Journal Article > ResearchFull Text
Am J Trop Med Hyg. 11 November 2013; Volume 90 (Issue 1); DOI:10.4269/ajtmh.13-0150
Mueller YK, Kolaczinski JH, Koech T, Lokwang P, Riongoita M, et al.
Am J Trop Med Hyg. 11 November 2013; Volume 90 (Issue 1); DOI:10.4269/ajtmh.13-0150
Between 2000 and 2010, Médecins Sans Frontières diagnosed and treated 4,831 patients with visceral leishmaniasis (VL) in the Pokot region straddling the border between Uganda and Kenya. A retrospective analysis of routinely collected clinical data showed no marked seasonal or annual fluctuations. Males between 5 and 14 years of age were the most affected group. Marked splenomegaly and anemia were striking features. An Rk39 antigen-based rapid diagnostic test was evaluated and found sufficiently accurate to replace the direct agglutination test and spleen aspiration as the first-line diagnostic procedure. The case-fatality rate with sodium stibogluconate as first-line treatment was low. The VL relapses were rare and often diagnosed more than 6 months post-treatment. Post-kala-azar dermal leishmaniasis was rare but likely to be underdiagnosed. The epidemiological and clinical features of VL in the Pokot area differed markedly from VL in Sudan, the main endemic focus in Africa.
Journal Article > LetterFull Text
Emerg Infect Dis. 1 March 2007; Volume 13 (Issue 3); 507-509.; DOI:10.3201/eid1303.060706
Kolaczinski JH, Worku DT, Chappuis F, Reithinger R, Kabatereine N, et al.
Emerg Infect Dis. 1 March 2007; Volume 13 (Issue 3); 507-509.; DOI:10.3201/eid1303.060706
Journal Article > ResearchFull Text
Int J Epidemiol. 9 January 2008; Volume 37 (Issue 2); DOI:10.1093/ije/dym275
Kolaczinski JH, Reithinger R, Worku DT, Ocheng A, Kasimiro J, et al.
Int J Epidemiol. 9 January 2008; Volume 37 (Issue 2); DOI:10.1093/ije/dym275
BACKGROUND: In East Africa, visceral leishmaniasis (VL) is endemic in parts of Sudan, Ethiopia, Somalia, Kenya and Uganda. It is caused by Leishmania donovani and transmitted by the sandfly vector Phlebotomus martini. In the Pokot focus, reaching from western Kenya into eastern Uganda, formulation of a prevention strategy has been hindered by the lack of knowledge on VL risk factors as well as by lack of support from health sector donors. The present study was conducted to establish the necessary evidence-base and to stimulate interest in supporting the control of this neglected tropical disease in Uganda and Kenya. METHODS: A case-control study was carried out from June to December 2006. Cases were recruited at Amudat hospital, Nakapiripirit district, Uganda, after clinical and parasitological confirmation of symptomatic VL infection. Controls were individuals that tested negative using a rK39 antigen-based dipstick, which were recruited at random from the same communities as the cases. Data were analysed using conditional logistic regression. RESULTS: Ninety-three cases and 226 controls were recruited into the study. Multivariate analysis identified low socio-economic status and treating livestock with insecticide as risk factors for VL. Sleeping near animals, owning a mosquito net and knowing about VL symptoms were associated with a reduced risk of VL. CONCLUSIONS: VL affects the poorest of the poor of the Pokot tribe. Distribution of insecticide-treated mosquito nets combined with dissemination of culturally appropriate behaviour-change education is likely to be an effective prevention strategy.