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Human African Trypanosomiasis (HAT), or sleeping sickness, is a neglected tropical parasitic disease of humans due to trypanosomes transmitted by tsetse flies (Glossina spp.) in sub-Saharan Africa. Comparable diseases (Animal African Trypanosomiasis—AAT—nagana) are present in domesticated animals and these are an important constraint to animal health and production in Africa (Jordan, 1986; Kabayo, 2002). For HAT, there is no vaccine, no chemoprophylaxis, and treatment is still long and difficult to administer despite recent improvements (Simarro et al., 2012). In most cases HAT is fatal if untreated. The disease affects rural communities in remote parts of Africa, particularly people working outdoors (e.g., farmers, foresters, fishermen, people collecting water) and hence at greater risk of being bitten by tsetse. Two flagellate protozoan parasites cause HAT. Trypanosoma brucei rhodesiense causes the rhodesiense form of the disease (currently 95% of all cases) in Central and West Africa (Simarro et al., 2010). Although it is accepted that tsetse control plays a central role in combatting the rhodesiense form of HAT (Welburn et al., 2009), this has not been the case for the gambiense form. Indeed in the strategy recommended by WHO to control sleeping sickness, active case detection and treatment has always been the first, it not the only method recommended, until very recently. Historically, there have been two clear justifications for this—(1) that vector control is not required and/or that (2) it is too expensive and difficult to organize; we will discuss both.

Is vector control needed to eliminate gambiense human African trypanosomiasis?