuals which form merozoites are termed
  schizonts, and those which produce spores are called sporonts. In
  contradistinction to sporogony (exogenous sporulation), the term
  schizogony (endogenous sporulation) is used.

  The more minute examination of these processes at last led to the
  discovery of sexual dimorphism, of copulation and of alternation of
  generations in the coccidia. Schuberg was the first to consider the
  possibility of copulation in coccidia; in addition to the formations
  which now are termed merozoites, he observed very diminutive
  bodies (“microsporozoites”) in the coccidia of the intestine of
  the mouse, which were able eventually to copulate. Labbé confirmed
  this observation in some of the species, and Simond expressed
  the opinion that bodies termed “chromatozoites” occurred in all
  coccidia. Copulation itself was then observed by Schaudinn and
  Siedlecki (1897). The copulating bodies were termed gametes. As,
  however, they differed considerably one from the other, the males
  were called microgametes (_i.e._, the microsporozoites of Labbé and
  the chromatozoites of Simond) and the females macrogametes. After
  copulation was completed sporogony took place, and in the cycle of
  development of one species this regularly alternated with schizogony
  (asexual multiplication). Schaudinn in 1900 described in detail the
  life-cycle of _Eimeria_ (_Coccidium_) _schubergi_.

  The recognition of this unsuspected complicated process was bound to
  effect reforms in the classification of the coccidia; and all the
  forms that had been regarded as developmental stages (_Eimeria_,
  etc.) had to be reconsidered.

_Occurrence._--The Coccidiidea in their mature condition usually live
within the epithelial cells of various organs, and by choice inhabit
those of the intestine and of its associated organs. They also occur
frequently in the excretory organs of mammals, birds, amphibia,
molluscs, arthropods, and may also be found in the testes and vas
deferens, but the statement that they live in hen’s eggs, as well as
in the oviducts of fowls, has not been confirmed.[171] Some species
inhabit the nuclei of cells, others live in the connective tissue, but
their presence in the latter situation is probably only secondary,
that is, they have only reached it from the epithelium of the affected

[171] Notwithstanding the progress made during the last decades, the
ova of helminthes and more particularly of trematodes, have been
mistaken for Coccidia. Thus Poschinger (_Zool. Anz._, 1819, ix, p. 471)
and Gebhard (_Virchow’s Arch._, 1897, No. 147, p. 536) mistook the ova
of _Distoma turgidum_, Brds., for Coccidia. Podwyssotzki (_Centralbl.
f. allg. Path._, 1890, i, p. 135) made a similar error with the ova
(and vitelline sacs) of a species of _Prosthogonimus_ (_Distoma ovatum_
of the authors); von Willach (_Arch. f. wiss. u. prakt. Thierheilk._,
1892, xviii, p. 242) mistook the ova of a nematode for Coccidia.

The size of the Coccidiidea, corresponding as a rule to the capacity
of their habitat, is usually small, but there are said to be species
that attain a diameter of 1 mm. Their form[172] is globular, oval,
or elliptical. External appendages are lacking, at least during
the trophic or vegetative period of their life, which is spent in
epithelial cells, within which they increase in size. Frequently one
only is present in each cell, but more can occur. The body substance
is composed of a more or less finely granular or distinctly alveolar
protoplasm which exhibits no differentiation into ecto- and endoplasm.
All species possess a nucleus that enlarges with their growth;
sometimes it only shows through the cytoplasm as a lighter spot, or may
even be quite concealed. It is vesicular, and besides containing very
delicate threads of chromatin in the clear nucleoplasm, it contains
generally only one large karyosome.

[172] The life-cycle given here is based on that of _Eimeria_
(_Coccidium_) _schubergi_, after Schaudinn (1900). See “Untersuchungen
über den Generationswechsel bei Coccidien,” _Zool. Jahrb., Abt. f.
Anat._, xiii, pp. 197–292, 4 plates.

The infected epithelial cells degenerate sooner or later as the
parasite feeds on them (fig. 67, II-IV). After their form has been
changed by the action of the growing parasite, they finally perish.
The cell membrane then alone surrounds the coccidia, which, at least
in the species sufficiently known, begin to propagate by an asexual
process (schizogony), the parasites themselves becoming schizonts, as
the initial stage is usually called. They differ from later stages
(sporonts or gametocytes), which resemble them in form, by the absence
of granulations in the cytoplasm, as well as by the vesicular nucleus.
The form is not always the same, for in some cases, at least, many
schizonts assume a globular form.

Schizogony (fig. 67, V-VII) commences with a division of the nucleus,
which takes place in different ways in the various species. This
finally leads to the formation of numerous daughter nuclei which
become smaller and smaller, and which collect beneath the surface of
the schizonts. In some species the daughter nuclei collect only in one
half of the schizont. A part of the protoplasm of the periphery now
divides around each daughter nucleus, the remaining part (residual
body) being left in the centre or on one side. The segments of the
divided cytoplasm, each containing a nucleus, assume a fusiform shape
and become merozoites, which very soon become free (fig. 67, VIII) and
leave the residual body. They are distinguishable from the very similar
sporozoites (fig. 67, I), as the merozoites possess a karyosome.

[Illustration: FIG. 67.--Life-cycle of _Eimeria_ (_Coccidium_)
_schubergi_, Schaud., from the intestine of _Lithobius_. (After
Schaudinn.) The infection is caused by a cyst (XX), containing spores,
which reaches the intestine of a _Lithobius_, where it discharges the
sporozoites (I). II, A sporozoite invading an intestinal epithelial
cell; III, intestinal epithelial cell with young trophozoite; IV,
intestinal epithelial cell with a globular schizont; V, nuclear
segmentation within the schizont; VI, the daughter nuclei arranging
themselves superficially; VII, formation of the merozoites; VIII,
merozoites that have become free, and which, penetrating into other
epithelial cells of the same intestine, repeat the schizogony
(II-VIII); IX and X, merozoites which, likewise invading the epithelial
cells of the same intestine, become sexually differentiated; XIa,
young macrogametocyte; XIb, older macrogametocyte; XIc, mature
macrogametocyte (discharging particles of chromatin); XIIa, young
microgametocyte; XIIb, older microgametocyte; XIIc, increase of nuclei
in the microgametocyte; XIId, the globular residual body around which
numerous microgametes have formed; XIIe, an isolated microgamete; XIII,
the mature macrogamete surrounded by numerous microgametes and forming
a cone of reception or fertilization prominence; XIV, shows the nucleus
of a microgamete that has penetrated and fused with the nucleus of the
macrogamete (fertilization)--the latter forms a membrane and becomes
an oöcyst; XV, XVI, XVII, nuclear segmentation in the oöcyst; XVIII,
oöcyst with four sporoblasts; XIX, the sporoblasts transformed into
spores, each containing two sporozoites; XX, the cyst introduced into
the intestine and liberating the sporozoites by bursting.]

  The merozoites move in a manner similar to that of the sporozoites.
  The movements consist either of slow incurvations with subsequent
  straightenings, or annular contractions along the entire extent
  of the body. In addition, there are gliding movements similar to
  those of many gregarines, and brought about in a like manner by the
  secretion at the posterior extremity of a gelatinous substance that
  hardens rapidly.

The merozoites do not gain the open in the usual way, but are destined
to infect still further the same host by actively penetrating into
other epithelial cells of the affected organ. Here they continue their
growth and may again and again undergo schizogony. In the Infusoria
the repeated segmentations finally cease and are renewed only after
a conjugation. This is likewise the case with the Coccidia, with the
difference that in the latter the two conjugating individuals (gametes)
are differently constituted one from the other, whereas in the
Infusoria they are almost always similar.

When the schizogony ceases, the merozoites, that had penetrated
the epithelial cells and become trophozoites there, consist of two
kinds of differently constituted individuals. One kind possesses a
clear cytoplasm (fig. 67, XII), the other an opaque, richly granular
cytoplasm (fig. 67, XI), while both possess a vesicular nucleus
with a karyosome. In order to continue their development, the more
granular individuals must be fertilized, and are therefore termed
either female gametes or, on account of their size, macrogametes.
The male individuals (microgametes) necessary to conjugation, are
formed in greater numbers from the less dense microgametocytes or
male mother-cells (fig. 67, XIId). They are slender bodies consisting
chiefly of nuclear substance, and in most species bear two flagella
of unequal length directed backwards, the place of insertion of which
varies according to the species (fig. 67, XIIe).

While the development of the microgametes is rapidly advancing a change
occurs in the nucleus of the female parent forms or macrogametocytes.
Parts of the karyosome are extruded (fig. 67, XIc), and the nucleus
loses at the same time its vesicular form. One macrogamete results,
after nuclear maturation, from one macrogametocyte. By this time
the macrogametes are capable of conjugation, and the process takes
place within the host, generally, however, outside the affected and
degenerated host cells. The microgametes that have now become free from
the very large residual body, crowd around the mature macrogametes,
which often send out a small prominence (“cone of reception” or
fertilization protuberance) for their reception (fig. 67, XIII). As
soon as a microgamete comes in contact with this and penetrates into
the cytoplasm of the macrogamete, the latter surrounds itself with
a membrane which prevents the intrusion of other microgametes. The
nucleus of the microgamete that has gained entry unites with the
nucleus of the macrogamete, which latter is afterwards capable of
forming the well-known spores. The parasite is now called an encysted
zygote or oöcyst. The oöcysts of some other members of the Coccidiidea,
_e.g._, _Eimeria avium_, can form their walls prior to fertilization.
In such cases, a weak spot is left at one place in the cyst wall,
forming a micropyle, that permits of the entry of the male, immediately
after which the micropyle is closed.

  The reduced nucleus of the macrogamete elongates on the entry of the
  microgamete, and becomes a fertilization spindle to which the male
  pronucleus (from the microgamete) becomes attached (fig. 67, XIV and
  XV). Thereupon the spindle divides into two daughter nuclei (fig. 67,
  XVI) which assume a round shape. The protoplasm at this stage may
  at once divide, or another segmentation of the daughter nuclei may
  first occur. In the former case the two halves divide again, so
  that finally four nucleated segments, the sporoblasts, are formed,
  whereas in the latter case the four sporoblasts appear simultaneously
  (fig. 67, XVII). In both cases a residual body of varying size is
  separated from the protoplasm of the oöcyst. As a rule the oöcysts
  have already been discharged from the body of the host, and in the
  manner described above, form the sporoblasts after a longer or
  shorter period of incubation.

The sporoblasts are originally naked, but each soon secretes a
homogeneous membrane, the sporocyst, in which it becomes enveloped
(fig. 67, XVIII). After the segmentation of the nucleus the contents
divide into two sickle-shaped sporozoites, in addition to which there
is generally also a residual body (fig. 67, XIX).

This terminates the development. The spores are intended for the
infection of other hosts. If they reach the intestine of suitable
hosts, either free or enclosed in the oöcyst wall, the action of the
intestinal juices causes them to open and permits the escape of the
sporozoites (fig. 67, XX). The latter move exactly like the merozoites
and soon make their way into epithelial cells (fig. 67, I), where they
become schizonts, and thus repeat the life cycle.

  Although our knowledge of the development of the coccidia is but of
  recent date, yet it already extends to a large number of species,
  which exhibit various deviations from the cycle of development
  described above. For instance, in addition to differences in the
  gametocytes, the schizonts of _Adelea_ and _Cyclospora_ also show
  differentiation and give rise to macromerozoites and micromerozoites,
  whilst in _Adelea_ and _Klossia_ a precocious association of the
  gametocytes precedes the true copulation of the ripe gametes.

The classification of the Coccidiidea is based chiefly on the number of
sporozoites found in each spore, and the number of sporocysts (spores)
found in one oöcyst. Léger[173] recognises two great legions, the
Eimeridea and the Adeleidea, the former comprising the greater number
of genera, including the genus of most economic importance, _Eimeria_.
It must be noted that, though a member of this genus may be frequently
referred to as _Coccidium_, strictly it should be termed _Eimeria_,
that name having priority. The name of the disease resulting from
the action of such parasites is, however, established and remains as

[173] _Arch. f. Protistenkunde_ (1911), xxii, p. 71.

Certain of the more important of the Coccidiidea may now be considered.

Genus. *Eimeria*, Aimé Schneider, 1875.

  Syn.: _Psorospermium_, Rivolta, 1878; _Cytospermium_, Rivolta,
  1878; _Coccidium_, R. Leuckart, 1879; _Pfeifferia_, Labbé, 1894;
  _Pfeifferella_, Labbé, 1899.

The Eimeria belong to Léger’s old family, the Tetrasporocystidæ, which
comprises forms producing oöcysts with four sporocysts, each containing
two sporozoites. The cysts are spherical or oval, as are also usually
the schizonts. The members of the genus are confined chiefly to
vertebrate hosts, the more important economically occurring in mammals
and birds. From the mammalian hosts very rarely the parasites may reach
man. _Eimeria_ (_Coccidium_) _avium_ of wild birds and poultry, and
_Eimeria stiedæ_ parasitic in rabbits, may be considered. There is a
general similarity in their life-cycles and each is of great practical

*Eimeria avium*, Silvestrini and Rivolta.

  _Eimeria avium_ is responsible for fatal epizoötics among game birds
  such as grouse, pheasants and partridges, and domestic poultry such
  as fowls, ducks, pigeons and turkeys, and can pass from any one of
  these hosts to any of the others with the same effect. The organism
  is parasitic in the alimentary tract of the host, affecting more
  especially the small intestine (duodenum) and the cæca, but in
  some cases penetrating to the liver and multiplying there (as in
  turkeys), producing necrotic cheesy patches, that ultimately become
  full of oöcysts. The gut is rendered very frail by the action of
  the parasites, its mucous membrane is greatly injured, and is often
  reduced to an almost structureless pulp, riddled with parasites
  (fig. 68). Infection is conveyed from host to host by the ingestion
  of food or drink contaminated with the oöcysts voided in the fæces of
  infected birds. Oval oöcysts from 24 µ to 35 µ long and from 14 µ to
  20 µ broad are the means of infection. The oöcysts develop internally
  four sporocysts or spores, from each of which two sporozoites are
  produced. The life-history[174] presents two phases: (1) The asexual
  multiplicative phase, schizogony, for the increase in numbers of the
  parasites within the same host; (2) the reproductive phase, following
  the formation of gametes (gametogony), leading to the production of
  resistant oöcysts, destined for the transference of the parasite to
  new hosts (sporogony).

[174] Fantham, H. B. (1910), “The Morphology and Life History of
_Eimeria_ (_Coccidium_) _avium_, a Sporozoön causing a fatal disease
among young Grouse,” _Proc. Zool. Soc. Lond._, 1910, pp. 672–691, 4
plates. Also Fantham, H. B. (1911), “Coccidiosis in British Game Birds
and Poultry,” _Journ. Econ. Biol._, vi, pp. 75–96.

  The oöcysts usually reach the duodenum unharmed, with food or
  drink. Under the influence of the powerful digestive juices
  (especially the pancreatic) now encountered, the oöcysts soften,
  as do the sporocysts, and ultimately two sporozoites emerge from
  each sporocyst. The sporozoites are from 7 µ to 10 µ long, and each
  is vermicular with a uniform nucleus (fig. 69, A). After a short
  period of active movement in the gut, each sporozoite penetrates an
  epithelial cell (figs. 68 _spz_, 69, B), and once within, gradually
  becomes rounded (fig. 69, B, C). It grows rapidly, feeding on the
  contents of the host cell and living as a trophozoite (fig. 69,
  _D_). When the parasite is from 10 µ to 12 µ in diameter, usually
  multiplication by schizogony (fig. 69, E-H) begins. The nucleus
  of the parent cell, now called a schizont, divides into a number
  of portions that become arranged at the periphery (fig. 69, E).
  Cytoplasm collects around each nucleus (fig. 69, E, F) and gradually
  a group of daughter individuals (merozoites) is produced (fig. 69,
  G), the nucleus of each merozoite showing a karyosome.

[Illustration: FIG. 68.--Small piece of epithelial lining of gut of
heavily infected Grouse chick, showing various stages in life history
of the parasite _Eimeria avium_; _par_, parasite (trophozoite); _mz_,
merozoite; _sch_, schizont; _spz_, sporozoite; _ooc_, oöcyst; ♂, male
gametocyte; ♀, female gametocyte. × 750. (After Fantham.)]

  The merozoites of _Eimeria avium_ are arranged “en barillet,” like
  the segments of an orange (figs. 68 _mz_, 69, G), therein differing
  from those of _E. schubergi_, which are arranged “en rosace.” They
  separate from one another (fig. 69, H), penetrate other epithelial
  cells, where they may, in turn, become schizonts. Eight to fourteen
  merozoites are usually formed by each schizont, twenty have been
  found, while in cases of intense infection when space has become
  limited, the number may be only four.

  After a number of generations of merozoites have been formed, a limit
  is reached both to the multiplicative capacity of the parasite and to
  the power of the bird to provide the invader with food. Consequently,
  resistant forms of the parasite are necessary, and the trophozoites
  begin to show sexual differentiation instead of forming schizonts,
  that is, gametogony commences.

  [Illustration: FIG. 69.--_Eimeria avium_. Diagram of life-cycle. For
  explanation see text. (After Fantham.)]

  Certain trophozoites store food and become large and granular. These
  are macrogametocytes (fig. 69, I, ♀). The microgametocytes (fig. 69,
  I, ♂) are smaller and far less granular. The macrogametocyte
  continues to grow, and becomes loaded with chromatoid and plastinoid
  granules (fig. 69, J, ♀), while the microgametocyte has its nucleus
  divide to form a number of bent, rod-like portions (fig. 69, J, ♂).
  The macrogametocyte gives rise to a single macrogamete, which forms
  a cyst wall for itself, leaving a thin spot (micropyle) for the
  entry of the male (fig 69, K, ♀). The microgametocyte gives rise to
  numerous small, biflagellate microgametes (fig. 69, K, ♂) around a
  large, central residual mass, from which they ultimately break free,
  and swim away. When a macrogamete is reached, the microgamete enters
  through the micropyle (fig. 69, L)--which then closes, thus excluding
  the other males--and applies itself to the female nucleus (fig. 69,
  M). Nuclear fusion occurs, the oöcyst (encysted zygote) being thus
  produced. Sporogony then ensues. The oöcyst (fig. 69, N) at first
  has its contents completely filling it. They then concentrate into
  a central spherical mass (fig. 69, O) which gradually becomes
  tetranucleate (fig. 69, P). Cytoplasm collects around each nucleus,
  and four sporoblasts are thus formed (fig. 69, Q). Each sporoblast
  becomes oval (fig. 69, R) and produces a sporocyst. Ultimately two
  sporozoites are formed in each sporocyst or spore, at first lying
  tête-bêche (fig. 69, S), but finally twisting to assume the position
  most convenient for emergence (fig. 69, T) when they reach a new
  host. The period of the life-cycle of _Eimeria avium_ (as well as
  the details of the life-cycle) was determined by Fantham to be from
  eight to ten days, of which period schizogony occupies four to five

  The method of infection[175] is contaminative, by way of food or
  drink. Young birds are especially susceptible to infection. Certain
  birds, particularly older ones, may act as reservoirs of oöcysts,
  being continuously infected themselves, without showing any marked
  ill effects from the parasite, but being highly infectious to
  other birds. Much moisture retards the development of sporocysts
  considerably. The duration of vitality of the infective oöcysts has
  been determined experimentally to extend well over two years, and in
  certain cases longer. _Eimeria avium_ is the causal agent of “white
  diarrhœa” or “white scour” in fowls, and of “blackhead” in turkeys.

[175] Fantham, H. B. (1910), “Experimental Studies on Avian
Coccidiosis, especially in relation to young Grouse, Fowls and
Pigeons,” _Proc. Zool. Soc. Lond._, 1910, pp. 722–731, 1 plate.

_Eimeria avium_ of birds and _E. stiedæ_ of rabbits closely resemble
one another, but are not the same parasite, for _E. avium_ is not
infective to rabbits, nor _E. stiedæ_ to poultry.

*Eimeria stiedæ*, Lindemann, 1865.

  Syn.: _Monocystis stiedæ_, Lindemann, 1865; _Psorospermium cuniculi_,
  Rivolta, 1878; _Cytospermium hominis_, Rivolta, 1878; _Coccidium
  oviforme_, Leuckart, 1879; _Coccidium perforans_, Leuckart, 1879;
  _Coccidium cuniculi_.

[Illustration: FIG. 70.--_Eimeria stiedæ_. Section through an infected
villus of rabbit’s intestine. × 260.]

_Eimeria stiedæ_ is parasitic in the gut epithelium (fig. 70), liver,
and epithelium of the bile ducts of rabbits, and is usually considered
to be the parasite very occasionally found in man. The life-cycle
resembles that of _Eimeria avium_ in its general outlines (see fig. 69)
and therefore will not be detailed in full here. The oöcysts (fig. 71)
are large, elongate-oval, greenish in fresh preparations and vary in
size from 24 µ to 49 µ long and 12·8 µ to 28 µ broad, the gut forms
being usually smaller than those occurring in the liver, owing to the
more confined space in which they are formed. Formerly, the parasites
in the liver were described under the name of _Coccidium oviforme_,
while those from the intestine were termed _Coccidium perforans_. This
distinction has now broken down.

[Illustration: FIG. 71.--_Eimeria stiedæ_, from the liver of the
rabbit, oöcysts in various stages of development. (After Leuckart.)]

[Illustration: FIG. 72.--_a_, _b_, spores of _Eimeria stiedæ_ (Riv.),
with two sporozoites and residual bodies; _c_ represents a free
sporozoite. (After Balbiani.)]

[Illustration: FIG. 73.--So-called swarm cysts (endogenous sporulation
or schizogony) of the Coccidium of the rabbit. The daughter forms are
called merozoites. (After R. Pfeiffer.)]

The oöcysts[176] are thick-walled, somewhat flattened at one pole,
where a large micropyle is present. Four egg-shaped spores (sporocysts)
are formed within, each about 12 µ to 15 µ long and 7 µ broad
(fig. 72). The oöcysts are voided with the fæces. Sporogony takes,
in nature, about three days in the excrement. Fæcal contamination of
the food of rabbits results, and coccidian oöcysts are swallowed.
Under the influence of the pancreatic juice of a new host, the
sporozoites (fig. 72, _a_--_c_) are liberated from the spores and
proceed to attack the epithelium and multiply within it, as in the
case of _Eimeria avium_. From the gut, infection spreads to the liver,
where multiplication of the parasite goes on actively, resulting in
the formation of the whitish coccidial nodules, which may be very
conspicuous (fig. 74). Proliferation of the connective tissue may occur
around the coccidial nodules, which then contain large numbers of
oöcysts in various stages of development. It is said that the oöcysts
in the older nodules do not seem to be capable of further development.
Schizogony (fig. 73) and gametogony in all stages can be found in both
liver and gut.

[176] For an account of the life-cycle of _Eimeria stiedæ_ consult
Wasielewski, Th. von (1904), “Studien und Photogramme zur Kenntnis der
pathogenen Protozoen,” Heft. 1 (Coccidia), 118 pp., 7 plates, Leipzig:
J. A. Barth. Also, Metzner, R. (1903), _Arch. f. Protistenk._, ii,
p. 13.

Young rabbits often die of intestinal coccidiosis before infection of
the liver occurs. The repeated schizogony of _Eimeria stiedæ_ in the
gut is sufficient to cause death.

[Illustration: FIG. 74.--_Eimeria stiedæ_. Section through coccidian
nodule in infected rabbit’s liver. × 55.]

  The disease of cattle popularly known as “red dysentery” is also
  ascribed to the action of _Eimeria stiedæ_. The fæces of infected
  cattle show blood clots of various sizes and in severe cases watery
  diarrhœa is present. Acute cases end fatally in about two days.
  Numerous oöcysts, considered to be those of _Eimeria stiedæ_, occur
  in the fæces, and there is a heavy infection of the gut, especially
  the large intestine and rectum, all stages of the parasite being
  found in the epithelium. It is suspected that cattle contract the
  disease by feeding on fresh grass contaminated with oöcysts. The
  disease is recorded from Switzerland and from East Africa.

As before mentioned, _Eimeria stiedæ_ is considered to be the
organism found in a few cases in man, possibly acquired by eating the
insufficiently cooked livers of diseased rabbits. These cases may now
be described.

(_a_) *Human Hepatic Coccidiosis.*

  (1) Gubler’s Case. A stone-breaker, aged 45, was admitted to a Paris
  hospital suffering from digestive disturbances and severe anæmia.
  On examination the liver was found to be enlarged and presented a
  prominent swelling, which was regarded as being due to Echinococcus.
  At the autopsy of the man, who succumbed to intercurrent peritonitis,
  twenty cysts were found averaging 2 to 3 cm. in diameter, and one
  measuring 12 to 15 cm. The caseous contents consisted of detritus,
  pus corpuscles, and oval-shelled formations, which were considered to
  be Distoma eggs, but which, in accordance with Leuckart’s conjecture,
  proved to be Coccidia.[177]

[177] Gubler, A., “Tumeurs du foie déterm. par des œufs d’helm....”
_Mem. Soc. Biol._, Paris, 1858, v, 2; and _Gaz. med. de Paris_, 1858,
p. 657; Leuckart, R., _Die menschl. Paras._, 1863, 1ST edition, i,
pp. 49, 740.

  (2) Dressler’s Case (Prague). Relates to three cysts, varying from
  the size of a hemp-seed to that of a pea, and containing Coccidia,
  found in a man’s liver.[178]

[178] Leuckart, R., _Die menschl. Paras._, 1863, 1st edition, i, p. 740.

  (3) Sattler’s Case (Vienna). Coccidia were in this case observed in
  the dilated biliary duct of a human liver.[179]

[179] Leuckart, R., _Die Paras. d. mensch._, 1879, 2nd edition, p. 281.

  (4) Perls’ Case (Giessen). Perls discovered Coccidia in an old
  preparation of Sömmering’s agglomerations.[180]

[180] Leuckart, R., _ibid._, p. 282.

  (5) Silcock’s Case (London).[181] The patient, aged 50, who had
  fallen ill with serious symptoms, exhibited fever, enlarged liver
  and spleen, and had a dry, coated tongue. At the autopsy numerous
  caseous centres, mostly immediately beneath the surface, were found,
  while the contiguous parts of the liver were inflamed. Microscopical
  examination demonstrated numerous Coccidia in the hepatic cells as
  well as in the epithelium of the biliary ducts. A deposit of Coccidia
  was likewise found in the spleen, which the parasites had probably
  reached by means of the blood-stream.[182]

[181] Silcock, “A Case of Parasit. by Psorospermia,” _Trans. Path.
Soc._, London, 1890, xli, p. 320.

[182] Pianese has confirmed the fact that Coccidia actually occur in
the blood of the hepatic veins of infected rabbits.

(_b_) *Human Intestinal Coccidiosis.*

  In two cadavers at the Pathological Institute in Berlin, Eimer[183]
  found the epithelium of the intestine permeated by Coccidia. Railliet
  and Lucet’s case may be traced back to intestinal Coccidia, which
  were found in the fæces of a woman and her child, who had both
  suffered for some time from chronic diarrhœa.[184] In other cases
  (Grassi, Rivolta), where only the existence of Coccidia in the fæces
  was known, it is doubtful whether the parasites originated in the
  intestine or in the liver.

[183] _Die ei- u. kugelf. Psorosp. d. Wirbelt._, 1870, p. 16.

[184] Railliet and Lucet, “Obs. s. quelq. Cocc. intest.,” _C. R. Soc.
Biol._, Paris, 1890, p. 660; Railliet, _Trait. Zool. med. et agric._,
2e éd., 1895, p. 140.

(_c_) *Doubtful Cases.*

  To these belong Virchow’s case[185] where, in the liver of an elderly
  woman, a thick walled tumour measuring 9 to 11 mm. was found.
  Among the contents of this tumour there were oval formations 56 µ
  long, surrounded by two membranes and enclosing a number of round
  substances. Virchow considered these foreign bodies to be eggs of
  pentastomes in various stages of development, others consider them to
  be Coccidia.

[185] _Arch. f. path. An._, xviii, 1860, p. 523.

  The Coccidia which Podwyssotzki claims to have seen in the liver of
  a man, not only in the liver cells, but also in the nuclei, are also
  problematic.[186] The parasite was called _Caryophagus hominis_.

[186] Podwyssotzki, “Ueb. d. Bedeut. d. Coccid. in d. Path. Leber des
Menschen,” _Centralbl. f. Bakt._, vi, 1889, p. 41.

  Again, other explanations can be given to an observation by Thomas,
  on the occurrence of _Coccidium oviforme_ in a cerebral tumour of a
  woman aged 40. The growth was as large as a pea and surrounded by a
  bony substance.[187]

[187] Thomas, J., “Case of Bone Formation in the Human Brain, due to
the Presence of _Coccidium oviforme_,” _Journal Boston Soc. Med. Sc._,
iii, 1899, p. 167; _Centralbl. f. Bakt._ [I] xxviii, 1900, p. 882.

Genus. *Isospora*, Aimé Schneider, 1881.

  Syn.: _Diplospora_, Labbé, 1893.

Belonging to the section _Disporea_, that is, forming only two spores,
each with four sporozoites.

*Isospora bigemina*, Stiles, 1891.

  Syn.: “_Cytospermium villorum intestinalium canis et felis_,”
  Rivolta, 1874; “_Coccidium Rivolta_,” Grassi, 1882; _Coccidium
  bigeminum_, Stiles, 1891.

This parasite lives in the intestinal villi of dogs, cats, and the
polecat (_Mustela putorius_, L.). According to Stiles,[188] the oöcyst
divides into two equal ellipsoidal portions or sporoblasts which
become spores and then each forms four sporozoites. The oöcysts of
this species vary from 22 µ to 40 µ in length and from 19 µ to 28 µ in
breadth. Each spore is 10 µ to 18 µ long and contains four sporozoites.
The parasites live and multiply, not only in the gut epithelium, but
also in the connective tissue of the intestinal submucosa. Wasielewski
has seen merozoites in the gut of the cat.

[188] “Notes on Paras.,” No. II, _Journ. of Comp. Med. and Vet. Sci._,
1892, xiii, p. 517.

_Isospora bigemina_ (fig. 75) appears to occur also in man, for Virchow
published a case which was communicated to him by Kjellberg, and
attributed the illness to this parasite.[189] Possibly also it would be
more correct to ascribe the observation of Railliet and Lucet, which
is mentioned under “Human Intestinal Coccidiosis,” p. 148, to this
species, as the Coccidia in that case were distinguished by their
diminutive size (length 15 µ, breadth 10 µ). The case communicated by
Grunow may also possibly refer to _Isospora bigemina_.[190] Roundish
or oval structures of 6 µ to 13 µ in diameter occurred in the mucous
membrane of the gut and in the fæces of a case of enteritis.

[189] _Arch. f. path. An._, 1860, xviii, p. 527.

[190] Grunow, “Ein Fall von Protozoën (Coccidien?) Erkrankung des
Darmes,” _Arch. f. exper. Path. und Pharm._, 1901, xlv, p. 262.

[Illustration: FIG. 75.--_Isospora bigemina_, Stiles (from the
intestine of a dog). _a_, Piece of an intestinal villus beset with
Isospora, slightly enlarged; _b_, _Isospora bigemina_ (15 µ in
diameter), shortly before division; _c_, divided; _d_, each portion
encysted forming two spores; _e_, four sporozoites in each part, on the
left seen in optical section, together with a residual body--highly
magnified. (After Stiles.)]


  In literature many other statements are found as to the occurrence
  of Coccidia-like organisms in different diseases of man. In some
  of the cases the parasites proved to be fungi. This was the case
  with the parasites of a severe skin disease of man, formerly called
  _Coccidioides immitis_ and _Coccidioides pyogenes_. Other statements
  are founded on misapprehensions, or are still much disputed. If
  reference is here made to “_Eimeria hominis_,” R. Blanchard, 1895,
  this is done on the authority of the investigator mentioned. The
  structures in question are nucleated spindle-shaped bodies of very
  different lengths (18 µ to 100 µ), which either occurred isolated or
  were enclosed in large globular or oval cysts, alone or with a larger
  tuberculated body (“residual body”). These formations were found by
  J. Künstler and A. Pitres in the pleural exudation removed from a man
  by tapping. The man was employed on the ships plying between Bordeaux
  and the Senegal River.

  Blanchard looks upon the fusiform bodies as merozoites and the cysts
  as schizonts of a Coccidium. On the other hand, Moniez declares the
  spindle bodies to be the ova and the supposed residual bodies to be
  “floating ovaries” of an Echinorhynchus.

  Severi’s “monocystid Gregarines,” which were taken from the lung
  tissue of a still-born child, are also quite problematical.

  No less doubtful are the bodies which Perroncito calls _Coccidium
  jalinum_, and which he found in severe diseases of the intestine in
  human beings, pigs, and guinea-pigs; Borini also reported another

Order. *Hæmosporidia*, Danilewsky emend. Schaudinn.

The Hæmosporidia are a group of blood parasites, comprising forms
differing greatly among themselves. Some of the forms need much further
investigation. However, there are certain true Hæmosporidia which
present close affinities with the Coccidia, leading Doflein to use the
term *Coccidiomorpha* for the two orders conjoined.

The Hæmosporidia present the following general characteristics:--

(1) They are parasites of either red or white blood corpuscles of
vertebrates during one period of their life-history.

(2) They exhibit alternation of generations--asexual phases or
schizogony alternating with sexual phases or sporogony--as do the

(3) There is also an alternation of hosts in those cases which have so
far been completely investigated. The schizogony occurs in the blood or
internal organs of some vertebrates while the sporogony occurs in an
invertebrate, such as a blood-sucking arthropod or leech.

(4) Unlike the Coccidia, resistant spores in sporocysts are not
generally produced, such protective phases in the life-cycle being
unnecessary, as the Hæmosporidia are contained within either the
vertebrate or invertebrate host during the whole of their life.

The Hæmosporidia may be considered for convenience under five main

(1) The _Plasmodium_ or _Hæmamœba_ type. This includes the malarial
parasites of man and of birds. The asexual multiplicative or
schizogonic phases occur inside red blood corpuscles and are amœboid.
They produce distinctive, darkish pigment termed melanin or hæmozoin.
Infected blood drawn and cooled on a slide may exhibit “exflagellation”
of the male gametocytes, _i.e._, the formation of filamentous male
gametes. The invertebrate host is a mosquito. The malarial parasites
of man are discussed at length on p. 155. Similar pigmented hæmamœboid
parasites have been described in antelopes, dogs, and other mammals,
and even reptiles.

(2) The _Halteridium_ type. The trophozoite stage inside the red blood
corpuscle is halter-shaped. Pigment is produced, especially near the
ends of the organism. The parasites occur in the blood of birds. The
invertebrate host of _H. columbæ_ of pigeons in Europe, Africa, Brazil
and India, is a hippoboscid fly, belonging to the genus _Lynchia_.

Halteridium parasites are common in the blood of passerine birds,
such as pigeons, finches, stone owls, Java sparrows, parrots, etc.
The Halteridium embraces or grows around the nucleus of the host red
cell without displacing the nucleus. Young forms and multiplicative
stages of _H. columbæ_ have been found in leucocytes in the lungs of
the pigeon (fig. 76, _8_-_12_). Male and female forms (gametocytes)
are seen in the blood (fig. 76, _3a_, _3b_). The cytoplasm of the
male gametocytes is pale-staining and the nucleus is elongate, while
the cytoplasm of the females is darker and the nucleus is smaller and
round. Formation of male gametes from male gametocytes (the so-called
process of “exflagellation”) may occur on a slide of drawn infected
blood, also fertilization, and formation of the oökinete, as first seen
by MacCallum. The correct generic name for Halteridia is, apparently,
_Hæmoproteus_. Wasielewski (1913), working on _H. danilewskyi_ (var.
_falconis_), in kestrels, finds that the halteridium may be pathogenic
to nestlings. The cycle of _H. noctuæ_ described by Schaudinn (1904)
lacks confirmation. The account of the life-cycle of _H. columbæ_ given
by Aragão (1908) is illustrated in fig. 76. It agrees with the work of
Sergent (1906–7) and Gonder (1915). Mrs. Adie (1915) states that the
cycle in _Lynchia_ is like that of a _Plasmodium_.

[Illustration: FIG. 76--_Hæmoproteus_ (_Halteridium_) _columbæ_.
Life-cycle diagram: 1, 2, stages in red blood corpuscle of bird; 3,
4, gametocytes (3_a_ ♂, 3b ♀); 5_a_, formation of microgametes; 6,
fertilization (in fly’s gut); 7, oökinete; 8–12, stages in mononuclear
leucocytes in lungs. (After Aragão.)]

(3) The _Leucocytozoön_ type. The trophozoites and gametocytes occur
within mononuclear leucocytes and young red cells (erythroblasts) in
the blood of birds. Laveran and França consider that the Leucocytozoa
occur in erythrocytes. The host cells are often greatly altered by
the parasites, becoming hypertrophied and the ends usually drawn into
horn-like processes (fig. 77), though some remain rounded. Leucocytozoa
are limited to birds, and very rarely produce pigment. Male and female
forms (gametocytes) are distinguishable in the blood (fig. 77), and the
formation of male gametes (“exflagellation”) may occur in drawn blood.

[Illustration: FIG. 77.--_Leucocytozoön lovati_. _a_, Male parasite
(microgametocyte), within host cell, whose ends are drawn out; _b_,
female parasite (macrogametocyte) from blood of grouse. × 1,800. (After

The Leucocytozoa were first seen by Danilewsky in 1884. They are
usually oval or spherical. It is not easy sometimes to distinguish the
altered host cell from the parasite, as the nucleus of the former is
pushed to one side by the leucocytozoön. The cytoplasm of the female
parasite stains deeply, and the nucleus is rather small, containing a
karyosome. In the male the cytoplasm stains lightly and the nucleus is
larger, with a loose, granular structure.

Many species of Leucocytozoa are recorded, but schizogony has only
been described by Fantham (1910)[191] in _L. lovati_ in the spleen of
the grouse (_Lagopus scoticus_), and by Moldovan[192] (1913) in _L.
ziemanni_ in the internal organs of screech-owls.

[191] _Annals Trop. Med. and Parasitol._, iv, p. 255.

[192] _Centralbl. f. Bakt._, Orig., lxxi, p. 66.

M. and A. Leger[193] (1914) propose to classify Leucocytozoa,
provisionally, according as the host cells are fusiform or rounded.

[193] _Bull. Soc. Path. Exot._, vii, p. 437.

(4) The _Hæmogregarina_ type. Included herein are many parasites of red
blood corpuscles, with a few (the leucocytogregarines) parasitic in the
white cells of certain mammals and a few birds. They are not amœboid
but gregarine-like, vermicular or sausage-shaped (fig. 78). They do
not produce pigment. They are widely distributed among the vertebrata,
but are most numerous in cold-blooded vertebrates (fishes, amphibia
and reptiles). The hæmogregarines of aquatic hosts are transmitted by
leeches, those of terrestrial hosts by arthropods.

The nucleus of hæmogregarines is usually near the middle of the
parasite, but may be situated nearer one end. The body of the
parasite may be lodged in a capsule (“cytocyst”). There is much
variation in size and appearance among hæmogregarines. Some are
small (_Lankesterella_); some attack the nucleus of the host cell
(_Karyolysus_); others have full grown vermicules larger than the
containing host corpuscle, and so the hæmogregarines bend on themselves
in the form of *U* (fig. 78, _b_). Schizogony often occurs
in the internal organs of the host, sometimes in the circulating blood.

The hæmogregarines occurring in the white cells (mononuclears or
polymorphonuclears) of mammals have been referred to a separate
genus, _Leucocytogregarina_ (Porter) or _Hepatozoön_ (Miller). Such
leucocytogregarines are known in the dog (fig. 79), rat, mouse,
palm-squirrel, rabbit, cat, etc. Schizogony of these forms occurs in
the internal organs, such as the liver, lung and bone-marrow of the
hosts. They are apparently transmitted by ectoparasitic arthropods,
such as ticks, mites, and lice.

[Illustration: FIG. 78.--Hæmogregarines from lizards, _a_, _H.
schaudinni_, var. _africana_, from _Lacerta ocellata_; _b_, _H. nobrei_
from _Lacerta muralis_; _c_, _H. marceaui_ in cytocyst, from _Lacerta
muralis_. (After França.)]

A few hæmogregarines are known to be parasitic in the red blood
corpuscles of mammals. Such are _H. gerbilli_ in the Indian field rat,
_Gerbillus indicus_; _H. balfouri_ (_jaculi_) in the jerboa, _Jaculus
jaculus_, and a few species briefly described from marsupials. These
parasites do not form pigment.

Strict leucocytic gregarines have been described from a few birds by
Aragão and by Todd.

The sporogony of hæmogregarines is only known in a few cases, and
in those affinity with the Coccidia is exhibited. In fact, the
Hæmogregarines are now classified by some authors with the Coccidia.

(5) The _Babesia_ or _Piroplasma_ type. These are small parasites of
red blood corpuscles of mammals. They do not produce pigment. They
are pear-shaped, round or amœboid in Babesia, bacilliform and oval
in other forms referred to this group. Piroplasms are transmitted by
ticks. These parasites are described at length on p. 172.

[Illustration: FIG. 79.--_Leucocytogregarina canis_. Life-cycle
diagram. Constructed from drawings by Christophers. (After Castellani
and Chalmers.) Schizogony occurs in the bone-marrow. The parasite is
transmitted from dog to dog by the tick, _Rhipicephalus sanguineus_,
development in which, so far as known, is shown on the right.]


Malaria, otherwise known as febris intermittens, chill-fever, ague,
marsh fever, paludism, etc., is the name given to a disease of man,
which begins with fever. It has been known since ancient times and is
distributed over almost all the world, although very unevenly, but does
not occur in waterless deserts and the Polar regions. In many places,
especially in the civilized countries of Central Europe, the disease
is extinct or occurs only sporadically, and large tracts of land have
become free from malaria.

The rhythmical course of the fever is characteristic. It begins
apparently suddenly with chilliness or typical shivering, whilst the
temperature of the body rises, the pulse becomes low and tense and the
number of beats of the pulse increases considerably. After half to
two hours the heat stage begins. The patient himself feels the rise
of his temperature (shown by feeling of heat, dry tongue, headache,
thirst). The temperature may reach 41°C or more. At the same time there
is sensitiveness in the region of the spleen and enlargement of that
organ. After four to six hours an improvement takes place, and with
profuse perspiration the body temperature falls rapidly, not often
below normal. After the attack the patient feels languid, but otherwise
well until certain prodromal symptoms (heaviness in the body, headache)
which were not noticed at first, denote the approach of another attack
of fever, which proceeds in the same way.

The intervals between the attacks are of varying length which permit of
a distinction in the kinds of fever. If the attacks intermit one day,
occurring on the first, third and fifth days of the illness and always
at the same time of day, it is termed _febris tertiana_; if two days
occur between fever days, it is called _febris quartana_. In the case
of the fever recurring daily, later writers speak of typical _febris
quotidiana_. But a quotidian fever may arise when two tertian fevers
differing by about twenty-four hours exist at the same time (_febris
tertiana duplex_). The patient has a daily attack, but the fever of the
first, third and fifth days differs in some point (hour of occurrence,
height of temperature, duration of cold or hot stage) from the fever
of the second, fourth and sixth days. Similarly, two or three quartan
fevers which differ by about twenty-four hours each may be observed
together (_febris quartana duplex_ or _triplex_); in the latter case
the result is also a quotidian fever.

Two kinds of tertian fever are differentiated--a milder form occurring
especially in the spring (spring tertian fever), and a more severe form
appearing in the summer and autumn in warmer districts, especially in
the tropics (_summer or autumn fever_, _febris æstivo-autumnalis_,
_febris tropica_, _febris perniciosa_). The latter often becomes a
quotidian fever.

All the afore-mentioned infections are termed acute. They are
distinguished from the very different _chronic malarial infection_ by
the frequent occurrence of relapses, which finally lead to changes
of some organs and particularly of the blood. The relapses are then
generally marked by an irregular course of fever.

The term masked malaria is used when any disturbance of the state
of health of a periodic character shows itself and disappears after
treatment with quinine.[194] Generally it is a question of neuralgia.

[194] Quinine is still almost exclusively the remedy used in the
treatment of malaria. It is prepared from the bark of the cinchona
tree. This important remedy was introduced into Europe in 1640 from
Ecuador by Juan del Vego, physician of the Countess del Cinchon.

  That intermittent fever was an infectious disease, although
  not one which was transmitted direct from man to man, had been
  assumed for a long time. Therefore it was natural, at a time when
  bacteriology was triumphing, to look for a living agent causing
  infection in malaria, which search was, seemingly, successful (Klebs,
  Tomasi-Crudeli, 1879). Hence it was not surprising that the discovery
  of the real malarial parasites in November, 1880, by the military
  doctor A. Laveran[195] in Constantine (Algeria), at first met with
  violent opposition, even after Richard (1882) had confirmed it and
  Marchiafava, Celli, Grassi and others, had further extended it.
  Not that the existence of structures found in the blood of malaria
  patients by Laveran and Richard was denied; on the contrary, the
  investigations of the opponents furnished many valuable discoveries,
  but the organisms were differently interpreted and considered to be
  degeneration products of red blood corpuscles. Only when Marchiafava
  and Celli (1885) saw movements in the parasites, which Laveran called
  _Oscillaria malariæ_ and later _Hæmatozoön malariæ_, was their animal
  nature admitted and the parasites were named _Plasmodium malariæ_.
  Shortly before this, Gerhardt (1884) had stated that the disease
  could be transmitted by the injection of the blood of a malarial
  patient to a healthy person.

[195] The discovery of Laveran is in no way lessened by the fact that
one investigator or another (according to Blanchard [_Arch. de Paras._,
vii, 1903, p. 152], P. F. H. Klencke in 1843) had seen, mentioned and
depicted malarial parasites. (_Neue phys. Abhandl. auf. selbständ.
Beob. gegr._, Leipzig, 1843, p. 163, fig. 25). In 1847 Meckel had
recognized that the dark colour of the organs in persons dead of
malaria was due to pigment. Virchow in 1848 stated that this pigment
occurred in blood cells. Kelsch in 1875 recognized the frequency of
melaniferous leucocytes in the blood of malarial patients. Beauperthuy
(1853) noticed that in Guadeloupe there was no malaria at altitudes
where there were no “insectes tipulaires,” and suggested that the
disease was inoculated by insects.

  This supplied the starting point for further investigations, which
  were made not exclusively, but principally, by Italian investigators
  (Golgi, Marchiafava and Celli, Bignami and Bastianelli, Grassi and
  Feletti, Mannaberg, Romanowsky, Osier, Thayer and others). In 1885
  Golgi described the asexual cycle in the blood, in the case of the
  quartan parasite. These investigations, after attention had been
  drawn by Danilewsky (1890) to the occurrence of similar endoglobular
  parasites in birds, were extended to the latter (Grassi and Feletti,
  Celli and Sanfelice, Kruse, Labbé and others).

  The result was as follows: Malaria in man (and birds) is the result
  of peculiar parasites included in the _Sporozoa_ by Metchnikoff,
  which parasites live in the erythrocytes, grow in size and finally
  “sporulate,” that is, separate into a number of “spores” which leave
  the erythrocytes and infect other blood corpuscles. Morphologically
  and biologically several species (and respectively several varieties)
  of malarial parasites may be distinguished, on which the different
  intermittent forms depend. Transmission of the blood of patients to
  healthy people produces a malarial affection which corresponds in
  character to the fever of the patient from whom the inoculation was
  made. The combined types of fever (tertiana duplex, quartana duplex
  or triplex) are explained by the fact that the patient harbours
  two or three groups of parasites which differ in their development
  by about twenty-four hours, whilst the irregular fevers depend on
  deviation from the typical course of development of the parasites. In
  addition to stages of the parasites which could easily be arranged
  in a developmental series concurrent with the course of the disease,
  other phases of the parasites also became known, such as spheres,
  crescents, polymitus forms, which seemed not to be included in the
  series and, therefore, were very differently interpreted.

  The decision reached at the beginning of the last decade of the
  last century, which found expression in comprehensive statements
  (Mannaberg, Ziemann and others), only concerned a part of the
  complete development of the malarial parasites. No one could with
  any degree of certainty demonstrate how man became infected, nor
  were there reliable hypotheses based on analogy with other parasites
  concerning the exit of the excitants of malaria from the infected
  person and their further behaviour. Numerous hypotheses had been
  advanced, but none was able to elucidate the various observations
  made from time to time in dealing with malaria. One hypothesis only
  seemed to have a better foundation. Manson (1894), who knew from
  his own experience the part played by mosquitoes in the development
  of Filaria from the blood of man, applied this also to the malarial
  parasites living in the blood, whereby at least the way was indicated
  by which the Hæmosporidia could leave man. The parasites were said
  finally to get into water through mosquitoes which had sucked the
  blood of malarial patients, and the germ spread thence to men who
  drank the water. In some cases the parasites were supposed to reach
  man by the inhaling of the dust of dried marshes. On the other
  hand, Bignami believed that the mosquitoes were infected in the
  open air by malarial parasites which occurred there in an unknown
  stage and the insects transmitted the germs to man when biting. R.
  Koch combined both hypotheses, without, however, producing positive
  proof. R. Ross, then (1897–8) an English military doctor in India,
  was the first to succeed in this. He had been encouraged by Manson
  to study the fate of malarial _Plasmodia_ which had entered the
  intestine of mosquitoes with malaria-infected blood, especially in
  the case of the _Plasmodium_ (_Proteosoma_) living in the blood of
  birds. He showed that the _Proteosoma_ penetrate the intestinal wall
  of the mosquitoes, grow and develop into large cysts which produce
  innumerable rod-like germs, which burst into the body cavity and
  penetrate the salivary glands. Ross allowed mosquitoes to suck the
  blood of birds affected by malaria, and some nine days later, let
  the infected mosquitoes which had been isolated suck healthy birds.
  After five to nine days _Proteosoma_ were found to occur in the blood
  of the birds used. The _Proteosoma_ and _Halteridium_ of birds were
  also further investigated by MacCallum (1897–8), Koch and others, and
  important results followed.

  In any case Ross (1898) had clearly established the importance
  of mosquitoes in the spread of malaria among birds. It was now
  only a question of proving whether, and how far, mosquitoes were
  concerned with human malaria. Ross himself worked to this end. Here
  the experiments of Italian investigators (Bignami, Bastianelli,
  Grassi)[196] were of importance. These investigators studied the fate
  of malarial parasites in man, produced malaria in men experimentally
  by the bites of infected mosquitoes, and established that only
  mosquitoes belonging to the genus _Anopheles_ were concerned, and
  not species of _Culex_. These latter are only able to transmit
  _Proteosoma_ to birds. It is true that _Culex_ can ingest the
  human malarial parasites, but the latter do not develop in them.
  Development only occurs in species of _Anopheles_. In _Anopheles_
  (and similarly for _Proteosoma_ in _Culex_) sexual reproduction takes
  place; crescents, spheres and polymitus forms are necessary stages of
  development in the mosquito.

[196] Grassi, B. (1901), “Die Malaria,” 250 pp., 8 plates. G. Fischer,

  With these discoveries the campaign against malaria became more
  definite. It was directed partly against the transmitters, whose
  biology and life-cycle were more thoroughly investigated, instead of
  merely against the infection of the adult _Anopheles_. The latter do
  not, as was believed for some time, transmit the malarial germs to
  their offspring. They always infect themselves from human beings,
  whereby the relapses appearing in early summer, and the latent
  infection, especially of children of natives, play a principal part
  (Stephens and Christophers, Koch). Further, the crusade was directed
  against the infection of man by the bites of _Anopheles_. Important
  results have been obtained in these directions. Low and Sambon in
  1900 lived in a mosquito-screened hut in a malarial part of the
  Roman Campagna for three of the most malarious months and did not
  contract the disease. In the same year Dr. P. T. Manson was infected
  with malaria by infected mosquitoes sent from Italy. The rôle of
  mosquitoes having been proved, it may be hoped that ultimately the
  eradication of malaria, or at least a considerable restriction of it,
  will be achieved.

  It is of importance to record that, although malarial parasites occur
  in mammals (monkeys, bats, etc.) the human ones are not transmissible
  to mammals, not even to monkeys. The species, therefore, are specific
  to the different hosts (Dionisi, Kossel, Ziemann, Vassall).

  An important work dealing with the modern applications of the
  mosquito-malaria theory in all parts of the Tropics was published by
  Sir Ronald Ross in 1911. It is entitled “The Prevention of Malaria”
  (John Murray, London, 21s.).


The commencement of the developmental cycle and of the infection of
man, is the sporozoites (fig. 80, _1_) which are passed into the
blood of a person by the bite of an infected mosquito. Prior to this
the parasites collect in the excretory ducts of the salivary glands
(fig. 80, _27_) of the _Anopheles_. The sporozoites are elongate
and spindle-shaped, 10 µ to 20 µ long and 1 µ to 2 µ broad, with an
oval nucleus situated in the middle. They are able to glide, perform
peristaltic contractions, or curve laterally. Schaudinn has studied
the penetration of the red blood corpuscles (fig. 80, _2_) by the
sporozoites in the case of the living tertian parasite. The process
takes forty to sixty minutes in drawn blood. After its entrance the
parasite, which is now called a trophozoite, contracts, and becomes an
active amœbula (fig. 80, _3_). It develops a food vacuole and grows at
the expense of the invaded blood corpuscle (fig. 80, _4_), which is
shown by the appearance of pigment granules (transformed hæmoglobin)
in it. When the maximum size is attained, multiplication by schizogony
(fig. 80, _5_-_7_) begins with a division of the nucleus, which is
followed by further divisions of the daughter nuclei, the number of
which varies up to 16 or even 32, depending on the species of the
parasite. Then the cytoplasm divides into as many portions as there
are nuclei, the result being a structure suggestive of the spokes of a
wheel or of a daisy, the centre of the resulting rosette being occupied
by dark pigment. Finally, the parts separate from one another, leaving
behind a residual body containing the pigment, and the daughter forms
issue into the blood plasma as merozoites (fig. 80, _7_). They are
actively amœboid (fig. 80, _8_) and soon begin to enter other blood
corpuscles of their host, for the entry into which thirty to sixty
minutes are necessary, according to Schaudinn’s observations.[197]

[197] It should be remembered that some authors (Laveran, Argutinsky,
Panichi, Serra) argue against the intra-globular position of
malarial parasites and state that they only adhere outwardly to
the red blood corpuscles. These views have recently been revived
by Mary Rowley-Lawson, and she states that the malarial parasite
is “extracellular throughout its life-cycle and migrates from red
corpuscle to red corpuscle destroying each before it abandons it.”
(_Journ. Exper. Med._, 1914, xix, p. 531.)

Here they behave like sporozoites which previously entered and again
produce merozoites. This process is repeated until the number of
parasites is so large that, at the next migration of the merozoites,
the body of the person infected reacts with an attack of fever,[198]
which is repeated with the occurrence of the next or following

[198] The incubation period, that is, the time between infection
and the first attack of fever, is ten to fourteen days; with severe
infection fewer days (minimum 5 to 6) are needed.

[Illustration: FIG. 80.--Life-cycle of the tertian parasite
(_Plasmodium vivax_). Figs. 1 to 17, × 1,200; figs. 18 to 27, × 600.
(After Lühe, based on figures by Schaudinn and Grassi.) 1, sporozoite;
2, entrance of the sporozoite into a red blood corpuscle; 3, 4, growth
of the parasite, now sometimes called a trophozoite; 5, 6, nuclear
division in schizont; 7, free merozoites; 8, the merozoites which have
developed making their way into blood corpuscles, (arrow pointing to
the left) and increase by schizogony (3–7); after some duration of
disease the sexual individuals appear; 9_a_-12_a_, macrogametocytes;
9_b_-12_b_, microgametocytes, both still in the blood-vessels of
man. If macrogametocytes (12_a_) do not get into the intestine of
_Anopheles_ they may perhaps increase parthenogenetically according
to Schaudinn (12_a_; 13_c_-17_c_). The merozoites which have arisen
(17_c_) become schizonts 3–7. The phases shown underneath the dotted
line (13–17) proceed in the stomach of _Anopheles_. 13_b_ and 14_b_,
formation of microgametes; 13_a_ and 14_a_, maturation of the
macrogametes; 15_b_, microgamete; 16, fertilization; 17, oökinete; 18,
oökinete in the walls of the stomach; 19, penetration of the epithelium
of the stomach; 20–25, stages of sporogony on the outer surface of
the intestinal wall; 26, migration of the sporozoites to the salivary
gland; 27, salivary gland with sporozoites.]

The growth and schizogony last different times, according to the
species of the parasite, about forty-eight hours in the case of the
parasite of febris tertiana or tropica, and seventy-two hours for the
quartan parasite. The various intermittent forms produced by them
depend on this specific difference in the malarial parasites.

The schizogony can, however, only be repeated a certain number of
times, supposing that the disease has not been checked prematurely by
the administration of quinine, which is able to kill the parasites.
It appears that after a number of attacks of fever the conditions of
existence in man are unfavourable for the malarial parasites, and
this brings about the production of other forms which have long been
known, but also long misunderstood (spheres, crescents, polymitus). The
merozoites in this case no longer grow into schizonts, or at least not
all of them, but become sexual individuals called gametocytes (fig. 80,
_9_-_12_), which only start their further development when they have
reached the intestine of _Anopheles_. This does not take place in
every case, nor with all the gametocytes which exist in the blood of
patients with intermittent fever. Of those parasites which remain in
the human blood the male ones (microgametocytes) soon perish, the
females (macrogametocytes) persist for some long time, and perhaps at
last acquire the capacity of increasing by schizogony. They might thus
form merozoites which behave in the body as if they had proceeded from
ordinary schizonts (fig. 80, _13c_-_17c_). If their number increases
sufficiently, in course of time the patient, who was apparently
recovering, has a new series of fever attacks, or relapses, without
there having been a new infection. This is the view of Schaudinn, who
from researches of his own concluded that relapses were brought about
by a sort of parthenogenetic reproduction of macrogametocytes. R. Ross,
on the contrary, believes that in the relatively healthy periods the
number of parasites in the blood falls below that necessary to provoke
febrile symptoms; relapses then result merely from increase in the
numbers of the parasites present in the individual. Ross’s view is now
generally accepted.

[Illustration: FIG. 81.--Stages of development of pernicious
or malignant tertian parasites in the intestine of _Anopheles
macultpennis_. (After Grassi.) _a_, macrogametocyte (crescent) still
attached to human blood corpuscles; _b_, macrogametocyte (sphere)
half an hour after ingestion by the mosquito; _c_, microgametocyte
(crescent) attached to the blood corpuscle; _d_, microgametocyte
(sphere) half an hour after ingestion; the nucleus has divided several
times; _e_, microgametes attached to the residual body (polymitus

[Illustration: FIG. 82.--Oökinete of the malignant tertian parasite
in the stomach of _Anopheles maculipennis_, thirty-two hours after
ingestion of blood. (After Grassi.)]

If the gametocytes, which are globular, or in the pernicious or
malignant tertian parasite crescentic (fig. 81), gain access to the
intestine of an Anopheline,[199] they mature. The macrogametocytes
extrude a part of their nuclear substance (fig. 80, _13a_, _14a_) and
thereby become females or macrogametes. The microgametocytes, on the
other hand, undergo repeated nuclear division, preparation for this
being made apparently whilst in the blood of man. This results in the
formation of threadlike bodies which move like flagella and finally
detach themselves from the residual body (fig. 80, _13b_, _14b_). These
are the males or microgametes[200] (fig. 80, _15b_).

[199] Schizonts ingested about the same time perish in the intestine of
the mosquito.

[200] If the microgametocytes are sufficiently mature the formation of
microgametes occurs in the blood of man as soon as it is taken from the
blood-vessel and has been cooled and diluted. Such a stage is called a
_Polymitus_ form, and the process has been called “exflagellation.”

Copulation takes place in the stomach of the Anopheline (fig. 80,
_16_). A microgamete penetrates a macrogamete and coalesces with it.
The fertilized females elongate very soon and are called oökinetes
or “vermicules” (figs. 80, _17_; 82). They penetrate the walls of the
stomach, pierce the epithelium (fig. 80, _18_, _19_), and remain lying
between it and the superficial stratum (tunica elastico-muscularis).
Then they become rounded and gradually develop into cysts which grow
larger and are finally visible to the naked eye, being called oöcysts
(figs. 80, _20_-_24_; 83). Their size at the beginning is about 5 µ,
the maximum that they attain is 60 µ, only exceptionally are they

[Illustration: FIG. 83.--Section of the stomach of an _Anopheles_, with
cysts (oöcysts) of the malignant tertian parasite. (After Grassi).]

The sporulation (figs. 80, _21_-_25_; 84), which now follows, begins
with repeated multiple fission of the nucleus. Long before the
definitive number of nuclei, which varies with the individual, is
attained the protoplasm, according to Grassi, begins to segment around
the individual large nuclei but without separating completely into cell
areas. According to Schaudinn, however, there is a condensation of the
outstanding protoplasmic strands. It is certain that the number of
nuclei increases with simultaneous decrease in size. They soon appear
on the surface of the strands or sporoblasts, surround themselves
with some cytoplasm and then elongate (fig. 84). In this manner the
sporozoites are formed and break away from the unused remains of the
cytoplasmic strands of the sporoblasts (fig. 80, _26_). The number
of the sporozoites in an oöcyst varies from several hundreds to ten

[Illustration: FIG. 84.--Four different sporulation stages of malarial
parasites from _Anopheles maculipennis_, much magnified. _a_-_c_, of
the malignant tertian parasite; _a_, four to four and a half days after
sucking; _b_ and _c_, five to six days after sucking; _d_, of the
tertian parasite, eight days after sucking. (After Grassi.)]

