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Major epidemics of meningococcal infections usually occur every 5-10 years within the African "meningitis belt;" they usually start in the middle of the dry season and end a few months later with the onset of the rains (Greenwood, 1984). Between February and April 1996, the disease affected thousands of people in parts of northern Nigeria, many of whom died (Angyo and Okpeh, 1997). This epidemic spread from the original meningitis belt to Kenya, Uganda, Rwanda, Zambia, and Tanzania (Hart and Cuevas, 1997). One of the environmental factors that predisposes to infection and epidemics is low humidity (Tikhomirov et al., 1997). However, a climate-meningitis association was not clear in parts of the Gulf of Guinea (Besancenot et al., 1997). That this disease has been limited to the semi-arid areas of Africa suggests that its transmission could be affected by warming and reduced precipitation.
From 1931 (when the disease was first described) until the end of the 1970s, Rift Valley fever (RVF) was considered to be a relatively benign zoonoses for humans that periodically developed in domestic animals (especially sheep) following heavy rains (Lefevre, 1997). Recent research indicates that although epizootics in east Africa are associated with an increase in rainfall, a similar association is unknown in west Africa (Zeller et al., 1997). Recent data from west Africa indicate that the risk of a new epizootic is increasing in the region (Fontenille et al., 1995), with significant exposure to the virus among livestock herders and wildlife rangers during the wet season (Olaleye et al., 1996). Following the 1997-1998 El Niño event in east Africa, an RVF outbreak in Somalia and northern Kenya killed as much as 80% of the livestock and affected their owners (WHO, 1998b). Many cases also were reported in Tanzania. In Mauritania, the human epidemic was linked to the epizootic disease (Jouan et al., 1989). Extensive research on mosquito vectors of RVF in Kenya (mainly Aedes and Culex spp.) has clearly linked the risk of outbreak with flooding (Linthicum et al., 1990). It can be expected that increased precipitation as a consequence of climate change could increase the risk of infections in livestock and people. Such new risks could cause major economic and health problems for herding communities in Africa.
Plague is a flea-borne disease with rodents as reservoirs. The population of rodents can increase suddenly following heavy rains as a result of abundance of food (e.g., grain). During drought, rodents may migrate into human dwellings in search of food. Development of fleas and the pathogens they carry can be accelerated by increased temperature. Plague outbreaks recently have been reported in Mozambique, Namibia, Malawi, Zambia, and Uganda (see WHO Outbreak Web site: <www.who.int/disease-outbreak-news>).
Pollution of streams, wells, and other sources of rural water supplies by flooding could introduce parasites such as giardia, amoeba, and cryptosporidium into drinking water (Alterholf et al., 1998). These parasites assume a new significance in HIV-infected individuals because of the latter's immunocompromised status (Mwachari et al., 1998). Extreme weather events such as El Niño have been associated with increased episodes of diarrhea.
Shifts in the epidemiology of schistosomiasis, onchocerciasis, and filariasis may take longer to become evident because these parasites are less sensitive to the effects of climate than diseases such as malaria. Changes in the impacts of climate on human trypnosomiasis may require substantial and permanent changes in tsetse fly ecology. Little or no data are available on this subject.
Biomass burning and massive importation of badly maintained vehicles could result in increased air pollution—which, combined with increasing temperature, would exacerbate health risks such as respiratory problems and eye and skin infections (Boko, 1988).
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