Overview
- Trypanosomosis in camels is a protozoal disease caused by Trypanosoma evansi (T. evansi) which is transmitted by hematophagous flies including Tabanus and Stomoxys.
- The trypanosomes that cause tsetse-transmitted trypanosomiasis (sleeping sickness)
- Dourine is a chronic venereal disease of horses that is transmitted during coitus and caused by T equiperdum. The disease is recognized on the Mediterranean coast of Africa and in the Middle East, southern Africa, and South America; distribution is probably wider.
- Chagas’ disease, or American trypanosomiasis, is a zoonotic, vectorborne disease transmitted by triatomine bugs and caused by T cruzi.
Transmission
Life Cycle
- Most tsetse transmission is cyclic and begins when blood from a trypanosome-infected animal is ingested by the fly. The trypanosome alters its surface coat, multiplies in the fly, then alters its surface coat again, and becomes infective. T brucei spp migrate within the tsetse from the gut and eventually to the salivary glands; the cycle for T congolense stops at the hypopharynx, and the salivary glands are not invaded; the entire cycle for T vivax occurs in the proboscis. Therefore, the location within the tsetse can be useful in identifying the parasite species. The animal-infective form in the tsetse salivary gland is referred to as the metacyclic form. The life cycle in the tsetse may be as short as 1 wk with T vivax or extend to a few weeks for T brucei spp.
Pathogenesis
- Infected tsetse inoculate metacyclic trypanosomes into the skin of animals, where the trypanosomes reside for a few days and cause localized inflammation (chancres). They enter the lymph and lymph nodes, then the bloodstream, where they divide rapidly by binary fission. In T congolense infection, the organisms attach to endothelial cells and localize in capillaries and small blood vessels. T brucei species and T vivax invade tissues and cause tissue damage in several organs.
- The immune response is vigorous, and immune complexes cause inflammation, which contributes to fever and other signs and lesions of the disease. Antibodies against the surface-coat glycoproteins kill the trypanosomes. However, trypanosomes have a large family of genes that code for variable surface-coat glycoproteins that are switched in response to the antibody response, evading immunity. This antigenic variation results in persistence of the organism. Antigenic variation has prevented development of a protective vaccine and permits reinfections when animals are exposed to a new antigenic type.
Clinical signs
- Severity of disease varies with species and age of the animal infected and the species of trypanosome involved. The incubation period is usually 1–4 wk. The primary clinical signs are intermittent fever, anemia, and weight loss. Cattle usually have a chronic course with high mortality, especially if there is poor nutrition or other stress factors. Ruminants may gradually recover if the number of infected tsetse flies is low; however, stress results in relapse.