  The sporulation is influenced in its duration by the external
  temperature (Grassi, Jansci, Schoo). In the tertian parasite it takes
  place quickest at a temperature of 25° to 30° C. and takes eight to
  nine days. A temperature a few degrees lower has a retarding effect
  (eighteen to nineteen days at 18° to 20° C). A still lower one has a
  restraining or even destructive effect. Temperatures over 35° C. also
  exercise a harmful effect. The malignant tertian parasite seems to
  need a somewhat higher temperature and the quartan parasite a lower

The sporozoites of the various malarial parasites show no specific
differences. They were stated by Schaudinn to occur in three forms,
and these were described as indifferent (neuter), female and male.
There is, however, little or no evidence for this hypothetical
differentiation. The last were said to perish prematurely, that is, in
the oöcyst. The others after the rupture of the oöcysts enter the body
cavity of the Anophelines, whence they are carried along in the course
of the blood. Finally they penetrate the salivary glands (fig. 80,
_27_) probably by their own activity, break through their epithelia and
accumulate in the salivary duct (fig. 80, _27_). At the next bite by
the mosquito they are transmitted to the blood-vessels of man.


  In view of the differences in opinion regarding “species” and
  “varieties,” the dispute whether the malarial parasites of man
  represent one species with several varieties, or several species is
  almost superfluous. If necessary two genera may be distinguished.

The parasites of the tertian and quartan fever are alike in that
their gametocytes have a rounded shape (figs. 80, _12_, _13_), whilst
the corresponding stages of the pernicious or malignant tertian
parasites are crescentic (figs. 81, 88). These differences are used
by some writers as the distinguishing characteristic of two genera:
_Plasmodium_, Marchiafava and Celli, 1885, for the first mentioned
species; _Laverania_, Grassi and Feletti, 1889, for the pernicious or
malignant tertian parasite. Whether there is a genuine quotidian fever
and accordingly a special quotidian parasite is still disputed.

  These parasites are treated in practical detail in Stephens and
  Christophers’ “Practical Study of Malaria,” 3rd edition, 1908.

*Plasmodium vivax*, Grassi and Feletti, 1890.

  Syn.: _Hæmamœba vivax_, Grassi and Feletti, 1890; _Plasmodium
  malariæ_ var. _tertianæ_, Celli and Sanfelice, 1891; _Hæmamœba
  laverani_ var. _tertiana_, Labbé, 1894; *Hæmosporidium tertianum*,
  Lewkowitz, 1897; _Plasmodium malariæ tertianum_, Labbé, 1899:
  _Hæmamœba malariæ_ var. _magna_, Laveran, 1900, p.p.; _Hæmamœba
  malariæ_ var. _tertianæ_, Laveran, 1901.

This species, _P. vivax_,[201] is the causal agent of the simple or
spring tertian fever and is, therefore, named directly the tertian or
benign tertian parasite (figs. 80, _3_-_8_; 85). During the afebrile
period in the patient, the young trophozoites or amœbulæ appear on or
in the red blood corpuscles as pale bodies of 1·5 µ to 2 µ diameter
which at first show only slow amœboid movements. Their nucleus is
difficult to recognize in the early stage. Soon the food vacuole is
formed and this grows concomitantly with the trophozoite and the
parasite has a ring-like appearance. Afterwards the vacuole diminishes,
and at this period the first brownish melanin granule appears. From
this time the activity and number of the pigment granules increase
with continuous growth. When the parasite has grown to about one-third
the diameter of the erythrocyte the latter shows characteristic red
Schüffner’s dots or “fine stippling,” after staining with Romanowsky’s
solution. Later, after about twenty-four hours, the blood corpuscles
begin to grow pale, then to increase in size, and after thirty-six
hours, that is, about twelve hours before the next attack of fever,
schizogony of the parasite is initiated by the division of the nucleus.
The parasite at this time occupies half to two-thirds of the enlarged
blood corpuscle. The daughter nuclei continue dividing until sixteen,
and occasionally twenty-four, daughter nuclei are produced. The pigment
which, up till now lies nearer the periphery, moves to the middle,
while the nuclei lie nearer the surface.

[201] See Schaudinn, F. (1902), _Arb. a. d. kaiserl. Gesundheits._,
xix, pp. 169–250, 3 plates.

[Illustration: FIG. 85.--Development of the tertian parasite in the red
blood corpuscles of man; on the right a “Polymitus.” (After Mannaberg.)
See also fig. 80, _3_--_7_.]

Around each nucleus a portion of cytoplasm collects and thus young
merozoites are produced. These separate from each other and from the
little residual masses[202] which contain the melanin and pass from
the blood corpuscles, which now can hardly be recognized, to the blood
plasma, where they soon attack new erythrocytes.

[202] The pigment masses (melanin or hæmozoin) are taken up by the
leucocytes, particularly the mononuclear ones, and are carried
especially to the spleen, and also to the liver and the bone-marrow.
From this circumstance arises the well-known pigmentation of the spleen
in persons who have suffered from malaria.

The migration of the merozoites initiates a new attack of fever and two
groups of tertian parasites in the blood, differing in development by
about twenty-four hours, are the conditions for febris tertiana duplex.

After a lengthy duration of fever the gametocytes (figs. 80, _9_--_12_)
appear. They are uninucleate. The microgametocytes are about the size
of fully developed schizonts, the macrogametocytes are somewhat larger.
Their further development takes place in Anophelines.

The chief distinctive characteristics of the simple tertian parasite,
as seen in infected blood, are:--(1) The infected red-cell is usually
enlarged; (2) the presence of fine red granules known as Schüffner’s
dots in the red blood corpuscles, after Romanowsky staining; (3)
the fragile appearance of the parasite compared with other species.
Large forms are pigmented, irregular and “flimsy-looking,” sometimes
appearing to consist of separate parts. Irregularity of contour is

Ahmed Emin[203] (1914) has described a small variety of _P. vivax_.

[203] _Bull. Soc. Path. Exot._, vii, p. 385.

*Plasmodium malariæ*, Laveran.

  Syn.: _Oscillaria malariæ_, Laveran, p.p., 1883; _Hæmamœba malariæ_,
  Gr. et Fel., 1890; _Plasmodium malariæ_ var. _quartanæ_, Celli et
  Sanfel., 1891; _Hæmamœba laverani_ var. _quartana_, Labbé, 1894;
  _Hæmosporidium quartanæ_, Lewkowitz, 1897; _Plasmodium malariæ
  quartanum_, Labbé, 1899; _Plasmodium golgii_, Sambon, 1902;
  _Laverania malariæ_, Jancso, 1905 nec Grassi et Fel. 1890; _Hæmomœba
  malariæ_ var. _quartanæ_; Lav., 1901.

_Plasmodium malariæ_ is the parasite of quartan malaria (fig. 86). The
trophozoites of the quartan parasite differ from the corresponding
stages of the tertian parasite in that their motility is less and
soon ceases. They differ also in their slower growth, by the early
disappearance of the food vacuole, by the more marked formation of
the dark brown pigment, and by the fact that the red blood corpuscles
attacked are not altered either in colour or size.

[Illustration: FIG. 86.--Development of the quartan parasite in the red
corpuscles of man--asexual stages. (After Manson.)]

When the parasites have grown almost to the size of the erythrocytes
schizogony occurs. The pigment granules arrange themselves in lines
radiating towards the centre and the merozoites are also radially
disposed in groups of 6, 8, 10 or even 12, but are often arranged less
regularly. The whole development, growth and schizogony, occupies
seventy-two hours.

The appearance of quartana duplex or triplex is conditional on the
presence in the blood of the patient of two or three groups of
_Plasmodia_ differing in their development by twenty-four hours.

The chief distinctive characters of the quartan parasite are: (1)
The erythrocyte is unchanged in size; (2) the rings are compact and
show pigment early; in the larger forms the chromatin is dense and
relatively plentiful; (3) the pigment, which is relatively well-marked,
may be arranged at the periphery.

*Laverania malariæ*, Grassi and Feletti, 1890 = *Plasmodium
falciparum*, Welch, 1897.

  Syn.: _Plasmodium malariæ_ var. _quotidianæ_, Celli et Sanf., 1891;
  _Hæmamœba malariæ præcox_, Gr. et Fel., 1892 (nec _H. præcox_,
  Gr. et Fel., 1890); _Hæmamœba laverani_, Labbé, 1894; _Hæmatozoön
  falciparum_, Welch, 1897; _Hæmosporidium undecimanæ_ and _H.
  sedecimanæ_ and _H. vigesimo-tertianæ_, Lewkowitz, 1897; _Hæmamœba
  malariæ parva_, Lav., 1900; _Plasmodium præcox_, Dofl., 1901;
  _Plasmodium immaculatum_, Schaud., 1902; _Plasmodium falciparum_,
  Blanch., 1905.

The names most commonly used for the parasite of malignant tertian
malaria are _Plasmodium falciparum_ and _Laverania malariæ_.

The summer and autumn fever (_febris æstivo-autumnalis_), also called
malignant tertian or sub-tertian, is caused by a malarial parasite
which is distinguished by the small size of its schizont, while the
gametocytes are crescentic (figs. 81, 88).

  Most authors identify this kind of fever or the parasites which
  cause it (_Laverania malariæ_) with the pernicious malaria of the
  tropics. Ziemann, however, repeatedly has drawn attention to certain
  small but definite differences between the usual malignant tertian
  or pernicious parasites which occur in the tropics and the tropical
  parasites of some malarial districts, particularly of West Africa,
  and insists that at least two varieties or sub-species occur. Other
  investigators distinguish from this or these forms a quotidian
  parasite. On the other hand, the assertion is made that there are no
  specific differences, but that the malignant or pernicious tertian
  parasite which normally needs forty-eight hours for its development
  in the blood of man, can also develop in twenty-four hours. The
  establishment of the duration of the development is a matter of
  especial difficulty, because the stages of schizogony are far less
  numerous in the peripheral blood than in that of the internal
  organs. It is also stated that the tropical parasite very seldom
  forms crescentic but rather rounded gametocytes. According to such
  an observation the organism would belong to _Plasmodium_ and not to
  _Laverania_. The question whether the tropical fevers are caused by
  two different parasites does not seem to be definitely settled.

The young trophozoite of the malignant, pernicious tertian, or
sub-tertian parasite (fig. 87) are but slightly active and are very
small, even after the formation of the comparatively large food
vacuole, which makes the body appear annular (“signet ring” stage).
Often two and even more parasites are found in one blood corpuscle.

Fully grown they only attain two-thirds or less of the diameter of
the erythrocytes, which display an inclination to shrink and then
appear darker than the normal (brass-coloured). In the early stage
dots or stippling--sometimes called Maurer’s dots--appear on the blood
corpuscles as in those attacked by the ordinary tertian parasite
(_Plasmodium vivax_), but the Maurer’s dots are relatively coarse and
few, and are not easily stained. These dots were first described by
Stephens and Christophers in 1900, and subsequently by Maurer in 1902.

About thirty hours after the entrance into the blood corpuscles, the
parasites are rarely found in the peripheral blood, but they are
present in the internal organs, and especially in the spleen. The
schizogony, which now begins in the internal organs, proceeds on the
same lines as that of the quartan parasite, that is, usually with the
merozoites radially arranged around a central agglomeration of dark
brown pigment.

[Illustration: FIG. 87.--The pernicious malignant or sub-tertian
parasite in the red corpuscles of man, asexual stages. (After Manson.)]

The number of merozoites formed is quoted differently, _e.g._, 8 to
24, on an average 12 to 16. However, according to the recent cultural
researches of J. G. and D. Thomson[204] (1913) the number of merozoites
of _P. falciparum_ is 32. D. Thomson, from examination of spleen smears
at autopsy, also concludes that the number of merozoites may reach 32.
During their formation the blood corpuscle which is attacked gets paler
and disintegrates.

[204] _Proc. Roy. Soc._, B, lxxxvii, p. 77.

[Illustration: FIG. 88.--The crescents of the malignant tertian
parasite. (After Mannaberg.) See also fig. 81.]

The gametocytes which finally appear are attenuated, curved bodies,
rounded at each end and known as crescents (figs. 81, 88), and are
provided with a nucleus and with coarse pigment masses. In the males
the pigment is more scattered than in the females, where it is around
the nucleus. Their length is 9 µ to 14 µ, and their breadth is 2 µ to
3 µ. At first they are still in the pale blood corpuscles, later they
free themselves and are found in numbers in the peripheral blood in
cases of pernicious malaria of Southern Europe and the tropics, while,
on the other hand, they occur much more rarely in the peripheral blood
in West African malignant tertian. Their further development takes
place under the same conditions as in the other malarial parasites.

[Illustration: FIG. 89.--Section through a tubule of the salivary gland
of an _Anopheles_ with sporozoites of the malignant tertian parasites;
on the left at the top a single sporozoite greatly magnified. (After

D. Thomson (1914),[205] from studies of autopsy smears, has shown that
crescents develop chiefly in the bone-marrow and spleen, and take
about ten days to grow into the adult state in the internal organs.
He believes that crescents are produced from ordinary asexual spores.
Quinine, he states, has no direct destructive action on crescents, but
it destroys the asexual source of supply.

[205] _Annals Trop. Med. and Parasitol._, viii, p. 85.

The sporozoites of _Laverania malariæ_ (_P. falciparum_) are
represented in fig. 89.

The principal distinctive characters of the malignant tertian parasite
are: (1) The ring forms are very small, occasionally bacilliform, and
may be marginal (“accolé” of Laveran); (2) the larger trophozoites
are often ovoid, and about one-third or one-half of the erythrocyte
in size; (3) the infected red cells sometimes show coarse stippling
(Maurer’s dots); (4) the gametocytes, or sexual forms, are crescentic
in shape.

J. W. W. Stephens (1914) has described a new malarial parasite of
man; it is called _Plasmodium tenue_. It is very amœboid, with scanty
cytoplasm and much chromatin, sometimes rod-like or irregular. The
parasite was described from a blood-smear of an Indian child. The
creation of a new species for this parasite has been criticized by
Balfour and Wenyon, and by Craig.

*Plasmodium relictum*, Sergent, 1907.

  Syn.: _Plasmodium præcox_, Grassi and Feletti, 1890; _Plasmodium
  danilewskyi_, Gr. et Fel., 1890; _Hæmamœba relicta_, Gr. et Fel.,
  1891; _Proteosoma grassii_, Labbé, 1894.

  Hæmamœboid, pigment-producing, malarial parasites are often found in
  birds. Like the human malarial parasites they have been variously
  named. Labbé created the genus _Proteosoma_ for them, and this name
  is still often used as a distinctive one unofficially. The correct
  name is stated to be either _Plasmodium relictum_ or _P. præcox_,
  or possibly even _P. danilewskyi_, assuming that there is only one
  species. The nomenclature of the malarial parasites is most confused.
  The avian malarial parasites are transmitted by Culicine mosquitoes.

  The organism was discovered by Grassi in the blood of birds in Italy,
  and causes a fatal disease in partridges in Hungary. Sparrows are
  affected in India, and it was this Plasmodium in which Ross first
  traced the development of a malarial parasite in a mosquito. The
  parasite may be transmitted from bird to bird by blood-inoculation,
  canaries being very susceptible.

  The principal stages of the avian plasmodium closely resemble those
  of the malarial parasites of man. In its earliest stage _P. relictum_
  is unpigmented, but soon the trophozoite grows and becomes pigmented,
  meanwhile displacing the nucleus of the avian red-blood corpuscle,
  a characteristic feature, distinguishing it from _Halteridium_.
  Schizonts are formed, each of which gives rise to about nine
  merozoites in the circulating blood. Sexual forms or gametocytes also
  occur in the blood. These develop in _Culex fatigans_, _C. pipiens_
  and _C. nemorosus_. Oökinetes or vermicules are formed in twelve
  to fifteen hours in the stomach of the mosquito, and in one to two
  days well-developed round oöcysts may be seen. In three to four days
  sporoblasts have formed within the oöcysts and young sporozoites
  begin to develop. In nine to ten days the oöcysts are mature, being
  filled with sporozoites. The oöcysts then burst and the sporozoites
  travel through the thoracic muscles to the salivary glands of the

  Neumann, experimenting with canaries, found that _Stegomyia fasciata_
  could transmit the infection, but less efficiently than species of


The successful cultivation of malarial parasites _in vitro_ was first
recorded by C. C. Bass and by Bass and Johns (1912).[206] Since then,
J. G. and D. Thomson,[207] and McLellan (1912–13), Ziemann[208] and
others have repeated the experiments.

[206] _Journ. Exptl. Med._, xvi, p. 567.

[207] _Annals Trop. Med. and Parasitol._, vi, p. 449; vii, pp. 153, 509.

[208] _Trans. Soc. Trop. Med. and Hyg._, vi, p. 220.


               |                  |                  |_Laverania malariæ_
    Character  |    _Plasmodium   |_Plasmodium vivax_|   _Plasmodium
               |     malariæ_     | (Benign tertian) |    falciparum_
               |     (Quartan)    |                  |(Malignant tertian)
  Schizogony   |Complete in       |Complete in forty-|Complete in forty-
               | seventy-two      | eight hours      | eight hours
               | hours            |                  | or less
  Trophozoite  |Smaller than _P.  |Young trophozoite |Young trophozoite
               | vivax_larger than| large.           | small
               | _L. malariæ_     |                  |
               |Pseudopodia not   |Long pseudopodia  |
               | marked or long   |                  |
  Movements    |Rather slow in    |Active amœboid    |Sometimes actively
               | immature forms   | movements        | motile
  Pigment      |Coarse granules,  |Fine granules,    |Granules fine and
               | peripherally     | with active      | scanty, movement
               | arranged, little | movement         | oscillatory
               | movement         |                  |
  Schizont     |Smaller than red  |Larger than red   |Smaller than red
               | corpuscle        | blood corpuscle  | corpuscle
  Merozoites   |6 to 12 forming   |15 to 20 regularly|8 to 32 (according
               | rosette          | arranged         | to different
               |                  |                  | authors) arranged
               |                  |                  | irregularly
  Gametocytes  |Spherical         |Spherical         |Crescentic
  Distribution |About equal number|Larger numbers in |Scanty in periph-
   of          | in peripheral and| visceral blood   | eral blood com-
   parasites in| visceral blood   |                  | pared with the
   vertebrate  |                  |                  | enormous numbers
   host        |                  |                  | in the internal
               |                  |                  | organs. The latter
               |                  |                  | part of the cycle
               |                  |                  | (schizogony) may
               |                  |                  | occur in the in-
               |                  |                  | ternal organs only
  Alterations  |Almost normal     |Pale and          |Corpuscle may be
   in          |                  | hypertrophied.   | shrunken and dark,
   erythrocytes|                  |Schüffner’s dots  | or may be colour-
               |                  | seen in deeply   | less. Maurer’s
               |                  | stained specimens| coarse dots some-
               |                  |                  | times seen

Essentially the method of cultivation, as used by Thomson, is
as follows: 10 c.c. of infected blood are drawn from a vein and
transferred to a sterile test tube, in which is a thick wire leading
to the bottom of the tube. One-tenth of a cubic centimetre of a 50 per
cent. aqueous solution of glucose or dextrose is placed in the test
tube, preferably before adding the blood. The blood is defibrinated
by stirring gently with the wire. When defibrination is complete the
wire and the clot are removed, and the glucose-blood is transferred,
in portions, to several smaller sterile tubes, each containing a
column of blood about one inch in height. The tubes are plugged and
capped and then transferred, standing upright, to an incubator
kept at a temperature of 37° C. to 41° C. The blood corpuscles soon
settle, leaving a column of serum at the top, to the extent of about
half an inch in each tube. The leucocytes need not be removed by
centrifugalization. J. G. Thomson (1913) and his collaborators did not
find it necessary to destroy the complement in the serum, and they
found that the malarial parasites developed at all levels in the column
of corpuscles, and not merely on the surface layer of the corpuscles as
first stated by Bass and Johns.

So far only the asexual generation of the malarial parasites has been
grown _in vitro_. Thomson rarely observed hæmolysis in the cultures.
Clumping of the malignant tertian parasites occurred. In cultures of
the benign tertian parasite (_Plasmodium vivax_) clumping was not
observed. J. G. and D. Thomson consider that this difference as regards
clumping explains why only young forms of malignant tertian are found
in peripheral blood, as the clumping tendency of the larger forms
causes them to be arrested in the finer capillaries of the internal
organs. It also explains the tendency to pernicious symptoms, such as
coma, in malignant tertian malaria. Further it was found from cultures
that _P. falciparum_ was capable of producing thirty-two spores
(merozoites) in maximum segmentation, while _P. vivax_ produced sixteen
spores (merozoites) as a rule, though the number might be greater than
sixteen. (Quartan parasites produce eight spores or merozoites in

It may also be mentioned here that _Babesia_ (_Piroplasma_) _canis_ has
been successfully cultivated _in vitro_ by Bass’s method. This has been
accomplished by Thomson and Fantham,[209] Ziemann, and Toyoda in 1913.
J. G. Thomson and Fantham used the simplified Bass technique recorded
above, namely, infected blood and glucose, incubating at 37° C. In
one of the _B. canis_ cultures, starting with heart blood of a dog
containing corpuscles infected with one, two, or, exceptionally, four
piroplasmata, Thomson and Fantham succeeded in obtaining a maximum of
thirty-two merozoites in a corpuscle. The cultures are infective to
dogs and sub-cultures have been obtained.

[209] _Annals Trop. Med. and Parasitol._, vii, p. 621.

Family. *Piroplasmidæ*, França.

The parasites included in this provisional family or group belong
to the Hæmosporidia. They are minute organisms, sometimes amœboid,
but usually possessing a definite form. They are endoglobular, being
contained within mammalian red blood corpuscles, but they produce no
pigment. The true Piroplasmata, belonging to the genus _Babesia_,
destroy the host corpuscles, setting free the hæmoglobin, which is
excreted by the kidneys of the cow, sheep, horse, dog, etc., acting
as host. The disease produced, variously called piroplasmosis or
babesiasis, is consequently characterized by a red coloration of the
urine known as hæmoglobinuria, or popularly as “red-water.” One of the
best known piroplasms is _Piroplasma bigeminum_ or _Babesia bovis_
(probably the latter name is correct), which is the causal agent of
“Texas fever” or “red-water” in cattle and is spread by ticks.

[Illustration: FIG. 90.--_Nuttallia equi_, life-cycle as seen in red
blood corpuscles in stained preparations of peripheral blood. (After
Nuttall and Strickland.)]

Of recent years, researches on the morphology of these blood parasites
has led to their separation into various genera and species. However,
our knowledge is still very far from complete. The various genera
recognized by França[210] (1909), and placed in a provisional family,
Piroplasmidæ, may be listed, though further research may lead to

[210] _Arch. Inst. Bact. Camara Pestana_, iii, p. 11.

(1) _Babesia_ (Starcovici) or _Piroplasma_ (Patton). Pyriform
parasites, dividing by a special form of budding or gemmation with
chromatin forking, as well as by direct binary fission. Parasitic in
oxen, dogs, sheep, horses, etc.

(2) _Theileria_ (Bettencourt, França and Borges). Rod-shaped and oval
parasites occurring in cattle and deer. _T. parva_ is the pathogenic
agent of African East Coast fever in cattle.

(3) _Nuttallia_ (França). Oval or pear-shaped parasites, with
multiplication in the form of a cross. _N. equi_[211] (fig. 90) of
equine “piroplasmosis” (nuttalliosis). _N. herpestidis_ in a mongoose.

[211] _Parasitology_, v (1912), p. 65.

(4) _Nicollia_ (Nuttall). Oval or pear-shaped parasites with
characteristic nuclear dimorphism, and with quadruple division at first
fan-like, then like a four-leaved clover. _N. quadrigemina_ from the

(5) _Smithia_ (França). Pear-shaped, single forms stretching across the
blood corpuscle. Multiplication into four in the form of a cross. _S.
microti_ from _Microtus arvalis_, _S. talpæ_ from the mole.

(6) _Rossiella_ (Nuttall). This belongs to the family Piroplasmidæ
of França. It is intracorpuscular and non-pigment forming, occurring
singly, in pairs, or occasionally in fours. It is usually round and
larger than Babesia. The parasite multiplies by binary fission. _R.
rossi_ in the jackal.

The genus _Babesia_ is the best known and most important, and will be
considered next.

Genus. *Babesia*, Starcovici, 1893.

  Syn.: _Pyrosoma_, Smith and Kilborne, 1893; _Apiosoma_, Wandolleck,
  1895; _Piroplasma_, W. H. Patton, 1895; _Amœbosporidium_, Bonome,

The organisms belonging to this genus are pyriform, round or amœboid.
The characteristic mode of division is as follows: Just before division
the parasite becomes amœboid and irregular in shape, (fig. 91, _1–5_)
with a compact nucleus. The latter gives off a nuclear bud. This
nuclear bud divides into two by forking (fig. 91, _6_, _7_). The
chromatin forks grow towards the surface of the body of the rounded
parasite, and then two cytoplasmic buds grow out. The forking nuclear
buds, which are *Y*-shaped, pass into the cytoplasmic outgrowths[212]
(fig. 91, _8_, _9_). The buds gradually increase in size at the
expense of the parent form until they become two pear-shaped parasites
joined at their pointed ends. The connecting strand shrinks and the
two daughter forms separate (fig. 91, _10–14_). The pyriform parasites
after having exhausted the blood corpuscle escape from it (fig. 91,
_15_), and seek out fresh host corpuscles, entering by the rounded,
blunt end (fig. 91, _1_). It is the pyriform phase of the parasite
which penetrates red blood corpuscles, not rounded forms, which
die if set free. The pyriform parasite, however, becomes rounded
(fig. 91, _2_, _3_), soon after its entry into a fresh host cell. This
interesting mode of division by gemmation and chromatin forking has
been made diagnostic of the genus _Babesia_ by Nuttall.[213] Rounded
forms of _Babesia_ divide by binary fission, and this direct method can
also be adopted by the other forms of Babesia.

[212] Nuttall and Graham-Smith, _Journ. Hyg._, vii, p. 232.

[213] “Piroplasmosis,” Herter Lectures, _Parasitology_, vi, p. 302.

[Illustration: FIG. 91.--_Babesia_ (_Piroplasma_) _canis_, life-cycle
in stained preparations of infected blood of dog. (After Nuttall and

  The distribution of the chromatin in the pear-shaped _Babesia_,
  as seen in _B. canis_ and _B. bovis_, is interesting. The main
  nuclear body consists of a karyosome surrounded by a clear area.
  There is also a loose (chromidial) mass of chromatin representing
  the remains of the chromatin forks seen during the formation of the
  parasite as a daughter form by gemmation. Occasionally there is
  a small dot or point, the so-called “blepharoplast” of Schaudinn
  and Lühe. This minute dot is not a flagellate blepharoplast, for
  there is no flagellate stage in the life-history of Babesia. These
  nuclear phenomena have been described by Nuttall and Graham-Smith
  and Christophers (1907)[214] for _B. canis_, by Fantham (1907)[215]
  for _B. bovis_, and by Thomson and Fantham (1913) from glucose-blood
  cultures of _B. canis_.

[214] _Sci. Mems. Govt. India_, No. 29.

[215] _Quart. Journ. Microsc. Sci._, li, p. 297.

Babesia are tick borne, as was first shown by Smith and Kilborne
(1893). The developmental cycle in the tick is incompletely known. The
best accounts are those of Christophers (1907)[216] for _B. canis_ and
Koch (1906) for _B. bovis_, and these accounts are supplementary. The
principal stages, so far as known, may be summarized thus:--

[216] _Sci. Mems. Govt. India_, No. 29.

  (1) The piroplasms taken by the tick in feeding on blood pass into
  the tick’s stomach. The pyriform parasites, which alone are capable
  of further development, are set free from the blood corpuscles. In
  about twelve to eighteen hours they become amœboid, sending out long,
  stiff, slender, pointed pseudopodia. The nucleus of each parasite
  divides unequally into two. Similar forms have been obtained in
  cultures. These stellate forms may be gametes, and according to Koch
  fuse in pairs.

  (2) A spherical stage follows, possibly representing the zygote. This
  grows, and a uninucleate globular mass results. This form is found in
  large numbers on the third day, according to the observations of Koch.

  (3) A club-shaped organism is next formed. This may represent an
  oökinete stage. The club-shaped bodies are motile and gregarine-like,
  and are about four times the size of the blood forms. These
  club-shaped bodies and subsequent stages were described by
  Christophers in the development of _B. canis_ in the dog-tick,
  _Rhipicephalus sanguineus_.

  (4) The club-shaped bodies pass from the gut of the tick into the
  ovary, and so get into the ova. There they become globular, and later
  are found in the cells of the developing tick-embryo. The parasites
  are, then, transmitted hereditarily. Similar globular bodies are
  found in the tissue cells of the body of tick nymphs which have
  taken up piroplasms. The globular stage was called the “zygote” by
  Christophers, but it may correspond to the oöcyst of Plasmodia.

  (5) The globular body divides into a number of “sporoblasts,” which
  become scattered through the tissues of the larval or nymphal tick,
  as the case may be.

  (6) The sporoblasts themselves divide into a large number of
  sporozoites, which are small uninucleate bodies, somewhat resembling
  blood piroplasms. The sporozoites collect in the salivary glands of
  the tick. They are inoculated into the vertebrate when the tick next

The chief species of _Babesia_ and their pathogenic importance may be
listed thus:--

(1) _Babesia bovis_ (Babes) produces infectious hæmoglobinuria of
cattle in Europe and North Africa. It is transmitted by _Ixodes
ricinus_. A similar parasite also occurs in deer.

(2) _Babesia bigemina_ (Smith and Kilborne) produces Texas fever,
tristeza, or red-water in cattle in North and South America, South
Africa and Australia. It is transmitted by _Boöphilus annulatus_ in
North America, by _B. australis_ in Australia, South America, and the
Philippines, and by _B. decoloratus_ in South Africa.

The parasite is from 2 µ to 4 µ long, and from 1·5 µ to 2 µ broad.

_Babesia bigemina_ may be the same parasite as _B. bovis_.

(3) _Babesia divergens_ (MacFadyean and Stockman) is a small parasite.
It is found in cattle suffering from red-water in Norway, Germany,
Russia, Hungary, Ireland, Finland, and France, and is transmitted by
_Ixodes ricinus_.

(4) _Babesia canis_ (Piana and Galli-Valerio) gives rise to malignant
jaundice or infectious icterus in dogs in Southern Europe, India,
and other parts of Asia and North Africa, where it is transmitted by
_Rhipicephalus sanguineus_. In Africa generally, especially South
Africa, the disease is transmitted by _Hæmaphysalis leachi_. _Babesia
canis_ varies from 0·7 µ to 5 µ, the size depending partly on the
number of parasites within the corpuscle. It averages about 3 µ. It
has been cultivated in Bass’ medium (glucose and infected blood), see
p. 172.

In India _Piroplasma gibsoni_ (Patton) infects hunt dogs and jackals.
It is annular or oval in shape.

(5) _Babesia ovis_ (Babes) produces “Carceag,” a disease of sheep in
Roumania, the Balkan Peninsula, Italy, and Transcaucasia. It varies in
size from 1 µ to 3 µ. It is transmitted by _Rhipicephalus bursa_. The
parasite has recently been recorded from Rhodesia.

(6) _Babesia caballi_ (Nuttall and Strickland) causes “biliary
fever” in equines. The parasite occurs in Russia, Roumania, and
Transcaucasia. It varies in size from 1 µ to 2 µ. It is transmitted by
_Dermacentor reticulatus_.

  It should be mentioned that _Nuttallia equi_ also causes
  “piroplasmosis” in equines, with symptoms of hæmoglobinuria and
  jaundice in Italy, Sardinia, many parts of Africa, Transcaucasia,
  India, and Brazil. In Africa it is transmitted by _Rhipicephalus
  evertsi_. It has been shown experimentally that a horse recovered
  from _Babesia caballi_ was susceptible to the inoculation of
  _Nuttallia equi_ blood.

(7) _Babesia pitheci_ (P. H. Ross) was found in a monkey,
_Cercopithecus_ sp., in Uganda. The pear-shaped forms measure 1·5 µ by
2·5 µ.

(8) _Babesia muris_ (Fantham)[217] was found in white rats. The
pyriform parasites are 2 µ to 3 µ long and 1 µ to 1·5 µ broad; oval
forms are 0·5 to 1·5 µ diameter.

[217] _Quart. Journ. Microsc. Sci._, 1, p. 493.

The usual symptoms of babesiasis (piroplasmosis) are high fever, loss
of appetite, hæmoglobinuria, icterus, anæmia, paralysis, and death in
about a week in acute cases. In chronic cases there is anæmia, and
hæmoglobinuria is less marked. When animals recover, there are still
some piroplasms left in the blood. “Recovered” or “salted” animals
are not susceptible to reinfection, but ticks feeding on them acquire
piroplasms, and are a source of danger to freshly imported animals.

  _Treatment._--Trypan-blue is the best drug, as shown by Nuttall
  and Hadwen[218] (1909). It should be administered intravenously
  in 1 to 1·5 per cent. aqueous solution. A dose of 5 to 10 c.c. is
  curative for dogs, one of 100 to 150 c.c. for horses and cattle.
  Unfortunately, the tissues are coloured blue by the drug. The
  “salted” animals, after trypan-blue treatment, still harbour the
  parasites in their blood for years.

[218] _Parasitology_, ii, p. 156.

Genus. *Theileria*, Bettencourt, França and Borges, 1907.

  The organisms belonging to this genus are rod-like or bacilliform,
  and coccoid or round.

  The best known of the species of Theileria is _T. parva_, the
  pathogenic agent of East Coast fever or Rhodesian fever in cattle in

*Theileria parva*, Theiler, 1903.

  Syn.: _Piroplasma parvum_.

In the blood corpuscles of infected cattle minute rod-like and oval
parasites are seen. Some are comma shaped and others are clubbed
(fig. 92, _1–12_). The rod-like forms measure 1 µ to 3 µ in length
by 0·5 µ in breadth; the oval forms are 0·7 µ to 1·5 µ in diameter.
The intracorpuscular parasites are said by R. Gonder (1910) to be
gametocytes, the rod-like forms being thought to be males, the oval
forms to be females. Free parasites are practically never seen in the
blood. It is known that it is impossible to produce the disease in
a healthy animal by blood inoculation, but only by intraperitoneal
transplantation of large pieces of infected spleen (Meyer). There may
be as many as eight parasites in a corpuscle. The chromatin is usually
at one end of the organism. In some parasites the appearance of the
chromatin suggests division, but such division, if it takes place, must
be very slow, as it has not been actually seen in progress. The red
blood corpuscles appear merely to act as vehicles for the parasites
(Nuttall, Fantham, and Porter).[219]

[219] _Parasitology_, ii, p. 325; iii, p. 117.

[Illustration: FIG. 92.--_Theileria parva._ 1–12, intracorpuscular
parasites, stained. (After Nuttall and Fantham); 13–18, Koch’s blue
bodies, from stained spleen smear; 17–18, breaking up of Koch’s body.
(After Nuttall.)]

  In the internal organs, especially the lymphatic glands, spleen
  and bone-marrow, are found multinucleate bodies known as Koch’s
  blue bodies (fig. 92, _13–18_). These are schizonts, according
  to Gonder.[220] The actual Koch’s blue bodies are said to be
  extracellular, but similar multinucleate bodies, schizonts, occur
  in lymphocytes. The schizonts divide and the merozoites resulting
  probably invade the red blood corpuscles in the internal organs.
  Gonder considers that the sporozoites injected by the tick collect in
  the spleen and lymphatic glands, penetrate the lymphocytes and give
  rise to the schizonts.

[220] _Zeitschr. f. Infekt. paras. Krankh. u. Hyg. d. Haustiere_, viii,
p. 406.

  Gonder has studied the cycle of _T. parva_ in the tick. He states
  that the gametocytes leave the host corpuscles and give rise to
  gametes, then conjugation occurs producing zygotes. The zygotes
  are then said to become active to form ookinetes, and to enter the
  salivary glands of the tick. Multiplication is said to occur therein,
  producing a swarm of sporozoites. This work needs confirmation.

  _T. parva_ is transmitted by _Rhipicephalus appendiculatus_, _R.
  simus_, _R. evertsi_, _R. nitens_, and _R. capensis_. The parasites
  are not hereditarily transmitted in _Rhipicephalus_, but when taken
  by the transmitter at one stage of its development the tick is
  infective in its next stage (_e.g._, if the larva becomes infected,
  then the nymph is infective; if the nymph becomes infected, then the
  adult is infective).

  An animal recovered from _Theileria parva_ is incapable of infecting
  ticks, but few animals recover from East Coast fever. Animals
  suffering therefrom do not show hæmoglobinuria.

*Theileria mutans*, Theiler, 1907·

  Syn.: _Piroplasma mutans_.

  This is transmissible experimentally by blood inoculation. It
  occurs in cattle in South Africa and Madagascar and is apparently
  non-pathogenic. No Koch’s blue bodies are formed. It is transmitted
  by ticks.

  _Theileria annulata_ (Dschunkowsky and Luhs) occurs in cattle in

  A Theileria (_T. stordii_) has been found in a gazelle (França, 1912).

Genus. *Anaplasma*, Theiler, 1910.

  This genus[221] may be mentioned here. The organisms included therein
  are, according to Theiler, coccus-like, consisting of chromatin,
  and are devoid of cytoplasm. They occur in the red blood corpuscles
  of cattle, causing a disease characterized by destruction of red
  cells, fever and anæmia, but with yellow urine. The disease is
  tick transmitted. The bodies now called _Anaplasma marginale_ were
  formerly described as marginal points. They multiply by simple
  fission. They are said by Theiler to cause gall-sickness in cattle in
  South Africa. Some authors doubt whether these bodies are organismal.

[221] _Bull. Soc. Path. Exot._, iii, p. 135.

Genus. *Paraplasma*, Seidelin, 1911.

Under this generic name Seidelin described certain bodies found
by him in cases of yellow fever in 1909. The type species is _P.
flavigenum_,[222] and is claimed by Seidelin to be the causal agent of
yellow fever.

[222] _Yellow Fever Bulletin_, i, p. 251.

_Paraplasma flavigenum_ occurs in the early days of the disease as
small chromatin granules with or without a faint trace of cytoplasm.
The bodies are usually intracorpuscular. Also, somewhat larger forms,
with distinct cytoplasm, are seen in small numbers. During the later
days of the disease still larger forms are found, and these occur
also in sections of organs (_e.g._, kidney) made post-mortem. Some of
these larger forms are perhaps schizonts. In the second period of the
disease possible micro- and macro-gametes may be found, some of which
are extracorpuscular. Some small free bodies have been seen. Recently
schizogony has been stated to occur in the lungs, and it is said that
guinea-pigs can be inoculated with _Paraplasma flavigenum_, and show
yellow pigment in the spleen.

Seidelin places _Paraplasma_ in the _Babesiidæ_, with resemblances
more particularly to _Theileria_. V. Schilling-Torgau and Agramonte
have criticized these findings; the former considers them to be the
resultant of certain blood conditions.

_P. subflavigenum_ was found by Seidelin in 1912 in a man suffering
from an unclassified fever in Mexico.

Further, it is now known that a Paraplasma occurs naturally in
guinea-pigs. More researches are needed on these matters, as some
writers (_e.g._, Wenyon and Low) claim that the bodies are not

|_Paraplasma flavigenum._--The Yellow Fever Commission (West Africa) |
|in their third report, dated 1915, have come to the conclusion that |
|there is no evidence that the bodies termed _Paraplasma flavigenum_ |
|are of protozoal nature or that they are the causal agents of yellow|
|fever.                                                              |

Sub-class. NEOSPORIDIA, Schaudinn.

Sporozoa in which growth and spore formation usually go on together.

Order. *Myxosporidia*, Bütschli.

[Illustration: FIG. 93.--Upper figure, part of a gill of a roach,
_Leuciscus rutilus_ (natural size), with two myxosporidia. Lower
figures, _a_, _b_, _d_, spores of myxosporidia from a pike, _Esox
lucius_. _c_, Spore from _Platystoma fasciatum_. (After J. Müller.)]

[Illustration: FIG. 94.--The tailless spore of _Myxobolus mülleri_,
with the polar bodies and their nuclei and the sporozoite. (After

  These parasites, which were discovered by Johannes Müller (1841),
  live principally in fishes, and occasionally cause destructive
  epizoötics amongst their hosts. Müller first observed them in
  the form of whitish-yellow pustules on the skin or on the gills
  of various fishes. These pustules contained masses of small
  shell-covered bodies with or without tails (“psorosperms,” see
  fig. 93). Similar bodies were also found in the air bladders of
  certain fish. Creplin (1842) demonstrated the resemblance of the
  cysts (“psorosperm tubes”) harbouring the psorosperms to the
  “pseudonavicella-cysts” of a gregarine, as described by v. Siebold.
  Dujardin (1845) considered that there was possibly some connection
  between the protoplasmic “psorosperm tubes” and the spores they
  contained, and the developmental stages of monocystid gregarines
  from the vesiculæ seminales of earth-worms. The relationship of the
  “fish psorosperms” was placed on a firmer basis by Leydig (1851)
  and Lieberkühn. The former found numerous forms in marine fish, and
  he discovered in species which live free in the gall bladder of
  cartilaginous fishes that the psorosperms originated in a manner
  similar to the gregarines. Lieberkühn (1854) studied the Myxosporidia
  in the bladder of the pike (fig. 93, _a_, _b_, _d_), and observed
  their amœboid movements, as well as the formation of the spores,
  from each of which a small amœboid body escaped, a discovery that
  was confirmed by Balbiani. The same author also found that spiral
  filaments were enclosed in the so-called polar body, _i.e._, the
  polar capsule of the psorosperm spores, and that these could be
  protruded (fig. 93, _d_, and fig. 95).

  The term Myxosporidia, which at the present day is universally
  applied to the “psorosperm tubes,” was introduced by Bütschli
  in 1881, who studied not only the structure and development of
  the spores, but also the protoplasmic body of the parasites
  (fig. 96), and confirmed the occurrence of numerous nuclei. Many
  authors have made important additions to our knowledge of the
  Myxosporidia: Perugia, Thélohan, Mingazzini, L. Pfeiffer, L. Cohn,
  Doflein, Mercier, Schröder and Auerbach; while the presence of this
  parasite outside the class of fishes has become known through Lutz,
  Laveran, and others. The species causing disease in fishes have been
  described by Ludwig, Railliet, Weltner, L. Pfeiffer, Zschokke, Hofer,
  Doflein, Gurley, Plehn, Schuberg, Fantham and Porter. With regard to
  classification the works of Thélohan (1895) and Gurley (1894) may be

[Illustration: FIG. 95.--Schematic representation of a spore of
_Myxobolus_. One polar capsule has protruded its filament; two nuclei
and a “vacuole” in the sporozoite. (After Doflein.)]

[Illustration: FIG. 96.--_Chloromyxum leydigi._ Active trophozoite
(parasitic in gall-bladder of skates, rays, dog-fish). _Ect_,
ectoplasm; _ps_, pseudopodia; _end_, endoplasm; _y_, yellow globules in
endoplasm; _sp_, spores, each with four polar capsules. × 525. (After

  The Myxosporidia live either free on the epithelial surface of hollow
  organs (gall or urinary bladder, renal tubules, but never in the
  intestine), or are enclosed in the tissues of their host. The gills
  and muscular system are their favourite habitat, but other tissues or
  organs may be attacked. Species of Myxosporidia are also known from
  Amphibia, Reptilia, and a few invertebrates.

  The free forms, which are often amœboid (fig. 96), move by the
  aid of variously shaped pseudopodia, have a constant form, or may
  exhibit contractions of the body. The tissue parasites often reach
  a considerable size, so that the integument of the host forms
  protuberances over them. They are of a roundish or irregular shape.
  Frequently they are enveloped in a connective tissue covering formed
  by the host.

  The protoplasmic body in the trophic phase (fig. 96) shows a distinct
  ectoplasm which is finely granular or sometimes striated, and an
  endoplasm which is coarsely granular and contains many nuclei as
  well as cell inclusions, such as crystals, pigment grains and fat
  globules. The nuclei originate by division from the primitive nucleus
  of the amœboid germ that issues from the spore. This amœbula may
  or may not live intra-cellularly during the early stages of its

  The multinucleate trophozoite of a Myxosporidian forms spores in
  its endoplasm practically throughout its whole period of growth
  (fig. 96). Vegetative reproduction by a process of external budding
  or plasmotomy may also occur, as in _Myxidium lieberkühni_ from the
  urinary bladder of the pike.

  The myxosporidian trophozoite may produce two spores within
  itself, when it is placed in the sub-order _Disporea_, or it may
  produce numerous spores, which is characteristic of the sub-order,
  _Polysporea_. The phenomenon of spore formation is not simple
  (fig. 97), and the spore itself is surrounded by a bivalved shell or
  sporocyst and contains polar capsules in addition to the amœboid germ
  (fig. 97, G, H). The valves of the sporocyst and the polar capsules
  are really differentiated nucleate cells, so that each spore is an
  aggregate of cells rather than one cell, though only a single amœbula
  issues from a spore. The accounts of spore formation vary somewhat
  according to the different workers.

  Spore formation is usually very complicated and there are differences
  of opinion as to the interpretation of various stages, particularly
  as to whether conjugation occurs therein. The process is initiated
  by the concentration of cytoplasm around one of the nuclei of the
  endoplasm, so that a small spherical mass or initial corpuscle is
  produced, the pansporoblast (Gurley) or primitive sphere (Thélohan).
  Some authors state that a pansporoblast really results from a
  conjugation of two initial corpuscles (fig. 97, A-D). Nuclear
  multiplication occurs within the pansporoblast (fig. 97, E), and
  sooner or later two multinucleate sporoblasts are formed within it
  (fig. 97, F). Each sporoblast gives rise to a single spore, which
  consists of a sporocyst or envelope composed of two valves each
  secreted by a cell, two polar capsules each secreted by a cell, and
  the sporoplasm or amœbula which becomes binucleate (fig. 97, G).
  During the process of spore formation (fig. 97) various vegetative
  and reduction nuclei may be produced, in addition to those which are
  essentially involved in spore formation, and the sporocyst cells may
  be developed early.

[Illustration: FIG. 97.--_Myxobolus pfeifferi._ Spore formation.
A, reproductive cell from plasmodial trophozoite; B, cell divided
unequally into two; C, smaller cell forming envelope to larger one; D,
pansporoblast formed by union of two forms like C; E, multinucleate
pansporoblast, two of the nuclei being those of the envelope; F,
pansporoblast divided into two multinucleate sporoblasts; G, spore
differentiation; _p_, two parietal cells forming sporocyst; _bc_, polar
capsules; _am_, binucleate amœbula; H, ripe spore in which the two
nuclei of the amœbula have fused. (After Keysselitz.)]

  Each spore contains two (figs. 94, 95) or more polar capsules which
  are clearly visible in the fresh condition. Each polar capsule is
  a hollow, more or less pear-shaped body, secreted by a cell and
  having a well defined contour. Within it, a long, delicate, elastic
  filament, the polar filament, is formed, and lies spirally coiled
  in the polar capsule until just before the emergence of the amœbula
  from the spore (fig. 95). The polar filament is ejected, probably
  under the influence of the digestive juice, when the spore reaches
  a new host, and serves to anchor the spore to the tissue with which
  it is in contact, and thus allow of the emergence of the amœbula in
  a situation suitable for its development. The polar capsule with its
  contained polar filament has been compared with the stinging cells or
  nematocysts of the Cœlentera, but it has a totally different function.

  The spores fulfil the purpose of effecting transmission to other
  hosts. Infection occurs by the ingestion of the parasites per os
  after their escape by some means from their host. Thélohan and
  others have demonstrated that the valves of the spores soon open
  under the influence of the digestive juices, thus allowing the young
  myxosporidia to escape. Their further history is unknown; but it may
  be surmised that they either travel direct to the organs usually
  affected (gall bladder, urinary bladder), or are distributed in the
  body by means of the circulatory or lymphatic systems.

  The Myxosporidia that invade tissues are often deadly to their
  hosts. They may be present in a state of “diffuse infiltration”
  when practically every organ of the body may be infected, as in
  barbel disease (due to _Myxobolus pfeifferi_). On the other hand,
  the parasites may be concentrated at one spot, when cysts, either
  large or small, are produced. Such cysts occur on the gills of many
  fishes. A few additional important pathogenic forms are _Myxobolus
  cyprini_, the excitant of “pockenkrankheit” of carp, and _Lentospora
  cerebralis_, parasitic in the skeleton of Salmonidæ and Gadidæ.
  The skeletons of the tail, fins and skull particularly are seats
  of infection, and from the skull the Lentospora can spread to the
  semicircular canals, resulting in loss of power to maintain its
  balance on the part of the fish. On this account the malady is
  termed “drehkrankheit.” Young fish are more particularly infected.
  _Myxobolus neurobius_ infects the spinal cord and nerves of trout.

  Myxosporidia are divided into two sub-orders--_Disporea_ and
  _Polysporea_--according to whether they form only two or several
  spores during their growth. The former include two genera limited to
  fishes, which are easily distinguishable by the shape of the spores:
  _Leptotheca_, Thél., with a rounded spore, and _Ceratomyxa_, Thél.,
  with a very elongate spore. The larger number of genera belong to the
  _Polysporea_, which are divided into three families:

    (1) Amœboid germ with a vacuole  {(a) With two polar capsules.--
          the contents of which do   {        _Myxidiidæ._
          not stain with iodine.     {(b) With four polar capsules.--

    (2) Amœboid germ with a vacuole stainable with iodine. Spores with
          two polar capsules.--_Myxobolidæ._

  For further subdivisions the differences in the spores are
  principally utilized.

Order. *Microsporidia*, Balbiani.

  These are the organisms discovered in the stickleback by Gluge in
  1834, and in _Coccus hesperidum_ by Leydig in 1853. They have since
  been found in numerous other arthropods, especially insects. They
  acquired particular importance when it was discovered that they
  were the cause of the “pébrine” disease (“gattina” of the Italians)
  which caused so much destruction amongst silkworms (_Bombyx mori_).
  Pasteur (1867–70) and especially Balbiani (1866) participated in the
  researches on _Nosema bombycis_, and it was the latter who classed
  the “pébrine bodies” or “psorospermia of the arthropoda” amongst the
  Sporozoa as Microsporidia (1882).[223] The complete life cycle of
  _N. bombycis_ was described in 1909 by Stempell. The Microsporidia
  are not confined to insects and arachnoids, they are now known to
  occur also in crustacea, worms, bryozoa, fishes, amphibians and
  reptiles. Certain tumours in fishes, similar to those formed by many
  Myxosporidia, are produced by Microsporidia. Fantham and Porter found
  that _Nosema apis_ was pathogenic to bees and other insects, and
  was the causal agent of the so-called “Isle of Wight” disease in
  bees[224] in Great Britain.

[223] _C. R. Acad. Sci._, Paris, xcv, p. 1168.

[224] _Annals Trop. Med. and Parasitol._, vi, pp. 145–214, 3 pls.

  The Microsporidia, as their name implies, form minute spores which
  usually are oval or pear-shaped. Each spore contains a single polar
  capsule which is not easily visible in the fresh state (fig. 98, _f_)
  and a single amœboid germ issues from the spore (fig. 99, _b_).

[Illustration: FIG. 98.--_Nosema apis._ Various stages in life-cycle.
_a_, planonts or amœbulæ from chyle stomach of bee; _b_, amœboid
planont creeping over surface of gut epithelial cell; _c_, uninucleate
trophozoite within epithelial cell; _d_, meront with nucleus divided
into four, about to form four spores; _e_, epithelial cell crowded
with spores; _f_, young spore; _g_, spore showing five nuclei, polar
filament ejected, and amœbula, about to issue. × 1,500, _a-e_; × 2,150,
_f-g_. (After Fantham and Porter.)]

  The life cycle of _Nosema apis_, parasitic in bees, may be taken
  as an example of that of a microsporidian. The infection of the
  host is initiated by the ingestion of spores of _N. apis_ in food
  or drink contaminated with the excrement of other infected bees.
  Under the influence of the digestive juice of the bee the spore-coat
  (sporocyst) softens, the polar filament is ejected and anchors the
  spore to the gut epithelium, and the minute amœbula contained in the
  spore emerges. The amœbula is capable of active amœboid movements
  (fig. 98, _b_) and so is termed the planont or wandering form
  (fig. 98, _a_). After a short time each planont penetrates between
  or into the cells of the epithelium of the gut, a few only passing
  through into the body cavity. Within the cells the amœbulæ become
  more or less rounded, lose their power of movement, and after a
  period of growth of the trophozoite (fig. 98, _c_) commence to divide
  actively, these dividing forms being known as meronts (fig. 98,
  _d_). Various forms of fission occur, and during this phase, termed
  merogony, the numbers of the parasite within the host are greatly
  increased, with concomitant destruction of the epithelium (fig. 98,
  _e_). After a time sporogony commences. The full-grown meront becomes
  successively the pansporoblast and sporoblast. Nuclear multiplication
  and differentiation ensue and five nuclei are ultimately produced. At
  the same time a sporocyst is secreted, and two vacuoles are produced
  within. One is the polar capsule, and within it the polar filament
  is differentiated; the other forms the posterior vacuole (fig. 98,
  _g_). Between the two vacuoles the body cytoplasm or sporoplasm forms
  a girdle-like mass. Of the nuclei, one regulates the polar capsule,
  two control the secretion of the sporocyst, and two remain in the
  sporoplasm. The polar capsule and polar filament are not usually
  visible in the fresh condition, but can be demonstrated by the use
  of various chemical reagents (fig. 100). The sporoplasm ultimately
  becomes the amœbula (fig. 98, _g_) which issues from the spore after
  the ejection of the polar filament.

[Illustration: FIG. 99.--_a_, section through the abdominal wall of
a silkworm, whose epithelial cells contain Microsporidia (_Nosema
bombycis_); _b_, a spore, the contents of which are escaping. (After

[Illustration: FIG. 100.--_Nosema bombycis_, Naeg. Spores treated with
nitric acid, thus rendering the polar capsule perceptible, and the
filament has protruded from one of the spores. (After Thélohan.)]

  A trophozoite (meront) of _N. apis_ becomes a single pansporoblast
  which gives rise to one sporoblast producing one spore, and this
  procedure is characteristic of the genus _Nosema_. In other genera
  the trophozoite may form more than one pansporoblast and each
  pansporoblast may form a variable number of spores in different
  cases. Various attempts at classification have been based on these
  characteristics. It must suffice here to note that in the cases where
  the trophozoite becomes one pansporoblast, the latter can produce
  four spores in the genus _Gurleya_, eight spores in _Thélohania_ and
  many spores in _Pleistophora_. In other cases, where the trophozoites
  give rise to many pansporoblasts, each of the latter may form many
  spores, as in the genus _Glugea_.

  A few pathogenic microsporidian parasites other than _N. apis_ may
  be mentioned. _N. bombycis_, causing pébrine in silkworms, may
  infect any or all the tissues of the host (fig. 99). The larvæ of
  the host, _i.e._, the “silkworms,” may become infected by eating
  food contaminated with spore-containing excrement of already
  infected silkworms. In cases of heavy infection the silkworm dies,
  but should the infection be less intense the larva becomes a pupa
  in which the parasite persists, so that the moth emerges from the
  cocoon already infected. Not only is the moth parasitized itself,
  but the Nosema reaches the generative organs of both sexes and
  penetrates the ovaries of the female, with the result that the ova
  are deposited infected. Such infected eggs are capable of developing,
  so that infection may be transmitted hereditarily as well as by the
  contaminative method. Infected eggs can be recognized by microscopic
  examination, as Pasteur showed, and thus preventive measures may be

  A microsporidian parasite is known to occur on the roots of the
  spinal and cranial nerves of _Lophius piscatorius_, the angler fish.
  This parasite is variously referred to the genera _Nosema_ and

  _Thélohania contejeani_, parasitic in the muscles of crayfish, is
  believed by some to be the causal agent of recent epizoötics among
  them, though others believe the disease to be really due to a
  bacillus. It may be that the one organism aids in the entry of the
  other into the host.

Order. *Actinomyxidia*, Stolč.

  A brief mention may be made of the Actinomyxidia (fig. 101), which
  were first described by Stolč in 1899 as parasites of Oligochætes.
  They have also been investigated by Mrazek, and a detailed study
  of certain species was made by Caullery and Mesnil (1905). The
  trophozoite is small and amœboid. The spores are large, and exhibit
  tri-radiate symmetry. Spore formation is complicated and sexual
  processes occur therein. Many amœbulæ are set free from each spore.

[Illustration: FIG. 101.--Spore of _Hexactinomyxon psammoryctis_. At
top of figure three polar capsules, one with polar filament extended.
× 450. (After Stolč.)]

Order. *Sarcosporidia*, Balbiani.

  The first member of this group was discovered by Miescher in 1843.
  This author found white filaments running parallel with the direction
  of the fibres in the voluntary muscles of mice. They were visible
  to the naked eye, and proved to be cylindrical tubes tapering at
  each end. They were as long as the muscular fibres, were enveloped
  in a membrane, and contained innumerable elongate or kidney-shaped
  bodies and a smaller number of little spherical forms. Th. v.
  Hessling confirmed (1853) the occurrence of these “Miescher’s tubes”
  within the muscular fibres, this author having discovered the same
  structures in the heart muscles of deer, cattle, and sheep. Both
  investigators considered them to be pathological transformations of
  the muscles. v. Siebold, from his own experiences, regarded them as
  fungus-like entophytes.

  Rainey (1858) discovered similar structures in the muscular system
  of pigs, and considered them to be early stages of _Cysticercus
  cellulosæ_, which error Leuckart rectified, simultaneously
  emphasizing their relationship with Myxosporidia. Both these authors
  found them in the muscular fibres, and both observed that they
  possessed a thick striated membrane. Manz (1867) published the
  results of more minute investigations on the structure and contents
  of the cylinders. This observer also recognized the disease in
  rabbits and attempted to cultivate the parasites. He also tried to
  induce experimental infection in guinea-pigs, rats, and mice, but the
  result was negative.

  However, domestic and wild mammals are not the only hosts of
  Sarcosporidia; these parasites are also harboured by birds. Thus,
  according to Kühn, they are found in the domestic fowl; according
  to Rivolta in _Turdus_, _Corvus_, and other birds; according to
  Stiles in North American birds; while Fantham found Sarcosporidia
  in the African mouse-bird, _Colius_. Reptiles also are parasitized
  occasionally. Bertram found them in the gecko, Lühe in the
  wall-lizard. It was found also that the Sarcosporidia could develop
  not only in the muscles but also in the connective tissue. This
  led to the foundation of a new, but provisional, classification by
  Blanchard, using the generic name _Miescheria_ for the parasites
  in the muscles and _Balbiania_ for those in the connective tissue.
  Finally, Sarcosporidia have also been observed in man.

  The relation of these parasites to certain diseases of domestic
  animals has been studied by veterinary surgeons. Sarcosporidia may
  cause fatal epizoötics among sheep.

  There is still a wide field open for research in regard to the
  structure and development of these parasites, and the manner in which
  the hosts become infected.

[Illustration: FIG. 102.--Longitudinal section of a muscle of the
domestic pig, with _Sarcocystis miescheriana_. × 30. (After Kühn.)]

[Illustration: FIG. 103.--Transverse section of the muscle of a pig,
with _Sarcocystis miescheriana_. × 38. (After Kühn.)]

The Sarcosporidia usually appear as elongate, cylindrical, or fusiform
bodies, rounded at both extremities and of various lengths and breadths
(fig. 102). In some species they may be from 16 mm. to 50 mm. long, as
in the sheep and roebuck. These bodies are the so-called sarcocysts or
Miescher’s tubes. They lie in transversely striated muscular fibres
which they distend more or less. The forms found in the connective
tissue are apparently parasites which originally inhabited the muscular
fibres, and only on disintegration of the fibres reached the connective
tissue, where they grow to large oval or globular bodies (fig. 105).
The mammalian muscles usually infected are those of the œsophagus,
larynx, diaphragm, body-wall, and the psoas muscles. The skeletal
muscles may be affected in acute cases, as well as those of the tongue
and eye. The heart muscles are sometimes parasitized.

  In fresh material cut into thin slices the parasites are
  frequently recognizable, even with the naked eye, because of their
  yellowish-white colour. Under the microscope they appear to be
  coarsely granular (fig. 103). Beginners may find some difficulty
  in distinguishing them from other foreign bodies, such as dead and
  calcified encapsuled Trichinæ, or from Cysticerci that have died
  and become calcified in the early stages, more particularly as the
  Sarcosporidia also occasionally may become calcified.

The Sarcosporidia are always enveloped in a membrane, which is
probably formed at an early stage. In a few cases it remains thin
and simple, in other cases a radially striated ectoplasmic layer is
present (figs. 104, 108), which has been variously described. From the
inner integument, which may be homogeneous or fibrous, thick or thin,
membranes or trabeculæ pass into the interior of the body, forming
anastomosing partitions, and so producing a system of chambers of
various sizes that do not communicate with one another (figs. 104,
108). These chambers are occupied by sickle- or bean-shaped bodies
(spores or sporozoites), or various developmental stages of them.
The oldest spores are found in the centre of the Miescher’s tubes or
trophozoites. If they are not liberated they die there, so that the
central chambers of the tube are empty and hollow.

