Could human infective ‘Trypanosoma evansi’ escape sub-Saharan Africa?

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Between the Tropics of Cancer and Capricorn can be found a diverse group of infectious diseases, most common in low income populations. These are called neglected tropical diseases (NTDs). One group of NTDs are the trypanosomiases, so called because they are caused by various species of trypanosomes (flagellated parasites).

Perhaps the most well-known trypanosome parasite is Trypanosoma brucei (T. brucei), which transmits among mammals via the bite of an infected tsetse fly. In parts of sub-Saharan Africa, this causes human African trypanosomiasis (HAT, or sleeping sickness) and animal trypanosomiasis (or nagana) in cattle. Another trypanosome species, T. evansi, is found in parts northern Africa, the Middle East and Southeast Asia, where it infects wild and domesticated animals to cause a disease called surra. It is thought that T. evansi originated in camels in Africa, partly because it occurs in all countries where camels are found. Surra causes thousands of animal deaths per year, resulting in significant economic losses due the amount of resources invested in therapeutic interventions.

Since tsetse flies are found only in Africa, African trypanosomes such as T. brucei have so far been confined to the continent. Some trypanosomes, including T. brucei, require the tsetse fly for the completion of their life cycle and for transmission, while others do not. T. evansi is unable to undergo development in the tsetse fly because some strains either lack certain components of its DNA, or because the DNA does not function properly. As a result, vampire bats in South America and biting insects in other endemic regions are responsible for the transmission of T. evansi. A combination of these factors has shed light on why T. evansi has been able to escape the ‘tsetse fly belt’ in sub-Saharan Africa and why it is one of the most geographically widespread trypanosomes.

Previous gene studies of T. evansi strains have found that some strains are genetically closer to strains of T. brucei than to each other. This fascinating insight suggests that T. evansi is not monophyletic, meaning that it has in fact evolved many times, possibly from different strains of T. brucei. Scientists from Kenya, Yale University and the University of Edinburgh have recently published data that supports this hypothesis, and that some T. evansi isolates from Kenya have indeed evolved many times from multiple strains of T. brucei.

The goal of this collaborative project was to quantify levels and patterns of genetic diversity between T. evansi and T. brucei, in order to understand the evolutionary origins of different T. evansi strains. To achieve this, the DNA of different strains of T. evansi was screened for genetic variation. This was carried out on T. evansi samples from a region in Kenya where T. brucei and T. evansi are both found, making it a location where the trypanosome host is likely to have shifted to camels. The climate of this region is semi-arid which lends itself to the husbandry of camels, cattle and goats; classic hosts of T. evansi and therefore supportive of this theory.

A total of 107 isolates of T. brucei and T. evansi from different mammalian hosts were analysed using polymerase chain reaction (PCR) tests and microsatellite genotyping. PCR is a technique used to create more copies of a specific target region of DNA. This allows for the identification and classification of DNA. Microsatellite genotyping is a tool which uses microsatellites (pieces of repetitive DNA in which short specific DNA patterns are repeated) to address questions about population genetics. This is useful because it helps to generate genetic maps which can reveal the levels of similarity between subspecies, groups and individuals. The data generated was analysed using STRUCTURE, a population analysis tool. STRUCTURE examines population structures and deduces the origins of individuals, or isolates exactly when genetic admixture occurs (i.e. when new genetic lineages are introduced into a population).

The results of this study suggest that some T. evansi isolates from Eastern Africa, an area where both T. evansi and T. brucei co-occur, likely evolved from different strains of T. brucei. Surprisingly, although all T. evansi strains share similar features (such as the ability to sustain mechanical transmission outside the tsetse belt, loss of functional DNA and the common disease symptoms they cause), there is a high degree of genetic variation amongst these isolates. This suggests that the aforementioned features of T. evansi have multiple origins, further implying that these complex traits have evolved multiple times. Furthermore, it is possible that T. evansi will continue to evolve new and more complex traits.

The results presented in this research have important epidemiological implications. They show that T. brucei strains from different genetic backgrounds can seemingly evolve to be transmitted by insects other than the tsetse fly.

So far there have only been a few cases of T. evansi infecting humans, the risk of this occurring more often is relatively small, and in order for the human disease to escape Africa a single strain of T. evansi would need to have the genes responsible for mechanical transmission and evasion of the human immune system. However, this prospect deserves attention, because it would allow sleeping sickness to escape sub-Saharan Africa, provoking significant worldwide consequences; a dangerous possibility given the fact that trypanosomes have been able to acquire both transmission and immune system evasion traits repeatedly. It is therefore important to understand the origin and dynamics of the spread of T. evansi from Africa to other continents, and the molecular basis by which T. evansi is able to bypass tsetse fly transmission.


This article was written by Zandile Nare and edited by Sam Stanfield.

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