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African trypanosomiasis (sleeping sickness) is a parasitic disease transmitted by tsetse flies of the genus Glossina and caused by a group of parasites called trypanosomes.1 West African trypanosomiasis, also called Gambian sleeping sickness, is caused by a subspecies of the extracellular flagellate Trypanosoma brucei known as Trypanosoma brucei gambiense. East African trypanosomiasis, also called Rhodesian sleeping sickness, is caused by T brucei rhodesiense. These diseases exist in Africa wherever the various species of Glossina (ie, the tsetse fly) are found.




African trypanosomiasis has a focal distribution but expands outward during epidemics. About 60 million people live in risk areas of African trypanosomiasis, and the World Health Organization estimates a continent-wide prevalence of both forms of African trypanosomiasis of 300,000 cases; an average of 30,000 new cases of the disease have been reported annually over the last 10 years, although underreporting rates are high.1 Thirty-six sub-Saharan countries are considered endemic for one or the other form of the disease despite that some of them have reported no cases in the last decade.2 The Gambian form is currently a major public health problem over vast areas of Africa from Sudan in the north to northwest Uganda to the Democratic Republic of the Congo to Angola in the south. This form represents more than 90% of reported cases.2 The Rhodesian form continues to present a serious health risk in the Lake Victoria Basin, particularly in eastern Uganda, and there are small pockets of disease endemic in other countries of east and central Africa. A line drawn from north to south through sub-Saharan Africa, roughly following the Rift Valley, differentiates the distribution of the 2 diseases with the Gambian form to the west and the Rhodesian to the east of this notional line.1T brucei rhodesiense is a zoonotic parasite, and wild and domestic animals serve as reservoirs. A number of domestic animals species, including pigs, dogs, goats, sheep, and cattle, may carry human-infective trypanosome species. For T brucei gambiense, the nature of animal reservoirs and its role in disease transmission is somewhat less certain.1




All members of the T brucei complex share a common morphology, biochemistry, and life cycle (eFig. 355.1). Infective metacyclic trypomastigotes are inoculated into subcutaneous tissue of a human or another mammalian host by a bite from the tsetse fly. They are converted to the pleomorphic blood forms: long, slender forms (20–40 by 1 μm) and stumpy forms (15–25 by 3.5 μm). Within the human host, trypomastigotes multiply in blood, lymph, and extracellular spaces. The central nervous system eventually is invaded, where multiplication continues unabated. The tsetse fly is infected with ingestion of a blood meal. Trypomastigotes differentiate into procyclic forms in the midgut where they multiply by binary fission and remain for the next 2 to 3 weeks. Finally, they enter the salivary glands and transform into infective metacyclic trypomastigote ...

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