[Illustration: FIG. 104.--_Sarcocystis miescheriana_ from pig. Late
stage in which body is divided into numerous chambers or alveoli, each
containing many spores. (From Wasielewski, after Manz.)]

In the youngest Sarcosporidia (40 µ in length) from the muscles of
the sheep there occur, according to Bertram, small roundish or oval
cells (4 µ to 5 µ), the nuclei of which are half their size, and are
embedded in a granular protoplasmic mass. In somewhat larger, and
therefore older, cylinders, the investing membrane of which already
shows both layers, the cells have become larger (to 7 µ) and are more
sharply outlined from each other (fig. 106). These uninucleate cells
may be considered as pansporoblasts. In each pansporoblast division
of the nucleus occurs (fig. 107), and meanwhile the pansporoblasts
become isolated within the chambers, the dividing partitions of which
originate from the granular protoplasm which is present between the
pansporoblasts. The numerous uninucleate daughter forms produced within
the chambers become spores direct (fig. 108).

The process commences in the centre of the cylinders or sarcocysts,
and then progresses towards the extremities, the parasites meanwhile
increasing in size, and new pansporoblasts being continually formed at
the extremities (fig. 107).

[Illustration: FIG. 105.--Transverse section of _Sarcocystis tenella_,
Raill. From the œsophagus of the sheep, _Ovis aries_. × 38. _a_,
marginal chambers filled with spores; _b_, connective tissue of the
œsophagus; _c_, muscles of the œsophagus.]

[Illustration: FIG. 106.--Young _Sarcocystis tenella_ of the sheep,
47 µ in length. (After Bertram.)]

[Illustration: FIG. 107.--End of a trophozoite of _Sarcocystis
miescheriana_ from the diaphragm of the pig, showing division in
pansporoblasts. × 800. (After Bertram.)]

[Illustration: FIG. 108.--_Sarcocystis blanchardi_ of the ox.
Longitudinal section of sarcocyst or Miescher’s tube. _a_, substance
of muscle fibre; _b_, envelope of sarcocyst; _c_, muscle nuclei; _d_,
spores in chambers; _e_, ground substance. × 400. (From Wasielewski,
after van Eecke.)]

The spores (sometimes called Rainey’s corpuscles), vary in shape
according to the species, but are also of different form individually.
They are mostly kidney-, bean- or sickle-shaped (fig. 109), and of
small size, sometimes reaching 14 µ by 3 µ to 5 µ. They are apparently
surrounded by a thin membrane, and at one extremity (according to the
discovery of L. Pfeiffer, confirmed by van Eecke, Laveran and Mesnil)
contain an obliquely striated body (fig. 109) often homologized with
the polar capsule, while the greater part of the spore is taken up by
the nucleate sporozoite. Several authors state that they have also
observed filamentous appendages (polar filaments) at one end of the
spores, and have seen two kinds of spores in the same Sarcosporidium.
Spores of various species of Sarcosporidia may contain metachromatic
granules, often centrally placed (fig. 109). These granules may be
metabolic or possibly may contain toxin (see below).

[Illustration: FIG. 109.--Spores of _Sarcocystis tenella_, Raill. _a_,
fresh, showing the polar capsule; _b_, stained, showing metachromatic
granules and nucleus. × 1,000. (After Laveran and Mesnil.)]

The gymnospores of _Sarcocystis muris_, from the mouse, show active
boring movements when kept in saline solution warmed to 35° or 37° C.
_S. muris_ is very deadly to its host. From their structure the
spores do not appear to have great powers of resistance to external
conditions. They measure 12 µ by 3 µ to 4 µ or less.

Laveran and Mesnil (1899) isolated a toxin from _S. tenella_ of
the sheep and called it sarcocystin. This substance is especially
pathogenic to experimental rabbits.

The duration of life of the Sarcosporidia is a comparatively long
one. The affected muscular fibres may remain intact and capable of
performing their functions for a long time, but at last they perish,
if the host lives long enough. Thus the Sarcosporidia of the muscles
are then enveloped only by sarcolemma, and finally, when this likewise
disappears, they fall into the intra-muscular connective tissue.
In many cases the Sarcosporidia die off within their hosts, this,
according to Bertram, being brought about by a disintegration of the
spores in the central chambers. In other cases the leucocytes play a
part in the destruction of the Sarcosporidia, and sometimes it happens
that lime salts are deposited in and around the vacant cylinders.

In some places pigs, sheep, mice and rats are infected with
sarcosporidiosis to a remarkable extent, in certain cases almost
reaching 100 per cent. Young animals also are infected, and perhaps
infection only takes place during youth.

Although the natural mode of transmission of the Sarcosporidia remains
to be determined, yet various experimental researches on the problem
are of interest and importance. Theobald Smith (1901) found that mice
could be experimentally infected with _S. muris_ by feeding them with
the flesh of other infected mice. The incubation period was a long one,
namely forty to fifty days. Thus, on the forty-fifth day after feeding
young Sarcosporidia were found, and seventy days after feeding spore
formation began. Ripe spores were found two and a half to three months
after the commencement of these experiments. This mode of infection--a
cannibalistic one--hardly seems likely to be the natural method for the
infection of sheep and ruminants generally. Smith’s researches have
been confirmed. Nègre[225] (1910) found that the fæces of mice fed on
infected muscular tissue were infective to other mice when ingested by
them. Negri[226] infected guinea-pigs with _S. muris_ by feeding them
on infected mouse flesh, and found that the parasite in guinea-pigs
showed different characters from those exhibited by it in mice.
Darling[227] also succeeded in infecting guinea-pigs with _S. muris_,
and Erdmann infected mice with _S. tenella_ (from the sheep).

[225] _C. R. Soc. Biol._, lxviii, p. 997.

[226] _Centralbl. f. Bakt._, Orig., xlvii, p. 612; see also xlvii,
p. 56; lv, p. 373.

[227] _Journ. Exptl. Med._, xii, p. 19.

According to Erdmann[228] (1910) the Sarcosporidian spore germinates
in the intestine of the host, which has recently ingested infected
material. The spore liberates its contained toxin--sarcocystin--which
acts upon the adjacent intestinal epithelium, whereby the latter is
shed, and an amœbula creeps out of the spore. The amœbula is able to
penetrate the denuded area and get directly into the lymph-spaces of
the submucous coat of the intestine. The first period of development,
lasting some twenty-eight to thirty days, is said to be passed in the
lymph-spaces of the intestine. Later the amœbula reaches a muscle
fibre. Writing in May, 1914, Erdmann[229] records the appearance of
small amœboid and schizogony forms six days after infection of the
host. Crawley[230] (1913) controverts some of these statements and
considers that the Sarcosporidian spore, still sickle-shaped, bores its
way into the epithelial cells of the intestine and comes to rest there.
The spore then becomes round or elliptical, and peripheral masses of
chromatin appear within it, suggesting schizogony. This happens about
twelve hours after feeding, and in twenty-four hours the spores appear
to have left the intestine. More recently (May, 1914), Crawley[231]
considers that there is sexual differentiation among the Sarcosporidian
spores, a few hours after their ingestion by the host.

[228] _Sitz. Gesell. naturf. Freunde zu Berlin_, p. 377.

[229] _Proc. Soc. Exper. Biol. and Med._, xi, p. 152.

[230] _Science_, xxxvii, p. 498.

[231] _Proc. Acad. Nat. Sci._, Philadelphia, May, 1914, p. 432.

Interesting discussions have occurred as to the site of the toxic
sarcocystin within the spore. Metachromatic granules occur in the
middle of the Sarcosporidian spore (fig. 109), and the toxin may be
contained in these grains, as they disappear, according to Erdmann,
before the amœbula penetrates the denuded intestinal wall. However, a
polar capsule, containing a polar filament, may be present at one end
of a Sarcosporidian spore. Laveran and Mesnil described a striated
area at the more pointed end of the spore of _S. tenella_, which area
they consider to represent a polar capsule. Fantham[232] (1913) found
a vacuole-like, polar capsule area in the spores of _S. colii_ from
the African mouse-bird. The sarcocystin may be contained in the polar
capsule. The nucleus of the spore is generally at the opposite, blunter

[232] _Proc. Cambr. Philosoph. Soc._, xvii, p. 221.

Again, various authors have stated that Sarcosporidian spores may occur
in the blood of the host at times. If so, then an intermediate host may
be concerned in their transmission. Perrin suggested that Sarcosporidia
might be spread by blow-flies and flesh-flies.

The classification of the Sarcosporidia as proposed by R. Blanchard,
which was based on their various habitats, can no longer hold, because
the same species may occur in the muscles as well as in the connective
tissue. For the present, the few species that are known may be placed
in one genus, _Sarcocystis_, Ray Lankester, 1882.

The following species of _Sarcocystis_ are of interest:--

_S. miescheriana_, Kühn, 1865, in the pig.

_S. bertrami_, Doflein, 1901, in the horse.

_S. tenella_, Railliet, 1886, in sheep. _S. tenella bubali_ in
buffaloes in Ceylon and Egypt.

_S. blanchardi_, Doflein, 1901, in cattle.

_S. muris_, Blanchard, 1885, in the mouse, to which it is lethal.

_S. hueti_, Blanchard, 1885, in the seal.

_S. colii_, Fantham, 1913, in the African mouse-bird, _Colius

Also various Sarcosporidia from antelopes, monkeys, opossum, birds, the
gecko and wall-lizard are known.

The spores of _S. muris_, _S. bertrami_, _S. tenella_, and _S. colii_
can multiply by longitudinal fission.


(1) Lindemann[233] found on the valves and in the myocardium of a
person who had died of dropsy certain brownish masses, 3 mm. in length
and 1·5 mm. in breadth which he regarded as gregarines. If these were
actually independent animal organisms it may be suggested that they
were Sarcosporidia. Rivolta (1878) named the species _S. lindemanni_.

[233] “Ueb. d. hyg. Bdtg. d. Gregarinen,” _Dtsche. Ztschr. f.
Staatsarzneikunde_, 1868, xxvi, p. 326.

(2) Rosenberg[234] found a cyst 5 mm. in length and 2 mm. in breadth
in a papillary muscle of the mitral valve of a woman, aged 40, who had
died from pleuritis and endocarditis. The cyst contained no scolex nor
hooklets of tænia. Numerous small refracting bodies, round, oval or
kidney-shaped, were found in a daughter cyst, as well as sickle-shaped
bodies. The description hardly appears to indicate Sarcosporidia.

[234] “Ein Befund von Psorosp. in Herzmusk d. Menschen,” _Ztschr. f.
Hygiene_, 1892, xi, p. 435.

(3) Kartulis[235] observed Miescher’s cylinders of various sizes in the
liver (?) and in the muscular system, of a Sudanese who had succumbed
to multiple abscesses of the liver and abdominal muscles. This may be
considered as the first actual case of the occurrence of Sarcosporidia
in man. Koch in 1887 described a case in Egypt.

[235] Kartulis, “Ueb. pathog. Protoz. b. Menschen,” _Ztschr. f. Hyg.
u. Inf._, 1893, xiii, p. 1. Compare also Braun, M., _Die Thier. Par.
d. Mensch._, 2nd Edit., Wrzbg., 1895, p. 92; Braun, M., “Z. Vork. d.
Sarcosp., b. Menschen,” _Centralbl. f. Bakt._ 1895, xviii, p. 13.

(4) The case reported by Baraban and St. Remy[236] was at once
demonstrated as certain. It related to a man who had been executed,
and in the laryngeal muscles of whom Sarcosporidia were found; the
length of the parasites varied between 150 µ and 1,600 µ, their breadth
between 77 µ and 168 µ. The affected muscular fibres were distended
to four times their normal thickness. This species was described by
Blanchard as “_Miescheria_” _muris_, but according to Vuillemin, it was
more probably _Sarcocystis tenella_ of the sheep.

[236] “Sur un cas de Tub. Psorosp. ob. chez l’homme,” _C. R. Soc.
Biol._, Paris, 1894 (x), I, p. 201. “Le Parasitisme d. Sarcosp. chez
l’homme,” _Bibliogr. Anat._ 1894, p. 79.

(5) Vuillemin has also described a case of Sarcosporidia found in the
muscles of a man who died from tubercle at Nancy. The author considered
that the parasite corresponded to _S. tenella_.

(6) Darling[237] (1909) found Sarcosporidia in the biceps of a negro
from Barbados.

[237] _Arch. Internal Med._, III, p. 183.

The Myxosporidia, Microsporidia, Actinomyxidia and possibly the
Sarcosporidia may be included within the section *Cnidosporidia*
(Doflein), since they possess spores containing polar capsules.

Order. *Haplosporidia*, Caullery and Mesnil.

  The Haplosporidia are a group of organisms having both a simple
  structure and life-history. The simplicity may represent a primitive
  condition or may be due to degradation resultant on parasitism, and
  thus it is possible that the group is not a homogeneous one. The
  order Haplosporidia was created by Caullery and Mesnil in 1899, and
  includes parasites of rotifers, annelids (fig. 110), crustacea, fish,
  prochordates and man. They may be present in the body cavity or
  alimentary tract, and can also occur in the septum nasi of man, in
  the nervous system of Cephalodiscus, and in tumours of fish.

  As the name implies, the spores of the Haplosporidia are simple,
  without polar capsules, and are uninucleate. In some genera, _e.g._,
  _Haplosporidium_, _Urosporidium_ (fig. 111) there is a spore-coat
  or sporocyst which may be elongate or spiny. The developmental
  cycle of a Haplosporidian, such as _Haplosporidium_ or _Bertramia_,
  begins with a small, uninucleate cell, often rounded, possessing a
  cell membrane that may be prolonged into processes. Growth takes
  place, coupled with an increase in the number of nuclei, so that a
  multinucleate trophozoite is produced. Later, this multinucleate
  trophozoite becomes segmented into a number of ovoid or spherical
  pansporoblasts, which give rise to few (one to four) spores. Such a
  spore, when set free, begins the life cycle over again.

  More recently (1905–1907) two important organisms have been
  described and included in this group, namely, _Neurosporidium
  cephalodisci_[238] (Ridewood and Fantham) from the nervous system
  of the prochordate, _Cephalodiscus nigrescens_, and _Rhinosporidium
  kinealyi_ (or _seeberi_) from the septum nasi of man. In the case of
  _Rhinosporidium_ and _Neurosporidium_, after the uninucleate spore
  has grown into a multinucleate trophozoite, the latter segments into
  uninucleate pansporoblasts, as in the preceding cases. A difference
  then occurs, for each pansporoblast enlarges, its nucleus divides
  and a “spore-morula” is formed. Thus a multinucleate pansporoblast
  or spore-morula, divided into many uninucleate sporoblasts (spore
  mother cells) is produced, and each sporoblast without further change
  becomes a uninucleate spore.

[238] _Quart. Journ. Microsc. Sci._, li, p. 81.

  The Haplosporidia have therefore been divided by Ridewood and Fantham
  (1907)[239] into two sections:--

[239] See Fantham, _Brit. Assoc. Reports_, 1907, p. 553.

  (1) The _Polysporulea_, wherein the pansporoblast gives rise to
  a number of spores (nine or more), _e.g._, _Rhinosporidium_,

  (2) The _Oligosporulea_, wherein the pansporoblasts give rise
  each to a few (four) spores or to only a single spore, _e.g._,
  _Haplosporidium_, _Bertramia_, _Cœlosporidium_, _Ichthyosporidium_.

[Illustration: FIG. 110.--_Haplosporidium heterocirri._ Section
throughout wall of the Polychæte worm, _Heterocirrus viridis_, showing
various developmental stages of the Haplosporidium. × 550. (After
Caullery and Mesnil.)]

[Illustration: FIG. 111.--Haplosporidian spores. _a_, _b_,
_Haplosporidium heterocirri_. _a_, fresh; _b_, after immersion in sea
water; _c_, _d_, _Urosporidium fuliginosum_. × 1000. (After Caullery
and Mesnil.)]

*Rhinosporidium kinealyi*, Minchin and Fantham, 1905.

_Rhinosporidium kinealyi_, parasitic in man, must now be considered in
greater detail. This organism was found in nasal polypus in India, and
has since been recorded from the ear as small nodules in the external
auditory meatus. The Indian cases came from the neighbourhoods of
Calcutta and Madras, and the parasite has been seen in Ceylon. Similar
structures have since been described from the United States and South

The Rhinosporidium polypus is said not to be particularly painful,
though nasal forms must interfere with breathing to some extent. The
first nasal polyp reported from India formed a vascular pedunculated
growth on the septum nasi and was about the size of a large pea or
raspberry. It was compared with a raspberry, being red in colour with a
number of small whitish dots upon its surface. When the tumour was cut,
a number of similar whitish dots were seen within. These were the cysts
of Rhinosporidium. According to Minchin and Fantham[240] (1905), they
vary considerably in size and measure up to 200 µ or 250 µ in diameter.
Each possesses a cyst wall which varies in thickness in different
cysts. Its outer wall is always firm and distinct, the inner limit
being less definite at times. Each large cyst is filled with numbers of
spherical or oval bodies, showing every gradation between small ones at
the periphery and large ones at the centre (fig. 112). Roughly, three
zones of parasites can be distinguished in a large cyst, a peripheral
set consisting of the youngest parasites, an intermediate group and a
central, oldest zone. A large cyst may possess a pore for the egress of
its contents. Some of the cysts show polar distribution of the zones.

[240] _Quart. Journ. Microsc. Sci._, xlix, p. 521.

The youngest forms of Rhinosporidium are difficult to detect. They are
small, granular masses, round, ovoid or irregular and at times even
amœboid in appearance. These are young trophozoites. They increase in
size, but encystment occurs early, the outer layer becoming firm so
that the organisms have a definite contour. Each is soon multinucleate
and the cytoplasm segments around the nuclei. The cyst thus becomes
full of uninucleate pansporoblasts or sporonts, with a peripheral
layer of undifferentiated protoplasm. The pansporoblasts grow in size.
In the larger cysts the formation of pansporoblasts progresses at
the expense of the peripheral layer of protoplasm, which, however,
continues to grow, so that the cyst as a whole increases in size. The
pansporoblasts at first are uninucleate (fig. 112, _a_), and then
undergo nuclear multiplication. This is well seen in the intermediate
zone of parasites, where the pansporoblasts show first one, then two,
then four or more spores (fig. 112, _b_), while in the oldest centrally
placed pansporoblasts, about a dozen or sixteen closely packed spores
(fig. 112, _c_), can be seen. The spore is small and rounded, and its
nucleus is clear and distinct. The fully formed pansporoblast or spore
morula becomes surrounded by a membrane.

Certain of the cysts have been found in a ruptured condition, whereby
the spores have been liberated into the surrounding tissue. It is
almost certain that the spores serve for the auto-infection of the
host, for though the tumours of Rhinosporidium seemed to have been
removed entirely, it has been found that they recur, some minute
fragment of the parasite having probably been left behind. The method
whereby the parasite reaches new hosts has not yet been determined,
and it would be of interest if its life-history could be more fully

[Illustration: FIG. 112.--_Rhinosporidium kinealyi._ Portion of ripe
cyst containing pansporoblasts of various ages. × 480. (After Minchin
and Fantham.)]

The Asiatic specimens of _R. kinealyi_ were first described in detail
by Minchin and Fantham (1905) from material briefly reported to the
Laryngological Society of London in 1903, by O’Kinealy. Material
obtained by Dr. Nair, of Madras, was described by Beattie[241] in 1906.
This material came from Cochin. Castellani and Chalmers have found
similar polypi in Ceylon.

[241] _Journ. Pathol. and Bacteriol._, xi, p. 270; and _Brit. Med.
Journ._, Nov. 16, 1907, p. 1402.

Wright[242] has described the parasite from Memphis, Tennessee.
Seeber[243] in 1896 described nasal polypi in Buenos Ayres, and in
1900 Wernicke named the parasite therein _Coccidium seeberi_. Seeber’s
parasite is a Rhinosporidium, _R. seeberi_, and may ultimately be found
to be the same as _R. kinealyi_. Ingram[244] reports Rhinosporidium
cysts, with pores in the cyst walls, in conjunctival polypus and in
papilloma of the penis in India. Zschokke has reported the presence of
_Rhinosporidium_ in horses in South Africa.

[242] _New York Med. Journ._, December 21, 1907, p. 1149.

[243] _La Ciencia Medica_ (Buenos Ayres), 1912.

[244] _Lancet_, September 3, 1910, p. 726.

Class IV. *INFUSORIA*, Ledermüller, 1763.

The Infusoria (or Heterokaryota, Hickson, or Ciliophora, Doflein)
include the Ciliata and the Suctoria. A few authorities, including
Braun, raise the Suctoria (or Acinetaria) to separate rank as a class,
but this is not widely followed.

The body of the Ciliata usually is bilaterally symmetrical and is
enveloped in a cuticle which has numerous openings for the protrusion
of the cilia. Most kinds have a fixed shape, whilst changes in the form
of others are brought about by the contractions of the body substance.
The latter exhibits hyaline ectoplasm, in which myonemes, and
occasionally also trichocysts (minute spindle-shaped bodies) appear,
and granular endoplasm which may contain numerous vacuoles. The cilia,
on whose various arrangements the classification is based, are always
processes of the ectoplasm. Their form varies; they may be hair-like,
or more rarely thorn-like, spur-like, or hook-shaped; undulatory
membranes also may occur, which are probably composed of fused cilia.

With the exception of some of the parasitic species, an oral cavity,
peristome or cytostome, is always present. It is frequently beset with
cilia or provided with undulatory membranes, which help to waft the
food inwards; sometimes there is an anal aperture (cytopyge) generally
placed at the opposite pole of the organism. A cytopharynx fringed with
cilia or sometimes with a specialized supporting apparatus is connected
with the peristome. Vacuoles form round the ingested food, and in many
species a constant rotation goes on in the endoplasm. Often one, and
sometimes two contractile vacuoles are present, the frequency of the
pulsations of which depends on the surrounding temperature. Sometimes
special conducting channels lead to the vacuoles, or there are outlet
channels leading to the exterior.

There is in almost every case a large nucleus (macronucleus), and lying
close up to it a small nucleus (micronucleus). The form of the large
nucleus varies according to the species. Numerous nuclei are not very
common, but these occur in _Opalina_, which lives in the hind-gut of
amphibia, and is also distinguished by the absence of an oral aperture.

Reproduction is effected by binary fission; less commonly, after
encystment, by multiple division, or by budding. The divisions can
be repeated many times, but finally cease, and then the conjugation
of two specimens brings about a regeneration, particularly of the
nuclei. Numerous examinations (Bütschli, Hertwig, Maupas, Calkins) have
demonstrated that after two individuals have associated by homologous
parts of the body, the micronucleus separates from the macronucleus,
becomes larger and divides twice by mitosis, so that four micronuclei
are present in each one of the two individuals forming the couple.
Three of these nuclei perish and become absorbed, the fourth gradually
passes to the portion of protoplasm connecting the two conjugants,
which has originated by absorption of the cuticle at the point of
contact of the conjugants. After a further division one micronucleus of
each conjugant passes over into the other conjugant, and fusion ensues
between the two micronuclei of each individual. Complicated changes and
divisions may occur, but only the main principles can be noted here.
A new nuclear body is thus formed in each conjugant, and soon divides
into two. Of the segments thus produced one becomes a micronucleus, and
one or several of the others, as the case may be, form or amalgamate
into a new macronucleus, the old macronucleus usually perishing or
becoming absorbed during the conjugation. Usually, sooner or later,
the two conjugants separate, or may have separated already, and again
multiply independently by fission until a series of divisions by simple
fission is again followed by conjugation. The theoretical significance
of conjugation cannot be dealt with fully here. It may be remarked,
however, that the macronucleus plays no part in it, but governs
entirely the metabolism of the Infusorian, whereas the micronucleus is
essentially a generative nucleus from which macro- and micro-nuclei are
again and again produced.

Encystment amongst the Infusoria is very general, and is essentially
a means of protection when the surrounding medium dries up. Doubtless
these cysts are frequently carried long distances by the wind, which
explains the wide geographical distribution of most species. Also,
multiplication often takes place in the encysted condition.

Some Infusoria live a free life, others are sedentary; the latter
form colonies in fresh as well as in salt water. Numerous species are
parasites of various lower and higher animals,[245] and a few also are
parasitic in man.

[245] It may be stated that numerous peculiarly shaped species live
in the stomach of ruminants, others in the colon of horses. Several
species are found in the rectum of frogs and toads; others, again, on
the surface of the bodies of fishes; and various other species exist in
and on the bodies of invertebrate animals.

The Prague zoologist, v. Stein, introduced a classification of the
Infusoria that has been almost universally adopted. It is founded on
the different position of the cilia on the body. Though, no doubt,
artificial, it is a convenient system. Bütschli has compiled a better
one.[246] But for our purpose Stein’s system is sufficient:--

[246] Bronn’s _Cl. u. Ordn. d. Thierr._, i, Protozoa, Part 3, Infusoria.

  Order 1. _Holotricha_, Infusoria with cilia that are evenly
  distributed over the entire body.

  Order 2. _Heterotricha_, ciliated all over like the _Holotricha_, but
  having stouter cilia about the peristome.

  Order 3. _Hypotricha_, only ciliated on the ventral surface.

  Order 4. _Peritricha_, with only a ring of spiral cilia, mostly

The Infusoria observed in man belong to the order _Heterotricha_, with
few exceptions.

Genus. *Balantidium*, Claparède et Lachmann.

  Heterotrichous Infusoria of oval or bag-like form and almost circular
  on transverse section; the anterior extremity narrowed, the posterior
  end broad and rounded off, or also narrowed; the peristome starting
  at the anterior end is broadest there and becomes narrower as it
  gradually obliquely approaches towards the posterior extremity. There
  are coarse cilia along the entire left border and the anterior part
  of the right border. Longitudinal striation is distinct and regular.
  There are two contractile vacuoles on the right, and occasionally
  also two or more to the left. The anus (cytopyge) is terminal. The
  macronucleus is usually horse-shoe or kidney-shaped, sometimes oval;
  the micronucleus contiguous. Reproduction is by binary fission and
  conjugation, and encystment occurs. The cysts are spherical or oval.
  These ciliates are parasitic in the large intestine of human beings
  and pigs, in Amphibia, and in the body cavity of polychæte Annelida.

*Balantidium coli*, Malmsten, 1857.

  Syn.: _Paramæcium coli_, Malmsten, 1857.

[Illustration: FIG. 113.--_Balantidium coli._ _a_, nucleus; _b_,
vacuole; _c_, peristome; _d_, bolus of food. (After Leuckart.)]

[Illustration: FIG. 114.--_Balantidium coli_, free and encysted;
_a_, anus or cytopyge; _n_, macronucleus; _b_, bolus of food. (After
Casagrandi and Barbagallo.)]

The body is oval, 60 µ to 100 µ in length (up to 200 µ according to
Janowski), and 50 µ to 70 µ in breadth. The peristome is funnel-shaped
or contracted, the anterior end being then broadened or pointed
according to the degree of contraction (figs. 113, 114). The ecto- and
endo-plasm are distinct, the latter is granular, containing drops of
fat and mucus, granules of starch, bacteria, and occasionally also red
and white blood corpuscles. There are usually two contractile vacuoles,
seldom more. The anus (cytopyge) opens at the posterior extremity. The
macronucleus is bean- or kidney-shaped, rarely oval; the micronucleus
is spherical.

_Balantidium coli_ lives in the large intestine of man, in the rectum
of the domestic pig, and has been found in monkeys. It propagates by
transverse division, but conjugation and encystment are known to take
place.[247] Transmission to other hosts is effected by the cysts of the
parasite (fig. 114).

[247] According to Gourvitch (“Bal. coli. Darmk. d. Menschen,” _Russ.
Arch. f. Path., klin. med. u. Bact._, Petrograd, 1896), the conjugated
Balantidia are supposed to fuse with each other and form oval cysts
two or three times the size of the free organisms, and to divide into
numerous globules within the cystic membrane; the process, however, has
hitherto not been confirmed. The supposed Balantidium cysts appeared in
two patients who were simultaneously suffering from _Dibothriocephalus
latus_, after the administration of anthelminthics. It therefore seems,
according to the description, that in reality these forms were actually
abnormally large, possibly swollen, young eggs of the tape-worm

_Balantidium coli_, first seen by Leeuwenhoek, was described by
Malmsten in 1857 in a man aged 35 years, who had two years previously
suffered from cholera, and since then had been subject to diarrhœa. The
examination showed an ulcer in the rectum above the mid sphincter ani,
in the sanguineous purulent secretion of which numerous Balantidia were
swimming about. Although the ulcer was made to heal, the diarrhœa did
not cease and the stools contained numerous Balantidia, the number of
which could only be decreased by extensive enemas of hydrochloric acid.

The second case related to a woman who was suffering from severe
colitis, and who died ten days after admission. The malodorous, watery
evacuations contained innumerable Balantidia, in addition to pus, and
at the autopsy the anterior portion of the large intestine was found to
be infested with them.

Subsequently this parasite has often been observed in human beings,
and various cases have been recorded. These occurred in Russia,
Scandinavia, Finland, Cochin China, Italy, Germany, Serbia, Sunda
Islands, Philippine Islands, China, and in other parts of Asia and in
America. Other cases were reported by Askanazy, Ehrnroth, Klimenko,
Nagel, Koslowsky, Kossler, Waljeff, Strong and Musgrave, Glaessner[248]
and others. Sievers found _B. coli_ very common in Finland.

[248] _Centralbl. f. Bakt._, Orig., xlvii, p. 351.

In the majority of the cases described by Sievers from Finland,
and in other cases from Central Europe, the patients suffered from
obstinate intestinal catarrh, which did not always cease even after
the Balantidia had disappeared. On the other hand, Balantidia have
occasionally still been found to persist, though in small numbers,
after the catarrh has been cured. Some authors, nevertheless, do
not regard Balantidia as the primary cause of the various diseases
of the large intestine, which often commence with the development of
ulcers, but they consider that they may aggravate these diseases and
render them obstinate. According to Solowjew, Askanazy, Klimenko and
Strong and Musgrave, however, the parasites penetrate the intestinal
wall, and give rise to ulcerations which may extend deeply into the
submucosa, and even be found in the blood and lymphatic vessels of the
intestinal wall. According to Stokvis, _B. coli_ occurs also in the
lung; at all events this author states that he found one living and
several dead paramæcia (?) in the sputum of a soldier, returned from
the Sunda Islands, who was suffering from a pulmonary abscess. Sievers
has shown that _B. coli_ might occur in persons not suffering from
intestinal complaints, but E. L. Walker[249] (1913) states that every
person parasitised with _B. coli_ is liable sooner or later to develop
balantidian dysentery.

[249] _Philip. Jl. Sc._, Sec. B, viii, p. 333.

Since Leuckart confirmed the frequent presence of _B. coli_ in the
rectum of pigs, and corresponding observations were made in other
countries, the pig is universally considered to be the means of the
transmission of Balantidium to man. The encysted stages only serve
for transmission, because, according to all observations, the free
parasites have a very small power of resistance. They perish when the
fæces have become cool; they cannot live in ordinary, slimy, or salt
water. As they are killed by acids even when much diluted, they cannot
pass through the normal stomach alive except under the most unusual
circumstances. The pigs, in whose intestines the Balantidium appears to
cause little or no disturbance, evacuate numerous encysted Balantidia
with the fæces, and their occasional transference to man brings about
their colonization there, but perhaps only when a disease of the colon
already exists.

Experimental transmission of the free parasites to animals (per os
or per anum) yielded negative results, even in the case of pigs.
Casagrandi and Barbagallo (1896), however, had positive, as well as
negative, results. They employed healthy young cats, or cats in which
catarrhal entero-colitis had been artificially induced (which in other
experiments is apt to cause the death of the animals experimented upon
in about six or seven days), or finally cats that had dilatation of
the rectum with alkaline reaction of the fæces. An attempt to infect
three healthy cats by injecting human fæces containing Balantidium
into the rectum proved negative, in so far as the fæces of the
experimental animals had an acid reaction and contained no Balantidia,
but at the autopsy performed eight days after infection a few encysted
parasites were found in the mucus of the ileum. In the case of four
cats suffering from entero-colitis, into which human fæces containing
Balantidia were introduced per os, Balantidium cysts were found in the
fæces three days after the last ingestion. Great numbers, moreover,
were found in the cæcum and the posterior part of the small intestine
at the autopsy of the animals, which died about eight days after the
commencement of the experiments. Actual colonization, therefore,
was not effected in either series of experiments. Free or encysted
Balantidia of pigs were used for further experiments. The experiments
proved negative when fæces containing cysts were injected into the
rectum of healthy cats (three experiments), or cats (two) suffering
from spontaneous intestinal catarrh, or when such material was
introduced per os into three healthy cats. In the case of two cats
with intestinal catarrh artificially produced, a small number of the
active Balantidia injected into the rectum remained alive. Larger
quantities of fæces containing encysted Balantidia were introduced into
two other cats affected with the same complaint. These, certainly, did
not appear in the fæces, but small numbers, free and alive, were found
in the cæcum. Similarly, encysted Balantidia were introduced into two
cats with dilated rectum, and whose fæces had an alkaline reaction.
In these cases no parasites appeared in the fæces, but three and five
days later, when the two animals were examined, a very small number
were discovered free in the large intestine. Klimenko did not succeed
in infection experiments with _B. coli_ on young dogs, whose intestines
had been artificially affected by disease.

More recent experiments by Brumpt have shown that young sucking pigs
can be infected with Balantidium from infected monkeys (_Macacus
cynomolgus_) and suffer heavily from the same, whereas the Balantidium
of the pig is rarely harmful to its host. This and previous experiments
may be thought to suggest that there are perhaps several pathogenic
species, and also that harmless strains of Balantidium may occur.
At the same time, it must be remembered that a large proportion of
the cases recorded of Balantidian colitis occur among swineherds
and butchers, that is, among people in frequent contact with pigs.
Morphologically, there are practically no differences between the
Balantidia found in man, monkeys and pigs, and it is probable that
one species only, under slightly different environmental conditions,
may be responsible for the colitis observed. In any case, efficient
prophylactic measures should be taken against balantidiasis in
countries where it may occur, by confining the pigs and not allowing
them to run in yards and dwellings.

E. L. Walker (1913) has given a good summary of work on balantidiasis.
His own researches in the Philippines showed that monkeys could be
infected by Balantidia both from pigs and men. Parasites may appear
in the stools only at infrequent intervals. He believes that the
ciliates are the primary etiologic factor in the symptoms and lesions
of balantidian dysentery.

Behrenroth (1913) has given an interesting account of _Balantidium
coli_ and its pathogenic significance.

*Balantidium minutum*, Schaudinn, 1899.

The body is of oval form, with the anterior extremity pointed, and
posterior extremity broad and rounded (fig. 115). The length is 20 µ
to 32 µ, and the breadth is 14 µ to 20 µ. The peristome, which is
fissure-like, extends to the centre of the body (fig. 115). The right
lateral border of the peristome is beset with cilia the same length as
those of the body, the left side terminates in a thin hyaline membrane
that extends towards the back, and can pass over to the right side. A
row of longer and stronger cilia (cirri) are on the left border of the
peristome. The cuticle is refractile, the ectoplasm hyaline and the
endoplasm granular, with numerous food vacuoles.

[Illustration: FIG. 115.--_Balantidium minutum._ _P_, peristome; _N_,
nucleus; _M_, micronucleus; _V_, contractile vacuole. Food vacuoles are
represented in the endoplasm. (After Schaudinn.)]

A single contractile vacuole lies dorsally and to one side at the
posterior extremity. The macronucleus, which is always spherical, is
central and is 6 µ to 7 µ in diameter. The micronucleus, close in front
of it, only measures 1 µ (fig. 115). The cysts are oval.

These parasites were found in numbers in the evacuations of a man
aged 30, who was born in Germany and had repeatedly travelled between
Hamburg and North America, where he made long stays. The patient came
to the Charité in Berlin to seek advice for constipation alternating
with diarrhœa accompanied by abdominal pain.

A second case (the parasite of which was described as _Colpoda
cucullus_ by Schulz) was observed in a patient in the same institution.

As, in both cases, the parasites only appeared during the diarrhœa,
and disappeared as soon as the fæces had assumed a normal consistency,
or could only be demonstrated in a few encysted specimens, it may be
assumed that the small intestine or the duodenum is their habitat.

Genus. *Nyctotherus*, Leidy, 1849.

  Flat, heterotrichous Infusoria, kidney- or bean-shaped. The peristome
  commences at the anterior pole of the body and extends along the
  concave side to the middle, where the oral aperture is situated. The
  cytopharynx is oblique and is more or less curved. The cytopyge is at
  the posterior extremity, where a single contractile vacuole is also
  situated. The macronucleus is almost in the centre of the parasite.
  The members of this genus live parasitically in the intestine of
  amphibia, insects and myriapods, and at least one species is found in

*Nyctotherus faba*, Schaudinn, 1899.

The body is bean-shaped, and a little flattened dorso-ventrally. It
is 26 µ to 28 µ long, 16 µ to 18 µ broad, and 10 µ to 12 µ thick
(fig. 116). The peristome is on the right border and extends to the
middle; at the left there are large adoral cilia, the cilia on the
right border not being larger than those on the body. The cytopharynx
is short, slightly curved and turned backwards. The contractile vacuole
is large, spherical, situated at the posterior extremity, and its
contents are voided through the anus at its left. The macronucleus is
in the centre of the body; it is globular (6 µ to 7 µ in size), and
contains four or five chromatin masses. The micronucleus lies close
to it, and is spherical or somewhat elongate measuring 1 µ to 1·5 µ
(fig. 116). The cysts are oval.

[Illustration: FIG. 116.--_Nyctotherus faba._ _P_, peristome;
_N_, nucleus; _M_, micronucleus; _V_, contractile vacuole. (After

This species has hitherto only been seen once in the same patient in
whom _Balantidium minutum_ was discovered.

*Nyctotherus giganteus*, P. Krause, 1906.

Under the name _Balantidium giganteum_ n. sp., P. Krause described
an Infusorian which was repeatedly observed with _Trichomonas
intestinalis_ in the alkaline evacuations of a typhoid patient in
Breslau. The body is ovoid, narrower and rounded anteriorly and
broader and stunted posteriorly. The peristome lies to one side; the
macronucleus is bean-shaped, the micronucleus small and globular;
one or two vacuoles are present. The anus is at the farther end. The
organism is 90 µ to 400 µ long, 60 µ to 150 µ broad (fig. 117). After
a prolonged stay outside the body, it becomes rounded and encystment
occurs. In the thermostat the Infusoria remain alive at 37° C. for five

The species, however, hardly belongs to _Balantidium_, but to all
appearances is a _Nyctotherus_ and is distinguished from _N. faba_ by
the difference in size.

[*Nyctotherus*] *africanus*, Castellani, 1905.

In the fæces of a native of Uganda who suffered from sleeping sickness
and diarrhœa and had in his intestine _Ascaris lumbricoides_,
_Trichocephalus trichiurus_ and _Ancylostoma duodenale_, Castellani
found a curiously shaped Infusorian, 40 µ to 50 µ long, and 35 µ
to 40 µ broad, with spherical macro- and micronucleus and a
contractile vacuole (fig. 118). He included the organism in the genus
_Nyctotherus_, perhaps wrongly, or the parasite may have been deformed.
After the patient’s death the same parasite was found in the intestine
and especially in the cæcum.

[Illustration: FIG. 117.--_Nyctotherus giganteus._ (After Krause.)]

[Illustration: FIG. 118.--_Nyctotherus africanus._ (After Castellani.)]

  G. Lindner, in Cassel, studied certain peritrichal Infusoria
  (stalkless Vorticella), and connected them, probably incorrectly,
  with the most varied diseases of man and domestic animals, even
  with Sarcosporidia of pigs. It may be mentioned that according to a
  communication by letter from Schaudinn, Vorticella may be found in
  freshly evacuated fæces, but always only after the administration of
  a water enema. In spite of this, several other investigators mention
  Vorticellæ as intestinal parasites of man.

  The _Chilodon dentatus_ (Ehrenberg) recorded in 1903 by J. Guiart as
  a parasite of man, which may be found in all infusions, can hardly
  have lived in the man from whose fæces it was cultivated, but may
  represent a chance admixture both in the fæces and the cultivations.
  _C. uncinatus_ was also found as a chance parasite of man by Manson
  and Sambon. According to Doflein[250] (1911) certain Chilodon-like
  organisms have been found by Selenew in prostate secretions in
  gonorrhœa. Other species of the genus _Chilodon_ are known, but only
  as ectoparasites (_e.g._, _Chilodon cyprini_, Moroff, 1902, from the
  skin and gills of diseased carp).

[250] _Lehrbuch der Protozoenkunde_, 3rd ed., p. 963.

  A number of other parasitic Ciliates are known, among which
  _Ichthyophthirius multifiliis_, destructive to fish, is important. It
  lives in the skin and the layers immediately below it, forming small
  whitish pustules which may become confluent. The pustules are most
  common on the head and fins, but occur also on the eyes and gills of
  the host. The young parasite, which is one of many formed in a cyst,
  is very small. At first it is free swimming, but soon attaches itself
  to the skin of a fish. It bores inwards and becomes surrounded by the
  irritated skin. There it attains a relatively large size, being 500 µ
  to 750 µ and occasionally more in diameter. The body has a rounded
  terminal mouth, short cytopharynx and a number of minute contractile
  vacuoles. The macronucleus is large and horseshoe-shaped; the small
  micronucleus is only seen in the very young animal. When full grown,
  the organism encysts and forces its way to the surface and bursts
  through, leaving a small, gaping wound behind. The cyst sinks to the
  bottom of the water, nuclear multiplication occurs and a number of
  young parasites are produced, which leave the cyst and either attack
  new hosts or else perish.

  _Opalina ranarum_, parasitic in the rectum and urinary bladder of
  frogs and toads, shows great degradation and simplification due
  to parasitism, possessing no separate micronuclei, no cytostome,
  cytopharynx or cytopyge. It has many macronuclei, and is a large
  parasite. During summer and autumn nuclear multiplication followed
  by division of the body occurs, the process being repeated after the
  daughter forms have grown to the size of their parent. In spring, the
  Opalina divide rapidly, but do not grow much before dividing again.
  Finally, tiny forms, containing three to six nuclei, encyst and pass
  from the host with the fæces. As these latter are greedily devoured
  by tadpoles, the _Opalina_ gain new hosts in which they develop.


The name Chlamydozoa was proposed by Prowazek in 1907 for a number of
minute, problematic organisms (fig. 119) believed to be the causal
agents of certain diseases in man and animals, such as vaccinia
and variola, trachoma, inclusion blenorrhœa in infants, molluscum
contagiosum, and bird epithelioma contagiosum. Other diseases possibly
due to Chlamydozoa[251] are hydrophobia, measles, scarlet fever,
foot-and-mouth disease, the “Gelbsucht” disease of silkworms, and
perhaps even typhus (Prowazek, 1913). The subject is difficult and
controversial and can only be briefly discussed here. It is known that
the viruses in all these diseases can pass through ordinary bacterial
filters, that is, they belong to the group of “filterable viruses.”
At such periods the organisms are extracellular or free. It is also
known that in many of these cases the virus produces definite and
characteristic reaction-products or cell-inclusions in the infected
cells, during the intracellular phase of the life-history of the
organism. As the organisms to be considered are problematic, it will be
convenient to summarize their history:--

[251] For a detailed account of the Chlamydozoa see Prowazek’s
_Handbuch der Pathogenen Protozoen_, Bd. i (1911–12). Leipzig, J. A.

(1) Cell-inclusions, usually named after their discoverers, have been
found in certain diseases, thus: In vaccinia Guarnieri’s bodies, in
scarlet fever Mallory’s bodies, in hydrophobia Negri’s bodies, in
trachoma Prowazek’s bodies occur.

(2) At first these characteristic cell-inclusions were considered to
be actual parasitic organisms causing the diseases in question. The
bodies received zoological names and attempts were made to work out
their supposed development cycles. The supposed parasites of vaccinia
and variola were referred to a so-called genus _Cytoryctes_, those
of hydrophobia to _Neuroryctes_, of scarlet fever to _Cyclasterium_,
while those of molluscum contagiosum were referred to the Coccidia.
Calkins in 1904 studied in detail the cell-inclusions of vaccinia
and small-pox, calling them _Cytoryctes variolæ_, Guarnieri. Calkins
considered that in the stratified cells of the epidermis they passed
through two cycles, the one cytoplasmic, the other intranuclear. The
first is the vaccinia cycle, the second the pathogenic (intranuclear)
variola cycle. It is hardly necessary to follow all Calkins’ stages

Negri (1909) described a cycle for _Neuroryctes hydrophobiæ_. Calkins
refers both _Cytoryctes variolæ_ and _Neuroryctes hydrophobiæ_ to the

Siegel (1905) described quite different organisms under the name
_Cytorhyctes_. He listed several species: _C. vacciniæ_; of vaccinia
and small-pox, _C. scarlatinæ_ of scarlet fever, _C. luis_ of syphilis
(this is probably the granule stage of _Treponema pallidum_), and _C.
aphtharum_ of foot-and-mouth disease.

(3) The afore-mentioned views were criticized, and the bodies were
not considered to be living organisms but merely reaction products or
cell-inclusions due to the effects of the virus on the host cells.
Thus Guarnieri’s bodies were stated to consist of extruded nucleolar
or plastin material, having no developmental cycle. It was further
asserted that infection could be produced by lymph in which Guarnieri’s
bodies had been destroyed. Similar assertions have been made regarding
the Negri bodies, and others. The _Cytoryctes_, _Neuroryctes_, etc.,
are considered, according to these views, to be degeneration products
of the nucleus or to be of a mucoid nature.

(4) More recently a positive belief has gained ground that there
are true parasitic organisms causing these diseases, and that the
parasites are very minute, being termed Chlamydozoa by Prowazek and
Strongyloplasmata by Lipschütz.

The Chlamydozoa are characterized by (_a_) their very minute size,
smaller than any bacteria, so that they can pass through bacterial
filters; (_b_) they pass through intracellular stages, in the cytoplasm
or the nucleus of the host cell, producing therein the reaction
products or inclusions in the cell already recorded as characteristic
or diagnostic of the diseases produced; (_c_) they pass through
definite developmental cycles. Such a cycle consists essentially of
growth and division. The mode of division of the Chlamydozoa resembles
that of the centriole of a cell, by the formation of a dumb-bell-shaped
figure. Two dots are observed connected by a fine line or strand which
becomes drawn out and finally snaps across the middle. Prowazek and
Aragão (1909) working on smallpox in Rio de Janeiro found that the
chlamydozoal granules passed through a Berkefeld filter and that the
filtrate was virulent. But if an “ultra-filter” were used, _i.e._, one
coated with agar, then the granules were retained and the filtrate
was no longer virulent. The surface of the ultra-filter was found to
contain many granules.

The Chlamydozoa are parasites of epiblastic tissues (_e.g._, epidermal
cells, nerve cells, conjunctival cells).

[Illustration: FIG. 119.--Chlamydozoa. Trachoma bodies in infected
epithelial cells of the conjunctiva. (_a_) initial bodies (above) and
cluster of elementary bodies (touching the nucleus); (_b_) cluster
of granules surrounded by mantles. × 2,000 approx. (Original. From
preparation by Fantham.)]

The life-history of a Chlamydozoön (fig. 119), such as that of
vaccinia, is, according to Prowazek, Hartmann and their school, as

1. The infection begins with _elementary bodies_ or _elementary
corpuscles_ which live at first extracellularly. An elementary body
is a minute speck of chromatin, apparently devoid of cytoplasm, which
can pass through a bacterial filter. It can enter a host cell, but the
entry is not a process of phagocytosis.

2. Inside the host cell the elementary body grows in size, and becomes
an _initial body_ (fig. 119, _a_).

3. A reaction on the part of the host cell results, for nucleolar,
plastin substance is extruded from the cell-nucleus and surrounds the
parasitic initial body. The latter is thus enveloped in a mantle (hence
the name Chlamydozoa, from χλαμὑς, a mantle), and the characteristic
cell-inclusion (Guarnieri’s body, Negri’s body, etc.) is produced. The
nucleolar, mantle substance probably represents the “cytoplasm” of
_Cytoryctes_, described by Calkins.

4. The body next breaks up into a number of smaller bodies known as
_initial corpuscles_. These, in their turn, divide by simple division
(in the manner already described) into numerous elementary bodies
(fig. 119). Thus, the life-cycle is completed.

The Chlamydozoa are, then, the minute granules inside the body of the
_Cytoryctes variolæ_ or the _Neuroryctes hydrophobiæ_, so that the
whole body of the _Cytoryctes_ or _Neuroryctes_ corresponds to the
mantle and parasite of the Chlamydozoön. The Cytoryctes group is said
to cause destruction of the host cell. The Cytoöikon group (_e.g._,
trachoma bodies) causes proliferation of the host cell.

In September, 1913, Noguchi[252] described the cultivation of the
parasite of rabies in an artificial medium, similar to that used by
him for the cultivation of _Spirochæta recurrentis_. The cultures were
stated to be infective to dogs, rabbits and guinea-pigs. Levaditi, in
December, 1913, stated that he had succeeded in cultivating spinal
ganglia of rabid monkeys in monkey plasma.

[252] _Journ. Exptl. Med._, xviii, p. 314.

Noguchi and Cohen (November, 1913)[253] have succeeded in cultivating
the so-called trachoma bodies, or at any rate bodies very closely
resembling them morphologically. The medium employed was Noguchi’s
ascitic fluid and rabbit kidney medium, as used for spirochætes. The
coarser cultural forms stained blue with Giemsa’s solution, the finer
ones stained red. Attempts to infect monkeys from the culture tubes

[253] _Idem_, p. 572.

From their behaviour on treatment with such reagents as saponin, bile
and sodium taurocholate, Prowazek considers that the Chlamydozoa
approach the Protozoa.

       *       *       *       *       *


*Sergentella hominis*, Brumpt, 1910.

Et. and Ed. Sergent in 1908 found vermiform bodies about 40 µ long by
1 µ to 1·5 µ broad in the blood of an Algerian suffering from nausea
and cold sweats, without other symptoms. The bodies were pointed at
each end, with a somewhat ill-defined nucleus in the middle. Their
systematic position is doubtful.

  |NOTE.--An Appendix on Protozoology will be found on pp. 733–752. |
  |This has been prepared in order to incorporate a number of new   |
  |additions to knowledge made since the body of the book was       |
  |printed off.                                                     |

B. *PLATYHELMINTHES*, or Flat Worms.


J. W. W. STEPHENS, M.D., B.C., D.P.H.

  DEFINITION: Bilaterally symmetrical animals without limbs, the form
  of which is leaf or tape-like, rarely cylindrical, and whose primary
  body cavity (segmentation cavity) is absent, the cavity being filled
  by a mesenchymatous tissue (parenchyma).

  The mouth is either situated at the anterior end of the body, or is
  shifted more or less backwards on to the flat ventral surface. The
  alimentary canal consists of a short fore-gut, which is frequently
  provided with a muscular pharynx, and of a simple forked or branched
  mid-gut; there is neither a hind-gut nor an anus; in one class, the
  Cestodes, the alimentary canal has entirely disappeared except for
  muscular remnants in the scolex.

  The INTEGUMENT OF THE BODY consists either of a ciliated epithelium
  of only one layer (Turbellaria), or of a cuticle and gland-like
  cells embedded in the parenchyma, or subcuticular layer (Cestodes,
  Trematodes). The dermo-muscular layer consists of annular,
  longitudinal, and even diagonal fibres, while the parenchyma is
  traversed by dorso-ventral fibres.

  The central NERVOUS SYSTEM, which is embedded in the parenchyma of
  the body, consists of cerebral ganglia, united together in the shape
  of dumb-bells, and of two or more longitudinal MEDULLARY FASCICLES,
  often forming transverse anastomoses. Organs of sense usually occur
  only in the free-living species, more rarely during the free-living
  stages of a few parasitic species and in a few ectoparasitic forms.

  [In Platyhelminthes simple eye-spots frequently occur, and in a few
  an auditory vesicle.]

  BLOOD-VESSELS and definite RESPIRATORY ORGANS are lacking [except
  in _Nemertinea_]; the EXCRETORY APPARATUS (formerly termed
  water-vascular system) is typical of the entire class. It commences
  in the interstices of the parenchyma, with peculiar terminal cells
  (ciliated funnels), which will be described later (p. 219), the
  capillary processes of which go on uniting into larger branches,
  and finally form two large collecting vessels, which, sometimes
  separately and sometimes united, open to the exterior through one,
  two, or numerous pores.

  Nearly all the Platyhelminthes are HERMAPHRODITIC, and in nearly all
  there are, in addition to the ovaries producing ova, other glands
  attached to the female genital apparatus, namely, the vitellaria or
  yolk glands, which provide a substance termed yolk, which serves
  as nourishment for the embryo. The fully formed eggs have shells
  and are “compound,” _i.e._, composed of the egg or ovarian cell,
  which is surrounded by numerous yolk cells or their products of
  disintegration. The two sexual openings usually lie close together,
  frequently in the fundus of a genital atrium; they are rarely
  separated from one another. Shell glands also usually occur (p. 221).

  Reproduction is sexual, often, however, combined with asexual methods
  of propagation (segmentation, budding). The Platyhelminthes live
  partly free in fresh or salt water, exceptionally also on land. The
  greater part, however, live as parasites on or in animals.


  _Class I._--*Turbellaria* (or Eddy Worms). Flat worms for the most
  part, free living, and always covered with a ciliated epithelium.

    _Order 1._--_Rhabdocœlida_, gut unbranched.

    _Order 2._--_Tricladida_, gut with three main branches.

    _Order 3._--_Polycladida_, a central gut with lateral cæca.
    Development direct or through metamorphosis. They live in fresh and
    salt water or on land; very seldom as parasites.

  _Class II._--*Trematoda* (Sucking Worms[254]). [Usually known as
  Flukes.--F. V. T.] Flat worms, living as ecto- or endoparasites, that
  are only ciliated in the larval condition, and in their adult state
  are covered with a cuticle, the matrix cells of which lie in the
  parenchyma. They have either one, a few, or several suckers,[255] and
  frequently also possess chitinous fixation and adhesive organs. The
  intestine is single, but generally bifurcated, and not uncommonly there
  are transverse anastomoses between the forks or diverticula on them.
  Excretory organs double, with two orifices at the anterior extremity
  or a single one at the posterior end. Development takes place by a
  metamorphosis or alternation of generations (p. 283). These worms are
  almost always hermaphroditic, with two or more female and one male
  sexual orifice. They live, almost without exception, as parasites on
  vertebrate animals, but the intermediate generations are passed in

[254] This grouping goes back to the year 1800, and was made by
J. G. H. Zeder, a physician and helminthologist of Forchheim, who
divided the helminths, which until 1851 were generally regarded as
a special class of animals, into the groups of round, hook, sucker,
tape and bladder worms, as which they are recognized up to the present
time. In 1809, K. A. Rudolphi gave them the names _Nematodes_,
_Acanthocephali_, _Trematodes_, _Cestodes_ and _Cystici_.

[255] A sucker or acetabulum (little cup) is a round, cup-shaped
muscular organ, the muscles of which are _sharply defined_ from those
of the body.

  _Class III._--*Cestoda* (Tapeworms). Endoparasitic flat worms without
  an alimentary canal. The larval stages are rarely ciliated, but are
  usually provided with six spines; the adult worm is covered with a
  cuticle, the matrix cells of which are embedded in the parenchyma. The
  body consists of a single segment (Cestodaria) or a chain of segments,
  in which case it consists of the scolex and the segments containing
  the sexual organs (proglottides) (Cestodes s. str.). The scolex is
  provided with various adhesive and fixation organs, and there are
  calcareous corpuscles in the parenchyma. Excretory organs symmetrical,
  opening at the posterior end. These worms are always hermaphroditic,
  and then possess one or two female and one male sexual orifice. During
  development a larval intermediate stage (“measle”) occurs and almost
  always in a different host to that in which the adult sexual worm
  lives. The adult stage is parasitic in vertebrate animals; but the
  larval stage may occur in invertebrates.

Class II. *TREMATODA*, Rud.

These worms are usually leaf- or tongue-shaped, but also barrel-shaped
or conical; they vary from 0·1 mm. to almost 1 m.[256] in length; most
of them, however, are small (5 mm. to 15 mm.). The surface on which
the orifice of the uterus and the male sexual opening are situated is
termed the ventral surface; the oral aperture, which also acts as anus,
is always at the anterior end in the sub-order _Prostomata_ (p. 230),
but in the sub-order _Gasterostomata_ it is ventral.

[256] _Nematobothrium filarina_, van Bened., on the branchial chamber
of the Tunny.

Suckers are always present and occur in varying numbers and positions
at the anterior extremities as well as on the ventral surface, and
occasionally on the lateral margin and on the dorsum; the beginning
of the intestine (mouth) is always surrounded by a sucker in the

In or near the suckers there may be chitinous hooks, claws or claspers,
or the surface of the body is more or less covered with spines, scales
or prickles; in one genus (_Rhopalias_) there are projectile tentacles
beset with spines on the sides of the anterior part of the body.

The body of adult Trematodes is covered by a homogeneous layer of
varying thickness, which either lies directly over the external layer
(basement membrane) of the parenchyma, or over the muscles embedded
in the parenchyma. This investing membrane (cuticle) arises from
pear-shaped or spindle-shaped cells arranged singly or in groups (which
lie between or internal to the diagonal muscles), and is connected with
them by processes; these cells one may regard as epithelial cells which
have sunk down, or possibly as parenchymatous cells. An epithelium of
one layer is also found on the body of young stages, but it disappears
during growth, and only occasionally do its nuclei persist until adult
life. In its place we then find the cuticle, which, moreover, extends
into all the body openings more or less deeply.

It is thus a debatable point whether the “investing layer” of flukes
is a cuticle--that is, consists of modified epithelial cells--or
whether it is a basement membrane, _i.e._, compressed and modified
connective tissue cells; in this latter case the true epidermis and
cuticle have been cast off. In the former case the epidermal cells are
the pear-shaped cells referred to above. According to recent authors
it consists of two parts, an outer true cuticle and an inner basement
membrane. There are also unicellular cuticular glands, lying isolated
or in groups, which are termed cephalic, abdominal, or dorsal glands
according to the position of their orifice.

The PARENCHYMA is a connective substance, the structure of which is
still a matter of dispute. It consists, according to some authors, of
multipolar cells, the offshoots from which anastomose with each other
so that a network, permeating the entire body and encompassing all the
organs, is produced. There exists also, as part of it, a homogeneous
matrix, in the form of lamellæ and trabeculæ that border small cavities
communicating with each other and filled with fluid. According to
other authors, the parenchyma of the Trematodes consisted originally
of cells, of which, however, only the cell membranes remain, while
the protoplasm has been liquefied except for small residua around
the nucleus. Between these cells an intercellular mass has appeared.
By partial absorption of the walls, adjoining spaces unite, and the
originally flat cell walls become transformed into trabeculæ. According
to this view the cavities filled with fluid are _intra_-cellular,
according to the former view _inter_-cellular. Pigment cells occur only
in a few species.

The MUSCULAR SYSTEM of the Trematodes is composed of (1) a
dermo-muscular tube, (2) the dorso-ventral or parenchymal muscles, (3)
the suckers, and (4) the special muscles of certain organs.

The dermo-muscular tube, which lies fairly close to the cuticle,
consists of annular, diagonal, and longitudinal fibres which surround
the entire body in one or several layers, and as a rule are more
strongly developed on the ventral surface as well as in the anterior
part of the body. The MUSCLES OF THE PARENCHYMA are found chiefly in
the lateral parts of the body and pass through the parenchyma in a
dorso-ventral direction; their diverging brush-like ends are inserted
on the inner surface of the cuticle (fig. 120).

[Illustration: FIG. 120.--Half of a transverse section through
_Fasciola hepatica_, L. 25/1. _Cu._, Cuticle with scales; under the
cuticle are circular muscles, and adjoining them the longitudinal
and diagonal muscles; internal to the latter are the matrix cells of
the cuticle; _I._, gut; the other similarly contoured cavities are
gut diverticula that have been transversely or obliquely sectioned;
_F.v.s._, vitellaria; _Ex.v._, excretory vessels; _T._, testes; _Md._,
median plane; the fibres passing from the ventral to the dorsal surface
are the muscles of the parenchyma. The parenchyma itself is omitted.]

The suckers are specially differentiated parts of the dermo-muscular
tube. Their concave inner surface is lined by the continuation of the
cuticle and their convex external surface is covered by a more dense
tissue that frequently takes the form of a refractive membrane, thus
separating them from the parenchymal muscles.

