Abstract

Lambwe Valley, situated close to Lake Victoria in western Kenya, is one of two remaining foci of sleeping sickness in Kenya. Ruma National Park occupies the valley floor, with a large mammal fauna including hyena, leopard, buffalo, bushpig and various species of antelope. Outside the park, the land is densely settled by subsistence farmers, mainly of the Luo tribe, who keep cattle, sheep and goats. The latter half of I980 saw a striking increase in the incidence of sleeping sickness in Lambwe Valley, with 68 cases reported by the end of the year, more than the cumulative total for the previous five years. This outbreak was curtailed by the aerial spraying of insecticide in I98 I, coupled with active case finding and treatment, and now there are only sporadic cases. At the time of the outbreak, the valley was massively infested with the tsetse fly, Glossina pallidipes; biconical trap catches of over 500 per day were not unusual. This tsetse population had been building up from reduced numbers left by the control operations of the early I97Os, and had come to infest not only the thickets in the game park itself, but also areas outside where people had settled. By the start of the 1980 outbreak most dogs had already died with ‘white eyes’, the cornea1 opacity characteristic of trypanosomiasis in the dog. Cattle were also heavily infected with trypanosomes and infection rates of over 50% with J. brucei-group trypanosomes were recorded. Clearly, the valley was undergoing a sudden upsurge of trypanosomiasis on all fronts. The most obvious explanation was that encroaching human settlement had brought humans and their livestock within range of the expanding fly population of the game park, but what other factors might have been involved? Mihok and colleagues’ have reanalysed the large data set on isoenzyme characterization of Lambwe Valley J. brucei spp isolates in an attempt to gain new insight into this question. The team from the International Centre of Insect Physiology and Ecology (ICIPE) W. Gibson

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