Trypanosoma brucei rhodesiense infection in a German traveller returning from the Masai Mara area, Kenya, January 2012

Wolf, Timo; Wichelhaus, Thomas A.; Göttig, Stephan; Kleine, Christian; Brodt, H.-R.; Just-Nuebling, G

doi:10.2807/ese.17.10.20114-en

Cited by 14 publications

(2 citation statements)

References 6 publications

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“…A summary of this case was reported through ProMED-mail on 22 February 2012 [1]. A similar case had been reported from Frankfurt, Germany, in a traveller who had visited the Masai Mara area in January 2012 [2], which is described further in this issue [3].…”

Section: Case Reportmentioning

confidence: 70%

Human African trypanosomiasis in a Belgian traveller returning from the Masai Mara area, Kenya, February 2012

et al. 2012

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A Belgian traveller was diagnosed with human African trypanosomiasis (HAT) due to Trypanosoma brucei rhodesiense nine days after visiting the Masai Mara area in Kenya. He presented with an inoculation chancre and was treated with suramin within four days of fever onset. Two weeks earlier, HAT was also reported in a German traveller who had visited the Masai Mara area. Because no cases have occurred in the area for over 12 years, this may indicate a focal cluster of HAT.

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Section: Case Reportmentioning

confidence: 70%

Human African trypanosomiasis in a Belgian traveller returning from the Masai Mara area, Kenya, February 2012

et al. 2012

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“…On a few occasions, cases in non-DEC reflect the occurrence of epidemic outbreaks of rhodesiense HAT in particular areas (e.g. Vwaza Marsh NP in 2019-2020 [25,[41][42][43][44], Masai Mara NR in 2012 [45][46][47][48][49] and Serengeti WR in earlier periods [50]).…”

Section: Discussionmentioning

confidence: 99%

Human African trypanosomiasis cases diagnosed in non-endemic countries (2011–2020)

et al. 2022

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Background Sleeping sickness, or human African trypanosomiasis (HAT), is transmitted by tsetse flies in endemic foci in sub-Saharan Africa. Because of international travel and population movements, cases are also occasionally diagnosed in non-endemic countries. Methodology/Principal findings Antitrypanosomal medicines to treat the disease are available gratis through the World Health Organization (WHO) thanks to a public-private partnership, and exclusive distribution of the majority of them enables WHO to gather information on all exported cases. Data collected by WHO are complemented by case reports and scientific publications. During 2011–2020, 49 cases of HAT were diagnosed in 16 non-endemic countries across five continents: 35 cases were caused by Trypanosoma brucei rhodesiense, mainly in tourists visiting wildlife areas in eastern and southern Africa, and 14 cases were due to T. b. gambiense, mainly in African migrants originating from or visiting endemic areas in western and central Africa. Conclusions/Significance HAT diagnosis in non-endemic countries is rare and can be challenging, but alertness and surveillance must be maintained to contribute to WHO’s elimination goals. Early detection is particularly important as it considerably improves the prognosis.

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Alternative oxidase inhibitors: Mitochondrion‐targeting as a strategy for new drugs against pathogenic parasites and fungi

Ebiloma

Balogun

Cueto-Díaz

et al. 2019

Medicinal Research Reviews

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The alternative oxidase (AOX) is a ubiquitous terminal oxidase of plants and many fungi, catalyzing the four‐electron reduction of oxygen to water alongside the cytochrome‐based electron transfer chain. Unlike the classical electron transfer chain, however, the activity of AOX does not generate adenosine triphosphate but has functions such as thermogenesis and stress response. As it lacks a mammalian counterpart, it has been investigated intensely in pathogenic fungi. However, it is in African trypanosomes, which lack cytochrome‐based respiration in their infective stages, that trypanosome alternative oxidase (TAO) plays the central and essential role in their energy metabolism. TAO was validated as a drug target decades ago and among the first inhibitors to be identified was salicylhydroxamic acid (SHAM), which produced the expected trypanocidal effects, especially when potentiated by coadministration with glycerol to inhibit anaerobic energy metabolism as well. However, the efficacy of this combination was too low to be of practical clinical use. The antibiotic ascofuranone (AF) proved a much stronger TAO inhibitor and was able to cure Trypanosoma vivax infections in mice without glycerol and at much lower doses, providing an important proof of concept milestone. Systematic efforts to improve the SHAM and AF scaffolds, aided with the elucidation of the TAO crystal structure, provided detailed structure‐activity relationship information and reinvigorated the drug discovery effort. Recently, the coupling of mitochondrion‐targeting lipophilic cations to TAO inhibitors has dramatically improved drug targeting and trypanocidal activity while retaining target protein potency. These developments appear to have finally signposted the way to preclinical development of TAO inhibitors.

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Trypanosoma brucei rhodesiense infection in a German traveller returning from the Masai Mara area, Kenya, January 2012

Cited by 14 publications

References 6 publications

Human African trypanosomiasis in a Belgian traveller returning from the Masai Mara area, Kenya, February 2012

Human African trypanosomiasis in a Belgian traveller returning from the Masai Mara area, Kenya, February 2012

Human African trypanosomiasis cases diagnosed in non-endemic countries (2011–2020)

Alternative oxidase inhibitors: Mitochondrion‐targeting as a strategy for new drugs against pathogenic parasites and fungi

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