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Water- and food-borne diseases tend to show marked seasonality, with peaks in early spring or summer. Higher temperatures favor microorganism proliferation and often are associated with an increase in gastrointestinal infections. Above-average temperatures in Peru during the 1997-1998 El Niño were associated with a doubling in the number of children admitted to the hospital with diarrhea (Checkley et al., 2000). Higher temperatures also can trigger spore maturation (e.g., Cyclospora cayetanensis—Ortega et al., 1993; Smith et al., 1997). In Peru, the incidence of cyclosporosis peaks in the summer months (Madico et al., 1997). Because climate change is expected to entail warmer springs and summers, additional cases of food-borne disease may occur, if current trends continue (Bentham and Langford, 1995). In most developed countries, food-borne disease incidence is increasing as a result of changes in behavior, consumption patterns, and commerce.
Major epidemics of meningococcal infection 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
et al., 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). The epidemic spread from the original meningitis belt to Kenya, Uganda,
Rwanda, Zambia, and Tanzania (Hart and Cuevas, 1997). One of the environmental
factors that predispose to infection and epidemics is low humidity (Tikhoumirov
et al., 1997). However, a climate-meningitis association was not clear in parts
of the Gulf of Guinea (Besancenot, 1997). The fact that this disease has been
limited to semi-arid areas of Africa suggests that its transmission could be
affected by warming and reduced precipitation.
Warm and humid conditions can promote fungal skin infections such as sporotrichosis (Conti Diaz, 1989). Decreases in humidity can lead to increased dispersion of particulate fungal spores, thereby increasing the risk of pneumonia caused by coccidioidomycosis (Durry et al., 1997; Schneider et al., 1997).
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