The principal mass of the suckers consists of muscular fibres which
run in three directions--equatorial, meridional and radial. The
equatorial fibres correspond to the annular muscles, the meridional
fibres to the longitudinal muscles, and the radial fibres to the
muscles of the parenchyma; the radial fibres are always the most
strongly developed. The function of these muscles is evident from
their position; the meridional fibres flatten the suctorial disc and
diminish the depth of its cavity, so that the internal surface may
adhere to the object to be held; if the equatorial fibres now contract,
the sucker rises by elongating longitudinally, and its inner surface
is drawn in by the contraction of the radial muscles. Thus the sucking
disc becomes adherent. Usually also there is a sphincter at the border
of the suckers, which plays its part during the act of adhesion by
constricting in a circular manner that part of the mucous membrane to
which it is attached. The loosening of the fixed sucker is effected
by relaxation chiefly of the radial fibres, by the contraction of the
meridional fibres and certain bundles of muscles situated at the base
and at the periphery of the suckers. The connective and elastic tissues
between the muscles of the suckers probably also take part in the

[Illustration: FIG. 121.--_Harmostomum leptostomum_, Olss., an immature
specimen from _Helix hortensis_. _Nervous system_, according to
Bettendorf. _A.s._, ventral sucker; _C.g._, cerebral ganglion; _Ex.p._,
excretory pore; _G.p._, genital pore; _O.s._, oral sucker; _M.d._,
dorsal medullary nerve; _M.l._, lateral medullary nerve; _N.ph._,
pharyngeal nerve; _M.v._, ventral medullary nerve. Magnified.]

Of the muscles of the organs which have developed from the parenchyma
muscles we may briefly mention those bundles that are attached to
certain parts of the genital apparatus, to the suckers, to the hooks
and claws, and also, at all events in _Fasciola hepatica_, to the
spines. The sheaths used for the projection of the tentacles of the
_Rhopaliadæ_ are also muscular.

The contractile elements consist of fibres of various lengths that are
mostly parallel to one another, and frequently anastomose; a cortical
substance finely fibrillated can usually be distinguished from an
internal homogeneous mass; large nucleated cells of uniform size are
always connected with them; these have been variously interpreted,
but have been proved to be myoblasts, one or more of their processes
constituting the muscular fibres.

The MOVEMENTS of the Trematodes consist in alterations of form and
position of the body, as well as in creeping movements.

In the NERVOUS SYSTEM (fig. 121) can be distinguished a cerebral
portion as well as strands (medullary strands) running from it, and
peripheral nerves. The cerebral portion always consists of two large
ganglia situated in the anterior end of the body which pass dorsally
over the œsophagus and are connected by means of a broad and thick
commissure composed of fibres only. From each ganglion three nerves
run anteriorly--the inner and dorsal nerve for supplying the anterior
dorsal part of the body; the median and ventral for the oral sucker;
and the exterior and lateral likewise for the supply of the sucker.

In a similar manner three strands run backwards from each ganglion--one
dorsal, one lateral and one ventral. The dorsal and ventral strands
become united and curve backwards; the symmetrical lateral strands
are connected by means of transverse commissures, the number of which
vary according to the species. Such commissures also exist between the
lateral and the two other strands on each side. There are ganglion
cells along the entire course of the posterior cords, more particularly
at the points of origin of the commissures. There also appears to be in
addition a fourth anterior and posterior pair of nerves, the front pair
for the oral sucker and the hind pair for the pharynx.

The peripheral nerves, which spring from the posterior strands as well
as from the commissures, either pass directly to the muscular fibres or
to the sensory cells that are situated at the level of the subcuticular
cells, or they reach these after the formation of a plexus situated
immediately beneath the dermo-muscular layer; the processes directed
outwards terminate in small vesicles in the cuticle.

As to other ORGANS OF SENSE, simple eyes, two or four in number, are
known in several ectoparasitic species as well as in a few free-living
larval stages (Cercariæ) of endoparasitic forms. In the adult stage,
however, they usually undergo complete atrophy.

The ALIMENTARY CANAL commences with an oral aperture, generally
terminal or sub-terminal (ventral) at the anterior extremity, which
leads into an oral cavity usually surrounded by a sucker; the
œsophagus, of various lengths, is directed backwards and is generally
surrounded by a muscular pharynx (fig. 122). In some cases there exists
between the sucker and pharynx, pharyngeal pouches (præpharynx). Sooner
or later the intestine divides into two lateral branches directed
backwards, both of which end blindly (cæca) at the same level.[257]
In many ectoparasites (_Monogenea_ [p. 222]) a connection exists
between the genital glands and one of the intestinal branches (ductus
vitello-intestinalis [fig. 123]).

[257] The following conditions represent deviations from this type: (1)
In _Gasterostomum_ the oral aperture is situated in the middle of the
ventral surface, and occasionally is even nearer to the posterior than
to the anterior end. There is no proper oral sucker, but the pharynx is
thus termed. (2) A few genera, such as _Gasterostomum_, _Aspidogaster_,
_Diplozoon_, etc., have only _one_ intestinal diverticulum, which is
undoubtedly to be taken as representing the primitive condition, as
it is also often found in the young stages of the _Trematoda_. (3)
The branches of the intestines are curved and united behind (several
_Tristomidæ_ and _Monostomidæ_), while in _Polystomum integerrimum_
(in the bladder of frogs) there are several commissures between the
intestinal branches, and in the _Schistosomidæ_ the united intestinal
branches proceed as one channel towards the posterior end. (4) The
termination of the two intestinal branches is not always on a level;
they are therefore of different lengths. (5) When the œsophagus is
very long the intestinal branches extend both forward and backward, so
that the gut exhibits the form of an *H*. (6) In the broad and flat
species the gut-forks form diverticula mostly externally but also
internally; these again may branch (fig. 139). (7) In a few cases
(_Nematobothrium_, _Didymozoon_) the intestine completely disappears up
to the pharynx.

The oral cavity, pharyngeal pouches, pharynx, and œsophagus are
lined with a continuation of the cuticle of the body; the gut cæca
are lined with tall cylindrical epithelium (fig. 120). The œsophagus
and intestinal branches often have also one layer of annular and
longitudinal muscles; the pharynx has essentially the structure of a
sucker (fig. 122).

[Illustration: FIG. 122.--Median section through the anterior part of
_Fasciola hepatica_: the oral sucker, pharyngeal pouches, pharynx,
œsophagus, cuticle with spines, and the body parenchyma.]

The accessory organs of the alimentary canal consist of groups of
unicellular SALIVARY GLANDS that discharge into the œsophagus in front
of or behind the pharynx, or even into the pharynx itself.

The food of the Trematodes consists of mucus, epithelial cells, the
intestinal contents of the hosts, and often also of blood, and this
not only in those species living in the vascular system, but also in
species living as ectoparasites or in the intestine or biliary passages
of their hosts.

[Illustration: FIG. 123.--_Polystomum integerrimum_, a monogenetic
fluke from the urinary bladder of the frog. _i._, intestine; _h._,
large hooks of the sucking disc; _h.k._, smaller hooklets; _l.c.v._,
longitudinal vitelline ducts; _o._, oral orifice; _Oot._, oötype;
_ov._, ovary; _s.p._, suckers of the disc; _tr.c.v._, transverse
vitelline ducts; _Ut._, uterus with ova; _v._, entrance to the vagina;
_v.d.e._, vas deferens; _v.d.i._, ductus vitello-intestinalis; the
vitellaria and testes are not shown. Magnified. (After Zeller.)]

[Illustration: FIG. 124.--_Allocreadium isoporum_, Looss. Excretory
apparatus. Of the other organs, the oral sucker, pharynx, genital pore,
ventral sucker, ovary and testes are shown; the cylindrical excretory
bladder is in the posterior end. 38/1. (After Looss.)]

The final products of assimilation dissolved in the fluids of the body
are distributed throughout the parenchyma and are thence expelled
by a definite tubular system (excretory apparatus, proto-nephridia,
formerly also termed the water-vascular system). This system, which is
distributed throughout the entire body (fig. 124), is symmetrically
developed, and, in the ectoparasitic Trematodes, it opens, right and
left, at the anterior end on the dorsal surface; in all other flukes,
however, it opens singly into the excretory pore (foramen caudale) at
the centre of the posterior border; in those cases, however, where a
sucker is present at the posterior end, as in the Amphistomata, the
excretory pore is situated on the dorsal surface close in front of the

The EXCRETORY SYSTEM[258] consists of several parts: (1) of the more or
less numerous terminal “flame” cells or funnel cells (figs. 124, 125);
(2) of the capillaries ending in them; (3) of larger vessels receiving
the capillaries; and (4) of the excretory bladder. Terminal cells and
capillaries may be compared to unicellular glands with long excretory
ducts; the cellular body (fig. 125) is comparatively large, stretched
longitudinally, more rarely transversely, and provided with numerous
processes, that are lost in the parenchyma; within is a conical cavity
(analogous to the secretory cavity of unicellular glands) which is
continued directly into the structureless capillary; at its blind end
is a bunch of cilia projecting into the cavity, and which, during life,
shows a flickering motion (ciliary flame). The nucleus is situated in
the protoplasm of the terminal cell at its blind end.

[258] The following description relates in the main to the _Distomata_.

The entire apparatus thus begins blindly--_i.e._, within the terminal
cells, to which must be ascribed the capacity of taking up from the
fluid that permeates the parenchyma the products which are first
collected into their own cavities and thence excreted by means of the
capillaries and vessels.

[Illustration: FIG. 125.--Terminal flame cell of the excretory system.
_n._, nucleus of cell; _c._, bundle of cilia forming the “flame”; _p._,
processes of cell extending into parenchyma; _d._, excretory capillary.

The vessels possess definite walls, consisting of a membrane and a
nucleated protoplasmic layer. They unite at many points on either side,
and again pass into other canals (COLLECTING TUBES), which finally,
travelling towards the posterior end, discharge into the excretory
bladder (fig. 124).

The form and size of the bladder vary much according to the different
species, but it always possesses its own flattened epithelium,
surrounded by circular and longitudinal muscles, the circular muscles
forming a sphincter around the opening. Frequently also the structure
of the bladder extends to the tubules discharging into it, which
therefore are not to be regarded as separate “vessels,” but rather
as tubular diverticula of the bladder, directed anteriorly. In some
few species the diverticula also branch and the branches anastomose,
so that a network of tubules ensues which receives the vessels or
capillaries. In such cases there are also ciliary tracts in the tubules.

The contents of the entire apparatus usually consist of a clear or
sometimes reddish fluid; in some species there are larger or smaller
granules, and occasionally also concretions occur.

[Illustration: FIG. 126.--Diagram of female genitalia. _Ov._, ovary;
_ovd._, oviduct; _L.c._, Laurer’s canal; _Rec. sem._, receptaculum
seminis; _Vit. R._, vitellarian reservoir; _t.v.d._, transverse
vitelline duct; _Oo._, oötype; _Sh. gl._, shell gland; _Rec. ut._,
receptaculum uterinum; _ut._, uterus. (The various parts are not to the
same scale.) (Stephens.)]

[Illustration: FIG. 127.--Diagram of male and part of female genitalia.
_ut._, uterus; _vag._, vagina; ♀, opening of vagina; _g.s._, genital
sinus; _g.p._, genital pore; ♂, opening of ejaculatory duct or vas
deferens; _c.s._, cirrus sac; _c._, cirrus; _p.p._, pars prostatica;
_s.v._, seminal vesicle; _e.j._, ejaculatory duct or vas deferens;
_v.e._, vas efferens; _t._, testis. (Stephens.)]

_Sexual Organs._--Nearly all the Trematodes are hermaphrodites,
and only a few (_Schistosomidæ_, _Koellikeria_) are sexually
differentiated. The sexual organs usually lie in the “central field”
limited by the gut cæca; the vitellaria, on the other hand, are, as a
rule, external to the gut cæca in the “lateral fields.”

The male apparatus[259] is composed of two variously formed testes
(fig. 127) (globular, oval, indented, lobed, or ramified), which may
lie side by side or one behind the other; from each testicle a tube
(vas efferens) originates; sooner or later, both tubes as a rule unite
to form the ejaculatory duct or vas deferens, which is frequently
enclosed in a muscular CIRRUS SAC, or more rarely passes directly into
the genital pore. The cirrus, which is the thick muscular terminal
portion of the vas deferens, can be everted and protruded from the
cirrus sac and serves as an organ of copulation. The walls of the
muscular portion of the tube (the cirrus) are attached to the walls of
the cirrus sac, and hence when the sac contracts the cirrus cannot be
protruded except by evagination of its lumen. Opening into the middle
portion of the vas deferens, and as a rule enclosed in the cirrus
sac, is found a mass of unicellular glands (prostate), the vesicula
seminalis (which is likewise within, or may also be outside the sac)
being the dilated first portion of the vas.

[259] The following description relates mainly to the _Distomata_.

The female genitalia (fig. 126) consist of an ovary, usually situated
in front of the testes, the form of which varies according to the
species, the usually double vitellaria, the ducts and a number of
auxiliary organs; the short oviduct directed towards the centre
arises from the ovary, and is connected in the median line with the
excretory duct of the vitelline glands. These grape-like glands possess
longitudinal excretory ducts, which assume a transverse direction
behind the ovary, unite together at the median line and form a single
duct, often dilated into a vitelline receptacle, that unites with
the oviduct. Near this point, moreover, there frequently opens a
canal (Laurer’s canal) which begins on the dorsal surface, and on the
inner end of which a vesicle filled with sperm (receptaculum seminis)
usually occurs (fig. 126). Moreover, there are also numerous radial
unicellular glands (shell glands) at or beyond the point of junction
of the oviduct, vitelline ducts and Laurer’s canal. In this portion
of the duct (oötype), which is usually dilated, the ovarian cells are
fertilized, surrounded with yolk cells and shell material, and as
ova with shells they pass into the uterus (a direct continuation of
the oviduct), which, with its many convolutions, occupies a larger
or smaller portion of the central field, and runs either direct to
the genital pore or, forming convolutions, first runs posteriorly and
then bends forward (descending and ascending limbs). In both cases
the terminal part lies beside the cirrus pouch and discharges beside
the male orifice either on the surface of the body or into a genital
atrium. The terminal portion of the uterus, which is often of a
particular structure, serves as a vagina (METRATERM).

The cirrus sac may include (1) the genital atrium (_i.e._, the common
sinus, into which the vas deferens and vagina may open), or (2) a
variable extent of the vas from cirrus to seminal vesicle. Thus the
latter may be outside the sac. In the absence of a sac, the genital
sinus may be surrounded by a pseudo-sucker, as in _Heterophyes_ (in
some cases the ventral sucker itself, from its close proximity to the
genital pore, serves as an accessory copulatory organ). In other cases
copulatory organs are formed by hooks projecting into the lumen of the
terminal portion of the vas.

The GENITAL PORE, which is the opening from the genital sinus on to
the surface, is generally situated at or near to the median line on
the ventral surface and in the anterior region of the body; in most of
the _Distomata_ it is in front of the ventral sucker, in other cases,
_e.g._, in the _Cryptocotylinæ_, it is behind.[260]

[260] The typical position of the genitalia is subject to many
deviations, which are of importance in the differentiation of the
genera and families. The following are some few of these deviations:
(1) The genital pore remains on the ventral surface, but is situated
beside or behind the ventral sucker, or it becomes marginal, and is
then found in front of or beside the oral sucker, or at a lateral edge,
or, finally, in the centre of the posterior border; the ducts also
correspondingly alter their direction. (2) The ovary usually lies in
front of the testes, not rarely, however, behind them or between them.
(3) The three genital glands mostly lie together close in front of, or
behind, the centre of the body; they may be moved far back, and may
incidentally become separated one from the other. (4) The vitellarium
may be single, in which case it then may lie in the central field.
(5) A few forms possess but one, others several or numerous testes.
Amongst the ectoparasitic trematodes there are also species with but
one testis; but they mostly have several. As a rule, their uterus is
short, but the oötype well developed. Special canals (vagina), single
or double, are used for copulation, not the uterus. The vitelline
ducts also communicate with the intestine through the canalis
vitello-intestinalis (fig. 123).

The spermatozoa do not differ essentially in their structure from those
of other animals; the ovarian or egg cells are cells without integument
and contain a large nucleus and a little protoplasm; the vitellaria
also produce nucleated cells, in the plasm of which there are numerous
yellow yolk granules; the yolk cells detach themselves, like the
ovarian cells, from the ovarium, and pass into the oviduct to surround
each ovarian cell in the oötype. They disintegrate sooner or later in
the completely formed egg and are utilized as food by the developing


(1) _Copulation._--Observation has demonstrated that the one or
two vaginæ occurring in the ectoparasitic Trematodes are utilized
as female organs of copulation, and that the copulation is cross;
it is also known that Laurer’s canal, which was formerly generally
regarded as the vagina, has only quite exceptionally, if at all,
served the digenetic Trematodes as such--it appears to be homologous
with the canalis vitello-intestinalis of the _Monogenea_[261]--but
the terminal portion of the uterus, termed the metraterm, is used
for copulation. Cross-copulation occurs as well as auto-copulation
and auto-fecundation. The spermatozoa subsequently pass through the
entire uterus, which is still quite short at the time the male organs
are matured; the maturation of which, as usually is the case in
hermaphrodites, precedes that of the female organs. It is only later
with the onset of egg formation that the uterus is fully developed.
Copulation, however, takes place also in the case of fully grown forms
with completely developed uteri.

[261] _Monogenea_: Trematoda in which the anterior sucker, if present,
is double. Development without an intermediate host.

[Illustration: FIG. 128.--Ovum of _Fasciola hepatica_, L., cut
longitudinally. The lid has been lifted in the process. Within the
egg are numerous yolk cells, and at the lid end there is the still
unsegmented ovum (dark). 240/1.]

[Illustration: FIG. 129.--Miracidium of _Fasciola hepatica_ that
has just hatched from the egg, with a distinct cuticular ciliated
epithelium. Magnified. (From Leuckart.)]

(2) _Formation of the Ova._--The ovarian cells arising from the
ovary first become mature after their entry into the oötype by the
formation of three polar bodies, fertilization then taking place. At
the same time as the ovarian cell a number of yolk cells from the
vitellarium and secretion, drop by drop, from the shell gland reach
the oötype.[262] The shell is then formed during the generally active
contractions of the oötype walls and then passes on into the uterus.
In the uterus of the endoparasitic trematodes the eggs accumulate more
and more, often in large quantities, while in ectoparasitic species
generally only one or some few eggs can be found. The completed ova
are of various forms and sizes. They are mostly oval, at all events in
the digenetic trematodes, and the yellowish or brown shell is provided
with an opening at one pole which is closed by a watch-glass-shaped
lid (operculum). Appendages (filaments) on the shell--at one or both
poles--are uncommon, but are the rule in the ova of the _Monogenea_
(ectoparasitic species).

[262] [Recent work (_e.g._, Goldschmidt, _Zool. Anzeiger_, xxxiv,
p. 482) has shown that the older views regarding the formation of
the egg must be modified. In certain species, at any rate, the shell
material is formed by the yellow droplets of the yolk glands and not
by the so-called shell gland (Mehli’s gland) secretion, which is clear
and watery. The function of this secretion accordingly still requires
explanation; according to Looss it serves as a covering secretion for
the egg-shell proper. It appears also that other granules, the yolk
granules as distinct from the shell drop granules, are not always used
up during the development of the embryo and hence do not function as
yolk, so these also when they exist, and frequently they are wanting,
must serve some other purpose, possibly that of imbibing water for the
use of the embryo.--J. W. W. S.]

(3) _Deposition of the Ova._--Soon after their formation, the
_Monogenea_ (ectoparasitic trematodes) deposit round the place of
their attachment on the skin or the gills or other organs of their
hosts, eggs which attach themselves by means of their filaments. The
embryonic development thus takes place outside the parent. This also
holds good for the eggs of many endoparasitic species, although as a
rule in these the eggs are always retained for a longer time in the
uterus. Moreover, they usually here undergo a part or a whole of their
development, and are eventually deposited in those organs in which the
adult forms are parasitic, but this is not always the case, as the egg,
_e.g._, of _F. hepatica_ appears in bile (and fæces) quite unchanged.
By the natural passages they eventually get out of the body, and in
cases where such do not exist, as in the case of the blood-vessels, the
eggs pass out by means of the kidneys.

(4) _The embryonic development_, after irregular segmentation of the
ovum into a number of blastomeres, leads to the formation of a solid
blastosphere or morula, which is surrounded by a cellular investing
membrane (yolk envelope), while the principal mass of the cells forms
the embryo, which uses for its nourishment the yolk cells, which have
in the meantime disintegrated (_cf._ footnote, p. 223). Usually,
after the ova have reached water the embryos hatch out, leaving the
yolk envelope in the egg-shell; in other cases, however, the embryos
only hatch out after having been subjected to the influence of the
intestinal juices, that is to say, in the intestine of an intermediate
host which has ingested with its food the ova that have escaped from
the primary host.

(5) _The post-embryonic development_ of the Trematodes is accomplished
in various ways; the process is the most simple in the ectoparasitic
species (_Monogenea_), the young of which should certainly be
regarded as larvæ, because they possess characteristics (cilia,
simple gut, etc.) that are lacking in the adult worms, but which,
nevertheless, pass into the adult state direct after a relatively
simple metamorphosis. In the _Holostomata_,[263] a group found chiefly
in the intestine of aquatic birds, and which rarely occur in other
vertebrates, the ova develop in water. The young are ciliated all over,
and, after having entered an intermediate host (leeches, molluscs,
arthropods, amphibians, fishes) living in the water, they undergo a
metamorphosis into a second larval stage; they then encyst and await
transmission into the final host, where they become adult Metastatic
trematodes, _i.e._, trematodes without asexually produced generations
(p. 229).

[263] _Holostomata_: Prostomata with (in addition to the oral and
ventral suckers) a third fixation apparatus, generally on a separate
part of the body.

In the remaining so-called digenetic trematodes (p. 230) one or two
asexual generations interpose between the miracidium and terminal
stage, so that quite a number of adult worms may originate from one
egg. Usually the young, which are termed MIRACIDIA[264] (fig. 129),
hatch in water, where they move with the aid of their cilia. Sooner
or later they penetrate into an intermediate host, which is always a
snail or a mussel, and while certain of their organs disappear, they
grow into a gutless germinal tube (SPOROCYST, fig. 131). These are
simple elongated sacs with a central body cavity. They may or may
not have excretory tubules. In these, according to the species, the
larval stages (CERCARIÆ) that will ultimately become adult worms are
produced, or another intermediate generation is first formed, _viz._,
that of the REDIÆ[265] (figs. 132, 133), which are always provided with
an intestine, and these then give rise to cercariæ (figs. 130, 134).
The cercariæ, as a rule, leave their host and move about in the water
with the assistance of their rudder-like tails. After a little time,
however, they usually again invade an aquatic animal (worms, molluscs,
arthropods, fishes, amphibians), then they lose their tails and become
encysted (fig. 135); here they wait until they attain, together with
their host, the suitable terminal host, and in this new situation they
establish themselves and reach maturity. Or, again, the cercariæ may
themselves encyst in water or on foreign bodies (plants) and wait until
they are taken up directly by the terminal host, _e.g._, sheep.

[264] [Also known as ciliated embryos.--F. V. T.]

[265] [In _Fasciola hepatica_ in the summer months the rediæ give rise
to daughter rediæ, which then give rise to cercariæ.--J. W. W. S.]

[Illustration: FIG. 130.--A group of cercariæ of Echinostoma sp. (from
fresh water). 25/1.]

Accordingly the following conditions are necessary for the completion
of the entire development: (1) The terminal host in which the adult
stage lives; (2) an intermediate host into which the miracidia
penetrate and in which they become sporocysts; (3) a second
intermediate host in which the cercariæ become encysted. In certain
species, as in _Fasciola hepatica_, this second host is omitted, as the
cercariæ spontaneously encyst on plants, or again (in other species)
encystment may occur within the first intermediate host, when, in
fact, the cercariæ (which in this case do not acquire an oar-like tail)
do not swarm out of, but encyst themselves within their sporocysts. The
development, moreover, may be further complicated by rediæ appearing
in addition to the sporocysts, though this occurs in the first
intermediate host and not in a second one.

Animals that harbour adult digenetic Trematodes thus become infected by
ingesting encysted cercariæ, which either occur (1) in certain animals
(second intermediate hosts) on which they feed, or (2) in water, or
(3) on plants, or finally (4) in the first intermediate host; whereas
animals harbouring encysted cercariæ have been directly infected by
the corresponding tailed stage, and animals harbouring germinal tubes
(sporocysts or rediæ) have been infected by the miracidia.

[Illustration: FIG. 131.--Development of _Fasciola hepatica_, L. _a_,
the miracidium in optical section showing cephalic lobe, X-shaped
eye-spot resting on the cerebral ganglion, two germ balls; below each
of these a flame cell, and still lower germ cells lying in a cavity
(primitive body cavity). _b_, young sporocyst with two eye-spots, and
germ balls; the cells lining the cavity are not shown. _c_, older
sporocyst with a young redia. Magnified. (After Leuckart.)]

Thus certain species of ducks and geese become infected with
_Echinostoma echinatum_ by devouring certain water-snails (_Limnæus_,
_Paludina_) in which the encysted cercariæ occur. Oxen become infected
with _Paramphistomum cervi_ (= _Amphistomum conicum_) by swallowing
with water, cysts of this species which occur at the bottom of puddles
and pits. Sheep are infected with _Fasciola hepatica_ by eating grass
to which the encysted cercariæ of the liver-fluke are attached;
our song-birds infect themselves or their young with _Urogonimus
macrostomus_ by tearing off pieces containing the corresponding
sporocysts which are full of encysted cercariæ from snails (_Succinea
amphibia_), which act as the first intermediate hosts, and eating, or
offering their young these pieces.

(1) The MIRACIDIA of the digenetic Trematodes are comparatively highly
organized, and the mode of their formation from the segmentation cells
of the ovum is only imperfectly known. They have a cuticular epithelium
(fig. 129) entirely or partly covered with cilia, beneath this a
dermo-muscular tube composed of circular and longitudinal muscles;
also, a simple gut sac with an œsophagus, occasionally also with
pharynx, salivary glands and boring spine, also a cerebral ganglion
on which, in some species, there are eyes (fig. 131, _a_). As to the
excretory organs, they are represented by two symmetrically placed
terminal flame cells, with excretory vessels opening separately; there
is a more or less ample (primary) body cavity between the parietes of
the body and the gut; from the cellular parietal lining of this cavity
single cells (germ cells) become free (fig. 131, _a_, _b_), and become
rediæ or cercariæ.

[The germ cells of the miracidium and the germ balls of the
sporocyst arise, according to some observers, by further division of
undifferentiated blastomeres; according to others from the cells of the
lining wall of its body cavity. It is from these free germ balls that
the redia stage is developed.

[In the germ ball or morula appears an invagination, giving rise to
the cup-shaped gastrula stage. This elongates and forms the REDIA
(fig. 131, _c_).

[In the interior of the redia cells are budded off and develop into
gastrulæ, as in the case of the sporocyst. These become a fresh
generation of rediæ or give rise to the third stage (CERCARIA).]

[Illustration: FIG. 132.--Young redia of _Fasciola hepatica_, with
pharynx and intestine, with a circular ridge anteriorly and a pair of
processes posteriorly and masses of cells (germ balls) in the interior.
Magnified. (From Leuckart.)]

[Illustration: FIG. 133.--Older redia of _Distoma echinatum_, with
rudimentary intestine _i._; cercariæ, _c._; germ balls, _b._; and birth
pore, _g._ Magnified.]

(2) The SPOROCYSTS, on the contrary, which are produced direct from the
miracidia, are very simple, as all the organs of the latter disappear,
even to the muscles and excretory organs, during or after penetration
into the intermediate host, whereas the budded and still budding cells
of the wall of the (primary) body cavity continue to develop rapidly
and form germ balls. The sporocysts when fully developed have the
appearance of tubes or fusiform bodies with rounded edge; they are
frequently of a yellow colour. Their length rarely exceeds a few
millimetres; in some species their size increases exceedingly through
proliferation, and they then occupy a large portion of the body of the
intermediate host.

(3) The REDIÆ (figs. 132, 133), on the other hand, are more cylindrical
and always have a simple intestine of varying length, provided with
a pharynx; they likewise possess, situated near the circular ridge,
a “birth pore” which serves for the exit of the cercariæ originating
within them.

[Illustration: FIG. 134.--Cercaria of _Fasciola hepatica_; the
cutaneous glands at the side of the anterior body. Magnified. (After

[Illustration: FIG. 135.--Encysted cercaria of _Fasciola hepatica_.
Magnified. (After Leuckart.)]

(4) The CERCARIÆ[266] are very different; typically they consist of the
anterior body and the oar-like tail at the posterior end (fig. 134).
The former, even to the genitalia, has the organization of the adult
digenetic Trematodes, and thus allows the easy recognition of at least
the characters of that large group to which the species in question
belongs. On the other hand, however, there are also organs that are
lacking in the adult form, such as, in many, the boring spine in the
oral sucker, or the eyes situated on the cerebral ganglion; moreover,
also, cutaneous glands (fig. 134), the secretion of which forms the
cyst membrane. The oar-like tail may be long or short (stumpy-tailed
cercaria) or entirely absent; its free end may be partly split (furcate
cercaria), or split to its base (_bucephalus_); in various forms also
the anterior end of the tail is hollow, and has enclosed within it the
anterior body, which is otherwise free. The size also of the cercaria
belonging to the different species is very diverse; in addition
to forms swimming in the water that have the appearance of minute
milky-white bodies, there are forms which measure as much as 6 mm. in

[266] The cercaria is the characteristic larval stage of the
Trematodes, and corresponds to a cysticercus or cysticercoid, though
there is the important difference that the cercaria has an enteric
cavity. According to some observers the enteron is represented by the
frontal sucker of some Cestodes, and by the rostellum of the majority
of others.

The sporocyst and redia are regarded as intercalated stages, _viz._,
as cercariæ exhibiting _pædogenesis_, _i.e._, development of young by
a parthenogenetic process from individuals (_i.e._, cercariæ) not yet

The encysted cercariæ (fig. 135) are globular or oval, and are
surrounded by a homogeneous membrane, which may be striated or contain
granules. The tail is always cast off when encystment occurs, and
organs peculiar to the cercaria stage (boring papilla, eyes) almost
entirely disappear. On the other hand, the genitalia appear or become
more or less highly developed, in extreme cases to such an extent that
they become functional, and after autocopulation the creatures produce
ova within the cysts.

The cycle of development of the digenetic Trematodes has hitherto
been generally explained as a typical ALTERNATION OF GENERATIONS, one
sexual generation regularly alternating with one or two asexually
reproducing generations. Recent authors, however, regard the cells
in the sporocysts from which rediæ or eventually cercariæ arise as
parthenogenetically developing ova, and the sporocysts as well as the
rediæ as generations propagating parthenogenetically. In this case,
however, it is an alternation of a sexual not with an asexual but with
firstly a parthenogenetic generation (the sporocyst), the central cells
of which are regarded as ova which develop parthenogenetically into the
redia, and this the second parthenogenetic generation finally produces
larvæ (cercariæ) capable of developing into the sexually mature form.

Other authors, again, regard the development of the Digenea as only a
complicated metamorphosis (p. 283), which is distributed over several
generations before it is concluded.


Endoparasitic Trematodes, as fully developed organisms, occur in
vertebrate animals only, with very few exceptions; they inhabit almost
all the organs (with the exception of the nervous and osseous systems
and the male genitalia), but by preference the intestine in all its
extent from the oral cavity to the anus; and, further, certain species
or groups inhabit only quite restricted parts of the intestine.
Besides in the intestine other species live in the liver, or in the
bile-ducts, or in the gall-bladder; other accessory organs of the
intestine, such as the pancreas, bursa Fabricii (of birds), are only
infected by a few species. Many inhabit the lungs, or the air sacs in
fowls, a few the trachea. Trematodes have also been known to occur in
the urinary bladder, the urethra and the kidneys of all classes of
vertebrates; they are also present in the vascular system of a few
tortoises, birds and mammals; in birds they even penetrate from the
cloaca into the oviducts, and are occasionally found enclosed in the
laid eggs; one species is known to occur in the cavum tympani and in
the Eustachian tube of a mammal (Dugong), another in the frontal sinus
of the polecat; several species infest the conjunctival sac under the
membrana nictitans of birds, one species even lives in cysts in the
skin of song-birds. In an analogous manner the ectoparasitic Trematodes
are not entirely confined to the surface of the body or the trachea
of the lower vertebrate animals; a few species appear exclusively in
the urinary bladder, in the œsophagus, and in the case of sharks in an
accessory gland of the rectum.

Trematodes live free and active within the organs attacked, though they
may attach themselves by suction for a longer or shorter period; in
other cases, however, they bore more or less deeply into the intestinal
wall with their anterior end, or lie in cysts of the intestinal wall
which only communicate with the lumen through a small opening; in those
species living in the lungs of mammals the host likewise produces a
cyst, which usually encloses two specimens; such association of a pair
is also observed in other situations, and, though this is the rule in
species sexually distinct, it is not entirely confined to these.

As regards the AGE attained by endoparasitic Trematodes, there are but
few reliable records, and these differ considerably; the overwhelming
majority of species certainly live about a year, or perhaps a little
longer, but there are some whose term of life extends to several or
many years.

Trematodes are but rarely found encysted in the higher vertebrate
animals; the condition, however, is more frequent in amphibians, and
especially in fishes, as well as in numerous invertebrate animals.


The following classification, partly artificial, partly natural,
embraces only the flukes found in man:--

Order. *Digenea*, v. Beneden, 1858.

  Anterior sucker single and median, present. Eggs few. The
  (specialized) terminal portion of the uterus serves as a vagina.
  Development indirect, _i.e._, an intermediate host is required.

Sub-order. *Prostomata*, Odhner, 1905.

  Mouth surrounded by the anterior sucker.

Group. *Amphistomata*, Rudolphi, 1801, ep., Nitzsch, 1819.

  Gut forked, two suckers, the posterior sucker (acetabulum) terminal
  or ventro-terminal behind the genitalia, or at most embraced by the
  vitellaria. Skin with no spines. Excretory bladder a simple sac
  opening dorsally near hind end. Testes in front of ovary. Genital
  pore, median in anterior third of body. Thick flukes, almost circular
  in cross section.

Family. *Paramphistomidæ*, Fischoeder, 1901.

  Amphistomata: Body not divided into a conical anterior portion and
  disc-like caudal portion. Ventral pouch absent.

Sub-family. *Paramphistominæ*, Fisch., 1901.

  Paramphistomidæ: Oral sucker without evaginations. Not in man.

Sub-family. *Cladorchiinæ*, Fisch., 1901.

  Paramphistomidæ: Oral sucker with evaginations; testes, two, deeply
  cleft (fig. 137). Genera: _Watsonius_, _Cladorchis_, etc.

Family. *Gastrodisciidæ*, Stiles and Goldberger, 1910.

  Amphistomata: With body divided into a conical cephalic and disc-like
  caudal portion (fig. 138). Posterior sucker ventro-terminal. Oral
  sucker with evaginations. Genera: _Gastrodiscus_ and _Homalogaster_.

Group. *Distomata*, Retzius, 1782.

  Gut forked, two suckers, the posterior sucker (acetabulum) ventral.
  It is always separated from the hind end by at least a part of the

Family. *Fasciolidæ*, Railliet, 1895.

  Large flat forms, genital pore _in front_ of ventral sucker, the
  latter powerful. Vitellariæ of numerous follicles, united by
  branching vitellarian ducts, at the sides of the body meeting
  posteriorly and extending ventrally and dorsally. Cirrus and vagina
  without spines. No crown of strong spines around sucker. Testes much
  branched. Uterus not well developed. Excretory bladder much branched.
  Eggs large.

Sub-family. *Fasciolinæ*, Odhner, 1910.

  Large or median forms, gut much branched. Body has a shoulder
  separating head from body. Receptaculum seminis absent. Ovary
  branched, ventral sucker in anterior part of body. Genus: _Fasciola_.

Sub-family. *Fasciolopsinæ*, Odhner, 1910.

  Shoulder absent. Receptaculum seminis present. Ovary branched, gut
  takes a zig-zag course with kinks on it, ventral sucker in anterior
  part of body. Genus: _Fasciolopsis_.

Family. *Opisthorchiidæ*, Braun, 1901, emend. auctor.

  Ovary in front of testes. Small to medium flukes, very transparent,
  tapering anteriorly. Vitellaria moderately developed not extending
  in front of sucker. Cirrus absent. Seminal vesicle a twisted tube
  free in parenchyma. Testes near hind end one behind the other, lobed
  or branched, but not dendritically. Excretory bladder *Y*-shaped,
  the two limbs short, the stem *S*-shaped passing between the testes.
  Receptaculum seminis well developed. Laurer’s canal present. Uterine
  coils transverse, numerous. Eggs small.

Sub-family. *Opisthorchiinæ*, Looss, 1899, emend. auctor.

  _Opisthorchiidæ_ in which the excretory pore is terminal. Excretory
  bladder long, dorsal to testes. Uterine coils not overlapping gut
  forks. Genera: _Opisthorchis_, _Paropisthorchis_, _Clonorchis_,
  _Amphimerus_, etc.

Sub-family. *Metorchiinæ*, Lühe, 1909.

  _Opisthorchiidæ_ in which the excretory pore is ventral. Excretory
  bladder short, ventral to testes. Uterine coils partly overlapping
  gut forks and extend anteriorly beyond the sucker. Vitellaria
  compressed on the sides of the body. Genus: _Metorchis_.

Family. *Dicrocœliidæ*, Odhner, 1910.

  Ovary _behind_ testes. Testes behind the ventral sucker, between it
  and the ovary. Body thin and transparent. Cirrus sac encloses the
  pars prostatica and seminal vesicle. Skin smooth. Gut forks do not
  reach posterior end. Receptaculum seminis and Laurer’s canal present.
  Vitellaria, moderate, lateral in mid-body slightly overlapping the
  gut. Uterus with an ascending and descending branch and numerous
  transverse coils extending to hind end. Eggs dark brown, 25 µ to
  60 µ. Excretory bladder tubular in posterior third or half of body.
  Parasitic in bile-ducts of mammals and birds. Genus: _Dicrocœlium_.

Family. *Heterophyiidæ*, Odhner, 1914.

  Ovary _in front_ of testes. Genital pore _behind_ or on a level with
  ventral sucker. Genital pore surrounded by a pseudo-sucker (_i.e._,
  its muscle is not sharply separated from but blends with the body
  muscles). Cirrus sac absent, consequently vesicula seminalis and pars
  prostatica lie free. Vagina and ejaculatory duct unite into a common
  duct before opening. Small and very small forms. Body covered with
  scales. Genera: _Heterophyes_, _Metagonimus_, etc.

Family. *Troglotremidæ*, Odhner, 1914.

  More or less flattened Distomes of compact form, 2 to 13 mm. long.
  Ventral surface flat or somewhat hollowed, dorsal surface _arched_.
  Skin completely covered with pointed spines. Musculature weakly
  developed also in the suckers in those forms that inhabit cysts. Gut
  with pharynx and a not very long œsophagus and cæca, which end more
  or less shortly before the hind end. Excretory bladder *Y*-shaped or
  tubular. Pars prostatica and seminal vesicle always distinct. Testes
  elongated, symmetrically placed in or behind the middle of the body.
  Ovary directly in front of the testes, right-sided, generally much
  lobed. Receptaculum seminis and Laurer’s canal present. Vitellaria
  generally well developed, exclusively or for the most part confined
  to _the dorsal surface_, leaving only a median band unoccupied.
  Uterus either very long, coiling here and there, or shorter and more
  convoluted. Eggs in first case small 17 µ to 25 µ, in the second much
  larger 63 µ to 85 µ or even 120 µ (?) long. Parasitic in carnivora or
  birds, generally occurring in pairs in cyst-like cavities. Genera:
  _Paragonimus_, _Pholeter_, _Collyriclum_, _Troglotrema_.

Family. *Echinostomidæ*, Looss, 1902.

  _More or less elongated flukes, small or very large, much flattened
  anteriorly, less so posteriorly, or even round. Suckers near one
  another, the anterior small and weak, the posterior large and
  powerful directed obliquely backwards. Surrounding the oral sucker
  dorsally and laterally but not ventrally is a fold or “collar”
  bearing a row or rows of pointed spines which are continued round
  laterally on to the ventral corners, the number being constant
  for each species, the corner spines large or specialized, skin
  anteriorly scaled or spiny. Alimentary canal consists of a pharynx,
  epithelial “pseudo-œsophagus” and gut cæca reaching to posterior
  end. Testes behind one another in hind body. Ovary on right side
  or median directly in front of the testes. Vitellaria lateral,
  usually extending to the hind end and not beyond the ventral sucker
  anteriorly. Genital pore just in front of ventral sucker. Uterus
  in transverse loops. Genital sinus absent or present. Receptaculum
  seminis and Laurer’s canal present. Eggs thin shelled and large,
  bright yellow, 65 µ to 120 µ long. Excretory bladder *Y*-shaped.
  Parasitic in gut of vertebrates, especially birds._

Sub-family. *Echinostominæ*, Looss, 1899.

  _Cirrus sac usually reaching to centre of ventral sucker, but not
  beyond. Cirrus long, usually without spines, coiled when retracted.
  Seminal vesicle tubular, twisted. On the head a ventral uniting ridge
  between the angles of the collar. Dorsal circlet of spines, single or
  double, not interrupted unless the collar itself is dorsally divided.
  Genera_: Echinostoma, etc.

Sub-family. *Himasthlinæ*, Odhner, 1910.

  Cirrus sac reaching far beyond ventral sucker. Cirrus armed with
  strong rose-thorn-shaped hooks. Vesicula seminalis tubular not
  coiled. Cervical collar not continued across ventral aspect. Spines
  on collar in one row. Body armed with fine needle-shaped spines.

Family. *Schistosomidæ*, Looss, 1899.

  Sexes separate. Genital pore behind the ventral sucker. Ventral
  sucker elevated above the surface. Pharynx absent. Gut forks reunite
  to form a single stem. In ♂ four or more testicular follicles. In ♀ a
  single ovary, just in front of the union of the gut forks. Vitellaria
  on either side of the united gut stem.


Family. *Paramphistomidæ*, Stiles and Goldberger, emend. 1910.

Sub-family. *Cladorchiinæ*, Fisch., 1901.

Genus. *Watsonius*, Stiles and Goldberger, 1910.

  _Cladorchinæ_.--Body pyriform. Ventral pouch absent. Acetabulum
  ventral or (?) ventro-subterminal, very large, margins projecting,
  aperture small. Genital pore in front of bifurcation of gut, not
  surrounded by a sucker; ductus hermaphroditicus apparently absent.
  Excretory pore at posterior end of excretory vesicle, behind Laurer’s
  canal. Oral sucker with a pair of irregularly globular suctorial
  pouches; œsophagus thickened distally; cæca long, not wavy; end in
  acetabular region.

  _Male Organs_.--Testes two lobed, smaller than acetabulum;
  longitudinally, nearly or quite coinciding; transversely they abut or
  slightly overlap; preovarial in equatorial and caudal thirds. Pars
  musculosa not largely developed; cirrus pouch absent.

  _Female Organs_.--Ovary and shell gland post-testicular. Vitellaria
  extend from gut fork to slightly beyond gut ending; uterus
  intercæcal, partly post-testicular. Laurer’s canal in front of
  excretory vesicle.

  _Type Species_.--_Watsonius watsoni_, Conyngham, 1904.

*Watsonius watsoni*, Stiles and Goldberger, 1910.

  Syn.: _Amphistomum watsoni_, Conyngham, 1904; _Cladorchis watsoni_,
  Shipley, 1905.

_Body_, 8 to 10 mm. long, by 4 to 5 mm. broad, by 4 mm. thick; tapers
anteriorly to 2·5 mm. Caudal extremity bluntly rounded, venter
surrounded by an elevated ridge, surface with transverse ridges best
defined ventrally. Genital pore median about one-quarter of body length
from anterior end at level of suctorial pouches. Acetabulum 1 mm. in
diameter, margin projecting, aperture small. Mouth in a groove with
digitate papillæ. Oral sucker very large, one-fifth of length of body,
with a pair of irregularly globular pouches. Œsophagus somewhat longer
than sucker. Excretory pore at the level of the acetabular aperture.
The vesicle extends from the plane of the transverse vitelline ducts to
centre of acetabulum.

[Illustration: FIG. 136.--_Watsonius watsoni_: ventral view. 4/1.
(After Shipley.)]

_Male Organs_.--Testes deeply notched adjoining one another. Vesicula
seminalis much coiled and dilated, pars musculosa not coiled. Pars
prostatica (?) dilated, ejaculatory duct long and narrow, opening on a
papilla; genital atrium papillated.

_Female Organs._--Ovary dorso-posterior of posterior testis. Shell
gland dorsal to ovary. Vitellaria ventral and lateral to gut cæca
extending from gut fork to equator of acetabulum. Uterus dorsal to
testes, ductus hermaphroditicus absent. Laurer’s canal opens in
dorso-median line slightly behind anterior border of sucker.

[Illustration: FIG. 137.--_Watsonius watsoni_: ventral projection
composed from a series of transverse sections. _o.s._, oral sucker;
_s.p._, suctorial pouch; _ga._, genital atrium; _d.e._, ejaculatory
duct; _es._, œsophagus; _e.g._, œsophageal ganglion; _p.p._, pars
prostatica; _p.m._, pars musculosa; _i._, gut; _ut._, uterus; _v.e._,
vas efferens; _v.e.s._, left vas efferens; _v.e.d._, right vas
efferens; _v.g._, vitellarium; _t._, testes; _ov._, ovary; _s.g._,
shell gland; _t.vd._, transverse vitelline duct. (After Stiles and

_Eggs._--123 µ to 133 µ long by 75 µ to 80 µ broad.

_Habitat._--Jejunum and duodenum of man, German West Africa. The
parasite has only been found once in man. The patient, a negro from
German West Africa, died at Zola, Northern Nigeria. The symptoms were
persistent watery diarrhœa without blood or mucus. The parasites were
also passed in the stools. It occurs also in monkeys.

Family. *Gastrodisciidæ*.

Genus. *Gastrodiscus*, Lkt., 1877.

  Acetabulum small, caudal and ventral margin raised, aperture
  relatively large. Genital pore without sucker. Excretory pore
  post-vesicular, posterior to opening of Laurer’s canal. Œsophagus
  with muscular thickening; cæca not wavy, long, end post-equatorial
  and post-testicular.

  _Male Genitalia._--Testes two, branched pre-ovarial.

  _Female genitalia._--Ovary and shell gland post-testicular.
  Vitellaria extracæcal; uterus intercæcal; Laurer’s canal entirely

  _Type._--_Gastrodiscus ægyptiacus_, Cobbold, 1876.

*Gastrodiscus hominis*, Lewis and McConnell, 1876.[267]

  Syn.: _Amphistomum hominis_, Lew. and McConn.

[267] Leiper places this species in a new genus _Gastrodiscoides_.
Genus _Gastrodiscoides_, Leiper, 1913, distinguished from
_Gastrodiscus_ by: (1) large genital cone; (2) position of genital
orifice; (3) disc without papillæ; (4) testes one behind the other.

[Illustration: FIG. 138.--_Gastrodiscus hominis._ Slightly magnified.
(After Lerckart.)]

_Body_, reddish in the fresh, 5 to 8 mm. long; posteriorly, 3 to 4 mm.
broad. The disc has incurved edges which are interrupted in front where
it joins the anterior cylindrical portion and posteriorly behind the
ventral sucker. The disc itself and ventral surface are covered with a
number of (microscopic) papillæ. Pharynx provided with two diverticula
or pouches. The bifurcation of the gut lies sometimes above, sometimes
below the level of the genital pore. The gut cæca end about the level
of the centre of the acetabulum.

_Genital Pore._--About the middle of the conical anterior portion. (It
appears to be surrounded by a muscular sucker.) Leiper (1913) describes
the ducts as discharging at the tip of a large fleshy papilla, the
surface of which bears cuticular bosses.

_Testes_ much lobed, the anterior is smaller than the posterior and
lies at about the level where the anterior conical portion joins the
disc. The posterior testis just in front of the anterior margin of the
acetabulum separated from it by the ovary. The ovary, somewhat oval in
shape or slightly constricted in the middle, lies slightly to the right
of the median line. Dorsal to it lies the well-developed shell gland,
Laurer’s canal opening in front of the excretory bladder. The excretory
bladder is a long sac with its opening at its posterior extremity
about the level of the middle of the acetabulum. The vitellaria are
restricted in extent. They do not extend forward beyond the anterior
border of the posterior testis. They are best developed in the area
between the acetabulum and the termination of the gut cæca.

The eggs are oval and measure 150 µ in length by 72 µ in breadth.

_Habitat._--Cæcum and large intestine of man. Also in the pig (5 per
cent.) in Annam.

_Distribution._--This parasite has been recorded from Assam (not
uncommon), British Guiana (Indian immigrants), and Cochin China.

_Gastrodiscus ægyptiacus_, Cobbold, 1876, and _G. secundus_, Looss,
1907, occur in the horse; _G. minor_, Leiper, 1913, in the pig in
Nigeria and Uganda.

Family. *Fasciolidæ*, Raill., 1895.

Sub-family. *Fasciolinæ*, Odhner, 1910.

Genus. *Fasciola*, L., 1758.

  The ventral sucker is situated at the level of the junction of the
  cone with the body, _viz._, at the level of the “shoulder,” and is
  large and powerful. The cuticle is covered with strong spines; the
  gut cæca run in the mid-line to the hind end, and are provided with
  numerous long lateral and fewer and shorter median branches. The
  ovary lies on one side in front of the transverse vitelline duct;
  the testes lie obliquely one behind the other. The uterus, in the
  shape of a rosette, lies in front of the genitalia. Laurer’s canal
  is present; the vesicula seminalis lies in the cirrus pouch; the ova
  are large, not very numerous, and only develop after they have been
  deposited. Parasites of the biliary ducts of herbivorous animals.

*Fasciola hepatica*, L., 1758.

  Syn.: _Distomum hepaticum_, Retz., 1786; _Fasciola Humana_, Gmel.,
  1789; _Distomum caviæ_, Sons., 1890; _Cladocœlium hepaticum_, Stoss.,

Length 20 to 30 mm., breadth 8 to 13 mm., cephalic cone 4 to 5 mm.
in length and sharply differentiated from the body by a shoulder on
each side. Spines in alternating transverse rows and extending on
the ventral surface to the posterior border of the testes, and on
the dorsal surface not quite so far. The spines are smaller on the
cephalic cone than on the posterior part of the body, where they are
discernible with the naked eye. The suckers are hemispherical, and
near each other; the oral sucker is about 1 mm. and the ventral sucker
about 1·6 mm. in diameter. The pharynx, which includes almost the
entire œsophagus, measures 0·7 mm. in length and 0·4 mm. in breadth.
The intestine bifurcates at the limit of the cephalic cone and the
branches are even here furnished with diverticula directed outwardly.
The ovary is ramified and situated in front of the transverse vitelline
duct, usually on the right side; the shell gland lies near the ovary
in the median line; posterior to the transverse vitelline ducts are
the greatly ramified testes, which occupy the greater portion of the
posterior part of the body, with the exception of the lateral and
posterior border; the long vasa efferentia only unite as they enter the
cirrus pouch. The vitellaria occupy the sides of the posterior part of
the body, commencing at the level of the ventral sucker and uniting
behind the testes. The ova are yellowish-brown, oval, operculated,
130 µ to 145 µ in length, 70 µ to 90 µ in breadth (average size 132 µ
by 70 µ).

[Illustration: FIG. 139.--_Fasciola hepatica_, L. From a specimen that
is not yet mature, showing the gut and its branches. 5/1.]

The Liver Fluke inhabits the bile-ducts of numerous herbivorous mammals
(sheep, ox, goat, horse, ass, rabbit,[268] guinea-pig, squirrel,
beaver, deer, roe, antelope, camel, kangaroo, and others), and is
distributed over the whole of Europe, though not to an equal extent. It
is further known in North Africa, in North and South America, as well
as in Australia; it is also found in Asia, as it has been reported from
Japan, China, and Tonkin (Gaide, two cases in man). In some districts
of Germany it is very frequent, and the slaughter-house statistics of
various places show that it is of daily occurrence. _Fasciola magna_
occurs in herbivora in America.

[268] [There does not seem to be any direct evidence of either rabbits
or hares normally being invaded by this fluke.--F. V. T.]

The liver fluke, however, is by no means a harmless parasite, for it
produces in domestic animals, more especially in sheep, a disease of
the liver that appears epidemically in certain years and districts, and
commits great ravages amongst the flocks.

[The following records show the enormous loss caused in sheep by this
parasite. In 1812, in the Midi, principally in the Departments of
the Rhône, Herault, and Gard, the disease was rampant; 300,000 sheep
perished in the Arles territory, and 90,000 in the Arrondissements of
Nîmes and Montpellier. In 1829 and 1830, in the Department of the
Meuse and near localities, not only sheep but oxen died in enormous
numbers; for instance, in the Arrondissement of Verdun out of 50,000
sheep 20,000 died, and out of 20,000 cattle 2,200 died. In England, in
1830, 2,000,000 sheep were carried off; whilst in 1862 60 per cent.
of the sheep died in Ireland; and in 1879 over 300,000 were lost in
England; whilst as late as 1891 one owner in the same country lost over
10,000 sheep (_Live Stock Journal_, October 30, 1891).--F. V. T.]

[Illustration: FIG. 140.--_Fasciola hepatica._ _M._, mouth; _Ut._,
uterine rosette; _Tr.c._, transverse vitelline ducts uniting to form a
vitelline receptacle in the mid-line; _E.d._, longitudinal vitelline
ducts; _V.s._, vitellaria. The clear space in the centre represents the
position of the ramifying testes and part of the gut. Natural size.
(Mull. fluid, alcohol, creosote, Canada balsam.)]

[Illustration: FIG. 141.--_Fasciola hepatica_, L. _I._, intestine;
_Vs._, vitellaria; _Ov._, ovary; _O._, oral aperture; _Ut._, uterus;
_S._, ventral sucker; _T._, testes. In front of the testes are seen
the transverse vitelline ducts uniting to form the pyriform vitelline
receptacle. Immediately in front of this the spherical shell gland. The
two vasa efferentia can also be seen running up in the mid-line. The
branches of the gut are only shown in the cephalic cone. (After Claus.)]

The disease usually commences towards the end of summer with an
enlargement of the liver, induced by the invasion of numerous
young flukes; in the autumn and winter the animals suffer from the
consequences of disordered biliary secretion; they become feverish,
emaciated, and anæmic, and lose their appetite. In consequence of the
consecutive atrophy of the liver, œdema and ascites set in, and many
animals succumb to this “liver rot.” On examination the liver is found
to be shrunken, the bile-ducts are enormously dilated and in parts
saccular and full of flukes. Should the animals survive this stage,
spontaneous recovery ensues in consequence of the flukes commencing to
leave the liver in the spring, but the liver remains changed and its
sale is prohibited[269] when the changes are extensive.[270]

[269] [This is not the case in Great Britain; fluky sheep are sent to
market, there being no danger to man from eating the flesh.--F. V. T.]

[270] As an example, this occurred in Berlin in the case of 19,034
oxen, 15,542 sheep, 1,704 pigs, and 160 calves in the period of
1883–1893; during which time 719,157 oxen, 1,519,003 sheep, 2,258,110
pigs, and 567,964 calves were slaughtered. As a matter of fact,
however, the number of infected beasts was really larger.

[The following stages may be noticed in sheep suffering from
fascioliasis. Gerlach recognized four stages, based on the varied
relations that the flukes contract with the liver of their host. These
periods are sometimes very marked, but at others, owing to subsequent
infections, the features become merged and so obliterated. But when a
single infestation occurs they are very marked.

[The first period is called the PERIOD OF IMMIGRATION. This occurs at
the fall of the year and generally passes unperceived, as the young
flukes do little harm to the liver. It varies from four to thirteen
weeks. Gerlach has remarked upon cases of death from apoplexy at this

[The second period is the PERIOD OF ANÆMIA. This occurs in November
and December. The sheep at first fatten rapidly, but later the mucous
membranes become pale and of a yellowish hue, and the sheep become
sluggish and cease to feed. The fæces are normal, but may contain fluke

[Illustration: FIG. 142.--_Fasciola hepatica_: egg from liver of sheep.
_o_, operculum, _e_, segmenting ovum. The rest of the space is occupied
by yolk cells, the granules in three only being shown. × 680. (After

[Illustration: FIG. 143.--_Limnæus truncatulus_, Müll., the
intermediate host of _Fasciola hepatica_. _a._, natural size; _b._,
magnified. (From Leuckart.)]

[The third period is the PERIOD OF WASTING. This corresponds with the
beginning of January--about three months after the entry of the larvæ.
Emaciation now becomes very marked, the skin and mucous membranes
blanched, temperature variable and marked by an irregular curve;
respiration laboured and quick; appetite regular; abortion frequently
occurs in pregnant ewes; pressure on the back causes the animals to
fall; local œdemas occur, the most perceptible in the submaxillary
space, extending below the larynx and over the cheeks and parotids
(called “bourse,” “boule” in France; “watery poke” or “cockered” in
England). Death usually occurs at this period, but a fourth stage may

[The fourth period is the PERIOD OF MIGRATION OF THE FLUKES. This
is a period of convalescence and recovery, generally in May and
June.--F. V. T.]

Oxen suffer less in general, but even in these animals “stray” hepatic
flukes are occasionally found in the lungs, enclosed in thick-walled

_Pathological Anatomy._--The bile-ducts are conspicuous on the surface
of the liver. They are thickened and much dilated and in parts
saccular, and considerable atrophy of the liver cells accompanies
the condition. Histologically there is immense proliferation of the
epithelium of the bile-ducts leading to “adenomata.”

The LIFE-HISTORY of the liver fluke was discovered by R. Leuckart and
P. Thomas. According to these investigators the elongated miracidium
(fig. 131, _a_) ciliated all over develops from the eggs a few weeks
after the latter (fig. 142) have reached the water, and after it has
become free the embryo penetrates and becomes a sporocyst (fig. 131,
_b_) in a water-snail (_Limnæus truncatulus_, Müll. = _L. minutus_,
Drap.) that is common in fresh water, and can live in the smallest
collection of water as well as in fields that have been flooded. The
sporocyst first of all produces rediæ, which remain in the same host
(and under certain circumstances, _e.g._ in summer, these develop
a second generation of rediæ), and these finally form cercariæ
(fig. 134). The latter become encysted on blades of grass and are taken
up by the respective hosts with their food; this takes place towards
the end of summer, while the sheep feeding on the pasture land in the
spring spread the eggs of the fluke, and sometimes the fluke itself, by
passing them with their fæces.

In districts where _Limnæus truncatulus_ is absent, analogous species
act as the intermediary hosts, of which one example according to Lutz
is _Limnæus oahuensis_ in the Sandwich Islands.

[The host in Europe is _Limnæus truncatulus_. This snail extends from
Siberia to Sicily and Algeria, and according to Captain Hutton is a
native of Afghanistan. It also occurs in Thibet, Amoor, Morocco,
Tunis, Canary Islands and the Faroe Islands. It deposits its eggs or
spawn upon the mud around ponds, ditches and streams. The eggs are laid
in batches of thirty to a hundred, each snail laying as many as 1,500
eggs; they are united into strips of a gelatinous substance. In about
two weeks young snails appear. It is amphibious, being more frequently
met with out of the water than in it. It occurs in elevated spots as
well as in low-lying districts. Moquin-Tandon found it at 4,000 feet
in the Pyrenees. In the allied species, _L. peregra_, the fluke will
develop up to a certain stage, but never completes all its varied

[In South America the host is probably _Limnæus viator_, Orb., and in
North America _Limnæus humilis_, Say.--F. V. T.]

In human beings as well as in some of the mammals quoted above, the
liver fluke is only a casual parasite, and hitherto only twenty-eight
cases have been observed in man; the infection was mostly a mild one
and there were no symptoms, or only very trifling ones; a few isolated
cases were only discovered _post mortem_. Occasionally, however, even
when the infection was inconsiderable, severe symptoms were set up,
which in isolated cases led to death. The symptoms (enlargement and
painfulness of the liver, icterus) merely pointed to a disease of the

_Diagnosis_ can only be established by finding eggs in the fæces. Care
should be taken not to confuse them with those of _Dibothriocephalus


[Illustration: FIG. 144.--Young _Fasciola hepatica_, soon after
entry into the liver. The intestinal cæca have lateral diverticula.
Magnified. (From Leuckart.)]

In North Lebanon, the liver fluke is, according to A. Khouri, a
frequent parasite of man, not in the liver, however, but in the
pharynx. The occurrence in this unusual site is effected by the eating
of raw infected livers, especially those of goats (_Capra hircus_). The
flukes thus taken in do not all reach the stomach, where they would
be soon killed, but some of them attach themselves to the pharyngeal
mucosa and to the adjoining parts, and there cause inflammation and
swelling, which lead to dyspnœa, dysphagia, dysphonia and congestion of
the head, sometimes even to still more severe symptoms, and even death.
The affection termed “Halzoun” lasts some hours or several days, and
after vomiting recovery sets in. In other cases man becomes infected in
the usual way by ingesting cysts attached to grass or the underside of
leaves of plants (_e.g._, Rumex sp.), where they are overlooked from
their scanty size (0·2 to 0·3 mm.).

[Illustration: FIG. 145.--_Fasciola gigantica._ × 6-1/2 (After Looss.)]

