Abstract

The two week period that stretches between the absorption of gametocytes from a malaria patient by a mosquito and the subsequent injection of sporozoites in another human host is a most fragile segment of the malaria cycle. There is non-randomness in the blood meal choice of anopheline vectors. Manipulations of the host by the parasite to satisfy the preferences of the vector might have contributed to the robustness of the malaria cycle. Indeed, although gametocytes do not directly cause symptoms, the acute and chronic clinical manifestations caused by asexual forms seem to be organized around their transmission: fever patterns and behavior modification, anemia and thrombocytopenia converge towards making malarious individuals a preferred and safer source of blood for the vector than non-malarious individuals. Malaria symptoms offer the vector its favorite cues: increased skin temperature, increased lactates, sweating, and CO(2) expiration. In addition, this tempting menu seems easier to absorb because of thrombocytopenia and reduced blood viscosity during anemia, and because behavior modification reduces mosquito avoidance and the risk of dying. The attractive cues may be characteristic symptoms of malaria but also slight infraclinical changes that mostly go unnoticed by the doctor but not by the vector. The manifestations of malaria are often seen as adaptive for the host, this article argues that on average they may also be adaptive for malaria parasites. Examining malaria as the extended phenotype of Plasmodium leads to new research questions.

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