Beyond Tsetse – Implications for Research and Control of Human African Trypanosomiasis Epidemics

Epidemics of both forms of human African trypanosomiasis (HAT) are confined to spatially stable foci in Sub-Saharan Africa while tsetse distribution is widespread. Infection rates of Trypanosoma brucei gambiense in tsetse are extremely low and cannot account for the catastrophic epidemics of Gambian HAT (gHAT) seen over the past century. Here we examine the origins of gHAT epidemics and evidence implicating human genetics in HAT epidemiology. We discuss the role of stress causing breakdown of heritable tolerance in silent disease carriers generating gHAT outbreaks and see how peculiarities in the epidemiologies of gHAT and Rhodesian HAT (rHAT) impact on strategies for disease control.

TrendsTsetse flies are historically linked with human African trypanosomiais (HAT). However, for Gambian HAT (gHAT), this link is not supported by field data, which show foci of disease unrelated either to tsetse distribution or fly infection rates.The focal nature of gHAT and Rhodesian HAT (rHAT) may relate to differences within human populations in susceptibility to or tolerance of trypanosome infection, evolved during the Bantu expansion period.Epidemics of gHAT emerge when trypanotolerant silent carriers of disease are stressed, particularly by famine, entraining epigenetic events and generational epidemic cycling.This view challenges present policy around diagnosis and treatment of gHAT that demands visualisation of parasites before treatment can commence. If HAT is to be eliminated as a public health problem by 2030, investments will be needed to improve early diagnosis paying special attention to women of child-bearing age.