
doi: 10.5772/29530
Trypanosomosis is an important disease of both humans and animals commonly found in most parts of Africa and South America (Swallow, 2000). The tsetse fly (Glossina) is responsible for biological (cyclical) transmission while haematophagus arthropod vectors of the family, Tabanidae, Stomoxynae and Hippoboscidae are responsible for its mechanical transmission (Soulsby, 1982). Transplacental transmission has also been recorded in cattle (Ogwu et al., 1992). Trypanosoma congolense, T. vivax and T. brucei have been reported to cause nagana in cattle while T. evansi caused surra in camels (Camelus dromedarieus) (Mbaya et al., 2010). In humans, Trypanosoma brucei gambiense and Trypanosoma brucei rhodeseinse are responsible for human sleeping sickness in West and East Africa respectively, while T. cruzi, transmitted by triatomid bugs (Triatoma magista) is responsible for transmitting chagas diseases to humans in South America (Solano et al., 2003). The T. brucei group of trypanosomes (T. brucei, T. b. gambiense, T. b. rhodesianse and T. evansi) mostly invade tissues (humoral) whereas, T. congolense and to a lesser extent T. vivax and T. cruzi predominantly restrict themselves to the blood circulation (haemic) (Igbokwe, 1994; Mbaya et al., 2011). The mechanism or pathophysiology of anaemia in trypanosomosis is complex and multifactorial in origin (Naessens et al., 2005). It initiates a cascade of events leading to haemolytic anaemia and cardiovascular collapse (Anosa, 1988). In human trypanosomosis, disseminated intravascular coagulation has been reported (Barret-Connor et al., 1973). Among the complex and multifactorial etiologies associated with the anaemia is haemolysin, a sensory/excretory product of living trypanosomes. This product is known to lyse red blood cells in the absence of antibodies (in-vitro) and haemodilution (in-vivo). This mechanism has been adequately described in gold fish (Carassius auratus) infected with Trypanosoma dahilewskyi (Nazrul-Islam and Woo, 1991) and in murine models infected with T. b. rhodesiense (Naessens et al., 2005).
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