Malaria, a disease caused by protozoan parasites of the genus Plasmodium, can substantially reduce host fitness in wild animals (Atkinson and Van Riper 1991; Schall 1996). In humans, the major disease syndromes – severe anemia, coma, and organ failure, as well as general pathology such as respiratory distress, aches, and nausea – cause considerable mortality and morbidity (Marsh and Snow 1997).
Biomedical research attributes malaria to red cell destruction, infected cell sequestration in vital organs, and the parasite-induced release of cytokines (Marsh and Snow 1997). But mechanistic explanations are just one type of explanation for any biological phenomenon, and, in recent years, evolutionary biologists have become interested in offering evolutionary explanations of infectious disease virulence. This is entirely appropriate (Read 1994). In the context of malaria, for example, the clinical outcome of infection has an important impact on parasite and host fitness and is – at least in part – determined by heritable variation in host and parasite factors (Greenwood et al. 1991). Yet in the recent rush to provide evolutionary explanations of disease, there has been, in our view, too little interaction between the models built by evolutionary biologists and reality. There is unlikely to be a simple, general model of virulence: the causes of disease and the fitness consequences for host and parasite are too variable. Instead, different models, and even different frameworks, will be relevant in different contexts.