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Measuring only 9–18 μm in length, T. congolense is the smallest of the African trypanosomes. It is monomorphic although short and long strains also occur. One of its characteristic features is the absence of a free flagellum although the cell tapers finely at the anterior end, so it is possible to believe mistakenly that one is present. The posterior end is blunt and the kinetoplast marginal. The undulating membrane is not pronounced but this together with the absence of a free flagellum does not restrict its ability to move – although authors differ in their opinion about whether its activity is active or sluggish.

Within the blood and lymphatic system of their mammalian host, the trypomastigotes of T. congolense multiply by dividing by longitudinal fission. Several tsetse fly species (e.g., Glossina morsitans) are responsible for transmitting T. congolense with different species being of particular importance in different areas. Following ingestion by a tsetse fly, the parasites differentiate into procyclic trypomastigotes and undergo a similar migration pattern a sequence of transformations to T. brucei. However, T. congolense does not invade the tsetse fly salivary glands. Instead, the epimastigotes attach themselves to the walls of the proboscis and after transforming into the metacyclic stage, the parasites migrate to the hypopharynx region. As in T. brucei, a form of sexual reproduction occurs in some strains of T. congolense.

Trypanosoma congolense occurs throughout southern, East and West Africa and infects many domestic mammals (e.g., cattle, sheep, horses, pigs, dogs) and wild game (e.g., antelopes, warthogs). Except in unusual circumstances, T. congolense does not present a risk to humans (Truc et al. 2013). In addition, although the trypanolytic activity of normal human serum normally kills T. congolense, some strains are resistant to it (Van Xong et al. 2002).

Trypanosoma congolense is of primary concern for its effect on domestic cattle, and it is a major cause of economic loss to cattle farmers throughout the affected regions. It is less harmful to other domestic animals and wild game. In susceptible cattle, T. congolense causes similar symptoms to T. brucei. Therefore, when farmers say that their animals are suffering from ‘nagana’, it could mean that either parasite is the cause. In addition, co‐infections are common. The disease may manifest itself in acute, chronic forms and mild forms. In the acute form, the disease causes anaemia, emaciation and a high parasitaemia in the peripheral circulation. The liver, lymph nodes and spleen enlarge, haemorrhages occur in the heart muscle and kidneys, and the infected animal may die in within 10 weeks of becoming infected. In the chronic form, the symptoms are less severe, and it may be difficult to find the parasites in the blood. There is enlargement of the lymph nodes and liver and signs of degeneration in the kidney, but the infected animal can recover after about a year. In mild infections, it may not be obvious that T. congolense is present. The pathology caused by T. congolense differs from that of T. brucei in that the parasites remain within the circulatory system and the central nervous system is not affected. Anaemia is the most characteristic feature of T. congolense infection and results from the destruction of red blood cells in the liver and spleen although other mechanisms (e.g., inflammatory processes) may also be involved (Noyes et al. 2009). Indigenous breeds of cattle, such as N’dama, are not resistant to T. congolense but have a genetic ability to limit the development of anaemia (Naessens 2006).