Multiple evolutionary origins of Trypanosoma evansi in Kenya

Abstract

Trypanosoma evansi is the parasite causing surra, a form of trypanosomiasis in camels and other livestock, and a serious economic burden in Kenya and many other parts of the world. Trypanosoma evansi transmission can be sustained mechanically by tabanid and Stomoxys biting flies, whereas the closely related African trypanosomes T. brucei brucei and T. b. rhodesiense require cyclical development in tsetse flies (genus Glossina) for transmission. In this study, we investigated the evolutionary origins of T. evansi. We used 15 polymorphic microsatellites to quantify levels and patterns of genetic diversity among 41 T. evansi isolates and 66 isolates of T. b. brucei (n = 51) and T. b. rhodesiense (n = 15), including many from Kenya, a region where T. evansi may have evolved from T. brucei. We found that T. evansi strains belong to at least two distinct T. brucei genetic units and contain genetic diversity that is similar to that in T. brucei strains. Results indicated that the 41 T. evansi isolates originated from multiple T. brucei strains from different genetic backgrounds, implying independent origins of T. evansi from T. brucei strains. This surprising finding further suggested that the acquisition of the ability of T. evansi to be transmitted mechanically, and thus the ability to escape the obligate link with the African tsetse fly vector, has occurred repeatedly. These findings, if confirmed, have epidemiological implications, as T. brucei strains from different genetic backgrounds can become either causative agents of a dangerous, cosmopolitan livestock disease or of a lethal human disease, like for T. b. rhodesiense.

Author summary

Trypanosoma evansi is an important pathogen of the camel and other livestock where it is a causative agent of surra (an economically burdensome disease). The T. evansi is found in Kenya and the rest of the world. This study indicates that T. evansi originated recently from multiple Trypanosoma brucei strains from different genetic backgrounds. This suggests multiple independent evolutionary origins of some complex traits that may have facilitated mechanical transmission in T. evansi and subsequently enabled the parasite to escape the obligate link with the African tsetse fly vector. This evolutionary origin appears to have occurred repeatedly. Our results provide a more comprehensive understanding of the epidemiology of surra, provide recommendations for future work, and indicate a need to consider the risk of horizontal transfer of epidemiologically relevant traits among different Trypanosoma genetic backgrounds in any control campaign. Thus, our study is an important contribution to the field, and represents an important step towards the ultimate aim of trypanosomiasis prevention and/or elimination.