As the liver fluke feeds on blood it is possible that it also reaches,
particularly when young, the circulatory system, and cases have been
known in which it has been carried by the blood into organs far
from its original situation. Such cases also have been repeatedly
observed in men. Probably the parasite described by Treutler, 1793, as
_Hexathyridium venarum_, which protruded from the ruptured anterior
tibial vein of a man, was a young liver fluke. A few adult specimens
were found by Duval in the portal and other veins _post mortem_ at
Rennes (1842) in a man, aged 49, and a similar statement is reported
by Vital from Constantine (1874). Giesker, in 1850, found two hepatic
flukes in a swelling on the sole of the foot of a woman. Penn Harris
states that he observed six specimens in Liverpool in a spontaneously
ruptured abscess of the occiput of a two months old infant. Another
case which, like the previous one, is reported by Lankester,[271]
relates to a sailor who suffered from an abscess behind the ear, and
from which a liver fluke was expelled. Finally, Dionis de Carrières
reports the case of a man, aged 35, in whose right hypochondriac region
a tumour the size of a pigeon’s egg had formed, and from which a young
liver fluke was extracted.

[271] In the English translation of Küchenmeister’s work on
Parasitology (London, 1857). The specimen is preserved in the Hunterian
Museum, London, and is an adult liver fluke, measuring 18 mm. in length
and 7 mm. in breadth.

From such records it is not impossible that _Distomum oculi humani_,
Ammon, 1833, as well as _Monostomum lentis_, v. Nordm., 1832, may
have been very young hepatic flukes that had strayed. Ammon found
four specimens (length 0·5 to 1 mm.) of his species (named _Distomum
ophthalmobium_ by Diesing in 1850) between the opaque lens and the
capsule of a five months old child in Dresden, and von Nordmann
discovered his _Monostomum lentis_ to the number of eight specimens
(only 0·3 mm. in length) in the opaque lens of an old woman. Minute
white bodies which Greef found in the cortex of the lens of a
fisherman, aged 55, removed on account of cataract, were with some
reserve regarded as Trematode larvæ. The fact that Ammon found that
the intestinal cæca of the worm discovered by him had no lateral
branches does not negative the above opinion, as in the liver fluke
the intestinal cæca are originally unbranched, and according to Lutz
they only develop lateral ramifications later, between the twelfth and
twenty-second day of infection (fig. 144).

*Fasciola gigantica*, Cobbold, 1856.

  Syn.: _Distomum giganteum_, Diesing, 1858; _Fasciola gigantea_,
  Cobbold, 1858; _Cladocœlium giganteum_, Stoss., 1892; _Fasciola
  hepatica_ var. _angusta_, Raill., 1895; _Fasciola hepatica_ var.
  _ægyptiaca_, Looss, 1896.

This species is closely allied to _Fasciola hepatica_, but is
distinguished by its elongated body, short cephalic cone, almost
parallel sides, larger ventral sucker, which is also closer to the oral
sucker, and by its larger eggs. Length up to 75 mm., width up to 12 mm.
Oral sucker 1 to 1·2 mm., ventral sucker up to 1·7 mm. in diameter.
Eggs 150 µ to 190 µ long by 75 µ to 90 µ broad.

_Habitat._--Bile-ducts of _Camelopardalis giraffa_, _Bos taurus_, _Bos
indicus_, _Bos bubalis_, _Ovis aries_ and _Capra hircus_.


This species has once been observed in man by Gouvea, in Rio de
Janeiro, in a French naval officer who became ill with fever, cough
and slight blood-spitting. The lungs were normal except for a sharply
circumscribed spot at the base of the left lung. Twenty days later
during a fit of coughing the patient spat up a fluke 25 mm. long,
characterized by its slender aspect and by the size of its ventral
sucker, and its close proximity to the oral sucker. Considering the
fact that Gouvea’s patient had spent many weeks in July of the same
year in Dakar (Senegambia), where according to Railliet _Fasciola
gigantica_ is common in slaughtered animals, and considering also the
characters of the fluke, Railliet rightly assumes that one had to do
with the African giant fluke and that the patient had infected himself
in Dakar.

Sub-family. *Fasciolopsinæ*, Odhner, 1910.

Genus. *Fasciolopsis*, Looss, 1898.

  Ventral sucker large, and elongated posteriorly into a sac. Cirrus
  pouch long and cylindrical, its greatest length being occupied by the
  sinuous tubular seminal vesicle, on which exists a peculiar cæcal
  appendage. Laurer’s canal present.

*Fasciolopsis buski*, Lank., 1857.

  Syn.: _Distomum buski_, Lank., 1857; _Dist. crassum_, Cobbold, 1860,
  _nec_ v. Sieb., 1836.

[Illustration: FIG. 146.--_Fasciolopsis buski_, Lank. _V.s._,
ventral sucker; _C.p._, cirrus pouch; _I._, intestinal fork; _S.v._,
vitellaria; _T._, testes; _O._, ovary; _Ms._, sucker; _Shg._, shell
gland; _Ut._, uterus. Magnified. (After Odhner.)]

The length of the body varies; it may measure 24 to 37 or even attain
70 mm.; the breadth is from 5·5 to 12 to 14 mm. In the pig the fresh
parasites measure, smallest, 12 to 8 mm.; largest, 35 to 16 mm. (Mathis
and Léger). Skin without spines, but according to Heanly always
present in man and pig specimens. The oral sucker measures 0·5 mm.
in diameter; the ventral sucker is three to four times as large; the
pharynx is globular, 0·7 mm. in diameter; the prepharynx is provided
with a sphincter; the intestinal cæca extend to the posterior border
with two characteristic curves, one at the anterior border of the
anterior testis, the other between the two testes. The genital pore is
at the anterior border of the ventral sucker; the cylindrical cirrus
pouch extends from behind the ventral sucker to half-way to the shell
gland. The seminal vesicle extends forwards within the cirrus pouch
as a convoluted tube. From its anterior portion is given off the
cæcal appendage, which has itself short lateral diverticula. It runs
backwards, ending blindly about 0·5 mm. from the posterior end of the
cirrus sac. The seminal vesicle is continued as the pars prostatica (?)
0·5 mm. long, and this by the very short ejaculatory duct (13 µ), and
finally by the fairly long cirrus, which is beset with very fine spines
except at either extremity. The ovary and shell gland are situated
at about the middle of the body with the testes behind them, and the
uterus in front. The vitellaria extend from the ventral sucker to the
posterior border. The eggs measure 120 µ to 130 µ in length and 77 µ to
80 µ in breadth, and resemble those of Echinochasma sp. in dogs. The
larval stages are said to occur in shrimps.

_Habitat._--Intestine of pig and man.

_Distribution._--In man: India, Siam, China, Assam, Sumatra. It is
common in Cochin China (16 out of 133 Annamites, Noc.), in Tonkin very
rare. Dr. J. Bell has sent me [J. W. W. S.] human specimens from Hong
Kong. In pigs: very common in South China (Heanly). Common in pigs in
Hong Kong. Sixteen out of 248 pigs (_i.e._, 6 per cent.) infected in

*Fasciolopsis rathouisi*, Ward, 1903.

  Syn.: _Distomum rathouisi_, Poirier, 1887.

[Illustration: FIG. 147.--_Fasciolopsis rathouisi_, Poir.: the mouth at
the top, and under it the genital pore and ventral sucker, behind which
again is the uterus. The vitellaria are at the sides, and posteriorly
in the central field the ramified testes; the ovary is in front of the
right testis. (After Claus.)]

Fifteen to 19 mm. long by 8·5 to 10·5 mm. broad by about 3 mm. thick.
Skin with spines (Leiper). Bluntly oval or elliptical with short
cephalic cone which is absent in _Fasciolopsis buski_. Oral sucker
subterminal, 0·25 to 0·29 mm. broad by 0·2 mm. in antero-posterior
diameter. Distant from ventral sucker by about twice its diameter.
Ventral sucker 1·32 to 1·38 mm. broad by 0·68 to 0·7 mm. in
antero-posterior diameter. Œsophagus extremely short. Cirrus sac
not conspicuous and straight as in _Fasciolopsis buski_, but is
convoluted. Testes one behind the other (according to Poirier they
lie beside one another), more compactly branched, broader and denser
than in _Fasciolopsis buski_. Ovary on right side, small, coarsely
branched. Uterus in broad, closely grouped coils, packed with ova
anterior to ovary. Vitellarian acini more numerous and somewhat
differently distributed. Eggs 150 µ by 80 µ, thin shelled. [H. B.
Ward, who has examined this species, and from whose account the
above is mainly taken, considers that it is a good species, although
the differences between it and _Fasciolopsis buski_ are slight,
while Odhner, who examined the original species, is of the opposite
opinion.--J. W. W. S.] The parasite appears to cause diarrhœa, wasting
and occasionally jaundice.

_Habitat._--Intestine of man.

_Distribution._--China, common in some parts (Goddard).

*Fasciolopsis goddardi*, Ward, 1910.

Twenty-one to 22 mm. long, 9 mm. broad. Skin with spines (Leiper).
Uterus very closely coiled, most striking character is the large size
of the vitelline acini. Imperfectly known.

_Distribution._--China (Shanghai).

*Fasciolopsis fülleborni*, Rodenwaldt, 1909.

The fully extended fluke is tongue-shaped, 50 by 14 mm.; two contracted
specimens measured 40 by 15 mm. and 30 by 16 mm. respectively. Skin
without spines, with according to Leiper cephalic cone not clearly
defined. Oral sucker circular, 0·75 mm. in diameter, slightly larger
than that of _Fasciolopsis buski_. Ventral sucker 2·6 mm. in diameter
(that of _Fasciolopsis buski_ 1·6 to 2 mm.). Length 2·9 mm. (as in
_Fasciolopsis rathouisi_), the excess of length over breadth being
due to the posterior elongated sac-like prolongation of the sucker.
Prepharyngeal sphincter present. Pharynx 0·7 mm. in diameter. Œsophagus
practically absent. Gut cæca similar to those of _Fasciolopsis buski_.

_Testes_--regularly branched, separated by an incurving of the cæca,
the anterior occupying a smaller area than the posterior.

_Ovary_--very small, as in _Fasciolopsis buski_, on the right side.

_Shell Gland_--almond-shaped, 2·3 by 1·2 mm. In _Fasciolopsis buski_ it
is round and smaller, 1 to 1·5 mm. in diameter.

_Vitellaria_--similar in distribution to those of _Fasciolopsis buski_,
but the acini are strikingly small.

[Illustration: FIG. 148.--_Fasciolopsis fülleborni_, ventral aspect.
(After Fülleborn.)]

_Cirrus Sac_--is the most characteristic feature of this species. It is
a powerfully built, convoluted sac standing out clearly on the body.
It is not a uniform, straight cylinder 0·25 to 0·33 mm. in diameter, as
in _Fasciolopsis buski_, but even in fully extended flukes is typically
convoluted. It is 1 mm. thick in the middle, but in other parts varies
much from this. The posterior end of the cirrus sac is at two-thirds or
more of the distance from ventral sucker to shell gland. In the case of
_Fasciolopsis buski_ the posterior end of the sac only extends half-way.

_Seminal Vesicle_--has a peculiar convoluted, saccular and angular
course, but the cæcal appendage characteristic of the genus appears to
be absent!

_Excretory System._--The main stem gives off very regular transverse
branches which are well seen posteriorly.

_Eggs._--100 µ by 73 µ. Thin shelled.

_Habitat._--Intestine. Mahommedan from Calcutta.

[It is evident that a re-examination of fresh material is required
before the validity of all these species can be accepted.--J. W. W. S.]

Family. *Troglotremidæ*, Odhner, 1914.

Genus. *Paragonimus*, Braun, 1899.

  Body egg-shaped or somewhat elongated, generally more broadly
  rounded in front than behind. Covered all over with spear-shaped
  spines _arranged in groups_. Gut cæca winding with dilatations
  or constrictions in parts. Ventral sucker in or in front of the
  middle of the body. Excretory bladder cylindrical, very long and
  broad, reaching in front to the bifurcation of the gut. The lateral
  excretory canals join the bladder only a little in front of the
  excretory pore. Genital pore median just behind the ventral sucker.
  Genital sinus duct-like. Cirrus sac absent. Male terminal organs very
  small. Ejaculatory duct present. Testes and ovary deeply lobed, the
  testes in or just behind the middle, the ovary somewhat laterally
  placed just _behind_ the ventral sucker. Uterus forms a coil behind
  the ventral sucker. Eggs rather large, thin shelled, the ovarian cell
  still unsegmented on deposition. Receptaculum seminis, small.

  Parasitic in the lungs of mammals, enclosed in cyst-like cavities,
  generally in pairs.

  _Type Species._--_P. westermanii_ in the tiger.

*Paragonimus ringeri*, Cobb., 1880.

  Syn.: _Distoma ringeri_, Cobb., 1880; _Distoma pulmonale_, Baelz,
  1883; _Distoma pulmonis_, Suga, 1883.

The body is of a faint reddish-brown colour and plump oval shape. The
ventral surface a little flattened; 7·5 to 12 mm. in length, 4 to 6 mm.
in breadth, and 3·5 to 5 mm. thick (in man). The oral sucker (0·75 mm.)
is subterminal; the ventral sucker (0·8 mm.) somewhat in front of the
middle of the body. Pharynx spherical, 0·3 mm. in diameter, or 0·4 by
0·3 mm.; œsophagus, 0·02 mm.; intestinal cæca convoluted, asymmetrical,
the first part having the same structure as the œsophagus. The cuticle
is covered with spines in groups; the excretory pore opens at the
posterior end rather on the ventral surface, the excretory ducts open
into the elongated bladder at the hind end near the pore. Genital pore
behind the ventral sucker and median. Genital sinus 0·2 mm. long with
thick wall, ejaculatory duct 0·13 mm., pars prostatica 0·2 mm., seminal
vesicle duct-like of irregular outline. Behind the sucker the ovary
on the left, and the closely packed uterine coil on the right (though
amphitypy of these two organs is common); the two irregularly lobed
testes lie side by side posteriorly. Vitellaria extensive, leaving only
a median dorsal and ventral space free. Seminal receptacle probably
absent; Laurer’s canal present. The eggs are oval, brownish-yellow,
fairly thin shelled, and measure on an average 81·2 µ by 49·2 µ.

[Illustration: FIG. 149.--_Paragonimus ringeri_, Cobb.: to the right,
dorsal aspect; to the left, ventral aspect. Natural size. (After

[Illustration: FIG. 150.--_Paragonimus ringeri_, Cobb.: diagram of
the internal organs. _a_, œsophagus; _b_, vitellaria (a portion only
shown); _c_, common genital duct; _d_, shell gland with oviduct,
Laurer’s canal and vitelline duct; _e_, ovary; _f_, vitelline
receptacle; _g_, excretory pore; _h_, oral sucker; _i_, pharynx; _k_,
gut; _l_, ventral sucker; _m_, uterine coils; _n_, vitellarian ducts;
_o_, vas efferens; _p_, testis. (After Kubo.)]

[Illustration: FIG. 150A.--_Paragonimus westermanii_, Kerb.: seen from
the ventral surface. Mouth, pharynx, intestinal cæca, at the sides
of which the vitellaria are observed. The genital pore is behind the
ventral sucker, and next to it, on the left, the ovary; on the right,
the uterus; the two testes posteriorly; the excretory vessel in the
middle, 10/1. (After Leuckart.)]

The following species are also known:--_P. westermanii_, Kerb., 1878,
in the tiger, and _P. kellicotti_, Ward, 1908, in the pig, dog, and
cat (N. America). Ward and Hirsch give the following differences
between the spines of the three forms:--

                 _P. ringeri._      _P. westermanii._  _P. kellicotti._
  Shape         Chisel-shaped,       Lancet-shaped,     Chisel-shaped,
                  moderately heavy.    very slender.      heavy.
  Distribution  Circular rows, in    Circular rows,     Circular rows,
                  groups.              in groups.         singly.

Two other species, _P. rudis_, Diesing, 1850, in a Brazilian otter
(_Lutra brasiliensis_) and _P. compactus_, Cobbold, 1859, in the Indian
ichneumon, are but little known.

_Habitat._--Lungs, pleuræ, and especially the bronchi of man and
dog. The alleged occurrence (of eggs) in other organs may be due to
confusion with those of _Schistosoma japonicum_.

_Distribution._--China, Korea, and especially in Japan, where,
according to Katsurada, there are no districts that are entirely
free from pulmonary flukes. The _mountainous_ provinces of Okayama,
Kumamoto, Nagano and Tokushima are the principal centres.

[Illustration: FIG. 151.--Egg of _Paragonimus ringeri_, Cobb., from
the sputum. Showing the ovarian cell and vitelline cells and granules.
1,000/1. (After Katsurada.)]

_Pathology._--The number present in the lung varies from two to twenty,
about. Usually one cyst contains one worm, but in the dog each cyst
contains two. The cysts admit the tip of the finger, and have a fibrous
wall 1 mm. thick. They originate partly from dilatation of bronchi and
bronchioles. Others arise from the inflammatory reaction of lung tissue
into which the worms have wandered. The worms and their eggs cause
bronchitis and peribronchitis, catarrhal, hæmorrhagic, or purulent,
and areas of consolidation. Areas containing eggs in their centre
resembling tubercle nodules are not uncommon, and extensive cirrhosis
of the lung may be found. As a result of these changes, emphysema and
bronchiectasis also occur.

As to the development, only the following details are known: that the
eggs, which before segmentation of the ovum reach the open in the
sputum and through being swallowed also in the fæces, develop in water
into a miracidium ciliated all over, which hatches and swims about
freely. According to Manson this takes place in four to six weeks.

Sub-family. *Opisthorchiinæ*, Looss, 1899.

Genus. *Opisthorchis*, R. Blanch., 1845.

  Opisthorchiinæ with lobed testes. Laurer’s canal present. Parasitic
  in the bile-ducts of mammals and birds.

*Opisthorchis felineus*, Riv., 1885.

  Syn.: _Distoma conus_, Gurlt, 1831 (_nec_ Creplin, 1825); _Distoma
  lanceolatum_, v. Sieb., 1836, v. Tright, 1889 (_nec_ Mehlis, 1825 =
  _Fasciolo lanceolata_, Rud., 1803); _Distoma sibiricum_, Winogr.,
  1892; _Distoma tenuicolle_, Mühl., 1896.

This parasite is yellowish-red in the fresh condition, and almost
transparent. The body is flat, with a conical neck at the level of the
ventral sucker marked by a shallow constriction; this, however, is only
noticeable in fresh and somewhat contracted specimens. Posteriorly
to the ventral sucker the lateral borders run fairly parallel; the
posterior end is either pointed or rounded off. The length and breadth
vary according to the contraction, being usually 8 to 11 mm. by 1·5
to 2 mm. The suckers are about one-fifth to one-sixth of the length
of the body distant from each other, and of about equal size (0·23 to
0·25 mm.). The œsophagus is hardly any longer than the pharynx, which
lies close behind the oral sucker; the intestinal cæca reach almost to
the posterior border and are often filled with blood. The excretory
pore is at the posterior extremity, and the excretory bladder forks in
front of the anterior testis. The testes in the posterior fourth of
the body lie obliquely one behind the other; the anterior one has four
lobes, the posterior one five lobes; the ovary is in the median line
transversely, simple or slightly lobed; behind it lies the large pear-
or retort-shaped receptaculum seminis and Laurer’s canal. The uterus
is in the median field. The vitellaria occupy the fairly broad lateral
areas, in about the central third of the body, beginning behind the
ventral sucker and terminating at about the level of the ovary; the
acini are small and arranged in groups of seven to eight, separated by
interstices. The genital pore is close in front of the ventral sucker.
The eggs are oval with sharply defined operculum at the pointed pole,
30 µ, by 11 µ.

  This species, which is frequently confused with others, inhabits
  the gall-bladder and bile-ducts of the domestic cat especially;
  but is also found in the dog, in the fox, and in the glutton
  (_Gulo borealis_). It has been observed in France, Holland, North
  Germany (being particularly frequent in East Prussia), in Russia,
  Scandinavia, Siberia, Japan, Tonkin, Hungary, and Italy. The North
  American form (from cats and _Canis latrans_) is a distinct species
  (_Opisthorchis pseudofelineus_).

In man this species was first found by Winogradoff in Tomsk (nine
cases), then by Kholodkowsky in a peasant from the neighbourhood of
Petrograd who had travelled a great deal in Siberia, and finally by
Askanazy in five persons who were natives of the East Prussian district
of Heydekrug. In Tomsk, _Opisthorchis felineus_ is the most frequent
parasite of man that comes under observation at _post mortem_ (6·45
per cent.), whereas _Tænia saginata_ has only been found in 3·2 per
cent., Echinococcus in 2·4 per cent., _Ascaris lumbricoides_ in 1·6 per
cent., and _Oxyuris vermicularis_ in 0·8 per cent. of the autopsies.
In the district of Heydekrug, however, the species in question is also
frequent, as in a few years five cases came to our knowledge (of which
three were diagnosed by the discovery of the eggs in the fæces).

[Illustration: FIG. 152.--Egg of _Opisthorchis felineus_, Riv. 830/1.]

[Illustration: FIG. 153.--_Opisthorchis felineus_: from the cat. _m._,
mouth; _p.b._, pharynx; _i._, gut; _g.p._, genital pore; _ac._, ventral
sucker; _ut._, uterus; _v.g._, vitellarium; _ov._, ovary; _s.g._, shell
gland; _r.s._, receptaculum seminis; _t._ testes; _ex. p._, excretory
pore. (After Stiles and Hassall.)]

In none of Winogradoff’s nine cases had the death of the patient been
caused direct by the parasites, yet more or less extensive changes
in the liver were found in all of them; such as dilatation of the
bile-ducts with inflammation and thickening of their walls, and foci
of inflammation or atrophy in the liver substance; icterus was present
five times and atrophy of the liver an equal number of times; ascites
was observed three times, and in two cases, probably of recent date,
the organ was enlarged. The number of parasites found fluctuated
between a few and several hundreds.

In two of Askanazy’s cases, which he examined more closely, carcinoma
which had developed at the places most invaded by flukes was found
at the _post-mortem_, so that perhaps there may be grounds for the
connection which the author seeks to establish between cancer of the
liver and the changes induced by the parasites; these changes consist
of numerous and even ramified proliferations of the epithelium
of the biliary duct into the connective tissue, which is likewise
proliferated. The number of worms found in one case amounted to over
100; in a second case, in which the parasites had also invaded the
pancreatic duct, their number was even larger.

Winogradoff as well as Askanazy found isolated flukes in the intestine

[Illustration: FIG. 154.--_Opisthorchis pseudofelineus_: from the
bile-duct of the cat (Iowa), _m._, oral sucker; _p.b._, pharyngeal
bulb; _es._, œsophagus; _i._, intestine; _va._, vagina; _g.p.m._, male
orifice; _ac._, ventral sucker; _ut._, uterus; _v.g._ vitellarium;
_s.g._, shell gland; _v.dt._, vitelline duct; _ov._, ovary; _r.s._,
receptaculum seminis; _L.c._, Laurer’s canal; _t._, testis; _ex.c._,
excretory bladder; _ex.p._, excretory pore. (After Stiles.)]

Unfortunately, nothing much is known of the history of the development
of _Opisthorchis felineus_; we only know that when deposited the eggs
already contain a ciliated miracidium, which, however, according to my
experience, does not hatch out in water, but only after the entry of
the eggs into the intestine of young _Limnæus stagnalis_; no further
development, however, occurs. Winogradoff states that he has seen the
miracidia hatch after the eggs had been kept in water for a month at
37° C.; and has even observed free miracidia in the bile of man and of
a dog respectively. Although the whole post-embryonal development of
the cat fluke remains yet to be investigated, Askanazy by a series of
experiments on cats and dogs has discovered the mode of infection. The
intermediate hosts are fish, and mainly the ide, in this country called
Tapar (_Idus melanotus_, H. and Kr.), and of subsidiary importance the
roach (_Leuciscus rutilus_). Both species of fish as well as others
are readily eaten raw by man on the Courland lagoon (Baltic). It is,
moreover, significant that those persons whom Askanazy found infected
with the cat fluke were also infected with _Dibothriocephalus latus_,
the intermediate host of which is also fish (Lota sp., Esox sp., Perca

In one of his nine cases Winogradoff also saw a small fluke covered
all over with spines, which he conjectured to be the young stage of
_Opisthorchis felineus_; as, however, according to my experience, this
species, even in smaller specimens, is always without spines, the above
hypothesis cannot be accepted. It is much more probable that one of
the other species that also invade the liver of cats may accidentally
be introduced into man; we know, in fact, that _Metorchis albidus_,
Braun, and _Metorchis truncatus_, Rud., are both covered with spines.
As, however, the spines of the first-named species are rather apt to
fall off, and also as it possesses a different shape (spatula-shaped),
it may be assumed that probably Winogradoff had found _Metorchis
truncatus_, Rud., 1819, in his patient.

Genus. *Paropisthorchis*, Stephens, 1912.

  Structure as in Opisthorchis, except that the ventral sucker and
  genital pore occur on the apex of a process or pedicle projecting
  from the anterior portion of the body. This process is about 1/2 mm.
  long, and is retractile.

*Paropisthorchis caninus*, Barker, 1912.

  Syn.: _Distoma conjunctum_, Lewis and Cunningham, 1872; _Opisthorchis
  noverca_, M. Braun, 1903 (_pro parte_); _Opisthorchis caninus_,
  Barker, 1912 (?).

Length varies from 2·75 to 5·75 mm. in preserved specimens, average
3·6 to 5·2 mm. Body uniformly spinose, though as a rule spines are not
present on the pedicle. Body slightly concavo-convex, the concavity
being ventral. Oral sucker 0·28 mm. Pharynx 0·224 by 0·184 mm.
Œsophagus 0·04 mm. Ventral sucker 0·176 mm. in diameter. Pedicle about
1/2 mm. long, may be completely retracted.

_Genital Pore_--opens on the apex of the pedicle in front of the
ventral sucker. Its exact position varies with the state of contraction
of the parts. In certain cases it actually opens within the cuticular
border of the sucker, in other cases it opens externally to the sucker
and anterior to it. The opening is covered with scales. The vas
deferens and uterus run alongside one another until they merge near the
apex of the pedicle into a common sinus.

_Vitellaria_--consist of eight acini on each side, extending from
slightly behind the base of the pedicle to the anterior border of the
ovary, or as far back as a line separating the posterior border of the
ovary from the anterior border of the anterior testis.

[Illustration: FIG. 155.--_Paropisthorchis caninus_: from the
bile-ducts of the pariah dog, India. _Acet. v._, ventral sucker; _Ut._,
uterus; _V. ex. lat_., longitudinal excretory duct; _V. sem._, seminal
vesicle; _Sem. rec._, seminal receptacle; _Ov._, ovary; _V. ex._,
excretory bladder; _Test. l._, left testis; _Test. r._, right testis;
_P. ex._, excretory pore. × 40. (After Stephens.)]

_Testes._--Anterior testis 0·496 by 0·44 mm.; posterior testis 0·52
by 0·48 mm., usually ovoid, though both may be regularly lobed. The
anterior testis is usually on the left side.

_Ovary_--multilobular, the lobes 6 to 8 being irregular in size and

_Shell Gland_--extensive and diffuse, occupying an area which
approximately corresponds with the loop of the transverse vitelline

_Seminal Receptacle_--globular, to the right of and dorsal to the
posterior lobe of the ovary.

_Laurer’s Canal_--generally runs from the end of the receptacle with a
single curve medially and backwards.

_Uterine Coils_--form loosely packed transverse coils terminating
slightly in front of the level of the first vitelline acini. From here
the uterus passes forwards into the pedicle to the left and ventral to
the seminal vesicle.

_Seminal Vesicle_--commences about the level of the first vitelline
acini. The coils displace the uterus ventrally and to the left. In
the pedicle the vesicle diminishes in extent and lies in its dorsal
(anterior) side.

_Habitat._--Liver of pariah dogs, India. In North-Western Provinces
about 40 per cent. are infected. This fluke appears to be different
from _Amphimerus_ (_Opisthorchis_) _noverca_ in man, as the latter
has not the pedicle on the summit of which lie the sucker and common
genital pore.

Genus. *Amphimerus*, Barker, 1912 (?).

  Structure as in Opisthorchis, except that the vitellaria are
  separated into two portions, an ant-ovarial and a post-ovarial.

[Illustration: FIG. 156.--_Amphimerus noverca_, Braun. o.s., oral
sucker; p.b., pharynx; ac., ventral sucker; ut., uterus; v.g.,
vitellarium; ov., ovary; v.d., vas efferens; ex.c., excretory canal;
t., testis. (After McConnell.)]

*Amphimerus noverca*, Barker, 1912 (?).

  Syn.: _Distomum conjunctum_, McConnell, 1876 (_nec_ Cobbold, 1859);
  _Opisthorchis noverca_, M. Braun, 1903 _pro parte_.

At the autopsy of two Mahommedans who died in Calcutta, McConnell found
a large number of Distomata in the thickened and dilated bile-ducts.
The worms were lancet-shaped, covered with spines, and measured 9·5
to 12·7 mm. in length and 2·5 mm. in breadth. The two suckers lie
very close to one another, the anterior one being larger than the
ventral; the genital pore opens immediately in front of the ventral
sucker; pharynx spherical; intestinal cæca extending far back. At
the commencement of the posterior third of the body the two testes,
somewhat apart, the anterior one roundish, the posterior one distinctly
lobed. The transverse and slightly lobed ovary in front of the
bifurcation of the *Y*-shaped excretory bladder, whence the uterus, in
convolutions barely spreading beyond the central field, extends to the
pore; the vitellaria in the lateral areas commence behind the ventral
sucker and extend to the testes. Cirrus pouch absent. Eggs oval, 34 µ
by 21 µ.

Genus. *Clonorchis*, Looss, 1907.

  Structure as in Opisthorchis, distinguished, however, by the branched
  testes situated one behind the other, the branches of which ventrally
  encroach upon the gut forks; dorsal to the testes the *S*-shaped
  excretory bladder, the main branches of which, arising at the level
  of the bifurcation of the gut, open into the bladder below its
  anterior end. Parasitic in the bile-ducts of mammals and man.

[Illustration: FIG. 157.--_Metorchis conjunctus_,[272] (Syn.: _Distomum
conjunctum_, Cobb., _nec_ Lew. and Cunn., _nec_ McConn.): from _Canis
fulvus_. _Vs._, ventral sucker; _I._, intestine; _Vsc._ vitellaria;
_Ex._, excretory bladder; _T._, testes; _O._, ovary; _Ms._, oral
sucker; _Ph._, pharynx; _Ut._, uterus. (After Cobbold.)]

[272] This species from _Canis fulvus_ was for long thought to be the
same as that here described as _Amphimerus noverca_. It probably does
not belong to the genus Metorchis.

*Clonorchis sinensis*, Cobbold, 1875.

  Syn.: _Distoma sinense_, Cobbold, 1875; _Distoma spathulatum_, R.
  Leuckart, 1876 (_nec_ Rudolphi, 1819); _Distoma hepatis innocuum_,
  Baelz, 1883.

In shape resembles _Opisthorchis felineus_, 13 to 19 mm. long, 3 to
4 mm. broad, at the beginning of sexual maturity 12 to 13 mm. long, 2·5
to 3 mm. broad. Oral sticker 0·58 to 0·62 mm., ventral sucker 0·45 to
0·49 mm. in transverse diameter. In the parenchyma numerous yellowish
or brownish granules, especially behind the oral sucker and at the
posterior end. Testicular branches very long, in the anterior testis
often four, in the posterior testis five branches. Ovary generally
with three large lobes and a smaller lobe. Vitellaria not always
symmetrical, generally extending laterally from the ventral sucker to
the ovary, interrupted in parts.

Eggs 26 µ to 30 µ by 15 µ to 17 µ. Average 29 µ by 16 µ.

[Illustration: FIG. 158.--_Clonorchis sinensis._ _C.L._, Laurer’s
canal; _Dst._, vitellaria; _Ex._, excretory bladder; _H._, testes;
_K._, ovary; _R.s._, receptaculum seminis; _Vd._, terminal section of
vas deferens. Magnified 4-1/2 times. (After Looss.)]

[Illustration: FIG. 159.--Ova of _Clonorchis sinensis_. The knobs on
the ends of the eggs are not shown. 900/1. (After Looss.)]

This (?) species was discovered in 1874 by McConnell, in Calcutta, in
the bile-ducts of a Chinaman who died shortly after being admitted into

_Habitat._--Bile-ducts of man, dog and cat.

_Distribution._--Especially in China, apparently rare in Japan.

*Clonorchis endemicus*, Baelz, 1883.

  Syn.: _Distoma sinense_ s. _spathulatum p.p._; _Distoma hepatis
  endemicum_ s. _perniciosum_, Baelz, 1883; _Distoma japonicum_, R.
  Blanchard, 1886.

Very similar to the previous species and consequently generally
confused with it. Length between 6 and 13 mm., width varying between
1·8 and 2·6 mm. Oral sucker 0·37 to 0·5 mm., usually 0·43 to 0·45 mm.
in transverse diameter; ventral sucker 0·33 to 0·45 mm., usually 0·37
to 0·40 mm. No pigment in parenchyma; anterior testis with four,
posterior testis with five branches. Vitellaria continuous, ova 26 µ by
13 µ to 16 µ.

_Habitat._--Bile-ducts of man, dog, cat and pig.

_Distribution._--This species occurs very frequently in man, in certain
districts of Japan, especially in the province of Okayama, Central
Japan, in particular localities of which above 60 per cent. of the
population are infected. The worms are sometimes found in enormous
numbers in the liver (upwards of 4,000), also in the pancreas and
rarely in the duodenum. It is common in Tonkin and Indo-China. Léger
in Tonkin found 50 per cent. of people apparently in normal health
infected, so that probably symptoms only arise when the infection is
intense. [The exact distribution of these two species is, however,
not precisely defined at present, as commonly no distinction is made
between them.--J. W. W. S.]

[Illustration: FIG. 160.--_Clonorchis endemicus._ × 6 about. (After

[Illustration: FIG. 161.--_Clonorchis endemicus_: eggs. The knobs on
the eggs are not shown. × 900. (After Looss.)]

Verdun and Bruyant deny, in opposition to Looss, the possibility of
being able to distinguish within the genus Clonorchis the two species
described, but they admit the justification for the new genus. They
also report the occurrence of _Opisthorchis felineus_ in man in Tonkin
(_Compt. Rend. Soc. de Biol._, lxii, 1907).

_Pathology._--Both species of Clonorchis give rise to grave symptoms.
The liver is generally enlarged, though when the infection has
lasted some time it begins to contract. The surface of the organ
is studded with white vesicles, and on cutting into it one sees
numerous cavities with thickened walls (distended bile-ducts) filled
with a brownish fluid containing innumerable eggs, which cause its
colour. Microscopically, the epithelium of the bile-ducts is either
(1) entirely destroyed, or (2) actively proliferates, forming an
adenomatous outgrowth. Occasionally this proliferation is not limited
by the wall of the bile-duct but penetrates it and leads to a growth
of numerous new ducts, forming a malignant biliary adenoma. The
bile-ducts have their connective tissue wall greatly sclerosed. These
fuse with one another, forming areas of sclerosis devoid of liver
tissue. As a result of these changes the liver cells atrophy and
undergo fatty pigmentary and granular degeneration. Besides these
changes, due probably to the toxic action of the flukes, mechanical
obstruction due to the actual plugging of the ducts by the flukes
causes retention of bile and icterus, and through pressure on veins,
ascites and hypertrophy of the spleen.

To what extent blood or bile respectively forms the food of the flukes
is uncertain.

_Life-history._--(Kobayashi, 1911, _Mitteilungen aus dem kaiserlichen
Institut für Infektions-Krankheiten zu Tokio_, pp. 58–62.)

It results from the work of Kobayashi in Japan that fresh-water fish
form the _second_ intermediate host for _Clonorchis endemicus_. He
fed cats with encysted flukes (cercariæ) from various fish and easily
succeeded in infecting them, _e.g._ a kitten, proved to be uninfected
by repeated examination of its fæces, was fed on infected fish; a month
later innumerable flukes were found in the bile-ducts, gall-bladder,
pancreas and even in the duodenum. The fish infected were _Leucogobis
güntheri_, _Pseudorasbora parva_, and to a less extent _Acheclognathus
lanceolata_, _Acheclognathus limbata_, _Paracheclognathus rhombea_,
_Pseudoperilampus typus_, _Abbottina psegma_, _Biwia zezera_ and
_Sarcocheilichthys variegatus_. The cysts occur throughout the muscles
and subcutaneous tissue of the fish. Length 0·13 mm., breadth 0·1 mm.
The cercaria lies folded in the cyst, length 0·5 mm. breadth 0·1 mm.
It tapers posteriorly. Skin at first covered with fine spines,
disappearing as they grow older. Body dotted with fine pigment.

The _first_ intermediate host is still unknown.

Sub-family. *Metorchiinæ*, Lühe, 1909.

Genus. *Metorchis*, Looss, 1899, emend. auctor.

  Hind end rounded. Gut forks reach extreme end. Testes only slightly
  lobed, filling the hind end.

*Metorchis truncatus*, Rud., 1819.

This species, which attains a length of 2 mm., is slender and conical,
the anterior end is pointed and the posterior truncated, and provided
with a muscular tuberosity that resembles a terminal sucker; for
this reason the discoverer of the species (Rudolphi) classed it with
the Amphistomes. The cuticle in the young, as well as in the adult
specimens, is entirely and closely covered with spines. Suckers about
equal in size (0·134 to 0·172 mm.); the ventral sticker lies somewhat
in front of the middle of the body. The pharynx is small (0·09 mm.),
the œsophagus minute, the intestinal cæca reach to the posterior
extremity. Between them, and in front of their blind ends, lie the two
elliptical testes, one generally a little in front of the other. In
front of them, either in the median line or somewhat laterally, the
spheroidal ovary is situated; in front, again, is the uterus, the coils
of which usually extend beyond the median field. The vitellaria are at
the sides of the central third of the body, thus commencing in front of
the ventral sucker; cirrus pouch absent; the genital pore is close in
front of the acetabulum. The excretory pore is terminal (?). Eggs 29 µ
by 11 µ.

_Metorchis truncatus_ lives in the bile-ducts of the seal, cat, dog,
fox, and glutton (_Gulo borealis_). The source of infection is unknown,
although one would suspect fish. Askanazy did not succeed in getting
this fluke in his feeding experiments, but another species, _Metorchis
albidus_, not uncommon in cats by feeding them on roach (_Leuciscus

[Illustration: FIG. 162.--_Metorchis truncatus_, Rud.: from the biliary
ducts of the domestic cat. _V.s._, ventral sucker; _I._, gut; _V.sc._,
vitellaria; _T._, testes; _O._, ovary; _R.s._, receptaculum seminis;
_Ut._, uterus. 25/1.]

Family. *Heterophyiidæ*, Odhner, 1914.

Genus. *Heterophyes*, Cobbold, 1866.

  Syn.: _Cotylogonimus_, Lühe, 1899; _Cænogonimus_, Looss, 1899.

  No crown of spines on head. Body divided into a narrow, movable,
  anterior part (neck), and a broader, less movable, posterior
  portion, which contains the genitalia. The suckers separated from
  one another by a space equal to half the length of the body or more;
  the pharynx is close behind the oral sucker; the œsophagus is long;
  the intestinal cæca extend to the posterior border; the genital pore
  is placed laterally, and behind the ventral sucker. Genital sucker
  provided with a circlet of chitinous rodlets, shaped like stags’
  horns. The testes are at the posterior end, the ovary in a median
  position in front of them. Laurer’s canal with receptaculum seminis
  present; the small vitellaria are at the sides of the posterior part
  of the body. Parasitic in the intestine of mammals and birds.

*Heterophyes heterophyes*, v. Sieb., 1852.

  Syn.: _Distomum heterophyes_, v. Siebold, 1852; _Heterophyes
  ægyptica_, Cobbold, 1866; _Mesogonimus heterophyes_, Railliet, 1890;
  _Cœnogonimus heterophyes_, Looss 1900; _Cotylogonimus heterophyes_,
  Braun, 1901.

Length up to 2 mm., breadth 0·4 mm.; the neck not sharply defined; in
life it stretches to double the length of the hind body. The scales
are rectangular, 5 µ to 6 µ by 4 µ, their posterior margin serrate
with seven to nine teeth. Cuticular glands are numerous on the ventral
surface, especially in the fore part of the body, and partly discharge
at the anterior border of the oral sucker. The oral sucker is 0·09 mm.,
the ventral sucker 0·23 mm. in diameter; the pharynx measures 0·05
to 0·07 mm. in length; the œsophagus is about three times as long;
posteriorly the intestinal cæca are directed one towards the other and
terminate beside the excretory bladder. Close in front of the posterior
ends of the intestinal branches are the two elliptical testes, which
are not exactly on the same level. In the middle in front of them is
the receptaculum seminis, and in front of the latter lies the spherical
or elliptical ovary. The two vasa efferentia unite to form the vas
deferens, which after a short course passes over into the angularly
bent seminal vesicle; after the entry of the prostatic glands it
becomes united with the metraterm (vagina), and the common duct opens
into the genital sucker. The latter is somewhat smaller than the
ventral sucker, lateral to and close (0·15 mm.) behind it, and bears
a not entirely closed ring of from seventy-five to eighty chitinous
rods (20 µ in length). The vitellaria on either side consist of about
fourteen acini. The uterus is spread almost throughout the entire
posterior part of the body. The eggs have thick shells with a knob
resembling that of Clonorchis eggs but not so prominent, and measure
30 µ by 17 µ; they contain a completely ciliated miracidium with a
rudimentary intestinal sac.

[Illustration: FIG. 163.--_Heterophyes heterophyes_, v. Sieb. _C._,
cerebral ganglion; _I._, intestinal cæca; _Ct.g._, cuticular glands;
_V.sc._, vitellaria; _Ut._, genital sucker; _T._, testes--the excretory
bladder between them; _L.c._, Laurer’s canal; _R.s._, receptaculum
seminis, with the ovary in front of it; _G.c._, ventral sucker; _Vs._,
vesicula seminalis, 53/1. On the left side above, an egg, 700/1, is
depicted, and below it three chitinous rodlets from the genital sucker.
700/1. (After Looss.)]

This species was discovered in 1851 by Bilharz in the intestine of
a boy who died in Cairo; a second case was only found in 1891 and
published by R. Blanchard, so that it appeared as if the species were
very scarce. According to Looss, this is, however, not the case, but
the species easily escapes notice on account of its small size. Looss
found it in Alexandria twice in nine autopsies, and once in Cairo, and
has recently stated that in man “it is not at all uncommon to meet with
the parasite in cadavers, and the eggs of the worm in the stools of the
patients.” Leiper records one case from Japan and one from China. The
parasites occupy the middle third of the small intestine, and even when
present in large numbers appear to be harmless.

This small species, according to Looss, frequently occurs in Egyptian
dogs, less so in cats, and has also been found in the fox, as well as
once in _Milvus parasiticus_; Janson also reports this species from the
intestine of the dog in Japan.

*Metagonimus*, Katsurada, 1913; Yokogawa, Leiper, 1913.

Resembles in general structure Heterophyes. In the arrangement of
its ventral genital suckers resembles but differs from that of
Tocotrema,[273] Looss. The ventral and genital suckers lie laterally
and on the right.

[273] In the genus Tocotrema the common genital duct opens into the
ventral sucker.

*Metagonimus yokogawai.* Katsurada, 1913.

  Syn.: _Yokogawa yokogawai_, Leiper, 1913.

[Illustration: FIG. 164.--_Metagonimus yokogawai_, Katsurada, 1913: the
spines are only shown over a small part of the skin. (After Leiper.)]

One to 1·5 mm. long, seldom 2·5 mm., and 0·4 to 0·7 mm. broad;
elliptical in shape. The body is thickly covered with nail-shaped
spines about 10 µ long. Oral sucker 77 µ, to 85 µ in diameter. Ventral
sucker characteristic and peculiar 0·12 to 0·14 mm. by 0·08 to 1 mm.
It is a sac-like organ placed deeply in the body, but does not open as
in other flukes on the ventral surface. Testes elliptical, not quite
symmetrically placed at the hind end of the body. Vesicula seminalis
retort-shaped, situated transversely, internal to the ventral sucker.
Pars prostatica present. Ejaculatory duct opens with the uterus into
a genital sinus, which, together with the internal opening of the
ventral sucker, opens into a pit at the front of the ventral sucker.
The opening of the genital sinus and that of the ventral sucker are
furnished with a complex muscular apparatus. Ovary spherical, 0·12 to
0·13 mm. in diameter, lies in the middle of the hind body. Receptaculum
seminis and Laurer’s canal present. Vitellaria in the hind half of the
body, consisting of about ten acini on each side. Shell gland to the
left of the ovary. Uterus forms three to four transverse coils. Eggs
elliptical, double contoured, yellowish-brown in colour. There is no
shoulder below the operculum as in the eggs of _Cl. sinensis_. At the
rounder end there is a thickening or knob different from the spine-like
or hook-like process seen in _Cl. sinensis_. Dimensions 28 µ by 16 µ.

_Habitat._--Mainly in upper or middle portion of jejunum, rarely in
cæcum. They penetrate deep into the mucosa, but not into the submucosa,
and _post mortem_ appear as a number of small brown points. They
frequently occur in the solitary glands, which they destroy. They cause
chronic catarrh of the gut. Parasitic in man and mammals.

_Geographical Distribution._--Japan.

_Life-history._--The cercarial stage occurs in a trout (_Plecoglossus
altivelis_) and seldom in Crassius sp. and Cyprinus sp. Infection takes
place through the eating of the fish raw. Seven to sixteen days later
eggs appear in the fæces (of dog).

Family. *Dicrocœliidæ*, Odhner, 1910.

Genus. *Dicrocœlium*, Dujardin.

  _Dicrocœliidæ_, with leaf-shaped bodies, pointed posteriorly and
  anteriorly. Greatest width behind the mid-line. Vitellaria double.
  The testes smooth or indented, lying symmetrically or obliquely
  beside or behind the ventral sucker. The ovary approaches the median
  line behind one testis. Parasitic in the liver and gall-bladder
  (rarely in the intestine) of members of all classes of vertebrate
  animals--by preference in birds and mammals.

[Illustration: FIG. 165.--_Dicrocœlium dendriticum_, Rud. _V.s._,
ventral sucker; _Cb._, cirrus pouch; _I._, intestinal cæca; _V.sc._,
vitellaria; _T._, testicles; _O._, ovary; _M.s._, oral sucker; _Ut._,
uterus. 15/1.]

*Dicrocœlium dendriticum*, Rud., 1819.

  Syn.: _Dicrocœlium lanceatum_, Stil. and Hass., 1896; _Fasciola
  lanceolata_, Rud., 1803 (_nec_ Schrank, 1790); _Distomum
  lanceolatum_, Mehlis, 1825; _Dicrocœlium lanceolatum_, Dujardin, 1845.

[Illustration: FIG. 166.--Eggs of _Dicrocœlium dendriticum_, Rud. To
the left seen flat, to right lying on one side. 600/1.]

[Illustration: FIG. 167.--Miracidia of _Dicrocœlium dendriticum_. _a_,
from the dorsum; _b_, from the side. (After Leuckart.)]

Body lancet-shaped, narrowing especially at the anterior extremity;
length 8 to 10 mm., breadth 1·5 to 2·5 mm., the greatest breadth
usually behind the middle of the body. Suckers distant from each
other by about one-fifth the length of the body; oral sucker about
0·5 mm., ventral sucker about 0·6 mm. Pharynx globular, adjoining
the oral sucker; œsophagus 0·6 mm. in length; intestinal cæca reach
to four-fifths of the body length. Genital pore at the level of the
bifurcation of the intestine; cirrus pouch small and slender. The
large, slightly lobed testes lie obliquely one behind the other behind
the ventral sucker; the ovary, which is considerably smaller, is placed
behind the posterior one; the vitellaria, commencing at the level
of the posterior testis, terminate far before the cæca. The uterus,
situated behind the ovary, extends throughout the posterior end, not
confined to the central field, but overlapping the lateral fields with
its transverse coils; at the posterior edge of the body it turns back
again and winds forwards to the ovary in transverse loops, then between
the testes, and finally, dorsal to the ventral sucker, terminates in
the genital pore. The thick-shelled eggs when young are yellowish,
when older dark brown. They measure 38 µ to 45 µ by 22 µ to 30 µ.
They contain an oval or roundish miracidium, only the anterior part
of which is ciliated, and which possesses a rudimentary intestinal
sac with a boring spine. The miracidia do not hatch out in water
spontaneously, but, according to Leuckart, in the intestines of slugs
(_Limax_, _Avion_), but they do not develop either in these (slugs) or
in water-snails.

The lancet fluke inhabits the biliary duct of herbivorous and
omnivorous mammals (sheep, ox, goat, ass, horse, deer, hare, rabbit,
pig), and is often found associated with the liver fluke; it is not,
however, so common nor so widely disseminated, nevertheless, it has
been met with outside of Europe, namely, in Algeria, Egypt, Siberia,
Turkestan, and North and South America.

In man it is still more uncommon than the liver fluke, and has hitherto
only been observed seven times (Germany, Bohemia, Italy, France, and
Egypt); it may, however, have occurred more frequently, and have been
overlooked, as in slight infections it produces no special symptoms.

The intermediate host is still unknown. Leuckart for some time held
the opinion that small species of _Planorbis_ from fresh water, which
contain encysted Distomata, were to blame, and he supported his views
by a feeding experiment which seemingly yielded positive results; this,
however, is not definitely proved. Piana’s statement that small land
snails are the intermediate hosts has also not been proved.

Family. *Echinostomidæ*, Looss, 1902.

Sub-family. *Echinostominæ*, Looss, 1899.

Genus. *Echinostoma*, Rud. 1809; Dietz, 1910.

Fore-body not bulging. Greatest width at or behind the ventral sucker.
Oral sucker not atrophied. Collar kidney-shaped with a double dorsally
unbroken row of spines, terminating in four to five angle spines. The
border spines of the aboral series not larger than the oral. Skin
spined or smooth. Body elongated. Uterus long with numerous transverse
coils. Ventral sucker in the anterior quarter of body. Cirrus sac
small, almost completely in front of the ventral sucker. Testes round
or oval, smooth incurved or lobed, in the hinder half of body. Ovary
median or lateral in front of testes. Vitellaria from hinder margin of
ventral sucker to end of body. Eggs oval, 84 µ to 126 µ by 48 µ to 82 µ.

The spines placed most ventrally, or those placed most medially on
ventral surface, are from differences of position or form termed
“angle” spines, the rest “border” spines.

_Type._--_Echinostoma echinatum_, Rud.

*Echinostoma ilocanum*, Garrison, 1908.

Length 4 to 5 mm., breadth 1 to 1·35 mm., thickness 0·5 to 0·6 mm. The
circum-oral disc 0·3 mm. broad, separated by a shallow groove from the
body. Crown of forty-nine spines and five to six angle spines on each
side continuous with an irregularly alternating series of fourteen
spines on the dorsum. Largest spines are 34 µ long, 8 µ thick at the
base. The remainder of the dorsal spines are 24 µ by 6 µ. Skin thickly
covered with scales on the margins of the body as far back as the
level of the hind testis. Oral sucker, 0·18 mm.; ventral sucker, 0·4
to 0·46 mm. Its anterior border about 0·07 mm. from the anterior end.
Pharynx 0·17 mm. long, 0·11 mm. broad. Testes about mid-line of the
body, much lobed; the lobes of the anterior testis run transversely,
while the axis of the posterior testis is longitudinal, as often
occurs in the _Echinostomidæ_. Cirrus sac reaches to the centre of
the ventral sucker. Ovary transversely oval in front of the testes.
Vitellaria commence about half-way between the ventral sucker and ovary
and extend to the posterior end. Eggs numerous, 92 µ to 114 µ by 53 µ
to 82 µ.

_Average._--99·5 µ by 56 µ.

_Habitat._--Gut of man (Filipinos), Philippine Islands.

[Illustration: FIG. 168.--_Echinostoma ilocanum._ _Vo._, oral sucker;
_Ph._, pharynx; _Cirre_, cirrus; _V.v._, ventral sucker; _Ut._, uterus;
_G.c._, ovary; _Ov._, shell gland; _T._, testes; _T.d._, vitellarium;
_C.ex._, excretory vesicle. (After Brumpt.)]

[Illustration: FIG. 169.--_Echinostoma ilocanum_, Garrison, 1908: head
end showing collar of spines, ventral view. (After Leiper.)]

*Echinostoma malayanum*, Leiper, 1911.

Twelve millimetres long, 3 mm. broad, 1·3 mm. thick. Ends bluntly
rounded. At the anterior end a ventral furrow on either side, one-third
the width of the body, marking off the circum-oral collar. Along its
edge is a row of forty-three spines extending across the middle line
dorsally but not ventrally. The spines vary in size from 0·07 mm.
in length (ventrally) to 0·05 to 0·016 mm. (dorsally). Cuticular
spines also exist on the ventral side as far back as posterior end
of body, but dorsally limited to a triangular area ending in front
of the ventral sucker. Oral sucker 0·07 mm. thick, occupying the
middle third of the circum-oral disc; pharynx 0·25 mm. in diameter;
œsophagus 0·04 mm. long; gut cæca simple, extending to end of body;
ventral sucker 0·9 mm. long by 0·75 mm. broad by 0·7 mm. deep; wall
about 0·25 mm. thick. The sucker is inclined at an angle of 40° to the
ventral surface. Testes lobed, one behind the other, behind the ventral
sucker. Cirrus pouch well developed, reaching to the posterior edge of
the sucker. Genital pore in the angle between neck and anterior lip
of ventral sucker. Ovary smooth, 0·3 mm. in diameter, 0·85 mm. behind
ventral sucker. Vitellaria very numerous, extending from posterior
margin of sucker to posterior end of body, where they intermingle. Eggs
few in number, brown and large.

_Habitat._--Gut of man (Tamils), Malay States.

[Illustration: FIG. 170.--_Echinostoma malayanum_, Leiper, 1912:
anterior end showing collar of spines, ventral view. (After Leiper.)]

Sub-family. *Himasthlinæ*, Odhner, 1910.

Genus. *Artyfechinostomum*, Clayton-Lane, 1915.

Crown of thirty-nine spines, continuous over dorsum. Two corner spines
long. Vitellaria extend from posterior margin of sucker to posterior
end of fluke. Eggs without filament. [Although the possession of strong
rose-thorn hooks is given by Odhner as a sub-family characteristic,
yet in this genus assigned to this sub-family they have not been
seen.--J. W. W. S.]

*Artyfechinostomum sufrartyfex*, Clayton-Lane, 1915.

Spirit specimens: 9 by 2·5 by 0·8 mm. thick. Ventral sucker
conspicuous, 1 mm. in diameter. Cirrus sac 2 mm. long. Testes lobed,
about 1·5 mm. in diameter. Posterior border of posterior testes 1 mm.
from posterior end. Vitellaria meet posteriorly behind the posterior

Family. *Schistosomidæ*, Looss, 1899.

Genus. *Schistosoma*, Weinl, 1858.

  Syn.: _Gynæcophorus_, Dies., 1858; _Bilharzia_, Cobb., 1859;
  _Thecosoma_, Moq. Tandon, 1860.

  The males have bodies that widen out considerably behind the ventral
  sucker, the lateral parts of which in-roll ventrally, forming the
  almost completely closed canalis gynæcophorus, within which the
  female is enclosed. There is no cirrus pouch. The male has five or
  six testes, the females are filiform; the uterus is long. There
  is no Laurer’s canal. The ova almost equally attenuated at either
  extremity; they have a small terminal spine, and are not provided
  with a lid. They contain a miracidium, ciliated on all sides, which
  is characterized by the possession of two large glandular cells,
  which discharge anteriorly beside the gastric sac. They live in the
  vascular system of mammals. (An allied genus [Bilharziella] lives in
  the blood-vessels of birds.)

*Schistosoma hæmatobium*, Bilharz, 1852.

  Syn.: _Distoma hæmatobium_, Bilh.; _Distoma capense_, Harley, 1864.

[Illustration: FIG. 171.--_Schistosoma hæmatobium_, Bil.: male carrying
the female in the canalis gynæcophorus. 12/1. (After Looss.)]

_The Male_ is whitish, 12 to 14 mm. in length, but is already
mature when 4 mm. long. The anterior end is 0·6 mm. or a little
over in length. The suckers are near each other, the oral sucker is
infundibular, and the dorsal lip is longer than the ventral one. The
ventral sucker is a little larger, 0·28 mm., and is pedunculated.
A little behind the ventral sucker the body broadens to a width of
1 mm., decreasing, however, in thickness; the lateral edges in-roll
ventrally, so that the posterior part of the body appears almost
cylindrical, 0·4 to 0·5 mm. in diameter; the posterior extremity is
somewhat more attenuated. The dorsal surface of the posterior part of
the body is covered with spinous papillæ. There are delicate spines
on the suckers, and larger ones invest the entire internal surface of
the gynæcophoric canal, as well as a longitudinal zone at the edge of
that side of the external surface that is covered by the other side
rolling over it. The œsophagus is beset with numerous glandular cells
(fig. 173), and presents two dilatations; the intestinal bifurcation is
close in front of the ventral sucker, the two branches uniting sooner
or later behind the testes into a median trunk, which may again divide
at short intervals. The excretory pore is at the posterior end, but
placed somewhat dorsally; the genital pore is at the beginning of the
gynæcophoric canal, thus behind the ventral sucker; into it opens the
vas deferens which, posteriorly, broadens into the seminal vesicle
and then continues as the vasa efferentia of the four or five testes
(fig. 173).

[Illustration: FIG. 172.--Transverse section through a pair of
_Schistosoma hæmatobium_ in copulâ. In the male the point of reunion of
the intestinal forks has been cut across. (After Leuckart.)]

[Illustration: FIG. 173.--Anterior end of the male _Schistosoma
hæmatobium_, Bilh. _V.s._, ventral sucker; _I._, gut cæca; _G.p._,
genital pore; _T._, testes; _O.s._, oral sucker; _Oe._, œsophagus with
glandular cells; _V.s._, vesicula seminalis. 40/1. (After Looss.)]

_The Female_--filiform, about 20 mm. in length, pointed at each
end, and measuring 0·25 mm. in diameter in the middle. Their colour
varies according to the condition of the contents of the intestine.
(Posteriorly they are dark brown or blackish.) The cuticle is smooth
except in the sucker, where there are very delicate spines, and at the
posterior end, where there are other larger spines. The oral sucker
is a little larger than the pedunculated ventral sucker (0·07 and
0·059 mm. respectively). The anterior part of the body, 0·2 to 0·3 mm.
in length; the œsophagus is as in the male. The intestinal bifurcation
is in front of the ventral sucker, the two branches uniting behind the
ovary and the trunk running in a zigzag manner to the posterior border.
There are indications of diverticula at the flexures. The ovary is
median. In young females it is of an elongated oval shape; in older
females the posterior end becomes club-shaped, whereas the anterior
end becomes attenuated; the oviduct originates at the posterior end,
but immediately turns forwards and joins the parallel vitelline duct
in front of the ovary (fig. 174), where the shell gland cells open;
the common canal becomes dilated to form the oötype, and then proceeds
as the uterus, with only slight convolutions, along the central field
to the genital pore, which lies in the middle line immediately behind
the ventral sucker. The single vitellarium starts behind the ovary and
extends to the posterior end. The acini are situated at the sides of
the excretory duct, which runs a median course. The eggs are compact
spindles, much dilated in the middle; they have no lid, and are
provided with a terminal spine (rudimentary filament) at the posterior
end, measuring 120 µ to 150 µ in length and 40 µ to 60 µ in breadth,
but vary in size and shape (fig. 175).

_Distribution._--In order to understand the distribution of the worms
and eggs in the body, it may be well to recall the blood supply of the
abdominal and pelvic organs. It is generally assumed that the early
life (? cercarial stage) of the worms occurs in the liver, and that
the young worms travel from here, where they are invariably found, to
their various sites along the portal vein and its tributaries and so
_against_ the blood stream. The tributaries of the portal vein are:--

(1) _Superior mesenteric_, the tributaries of which are: (_a_) the
veins of the small intestine; (_b_) ileo-colic; (_c_) right colic;
(_d_) middle colic; (_e_) right gastro-epiploic; and (_f_) inferior
pancreatic. By these paths infection of the small intestine, ascending
and transverse colon and pancreas would occur.

(2) _Splenic._ (Ova have been recorded by Symmers in the spleen.)

(3) _Inferior mesenteric_, the tributaries of which are (_a_)
superior hæmorrhoidal veins from the upper part of the hæmorrhoidal
plexus; (_b_) sigmoid veins from sigmoid flexure and lower portion of
_descending_ colon; (_c_) left colic vein draining descending colon.

The superior hæmorrhoidal veins form a rich plexus in the rectum, and
below this level in the upper and middle parts of the anal canal. The
plexus forms two networks, an _internal_ plexus in the submucosa and
an external on the outer surface. The _internal_ plexus opens at the
anal orifice into: (_a_) branches of the inferior hæmorrhoidal vein
(from the pudic); (_b_) the external plexus. The _external_ plexus
gives off: (_a_) inferior hæmorrhoidal opening into internal pudic
(of _internal iliac_ vein); (_b_) mid-hæmorrhoidal into _internal
iliac_ or its branches; and (_c_) superior hæmorrhoidal opening into
inferior mesenteric. The external plexus further communicates with the
vesico-prostatic plexus. The vesico-prostatic (vaginal) plexus opens
into the _vesical veins_, which drain into the interior iliac vein.
This plexus also receives afferents from the pudendal plexus, the chief
tributary of which is the dorsal vein of the penis. The pudendal plexus
also receives branches from the inferior pudic and the anterior surface
of the bladder.

