Anemia due to Plasmodium falciparum infection is a major health problem in endemic areas for young children and pregnant women. The anemia is caused by excess removal of nonparasitized erythrocytes in addition to immune destruction of parasitized red cells, and impaired compensation for this loss by bone marrow dysfunction. The pathogenesis is complex, and a predominant mechanism has not been identified. Certain parasite and host characteristics may modify the anemia. Concomitant infections and nutritional deficiencies also contribute to anemia and may interact with the malarial infection. Few preventive strategies exist, and the management of severe malarial anemia with blood transfusion carries a risk of HIV transmission. The current increase in malaria-specific childhood mortality in sub-Saharan Africa attributed to drug-resistant P. falciparum infection is likely partly related to an increase in severe anemia. This review summarizes recent findings on the pathogenesis and epidemiology of malarial anemia.
Division of Medicine, Unit of Infectious Diseases, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden and Department of Infectious Diseases, Sundsvall Hospital, Sundsvall, Sweden.
Correspondence to Håkan Ekvall, MD, PhD, MPH, DTMH, Division of Medicine, Unit of Infectious Diseases, Karolinska Institute, Karolinska Hospital, 171 76 Stockholm, Sweden; e-mail: email@example.com