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In January 2012, a case of Human African Trypanosomiasis (HAT) has been identified in Germany in a traveller returning from the Masai Mara area in Kenya. The 62-year-old man had travelled to the Masai Mara game park from 18 to 19 January 2012 and developed fever on 28 January. The infection with Trypanosoma brucei rhodesiense was confirmed by laboratory testing three days hereafter.

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.

Background & Objectives: In Kenya, sleeping sickness (SS) caused by Trypanosoma brucei rhodesiense is confined to the Nyanza and Western Provinces tsetse belts. Over the last two decades, the disease has exhibited great spatial variability in its spread and distribution. The objectives of the study were to map the spatial and temporal distribution of SS and determine possible risk factors associated with the disease in western Kenya., Methods: Geographical coordinates of villages were obtained using a Global Positioning System (GPS). SS data were analyzed retrospectively and the mapping of villages was done using MapInfo Software. Epidemiological data of villages affected by SS were then correlated to human and cattle population., Results: SS has spread northwards affecting the western parts of Busia, Teso, and of Bungoma districts in the late 1990s. Most of the SS cases were reported between March and June. The mainly affected age groups were from 20 to 49 years. SS was highest in areas with low human population density, ranging from 0-340/km2 and high livestock population, ranging from 5000 to 10,000 cattle., Interpretation & Conclusion: There was a shift of SS occurrence from the old foci into new foci occurring at low transmission levels and causing occasional epidemic outbreaks. The study concludes that seasons influenced disease incidences with higher numbers of SS cases being recorded during the wet seasons. Gender and age determined the disease occurrence with most productive age groups being at higher risk. Areas with high livestock populations had low human population densities and had higher SS cases.

The human serum resistance associated (SRA) gene has been found exclusively in Trypanosoma brucei rhodesiense, allowing the unequivocal detection of this pathogen in reservoir hosts and the tsetse vector without recourse to laborious strain characterisation procedures. We investigated the presence of the SRA gene in 264 T. brucei ssp. isolates from humans, domestic animals and Glossina pallidipes from foci of human trypanosomiasis in Kenya and Uganda. The SRA gene was present in all isolates that were resistant to human serum, and absent from all serum sensitive isolates tested. Further, the gene was present in all isolates that had previously been shown to be identical to human infective trypanosomes by isoenzyme characterisation. The SRA gene was detected in isolates from cattle, sheep, pigs, dog, reedbuck, hyena and G. pallidipes from sleeping sickness foci, but was not found in Trypanosoma evansi or in Trypanosoma brucei gambiense isolates. The present study indicates that the SRA gene may be invaluable in detecting and differentiating T. brucei rhodesiense from other T. brucei ssp. in reservoir hosts and tsetse.