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Malaria in Pregnancy: Linking Immunity and Pathogenesis to Prevention

Pregnant women are susceptible to malaria during pregnancy. Plasmodium falciparum, which sequesters in the placenta, causes the greatest disease, contributing significantly to maternal and infant mortality. Parasitized cells in the placenta express unique variant surface antigens (VSA), predominantly the VAR2CSA protein, and lack of immunity to these pregnancy-specific variant surface antigens explains some of the pregnancy-associated malaria susceptibility. Changes in acquired cellular immunity during pregnancy also appear important. Placental inflammatory responses, particularly monocyte infiltrates, predispose to fetal growth restriction and maternal anemia. Preventing malaria in pregnancy relies on insecticide treated bed nets, intermittent preventive treatment with antimalarials such as sulphadoxine–pyrimethamine, and potentially relies on the development of effective vaccines. The optimal deployment of each may depend heavily on the relationship between the timing of placental malaria infection and its deleterious consequences. Improved understanding of the relationship between pathogenesis, immunity, and pregnancy outcome will allow better targeting of our interventions to prevent the consequences of malaria in pregnancy.

Received August 21, 2006. Accepted for publication April 5, 2007.

Acknowledgments: Sarah Landis drafted Figure 1. The authors thank Philippe Boeuf for critical reading of the manuscript.

Financial Support: SJR is supported by a Wellcome Trust Senior Research Fellowship ref 063215 and by the National Health and Medical Research Council of Australia.

^* Address correspondence to Stephen J. Rogerson, Department of Medicine (RMH/WH), Post Office Royal Melbourne Hospital, Parkville VIC 3050, Australia. E-mail: sroger{at}unimelb.edu.au

Authors’ addresses: Stephen J. Rogerson, Department of Medicine (RMH/WH), Post Office Royal Melbourne Hospital, Parkville VIC 3050 Australia, Tel: +61 3 8344 3259, Fax: +61 3 9347 1863. Victor Mwapasa, Department of Community Health, College of Medicine, University of Malawi, Blantyre, Malawi, Tel: +265 677 245, Fax: +265 674-700. Steven R. Meshnick, Departments of Epidemiology and of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC, Tel: +919 966 7414, Fax: +919 966 2089.

Reprint requests: Stephen J. Rogerson, Department of Medicine (RMH), University of Melbourne, Post Office, Royal Melbourne Hospital Victoria 3050, Australia. Tel: +61 3 8344 3259, Fax: +61 3 9347 1863, E-mail: sroger{at}unimelb.edu.au