Reemergence of Epidemic Malaria in the Highlands of Western Kenya

1998 
This study investigated reports of epidemic malaria in a highland area of Kenya traditionally thought to be free of malaria to 1) formulate recommendations for reducing disease incidence and preventing future epidemics and 2) determine whether malaria was imported or was due to local transmission. The factors necessary for malaria transmission are the Plasmodium parasite, the Anopheles mosquito vector, and the human host. Both parasite and vector are affected by temperature and rainfall. Although temperature extremes kill Anopheles mosquitoes, higher temperatures (15°C–30°C) increase their rate of development. The gonotrophic cycle (interval between blood meals) shortens with increasing temperature, and the effect of a small temperature increase is greatest at the cooler ambient temperatures. Thus, a small rise in temperature from 19°C to 21°C shortens the gonotrophic cycle from 4 to 3 days and increases the vectorial capacity of the mosquito (1). Altitude is thought to be a proxy for temperature, so the actual limiting factor for malaria at high altitude is the effect of the lower temperature on the parasite (2). Despite the effect of altitude on ambient temperature, microclimatic factors (e.g. heated houses) can play an important role in facilitating malaria transmission and epidemics at higher elevations. Unlike the parasite, the mosquito vector can commonly be found at altitudes from >1,600 m (3,4) to 3,000 m, demonstrating that the limiting factor for malaria transmission at high altitude is the survival of the Plasmodium parasite. The Anopheles population is very sensitive to rainfall, which increases the availability of mosquito breeding sites. A. gambiae, the primary malaria vector of western Kenya, lays its eggs in small pools and puddles; in this region, rainfall of 150 mm per month leads to rapid expansion of the A. gambiae population (3,5) and hence increased risk for malaria transmission. Finally, epidemic malaria requires sufficient numbers of human gametocyte carriers (to infect Anopheles mosquitoes) and nonimmune human hosts (to acquire clinical infection). Malaria did not exist in the western Kenya highlands until the second decade of the 20th century (6). In 1901, completion of a railway from the Kenya coast across the highlands and down to Lake Victoria and increased road transport facilitated the gradual spread of infective mosquitoes into the highlands from the low-lying hyperendemic-disease areas (5). The development of tea estates and agriculture in the highlands, with the concomitant clearing of the forests, provided suitable mosquito breeding grounds. Finally, importation of infected laborers completed the conditions necessary for malaria transmission. Reemergence of Epidemic Malaria in the Highlands of Western Kenya
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