78 THE ANIMAL PARASITES OF MAN 



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 /). 

 Laveran's views on these bodies have already been given on p. 74. 



(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 1 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 2 (1911) found a similar periodic, cyclical variation in the try- 

 panosomes 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. rhodes- 

 iense 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. 



In sheep and goats T. rhodesiense causes an acute disease, marked 

 by high fever, oedema of the face, and keratitis, as shown by Bevan 

 and others, death resulting after a relatively short period. T. gam- 

 biense gives rise, in these animals, to no symptoms except fever, which 

 may be overlooked. T. rhodesiense produces keratitis in dogs. 



Stannus and Yorke (1911) observed T. rhodesiense in animals 

 inoculated from a case of sleeping sickness in Nyasaland. Sir D. Bruce 

 and his colleagues 3 have shown (1912) that T. rhodesiense is the 



1 Proc. Roy. Soc., B, Ixxxii, p. 411. ~ Annals Trop. Med. and Paras //<?/., iv, p. 417. 



3 Proc. Roy. Soc., B, Ixxxv, p. 423. 



