History of Sleeping Sickness in East Africa

Abstract

SUMMARY The history of human sleeping sickness in East Africa is characterized by the appearance of disease epidemics interspersed by long periods of endemicity. Despite the presence of the tsetse fly in large areas of East Africa, these epidemics tend to occur multiply in specific regions or foci rather than spreading over vast areas. Many theories have been proposed to explain this phenomenon, but recent molecular approaches and detailed analyses of epidemics have highlighted the stability of human-infective trypanosome strains within these foci. The new molecular data, taken alongside the history and biology of human sleeping sickness, are beginning to highlight the important factors involved in the generation of epidemics. Specific, human-infective trypanosome strains may be associated with each focus, which, in the presence of the right conditions, can be responsible for the generation of an epidemic. Changes in agricultural practice, favoring the presence of tsetse flies, and the important contribution of domestic animals as a reservoir for the parasite are key factors in the maintenance of such epidemics. This review examines the contribution of molecular and genetic data to our understanding of the epidemiology and history of human sleeping sickness in East Africa.

Sleeping Sickness in Southeastern Uganda: A SystemsApproach

“…This inherently low transmission potential is influenced by the infectivity of T. brucei spp., which is lower than that of other major tsetse-transmitted trypanosomes. Transmission is favored by a large ratio of flies to humans, a relatively high prevalence of infection in flies and humans, and a high level of contact between flies and hosts (Rogers, 1988;Rogers and Williams, 1993;Hide, 1999). This low transmission potential is responsible for the typical pattern of sleeping sickness in Uganda: generally very low levels of sleeping sickness interrupted by distinct epidemics.…”

“…In another example of the importance of scale, genetic research conducted on the microscopic scale allows for the identification of trypanosome species, strains, genotypes, and isolated clusters (Hide et al, 1996;Hide, 1999). This research has contributed to the understanding of sleeping sickness patterns at the regional and national scales, revealed new information on which trypanosome species may have caused the 1900-1920 Ugandan outbreak (Hide et al, 1996;Welburn et al, 2001), and highlighted the role of cattle movements in parasite spread (Fèvre, 2001;Fèvre et al, 2001).…”

“…The epidemiology, pathology, and ecology of T. b. rhodesiense vary significantly from the more chronic form of sleeping sickness, caused by T. b. gambiense (Mbulamberi, 1994). Early symptoms of acute sleeping sickness include headache, fever, anxiety, and confusion, followed by disruption of sleeping patterns, slurred speech, mental confusion, coma, and eventual death within 6 to 12 months if untreated (Hide, 1999). Trypanosomes infect many species, including cattle and other livestock.…”

“…A second subspecies, T. b. gambiense, causes a chronic form of sleeping sickness and is prevalent predominantly in western and central Africa and southern Sudan. Sleeping sickness has continued to be a significant public health burden in southeastern Uganda, with epidemics in 1901-1915, 1940-1946, and 1976-1989(MacKichan, 1944Hide, 1999;Fèvre et al, 2004). More recently, the spread of sleeping sickness into areas previously thought to be free from the disease has highlighted gaps in the ability of current research to explain and predict the distribution of infection .…”

Multiplex-endonuclease genotyping approach (mega): a tool for the fine-scale detection of unlinked polymorphic DNA markers

“…For epidemiological identification and tracking of the subspecific strains, T. b. garnbiense can be distinguished from T. b. brucei and T. b. rhodesiense (Hide et al 1998;Agbo et al 2002). However, the distinction between T. b. brucei and T. b. rhodesiense has always been more difficult to determine (Godfrey et al 1990;Hide 1999;Agbo et al 2002). Resistance to normal human serum (equivalent to human infectivity) is an important trait that distinguishes T. b. gambiense and T. b. rhodesiense (which are resistant) from T. b. brucei strains (which are sensitive).…”