Abstract
Blood-parasite protozoa are causative agents of some of the major tropical or infectious diseases for humans and animals, such as Plasmodium for malaria (about 270 million infected people), Trypanosoma cruzi for Chagas' disease (about 18-20 million individuals), African trypanosomes for human and bovine trypanosomiasis, and Babesia for cattle and dogs. The absence of efficient vaccines against these diseases, the absence or the high toxicity of the few drugs against American and African trypanosomiasis, and the emergence of chemoresistance against Plasmodium falciparum emphasize the necessity to propose new antiparasitic strategies. Among these strategies, the biological strategy is based on the identification of key molecules for parasite development such that structural analogs can be designed that are parasite-specific or sufficiently inactive for the host. This requires a careful biochemical analysis of each step of the parasite life cycle. For blood-parasite protozoa, the lipid metabolism required for membrane biogenesis, antimicrotubular drugs or inhibitors of the mitotic spindle, and drug targeting offer new trends in chemotherapy against Plasmodium, Babesia, and trypanosomes.
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