There is thus a communication between the portal vein and the vena cava
by means of these plexuses, _viz._, through the inferior and middle
hæmorrhoidals, and by the inferior hæmorrhoidals to the bladder and
thence by the vesical veins or the pudic to the caval system (interior

It is thus by the inferior mesenteric and its tributaries that the
worms reach the descending colon, rectum, anal canal, and eventually
the bladder, and in some cases the caval system.

Before considering what is actually found _post mortem_ in these veins
and the organs drained by them, we may further recall the fact that the
calibre of “medium” veins is 4 to 8 mm., “small” veins less than 40 µ
in diameter and capillaries 8 µ to 20 µ. Further, the maximum diameter
of the male worm is 1 mm., that of the female 280 µ and eggs _in utero_
80 µ to 90 µ long by 30 µ to 40 µ.

_Liver and Portal Vein._--Here worms are most easily found _post
mortem_. Often only males are found and these of the same size, and
if females occur only a few worms are found in copulâ. The worms are
frequently not full size and the males may contain no free spermatozoa
in their testes, and as regards the females some may be fertilized,
others not, as shown by the presence or absence of spermatozoa in
the seminal receptacle or uterus. In either case they may contain
eggs--_lateral-spined_--usually one, less often two, but there may be
as many as five or six. These eggs may also show some abnormality,
which takes the form of: (1) abnormal contents, _viz._, disintegrating
yolk cells with or without an ovarian cell; (2) abnormal shape but with
normal contents and probably represented by the collapsed and empty
egg-shells which are found in the tissues.

As to the interpretation of these facts, Looss believes that these
lateral-spined eggs are products of young females whose egg-laying is
not at first properly regulated. The shape that the eggs take, _viz._,
with a lateral spine, is determined by an excess of material--ovarian
and yolk cells--being present in the oötype. The shape of eggs depends
upon the position they have in the oötype during their formation. In
young females an excess of cells--yolk cells especially--accumulates,
distending not only the dorsal wall but a portion also of the short
duct joining the oötype to the uterus. The result of this is that
the axis of the oötype and egg is almost transverse to the body, and
the posterior funnel-shaped portion of the oötype, instead of being
terminal, has now a lateral or rather a ventral position, so that the
spine which occupies this portion, instead of being terminal, is now
lateral. It is noteworthy that these lateral-spined eggs are thicker,
owing to the excess of material present, and not uncommonly have a
curved anterior border, due to a projection of the anterior end into
the anterior opening of the oötype.

As these eggs are being laid by females in the portal vein they are
carried back to the liver by the blood stream. The liver is one of the
commonest sites for these eggs; also terminal-spined eggs may be found
here for the same reason.

_Hæmorrhoidal Veins._--Mature worms, generally in copulâ, are usually
found here, though young not fully grown females may also occur. The
tissues of the rectal wall (or colon) show, as a rule, large quantities
of lateral-spined eggs, though less often only terminal-spined eggs may
be found.

_Vesico-prostatic Plexus._--Worms in copulâ are found in the veins of
the submucosa in the bladder, and the eggs in the mucosa, and those
voided are usually terminal-spined, though lateral-spined eggs are not
so rare as generally thought. The problem next arises as to how the
eggs get to the lumen of the gut or bladder.

The female worm is 280 µ in diameter. Veins in the submucosa of the
rectum less than 178 µ in diameter are not affected with endophlebitis.
It is probable that the female even by stretching could not penetrate
much beyond this. Eggs are probably then laid in the submucosa as near
the muscularis mucosa as possible. Now if the eggs are laid in a vein
of larger calibre than the worm fills, the eggs would be carried back
to the inferior mesenteric vein, so that presumably the worm must
succeed in blocking the vein already narrowed by endophlebitis, so that
by the stasis which ensues the eggs may escape from the veins. How this
occurs is not exactly known; it is not necessarily due to the spine,
as the same escape into the tissues occurs in spineless eggs, such
as those of _Schistosoma japonicum_. The eggs, then, pass as foreign
bodies through the tissues. Another hypothesis is that the worms leave
the veins in order to lay their eggs, but the evidence is against this.

_Caval System._--Occasionally worms that have passed through the
vesical plexus may be found in the iliac vein, inferior vena cava, and
even the lungs. If the worms are young they contain a lateral-spined
egg; if adult, numerous (50 to 100) terminal-spined eggs.

_Lungs._--When the liver is strongly infected with (terminal-spined)
eggs it is possible that by passive movements some may pass into the
intralobular veins, and thence by the inferior vena cava to the lungs.

_Gall-bladder._--Similarly terminal-spined eggs pass into the
bile-capillaries and gall-bladder (where they may be abundant), and so
into the fæces.

_Detection of Eggs._--Occasionally eggs may be found in various other
parts of the body. They are best detected by macerating pieces of the
tissue in question in about 1/4 per cent. hydrochloric acid at 50 to
60°C. (Looss).

Pathological changes:--

_Rectum._--These have been studied thoroughly by Letulle in the case of
an apparently pure infection of the rectum.[274] They take the form of
a chronic diffuse inflammation, which may result in--(1) ulceration, or
(2) hyperplasia of the mucosa, producing adenomata.

[274] It is noteworthy that in this almost classical case no worms were
found in any of the sections. It is further noteworthy that the eggs in
the rectum showed great irregularity of form. Eggs with a spine at each
end were not uncommon; exceptionally eggs with two polar spines and one

_Ulcerative Form._--The _mucosa_ is transformed into a mass of vascular
connective tissue. The connective tissue spaces next become invaded
by numerous mononuclear cells. The tissue itself undergoes diffuse
sclerosis, becoming hard and fibroid. Eventually ulcerative necrosis
sets in. During these changes the Lieberkühn glands are destroyed. The
process does not extend to the submucosa, in this respect differing
from that in chronic dysentery.

_Hyperplastic Form._--The Lieberkühn glands of the mucosa at first
hypertrophy; then there is an actual hyperplasia resulting in
adenomata. The interstitial tissue of the glands is also greatly
hypertrophied, giving rise to very vascular granulations. These growths
are often hollow and contain worms. Many eggs are found in the mucosa
on their way to the lumen of the gut.

The _muscularis mucosa_ is thickened up to twice or even ten times the
normal. Its vessels are dilated (36 µ to 80 µ), but they do not allow
of the passage of worms.

The _submucosa_ is profoundly changed; rigid and hard instead of
supple. It is here that the greatest number of eggs occur. A remarkable
condition of endophlebitis exists in the veins of the submucosa, not
only in the smaller ones but also in the larger ones (370 µ by 270 µ).
This endophlebitis results in a more or less complete occlusion of the
vessels of the lumen.

The _muscular coats_ are free from change, also their veins.

The _Serous Coats_.--The veins about 1,900 µ, also show endophlebitis.
Besides the rectum, in extreme cases even the transverse colon, the
cæcum and small intestine may be affected.

_Bladder._--In the early stages the mucosa is deep red and swollen
like velvet, or there may be localized patches of hyperæmia or
extravasation. The subsequent changes take two chief forms:--

(1) _Sandy Patches._--The mucosa looks as if it were impregnated with a
fine brownish or yellowish powder (myriads of ova). This is accompanied
by a gradual hypertrophy and new formation of connective tissue, so
that dry, hard or plate-like patches with this sandy appearance arise;
the thickening eventually affects all the coats of the bladder. In the
older patches many of the eggs are calcified. These patches sooner
or later break down, ulcerate and necrose. Phosphatic deposits are
abundant and stone is common. These patches are not found in the rectum.

(2) _Papillomata._--Where the inflammatory change produced by the eggs
gives rise to hypertrophy and hyperplasia of the mucosa, papillomata
result, the axis of which is formed by connective tissue of the
submucosa. These are most variable in shape and form and bleed readily,
and sometimes contain cavities of extravasated blood.

As in the rectum, it is in the submucosa that eggs are most abundant,
and worms in copulâ occur in the veins of this layer, but endophlebitis
is not as general as described in the rectum. Malignant disease of
the bladder is not an uncommon sequela of bilharziasis. Besides the
bladder, the ureters and kidneys may in advanced cases be involved. The
prostate and vesiculæ seminales are commonly diseased. Eggs have been
recorded in the semen. The urethra is frequently attacked; the vagina
in the female.

Eggs also occur in the lymphatic glands of the gut.

_Geographical Distribution._--East Africa: Nile Valley, Red Sea Coast,
Zanzibar, Portuguese East Africa, Delagoa Bay, Natal, Port Elizabeth.

South Africa: Cape Colony, Orange Free State, Transvaal, Mauritius,
Bourbon, Madagascar.

West Africa: Angola, Cameroons, Gold Coast, Gambia, Senegal, Sierra
Leone, Lagos, Nigeria.

North Africa: Tripoli, Tunis, Algeria, parts of the Sahara.

Central Africa: Sudan, various portions. Uganda, Nyasaland.

It occurs with varying frequency in these regions. It is probably more
widely spread than this list implies, as undoubtedly many cases are
seen which are not recorded.

Isolated cases have been recorded from Arabia, India,[275] Greece,

[275] In a case from Madras, recorded by Stephens and Christophers,
the eggs were long and spindle-shaped, quite unlike the eggs of
_Schistosoma hæmatobium_.

[Illustration: FIG. 174.--_Schistosoma hæmatobium_, Bilh.: genitalia of
the female. _V.s._, ventral sucker; _I._, gut cæca; _V.d._, vitelline
duct; _V.sc._, vitellarium; _O._, ovary; _Oe._, œsophagus; _Sh._, shell
gland; _U._, uterus. Magnified. (After Leuckart.)]

The means by which infection is brought about are still uncertain; we
only know that the miracidia (fig. 175) enclosed in the discharged
eggs do not hatch if the eggs remain in the urine, but after cooling
perish. As soon, however, as the urine is diluted with water the shell
swells, generally bursting lengthways, and releases the miracidium from
its investing membrane, so that it can swim about with the aid of its
cilia. In its structure it differs but little from the miracidium of
_Fasciola hepatica_, as, for instance, in the lack of eyes; the two
large gland cells situated on either side of the intestinal sac are
also present in the miracidia of _Fasciola hepatica_.

_Sarcode Globules._--This is a term applied to certain globules which
at times appear in the miracidium and are later ejected. Some authors
consider them as indicative that the miracidium has developed into a
sporocyst, but Looss considers them to be degeneration products.

The Bilharzia mission, under R. T. Leiper, sent to Egypt by the War
Office early in 1915, reports that cercariæ of bilharzia type were
recognized in four of the commonest fresh-water molluscs around Cairo.

With material obtained from naturally infected _Planorbis boissyi_
acute bilharziosis was experimentally produced in rats, mice, and
monkeys. Infection takes place experimentally through the skin and also
through the mucous membrane of the mouth and œsophagus. The miracidium,
after entering the mollusc, develops into a sporocyst. This gives rise
not to rediæ, but to secondary sporocysts, which, in turn, produce
cercariæ. These, like the adult worm, differ from other distomes in
lacking a muscular pharynx.

*Schistosoma mansoni*, Sambon, 1907.

According to Manson, Sambon and others, the eggs with lateral spines
belong to a species different from _Schistosoma hæmatobium_. Infections
with this species only are said to occur in the Congo, Southern States
of North America, West Indies (Guadeloupe) and Brazil (Bahia). The
following characters, according to Flu, differentiate this species: (1)
In the male the transition from the anterior portion of the worm to
the lateral fields (the infolded portions which form the gynæcophoric
canal) is not a gradual one as in _Schistosoma hæmatobium_, but in this
case the lateral fields rise suddenly, almost at right angles to the
anterior portion. (2) The ovaries have a well-marked convoluted course
as in no other schistosome. (3) The oötype is symmetrical in reference
to the long axis of the body, its duct being lateral on the ventral
side (Looss’ explanation of this we have already given). (4) The worms
live exclusively in portal vein and tract. (As lateral-spined eggs
occur also in the bladder, this is not exactly true.)

[Illustration: FIG. 175.--Ovum of _Schistosoma hæmatobium_, Bilh., with
miracidium, which has turned its anterior end towards the posterior end
of the egg. 275/1. (After Looss.)]

  |*Schistosoma hæmatobium*, Bilharz, 1852.                          |
  |                                                                  |
  |Male, four or five large testes. Gut forks unite late, so that the|
  |single gut stem is short. Female, ovary in posterior half of body.|
  |Uterus very long, voluminous, with many terminal-spined eggs, some|
  |lying in pairs. Vitellaria in posterior fourth of body. Cercariæ  |
  |in _Bullinus contortus_ and _Bullinus dybowski_ (syn.: _Physa     |
  |alexandrina_) in Egypt.                                           |
  |                                                                  |
  |                                                                  |
  |*Schistosoma mansoni*, Sambon, 1907.                              |
  |                                                                  |
  |Male, eight small testes. Gut forks unite early, so that the      |
  |single gut stem is very long. Females, ovary in anterior half of  |
  |body. Uterus very short; usually only one lateral-spined egg at a |
  |time _in utero_. Vitellaria occupy posterior two-thirds of body.  |
  |Cercariæ in _Planorbis boissyi_ in Egypt.                         |
  |                                                                  |
  |The above morphological descriptions are founded on worms of each |
  |species, derived from experimentally infected mice (Leiper, R. T.,|
  |_Brit. Med. Journ._, March 18, 1916, p. 411).                     |

*Schistosoma japonicum*, Katsurada, 1904.

  Syn.: _S. cattoi_, Blanchard, 1905.

_Male._--Eight to 19 mm., but extreme limits are 5 to 22·5 mm.
Consists of a short fore-body, separated by the ventral sucker from
the hind-body. The ventral sucker is stalked and somewhat larger than
the oral sucker. Both suckers are larger than the corresponding
ones in _S. hæmatobium_. Body usually smooth, but in the fresh
state numerous fairly evident spines along the margin of the canal.
Œsophagus: two bulbs. The junction of the gut forks more posterior than
in _S. hæmatobium_, the median united gut stem occupying a quarter to
one-fifth to one-sixth of the body length. An excretory canal runs
along each side of the body, opening into the dorsal excretory pore.
Testes irregularly elliptical, six to eight in number, in the anterior
part of hind-body. The vasa efferentia unite into a common vas deferens
which opens directly behind the ventral sucker. The seminal vesicle
lies just behind this.

[Illustration: FIG. 176.--_Schistosoma japonicum_: anterior end with
testes; posterior end with point of union of cæca. Length of worm about
10 mm. (After Katsurada.)]

_Female._--Up to 26 mm., generally thinner than the male. Surface
smooth. Suckers armed with fine spines. Ventral sucker larger than
oral. Body thicker behind the region of the ovary. The gut forks unite
immediately behind the ovary. The united gut much thicker than in _S.
hæmatobium_. Ovary elliptical, almost in the mid-body, its hinder
portion dilated. The oviduct arises from its posterior end and then
runs sinuously forward, where it is joined by the vitellarian duct;
the vitellarium well developed, extending from behind the ovary almost
but not quite to the posterior end as in _S. hæmatobium_. Shell gland
ducts enter at the junction point of oviduct and vitelline duct. The
canal here forms an oötype and then proceeds as the uterus to open
directly behind the ventral sucker. The uterus occupies almost half
the hind-body. In _S. hæmatobium_ this is not so. The uterine canal is
cleft-like, _i.e._, its dorso-ventral diameter is much greater than its
lateral diameter. The number of eggs varies from about 50 to 300 from
observations made in various hosts.

_Eggs._--_In utero_ assume various shapes, as they are soft; the lumen
of the uterus is narrow. Outside they are oval, faint yellow, double
contoured. In fæces the eggs measure 83·5 µ, by 62·5 µ (man); 85 µ by
61·5 µ (cattle); 98·2 µ by 73·8 µ (dog). The eggs have either small
lateral spines or thickenings, and Looss at the opposite side has
described cap-like thickenings. The eggs in the tissues undergo various
deformities, and may contain a miracidium, as also the eggs in fæces
do; or the contents may consist of granular matter or amorphous masses
or they may be calcified. Lymphocytes and giant cells may also invade
the eggs.

[Illustration: FIG. 177.--_Schistosoma japonicum_, male and female in
copulâ. × 60. (After Katsurada.)]

[Illustration: FIG. 178.--_Schistosoma japonicum_: eggs from human
liver, showing “spines” and “hoods” at opposite pole. (After Looss.)]

_Mode of Infection._--The miracidia hatch in water in as little as
fifteen minutes, but the majority in one to three hours. They will
live in water for about twenty-four hours. In water they undergo a
transformation into “larvæ,” which then penetrate the skin, as has been
shown by Japanese writers to hold good for man, cattle, dog and cat.
The penetration of the skin is attended with an eruption on the legs,
“Kabure.” The exact route by which the worms reach the portal vein
is uncertain. Infection in Japan takes place from spring to autumn,
especially May to July, when the soil is contaminated with manure
of cattle infected with _S. japonicum_. They also appear to develop
in molluscs. Leiper and Atkinson found cercariæ (in sporocysts) in
the liver of a mollusc, _Katayama nosophora_. They infected mice by
immersing them in water containing liver emulsion and so free cercariæ,
thus confirming the similar results of Miyairi and Suzuki.

[Illustration: FIG. 179.--_Schistosoma japonicum_: from dog. Uterine
egg. × c. 800. (After Katsurada.)]

[Illustration: FIG. 180.--_Schistosoma japonicum_: from dog. × c. 800.
(After Katsurada.)]

[Illustration: FIG. 181.--_Schistosoma japonicum_: from dog. Egg from
fæces. × c. 800. (After Katsurada.)]

_Habitat._--The worm occurs in Japan, China, and the Philippines. The
normal host is man and mammals. Cattle, dog and cat are often found
naturally infected. Mice can also be experimentally infected. Their
seat of election is the portal vein and its branches, especially the
mesenteric veins. They either swim free in the blood or remain fixed
by their suckers to the intima of the vessels. They have also been
found in the vena cava and right heart of a cat, but not so far in the
vesical plexus.

Eggs are found in the submucosa and mucosa of the gut, especially the
colon, and at times in the serosa and subserosa of the small intestine,
where they give rise to new growths. Occasionally eggs are found in the
brain. The life of the worms is at least two years.

_Pathogenic Effects._--Anæmia through loss of blood due to worms;
enlarged spleen, toxic in origin (?); phlebitis, thrombosis, due to
portal stasis; the eggs, however, cause the greatest mischief. They
are carried by the circulation to various organs where they produce
inflammation, granulation tissue, and later connective tissue.

_Liver._--The eggs reaching this organ give rise to granulomata and
hence enlarged liver, and later, when connective tissue is formed, to
contraction. The surface is rough and irregularly granular, “parasitic
embolic cirrhosis” of Yamagiwa.

[Illustration: FIG. 182.--_Schistosoma japonicum_: section through the
gut of a Chinaman showing eggs. × 58. (After Catto.)]

_Gut._--The eggs in the mucosa and submucosa cause catarrh and
destruction of tissue or new growth. In the small intestine the eggs
are mainly in the serosa and subserosa, where they give rise to
polypoid or branched growths.

_Spleen._--Enlarged, at first due to toxin (?) and later due to portal
stasis. Eggs in the spleen are uncommon.

_Ascites_ also arises from the portal stasis, and is generally present
in advanced cases.

Eggs may be found in many other situations: glands (numerous),
mesentery, stomach, pancreas, kidney, etc. The bladder remains free.

[Illustration: FIG. 183.--_Schistosoma japonicum_: liver showing eggs
in the intra- and interlobular connective tissue. × c. 80. (After

Class III. *CESTODA*, Rud., 1808.

  Tapeworms have been known from ancient times--at all events, the
  large species inhabiting the intestines of man--and there has never
  been a doubt as to their animal nature. The large cysticerci of the
  domestic animals (occasionally of man also) have been known for an
  equally long period, but they were generally regarded as growths,
  or “hydatids,” until almost simultaneously Redi in Italy, and
  Hartmann and Wepfer in Germany, concluded from their movements and
  organization that they were of animal nature. From that time the
  cysticerci have been included amongst the other intestinal worms, and
  Zeder (1800) established a special class (_Cystici_, Rud., 1808) for
  the bladder worms. Things remained in this condition until the middle
  of the last century, when Küchenmeister, by means of successful
  feeding experiments, demonstrated that the cysticerci were definite
  stages of development of certain tapeworms. Before Küchenmeister, E.
  Blanchard, van Beneden, and v. Siebold had held the same opinion in
  regard to other asexual Cestodes.

  Since the most remote period another question has again and
  again occupied the attention of naturalists, the question of the
  morphological nature--that of the INDIVIDUALITY OF THE TAPEWORM. The
  ancients, who were well acquainted with the proglottids (_Vermes
  cucurbitani_) that are frequently evacuated, were of the opinion
  that the tapeworm originated through the union of these separate
  proglottids, and this view was maintained until the end of the
  seventeenth century. In 1683 Tyson discovered the head with the
  double circlet of hooks in a large tapeworm of the dog; Redi (1684)
  was also acquainted with the head and the suckers of several Tæniæ.
  Andry (1700) found the head of _Tænia saginata_, and Bonnet (1777)
  and Gleichen-Rusworm (1779) found the head of _Dibothriocephalus
  latus_. Consequently most authors, on the ground of this discovery,
  considered the tapeworm as a single animal, that maintains its hold
  in the intestine by means of the head, and likewise feeds itself
  through it. The fact was recognized that there were longitudinal
  canals running through the entire length of the worm, and it was
  thought that these originated in the suckers, and that the entire
  apparatus was an intestine. As, moreover, the segments form at the
  neck, and are cast off from the opposite extremity, the tapeworm
  was also compared with the polyps, which were formerly regarded as
  independent beings.

  Steenstrup, in his celebrated work on the alternation of generations
  (1841), was the first to give another explanation. This has been
  elaborated still further by van Beneden, v. Siebold and Leuckart,
  and until a few years ago all authorities adopted his views.
  According to this view, the tapeworm is composed of numerous
  individuals, something like a polyp colony, and, in addition to the
  proglottids--the sexual individuals which are usually present in
  large numbers--there is ONE individual of different structure, the
  _scolex_, which not only fastens the entire colony to the intestine,
  but actually produces this colony from itself, and therefore is
  present earlier than the proglottids. The scolex is a “nurse,”
  which, though itself produced by sexual means, increases asexually
  like a _Scyphistoma_ polyp; the tapeworm chain has therefore been
  termed a _strobila_. Consequently the development of the tapeworms
  was explained by an alternation of generations. In support of this
  opinion it was demonstrated not only that the adult sexual creatures,
  the proglottids, can separate from the colony and live independently
  for a time, but that in certain Tæniæ, and especially in many
  Cestodes of the shark, the proglottids detach themselves long before
  they have attained their ultimate size, and thus separated continue
  to develop, grow and finally multiply; the scolex also exhibits a
  certain independence in so far as, though not, as a rule, capable of
  a free life, yet it in some cases lives as a free being, partly on
  the surface of the body of marine fishes and partly in the sea. With
  the more intimate knowledge of the development of the cysticerci,
  the independent nature of the scolex was recognized. It is formed by
  a budding of the bladder that has developed from the oncosphere, in
  some cases (Cœnurus) in large numbers, in other cases (Echinococcus)
  only after the parent cyst has developed several daughter cysts.
  Released from its mother cyst and placed in suitable conditions,
  it goes on living, and gives rise at its posterior end by budding
  to the strobila, the proglottids of which eventually become sexual

  In order to make this clearer we will briefly summarize what takes
  place in the jelly-fishes.

  By _metamorphosis_ is meant a developmental change in the _same_
  individual, while alternation of generations, or _metagenesis_,
  implies a stage in which _reproduction_ of individuals takes place by
  a process of budding or fission. This _asexual_ reproductive stage
  _alternates_ with the _sexual_ mode of reproduction. Thus in the
  development of the Scyphozoa (jelly-fishes) we have:--

  (1) The fertilized egg cell divides regularly and forms a _morula_.

  (2) By accumulation of fluid in the interior this becomes a closed
  sac with a wall formed of a single layer of cells, forming the
  _blastosphere_ or _blastula_.

  (3) One end of the sac is invaginated, forming a _gastrula_.

  (4) The gastrula pore or mouth closes, forming again a sac, the walls
  of which have two layers, forming a _planula_.

  (5) This becomes fixed to a rock, an invagination forms at one end,
  a depression--the stomodæum--communicating with the enteric cavity.
  Tentacles grow out and we have a _Scyphozoön polype_, _Scyphistoma_
  or _Scyphula_. It is to this stage that Steenstrup gave the name
  “nurse” (“wet-nurse”), because it nourished or produced asexually the
  succeeding forms.

  (6) _Asexual reproduction_ by transverse fission occurs in this,
  forming a pile of saucer- or pine-cone-like animals which before this
  time had been considered to be a distinct animal, which was called
  _strobila_ from its resemblance to a pine-cone. This is the alternate

  (7) The individuals of the strobila become free and are called

  (8) These develop finally into adult sexual jelly-fish, _Scyphozoa_,
  so that comparing a tapeworm with this we have (_a_) egg, (_b_)
  scolex (= Scyphula or “nurse”), (_c_) asexual reproduction of the
  tapeworm chain (= strobila), (_d_) development of the individuals of
  the chain (proglottids) into sexual adults.

  Van Beneden’s terminology for these stages is the following: Ciliated
  embryo = protoscolex; scyphistoma = deutoscolex (or scolex); free
  Ephyrula = proglottis. According to this view, as is the case in many
  endoparasitic Trematodes, asexual reproduction by budding occurs
  at two stages of the whole cycle of development, _viz._ (1) in the
  formation of the scolex by budding from the bladder (“nurse”), (2) in
  the formation of the strobila by budding from the scolex (“nurse”).

  But in cysticercal larval forms it appears that the scolex does not
  arise in this way but is simply a part of the proscolex (hexacanth
  embryo), becoming invaginated into it for protection, so that there
  is no asexual gemmation here. It has been questioned also whether
  the strobila also arises by gemmation. If it does, the tapeworm is a
  _colony_ of zoöids produced by budding from the asexual scolex; if
  it is not produced in this way, then the tapeworm is to be regarded
  as an _individual_ in which growth is accompanied by segmentation.
  Against the “colony” view are the facts that the muscular, nervous,
  and excretory systems are continuous throughout the worm, and that
  some tapeworms, such as _Ligula_, are unsegmented.

  Finally, if the tapeworm is an individual the question arises
  which is the head end. As new segments are formed at the neck,
  and as this point in annelids is the antepenultimate segment, the
  scolex must be the last or posterior segment. The caudal vesicle
  or bladder of larval forms is consequently anterior. According to
  this view, in tapeworms as among many endoparasitic flukes, an
  _asexual_ multiplication occurs at two points of the whole cycle
  of development, which is as follows: (1) egg, (2) oncosphere or
  hexacanth embryo, (3) bladder (cysticercus or hydatid), (4) (after
  digestion of the bladder) by budding, the scolex, (5) by budding from
  the scolex the sexual proglottids, (6) the egg; (4) and (5) being the
  two asexual stages.


If we except the tapeworms with only one proglottis, the CESTOIDEA
MONOZOA, Lang = _Cestodaria_, Monticelli, we can always distinguish in
the Cestodes, in the narrower sense, one scolex or head and a large or
small number of segments (proglottids). The SCOLEX serves the entire
tapeworm for fastening it to the internal surface of the intestinal
wall, and therefore carries at its end various organs which assist
in this function, and which are as follows: (i) SUCTORIAL ORGANS,
_i.e._, the four suckers (acetabula), which are placed crosswise at the
circumference of the thickened end of the scolex; further, the double
or quadruple groove-like suckers (bothridia), which are diversely
shaped in the various genera and families.[276] (2) FIXATION ORGANS
(hooklets)[277] that likewise occur in varying numbers and different
positions; they may be in the suckers, or outside them on the apex of
the scolex; for instance, in many of the _Tæniidæ_ they appear in a
circle around a single protractile organ, the rostellum, or the latter
may be rudimentary, and is then replaced by a terminal sucker. (3)
PROBOSCIS. One family of the Cestodes, the _Rhynchobothriidæ_, carries
four proboscides, moved by their own muscular apparatus, on the scolex,
and they are beset with the most diverse hooks. (4) TENTACLE-LIKE
formations are only known in one genus (Polypocephalus).

[276] They may remain simple, and are then not separated from the
remaining muscles of the scolex; or they project as roundish or
elongated structures over the scolex, hollow on their free surface, and
often divided into numerous areas by muscular transverse ribs. They may
also carry accessory suckers on their surface.

[277] The various parts of a hooklet are thus named from the point
backwards: (1) blade or prong, (2) guard or ventral or posterior root,
(3) handle or dorsal or anterior root.

The thickened part of the scolex that carries the suckers is usually
called the head; the following flat (unsegmented) part connecting
it with the proglottids is called the neck, and is sometimes quite
small. In a few cases the entire scolex (or head) disappears, and its
function is then undertaken by the contiguous portion of the chain of
proglottids, which is transformed into a variously shaped PSEUDO-SCOLEX.

The proglottids are joined to the scolex in a longitudinal row, and are
arranged according to age in such a manner that the oldest proglottis
is farthest from the scolex, and the youngest nearest to it.

The number of segments varies, according to the species, from only a
few to several thousands; they are either quadrangular or rectangular;
in the latter case their longitudinal axis falls either longitudinal
or transverse to that of the entire chain, according as the segments
are longer than broad or broader than long. When the number of segments
is very large, the youngest ones are, as a rule, transversely oblong,
the middle ones are squarish, and the mature ones longitudinally
oblong. The posterior border of the segments, as a rule, carries a
longitudinal groove for the reception of the shorter anterior border
of the following proglottis. The two lateral borders of the segment
are rectilinear, but converge more or less towards the front, or they
are bent outwards. In most of the Cestodes the segments, just as the
neck, are very flat; in rare cases their transverse diameter is equal
to their dorso-ventral diameter. As a rule the segments, singly or
several united together, detach themselves from the posterior end, in
many cases only after complete maturity is attained, and in others
much earlier; they then continue to live near their parent colony, to
still call it by that name, in the same intestine and continue their
development. Even when evacuated from the intestine the proglottids
under favourable circumstances can continue to live and creep about,
until sooner or later they perish.

The first proglottis formed, and which in a complete tapeworm [_i.e._,
sexually complete] is the most posterior, is as a rule smaller and
of different shape, it also frequently remains sterile, as likewise
happens in the next (younger) segments in a few species; otherwise,
however, sooner or later the generative organs develop in all the
segments, mostly singly, sometimes in pairs; in the latter case they
may be quite distinct from each other or possess some parts in common.
The term “mature” is used for a proglottid that has the sexual organs
fully developed, while “gravid” is used for one containing eggs. Most
of the species combine male and female genitalia in the same segment,
only a few are sexually distinct (Diœcocestus). In the hermaphrodite
species one male and one female sexual orifice are always present,
and, in addition, there may be a second female orifice, the uterine
opening; as a rule, however, this is lacking, and in one sub-family,
the _Acoleinæ_, to which also the genus Diœcocestus belongs, the other
sexual orifice, the opening of the vagina, is also absent. The position
of these orifices varies; the cirrus and vagina usually open into a
common atrium on one lateral border or on a surface of the segments;
the orifice of the uterus may be on the same surface or on the opposite

The surface on which the uterus opens is termed the VENTRAL SURFACE;
if this orifice is absent, one must depend on the ovary, which almost
always approaches one of the two surfaces; this surface is then called
the ventral.

The length of the Cestodes--independently of their age--depends on the
number and size of the segments, as well as on their contraction; the
smallest species (_Davainea proglottina_) is 0·5 to 1·0 mm. in length;
the largest may attain a length of 10 m., and even more.

The entire superficial surface of the tapeworms is covered with a
fairly resistant and elastic layer, which exhibits several indistinctly
limited layers and which is usually called a cuticle, which also covers
the suckers, and is reflected inwardly at the sexual orifices. In
some species fine hairs appear, either on the entire body or only in
the region of the neck, on the external surface. In the cuticle there
can be recognized, besides the pores, which no doubt are concerned
with nutrition, spaces in which lie the ends of sensory cells. Close
under the cuticle lies the external layer of the parenchyma (basal
membrane), and below this the circular and longitudinal muscles forming
the dermo-muscular coat. The matrix cells of the cuticle occur as in
the Trematodes, only on the inner side of the peripheral muscles in
the external zone of the parenchyma; they are fusiform cells, forming
one or two layers, but are not arranged in the manner of epithelial
cells (fig. 184, _Sc.c._). They have fine branching processes which
run between the dermal muscles, pass through the basal membrane and
penetrate the internal surface of the cuticle with small pistil-like
enlargements, expanding on the internal surface of the cuticle into a
thin plasma layer.

[Illustration: FIG. 184.--Schematic representation of a small part of
a transverse section of _Ligula_ sp. _Bs._, basal membrane; _Cu._,
cuticle; at its base are the endplates of the subcuticular (epithelial)
cells; in the centre a cuticular sense organ, _O.s._; _F.v.s._,
vitelline follicle; _Exc._, excretory vessel; _C._, calcareous
corpuscle; _L.m._, longitudinal muscles; _M.c._, myoblast; _P.m._,
parenchymatous or dorso-ventral muscles; _Pl._, plexus of nerve fibres;
_A.m._, circular muscles; _Sc.c._, subcuticular or matrix cell; _T.c._,
terminal flame cell. 500/1. (After Blochmann.)]

In addition to the above mentioned, there are other cuticular
formations occurring on the cuticle of some Cestodes, such as immobile
hairs and variously formed hooks, such as are seen principally on the
scolex. Their development is only roughly known in a few species;
they are usually already present in the larval stage, and of the same
arrangement and shape as in the fully developed tapeworms; a matter
of importance, because by these structures larvæ can be recognized as
being those of a certain species of tapeworm.

The CUTICULAR GLANDS in Cestodes are scarce.

The PARENCHYMA forms the chief tissue of the entire body, and in all
essentials its structure is similar to that of the Trematodes.

The same doubt exists here also as to the nature of the parenchyma.
Recent authors consider that it consists of highly branched cells,
the processes of which ramify in all directions. These cells lie in a
non-cellular matrix containing fluid vacuoles. This matrix spreads in
between and so breaks the continuity of the epidermal cells.

[Illustration: FIG. 185.--Half of a transverse section through a
proglottis of _Tænia crassicollis_. Cu., cuticle; _Ex.v._, external
excretory vessel, to the right of which there is the smaller internal
one; _T._, testicular vesicles; _L.m._, longitudinal muscles (outer
and inner); _M.f._, lateral nerve with the two accessory nerves;
_Sc.c._, subcuticular matrix cells; _Sm.f._, submedian nerve; _Tr.m._,
transverse muscles; _Ut._, the uterus, and the middle of the entire
transverse section. 44/1.]

In the parenchyma of almost all the Cestodes there are found in adult
specimens, as well as in larvæ, light-refracting concentrically
striated structures, of a spherical or broad elliptical shape, which,
on account of their containing carbonate of lime, are termed CALCAREOUS
CORPUSCLES (fig. 184, _C._). Their size, between 3 µ and 30 µ, varies
according to the species; their frequency and distribution in the
parenchyma also varies, but they are chiefly found in the cortical
layer. They are the product of certain parenchymatous cells, in the
interior of which they lie like a fat globule in a fat cell, but
according to others they are _intercellular_ in origin.

The MUSCULAR SYSTEM of the proglottids is composed of--(1) the
subcuticular muscles (figs. 184 and 185), as a rule consisting of
a single layer of annular muscles; (2) longitudinal muscles; (3)
dorso-ventral fibres extending singly from one surface to the other,
and at both ends expanding in a brush-like manner, and inserted into
the basal membrane, consisting of an outer, more numerous, and an
inner, less numerous but more powerful layer (the number of bundles
in this layer being in certain cases of specific importance); (4)
transverse fibres, the elements of which penetrate to the borders
of the segments, thus passing through the longitudinal muscles and
reaching the cuticle. In the region of the septa the transverse and
dorso-ventral muscles form a kind of plate.

The mass of parenchyma bounded by the transverse muscles is termed
the MEDULLARY layer, while the mass lying outside them is termed the

It was known long ago that the myoblasts adhere to the dorso-ventral
fibres as thickenings, but it is only recently that large star-shaped
cells (fig. 184), separated from but connected with them by processes,
have been recognized as the myoblasts of other fibres (Blochmann,

Within the scolex the direction and course of the muscular layers

The SUCKERS are parts of the musculature, locally transformed, with a
powerful development of the dorso-ventral muscles, now become radial

The ROSTELLUM of the armed Tæniæ, like the proboscis of the
_Rhynchobothriidæ_, also belongs to the same category of organs.

[Illustration: FIG. 186.--_Dipylidium caninum_: from the cat. In the
upper figure the rostellum is retracted, in the lower protruded, _a_,
sucker; _b_, hooks of rostellum; _B_, enlarged hook; _c_, apical
aperture on scolex; _d_, longitudinal muscles; _e_, circular muscles.
(After Benham.)]

In the simplest form, the rostellum, or top of the head (as in
_Dipylidium caninum_), appears as a hollow oval sac, the anterior part
of which, projecting beyond the upper surface of the head, carries
several rows of hooks (fig. 186). The entire internal space of the sac
is occupied by an elastic, slightly fibrous mass, while the anterior
half of the surface of the rostellum is covered by longitudinal fibres
and the posterior half by circular fibres. On contraction of the latter
the entire mass is protruded through the apical aperture, the surface
of the rostellum becomes more arched, and the position of the hooks is,
in consequence, altered. The rostellum of the large-hooked _Tæniidæ_,
which inhabit the intestine of man and beasts of prey, is of a far more
complicated structure, for, in addition to the somewhat lens-shaped
rostellum carrying the hooks on its outer surface, there are secondary
muscles grouped in a cup-like manner (fig. 187). Every change in the
curvature of the surface of the rostellum induces an alteration in the
position of the hooks. In the hookless _Tæniidæ_ the muscular system of
the rostellum is altered in a very different manner; in a few forms a
typical sucker appears in its place.

The NERVOUS SYSTEM commences in the scolex and runs through the
neck and the entire series of proglottids. Within the proglottids it
consists of a number of longitudinal nerve fibres of which those at
each lateral border are usually the largest. In the Tæniæ the lateral
nerves are accompanied both dorsally and ventrally by a thinner nerve
(accessory nerve) (fig. 185); on each surface, moreover, between the
lateral nerve and the median plane, there are two somewhat stronger
bundles (sub-median), so that there is a total of ten longitudinal
nerve bundles. They lie externally to the transverse muscle plates,
and the lateral and accessory bundles lie externally to the principal
excretory vessels, and are everywhere connected by numerous anastomoses
and secondary anastomoses; one typical ring commissure is usually found
at the posterior border of the segments. In the _Bothriocephalidæ_ the
distribution of the nerve bundles is different (for instance, two lie
in the medullary layer), or they are split up into a larger number
of branches. In the scolex the nerve bundles are connected in a very
remarkable manner by commissures with that which is generally termed
the central part of the entire nervous system. There occurs normally
a commissure between the two lateral nerves; at the same level, the
dorsal and ventral median nerves are also connected at each surface as
well with each other as with the lateral nerves, so that a hexagonal or
octagonal figure is formed. The so-called apical nerves pass from this
commissural system anteriorly, embrace the secondary muscular system of
the rostellum semicircularly, and form an annular commissure (rostellar
ring) at the inner part of the rostellum.

[Illustration: FIG. 187.--Longitudinal section of the head and neck of
_Tænia crassicollis_, showing the lens-shaped muscular rostellum, with
two hooks lying in the concentric cup-like mass of muscles. _L.m._,
longitudinal muscles of the neck; _L.f._, left lateral nerve; _G._,
ganglion; _S.c._, subcuticular layer; _W_{1}_, external, _W_{2}_,
internal excretory vessel. 30/1.

The peripheral nerves arise from the nerve bundles as well as from the
commissures situated in the scolex; some go direct to the muscles,
while others form a close plexus of nerves external to the inner
longitudinal muscles, which plexus likewise sends out fibres to the
muscles, but principally to numerous fusiform sense organs (fig. 184,
_Pl._); they lie internal to the subcuticular cells and, piercing the
cuticle with their peripheral processes, end as projecting “receptor”
hairs. Higher organs of sense are not known.

The EXCRETORY APPARATUS of the Cestodes is similar to that of other
flat worms. The terminal (flame) cells, which hardly differ in
appearance from those of the Trematodes, are distributed throughout
the parenchyma, but are more common in the cortical than in the
medullary layer (fig. 184, _T.c._). Before opening into a collecting
tube, the capillaries run straight, tortuously, or in convolutions,
anastomosing frequently with one another or forming a _rete mirabile_.
The collecting tubes, which have their own epithelial and cuticular
wall, and which also appear to be provided with muscular fibres, occur
typically as four canals passing through the entire length of the worm
(fig. 189); they lie side by side, two (a wider thin-walled ventral,
and a narrower thick-walled dorsal one) in either lateral field; in
the head the two vessels on each side unite by means of a loop, at
the posterior extremity they open into a short pyriform or fusiform
terminal bladder which discharges in the middle of the posterior edge
of the original terminal proglottis.

[Illustration: FIG. 188.--_Tænia cœnurus_, head and part of neck
showing nervous system. Enlarged. (After Niemiec.)]

This primitive type (fig. 189) of arrangement of collective tubes is
subject to variation in most Cestodes, in the scolex as well as in
the segments. Indeed, even the lumen of the four longitudinal tubes
does not remain equal, as the dorsal or external tubes are more fully
developed and become thicker, whereas the ventral or internal ones
remain thin, and in some species quite disappear in the older segments
(figs. 185, 187). Moreover, very frequently connections are established
between the right and left longitudinal branches, as in the head,
where a “frontal anastomosis” develops, which in the _Tæniidæ_ usually
takes the form of a ring encircling the rostellum (fig. 190), and in
the segments of a transverse anastomosis at each posterior border,
especially between the larger branches, and more rarely between the
smaller collecting tubes also (fig. 191).

The so-called “island” formation is another modification, _i.e._, at
any spot a vessel may divide and after a longer or shorter course the
two branches reunite, and this may appear in the collecting tubes
themselves as well as in their anastomoses. The above-mentioned ring
in the frontal commissure of the _Tæniidæ_ is such an island; similar
rings also frequently encircle the suckers (fig. 190). In extreme cases
(_Triænophorus_, _Ligula_, _Dibothriocephalus_, etc.) this island
formation extends to all the collecting tubes and their anastomoses.
Instead of two or four longitudinal canals only, connected by
transverse anastomoses at the posterior border of the segments, there
is an irregular network of vessels, situated in the cortical layer,
from which the longitudinal branches, having again subdivided, can only
be distinguished at intervals, and even then not in their usual number.

[Illustration: FIG. 189.--Young _Acanthobothrium coronatum_, v.
Ben., with the excretory vessels outlined. Slightly enlarged. (After

[Illustration: FIG. 190.--Scolex of a cysticercoid from _Arion sp._,
with the excretory vessels outlined. (After Pintner.)]

The opening of the longitudinal branches at the posterior end requires
more accurate investigation; it is true that a single terminal
bladder is mentioned as being present in many species, but this is
also disputed; when the original end proglottis has been cast off,
the longitudinal branches discharge separately. Some species possess
the so-called foramina secundaria, which serve as outlets for the
collecting tubes; they are generally at the neck, but may be situated
on the segments.

The contents of the excretory vessels is a clear fluid, the
regurgitation of which is prevented by the valves present at the points
of origin of the transverse anastomoses. The fluid contains in solution
a substance similar to guanine and xanthine.

_Genital Organs._--With the exception of one genus (_Diœcocestus_,
Fuhrm.), in which the species are sexually differentiated, all the
Cestodes are hermaphroditic; the genitalia develop gradually in the
segments (never in the scolex), the male organs, as is usual in
hermaphroditic animals, forming earlier than the female. The youngest
proglottids generally do not exhibit even traces of genitalia: these,
as a rule, develop first in the older segments, and the development
proceeds onwards from segment to segment. In a few exceptional cases
(_Ligula_) the sexual organs are already developed in the larval stage,
but are only functional after the entry of the parasite into the final

[Illustration: FIG. 191.--Proglottis of _Tænia saginata_, Goeze,
showing genitalia. _C._, transverse excretory canal; _N._, lateral
longitudinal nerve; _W._, longitudinal excretory canal; _T._, testicles
scattered throughout the proglottis; _Ut._, opposite the central
uterine stem (a closed sac); _Ss._, genital pore leading into the
genital sinus; above the cirrus and coiled vas deferens (_V.d._), below
the vagina (_Vag._), bearing near its termination a dilatation, the
seminal receptacle; _Vsc._, the triangular vitellarium, and above it
(_Shg._) the shell gland; leading from this to the uterus is seen the
short uterine canal, on either side of this the two lobes of the ovary
(_Ov._). 10/1.]

With the exception of the end portions of the vagina, cirrus and
uterus, all the parts of the genital apparatus lie in the medullary
layer, except only the vitellaria, which in many species are in the
cortical layer. The male apparatus consists of the testes, of which,
as a rule, there are a large number,[278] and which lie dorsal to the
median plane (fig. 185, _T._); a vas efferens arises from each testis,
unites with contiguous vasa, and finally discharges into the muscular
vas deferens that is situated in about the middle of the segment.
According to the position of the genital pore, the vas deferens opens
on the lateral margin or in the middle line in the front of the
segment; it is much convoluted or twisted, and frequently possesses a
dilatation termed the vesicula seminalis. It finally enters the cirrus
pouch, which is usually elongated; within the cirrus pouch lies the
protrusible cirrus, which is not uncommonly provided with hooklets.

[278] There are, however, tapeworms with only one, others with only two
or three testes in each segment.

[Illustration: FIG. 192.--_Dibothriocephalus latus._ Upper figure:
female genitalia, ventral view. Lower figure: male genitalia, dorsal
view. The central portion only of the proglottis is shown. _a_,
cirrus sac; _b_, partly everted cirrus; _c_, genital atrium and pore;
_d_, vaginal pore; _e_, uterus; _f_, uterine pore; _g_, vagina; _h_,
ovary; _i_, shell gland; _j_, vitelline duct; _k_, lateral nerve; _l_,
vitellarium; _n_, vas deferens (muscular portion); _p_, vas deferens;
_q_, seminal vesicle; _r_ and _x_, vasa efferentia; _s_, lateral
excretory canal; _t_, testicular follicles. (After Benham and Sommer
and Landois.)]

The male sexual orifice almost always opens with that of the vagina
into a genital atrium, the raised border of which rises above the edge
of the segment and forms the genital papilla (fig. 191).

[Illustration: FIG. 193.--Diagram of genitalia of a Cestode. _g.p._,
genital pore; ♀ ♂, male and female ducts opening into genital sinus;
_c.s._, cirrus sac; _v.d._, coiled vas deferens (“outer seminal
vesicle”); _vag._, vagina; _sem. rec._, seminal receptacle; _sp. d._,
spermatic duct; _C.c._, fertilization canal; _vit. d._, vitelline duct;
_sh. g._, shell gland; _ut. c._, uterine canal; _ut._, uterus; _Ov._,
ovary; _p_, pumping organ. _Cf._ figs. 191 and 233. (Stephens.)]

The vagina, like the vas deferens, usually runs inwardly and
posteriorly, where it forms a spindle-shaped dilatation (receptaculum
seminis); its continuation, the spermatic duct, unites with the
oviduct, the common duct of the ovaries (fig. 191). The ovaries,
usually two in number, are compound tubular glands in the posterior
half of the proglottis, which extend into the medullary layer, but
ventral to the median plane.

At the origin of the oviduct there is frequently a dilatation provided
with circular muscles (suction apparatus), which receives the ovarian
cells and propels them forward. After the oviduct has received the
spermatic duct the canal proceeds as the fertilization canal, and after
a very short course receives the vitelline duct or ducts, and then the
numerous ducts of the shell glands (oötype). [Although the nomenclature
of these parts varies, we may consider the oviduct as extending from
the ovary to the shell gland and as receiving the spermatic duct and
then the vitelline duct and the ducts of the shell gland. The short
piece into which the shell gland ducts open corresponds to the oötype
in the flukes, but in the tapeworms this portion of the canal is seldom
dilated. From this point the oviduct is continued as a shorter or
longer tube, the uterine canal or true oviduct opening into the uterus
proper.--J. W. W. S.] The vitellarium may be single, but often exhibits
its primitive duplication more or less distinctly, in which case it is
situated at the posterior border of the segments in the medullary layer
(fig. 191). The original position of the double organ is, moreover, the
same as in the Trematodes, _i.e._, at the sides of the proglottids, and
thence eventually extending more or less on both surfaces (figs. 192
and 194); the gland is then distinctly grape-like and the follicles lie
mostly in the cortical layer.

[Illustration: FIG. 194.--Part of a transverse section through a
proglottis of _Dibothriocephalus latus_. _Ct._, cuticle; _C._,
cirrus; _Vvs._, vitelline follicles; _L.M._, longitudinal muscles;
_T._, testicles; _M._, medullary nerve; _S.c._, subcuticle; _T.m._,
transverse muscles; _Ut._, uterus. 20/1.]

The egg cell that has been fertilized and supplied with yolk cells
receives the shell material at the point of entry of the shell gland
ducts, and, as a complete egg, then moves onward to the uterus. In
those cases in which the uterus in its further course presents a
convoluted canal, and may form a rosette (pseudo-phyllidea), there is
an external opening which is usually separate from the genital pore,
and lies on the same or the opposite surface. In all other cases,
however, the uterus terminates blindly and is represented by a longer
or shorter sac lying in the longitudinal axis (fig. 191), but in many
forms transversely. With the accumulation of eggs it becomes modified
in various ways: (1) it sends out lateral branches (fig. 241), or
(2) forms numerous isolated sacs (PARENCHYMAL CAPSULES) containing
single eggs or groups of eggs (fig. 217); further, (3) in some cases
at the blind end one or more special thick-walled cavities are formed
(PARUTERINE ORGANS or UTERINE CAPSULES), in which all or most of the
eggs are collected, the uterus then undergoing atrophy.

In species in which the uterus lacks an opening, simultaneously with
the growth of this organ an atrophy of the male apparatus, at least
of the testes and their excretory ducts, takes place; this atrophy
also frequently occurs in the female glands, so that the entire mature
segments have besides the uterus only traces of the genitalia left.

In the _Acoleïnæ_ the vagina is more or less extensively atrophied, and
in any case has no external opening.

A number of genera are distinguished by the duplication of the
genitalia in every segment; the genital apparatus in its entirety, or
with the exception of the uterus, is double, or the genital glands and
the uterus are single, but the cirrus, vas deferens and vagina are

On comparing the genitalia of the Trematodes and Cestodes the parts
will be found to agree, but the vagina of the Cestodes corresponds
with the uterus of the Trematodes, and the uterus of the tapeworms to
Laurer’s canal of the Trematodes, which in most of the Cestodes has
lost its external orifice.


_Copulation._--As each proglottis possesses its own genital apparatus,
and male as well as female organs are present, the following processes
may occur: (1) self- or auto-fecundation (without immissio cirri); (2)
self- or auto-copulation (with immissio cirri); (3) cross-copulation
between proglottids of the same or different chains (of the same
species); and (4) cross-copulation in the same proglottis in species
with double genital pores. These various modes have actually been

In those species which lack the vagina (_Acoleïnæ_) it appears that
the cirri, which are always furnished with hooks, are driven into the
tissues and for the most part reach the receptaculum seminis.

The _eggs_ of all Cestodes are provided with shells, but the shells,
like their contents, vary. In genera that possess a uterine pore the
mature eggs frequently do not differ from those of the Distomata; they
have a brown or yellow shell of oval form provided with an operculum,
and contain a number of yolk cells in addition to the fertilized
ovarian cell (fig. 128), but in other genera (with a uterine pore) the
lid is absent and the egg-shell is very thin, the eggs of these genera
resembling those of Cestodes in which the secretion of the vitellarium
is a light albumin-like substance that contains only a few granules,
and in which the egg-shell is very delicate and without operculum.

The eggs of _Tæniidæ_, for example, at first consist of egg-shell
(oötype), ovum and yolk cells. The egg-shell is as a rule soft,
colourless and frequently deciduous, and the yolk is scanty in amount
and contains few granules. The eggs are, moreover, more complicated
than this. They enlarge and change their shape and various envelopes
are developed around the embryo. The egg-shell proper often disappears,
and one or more embryonal envelopes, or protoplasmic layers, arise,
so that eventually it is difficult to say whether the whole egg is
present, and, if not, what the layers that remain really are.

[Illustration: FIG. 195.--Egg of _Diplogonoporus grandis_, showing the
morula surrounded by yolk cells and granules. 440/1. (After Kurimoto.)]

[Illustration: FIG. 196.--Uterine egg of _Tænia saginata_, G. Uterine
shell with filaments; the oncosphere with embryonal shell (embryophore)
in the centre. 500/1. (After Leuckart.)]

The _embryonal development_ in most species takes place during the stay
of the eggs in the uterus; in other species it takes place after the
eggs have been deposited and are in water. Separate cells or a layer
of cells always separate from the segmentation cells, as well as from
the cells of the developing embryo, and form one or more envelopes
round the embryo; usually two such envelopes are formed, the inner
one of which stands in intimate relationship with the embryo itself
and is often erroneously termed the egg-shell, but more correctly the
embryonal shell or _embryophore_. In some species it carries long
cilia, as in _Dibothriocephalus latus_, by aid of which the young swim
about when released from the egg-shell; as a general rule, however,
there are no cilia and this envelope is homogeneous, or is composed
of numerous rods and is calcified, as in _Tænia_ spp. (fig. 197). The
second outer envelope (“yolk envelope”) (fig. 207, 3) lies close within
the true (oötype) egg-shell, and remains within it when the embryo
hatches out, and in many species, as in _Tænia_ spp., it perishes at
the end of the embryonal development with the delicate egg-shell which
was formed in the oötype, so that one observes not the entire egg with
egg-shell but only the embryo in its embryonal shell, _viz._, the
embryophore (fig. 197, _a._).

The embryo (the ONCOSPHERE) enclosed within the embryonal shell
(embryophore) is of spheroidal or ovoid form (fig. 197, _b._), and
is distinguished by the possession of three pairs of spines, a few
terminal (flame) cells of the excretory system, and muscles to move the

NO FURTHER DEVELOPMENT of the oncosphere takes place, either in the
parent organism or in the open; in fact, in all cases in which the
oncospheres are already formed within the proglottids they do not
become free, but remain in their shell; it is only when the oncospheres
are provided with a ciliated embryophore that they leave the egg-shell,
and they even cast this ciliated envelope after having swum about in
water by its means for a week or so. Sooner or later, however, all the
oncospheres leave the host that harbours the parental tapeworm and
reach the open, either still enclosed in the uterus of the evacuated
proglottids, after the disintegration of which they then become free,
or after being deposited as eggs in the intestine of the host; they
then leave it with the fæces. In the former case also, the slightest
injury to the mature proglottids while still in the intestine suffices
to allow a part of the oncospheres in their embryophores to be released
and mingled with the fæces. Here they are the generally, but falsely,
so-called Tæniæ “eggs.” For, as stated above, the “yolk” envelope and
the true shell deposited in the oötype have before this disintegrated.

[Illustration: FIG. 197.--_a._, oncosphere, in its radially striated
embryophore (erroneously termed egg-shell) of _Tænia africana_. Greatly
magnified. (After von Linstow.) _b._, freed oncosphere of _Dipylidium
caninum_. (After Grassi and Rovelli.) Both oncospheres show six spines.]

In other cases, _e.g._, _Hymenolepis_ spp., the uterine (oötype) shell
persists in fæces (fig. 230).

In any case the oncospheres must be transmitted into suitable animals
to effect their further development; in only very rare cases might
an active invasion be possible, as, for instance, takes place with
the miracidia of many Trematodes. The entry into an animal is, as a
rule, entirely passive, that is to say, the oncospheres are swallowed
with the food or water. Many animals are coprophagous and ingest the
oncospheres direct with the fæces; others swallow them with water,
mud, or food contaminated by such fæces. Infection is easily produced
artificially by feeding suitable animals with mature proglottids of
certain Cestodes or introducing the oncospheres with the food. As
the mature tapeworm frequently finds the conditions suitable for
its development in only one species of host, or in species nearly
related, and perishes when artificially introduced into other hosts,
experiment has taught us that to succeed in cultivating the oncospheres
certain species of animals are necessary. Thus we are aware that the
oncospheres of _Tænia solium_, which lives in the intestine of man,
develop only in the pig, and only quite exceptionally develop into the
stage characteristic of all Cestodes--the cysticercus in the wide sense
of the word--in a few other mammals. The oncospheres of _T. saginata_
develop further only in the ox; those of _T. marginata_ (of the dog) in
the pig, goat, and sheep; those of _T. serrata_ (of the dog) in hares
and rabbits; those of _Dipylidium caninum_ (of the dog and cat) in
parasitic insects of the dog and cat, etc. It is not unusual that young
animals only appear to be capable of infection, while older animals of
the same species are not so.

Once introduced into a suitable animal, which is only exceptionally
the same individual or belongs to the same species as the one which
harbours the adult tapeworm, the oncosphere passes into the larval
stage common to all Cestodes, but varying in structure according to the
species. In the simplest case--as, _e.g._, in _Dibothriocephalus_--such
a larva resembles the scolex of the corresponding tapeworm, only that
the head, provided with suckers, is retracted within the fore-part of
the neck. Such a larval form is known as a _plerocercoid_ (πλήερης,
full; κέρκος, tail). They differ from the cysticercoids in being solid
larval forms, elongated, tape-like or oval, with the head invaginated.
The conditions appear to be similar in _Ligula_, _Schistocephalus_,
_Triænophorus_, but here the larvæ are very large, indeed as large in
the first-mentioned genera as the tapeworms originating from them,
and the sexual organs are already outlined; doubtless, however, this
stage is preceded by one that corresponds to the scolex of the genus in
question, and which represents the actual larval stage. In such cases
the development of the body of the tapeworm from the scolex has already
begun within the first or intermediate host; in other cases, except in
the single-jointed (monozootic) Cestodes, this only takes place in the
definitive host. The direct metamorphosis of the oncosphere into the
larval forms termed PLEROCERCOID has hitherto not been investigated,
although _Ligula_, _Schistocephalus_ and _Bothriocephalus_ are very
common parasites, but many circumstances point to the conclusions
arrived at by us and by other observers. In the larval stages of other
tapeworms we can always distinguish the scolex and a caudal-like
appendage, vesicular in the cysticerci (fig. 200), compact in the
cysticercoids (fig. 231). The scolex alone forms the future tapeworm,
the variously formed appendage perishing.

It has now been proved that the appendage, the caudal vesicle,
originates direct from the body of the oncosphere, and therefore
is primary, and that the scolex only subsequently forms through
proliferation on the surface of this appendage. On account of this
origin the scolex is generally regarded as the daughter, and the part
usually designated as the appendage as the mother, originating from the

Accordingly, two modes of development of the larval stage may be
distinguished; in the one case, plerocerci and plerocercoids, the
oncosphere changes directly into the scolex, thus forming the body of
the tapeworm within the primary host; in the other case, cysticerci and
cysticercoids, the scolex only forms secondarily in the transformed
body of the oncosphere, which later on perishes, the scolex alone
remaining as the originator of the tapeworm colony.

We may summarize briefly what has been said regarding these larval
forms. We have, firstly, solid larval forms without any bladder. These
arise _directly_ from the oncosphere and are of two kinds, plerocercus
and plerocercoid. _Plerocercus_ is a solid _globular_ larva with the
head invaginated into the posterior portion. _Plerocercoid_ (fig. 208)
is a solid _elongated_ larva also with the head invaginated into
the posterior portion, which is sometimes very long. Secondly, we
have larval forms with bladders from which the scolices arise thus
_indirectly_ from the oncosphere. They are of two kinds, cysticercoid
and cysticercus.

_Cysticercoid._--The bladder is but slightly developed and is usually
absorbed again. The anterior portion is, moreover, retracted into
the posterior, and in some cases there is a long or a stumpy tail
(figs. 220, 231).

_Cysticercus_, or true bladder worms. (These may be divided into
(1) cysticercus proper, consisting of a bladder and one scolex; (2)
cœnurus, a bladder and many scolices; (3) echinococcus, a bladder in
which daughter bladders or cysts are developed, and then in these
multiple scolices.)

[Illustration: FIG. 198.--Diagram of a cysticercoid. _Cf._ figs. 220,
227. _c.v._, caudal vesicle or bladder (small); _sec. c._, secondary
cavity caused by the growth forward of the hind-body; _t._, tail
bearing six spines. (Stephens.)]

[Illustration: FIG. 199.--Diagram of a cysticercus. _c.v._, caudal
vesicle or bladder; _i._, invagination of wall of bladder. (Stephens.)]

In the case of cysticerci a papilliform invagination forms, projecting
into the interior of the bladder (fig. 201). The layer of cells forming
the papilla becomes divided into two laminæ, the outer[279] of which
forms a kind of investing membrane (receptaculum capitis) for the
papilla. The head and suckers are now developed on the walls bounding
the axial lumen of the papilla. The papilla eventually evaginates, so
that the receptaculum capitis now forms the inner surface of the hollow
head, which eventually becomes solid.

