Synonyms: J. cazalboui, T. viennei, T. bovis, T. angolense, T. caprae.
Disease: Souma. T. vivax is also sometimes found in mixed infections of cattle with T. congolense and T. brucei.
Hosts: Cattle, sheep, goats, camels, horse. Antelopes and the giraffe are reservoir hosts in Africa, and the deer (Odocoileus gymnotis) 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. Central 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 u 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 species. 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 infected. 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 mechanical.
Pathogenesis: T. vivax is most important 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 cause a mild disease, but in West Africa they are usually fatal in some types of cattle. Virulent strains may also occur in East Africa. Unsworth (1953) found that T. vivax is highly pathogenic for zebu cattle in laboratory infections, and that when these cattle were exposed to infection under natural conditions in Nigeria, all of them died.
Camels are less seriously affected than cattle. T. vivax is apparently more pathogenic for sheep than other trypanosomes, and may be found in the central nervous system. It is apparently less pathogenic for goats. It causes a chronic disease, often with spontaneous recovery, in horses. It is not pathogenic for dogs, pigs and monkeys, and only slightly so for the common laboratory rodents.
The signs of disease are similar to those caused by T. congolense. There is a wide variation in virulence between different strains, but the virulence of any particular strain tends to remain constant.
Diagnosis: T. vivax is detected most readily in lymph node smears. Large numbers are found in the blood only in early infections. Inoculation of laboratory animals is not particularly satisfactory; inoculation of sheep or goats is better, the trypanosomes appearing in 7 to 10 days.
Cultivation: Same as for other trypanosomes.
Treatment: T. vivax can be successfully treated with the same drugs and in the same dosages as T. congolense. It is perhaps slightly more resistant, but not significantly so.
Control: Control measures are the same as those for T. congolense infections. In areas where tabanids are the vectors, measures directed against these flies should be practiced.
This species is similar to T. vivax, differing from it morphologically only in being smaller. It is 12 to 20 u long, with an average of about 16 u. It occurs in cattle, sheep, goats and antelopes, causing a disease similar to that caused by T. vivax (Wilson, 1949). Laboratory rodents are refractory to infection. T. uniforme occurs only in Uganda and the Belgian Congo. It is transmitted by tsetse flies in the same way as T. vivax.