Trypanosoma brucei — Overview

African Sleeping Sickness Trypanosome learn more about names for this taxon

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Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense are protozoan parasites that are the cause of nearly all human African trypanosomiasis (HAT, or African sleeping sickness); the subspecies Trypanosoma brucei brucei infects domestic and wild animals but usually not humans (but see the phylogeographic analysis by Balmer et al. 2011, which concludes that these three "subspecies" are not actually genetically or historically distinct lineages). These extracellular parasites are transmitted by the bite of Glossina tsetse flies. For the most part, at least, Trypanosoma brucei rhodesiense occurs in eastern and southern Africa and Trypanosoma brucei gambiense (which accounts for most cases of HAT) occurs in central and western Africa--although continued expansion of T. brucei rhodesiense to the northwest (e.g., by trade in infected cattle) may eventually result in overlapping ranges (Picozzi et al. 2005). HAT is limited to sub-Saharan Africa by the range of its tsetse fly vector. As of 2010, the best available estimates suggested a total of about 50,000–70,000 cases of HAT in the world. Left untreated, HAT leads to coma and death. Trypanosoma brucei gambiense infection is characterised by a chronic progressive course. The estimated average duration of infection is around 3 years, evenly divided between an initial haemolymphatic stage and a subsequent meningoencephalitic stage, during which the central nervous system is invaded. Abnormal sleep patterns are a leading symptom of the second stage (and account for the disease's colloquial name). Trypanosoma brucei rhodesiense disease is typically acute, with death occurring within weeks or months. (Fevre et al. 2008; Brun et al. 2010)

Three major HAT epidemics are known to have ravaged Africa in modern history. The first, which largely affected equatorial Africa, took place between 1896 and 1906, killing an estimated 800,000 people. The second major epidemic occurred between 1920 and the late 1940s and prompted the colonial powers to invest in vector control and in mobile teams to undertake active surveillance of the population--two strategies that remain the pillars of control today. These control mechanisms were effective, and the disease was almost eradicated in the early 1960s. However, with the advent of political independence across the continent came a collapse of surveillance and control activities in most countries with endemic HAT, often exacerbated by civil conflicts. This collapse led to a progressive re-emergence of the disease, which reached a peak in the late 1990s in the Democratic Republic of the Congo (DRC), Angola, Central African Republic, southern Sudan, and Uganda. Subsequent to this peak of infection in the 1990s, increased control activities have succeeded in rolling back disease related to Trypanosoma brucei gambiense in several countries. (Brun et al. 2010 and references therein)

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