[279] _I.e._, regarded from the interior or centre of the invagination.

Our knowledge of the development of cysticerci in the wide sense of
the word is limited almost exclusively to that of a few true “bladder
worms” (cysticerci); in other cases we know either only the terminal
stage, _i.e._, the complete larva, or, exceptionally, one of the
intermediate stages, but we are not acquainted with a complete series;
the description must therefore be incomplete.

We know from feeding experiments that, after the introduction of mature
proglottids or of the fully developed ova of _Tænia crassicollis_ (of
the cat) into the stomach of mice, the oncospheres escape from the
shell in the middle portion of the small intestine, and a few hours
later penetrate into the intestinal wall by means of a boring movement;
they have been found in this position twenty-seven to thirty hours
after the infection. By means of this migration, for which purpose they
employ their spines, they attain the blood-vessels of the intestine;
indeed, already nine hours after the infection and later they are found
in the blood of the portal vein, and in the course of the second day
after infection they are found in the capillaries of the liver, which
these larvæ do not leave.

Leuckart, in experimental feeding of rabbits with oncospheres of
_Tænia serrata_ (of the dog), found free oncospheres in the stomach of
the experimental animal, but not in the intestine: however, he came
across them again in the blood of the portal vein. The passage through
the blood-vessels to the liver is the normal one for those species
of _Tænia_ the eggs of which become larvae in mammals; even in those
cases in which the oncospheres develop further in the omentum or in
the abdominal cavity (_Cysticercus tenuicollis_, _C. pisiformis_),
there are distinct changes observable in the liver that lead one to the
conclusion that there has been a secondary migration out of the liver
into the abdominal cavity. Indeed, one must not imagine that the young
stages of the Cestodes are absolutely passive; once they have invaded
an organ they travel actively, and leave distinct traces of their

In other cases the oncospheres leave the liver with the circulation,
and are thus distributed further in the body; they may settle and
develop in one or more organs or tissues. Many oncospheres may, by
travelling through the intestinal wall, penetrate through it and
attain the abdominal cavity direct; some, perhaps, pass also into the
lymph stream. Where there are no blood and lymphatic vessels in the
intestinal wall, as in insects, the oncospheres attain the body cavity
or its organs direct; in short, they never remain in the intestinal
lumen itself, and only rarely--as in _Hymenolepis murina_ of the
rat--do they remain in the intestinal wall.

  When the infection has been intense, and the body is crowded with
  numerous oncospheres, acute feverish symptoms, are induced, to which
  the infected animals usually succumb (“acute cestode tuberculosis”);
  while in other cases the alterations in the organs attacked--as the
  liver in mice and the brain in sheep--may cause death.

Sooner or later the oncospheres of tapeworms come to rest, and are
first transformed into a bladder, which may be round or oval according
to the species. The embryonal spines disappear sooner or later, or
remain close together or spread over some part of the bladder wall
(fig. 200). Their discovery by V. Stein in the bladder worm of the
“meal worm” (the larva of a beetle, _Tenebrio molitor_) first led to
the conclusion that bladder worms (cysticerci) actually originate from
the oncospheres of _Tæniidæ_.

[Illustration: FIG. 200.--Diagram of development of a cysticercus. 1,
solid oncosphere with six spines; 2, bladder formed by liquefaction of
contents; 3, invagination of bladder wall; 4, formation of rostellum
(with hooklets) and suckers at the bottom of the invagination; 5,
evagination of head; 6, complete evagination effected by pressure.

The bladder may remain as a bladder, and then by proliferation the
scolex forms on its wall (fig. 202), or it may divide into an anterior
so-called “cystic” portion and a solid tail-like appendage of various
lengths, on which the embryonal hooks are to be found, and this is
particularly the case in those larval forms (cysticercoids), _e.g._,
those of _Dipylidium caninum_, that develop in invertebrate animals,
such as Arthropoda.

As mentioned above one may regard the scolex as an individual that
originates through proliferation of the wall of the parent cyst, mostly
singly, but in those cysticerci that are termed cœnurus (fig. 201)
many scolices occur, whereas in those called echinococcus the parent
cyst originating from the oncosphere of _Tænia echinococcus_ (of the
dog) first produces a number of daughter cysts, which in their turn
form numerous scolices. Echinococcus-like conditions also occur in
cysticercoids, as, for instance, in those peculiar to earthworms; and
similar conditions prevail in a larval form known as _Staphylocystis_,
found in the wood-louse (_Glomeris_). Thus it happens in these cases
that finally _one_ tapeworm egg produces not _one_, but numerous
tapeworms, for, under favourable conditions, each scolex can form a

[Illustration: FIG. 201.--Section through a piece of a _Cœnurus
cerebralis_, with four cephalic invaginations in different stages of
development. At the bottom of the invaginations the rostellum, hooks
and suckers develop. (From a wax model.)]

[Illustration: FIG. 202.--Median section through a cysticercus, with
developed scolex at the bottom of the invagination. (After Leuckart.)]

  The rudiment of the scolex appears as a hollow bud, the cephalic
  invagination usually directed towards the interior of the bladder
  cavity; on its invaginated surface arise the four suckers, and the
  rostellum with the hook apparatus is formed in its blind end; we
  thus get a Tænia head, but with the position of the parts reversed
  (fig. 201). In many cysticerci the head rises up from the base of the
  cephalic invagination and is then surrounded by the latter. A more
  or less elongated piece of neck also develops, and even proglottids
  may appear, as in _Cysticercus fasciolaris_ (the larva of _Tænia
  crassicollis_ of the cat) of the Muridæ, a process somewhat analogous
  to that of Ligula, etc.

The period that elapses from the time of infection till the cysticercus
is fully developed varies according to the species; the cysticercus of
_Tænia saginata_ requires twenty-eight weeks, that of _T. marginata_
seven to eight weeks, that of _T. solium_ three to four months, and
that of _T. echinococcus_ longer still.

[Illustration: FIG. 203.--_Cysticercus pisiformis_ in an evaginated
condition, with neck, fore-body and bladder, with excretory network in
its wall. 18/1.]

With one single exception (_Archigetes_) the larvæ do not become
sexually mature in the organ where they have developed; they must
enter the terminal host, a matter that is usually purely passive, the
carriers of the larvæ or infected parts of them being usually devoured
by other animals. In this manner, for instance, the larvæ (_Cysticercus
fasciolaris_) found in mice and rats reach the intestine of cats;
those of the hare and rabbit (_C. pisiformis_) reach the intestine
of dogs; those of the pig (_C. cellulosæ_) are introduced into man;
those of insects are swallowed by insectivorous birds; those of
crustaceans are ingested by ducks and other water fowl; perhaps, also,
the infection of herbivorous mammals is caused by their accidentally
swallowing smaller creatures infected by larvæ. Indeed, the researches
of Grassi and Rovelli have taught us that such an intermediate host
is not always necessary; _Hymenolepis murina_ of rats and mice in its
larval stage lives in the intestinal wall of these rodents, and as a
larva it passes into the intestinal lumen and develops into a tapeworm
in exactly the same way as the larvæ of other species that reach the
intestine of the terminal host by means of an intermediate carrier.
Probably this curtailed manner of transmission also occurs in many
other species. In some cases the larvæ actively quit the body of the
intermediate host, as in the case of _Ligula_ and _Schistocephalus_,
which travel out of the body cavity of infected fish and reach the
water, where they may be observed in hundreds in summer, at all events
in some localities. The larval stage of _Calliobothrium_--wrongly
termed _Scolex_--has been observed swimming free in the sea, and
the scolices of _Rhynchobothrium_, without their mother cysts, have
been observed free within the tissues of several marine animals.
In any case there is almost always a change of hosts, even in the
single-jointed Cestodes, for the larva of _Caryophyllæus_, which lives
in fishes of the carp family, is found in limicoline Oligochætes,
that of _Gyrocotyle_ (Chimæra) in shell-fish (Mactra), and different
conditions can hardly be possible for _Amphilina_. _Archigetes_ alone
becomes sexually mature in the larval stage, but the life-history of
this creature is not well known, so that it is not impossible that the
attainment of sexual maturity as a larva in invertebrates (Oligochætes)
is perhaps abnormal, and somewhat analogous to the maturity of some
encysted Trematodes.

The METAMORPHOSIS OF THE LARVA into the tapeworm is rarely accomplished
in a simple manner; the transformation, however, is not complex in
the single-jointed Cestodes, nor in _Ligula_ and _Schistocephalus_;
the latter is swallowed by birds (_Mergus_, _Anas_, etc.), produces
eggs after only a few days, and very soon quits the intestine of
its terminal host. In all other cases it is the scolex only which,
by proliferating at its posterior extremity, forms the proglottids,
after having invaded as a larva the intestine of a suitable host.
The mother cysts, or what corresponds to them, die, are digested,
absorbed, or perhaps even eliminated; on the contrary, segments found
on the scolex during the larval stage, also in the case of _Cysticercus
fasciolaris_, are retained. It is not certain whether the larvæ of
_Dibothriocephalus_ lose any part.

The time required by the scolex to complete the entire chain of
proglottids does not depend only on the number it has to produce,
for _Tænia echinococcus_, which, as a rule, only possesses three or
four segments, takes quite as long a time for their growth (eleven to
twelve weeks) as _T. solium_ with its numerous segments; _T. cœnurus_
is fully developed in three to four weeks, and the same holds good for
_Dibothriocephalus latus_, which possesses many more segments than the
above-mentioned Tænia of the dog. In a number of species it has been
possible to determine fairly accurately the average daily growth; for
instance, in _Dibothriocephalus latus_ the daily growth is 8 cm., in
_Tænia saginata_ 7 cm., etc.

The history of the development of the Cestodes demonstrates that
persons and beasts harbouring larval tapeworms have become infected by
having swallowed the oncospheres of the species of tapeworm to which
they belong. In regard to _Hymenolepis murina_ alone, it is known that
the introduction of the oncospheres into those species of animals which
harbour the adult tapeworm leads to the formation of the latter after
the development of a larval stage in the intestinal wall; nevertheless,
only young animals (rats) are capable of infection, for a previous
infection, or the presence of mature tapeworms in the intestine,
appears to produce a kind of immunity.


In their adult stage, the tapeworms inhabit almost exclusively the
alimentary canal of vertebrate animals, with but few exceptions the
small intestine, and a few species select definite parts of it. A small
number of _Rhynchobothriidæ_ of marine fishes live apparently always
in the stomach, while in rays and sharks the spiral intestine is their
exclusive site. Bothriocephali generally attach themselves with their
head on to the appendices of the pylorus of fishes; other species
(_Hymenolepis diminuta_) occasionally fix their head in the ductus
choledochus, and this is more frequent still in the tapeworms of the
rock badger (_Hyrax_), which occasionally penetrate entirely into the
biliary ducts. _Stilesia hepatica_, Wolffh., has so far only been found
in the bile-ducts of its host (sheep and goat, East Africa).

In the disease of sheep induced by Cestodes, the worms have been
observed also in the pancreas. Specimens found in the large intestines
were probably being evacuated.

The Cestodes are looked upon as fairly inert creatures, this opinion
having been formed by observing their condition in the cold cadavers of
warm-blooded animals. Actually, however, they are exceedingly active,
and accomplish local movements within the intestine, for they have been
found in the ducts communicating with the bowel, or in the stomach,
and may even make their way forward into the œsophagus.

They also invade other abdominal organs through abnormal
communications, or through any that may be temporarily open between the
intestine and such organs; they thus reach the abdominal cavity or the
urinary bladder, or they work their way through the peritoneum.

They produce changes in the intestinal mucous membrane at the place of
their attachment, the alterations varying in intensity according to the
structure of the fixation organs. The mucous membrane is elevated in
knob-like areas by the suckers; the epithelial cells become atrophied
or may be entirely obliterated. _Dipylidium caninum_ bores into the
openings of Lieberkühn’s glands with its rostellum, dilating the
lumen to two or three times its normal size, while the suckers remain
fixed between the basal parts of the cells. Species with powerful
armatures penetrate deeper into the submucosa, and some that are not
provided with exceptionally strong armatures, or are even unarmed,
may be actually found with the scolex embedded in the muscles of the
intestinal walls or even protruding beyond (_Tænia tetragona_, Mol., in
fowls, etc.). Other species, again, even cause perforation of the walls
of the intestine of their hosts.

It is generally assumed that tapeworms, which almost without exception
live in the gut of vertebrates, get their nutriment from the gut
contents, which apparently they absorb through the whole body surface
(cuticular trophopores). In favour of this view is the existence
of fat drops in the proglottids, the identity in colour in certain
forms between that of the fresh worm and the gut contents and the
passage of certain substances derived from medicines (iron and mercury
preparation) into the worms in the gut, etc. Whether the suckers are
concerned in the absorption of nutriment and to what extent is still

THE LENGTH OF LIFE OF THE ADULT TAPEWORM certainly varies; as a rule
it appears to last only about a year; in other cases (_Ligula_) it
averages only a few days, but we are likewise aware that certain
species of Cestodes of man attain an age of several or many years
(thirty-five). The natural death of Cestodes often appears to be
brought about by alterations in the scolex, such as loss of the hooks,
atrophy of the suckers and rostellum, finally the dropping off of the
scolex; it is unknown whether a chain of segments deprived of its
scolex then perishes or whether it first attains maturity. It has
already been mentioned that in a few species the foremost proglottids
are transformed into organs of fixation on the normal loss of the

  Abnormalities and malformations are encountered relatively frequently
  in the Cestodes--such as abnormally short or long segments;
  the so-called triangular tapeworms, which--if belonging to the
  _Tæniidæ_--always possess six suckers; often also club-shaped
  segments occur between normal ones, or there may be a defect in
  one segment or in the centre of a number following one another
  (fenestrated segments); bifurcated chains of segments have likewise
  been observed, as well as incomplete or complete union of the
  proglottids, abnormal increase of the genital pores, reversion of
  the genitalia. Besides the above-mentioned increase of the number
  of suckers on the scolex (in Tæniæ), there may be a decrease in
  the number; in other cases the crown of hooks may be absent, or
  abnormally shaped hooks may be formed.


Order. *Pseudophyllidea*, Carus, 1863.

  Scolex without proboscis or rostellum. Head “stalk” absent.

  Scolex never with four, generally with two (or one terminal)
  bothria.[280] Vitellaria numerous. Uterine opening present. Genitalia
  do not atrophy when uterus is developed. In large majority of
  proglottids eggs (or, if formed, their contents) are at the same
  stage of development.

[280] _Bothridia_ or “_phyllidia_” are _outgrowths_ from the scolex.
They are concave and extremely mobile. By some authors the term
“_phyllidium_” is used for the outgrowth, and the term “_bothridium_”
is restricted to the muscular cup. _Bothria_, on the other hand, are
grooves more or less wide, the musculature of which is only slightly
developed and is not separated off internally from the parenchyma.
_Acetabula_, or suckers in the usual sense, are hemispherical cups,
without lips and with musculature separated internally from the

Family. *Dibothriocephalidæ*, Lühe, 1902.

  Syn.: _Diphyllobothriidæ_, Lühe, 1910.

  Genitalia repeated in each proglottid (polyzootic Cestodes). Ventral
  and dorsal surfaces flat. Cirrus unarmed. Cirrus and vagina if
  non-marginal open on the same surface as the uterus. Uterus long,
  convoluted, often forming a “rosette,” never dilates into a uterine
  cavity. Eggs thick shelled, operculated, constantly being formed in
  mature proglottids.

Sub-family. *Dibothriocephalinæ*, Lühe, 1899.

  Syn.: _Diphyllobothriinæ_, Lühe, 1910.

  Segmentation distinct. Scolex unarmed, elongated, sharply separated
  (generally by a neck) from the first proglottis. Cirrus and vagina
  open ventrally. Genital pores non-alternating. Vas deferens
  surrounded by a muscular bulb. Receptaculum seminis large, sharply
  separated from the spermatic duct.

Order. *Cyclophyllidea*, v. Beneden.

  Four suckers always present. Uterine opening absent. Vitellarium
  single. Genitalia atrophy when uterus is fully developed.

Family. *Dipylidiidæ*, Lühe, 1910.

  Rostellum if present armed. Suckers unarmed. Uterus breaks up into
  egg capsules. Paruterine organs absent.

Family. *Hymenolepididæ*, Railliet and Henry, 1909.

  Segment always broader than long. Genitalia single. Longitudinal
  muscles in two layers. Genital pores unilateral. Testes one to four.
  Uterus persistent, sac-like. Eggs with three shells.

Family. *Davaineidæ*, Fuhrmann, 1907.

  Rostellum cushion-shaped. Armed with numerous (sixty to several
  thousand) hammer-shaped hooks in two (rarely one) rows.

Sub-family. *Davaineinæ*, Braun, 1900.

  Suckers armed. Uterus breaks up into egg capsules. Paruterine organs

Family. _Tæniidæ_, Ludwig, 1886.

  Suckers unarmed. Uterus with median longitudinal stem and lateral
  branches. Female genitalia at the hind end of the proglottis. Genital
  pore irregularly alternating. Testes numerous in front of female
  genitalia. Ovary with two lobes (wings). Vitellarium behind the
  ovary. Embryophore radially striated.


Most of the species to be mentioned live in man in their adult stage
and occupy the small intestine; man is the definite host of these
parasites, but is not the specific host for all the species; some of
these species, as well as others (of mammals), may occur in man also in
the larval stage.

Family. *Dibothriocephalidæ.*

Sub-family. *Dibothriocephalinæ.*

Genus. *Dibothriocephalus*, Lühe, 1899.

  Syn.: _Diphyllobothrium_, Cobbold, 1858; _Bothriocephalus_, p. p.
  Rud., 1819; _Dibothrius_, p. p. Rud., 1819; _Dibothrium_, p. p.
  Dies., 1850.

  Scolex egg-shaped; dorsal and ventral bothria elongated, moderately
  strong, cutting rather deeply into the head; genitalia single in
  each proglottis; papillæ in the vicinity of the genital atrium; the
  testes and vitellaria are in the lateral fields, the former in the
  medullary layer, the latter in the cortical layer on both surfaces,
  and occasionally extending to the median line; the ovary ventral,
  the shell gland dorsal. The uterus is in the central field, taking a
  zigzag course, and frequently forms a rosette.

*Dibothriocephalus latus*, L., 1748.

  Syn.: _Tænia lata_, L., 1748; _Tænia vulgaris_, L., 1748;
  _Tænia grisea_, Pallas, 1796; _Tænia membranacea_, Pall., 1781;
  _Tænia tenella_, Pall., 1781; _Tænia dentata_, Batsch, 1786;
  _Bothriocephalus latus_, Bremser, 1819; _Dibothrium latum_,
  Dies., 1850; _Bothriocephalus cristatus_, Davaine, 1874[281];
  _Bothriocephalus balticus_, Kchnmstr., 1855; _Bothriocephalus
  latissimus_, Bugn., 1886.

[281] Until recently this worm, which was understood to belong
to a separate species, was proved on examination by R. Blanchard
(“Mai. Par.,” 1896), to be _Dibothriocephalus latus_. Compare also
Galli-Valerio, in _Centralbl. f. Bakt., Path. und Infektionskr._, 1900
(1), xxvii, p. 308.

Length 2 to 9 m. or more; colour yellowish-grey; after lying in water
the lateral areas become brownish and the uterine rosette brown. The
head is almond-shaped, 2 to 3 mm. in length, the dorso-ventral axis is
longer than the transverse diameter; the head, therefore, generally
lying flat, conceals the suctorial grooves at the borders; these
suckers are deep and have sharp edges (fig. 205). The neck varies in
length according to the degree of contraction and is very thin; there
are 3,000 to 4,200 proglottids and there may be more; their breadth is
usually greater than their length, but in the posterior third of the
body they are almost square, and the very oldest are not uncommonly
longer than they are broad. There are numerous testes situated dorsally
in the medullary layer of the lateral fields; the vas deferens
(fig. 192) passes dorsally in transverse loops in the central field
anteriorly and forms a seminal vesicle before its entry into the large
cirrus pouch.

The orifice of the vagina is close behind the orifice of the cirrus;
the former passes almost straight along the median line posteriorly,
and widens into a receptaculum seminis shortly before its junction
with the oviduct; the ovary is bilobed, in shape like the wings of
a butterfly, ventrally in the medullary layer; the shell glands lie
in the posterior recess of the ovary; the uterus, forming numerous
transverse convolutions, passes ventral to the vas deferens forwards.
Eggs (fig. 207) large, with brownish shells and small lids, 68 µ to
71 µ by 45 µ; the ovarian cell, which is already, as a rule, in process
of segmentation, is surrounded by numerous large yolk cells; the
proglottids nearest the posterior extremity are frequently eggless.

[Illustration: FIG. 204.--Various chains of segments of
_Dibothriocephalus latus_, showing the central uterine rosette.
(Natural size.)]

[Illustration: FIG. 205.--Transverse section of the head of
_Dibothriocephalus latus_. 30/1.]

[Illustration: FIG. 206.--Fairly mature proglottis of
_Dibothriocephalus latus_. The vitellaria are at the sides; the uterus,
filled with eggs, is in the middle, also the vagina (the dark stripe
passing almost straight from the front to the back), and the vas
deferens (almost hidden by the uterus). Above in the centre is the
cirrus sac, and below the shell gland and ovary are seen. 15/1. (From a
stained preparation.)]

The eggs, which are deposited in the intestine and evacuated with
the fæces, hatch in water after a fortnight or more; the embryonal
integument (embryophore) of the oncosphere is provided with cilia;
after bursting open the lid of the egg the oncosphere in its
embryophore (fig. 207) reaches the water and swims slowly about; often
it slips out of its ciliated embryophore, sinks to the bottom and is
capable of a creeping motion; sooner or later it dies in the water.
The manner and means of its invasion of an intermediate host are
still unknown; yet we are aware that the larval stage (plerocercoid,
fig. 208), which resembles the scolex and may reach a length of 30 mm.,
lives in the intestine, in the intestinal wall, in the liver, spleen,
genital glands and muscular system (fig. 209) of various fresh-water
fish, the pike (_Esox lucius_), the miller’s thumb (_Lota vulgaris_),
the perch (_Perea fluviatilis_), _Salmo umbla_, _Trutta vulgaris_, _Tr.
lacustris_, _Thymallis vulgaris_ (grayling), _Coregonus lavaretus_,
_C. albula_ (in Europe) and _Onchorhynchus perryi_ (in Japan). The
transmission of the plerocercoids from these fish to the dog, cat and
man (Braun, Parona, Grassi and Ferrara, Grassi and Rovelli, Ijima,
Zschokke, Schroeder) leads to the development of the broad tapeworm,
the growth of which is rapid. In my experiments on human beings the
average number of proglottids formed per diem averaged thirty-one to
thirty-two for five weeks, with a length of 8 to 9 cm. According to
Parona the eggs appear twenty-four days after man has been infected.
Zschokke found the average growth in the experimental infection of man
between 5·2 and 8·2 cm. per diem, and the person experimented upon by
Ijima evacuated a piece of a _Dibothriocephalus latus_, 22·5 cm. in
length, only twenty-one days after the infection.

[Illustration: FIG. 207.--_Dibothriocephalus latus_: development of
egg. 1, segmentation complete; some cells of the blastosphere have
migrated through the yolk and have flattened to form _c_, the yolk
envelope; others form a layer of flattened cells (_e_) forming the
embryophore; the remaining cells (_d_) of the blastosphere form the
hexacanth embryo. 2, embryophore (_e_) is becoming thicker. 3, the
ciliated embryo has been pressed out of the shell; _s′_, the operculum;
_c_, the yolk envelope remaining in the shell (_s_); _y_, the yolk
consisting of separate cells. 4, a free-swimming larva much swollen by
the water. (After Benham and Schauinsland.)]

The “broad tapeworm” is a frequent parasite of man in some districts,
but it also occurs in the domestic dog, and on rare occasions is found
in the domestic cat (together with _Dibothriocephalus felis_, Crepl.)
and fox. French Switzerland and the Baltic Provinces of Russia are the
centres of distribution; from the former districts the distribution
radiates to France and Italy (Lombardy, Piedmont); from the Baltic
Provinces over Ingermanland to Petrograd, over Finland to Sweden (on
the shore of the Gulf of Bothnia), in a southerly direction to Poland,
and into the Russian Empire and across it to Roumania, and towards
the west along the coast of the Baltic Sea to the North Sea, where,
however, its frequency considerably diminishes (Holland, Belgium, and
the North of France).

In Turkestan and Japan the “broad tapeworm” is the most frequent
parasite of man; it has been reported in Africa from the vicinity
of Lake N’gami as well as from Madagascar; cases, in part at least
imported, have also come under observation in North America.

[Illustration: FIG. 208.--Plerocercoid of _Dibothricephalus latus_.
_A._, with the head evaginated; _B._, with the head invaginated. From
the muscle of the pike.]

[Illustration: FIG. 209.--A piece of the body wall of the Burbot, _Lota
vulgaris_. The tangential section has exposed the muscles of the trunk,
with a plerocercoid of _Dibothriocephalus latus_. Natural size.]

In Germany _Dibothriocephalus latus_--apart from the fact that it
is undoubtedly imported from Switzerland, Russia or Italy--is
particularly frequent in East Prussia amongst the inhabitants of the
Courland Lagoon district, on the Baltic; it is, moreover, also found in
the Province and even in the City of Königsberg. In West Prussia and
Pomerania it is very much scarcer.

It is also found in Munich and in the vicinity of the Lake of Starnberg

Krabbe found it in 10 per cent. of the sufferers from tapeworms in
Denmark; Szydlowski found the ova of this worm in Dorpat in 10 per
cent. of the fæces examined; Kruse found the worm in 6 per cent. of
_post-mortems_; Kessler, in Petrograd, found the eggs in the fæces in
7·8 per cent.; at _post-mortems_ he found the worms in 1·17 per cent.,
though Winogradoff only found it in 0·8 per cent. In Moscow, according
to Baranovsky, 8·9 per cent. of the fæces examined contained the ova of
_Dibothriocephalus_. In the interior and southern provinces of Sweden
the worm, according to Lönnberg, is only found sporadically, but, on
the other hand, in Angermanland about 10 per cent. of the population
is affected; while again in Norbotten the majority of persons are
affected, and in Haparanda the entire population (with the exception
of infants) harbour this parasite. In Switzerland _D. latus_ is very
frequent in close proximity to the lakes of Bieler, Neuchatel, Morat
and Geneva (according to Zaeslin 10 to 15 to 20 per cent. of the
population are affected); the parasite is less frequent in districts
one to four hours removed from these lakes.

Of the fish from Swiss lakes examined by Schor those from Lake Geneva
were most commonly infected, and especially _Lota_ sp. and _Perea_ sp.

The frequency and distribution have, nevertheless, decreased
perceptibly in places; at the commencement of the eighteenth century
the broad tapeworm was very common in Paris, at the present date it
only occurs when imported (Blanchard); in Geneva, also, according to
Zschokke, it has become rarer (formerly 10 per cent., now only 1 per

The disturbances produced in man by the presence of broad tapeworms
are, as a rule, very trifling; in other cases they produce partly
gastric disorders and partly nervous symptoms; in a number of cases,
again, they set up severe anæmia, apparently caused by toxins
produced by the worms and absorbed by the host. There is no danger
of auto-infection, as the larval stage lives only in fishes, not in
warm-blooded animals. The case reported by Meschede (ova like those of
_Dibothriocephalus latus_ in the brain of a man who had suffered from
epilepsy for six years) must be otherwise explained.

Human beings, like other hosts, can only acquire the broad tapeworm by
ingesting its plerocercoids with the previously mentioned fresh-water
fishes; the opportunity for such infection is afforded the more readily
by the fact that not only do the lower classes not pay sufficient
attention to the cooking of fish, so that all the larvæ that are
present may be killed, but also in certain localities the custom exists
of eating some parts of these fishes in a raw condition; even the
mere handling of the usually severely infected intermediary hosts may
occasionally cause infection. The plerocercoids are as well known as,
but differ materially in appearance from, the cysticerci (_Cysticercus
cellulosæ_) of pig’s flesh. In Germany the occurrence of the
plerocercoids of _Dibothriocephalus latus_ has been confirmed in the
pike, miller’s thumb and perch of East Prussia, and more particularly
in those taken from the Courland Lagoon.

The life of _D. latus_ is a very long one (six to fourteen years), as
is deduced from persons who have left _D. latus_ regions after they
have been infected.

According to the experiments of M. Schor, plerocercoids of _D. latus_
placed in slowly warmed water completely lose their movement at 54° to
55° C.; they survive the death of their host for several days; they
are killed by low temperatures -3° to +1° C. in two days; strong acids
and salt solutions kill them at once, also high temperatures, but all
the same at least ten minutes is required in boiling or frying fish in
order to kill the plerocercoids with certainty.

*Dibothriocephalus cordatus*, R. Lkt., 1863.

  Syn.: _Bothriocephalus cordatus_, R. Lkt.

[Illustration: FIG. 210.--Cephalic end of _Dibothriocephalus
cordatus_; on the left viewed sideways, on the right from the dorsal
surface, showing a suctorial groove. (After Leuckart.)]

Length, 80 to 115 cm.; the head is heart-shaped and measures 2 by 2 mm.
The suctorial grooves are on the flat surface; the segments commence
close behind the head and increase rapidly in breadth. At only 3 cm.
behind the head they are already mature; the greatest breadth attained
by them averages 7 to 8 mm., the length 3 to 4 mm.; the number of
proglottids averages 600; the most posterior ones are usually square.
The uterine rosette is generally formed of six to eight lateral loops.
The eggs are operculated and measure 75 µ by 50 µ.

_Dibothriocephalus cordatus_ is a common parasite of the seal, the
walrus and the dog in Greenland and Iceland, occasionally of man also.
No doubt its larva lives in fishes.

  The statement that _D. cordatus_ also occurs in Dorpat in human
  beings has been proved erroneous (_Zool. Anzeiger_, 1882, v,
  p. 46), as also has the report that this worm lives in hares in the
  neighbourhood of Berlin, whither it was supposed to have been carried
  by Esquimaux dogs (Rosenkranz in _Deutsch. med. Wochenschr._, 1877,
  iii, p. 620). The parasite stated by the author to be _D. cordatus_
  is _Tænia pectinata_, Goeze, which has been known since 1766.

*Dibothriocephalus parvus*, Stephens, 1908.

Largest gravid segments 5 by 3 mm. Uterus forms a central rosette
with four to five loops on each side of median line. In a proglottid
measuring 3·5 by 2·25 mm. the genital atrium is situated 0·4 to
0·5 mm. behind the anterior margin and the uterine opening the same
distance behind the genital atrium. Calcareous corpuscles absent in the
preserved specimens. Eggs operculated, 59·2 µ by 40·7 µ.

Distinguished from _Dibothriocephalus latus_--(1) by the size of gravid
segments (the minimum width of gravid segments of _D. latus_ is 10
to 12 mm., so that _D. parvus_ is a much smaller worm); (2) quadrate
segments of _D. latus_ measure 6 by 6 mm., those of _D. parvus_ 4 by
4 mm.; (3) by the eggs.

From _D. cordatus_ it is distinguished by--(1) _D. cordatus_ has only
fifty immature segments, _D. parvus_ has at least 200, possibly more;
(2) mature segments of _D. cordatus_ measure 7 to 8 mm., maximum width
of _D. parvus_ is 5 mm.; (3) quadrate segments of _D. cordatus_ measure
5 to 6 mm.; (4) _D. cordatus_ has six to eight uterine loops; (5) _D.
cordatus_ measures 75 µ to 80 µ by 50 µ.

_Habitat._--Intestine of man (Syrian, in Tasmania).

Genus. *Diplogonoporus*, Lönnbrg., 1892.

  Syn.: _Krabbea_, R. Blanch., 1894.

The scolex is short and has powerful suctorial grooves; no neck; the
proglottids are short and broad; there are two sets of genital organs
side by side in each segment, which in all essentials resemble the
single one of _Dibothriocephalus_.

Parasitic in whales and seals, occasionally in man.

*Diplogonoporus grandis*, R. Blanch., 1894.

  Syn.: _Bothriocephalus_ sp., Ijima et Kurimoto, 1894; _Krabbea
  grandis_, R. Blanch.

Scolex unknown; chain of proglottids over 10 m. in length, 1·5 mm.
broad anteriorly, 25 mm. broad posteriorly. The proglottids are very
short (0·45 mm.), but 14 to 16 mm. broad. On either side to the right
and left of the worm, along the entire ventral surface, there is a
longitudinal groove; these grooves are nearer to each other than to
the lateral margin; in them lie the genital pores, and they are in the
same sequence as in _Dibothriocephalus_; corresponding to the scanty
length (0·45 mm.) of the proglottids, the ovary is only developed
transversely; the uterus only makes a few loops. Eggs (fig. 195) thick
shelled, brown, 63 µ by 48 µ to 50 µ. This parasite has hitherto been
observed twice in Japanese. Similar species are known in Cetacea and

[Illustration: FIG. 211.--_Diplogonoporus grandis_, Lühe, 1899: ventral
view of a portion of the strobila, showing two rows of genital pores
and partially extruded cirri. (After Ijima and Kurimoto.)]

[Illustration: FIG. 212.--_Diplogonoporus grandis_: ventral view
(diagrammatic) of genitalia of left side; _cir_, cirrus; _cir.o_,
cirrus opening; _dtg._, vitelline duct; _ov._, ovary; _ovd._, oviduct;
_sb._, receptaculum seminis; _ut._, uterus; _ut.o._, uterine pore;
_vag._, vagina; _vag.o._, vaginal pore; _vd_, vas deferens. × 150.
(After Ijima and Kurimoto.)]

*Sparganum*, Diesing, 1854.

The term _Sparganum_, invented by Diesing, is used as a group name of
larval bothriocephalid Cestodes whose development is not sufficiently
advanced to enable them to be assigned to any particular genus.

*Sparganum mansoni*, Cobb., 1883.

  Syn.: _Ligula mansoni_, Cobbold, 1883; _Bothriocephalus linguloides_,
  R. Lkt., 1886; _Bothriocephalus mansoni_, R. Blanch., 1886.

These plerocercoids were discovered in 1882 by P. Manson during
the _post-mortem_ on a Chinaman who had died in Amoy, twelve
specimens being found beneath the peritoneum and one free in the
abdominal cavity. Cobbold described them as _Ligula mansoni_, and
Leuckart, who contemporaneously reported a case in Japan, termed them
_Bothriocephalus liguloides_. Ijima and Murata reported eight further
cases, and Miyake records nine further cases, seven of which are
recorded in Japanese literature.

[Illustration: FIG. 213.--Cephalic end of _Sparganum mansoni_, Cobb.
(After Leuckart.)]

[Illustration: FIG. 214.--_Sparganum mansoni_: on the right in
transverse section. Natural size. (After Ijima and Murata.)]

The plerocercoid, which hitherto alone is known to us, attains a length
of 30 cm. and a breadth of 3 to 6 to 12 mm. The ribbon-shaped body is
wrinkled, the lateral borders are often somewhat thickened, so that
the transverse section has the form of a biscuit; the anterior end
is usually wider and has the head provided with two weak suctorial
grooves, either retracted or protracted.

The parasite makes migrations within the body, and thus may reach the
urinary passages; then it is either evacuated with the urine or has
to be removed from the urethra; not rarely it causes non-inflammatory
tumours on various parts of the skin, which are at times painful and at
times vary in size.

Nothing is known of its development and origin.

*Sparganum proliferum*, Ijima, 1905.

  Syn.: _Plerocercoides prolifer_, Ijima, 1905; _Sparganum prolifer_,
  Verdun, Manson, 1907.

These plerocercoids produce an acne-like condition of the skin.
The condition is really one of capsules in great abundance in the
subcutaneous tissue and less so in the corium and in the intermuscular
connective tissue. The encapsuled worms in the corium feel like
embedded rice grains and raise the epidermis, giving rise to an
acne-like condition. Many thousands occur scattered over the body; in
Ijima’s Japanese case there were over 10,000 in the left thigh. The
worms when they first appear in the skin cause itching. The capsules
are ovoid, generally about 1 to 2 mm. in diameter, but they may be
smaller and also much larger. The larger ones occur in the subcutaneous
tissue. The capsules consist of dense tough connective tissue.

Each capsule, as a rule, contains one worm, but as many as seven may
occur. The skin of areas that have been long infected is swollen and
indurated or adherent, giving a somewhat elephantoid appearance. The
subcutaneous tissue is thick and filled with slimy fluid or in other
parts sclerosed.

[Illustration: FIG. 215.--_Sparganum prolifer_: left with buds, right
extended. × 4. (After Ijima.)]

[Illustration: FIG. 216.--_Sparganum proliferum._ × 10. (After Stiles.)]

_The Worm._--The chief peculiarity is its irregular shape and its
reproduction in the larval stage by forming supernumerary heads, which
are supposed to wander about the body.

The simplest forms are thread-like bodies, flat or round, 3 mm. long
and 0·3 mm. in diameter, but they may be 12 mm. long by 2·5 mm. broad.
The narrow end is the head, which in life invaginates and evaginates,
but there is no indication of any suckers, except an inconstant
terminal depression. In addition to these simple forms the most
complicated and irregular forms occur, due to the formation of buds
(heads) at various parts. The detachment and growth of a head account
for the presence of more than one worm in a cyst. The irregularity in
form is also increased by the presence in the subcuticular tissue of
the worm of _reserve food bodies_. These bodies are supposed to be of
this nature and are spherical, 100 µ to 300 µ in diameter, but also
much elongated.

_Calcareous bodies_ in the Japanese worms were 7·5 µ to 12 µ; in the
Florida worms 8·8 µ to 17·6 µ.

_Mode of Infection._--Probably from eating uncooked fish.

_Distribution._--Japan, Florida.

Family. *Dipylidiidæ*, Lühe, 1910.

Genus. *Dipylidium*, R. Lkt., 1863.

  Rostellum retractile, with several rings of alternating hooks; the
  latter with a disc-like base, having the shape of the thorns of a
  rose. Genital pores opposite; genitalia double. Testes very numerous
  in the central field; ovary with two lobes; the vitellaria, which are
  smaller, behind them; the uterus forms a reticulum, in the network of
  which the testicular vesicles lie; later on it breaks up into sacs
  enclosing one or several eggs. The eggs have a double shell.

*Dipylidium caninum*, L., 1758.

  Syn.: _Tænia canina_, L., 1758, p. p.; _Tænia moniliformis_, Pallas,
  1781; _Tænia cucumerina_, Bloch, 1782; _Tænia elliptica_, Batsch,
  1786; _Dipylidium cucumerinum_, Lkt., 1863.

[Illustration: FIG. 217.--_Dipylidium caninum_: on the left, the
scolex, neck and the first proglottids; on the right, at the top, a
packet of ova; below, hooks of the rostellum, side and front views;
below, an ovum. Various magnifications. (After Diamare.)]

[Illustration: FIG. 218.--_Dipylidium caninum_; egg showing _a_,
egg-shell (vitelline membrane of Moniez); _b_, albuminous coat; _c_,
internal shell formed of or secreted by an outer layer of blastomeres
(Moniez); _d_, hexacanth embryo. (After Benham and Moniez.)]

This worm measures 15 to 35 cm. in length and 1·5 to 3 mm. in breadth.
The scolex is small, rhomboidal, and has a club-shaped rostellum on
which there are, in three to four rings, forty-eight to sixty hooks
resembling rose thorns, the size of those in the foremost being 11 µ
to 15 µ and those in the hindmost ring 6 µ. The neck is very short,
the most anterior segments broad and short, the middle as long as they
are broad; the mature segments are longer than wide (6 to 7 mm. by 2
to 3 mm.), fairly thick, are frequently of a reddish colour, and when
cast off resemble cucumber seeds. The genital pores lie symmetrically
at the lateral margins; the roundish egg sacs, arising from the
uterine reticulum, contain eight to fifteen eggs embedded in a reddish
cement substance (in life). The eggs are globular (43 µ to 50 µ,); the
embryonal shell (embryophore) is thin, the oncosphere measures 32 µ to
36 µ. Surrounding the embryophore is an albuminous coating, and outside
this the thin vitelline envelope (fig. 218).

[Illustration: FIG. 219.--_Dipylidium caninum_: central portion of a
proglottis. _C.p._, cirrus sac; _V.s._, vitellaria; _Ex.v._, excretory
vessels; _T._, testicles lying in the meshes of the uterine reticulum
which laterally forms pouches; _O._, ovary; _U._, reticulum of uterus;
_V._, vagina and seminal receptacle (below ovary). Magnified. (After
Neumann and Railliet.)]

[Illustration: FIG. 220.--_Dipylidium caninum_: development of embryo.
1, solid hexacanth embryo; 2, primitive lacuna (_a_) in the embryo; 3,
elongation of hinder part, rudiments of sucker and rostellum appearing;
4, “body” and “tail” distinct, (_b_) and (_c_) excretory system; 5,
fore-body invaginates into hind-body, excretory bladder has a pore; 6,
tail has dropped off; scolex growing up into secondary cavity formed by
fore-body; the primitive cavity has been absorbed at stage 4. (After
Benham, Grassi and Rovelli.)]

_Dipylidium caninum_ is a common intestinal parasite of dogs, in
which it grows larger (_Tænia cucumerina_, Bloch) than in cats (_T.
elliptica_, Batsch); it has, however, also been found in jackals, as
well as in human beings, though in the latter it is of comparatively
rare occurrence (twenty-four cases), and almost always affects
children, generally of tender age. One-third of all the cases in
children were sucklings, about a quarter of all the cases recorded were
adults, and these occurred throughout all Europe with the exception of
Spain and Italy.

[Illustration: FIG. 221.--Larva (cysticercoid) of _Dipylidium caninum_,
consisting of body and tail. The latter is solid and bears on it the
embryonal spines. The bladder, which was only slightly developed, has
disappeared, and the fore-part of the body bearing the rostellum is now
seen invaginated into the hind portion. The hooklets are shown in front
of the excretory system which has now developed. At a further stage
the tail drops off; the head now evaginates, but is still enclosed in
a double-walled sac formed by the prolongation upwards on each side of
the topmost parts of the body shown in the figure. _Cf._ fig. 220, 6.
Enlarged. (After Grassi and Rovelli.)]

The proglottids, which leave the intestine spontaneously, are
recognizable by the naked eye on account of their form and reddish
colour, as well as their two genital pores. As a rule, the presence of
this parasite sets up no marked symptom in the patient.

The corresponding larval form (cysticercoid) lives in the louse of
the dog (_Trichodectes canis_), a fact that was first established by
Melnikow and Leuckart; according to Grassi and Rovelli, as well as
Sonsino, it also lives in the flea of the dog (_Ctenocephalus canis_)
and in the flea of man (_Pulex irritans_), but not in its larva.
The adult segments, which also leave the rectum of dogs and cats
spontaneously, creep about around the anus and get into the hair, and
are thus partly dried and disintegrated. Part of the segments, or the
oncospheres released by disintegration, are then taken up by lice and
fleas, within which they develop into larvæ (cysticercoids). Dogs and
cats are thus infected by their own skin parasites, which they bite
and swallow whilst gnawing at their fur. The infection of human beings
must occur in an analogous manner, by transmission of the cysticercoids
present on the lips or tongue of dogs when the latter lick them, or it
may be that the vermin of cats and dogs harbouring cysticercoids are
accidentally and directly swallowed by human beings.

Family. *Hymenolepididæ*, Railliet and Henry, 1909.

Genus. *Hymenolepis*,[282] Weinland, 1858.

[282] The genus is by some authors divided into two
sub-genera--Hymenolepis, s. str., and Drepanidotænia, Raill.

_Drepanidotænia._--Body, broad lanceolate, testes three, female
genitalia antiporal beside the testes. Scolex small, with eight
hooks. Neck very short, longitudinal muscle bundles very numerous. No
accessory sac opening into genital atrium.

_Hymenolepis._--Narrow, female genitalia ventral to or between testes.

  Accessory sac (opening into genital atrium) usually absent. Vas
  deferens with an external (outside cirrus sac) and an internal
  (inside cirrus sac) “seminal vesicle.” Three testes in each
  proglottis. The eggs are round or oval with two to four distinct
  envelopes. In mammals and birds.

*Hymenolepis nana*, v. Sieb., 1852.

  Syn.: _Tænia nana_, v. Sieb., 1852, _nec_ van Beneden, 1867; _Tænia
  ægyptiaca_, Bil., 1852; _Diplacanthus-nanus_, Weinld., 1858; _Tænia_
  (_Hymenolepis_) _nana_, Lkt., 1863.

The worm is 10 to 45 mm. in length and 0·5 to 0·7 mm. in breadth; the
head is globular, 0·25 to 0·30 mm. in diameter. The rostellum has a
single circlet consisting of twenty-four or twenty-eight to thirty
hooks, which are only 14 µ to 18 µ in length. The neck is moderately
long; the proglottids are very narrow, up to 200 in number, 0·4 to
0·9 mm. in breadth, and 0·014 to 0·030 mm. in length. The eggs are
globular or oval, 30 µ to 37 µ to 48 µ; the oncospheres measure 16 µ
to 19 µ in diameter, with two coats, separated by an intervening
semi-fluid substance (fig. 224).

This species was discovered by Bilharz in Cairo in 1851; it was found
by him in great numbers in the intestine of a boy who had died of
meningitis. For several years this was the only case, until 1885,
since when numerous cases have come to light. Spooner (1873) even
reported a case from North America, which may, however, have related
to _Hymenolepis diminuta_. In Europe the worm is particularly frequent
in Sicily, but it has also been repeatedly observed in North Italy;
it has, moreover, been reported from Russia, Servia, England, France,
Germany, North and South America, the Philippines, Siam and Japan, in
all over 100 cases. Notwithstanding its small size this worm causes
considerable disorders in its hosts--mostly children--as it sets up
loss of appetite, diarrhœa, various nervous disturbances, and even
epilepsy; all these symptoms, however, disappear after the expulsion of
the parasites, which are generally present in large numbers.

[Illustration: FIG. 222.--_Hymenolepis nana_, v. Sieb. About 12/1.
(After Leuckart.)]

[Illustration: FIG. 223.--_Hymenolepis nana_: head. Enlarged. (After

[Illustration: FIG. 224.--_Hymenolepis nana_: an egg. Highly magnified.
(After Grassi.)]

[Illustration: FIG. 225.--Longitudinal section through the intestinal
villus of a rat, with the larva (cysticercoid) of _Hymenolepis murina_.
Magnified. (After Grassi and Rovelli.)]

[Illustration: FIG. 226.--_Hymenolepis nana_ (_murina_): cross section
of proglottis from a rat. _c.p_., cirrus sac; _rec. sem._, receptaculum
seminis; _s.g._, shell gland; _ov._, ovary; _t._, testis; _cort.
par._, cortical parenchyma; _m.l.n._, main lateral nerve; _ex. can._,
excretory canal; _y.g._, vitellarium. (After v. Linstow.)]

[Illustration: FIG. 227.--_Hymenolepis nana_: longitudinal section of
an embryo. _bl.p._, anterior opening of secondary cavity; _caud._,
caudal appendage; _pr. cav._, primary cavity; _sec. cav._, secondary
cavity. Enlarged. (After Grassi and Rovelli.)]

The development as well as the manner of infection is still unknown;
Grassi is of opinion that _Hymenolepis nana_ is indeed merely a variety
of _Hymenolepis murina_, Duj., which lives in rats. According to
Grassi direct development takes place with omission of the intermediate
host, but with the retention of the larval stage; that is to say, rats
infect themselves directly with _Hymenolepis murina_, by ingesting the
mature segments or oncospheres of this species, from which subsequently
the small larvæ originate in the intestinal wall (fig. 225); when fully
developed they fall into the intestinal lumen and become tapeworms.
The identity of the two forms has nevertheless been disputed (Moniez,
R. Blanchard, v. Linstow), though their near relationship cannot be
denied. Grassi gave mature segments of _Hymenolepis murina_ to six
persons, but only one person evacuated a tapeworm. This, however,
proves nothing in a district where _Hymenolepis nana_ frequently
occurs in man; it was, moreover, not possible to infect rats with
segments of _Hymenolepis nana_ (of man). Accordingly this form may
represent an independent species, which, however, like _Hymenolepis
murina_, also omits an intermediate host.

*Hymenolepis diminuta*, Rud., 1819.

  Syn.: _Tænia diminuta_, Rud., 1819; _Tænia leptocephala_, Crepl.,
  1825; _Tænia flavopunctata_, Weinld., 1858; _Tænia varesina_, E.
  Parona, 1884; _Tænia minima_, Grassi, 1886.

This species measures 20 to 60 cm. in length, and up to 3·5 mm. in
breadth; there are from 600 to 1,000 segments. The head is very small
(0·2 to 0·5 mm.), it is club-shaped and has a rudimentary unarmed
rostellum; the neck is short; the mature segments are 3·5 mm. in
breadth, 0·66 mm. in length; the eggs are round or oval. The outer
egg-shell is yellowish and thickened, with indistinct radial stripes;
the inner embryonal shell (embryophore) double, thin; the outer layer
is somewhat pointed at the poles; oncosphere 28 µ by 36 µ. Between the
inner and outer shells is a middle granular layer.

[Illustration: FIG. 228.--_Hymenolepis diminuta_: scolex. Magnified.
(After Zschokke.)]

[Illustration: FIG. 229.--_Hymenolepis diminuta_: two proglottids
showing testes (3), ovary and vagina. Slightly enlarged. (After

[Illustration: FIG. 230.--_Hymenolepis diminuta_: egg from man. (After

_Hymenolepis diminuta_ lives in the intestine of rats--_Mus decumanus_
(the sewer rat), _Mus rattus_ (the black rat), and _Mus alexandrinus_,
rarely in mice; it is occasionally also found in human beings.

Weinland described it from specimens collected by Dr. E. Palmer in
1842, in Boston, from a child aged 19 months, as _T. flavopunctata_.
A second case relating to a three year old child, from Philadelphia,
was only reported in 1889 by Leidy; a third case was simultaneously
reported of a two year old girl in Varese (_T. varesina_); and Grassi
described another case relating to a twelve year old girl from Catania
(Sicily). Sonsino and Previtera reported the same species in Italy,
Zschokke in France, Lutz and Magalhães in South America, and Packard
in North America: a total of twelve cases, five from America, the rest
from Europe (Ransom).

According to Grassi and Rovelli the larval stage lives in a small
moth (_Asopia farinalis_), as well as in its larva, in an orthopteron
(_Anisolabis annulipes_), and in coleoptera (_Acis spinosa_ and
_Scaurus striatus_). Experimental infections have been successful on
rats as well as on human beings. In America other species of insects
may be the intermediary hosts.

[Illustration: FIG. 231.--_Hymenolepis diminuta_: cysticercoid from the
rat flea (_Ceratophyllus fasciatus_). _a_, remains of primary vesicle;
_b_, fibrous layer; _c_, radially striated layer resembling cuticle;
_d_, layer of columnar cells; _e_, parenchymatous layer of irregularly
disposed cells; _f_, parenchymatous layer. (Stephens, after Nicoll and

Nicoll and Minchin[283] found in the body cavity of 4 per cent. of rat
fleas (_Ceratophyllus fasciatus_) the cysticercoid of _Hymenolepis
diminuta_. That it belonged to this species was shown by its unarmed
rostellum and by feeding; 340 fleas were fed to white rats and
fourteen worms obtained, _i.e._, about 4 per cent., thus corresponding
to the infection of the fleas. The development in the flea probably
begins in the pupal stage, the eggs being ingested by the older flea
larvæ. The larva is 0·31 by 0·25 mm.; tail 0·8 mm., scolex 0·075 by
0·09 mm., suckers, 0·055 mm. in diameter. Microscopically it shows--(1)
externally a radially striated layer resembling cuticle, (2) a layer of
columnar cells, (3) parenchymatous layer continuous with the tail, (4)
fibrous layer around the small caudal vesicle, then the parenchymatous
scolex at the bottom of the secondary cavity.

[283] _Proc. Zool. Soc._, 1911, p. 9.

Nicoll and Minchin (_loc. cit._) found a cysticercoid[284] in the rat
flea _Ceratophyllus fasciatus_ which was probably that of _Hymenolepis
murina_. Body 0·16 mm., tail 0·19 mm., scolex 0·096 mm. in diameter.
Rostellum has twenty-three spines in a single row. Length 0·017 mm.,
handle 0·01 mm., guard 0·007 mm., prong 0·007 mm. Sucker 0·042 mm.
Although this cycle, then, for _H. murina_ also exists, it is not
probable that rats (or man in the case of _H. nana_ if this be
considered distinct) infect themselves in this way, as they hardly
ingest all the necessary fleas to account for the massive infection
which frequently exists in rats (and man), so that Grassi’s cycle holds
good as the predominant method. _Xenopsylla cheopis_ has also been
found by Johnston to harbour both cysticercoids in Australia.

[284] A third cysticercoid resembling this, but without hooks, has also
been found.

*Hymenolepis lanceolata*, Bloch, 1782.

  Syn.: _Tænia lanceolata_, Bloch, 1782; _Drepanidotænia lanceolata_,
  Railliet, 1892.

[Illustration: FIG. 232.--_Hymenolepis lanceolata_. Natural size.
(After Goeze.) To the right above, two hooks. 120/1. (After Krabbe.)]

[Illustration: FIG. 233.--_Hymenolepis lanceolata_: diagram of female
genitalia. _ov._, ovary; _ovd._, oviduct; _rec. sem._, receptaculum
seminis; _s.g._, shell gland; _ut._, uterus; _y.g._, vitellarium.
(After Wolffhügel.)]

The parasite measures 30 to 130 mm. in length and 5 to 18 mm. in
breadth; the head is globular and very small; the rostellum is
cylindrical, with a circlet composed of eight hooks (31 µ to 35 µ in
length). The neck is very short. The short segments increase gradually
and equally in breadth, but only a little in length; the female
glands lie on the side opposite to that on which the genital pore is
situated; the three elliptical testes are on the same side as the
pores; the cirrus is armed and slender. The eggs have three envelopes
and are oval (50 µ by 35 µ), the external envelope is thin, the middle
intermediate layer or envelope is not so marked as in _H. diminuta_,
and the internal one is very thin and sometimes has polar papillæ, as
in _Hymenolepis diminuta_ and _H. nana_.

It inhabits the intestine of the following birds: Domesticated ducks
and geese, the Muscovy duck (_Cairina moschata_), white-headed duck
(_Erismatura leucocephala_), the pochard (_Nyroca rufina_), and the
flamingo (_Phœnicopterus antiquorum_). It has been recorded from Great
Britain, France, Denmark, Austria and Germany.

Zschokke reports the receipt of two specimens which a twelve year old
boy in Breslau evacuated spontaneously at two different times.

The corresponding larva, according to Mrázek, lives in fresh water
_Cyclops_; according to Dadai it is likewise found in another copepod,
_Diaptomus spinosus_, but the hooks of Dadai’s larva differed in size.

Family. *Davaineidæ*, Fuhrmann, 1907.

Sub-family. *Davaineinæ*, Braun, 1900.

Genus. *Davainea*, R. Blanch., 1891.

  The large scolex is more or less globular, much wider than the
  rostellum, which is furnished with two rings of very small and
  numerous hooks. Neck absent, proglottids few, genitalia single.
  Parasitic chiefly in birds.[285]

[285] [The larval stage of the Davaineas occurs in slugs (_Limax_) and
snails (_Helix_).--F. V. T.]

*Davainea madagascariensis*, Davaine, 1869.

  Syn.: _Tænia madagascariensis_, Dav.; _Tænia demerariensis_, Daniels,

This worm measures 25 to 30 cm. in length; the head has four large
round suckers; the rostellum has ninety hooks (18 µ in length); there
are 500 to 700 segments, of which the last 100 are filled with eggs and
form half of the entire worm. The segments, when mature, measure 2 mm.
in length by 1·4 mm. in breadth; genital pores unilateral; about fifty
testes; the uterus consists of a number of loops, which at each side
are rolled up into an almost spherical ball; when filled with eggs the
convolutions unwind, permeate the segment and then lose their wall; the
eggs lying free in the parenchyma become finally surrounded, one, or
several together, by proliferating parenchymatous cells; this is how
the 300 to 400 egg masses, taking up the entire mature segment, are
formed. The globular oncosphere (8 µ) is surrounded by two perfectly
transparent shells, the outer of which terminates in two pointed

[Illustration: FIG. 234.--Scolex of _Davainea madagascariensis_. The
hooks have fallen off. 14/1. (After Blanchard.)]

_Davainea madagascariensis_ has hitherto been found in man only (eight
times). Davaine described this species from fragments sent to him from
Mayotta (Comoro Islands), which were found in two Creole children.
Chevreau observed four cases in Port Louis (Mauritius), likewise
in children; Leuckart received the first perfect specimen--it was
obtained from a three year old boy, the son of a Danish captain, in
Bangkok; Daniels, at the _post-mortem_ of an adult native of George
Town, Guiana, found two specimens (_Tænia demerariensis_); and finally
Blanchard describes another perfect specimen which was in Davaine’s
collection of helminthes in Paris, and which was obtained from a little
girl 3 years old, of Nossi-Bé (Madagascar). The intermediate host is

*Davainea (?) asiatica*, v. Linst., 1901.

  Syn.: _Tænia asiatica_, v. Linstow.

There exists only one headless specimen of this species, which is
not quite adult, and which is preserved in the Zoological Museum of
the Imperial Academy of Science in Petrograd. It came from a human
being and was found by Anger in Aschabad (Asiatic Russia, near the
northern frontier of Persia). The specimen measures 298 mm. in length.
The breadth anteriorly is only 0·16 mm., the posterior part measures
1·78 mm. across. The number of segments is about 750. The genital pores
are unilateral; the testes are globular and lie in a dorsal and ventral
layer in the medullary layer; the cirrus pouch is pyriform, 0·079 mm.
in length and 0·049 mm. in breadth; the female glands lie in the
fore-part of the segments, the ovary reaching to the excretory vessels;
the vitellarium is small and round. The vagina has a large fusiform
receptaculum seminis; the uterus breaks up into sixty to seventy large,
irregularly polyhedric eggsacs.

Family. *Tæniidæ*, Ludwig, 1886.

Genus. *Tænia*, L., 1758.[286]

  With the characters of the family. In the genus Cladotænia recognized
  by some authors, the testes encroach on the mid field and the uterine
  stem reaches the anterior end of the segment.

[286] The Greeks termed the tapeworms ἕλμινθες πλατεῖαι, more rarely
χηρία (= fascia); the Romans called them _tænia_, _tinea_, _tæniola_,
later _lumbrici_, usually with the addition _lati_, to distinguish
them from the _Lumbrici teretes_ (_Ascaridæ_). The proglottids were
called _Vermes cucurbitini_; the cysticerci χάλαζαι (hailstones),
later hydatids. Plater (1602) was the first to differentiate _Tænia
intestinorum_ (= _Bothriocephalus latus_) amongst the _Lumbrici lati_
of man from _Tænia longissima_ (= _Tænia solium_). The term _solium_
was already used by Arnoldus Villanovanus, who lived about 1300; and,
according to him, it signifies “cingulum” (belt, chain), while N.
Andry, in 1700, traces this word from “solus,” because the worm occurs
always singly in man. Leuckart and Krehl derive the word “solium”
from the Syrian “schuschl” (the chain), which in Arabian has become
“susl” or “sosl,” and in Latin has become “sol-ium.” What Linnæus
described under the term _Tænia solium_ was really _Tænia saginata_;
the latter was first distinguished by Goeze, but was forgotten until
Küchenmeister, in 1852, again called attention to the differences.

*Tænia solium*, L., _p. p._, 1767.

  Syn.: _Tænia cucurbitina_, Pall., 1781; _Tænia pellucida_, Goeze,
  1782; _Tænia vulgaris_, Werner, 1782; _Tænia dentata_, Gmel., 1790;
  _Halysis solium_, Zeder, 1800; _Tænia humana armata_, Brera, 1802;
  _Tænia_ (_Cystotænia_) _solium_, Lkt., 1862.

The average length of the entire tapeworm is about 2 to 3 m., but may
be even more; the head is globular, 0·6 to 0·8 to 1·0 mm. in diameter.
The rostellum is short with a double circlet of hooks, twenty-two to
thirty-two in number, usually twenty-six to twenty-eight; large and
small hooks alternate regularly; the length of the large hooks is
0·16 to 0·18 mm., of the small ones 0·11 to 0·14 mm. The rostellum is
sometimes pigmented. The suckers are hemispherical, 0·4 to 0·5 mm.
in diameter. The neck is fairly thin and long (5 to 10 mm.). The
proglottids, the number of which averages from 800 to 900, increase in
size very gradually; at about 1 m. behind the head they are square and
have the genitalia fully developed. Segments sufficiently mature for
detachment measure 10 to 12 mm. in length by 5 to 6 mm. in breadth. The
genital pores alternate fairly evenly at the lateral margin a little
behind the middle of each segment. The fully developed uterus consists
of a median trunk, with seven to ten lateral branches at either side,
some of which are again ramified. The eggs are oval, the egg-shell
very thin and delicate; the embryonal shell (embryophore) is thick,
with radial stripes; it is of a pale yellowish colour, globular, and
measures 31 µ to 36 µ in diameter; the oncospheres, with six hooks, are
likewise globular, and measure 20 µ in diameter (fig. 238).

