Abstract

A causative agent of sleeping sickness, Trypanosoma brucei rhodesiense, is differentiated from the morphologically identical parasite of animals Trypanosoma brucei brucei by its ability to infect humans. Epidemiological theory predicts that where these two subspecies coexist, the prevalence in non-humans of T. b. rhodesiense will exceed that of T. b. brucei. However, field observations suggest that the opposite is true, with T. b. brucei predominating. Here, we hypothesize that this discrepancy between theory and observations results from a reduction in fitness of T. b. rhodesiense relative to T. b. brucei when outside humans. The hypothesis is sufficient to reconcile theoretical predictions with field observations, and is consistent both with experimental data on parasite maturation probabilities in tsetse and growth rates in non-human serum. Further experiments to elucidate possible fitness costs of human-serum resistance could have significant implications for T. b. rhodesiense control.

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