THE HEMOFLAGELIATES 



57 



It is only slightly pathogenic for sheep 

 and goats, and apparently non-pathogenic 

 for cattle, horses or dogs, altho it may 

 infect them. The rabbit appears to be the 

 only susceptible laboratory animal. There 

 is a great deal of variation in pathogenicity 

 between strains, and indeed marked 

 changes can occur in the pathogenicity of 

 a single strain. 



T. slniiae occurs mostly in East 

 Africa and the Belgian Congo, but it has 

 also been found in other parts of Africa 

 where T. co)igolense occurs. 



T. simiae differs morphologically 

 from T. congolense in being polymorphic 

 instead of monomorphic. It varies in 

 length from 12 to 2^\i. About 90% of its 

 forms are long and stout, with a conspicu- 

 ous undulating membrane, about 7% are 

 long and slender with an inconspicuous un- 

 dulating membrane, and about 3% are 

 short, with an inconspicuous undulating 

 membrane. A free flagellum is usually 

 absent, but has been reported in from 1 to 

 4% of different strains. 



This species is transmitted in the 

 warthog reservoir host by tsetse flies, in- 

 cluding Glossliia morsitans and G. brevi- 

 palpis, in which it develops in the midgut 

 and proboscis. Tsetse flies also transmit 

 it to swine, but once it has been introduced 

 into a herd, it can apparently be trans- 

 mitted mechanically by horseflies and 

 other blood-sucking flies (Unsworth, 1952). 



T. simiae is more resistant to drugs 

 than the other African trypanosomes. 

 Antrycide methyl sulfate is probably the 

 best drug, but it may not be completely 

 effective. It is injected subcutaneously 

 at the rate of 5 mg/kg; more than one in- 

 jection is probably necessary. 



Control measures are the same as 

 for T. briicei. In addition, horseflies and 

 other biting flies should be controlled. 



Disease : Souma. T. vivax is also 

 sometimes found in mixed infections of 

 cattle with T. congolense and T. briicei. 



Hosts : Cattle, sheep, goats, camels, 

 horse. Antelopes and the giraffe are res- 

 ervoir hosts in Africa, and the deer (Odo- 

 coileiis g\'))inolis) in Venezuela (Faisson, 

 Mayer and Pifano, 1948). The pig, dog 

 and monkey are refractory to infection. 

 The small laboratory rodents are difficult 

 to infect. 



Location : Blood stream, lymph. Cen- 

 tral nervous system infections have been 

 described in sheep. 



Geographic Distribution : T. vivax 

 is found thruout the tsetse fly belt in Africa. 

 It has, however, spread beyond this region 

 to other parts of Africa and to Central 

 America, South America, the West Indies 

 and Mauritius. 



Morphology : T. vivax is 20 to 27 ji 

 long and monomorphic. The posterior end 

 is typically rounded, a free flagellum is 

 always present, the kinetoplast is large 

 and terminal, and the undulating membrane 

 is inconspicuous (Fairbairn, 1953). 



Life Cycle : The original vectors of 

 T. vivax and still the most important in 

 Africa are tsetse flies, including Glossina 

 morsitans, G. tachinoides and other spe- 

 cies. Development takes place only in the 

 proboscis. The trypanosomes turn into 

 the crithidial form, multiply in this form 

 and then turn into metacyclic, infective 

 trypanosomes which pass to the hypopharynx 

 and infect new hosts when the tsetse flies 

 bite. The flies become infectious as early 

 as 6 days after they themselves were in- 

 fected. 



Horseflies and other tabanids may act 

 as vectors; they are the only ones in the 

 New World and in Africa outside the tsetse 

 zone. In this case transmission is mechan- 

 ical. 



TRYPANOSOMA VIVAX 

 ZIEMANN, 1905 



Synonyms : T. cazalboui, T. viennei, 

 T. bovis, T. angolense, T. caprae. 



Pathogenesis : T. vivax is most im- 

 portant in cattle, in which the disease is 

 similar to that caused by T. congolense. 

 According to Fairbairn (1953), T. vivax 

 infections of cattle in East Africa usually 