  Malformations are not so common as in _T. saginata_; they consist in
  two or several proglottids being partly or entirely fused, formation
  of single club-shaped segments, fenestration of long or short series
  of segments and so-called double formation, in which the head has six
  suckers and the segments exhibit a *Y*-shaped transverse section. The
  oncospheres occasionally also possess more than six hooklets. Very
  slender specimens have led to the description of a particular species
  or variety (_T. tenella_).

In its fully developed condition _T. solium_ is found exclusively in
man; the head is usually attached in the anterior third of the small
intestine and the chain, in numerous convolutions, extends backwards;
a few mature detached proglottids usually lie at the most posterior
part, and these are usually evacuated during defæcation. In exceptional
cases single proglottids or whole worms may reach contiguous organs
if abnormal communications with them exist; thus they may reach the
abdominal cavity and the urinary bladder, or they may be found in a
so-called worm abscess of the peritoneum; occasionally, in vomiting,
single segments or several together may be brought up. Exceptionally it
induces severe anæmia.

[Illustration: FIG. 235.--Two fairly mature proglottids of _Tænia
solium_, showing ovaries (one bi-lobed), vitellaria, central uterine
stem, cirrus and vas deferens (above), vagina (below), testes
(scattered), longitudinal and transverse excretory vessels.]

[Illustration: FIG. 236.--Head of _Tænia solium_. 45/1.]

The _larval stage_ (_Cysticercus cellulosæ_) that gives rise to _Tænia
solium_ lives normally in the intramuscular connective tissue and other
organs of the domestic pig, but it is known to exist also in a few
other mammals, such as the wild boar, the sheep,[287] the stag, dog,
cat, brown bear and monkey, as well as in man. The cysticercus of
the pig is an elliptical vesicle with a longitudinal diameter of 6 to
20 mm., and a transverse diameter of 5 to 10 mm.

[287] The larvæ which on rare occasions are found in the muscular
system of sheep are either strayed specimens of _Cysticercus
tenuicollis_, which normally develop in organs of the abdominal cavity,
and appertain to _Tænia marginata_ of the dog, or actually _Cysticercus
cellulosæ_. (_Cf._ Bongert, in _Zeitschr. f. Fleisch- u. Milchhyg._,
1899, ix, p. 86.)

Even with the naked eye a white spot may be observed in the centre
of the long equator, this being the invaginated head; it is easy to
make it project by pressing on the vesicle (after tearing off with the
finger-nail the investing connective tissue), and on examining it under
the microscope one can convince oneself that it corresponds with the
head of _Tænia solium_.

[Illustration: FIG. 237.--Large and small hooks of _Tænia solium_.
280/1. (After Leuckart.)]

[Illustration: FIG. 238.--_Tænia solium._ 21, Egg with external
membrane; 22, without (embryophore). (After Leuckart.)]

[Illustration: FIG. 239.--Two mature proglottids of _Tænia solium_ with
fully developed uterus. 2/1.]

Numerous experiments have proved that the _Cysticercus cellulosæ_
of the pig, if introduced into the intestine of man, grows to a
_Tænia solium_ (Küchenmeister, 1855; Humbert, 1856; Leuckart, 1856;
Hollenbach, 1859; Heller, 1876); the cysticercus has frequently also
been cultivated purposely by feeding pigs with mature proglottids of
_T. solium_ (P. J. van Beneden, 1853; Haubner and Küchenmeister, 1855;
Leuckart, 1856; Mosler, 1865; Gerlach, 1870; etc.), but success did not
attend the efforts to make _Cysticercus cellulosæ_ establish themselves
in the intestines of pigs, dogs, guinea-pigs, rabbits and monkeys
(_Macacus cynomolgus_), and so become adult Tæniæ; the attempts, also,
to infect dogs with cysticerci by means of ova were likewise, as a
rule, abortive.[288]

[288] According to Gerlach only young pigs (up to 6 months old) are
capable of infection, and perhaps the failure may have been due to the
animals chosen for experiment being of the wrong age.

  The development of _Cysticercus cellulosæ_ takes two and a half
  to three or four months; it is not known how long the cysticerci
  remain alive in animals; not uncommonly they perish at earlier or
  later stages, and become calcified or caseated. Extracted cysticerci
  die in water at a temperature of 47° to 48° C., in flesh at normal
  temperature they remain alive for twenty-nine days or more. On
  account of the present rapid means of pickling and smoking meat, the
  cysticerci as a rule are not killed, also the effect of cold on them
  for some time in cold chambers of slaughterhouses is not lethal, but
  freezing is fatal (Ostertag).

There is not the least doubt that human beings are almost exclusively
infected with _Tænia solium_ by eating pork containing cysticerci in
a condition that does not endanger the life of the cysticerci. The
infection may likewise be caused in man by eating the infected meat of
other animals subject to this species of bladder worm, mainly, as a
matter of fact, deer and wild boar.

  The frequency of cysticerci in pigs’ flesh has considerably decreased
  since the introduction of meat inspection; in the Kingdom of Prussia
  there was on an average 1 infected pig to every 305 slaughtered
  between 1876 to 1882; from 1886 to 1889, there was 1 to 551; from
  1890 to 1892, there was 1 to 817; in 1896, 1 to 1,470; and in 1899, 1
  to 2,102; in the Kingdom of Saxony in 1894 there was 1 infected pig
  to every 636; in 1895 there was 1 to every 2,049, and in 1896 only 1
  infected pig was found of 5,886 slaughtered. In South Germany pigs
  with cysticerci are very rare, but are more frequent in the eastern
  provinces of Prussia; in 1892 the number of infected pigs compared
  with the total slaughtered was as follows:--

  In the district of Marienwerder                           1 :    28
    "      "         Oppeln                                 1 :    80
    "      "         Königsberg                             1 :   108
    "      "         Stralsund and Posen                    1 :   187
    "      "         Danzig, Frankfort a. O. and Bromberg   1 :   250
  As compared with the district of Arnsberg                 1 :   865
        "      "           "       Coblenz                  1 :   975
        "      "           "       Düsseldorf               1 : 1,070
        "      "           "       Münster and Wiesbaden    1 : 1,900

  The average for the whole of Prussia in the same year was 1 : 1,290;
  for the eastern provinces, on the other hand, 1 : 604. Even more
  unfavourable are the proportions in Russian Poland (over 1 per
  cent. of pigs measly), in Prague (over 3 per cent.), in Bosnia and
  Herzegovina (6 to 7 per cent.). The cause for this is most likely
  attributable to the manner in which the pigs are kept. When allowed
  to be in the farmyards of the small farmers for the whole day, or
  allowed to wander in the village streets and pasture lands, they are
  more liable to take up the oncospheres of the _T. solium_ than when
  shut up in good pig-styes.

The geographical distribution of _T. solium_ generally corresponds
with that of the domestic pig and the custom of eating pork in any
form insufficiently cooked or raw. There are, or were, some isolated
districts in Germany, France, Italy and England where the “armed
tapeworm” was frequent (for instance, Thuringia, Brunswick, Saxony,
Hesse, Westphalia, whereas it is and was very scarce in South Germany);
it is thus easily understood why it occurs very rarely in the East, in
Asia and in Africa, in consequence of the Mahommedans, Jews, etc.,
not eating pork. In North America, also, _T. solium_ is very rare; the
tapeworm which is known there by this name is generally _T. saginata_,
Stiles. During the last decade _T. solium_ infection has, however,
very markedly decreased in North and East Germany in consequence of
the precautions exercised by the public in the choice of pork to avoid
trichinosis, especially, however, because measly meat must be sold as
such and must be thoroughly cooked before being placed on the market;
indeed, if badly infected it may not be sold for food, but can be
turned to account for industrial purposes.

The occurrence of _Cysticercus cellulosæ_ in man has been known since
1558 (Rumler, _Obs. med._, liii, p. 32); there is hardly an organ in
man in which cysticerci have not been observed at some time; they are
most frequently found in the brain,[289] where they grow to a variety
known as _Cysticercus racemosus_; next in frequency they are found in
the eye, in the muscular system, in the heart, in the subcutaneous
connective tissue, the liver, lungs, abdominal cavity, etc. The number
of cysticerci observed in one man varies between a few and several
thousands. Of the sexes, men are most subject (60 to 66 per cent. of
the number attacked). The disturbances caused in man by cysticerci
vary according to the nature or position of the organs attacked; when
situated in the cerebral meninges they have the same effect as tumours.

[289] Dressel, for instance, examined eighty-seven persons suffering
from cysticercus, and found it seventy-two times in the brain, thirteen
times in the muscles; K. Müller, in thirty-six cases, found it
twenty-one times in the brain, twelve times in the muscles, three times
in the heart; Haugg, in twenty-five cases, found it thirteen times in
the brain, six times in the muscles, twice in the skin, etc. According
to Graefe, amongst 1,000 ophthalmic cases in Halle and Berlin, there
was one with cysticercus in the eye; in Stuttgart there was only one in
4,000, in Paris one in 6,000, and in Copenhagen one in 8,000.

During the last decades, however, these cases have also become less
common. In Rudolphi’s time 2 per cent. of _post-mortems_ in Berlin
showed cysticerci; in the ’sixties, according to Virchow, about the
same; in 1875 the number fell to 1·6 per cent.; in 1881 to 0·5 per
cent.; in 1882 to 0·2 per cent.; in 1900 to 0·15 per cent., and in
1903 to 0·16 per cent. Hirschberg between 1869 and 1885 discovered
cysticerci in the eye seventy times in 60,000 ophthalmic cases, but
during the following six years the parasite was only present twice
amongst a total of 46,000 cases of ophthalmic diseases, and since 1895
no ophthalmic case has been met with.

The infection of human beings with the cysticerci can only take place
by the introduction of the oncospheres of _Tænia solium_ into the
stomach with vegetable foods, salads that have been washed in impure
water containing oncospheres, also by drinking contaminated water;
the carriers of _T. solium_, moreover, infect themselves still more
frequently through uncleanliness in defæcation, the privies in public
localities and many private houses affording striking testimony of
this. The minute oncospheres can thus easily reach the fingers and
thence the mouth (as in twirling the moustache, biting the nail).
More rarely a third manner of transmission or internal auto-infection
may possibly take place, as when, in the act of vomiting, mature
proglottids near the stomach are drawn into it; the oncospheres or
segments there retained are then in the same position as if they had
been introduced through the mouth.

  On account of these dangers of internal or external auto-infection,
  it is therefore the duty of the medical attendant, after recognizing
  the presence of tapeworms, to expel them,[290] and in doing so to
  employ every possible means to prevent vomiting setting in; it is,
  however, equally important to take the necessary steps to destroy the
  parasites evacuated. It may be incidentally mentioned that in using
  certain remedies the scolex not rarely remains in the intestine; the
  cure in such cases has not been accomplished, as the scolex again
  produces new proglottids, and after about eleven weeks the first
  formed ones are again mature and appear in the fæces.

[290] The diagnosis as a rule is not difficult; the patients themselves
frequently observe the pumpkin seed-like segments in the fæces. But in
such cases the diagnosis must still be confirmed. In other cases the
discovery of the oncospheres in their embryonal shells (embryophores),
which cannot be confounded with the other constituents of the fæces,
gives complete certainty, although the differential diagnosis between
_T. solium_ and _T. saginata_ is hardly possible from the embryophores;
but, if evacuated segments are placed between two slides and lightly
pressed, the species is easily recognizable by the shape of the uterus
(_cf._ figs. 239 and 241).

  Amongst the cysticerci also many malformations appear; thus absence
  of the rostellum and the hooks, or double formation with six suckers,
  or abnormalities of growth on account of the surroundings, which have
  had a special name given to them, _viz._, _Cysticercus racemosus_,
  Zenk. (= _C. botryoides_, Hell.; _C. multilocularis_, Kchnmstr.);
  these forms are more especially found at the base of the brain, are
  irregularly ramified and often without the head.

A certain interest is attached to those forms that have led to the
establishment of a distinct species:--

*Cysticercus acanthotrias*, Weinld., 1858.

  In making the autopsy of a white Virginian woman who had died of
  phthisis, a cysticercus was found in the dura mater, and eleven or
  twelve specimens in the muscles and subcutaneous tissue. Weinland
  and Leuckart, who examined the specimens, found that they resembled
  _Cysticercus cellulosæ_ in form and size, but that they carried on
  the rostellum a triple crown, each consisting of fourteen to sixteen
  hooks, which differed from the hooks of _C. cellulosæ_ or of _Tænia
  solium_ by the greater length of the posterior root process and the
  more slender form of the hooks; the large hooks measured 0·153 to
  0·196 mm., the medium-sized hooks, 0·114 to 0·14 mm., and the small
  ones 0·063 to 0·07 mm.

On account of these differences a distinct species of cysticercus was
established, and this naturally presupposed a corresponding species
of Tænia (_T. acanthotrias_, Lkt.); this could be done with justice
so long as the case remained isolated, _i.e._, in America, as there
was the possibility of the corresponding Tænia being found. In this
respect, however, the position has changed; Delore first described a
cysticercus the size of a nut from the biceps muscle of the arm of a
silk-worker in Lyons; according to Bertolis this specimen possessed
hooks of three different sizes, the dimensions of which corresponded
with the figures given by Weinland and Leuckart; the correctness of
the diagnosis could hardly be doubted, as Bertolis was known to be a
very exact observer. A second case has become known through Cobbold,
who regards a specimen of a cysticercus in Dallinger’s collection as
likewise belonging to _Cysticercus acanthotrias_; this specimen also
came from a man’s brain; finally a third case, also from France, has
been published by Redon. This author, amongst numerous _C. cellulosæ_
of a man, found one that had forty-one hooks in three rows, and he
was the first to express the opinion that _C. acanthotrias_ does
not represent a distinct species, but is only an abnormality of _C.
cellulosæ_. This view was also taken by Blanchard and Railliet, and is
probably correct, as the discovery of the large corresponding Tænia
furnished with three rows of hooks is not to be expected in European
beasts of prey, and in Redon’s case _C. acanthotrias_ as well as _C.
cellulosæ_ occurred simultaneously.

The duration of life of _C. cellulosæ_ in man is very long; cysticerci
of the eye have been known to persist for twenty years, and in
cysticercus of the brain ten to nineteen years may elapse from the
first appearance of cerebral symptoms until death. Dead cysticerci may
shrivel up or become calcified, perhaps also undergo fatty degeneration
and then absorption. Finally, it may be mentioned that if particular
proof is required that _C. cellulosæ_ of man belongs to the cycle of
development of the _Tænia solium_, such proof has been furnished by

  NOTE.--_Tænia tenella_, mentioned on p. 332, was ascribed by Cobbold
  to cysticerci of the muscular system of sheep. It has, however,
  been demonstrated that these cysticerci belong to the cycle of
  development of _Tænia marginata_ (dog) (_Cysticercus tenuicollis_,
  from the omentum of sheep); but as already stated _C. cellulosæ_ also
  occurs in sheep. Chatin himself swallowed the cysticercus, which
  Cobbold termed _C. ovis_, without causing a Tænia to develop in his
  intestine. Müller also vainly sought to induce infection with _C.
  tenuicollis_ in his own person. On the other hand, the feeding of
  a dog with _Cysticercus ovis_ resulted in the production of _Tænia

*Tænia bremneri*, Stephens, 1908.

Characterized by the large size of the gravid segments. The largest was
32 by 9 mm. Smallest 21 by 6 mm. Average 28·6 by 8·5 mm. Mode 21 by
6 mm. Uterine branches twenty-two to twenty-four in number. Calcareous
bodies numerous, 15·2 µ in diameter. Eggs maximum 45·6 µ by 41·8 µ.
Smallest 34·2 µ by 30·4 µ. Mode 38 µ by 30·4 µ.

*Tænia marginata*, Batsch, 1786.

  Syn.: T. e. _Cysticerco tenuicolli_, Küchenmeister, 1853.

  This species, which in structure resembles _Tænia solium_, lives
  in the intestine of the dog and the wolf. It attains 1·5 to 4 m.
  in length, possesses a double crown of thirty to forty hooks, on
  an average thirty-six to thirty-eight hooks, and in its larval
  stage (_Cysticercus tenuicollis_) lives in the peritoneal cavity of
  ruminants and the pig, occasionally in the monkey and squirrel.

[Illustration: FIG. 240.--Large and small hooklets of _Tænia
marginata_. 280/1. (After Leuckart.)]

  It is included in this work because, according to one statement,
  _C. tenuicollis_ is supposed to have been observed in man in North
  America; but the case is not quite certain, as the number of hooks
  was less than in _C. tenuicollis_ and coincided with _C. cellulosæ_,
  although the size of the cysticercus appeared to point to _C.
  tenuicollis_. A yet earlier statement of Eschricht, that _Cysticercus
  tenuicollis_ had been observed in Iceland in the liver of a man, is
  undoubtedly due to an error.

*Tænia serrata*, Goeze, 1782.

  This parasite attains a length of from 0·5 to 2 m., possesses a
  double crown of thirty-four to forty-eight (mostly forty) hooks. It
  lives exclusively in the intestine of the dog, the corresponding
  cysticercus (_Cysticercus pisiformis_) living in the mesentery of the
  hare and rabbit. We mention this species with all reserve amongst
  the parasites of man, because Vital states that he has observed it
  twice in Constantine (Algeria) in human beings. The data, however,
  are not sufficient to characterize the species. It is highly probable
  that they relate to _Tænia solium_. Galli-Valerio even swallowed five
  specimens of _Cysticercus pisiformis_, but without result.

*Tænia crassicollis*, Rud., 1810.

  I only mention this species from the intestine of the domestic cat
  because Krabbe regards its occurrence in man as possible. It attains
  a length of 60 cm. and is armed; its cysticercus (_Cysticercus
  fasciolaris_) lives in the liver of mice and rats. In Jutland,
  according to Krabbe, chopped-up mice (spread on bread) are eaten
  raw, being a national remedy for retention of urine, and this custom
  affords the possibility of the introduction of _C. fasciolaris_ into
  the intestine of man (_Nord. med. Arkiv_, 1880, xii).

*Tænia saginata*, Goeze, 1782.

  Syn.: _Tænia solium_, L., 1767 (_pro parte_); _Tænia cucurbitina_,
  Pallas, 1781 (p.p.); _Tænia inermis_, Brera, 1802. Moquin-Tandon,
  1860; _Tænia dentata_, Nicolai, 1830; _Tænia lata_, Pruner,
  1847; _Bothriocephalis tropicus_, Schmidtmuller, 1847; _Tænia
  mediocanellata_, Küchenmeister, 1855; _Tænia zittavensis_,
  Küchenmeister, 1855; _Tænia tropica_, Moquin-Tandon, 1860; _Tænia_
  (_Cystotænia_) _mediocanellata_, Leuckart, 1863.

The length of the entire tapeworm averages 4 to 8 to 10 m. and more,
even up to 36 m. According to Bérenger-Feraud it attains a length of
74 m. (?) The head is cubical in shape, 1·5 to 2 mm. in diameter; the
suckers are hemispherical (0·8 mm.) and are frequently pigmented;
there is a sucker-like organ in place of the rostellum, and this also
is frequently pigmented. The neck is moderately long and about half
the breadth of the head; the proglottids, the number of which averages
more than 1,000, gradually increase in size; the mature detached
segments are shaped exactly like pumpkin-seeds, and are about 16 to
20 mm. in length and 4 to 7 mm. in breadth. The genital pores alternate
irregularly and are situated somewhat behind the middle of the lateral
margin. There are twenty to thirty-five lateral branches at each side
of the median trunk of the uterus, and these again ramify. The eggs
are more or less globular, the egg-shell frequently remains intact and
carries one or two filaments; the embryonal shell (embryophore) is
thick, radially striated, is transparent and oval; it is 30 µ to 40 µ
in length, and 20 µ to 30 µ in breadth. Several segments simultaneously
are usually passed spontaneously with defæcation.

[Illustration: FIG. 241.--Mature segment of _Tænia saginata_, G., with
distended uterus. 2/1.]

[Illustration: FIG. 242.--Cephalic end of _Tænia saginata_ in the
contracted condition. 8/1.]

[Illustration: FIG. 243.--_Tænia saginata._ 19, egg with external
shell. 20, without (embryophore). (After Leuckart.)]

  Malformations are not uncommon, and resemble those of _Tænia solium_;
  a triangular form has been termed _T. capensis_ by Küchenmeister, and
  _T. lophosoma_ by Cobbold, names that naturally possess as little
  value as does the term _T. fenestrata_ for fenestrated specimens.
  Moreover, _T. solium_, var. _abietina_, Weinld., 1858, which was
  evacuated by an Indian, was probably a _T. saginata_ with somewhat
  close uterine branches. It is regarded by Stiles and Goldberger as a
  doubtful subspecies.

_T. saginata_ in its adult condition lives exclusively in the
intestinal canal of man.[291] The corresponding cysticercus is
_Cysticercus bovis_, and is found almost exclusively in the ox; it is
small, 7·5 to 9 mm. in length and 5·5 mm. in breadth, may easily escape
notice, and requires from three to six months for its development.
Numerous experiments have confirmed the connection of _Cysticercus
bovis_ with _Tænia saginata_; indeed, the cysticercus was only
discovered by feeding experiments after attention had been called to
the ox as the probable intermediary host of this Tænia.

[291] Abnormal migrations of this species have also been known.
Compare, amongst others, Stieda, A., “Durchbohr. d. Duod. u.
d. Pancreas durch eine Tænia,” _Centralbl. f. Bakt., Path. und
Infektionsk._, 1900, xxviii (1), p. 430.

  Medical men observed that weakly children who were ordered to eat
  raw scraped beef to strengthen them contracted _T. saginata_. It
  was found, moreover, that Jews, who are prohibited from eating pork
  from religious motives, suffered especially from _T. saginata_;
  when _T. solium_ was found to occur in a Jew he often confessed to
  having eaten pork; and finally it was found that certain nations--for
  instance, the Abyssinians--frequently harbour _T. saginata_, and only
  eat beef--raw by preference.

  These observations led Leuckart, in 1861, to feed young calves
  with the proglottids of _T. saginata_ in order to discover the
  corresponding cysticercus, which was then not known. This experiment
  was successful. Similar experiments, with similar results, were
  then conducted by Mosler (1863), Cobbold and Simonds (1864 and
  1872), Röll (1865), Gerlach (1870), Zürn (1872), Saint Cyr, Jolicœur
  (1873), Masse and Pourquier (1876), and Perroncito, in 1876. The
  attempts to infect goats, sheep, dogs, pigs, rabbits and monkeys were
  unsuccessful. Only Zenker and Heller were able to infect kids, and
  Heller infected one sheep, but these are exceptions.

[Illustration: FIG. 244.--A piece of the muscle of the ox, with three
specimens of _Cysticercus bovis_. Natural size. (After Ostertag.)]

Artificial infections of human beings with _Cysticercus bovis_ to
obtain the tapeworm were less numerous, and indeed quite superfluous,
yet this was also done by Oliver (1869) in India, and Perroncito (1877)
in Italy. The experiments of the latter prove that the extracted
cysticerci of the ox certainly perish in water at 47° to 48° C.

  It is a remarkable circumstance that, at least as regards Central
  Europe, _C. bovis_ in the ox, after natural infection, was so seldom
  found that almost every case was published as a rarity; whereas the
  Tænia is very frequent in man. The reason for this is that in Germany
  cattle are not severely infected, and that the small, easily dried-up
  cysticerci easily escape notice in the large body of the host.
  Hertwig, the late director of the town cattle market in Berlin, in
  1888, pointed out that the cysticercus of the ox is found chiefly in
  the musculi pterygoide externi and interni, and since that time a far
  greater number of infected oxen have been found in Berlin.

      Year   | Number of oxen | Infected | Proportion
             |  slaughtered   |          |
     1888–89 |    141,814     |   113    |  1 : 1,255
     1889–90 |    154,218     |   390    |  1 :   395
     1890–91 |    124,593     |   263    |  1 :   474
     1891–92 |    136,368     |   252    |  1 :   541
     1892–93 |    142,874     |   214    |  1 :   672

  Since 1892 an increase has taken place in the number of oxen infected
  with cysticercus, but this is probably attributable to the more
  general and searching examinations. In the slaughter-houses of
  Prussia the number of infected beasts was as follows:--

    1892      567
    1893      686
    1894      748
    1895    1,143
    1896    1,981
    1897    2,629

  The condition was most frequent in Neisse (3·2 to 4 per cent.),
  Eisenach (1·91 per cent.), Ohlau (1·57 per cent.), Oels i. Schles.
  (1 per cent.), Marienwerder (0·34 to 1·2 per cent.). The flesh of
  oxen only slightly infected (containing not more than ten living
  cysticerci) is sold in pieces of not more than 5 lb. to consumers
  after having been rendered innocuous by cooking, or by pickling for
  twenty-one days in 25 per cent. salt brine, or hanging for twenty-one
  days in suitable refrigerators; oxen in which only one cysticercus is
  found are allowed free commerce, and those strongly infected (_i.e._,
  containing more than ten living cysticerci) may only be used for
  industrial purposes.

  It is a striking fact that more bulls than cows are infected
  (according to Reissmann, in Berlin, from 1895 to 1902, 0·446 per
  cent. bulls, 0·439 per cent. oxen, and 0·262 per cent. cows), the
  explanation of which, according to Ostertag, is that most oxen are
  killed when young, when also infection most readily takes place, and,
  further, that the larva later on in life can be completely atrophied.

The cysticercus of the ox has hitherto been found in man on very rare
occasions. Arndt (_Zeitschr. f. Psychiat._, xxiv) mentions a case in
the brain, Heller in the eye, and Nabiers and Dubreith also in the
brain (_Journ. méd. Bordeaux_, 1889–1890, p. 209); but the diagnoses
are not quite certain, as absence of hooks occasionally occurs in
_Cysticercus cellulosæ_.

_Tænia saginata_ is the most frequent tapeworm of man (with the
exception of _Dibothriocephalus latus_ in a few districts), and the
parasite is widely distributed over the surface of the globe; it has
been known in the East for ages, so far as data are available; it is
frequent in Africa, America, and Europe. Its frequency has perceptibly
increased during the last few years, but a decrease should soon take
place in consequence of the extent and improvement of the official
inspection of meat.

The following table shows the relative frequency of the Cestodes of

                  |         |Number of |   _T.    |  _T.  |_Dibr.|_Dipyl.|Undeter-
       Author     |  Year   |  cases   |saginata_ |solium_|latus_|canin._| mined
  Parona (Milan)  |  1899   |   150    |   121    |   11  |   4  |  --   |   14
  Parona (Italy)  | 1868–99 |   513    |   397    |   71  |  26  |  --   |   19
  Krabbe (Denmark)|  1869   |   100    |    37    |   53  |   9  |   1   |   --
    "        "    | 1869–86 |   200    |   153    |   24  |  16  |   8   |   --
    "        "    | 1887–95 |   100    |    89    |   --  |   5  |   6   |   --
    "        "    |1896–1904|    50    |    41    |    1  |   5  |   3   |   --
  Blanchard       |  1895   |     ?    | 1,000    |   21  |  --  |  --   |   --
   (Paris)        |         |          |          |       |      |       |
  Stiles          |  1895   |{more than|more than}|   --  |   3  |  --   |   --
   (United States)|         |{  300    |   300   }|       |      |       |
  Schoch          |  1869   |    19    |    16    |    1  |   2  |  --   |   --
   (Switzerland)  |         |          |          |       |      |       |
  Zaeslein        |  1881   |     ?    |   180    |   19  |   ?  |       |
   (Switzerland)  |         |          |          |       |      |  --   |   --
  Kessler         |  1888   |     ?    |    22    |   16  |  47  |  --   |   --
   (Petrograd)    |         |          |          |       |      |       |
  Mosler          |  1894   |   181    |   112    |   64  |   5  |  --   |   --
   (Greifswald)   |         |          |          |       |      |       |
  Bollinger       |  1885   |    25    |    16    |    1  |   8  |  --   |   --
   (Munich)       |         |          |          |       |      |       |
  Vierordt        |  1885   |   121    |   113    |    8  |  --  |  --   |   --
   (Tübingen)     |         |          |          |       |      |       |
  Mangold         | 1885–94 |   128    |   120    |    6  |   8  |  --   |   --
   (Tübingen)     |         |          |          |       |      |       |

*Tænia africana*, v. Linst., 1900.

[Illustration: FIG. 245.--Mature segment of _Tænia africana_. The ovary
is in the middle, and behind it are the shell gland and vitellarium;
at the sides are the testicles, and externally the excretory canals;
the cirrus pouch, the vas deferens and the vagina are on the left.
Magnified. (After v. Linstow.)]

This worm measures over 1·3 m. in length. The segments are all broader
than they are long. The scolex is unarmed and is provided with an
apical sucker (0·16 mm.). The parasite measures 1·38 mm. in breadth,
1·03 mm. in width; the suckers measure 0·63 mm. in diameter. The neck
is very short and somewhat broader than the scolex; number of segments
about 600; the hindmost segments measure 7 mm. in length and 12 to
15 mm. in breadth. The genital pores alternate irregularly in the
middle of the lateral margin; the testes are very numerous and occupy
the entire medullary layer; the vas deferens is much convoluted; the
cirrus pouch is pyriform and thick walled; the cirrus and vagina
are beset with bristles directed outwards; the receptaculum seminis
is fusiform; the ovary is large and double, and consists of radially
placed club-shaped tubes that do not anastomose and do not branch;
the vitellarium is at the posterior border of the proglottids, the
round shell gland in front of it; the uterus consists of a median
trunk and fifteen to twenty-four non-ramified lateral branches on each
side; the embryonal shell is thick and has radial stripes--it may be
round (31·2 µ to 33·8 µ) or oval (39 µ, by 33·8 µ); the spines of the
oncospheres measure 7 µ to 8 µ in length (fig. 197).

[Illustration: FIG. 246.--Proglottis of _Tænia africana_, with uterus.
Magnified. (After v. Linstow.)]

[Illustration: FIG. 247.--Head of _Tænia africana_; apical surface.
Magnified. (After v. Linstow.)]

At present only two specimens are known; they came from a black soldier
from the vicinity of Lake Nyasa. The cysticercus is unknown; perhaps it
lives in the zebu, the flesh of which the Askaris are in the habit of
devouring uncooked.

*Tænia confusa*, Ward, 1896.

Length 8·5 m., breadth about 5 mm. The scolex is unknown; there is
no neck; number of proglottids 700 to 800, always longer than they
are broad; the hindmost measure 35 mm. in length, 4 to 5 mm. in
breadth; the genital pores alternate irregularly behind the middle
of the lateral margin; testicles numerous; vas deferens not much
coiled; the cirrus pouch thick walled, elongated and club-shaped, with
globular vesicula seminalis; the cirrus is beset with little hairs;
the receptaculum seminis is globular; ovary small, double; each half
is bean-shaped; vitellarium narrow, triangular; shell gland globular;
uterus with median trunk and fourteen to eighteen short ramified
lateral branches on either side. The embryophores are oval (39 µ by
30 µ), thick and radially striated.

[Illustration: FIG. 248.--_Tænia confusa_: mature segment showing
central uterine stem, bilobed ovary, globular shell gland, triangular
vitellarium, scattered testes, cirrus, vas deferens, and vagina. 15/1.
(After Guyer.)]

[Illustration: FIG. 249.--_Tænia confusa_: gravid segment. 25/1. (After

Of this species only two specimens have been recorded; they occurred in
human beings and were sent at different times to the first describer
of them by a doctor in Lincoln (Nebr.). Perhaps _Tænia solium_, var.
_abietina_, Weinld., which was found in a Chipeway Indian, is of the
same species in spite of the shorter segments.

*Tænia echinococcus*, v. Sieb., 1853.

  Syn.: _Tænia nana_, v. Ben., 1861 (_nec_ v. Sieb., 1853);
  _Echinococcifer echinococcus_, Weinld., 1861.

_Tænia echinococcus_ measures 2·5 to 5 or 6 mm. in length; the head
is 0·3 mm. in breadth, and has a double row of twenty-eight to fifty
hooklets (on an average thirty-six to thirty-eight) on the rostellum.

The size and form of these hooklets vary (the larger ones are 0·040
to 0·045 mm. in length, the smaller ones are 0·030 to 0·038 mm. in
length). The suckers measure 0·13 mm. in diameter; the neck is short;
there are only three or four segments, the posterior segment being
about 2 mm. in length and 0·5 mm. in breadth. The genital pores
alternate; there are forty to fifty testicles; the vas deferens
is spirally coiled; the cirrus pouch is pyriform. The ovary is
horseshoe-shaped with the concavity directed backwards; the vitellarium
double, each half almost bean-shaped, at right angles to the plane of
the segment; the shell gland is round. The median trunk of the uterus
is dilated when filled with eggs and (instead of lateral branches)
has lateral diverticula. It is not unusual for the eggs to form local
heaps. The embryonal shell (embryophore) is moderately thin, with
radial striæ, almost globular, 30 µ to 36 µ in diameter.

[Illustration: FIG. 250.--_Tænia echinococcus_: the cirrus sac, the
vagina, uterus, ovary, shell gland and vitellarium, and the testicles
at the sides are recognizable in the second proglottis; the posterior
proglottis shows the uterus partly filled with eggs, as well as the
cirrus sac and the vagina. 50/1.]

When mature this parasite lives in the small intestine of the domestic
dog, the jackal, and the wolf, and apparently also in _Felis concolor_,
and is usually present in great numbers; it can also be transmitted
experimentally to the domestic cat, one successful result out of seven
(Dévé).[292] The larval stage (_Echinococcus polymorphus_) lives in
various organs--chiefly in the liver and lungs--of numerous species
of mammals (twenty-seven), especially in sheep, ox and pig, and it is
even not uncommon in man, though the Tænia itself has never been found
in a human being; accordingly man can only acquire the echinococcus by
ingesting the eggs of the “dog worm.” The dogs disseminate the eggs of
_Tænia echinococcus_ wherever they go, or carry them to their mouths
and coats by biting up the evacuated segments, and are thus able to
transmit them directly to human beings (by licking them or making use
of the same crockery, etc.). In other cases the oncospheres, enclosed
in the embryophores, must withstand desiccation for a time and then (as
when the dogs are “kissed” or otherwise caressed) are transmitted into
or on to man. As echinococcus disease in man is always very dangerous,
it would be a matter of general interest to prevent dogs being
infected by destroying the echinococci,[293] and all measures would be
justifiable which would diminish the superfluous number of house-dogs
(for instance, high taxes); measures should also be adopted to limit
the association of men with dogs, particularly in such frequented
places as restaurants, railway carriages and tram-cars.

[292] In Iceland 28 per cent. of the dogs are infected with this Tænia,
in Lyons 7·1 per cent., in Zurich 3·9 per cent., in Berlin 1 per cent.,
and in Copenhagen 0·4 per cent. In Australia even 40 to 50 per cent. of
the dogs are affected. It is, however, a question whether, in addition
to _Tænia echinococcus_, a second analogous form is not involved, as
the form from _Canis dingo_ attains a length of 10 to 30 mm.

[293] Mosler, F., “Ueb. Mittel z. Bekampfg. endem. vork.
Echinococcuskrank.,” _Deutsch. med. Zeit._, 1889, No. 72.

  Echinococcus is very common in slaughtered animals; in Germany,
  however, the figures in the reports of the abattoirs present an
  erroneous view in so far as, besides the total number of animals
  slaughtered, only the numbers of those organs (liver and lungs) are
  published that were so severely infected with echinococci that, even
  when the parasites were “shelled” out, the flesh could not be placed
  upon the market and was therefore “condemned.”

  In Berlin the following animals were slaughtered:--

    Year | 1889–90 | 1890–91 | 1891–92 | 1892–93 | 1896–97 |  1902
   Oxen  | 154,218 | 124,593 | 136,368 | 142,874 | 146,612 | 153,748
   Sheep | 430,362 | 371,943 | 367,933 | 355,949 | 395,769 | 434,155
   Pigs  | 442,115 | 472,859 | 530,551 | 518,073 | 694,170 | 778,538

  During the same years the following were condemned in consequence of
  being infected with echinococci:--

       |Lung |Liver|Lung |Liver|Lung |Liver|Lung |Liver|Lung |Liver|Lung  |Liver
  Oxen |7,266|2,418|5,792|1,938|4,497|1,721|2,563|  739|3,284|1,156| 2,507|  791
  Pigs |6,523|5,078|5,083|3,735|6,037|4,374|6,785|4,312|7,888|5,398| 9,544|9,233

  Nevertheless there are statistics that give the total number of
  animals infected with echinococcus:--

   Author |    Place    |     Oxen     |    Sheep     |     Pigs
  Längrich|Rostock i. M.|26·2 per cent.|37·0 per cent.| 5·4 per cent.
  Olt     |Stettin      | 7·1    "     |25·8    "     | 7·3   "
  Steuding|Gotha        |24·6    "     |35·4    "     |21·4   "
  Prettner|Prague       |23·2    "     | 5·5    "     |      ?

  In Güstrow, in Mecklenburg, half of the animals slaughtered are said
  to be infected with echinococcus; in Wismar 25 per cent. of the oxen,
  15 per cent. of the sheep and 5 per cent. of the pigs are infected;
  according to Mayer, in Leipzig, 3·79 per cent. native pigs, 24·47
  per cent. Hungarian pigs, and 13·09 per cent. of sheep were infected
  with echinococcus; at the same time it was stated that in regard
  to the native pigs the liver was more frequently affected than the
  lungs (3·81 per cent. as compared with 0·26 per cent.); in sheep the
  lungs were more frequently infected (12·71 per cent. to 3·73 per
  cent.), whereas in the Hungarian pigs both organs were almost equally
  infected (14·78 per cent. to 12·03 per cent.).

  The data of Lichtenheld, in Leipzig, give the frequency with which
  various organs were affected, as shown in the following table:--

             | Cattle  |       Pigs        |  Sheep  | Horses
             |         |    ♂    |    ♀    |         |
             |per cent.|per cent.|per cent.|per cent.|per cent.
  Lungs      |  69·3   |  16·2   |  21·4   |  52·2   |   5·5
  Liver      |  27·0   |  74·2   |  72·0   |  44·9   |  94·5
  Spleen     |   2·2   |   3·2   |   2·7   |   2·9   |   --
  Heart      |   0·75  |   3·2   |   1·3   |   --    |   --
  Kidneys    |   0·75  |   3·2   |   1·3   |   --    |   --
  Sub-       |         |         |         |         |
   peritoneal|         |         |         |         |
   tissue    |   --    |   --    |   1·3   |   --    |   --


[Illustration: FIG. 251.--_Echinococcus veterinorum_: the fibrous sac
enclosing the echinococcus has been opened and laid back in five parts,
so that the surface of the bladder worm may be seen, with the brood
capsules, visible to the naked eye, showing through it. Natural size.
(After Leuckart.)]

An echinococcus is a spherical or roundish bladder full of a watery
liquid, which originates by liquefaction of the oncosphere, and in man
may attain the size of a child’s head, but remains smaller in cattle
(the size of an orange or apple). The thin wall of the bladder is
composed of an external laminated cuticle (ectocyst) and an internal
germinal or parenchymatous layer (endocyst). The latter again exhibits
two layers: an outer layer of small cells that are less sharply
defined, and an inner layer of larger cells. It contains, in addition,
calcareous corpuscles, muscular fibres and excretory vessels. It is
rich in glycogen.

[Illustration: FIG. 252.

FIGS. 252 and 252A.--Diagrams of mode of formation of brood capsule and
scolices. (1) Wall of mother cyst, consisting of ectocyst and endocyst;
(2) theoretical stage of invagination of wall; (3) a brood capsule with
the layers of the wall in the reverse position to that in the mother
cyst; (4) evagination of wall; (5) invagination; (6) fusion to form the
solid scolex; (7) invagination of fore-part of scolex into hind-part.
(_Note._--The size of the scolex is much out of proportion to the brood
capsule.) (Stephens.)]

The development in cattle often remains stationary at the bladder
stage, and they are then called “acephalocysts,” or _Echinococcus
cysticus sterilis_. According to Lichtenheld, sterile cysts occur in
80 per cent. of cases in cattle, in 20 per cent. in pigs, and in 7·5
per cent. in sheep. In other cases large numbers of small, hollow
BROOD CAPSULES are formed in the germ layer, but are not arranged in
any particular order. The order of the layers is just the reverse
in them to what it is in the parent cyst, that is to say, they have
inside a thin non-laminated cuticle and the parenchymatous layer on
their external surface. These, theoretically at least, may be regarded
as invaginations of the bladder wall giving rise to a cavity with the
cuticle internal and the parenchymatous layer external. If we suppose
the orifice to close, we should then get an isolated cavity with
cuticle internal and parenchymatous layer external, as in the brood
capsule (fig. 252). If we next suppose an evagination of the wall of
the brood capsule to occur at one point we should get a hollow process
_lined_ with cuticle; at the bottom of this we get the scolex and
hooklets formed, and a little higher up the tube the suckers (fig. 252,
4). If this hollow scolex is now pictured as being invaginated we get
a hollow scolex _covered_ with cuticle and lined by a parenchymatous
layer projecting into the cavity of the brood capsule. The two sides of
this hollow scolex now fuse and we get a solid scolex projecting into
the cavity. Finally, if we imagine once more the rostellum and suckers
invaginated into the posterior part of the scolex we get the condition
as frequently found in the brood capsules, _i.e._, a scolex covered
with cuticle projecting into the cavity, with the rostellum and suckers
invaginated into the posterior portion of the scolex (fig. 252A, 7).

[Illustration: FIG. 252A.]

A large hydatid may contain many thousands of brood capsules. Each
brood capsule is about as big as a pin’s head, and may contain ten to
thirty or more scolices. The delicate wall of the brood capsules may
rupture, so that the scolices are now free in the mother cyst. These
free scolices and also free brood capsules constitute what is known as
“hydatid sand,” which settles at the bottom of a glass when hydatid
fluid is poured into it. This form occurs chiefly in domesticated
animals and is termed _E. veterinorum_, Rud., or _E. cysticus fertilis_.

In man, and only rarely in cattle, the mother cyst first forms
“daughter cysts” (_E. hominis_, Rud. [fig. 255]), which, though smaller
than the “mother cyst,” resemble it in the structure of their walls;
thus they are covered externally by a laminated cuticle and internally
by the parenchymatous layer. They originate:

[Illustration: FIG. 253.--Section through an invaginated echinococcus
scolex. _Cf._ fig. 252A, 7. × 300. (After Dévé.)]

[Illustration: FIG. 254.--A piece of the wall of an _Echinococcus
veterinorum_ stretched out and seen from the internal surface. A few
brood capsules (the outline of which is only faintly shown), with
scolices directed towards their interior and exterior. 50/1.]

(1) Between the laminæ of the cuticle of the mother cyst from small,
detached portions of the parenchymatous layer; during their growth
they bulge inwardly or outwardly and may separate themselves entirely
from their parent cyst. In the latter case they lie between the mother
cyst and the capsule of connective tissue formed by the host (_E.
granulosus_ or _E. hydatidosus exogenus_); when growing inwardly they
reach the interior of the mother cyst (_E. hydatidosus endogenus_).
Their number is very variable and does not depend on the size of the
mother cyst. They are as big as, or bigger than, gooseberries.

(2) According to some authors, endogenous daughter cysts arise also
from a _metamorphosis of scolices_ that have separated off from the
brood capsule. This takes place in the following way: Fluid accumulates
in the interior of the scolex, so that eventually nothing remains
except a sac consisting of cuticle lined by parenchyma. The cuticle
gradually thickens and several layers form (fig. 257).

[Illustration: FIG. 255.--_Echinococcus hominis_ in the liver. The
fibrous capsule and the wall of the echinococcus have been incised,
so that the endogenous daughter cysts may be seen. Reduced. (After
Ostertag, from Thoma.)]

[Illustration: FIG. 256.--Section through an echinococcus scolex in
process of vesicular metamorphosis, twenty-six days after insertion in
the pleural cavity. × 250. (After Dévé.)]

(3) _Transformation of Brood Capsules into Daughter Cysts._--This is
also held to be possible by various observers. New epithelial layers
are deposited between the cuticle which lines the brood capsule and
the outer parenchymatous layer. This parenchymatous layer gradually
disappears and a new parenchymatous layer forms in the interior from
the parenchyma of the scolex or scolices. Although it appears strange
that a completely formed scolex with specifically differentiated
tissues and organs should retrogress to more primitively organized
matter, and again become a proliferating bladder, yet we can hardly
doubt that the older observations, regarding such a vesicular
metamorphosis, of Bremser (1819), v. Siebold (1837), Naunyn (1862),
Rasmusser (1866), Leuckart (1881), Alexinsky (1898), Riemann (1899),
Dévé (1901), and Perroncito (1902) are correct.

(4) Further, _a fourth method_ of formation of daughter cysts is
described by Naunyn as occurring in sterile hydatids, _i.e._, those
containing no brood capsules. In this case a portion of the mother wall
of the hydatid gets constricted off.

[Illustration: FIG. 257.

Figs. _257_ and 257A.--Diagram of transformation of a scolex into a
daughter cyst (1 to 3): 1, scolex in brood capsule; 2, liquefaction
of scolex; 3, daughter cyst; and (4 to 6) of a brood capsule into
a daughter cyst; 4, brood capsule with scolex; 5, deposition of
new epithelial layers on the inner layer of the parenchyma; 6,
disappearance of outer parenchyma and formation of inner parenchyma
from the parenchyma of scolex, which has now disappeared. (_Note._--The
scolices are out of proportion to the brood capsules and to the
daughter cysts. Stephens.)]

It has also been established that not only daughter cysts transplanted
into animals develop further (Lebedeff, Andrejew, Stadnitzky,
Alexinsky, Riemann), but that this also holds good if only hydatid
_scolices_ from man or animals are transplanted into animals
(rabbits). They develop into echinococci and can then give rise to
brood capsules and scolices. As Dévé further established, hydatid
_scolices_ are not capable of developing in guinea-pigs, while
corresponding experiments with rabbits are in the large majority of
cases successful where the scolices are introduced subcutaneously
or into the pleural or peritoneal cavities. It is only in the case
of _daughter cysts_ that further growth is obtained in the case of
guinea-pigs. Finally it appears, as has been already stated, that brood
capsules can transform themselves into daughter cysts, but according to
Dévé only within the mother cyst, not after transplantation. Daughter
cysts that have been formed in the mother cyst of man and animals
behave themselves just as the mother cyst does, _i.e._, they can remain
sterile, or give rise to brood capsules and scolices, or even again
to fresh cysts--granddaughter cysts. The mother cyst can also die, so
that the daughter cysts then lie in the cavity of the connective tissue
capsule. The number of the daughter cysts in either case may attain
several thousands.

[Illustration: FIG. 257A.]

  The echinococcus fluid, which originally is formed from the blood
  of the host, is light yellow, with a neutral or slightly acid
  reaction; its specific gravity averages 1009 to 1015. It contains
  about 1·5 per cent. of inorganic salts, half of which is common salt;
  in addition (besides water) it contains sugar, inosite, leucine,
  tyrosin, succinic acid (associated with lime or soda) and albumens
  which are not coagulated by heat; occasionally also the fluid has
  been found to contain hæmatoidin and uric acid salts (in echinococcus
  of the kidneys), which doubtless demonstrates that the echinococcus
  liquid originates from the host. It has been generally assumed that
  echinococcus fluid contains a toxic substance the escape of which
  into the body cavity (at operation or by bursting of a hydatid
  cyst) produces more or less severe symptoms (fever, peritonitis,
  urticaria), so much so that one speaks of hydatid intoxication. The
  investigations of Kobert, Joest, etc., have, however, shown the
  harmlessness of fresh undecomposed hydatid and cysticercus fluid for
  rabbits, mice and guinea-pigs, whether inoculated intraperitoneally,
  subcutaneously or intravenously. Contrary data or clinical experience
  must accordingly depend on other factors.

According to the researches of Leuckart, the growth of the echinococcus
is very slow; four weeks after infection the average size is only 0·25
to 0·35 mm., at the age of eight weeks it is 1 to 2·5 mm., and at this
period the formation of the central cavity commences; at the age of
five months, and with a size of 15 to 20 mm., the first brood capsules
with scolices are formed. The consequence of this gradual increase of
size is that the organ attacked can maintain its functions by vicarious
hypertrophy, and that many echinococci induce no special symptoms and
cannot even be diagnosed, the latter circumstance being due to their
hidden position.

The echinococcus cannot be said to be scarce in man, as is shown by the
following table for Central Europe:--

         Place        |       |    No. of    |No. of cases|Percentage
                      |Period |_post-mortems_| of echino. |
  Rostock             |1861–83|     1,026    |     25     |   2·43
  Greifswald          |1862–93|     3,429    |     51     |   1·48
  Jena                |1866–87|     4,998    |     42     |   0·84
  Breslau             |1866–76|     5,128    |     39     |   0·761
  Berlin              |1859–68|     4,770    |     33     |   0·69
  Würzburg            |   --  |     2,280    |     11     |   0·48
  Göttingen           |   --  |       639    |      3     |   0·469
  Dresden             |1852–62|     1,939    |      7     |   0·36
  Münich              |1854–87|    14,183    |     35     |   0·25
  Vienna              |  1860 |     1,229    |      3     |   0·24
  Prague              |   --  |     1,287    |      3     |   0·23
  Kiel                |1872–87|     3,581    |      7     |   0·19
  Zürich, Basle, Berne|   --  |     7,982    |     11     |   0·13
  Erlangen            |1862–73|     1,755    |      2     |   0·11

These, however, are only cases that have become known by _post-mortem_;
in addition, there are cases that have been treated medically, of which
there are a few statements, at all events relating to the principal
districts of Germany. According to Madelung, one case of echinococcus
occurs in every 1,056 inhabitants in the town of Rostock, in the
district of Rostock one to every 1,283, in Schwerin one to every 5,887,
and in Ludwigsort one to every 23,685; according to Peiper, in Upper
Pomerania one case occurs to every 3,336, in the district of Greifswald
one to every 1,535 inhabitants. The northern districts of Pomerania are
more affected than the southern ones.

  Accordingly, echinococcus is also considerably more frequent in
  cattle in Pomerania. On an average in Germany 10·39 per cent. oxen,
  9·83 per cent. sheep, and 6·47 per cent. pigs are infected, whereas
  in Upper Pomerania 37·73 per cent. oxen, 27·1 per cent. sheep, and
  12·8 per cent. pigs are infected; in Greifswald, indeed, 64·58 per
  cent. oxen, 51·02 per cent. sheep, but only 4·93 per cent. pigs are
  infected. In accordance with these figures _Tænia echinococcus_ must
  be frequent in dogs in Pomerania, especially in Upper Pomerania; on
  the other hand, the conjecture that the frequency of echinococcus in
  Mecklenburg is explained by the occurrence of _Tænia echinococcus_ in
  foxes has not been confirmed, as the fox does not harbour this worm
  in Mecklenburg.

Beyond the European continent, echinococcus is frequent in the
inhabitants of Iceland, Argentine, Paraguay and Australia. In Iceland,
according to Finsen, 1 in every 43 inhabitants is affected with
echinococcus; according to Jonassen the proportion is 1 to 63; this
is due to the habits of the people of Iceland or, in fact, to the
frequency of _Tænia echinococcus_ in dogs, and the prevalence of the
hydatid in cattle. In certain districts of Australia it is just as
frequent. In Cape Colony, Egypt and Algeria echinococcus is not rare,
but it is scarce in America and in Asia, with the exception of the
nomadic tribes of Lake Baikal.

[Illustration: FIG. 258.--Hooklets of echinococcus. _a_, of
_Echinococcus veterinorum_; _b_, of _Tænia echinococcus_, three weeks
after infection; _c_, of the adult _Tænia echinococcus_; _d_, the
three forms of hooklets outlined one within the other. 600/1. (After

Echinococcus attacks persons of every age, though it is rare in
children up to 10 years of age and in old people. It occurs most
frequently between the ages of 21 and 40 years. According to all
statistics it preponderates in women (about two-thirds of the cases).
The liver is its favourite seat (57·1 per cent. of the cases); next
in order come the lungs (8 per cent.), kidneys (6 per cent.), cranial
cavity, genitalia, organs of circulation, spleen (3·8 per cent.), etc.
As a rule one organ only is invaded; multiple occurrence may originate
from one infection, or eventually from a later infection (?), or it may
come to pass that from some cause (through the spontaneous rupture of
an echinococcus, or the rupture of one caused by an injury or surgical
operation) daughter cysts, brood capsules or scolices escape into the
abdominal cavity,[294] where they settle or become transformed and
go on growing. In the distribution of this secondary echinococcus
the great powers of motility of the free scolices must be taken into
account (Sabrazès, Muratet, and Husnot).

[294] In such cases the toxic effects of the echinococcus fluid
usually--if not always--manifest themselves. Such effects are
manifested by severe symptoms of poisoning being set up, by urticaria,
peritonitis, and ascites, and not infrequently they cause a fatal

  Human echinococci may also die at various stages of development,
  become caseous or calcified, or may be absorbed, the cause for this
  being either disease of the hydatid itself or inflammation of its
  connective tissue capsule; the discovery of the laminated cuticle,
  which has great powers of resistance, or the finding of the hooklets
  of the scolices is sufficient to form a conclusion as to the nature
  of such formations.

Siebold (1853) was the first to rear _Tænia echinococcus_ in the dog
by feeding it with the echinococcus of cattle and especially of sheep.
Küchenmeister, van Beneden, Leuckart, Railliet and others obtained
similar results, and Thomas, Naunyn, Krabbe and Finsen succeeded in
rearing _T. echinococcus_ in dogs from the bladder worms of human
beings; these grow comparatively slowly (one to three months[295])
and only during the process of growth develop their hooklets in their
definite form (fig. 258). It lies in the nature of things that dogs,
whether experimentally or naturally infected, almost always harbour
_T. echinococcus_ in large quantities. That cats exceptionally harbour
these worms has been already mentioned (Dévé). Finally, Leuckart
infected young pigs by feeding them with mature segments.

[295] According to Perroncito the scolices had not formed proglottids
nine days after feeding, but the latter were present twenty-four days
after feeding, although the formation of eggs had not begun.

*Echinococcus multilocularis* (alveolar colloid).

In addition to the form of echinococcus already described, and which is
also frequently termed _Echinococcus unilocularis_, there is a second
form which occurs in man as well as in animals, and which is termed _E.
multilocularis_, s. _alveolaris_ (alveolar colloid).

It was originally regarded as a tumour; its animal nature was first
established by Zeller and R. Virchow. The parasite, which varies in
size from that of a fist to a child’s head, presents a collection
of numerous cysts, measuring between 0·1 and 3 to 4 mm. to 5 mm. in
diameter, which are embedded at first in a soft, connective tissue
stroma; the cut surface has therefore a honeycomb appearance. The cysts
are surrounded by a pellucid and laminated cuticle, and each according
to its size encloses either a small-celled tissue or a cavity lined by
a parenchymatous layer; the fluid contained in such a cavity may be
transparent, or is rendered opaque by globules of fat, bile-pigment,
hæmatoidin and fat crystals. According to some authors all or most of
these cysts intercommunicate; others state that this is the case at
least as regards the cuticle. The scolices are by no means found in
all the cysts, and when present only a few, rarely half, of the cysts
contain scolices (one or more); it is supposed that at least some of
these scolices are formed in brood capsules, and that the former are
capable of undergoing a cystic metamorphosis.

One circumstance is peculiar to the multilocular echinococcus of man,
namely, the disintegration that sets in at certain stages; in the
centre of the parasite a cavity forms that frequently becomes very
large and is filled with a purulent or brownish or brownish-green
viscid fluid; in this fluid one finds shreds of the wall of the
cavity, calcareous bodies, echinococcus cysts, also scolices and
hooklets, as well as fat globules and crystals of hæmatoidin,
margarine and cholesterin and concretions of lime. Such ulcerative
processes, according to Ostertag, are never present in the multilocular
echinococcus of oxen,[296] in which the separate cysts are larger and
the connective tissue integument less powerfully developed.

[296] This may perhaps be explained by the fact that the hosts are
slaughtered before the parasites have attained the size or other
conditions necessary to disintegration.

[Illustration: FIG. 259.--_Echinococcus multilocularis_ in the liver of
the ox. Natural size. (After Ostertag.)]

Hardly anything positive is known with regard to the development of
the alveolar echinococcus; its peculiar conformation is attributed by
some to enormous infection of oncospheres, by others to the abnormal
situation of one oncosphere; a few authors ascribe it to infection
of lymphatic vessels, others to infection of the biliary ducts or to
peculiarities of the surrounding hepatic tissue; Leuckart ascribes it
to a grape-like variety of form which continues budding; a few more
recent authors consider multilocular echinococcus to be specifically
different from unilocular echinococcus, and therefore also different
the species of Tænia arising from them. Melnikow-Raswedenkow is also
of this opinion. According to this author the oncospheres infect
the lumen of a branch of the portal vein in Glisson’s capsule of
the liver and grow into an irregularly shaped formation (chitinous
coil), which breaks through the vascular walls and thus forms the
alveoli. So far the data coincide well with Leuckart’s opinion of
the original grape-like form of the _Echinococcus multilocularis_;
according to Melnikow-Raswedenkow the “granular protoplasmic
substance” (parenchymatous layer) is not only present in the interior
of the loculi but also outside, and, moreover, “ovoid embryos”
are supposed to develop in the chitinous coils, which, “thanks to
their amœboid movements, reach the lumen of a vessel, where, under
favourable circumstances, they begin to develop further,” that is to
say, they become “chitinous cysts with fantastic outlines,” or also
“single-chambered chitinous cysts”; scolices may develop in both. Dévé,
however, considers that these embryos are only prolongations of the
protoplasmic layer which secondarily cuticularize.

  The multilocular echinococcus, which in man produces a severe disease
  and almost always leads to premature death, infects most frequently
  the liver, but may also be found primarily in the brain, the spleen
  and the suprarenal capsule; from the liver by means of metastasis it
  may reach the most various organs, especially those of the abdomen,
  but also the lungs, the heart, etc. Up to 1902, 235 cases have been
  described and up to 1906, 265, being 70 from Russia, 56 from Bavaria,
  32 from Switzerland, 30 from the Austrian Alps, 25 from Würtemberg;
  the remaining cases are distributed over Central Germany, Baden,
  Alsace, France, Upper Italy, North America. In some the origin is
  doubtful; in any case after Russia, the mountainous South of Europe
  is the principal region of distribution. As to the domesticated
  animals, the same parasite is found principally in the ox (according
  to Meyer, in Leipzig, in 7 per cent. of the oxen affected with
  echinococcus); it is rarer in the sheep and very scarce in the pig.

It has already been mentioned above that recently the multilocular
echinococcus has been stated to be specifically different from hydatid
or unilocular echinococcus. To this may be added the fact that
Mangold, who fed a young pig with oncospheres of a Tænia reared from
the multilocular echinococcus, found two growths in the liver four
months later, which he took to be _E. multilocularis_, and consequently
one has to assume the existence of two different worms. The chief
defender of this view, already put forward by Vogler, Mangold, and
Müller, is Possett. He bases his opinions on (1) the more restricted
distribution of the multilocular hydatid, the former occurring in
districts where only cattle are raised, the latter where sheep-breeding
is established; (2) that those engaged in looking after sheep are
attacked by multilocular, whereas those looking after cattle are
attacked by unilocular hydatid; (3) that among the cases of unilocular
hydatid occurring in the distribution areas of multilocular hydatid no
transitions between the two forms are observed; (4) on the difference
in the hooks both in the hydatid as well as in the Tænia stage; the
hooks of _Tænia echinococcus_ are plump, sharply curved, and have a
short posterior root process the length of which is to that of the
total length as 1 to 4·7, whereas on the contrary the hooks of the
alveolar echinococcus are more slender, slightly bent, and have a long
posterior root process (1 to 2·5); and (5) on the form of the uterus,
which in the alveolar Tænia has the form of a spherically distended sac


(1) _Precipitin Reaction._--Mix equal parts of hydatid fluid (of
the sheep) and serum of patient. Keep at 37° C. The reaction is not
decisive as it may be given by normal sera.

(2) _Complement Deviation._--Required: (1) Hydatid fluid of sheep
(antigen), (2) guinea-pig complement, (3) patient’s serum, (4) red
cells of sheep, (5) hæmolytic serum (of rabbit) against sheep’s red
cells, (6) 0·8 per cent. salt solution. Mix the antigen + patient’s
serum (heated) + complement + salt solution at 37° C. for one hour. Add
red cells of sheep + hæmolytic serum. Allow to stand for half an hour
at 37° C. It is imperative to make adequate control observations. An
example will indicate the method. Salt solution 1·3 c.c. + patient’s
serum (heated) 0·2 c.c. + hydatid fluid 0·4 c.c. + complement 0·1 c.c.
of serum diluted to a quarter strength + hæmolytic serum and red cell
emulsion 1 c.c. Result: no hæmolysis, _i.e._, the patient’s serum
contains specific (echinococcus) antibodies.



J. W. W. STEPHENS, M.D., B.C., D.P.H.

  Bilaterally symmetrical animals, without limbs and with a body
  cavity in which the gut or other organs float. They are generally

Class. *NEMATODA.*

  Nemathelminthes with an alimentary canal.

  Nematodes are as a rule elongated round worms of a filiform or
  fusiform shape; their length varies according to the species from
  about 1 mm. to 40 to 80 cm. The outer surface of the body is
  smooth or annulated, and at certain points provided with papillæ,