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Epidemiology, pathogenesis, and prevention of African trypanosomiasis

Authors
Sanjeev Krishna, MA, BMChB, DPhil, FRCP, ScD, FMedSci
August Stich, MD, MSc, DTMH
Section Editor
Peter F Weller, MD, FACP
Deputy Editor
Elinor L Baron, MD, DTMH

INTRODUCTION

Human African trypanosomiasis (HAT), also known as sleeping sickness, is caused by protozoan parasites transmitted via the bite of a tsetse fly [1]. There are two forms of the disease: an acute form occurring mainly in East Africa and caused by Trypanosoma brucei rhodesiense and a more chronic form occurring mainly in West and Central Africa, caused by Trypanosoma brucei gambiense (table 1) [2,3]. These two species have identical morphologic appearances and both are transmitted by tsetse flies of the genus Glossina. However, the clinical features of infection differ in presentation and prognosis [3,4].

Other Trypanosoma species include T. brucei subspecies brucei, T. lewisi, T. congolense, and T. evansi [4-10] Serum resistance factors lyse animal trypanosomes (including Trypanosoma evansi) and prevent infection in humans, unless there is a host genetic deficiency for these factors [5].

The epidemiology, lifecycle, and prevention of African trypanosomiasis will be reviewed here. The clinical manifestations, diagnosis, and treatment of these infections are discussed separately. (See "Clinical manifestations, diagnosis, and treatment of African trypanosomiasis".)

EPIDEMIOLOGY

There are two forms of human African trypanosomiasis (HAT): an acute form occurring mainly in East Africa and caused by Trypanosoma brucei rhodesiense and a more chronic form occurring mainly in West and Central Africa caused by Trypanosoma brucei gambiense [2]. T. b. gambiense generally causes endemic disease with chronic manifestations (the mean duration of the meningoencephalitic stage is approximately 250 days [11]), while T. b. rhodesiense is an acute epidemic disease (table 2).

In the last century, there have been three severe epidemics of African trypanosomiasis: one between 1896 and 1906, mostly in Uganda and the Congo Basin; one in the 1920s in several Central African countries; and one that began in 1970, which is abating. The 1920s epidemic was arrested using mobile teams that systematically screened millions of at-risk individuals. The disease practically disappeared between 1960 and 1965, and, subsequently, surveillance was relaxed. Civil wars, displacement of people, economic difficulties, and slackening in vector control measures subsequently allowed reemergence of disease in several foci.

            

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Literature review current through: Nov 2016. | This topic last updated: Wed Apr 27 00:00:00 GMT+00:00 2016.
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