Abstract
African trypanosomiasis is caused by salivarian trypanosomes that are extracellular parasites affecting humans, livestock and game animals around the world. There are only three salivarian trypanosomes that can infect humans. Both Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense cause human African trypanosomosis (HAT) or ‘sleeping sickness’. Trypanosoma evansi is the third salivarian trypanosome that has been identified in several human patients. As for the zoonotic nature of trypanosomiasis, only T. b. rhodesiense fits the narrow definition of this classification, with the main parasite reservoir for this human pathogen found in animals. For T. b. gambiense the classification is more complex, as these trypanosomes belong either to a rather homogenous collection of ‘Group 1’ parasites or a more heterogeneous ‘Group 2’ cluster. Here, the definition of zoonosis would apply to the Group 2 trypanosomes, while Group 1 gambiense parasites are anthroponotic. T. evansi, the third salivarian trypanosome, occasionally cause atypical human trypanosomosis (aHT). This form of trypanosomiasis has so far only been reported outside Africa.
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Acknowledgement
The work of the co-authors mentioned in this chapter was supported by research grant of the Foundation for Scientific Research/Funds voor Wetenschappelijk Onderzoek – Vlaanderen (G013518N), an UGent BOF startkrediet (01N01518) and the Strategic Research Program of the Vrije Universiteit Brussel (SRP63). The funders had no role in any of the study designs, data collection and analysis, decision to publish or preparation of this manuscript.
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Case Study
Case Study
As there are many typical case reports of both rhodesiense and gambiense HAT available, one report that stands out is the identification of an atypical T. evansi HT infection in 2015. This was the first HT infection diagnosed at both serological and molecular level in Southeast Asia. The report covers the case of a 38-year-old woman who presented to a healthcare facility in southern Vietnam. Her symptoms included non-species issues such fever, headache and joint pain. Interestingly, the report included the APOL1 measurement in the patient’s blood, showing that there was no genetic deficiency that could easily explain the susceptibility to infection. This report followed a decade of APOL1 research, where a consensus grew that this molecule was indeed the most important factor in the trypanolytic activity of human serum. Hence, with full trypanolytic activity being present in this case, it remains to be discovered how some T. evansi trypanosomes survive in human blood, while being devoid of the known T. b. rhodesiense and T. b. gambiense resistance factors.
Research Question
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Can anti-trypanosome immunity be induced by vaccination, and can vaccine-induced memory against any trypanosome target be recalled upon infection fast enough to stop the imitation of immune destruction by the parasite?
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Does host pathology and inflammation contribute directly to the signals that drive quorum sensing during peak parasitaemia?
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Which mechanisms allow T. b. gambiense Group 2 and T. evansi to avoid APOL1-mediated trypanolysis in aHT?
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What is the mechanism of the uptake of the major trypanolytic factor, i.e. TLF2, and which resistance mechanism is operated by T. b. gambiense Group 1 parasites that allows survival in human serum?
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Magez, S., Nguyen, H.T.T., Torres, J.E.P., Radwanska, M. (2022). African Trypanosomiasis. In: Parija, S.C., Chaudhury, A. (eds) Textbook of Parasitic Zoonoses. Microbial Zoonoses. Springer, Singapore. https://doi.org/10.1007/978-981-16-7204-0_12
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