Immunization. gQ5 



trypanosomes, indicates that strictly specific immune bodies develop in the affected 

 animals. Such, however, have not yet been demonstrated with certainty in an 

 objective manner. In this regard the complement fixation method, in which blood 

 containing parasites or material from organs was used as antigen, gave uncertain 

 and varying results (Weber, Manteufel & Woithe). Better results were obtained 

 by Levaditi & Mutermilch, when they carried out experiments with trypanosomes 

 separated from blood corpuscles. They could always demonstrate complement 

 fixing bodies in the serum of guinea pigs treated with trypanosome extract or in 

 the course of infection. These substances were specific for the genus trypanosoma, 

 but not for the individual species and varieties, therefore they could not be differen- 

 tiated by this method. Further, the complement fixing substances proved different 

 from the trj^^anolysines, which form in great numbers at the height of the infec- 

 tion (see p. 801), and exert their dissolving action also in test tube experiments. 



According to Laveran & Mesuil, human blood serum has a similar destructive 

 action on the trypanosomes of nagana, surra and mal de caderas, as the arsenic 

 acid. Serum of animals, even of those which have recovered from the disease, 

 or which have been repeatedly infected, has no such action, and on the other hand 

 the human serum is harmless for the trypanosomes of sleeping sickness. 



Literature. Nocard & Leclainche, Maladies microbiennes, Paris 1903. II. 575. 

 — • Laveran & Mesnil, Trypanosomes et trypanosamiases, Paris 1904. — Liihe, Handb. 

 d. Tropenkrkh., 1906. III. 92. — Sander, ibid., 690. — Nocht & Mayer, Hdb. d. p. 

 M. Erganzgsb., 1906. 1. — Sauerbeck, Ergebn. d. allg. Path., 1906. X. 305. — 

 Kaestner, ibid., 1907. XI./l. 455. — Ehrlich B. kl. W., 1907. Nr. 9-12. — Man- 

 teufel & Woithe, Arb. d. G.-A., 1908. XXIX. 452. — Koch, Beck & Kleine, ibid., 

 1909. XXI. 1. — Levaditi & Yamanouehi, Soe. biol., 1908. LXV. 23. — Levaditi 

 & Mutermilch, Z. f. Immf., 1909. II. 702. — Kleine, D. m. W., 1909. 924 u. 1257. 

 — Doflein, Protozoenkunde, 11. Aufl. 1909. 350. (Mostly with literature.) 



(a) Nagana. 



{Tsetse disease.) 



History. The disease was described as a destructive cattle 

 disease by Livingstone (1857) during his voyage in Zambesia, and was 

 connected by him with the sting of the native tsetse fly. Its cause was 

 discovered by Bruce in 1894, in the territory of the Zulu Kaffirs, 

 (nagana=without strength, debilitated), and the first detailed descrip- 

 tions of the clinical symptoms were also made by him. Shortly after- 

 Avard the disease, as well as its cause was investigated thoroughly by 

 Kanthack, Durham & Blandford and by Plimmer & Bradford, while 

 Theiler deserves special credit for the epidemiology. The problem of 

 the propagation of the nagana trypanosomes was studied by Koch and 

 recently by Kleine and Battaglia, while McNeal, and Laveran & Mesnil 

 were successful in their artificial cultivation. 



Occurrence. The disease used to be spread widely through 

 the entire Central and South Africa, wdiere it annihilated at 

 times the cattle of entire districts. Eecently it disappeared 

 from the south, so that at present it occurs only in some out- 

 of-the-way localities of Zulu land. The infected territory was 

 limited partly by the driving northwards of the game, prin- 

 cipally however by the invasion of rinderpest in 1896 and 1897, 

 as at that time besides cattle, numerous game animals and 

 buffaloes fell victims, and at the same time the tsetse fly also 

 disappeared from those localities (Theiler). 



Trypanosome affections occur also in Northern Africa, but the 

 classification of these, with the exception of dourine, has not been cleared 



