Abstract
Human African trypanosomiasis (HAT) is caused by two subspecies of trypanosomes, Trypanosoma brucei gambiense and T.b. rhodesiense. Clinically, the disease is characterized by an early stage during which patients report non-specifi c symptoms such as fever and malaise, and trypanosomes are found in the blood or in lymph node aspirates. While in the case of T.b. rhodesiense this early stage develops within days of the infective bite and rapidly progresses over days or weeks to a severe disease, patients with T. b. gambiense HAT can remain asymptomatic for months or years, or have only intermittent fever. Eventually, when the disease progresses to the late stage with involvement of the central nervous system (CNS), the patients develop somnolence, constant headaches, behavior changes or other neurological symptoms, and trypanosomes are now found in the cerebrospinal fl uid (CSF). If untreated, this is ultimately fatal within a few months. HAT is endemic only in sub-Saharan Africa between latitudes 15° north and 15° south, corresponding to the distribution of its vector (1, 2). T.b. gambiense HAT is endemic in western and central Africa and T.b. rhodesiense HAT in eastern and southern Africa. Uganda is the only country where both subspecies are present. The disease re-emerged in several countries in the 1990s, following the breakdown of control programs so that the distribution of sleeping sickness nowadays parallels that of wars that have recently devastated parts of Africa, with the highest incidences occurring in the Democratic Republic of Congo (DRC), Angola, and Sudan. The total number of cases is estimated to be ≈100,000 per year, with at least one-third of them remaining undetected and untreated (2). In 2000, WHO estimated that the burden of HAT corresponded to 66,000 deaths per year and 2.05 million disability-adjusted life-years lost (3). The highest incidence is seen in DRC, where 20–25,000 cases are reported annually; given the breakdown of its health system, the true incidence could be at least twice as high (4). DRC is followed by Angola (≈12,000 cases), southern Sudan (several thousands), Congo-Brazzaville and Central African Republic (≈1,000 cases) while the incidence is much lower in Gabon, Cameroon, and Equatorial Guinea. In West Africa, the disease has disappeared from several countries for ecologic reasons, but a few hundred cases are diagnosed each year in Cote d’Ivoire, Guinea, and Nigeria. In East Africa, an epidemic of Rhodesian HAT in the historical Busoga focus of southeastern Uganda has been much reduced by tsetse fl y trapping and case fi nding and only a few hundreds cases are now reported (5). There remains, however, Gambian HAT in the northwest of the country. Only residual T.b. rhodesiense HAT endemicity occurs elsewhere in eastern and southern Africa, with ≈200 reported cases per year in Tanzania, and fewer cases in Zambia, Kenya, Malawi, and Mozambique. Each year, a few dozen cases of T.b. rhodesiense trypanosomiasis are diagnosed in tourists who visited the game parks of East and Southern Africa (6), while ≈20 cases of T.b. gambiense HAT are diagnosed in Africans who have migrated outside the endemic areas (7). The determinants of the epidemiology of T.b. gambiense HAT are: (a) the long duration (months to years) of infection in human hosts with intermittent parasitemia; (b) man-fl y contact and infection rates among the tsetse vector; (c) and the impact of active case fi nding (1). In contrast, T.b. rhodesiense trypanosomiasis is a zoonosis and to some extent an occupational disease, with game animals and cattle harboring the parasite and sustaining the sporadic human disease (1). Interhuman spread occurs during epidemics but generally this subspecies offers less potential for large-scale spread because of its acute nature. So far, there is no evidence of an interaction between HAT and HIV infection, but this would need to be examined again now that HIV has spread to rural areas (8). The overwhelming majority of cases of both T.b. gambiense and T.b. rhodesienese African trypanosomiasis are diagnosed and treated in rural African hospitals with only the most basic laboratory back-up. The diagnosis is generally J. Pepin ( ) Center for International Health, University of Sherbrooke, QC, Canada jacques.pepin@usherbrooke.ca
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