ECOLOGY, COMMENSALISM AND PARASITISM 383 



cause of surra in horses; T. hippicum in mules; T. venezuelensis in 

 horses and dogs; T. equinum of horses and others. In leeches also 

 with inoculative infection, the trypanosomes accumulate in the 

 mouth region. 



Development in the posterior station of invertebrates, with con- 

 taminative infection, is characteristic not only of T. lewisi in the 

 rat flea but of the majority of small mammalian trypanosomes. 



Trypanosoma equiperdum, the cause of dourine in horses, has no 

 invertebrate host, transmission occurring at coitus. 



The genus Schizotrypanum chagas differs from Trypanosoma in 

 having an intracellular leishmania phase in tissues of the vertebrate 

 host. It was discovered in the form of crithidia by Chagas in Brazil 

 in 1907, in the posterior gut of the biting bug Triatoma megista. 

 When inoculated in a marmoset, they gave rise to typical trypano- 

 somes which Chagas called Schizotrypanum cruzi. Later Chagas 

 found them in cats and in children and associated them with a 

 widely-spread disease of unknown etiology now generally known as 

 Chagas' disease. The trypanosomes do not reproduce as free 

 flagellates but may enter nearly any type of cell of the body where, 

 as Leishmania forms, they reproduce by active division. Another 

 species, S. pipistrelli, was found by Chatton and Courrier (1921) 

 in the bat Vesperugo pipistrellus, in which it forms large (up to 200/1) 

 reproductive cysts in various organs of the bat. 



Human trypanosomiasis, known as sleeping sickness in Africa, is 

 essentially a disease of the lymphatics. This, however, is a later 

 stage of the disease which, as Bruce demonstrated, begins as an 

 irregular fever which was known clinically as Gambia fever before 

 its relation to sleeping sickness was discovered. At this time the 

 flagellates are multiplying in the blood and may be detected by 

 direct examination more readily than at other times. Their accu- 

 mulation leads to antibody formation and the trypanosomes are 

 destroyed in large numbers, the irregular fever being due to the 

 liberation of endotoxins through disintegration of the parasites. 

 Search for living forms of trypanosomes during the febrile period is 

 thus almost invariably negative. 



In this early period, which may last from one or two weeks to 

 several years, there is little or no evidence of glandular swelling 

 (Bruce, Kleine, Thiroux, et at.), indicating that the trypanosomes 

 have not yet become established in the lymphatic system. The use 

 of medicaments (atoxyl, urotropine, tartar emetic, etc.) at this 

 period is usually successful and a cure results, but when the try- 

 panosomes have become established in the lymphatics they are less 

 easily reached, and once established in the cerebrospinal fluid the 

 disease is incurable (Reichenow-I)oflein). Here the trypanosome 

 multiplication is rapid and at the same time the lymphocytes become 

 markedly increased in number. The peculiar nervous and psychic 



