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.