Plasmodium in the placenta: parasites, parity, protection, prevention and possibly preeclampsia.

The epidemiology of pregnancy malaria infection and disease is complex but reflects underlying interactions between the Plasmodium falciparum parasite, the mother, and the foetus. Parasites sequester in the human placenta by binding to chondroitin sulfate A (CSA), a novel receptor that does not commonly support binding of other parasites. Women become resistant to P. falciparum malaria over successive pregnancies as they acquire antibodies against the CSA-binding placental parasite forms. Due to acquired immunity, placental malaria is briefer and less inflammatory in multigravid women than primigravid women, and these parity differences may account for the different outcomes these women and their offspring experience. Commonly recognized sequelae of malaria-like maternal anaemia and low birth weight primarily occur in first and second pregnancies. Hypertension may result from maternal-foetal conflict over the inflammatory response to placental malaria, and occurs in young, first-time mothers. Placental malaria can either increase or decrease parasitaemia risk in the offspring, depending on the mother's parity. The burden of disease due to pregnancy malaria, and the benefits of an effective vaccine, may be much greater than is currently appreciated.