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Human African trypanosomiasis (HAT), or sleeping sickness, is a vector-borne parasitic disease that is restricted to sub-Saharan Africa. It is caused by extracellular protozoa belonging to the genus Trypanosoma, which are transmitted by the bite of a blood-feeding insect, the tsetse fly (Diptera; Glossina). Two human-pathogenic subspecies of trypanosomes, T. brucei gambiense and T. brucei rhodesiense, cause different forms of the disease: the slow-progressing form (gambiense-HAT) which is endemic in western and central Africa, and the faster progressing form (rhodesiense-HAT) found in eastern and southern Africa.1 About 97% of cases of HAT are due to T. b. gambiense. HAT still has a severe social and economic impact in various countries in sub-Saharan Africa, with an estimated 55 million people at risk and over 10 million people living in areas where gambiense-HAT is considered a public health problem.2 Sleeping sickness has been responsible for devastating epidemics in the twentieth century. However, due to increased disease surveillance efforts and large-scale use of control tools, major improvements have been achieved during the last two decades. Today, the number of newly reported cases is low. The World Health Organization (WHO) has targeted the elimination of HAT as a public health problem by 2020 with a target of fewer than 2000 reported cases per year.2–5 For T. b. rhodesiense-HAT, sporadic cases are diagnosed outside endemic African countries, mainly among travelers from Europe and the United States returning from visits to east African game parks, as well as expatriates and migrants.5–8


T. brucei is a digenetic parasite that is transmitted between mammals by the blood feeding tsetse fly (Fig. 133-1). During its life cycle, the parasite undergoes complex developmental changes in the mammalian host and tsetse fly vector. In the mammalian bloodstream, two life cycle stages are recognized: the proliferative long slender form and the short stumpy trypanosome form. The latter is preadapted for survival in the tsetse fly midgut when ingested during the fly’s blood meal. In addition to blood, T. brucei parasites colonize the interstitial spaces of several other tissues, including brain, adipose tissue, and skin.9–13 When ingested by the tsetse fly through a blood meal on an infected host, the parasite must go through an obligatory and complex life cycle in the alimentary tract and salivary glands of the fly.14 Here, the final developmental stage is the infectious metacyclic stage that is injected into the mammalian host skin through the bite of the infected fly.

FIGURE 133-1

The tsetse fly, vector of the parasites causing human African trypanosomiasis. (Source: Luc Verhelst, Institute of Tropical Medicine Antwerp.)

Both sexes of adult tsetse feed exclusively on vertebrate blood every 2–5 days and can contribute to the transmission of the trypanosome.15 Tsetse flies have a ...

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