Blood-parasite protozoa are causative agents of some of the major trop
ical or infectious diseases for humans and animals, such as Plasmodium
for malaria (about 270 million infected people), Trypanosoma cruzi fo
r Chagas' disease (about 18-20 million individuals), African trypanoso
mes for human and bovine trypanosomiasis, and Babesia for cattle and d
ogs. The absence of efficient vaccines against these diseases, the abs
ence or the high toxicity of the few drugs against American and Africa
n trypanosomiasis, and the emergence of chemoresistance against Plasmo
dium falciparum emphasize the necessity to propose new antiparasitic s
trategies. Among these strategies, the biological strategy is based on
the identification of key molecules for parasite development such tha
t structural analogs can be designed that are parasite-specific or suf
ficiently inactive for the host. This requires a careful biochemical a
nalysis of each step of the parasite life cycle. For blood-parasite pr
otozoa, the lipid metabolism required for membrane biogenesis, antimic
rotubular drugs or inhibitors of the mitotic spindle, and drug targeti
ng offer new trends in chemotherapy against Plasmodium, Babesia, and t
rypanosomes.