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IMMUNE COMPLEX LEVELS IN CHILDREN WITH SEVERE PLASMODIUM FALCIPARUM MALARIA

Malaria infection leads to the formation of circulating immune complexes. However, it is unclear whether these complexes play a role in the pathogenesis of complicated Plasmodium falciparum malaria. This study aimed at determining if there are differences in the levels of immune complexes between children with severe malaria-associated anemia and cerebral malaria and between each of these two groups and their respective uncomplicated symptomatic malaria or healthy asymptomatic controls. Children with severe malaria-associated anemia and cerebral malaria had significantly higher immune complex levels than their respective controls, but there were no significant differences in the levels between the two severe malaria groups. In addition, there was an inverse relationship between the hemoglobin levels and immune complex levels in the severe anemia controls, suggesting that immune complexes may contribute to erythrocyte destruction in these children. These results suggest that immune complex levels alone cannot account for the differences in the distinct clinical presentation between severe malaria-associated anemia and cerebral malaria.

Received May 9, 2004. Accepted for publication July 7, 2004.

Acknowledgments: We would like to thank the children who participated in our studies as well as their parents for their willingness to contribute to this research endeavor. In addition, we are indebted to our dedicated staff of clinicians, nurses, drivers, and field workers who made these studies possible. We are grateful to Dr. John Rowlands of the Biometrics Unit, International Livestock Research Institute, Nairobi, Kenya, for statistical support. This work is published with the permission of the Office of the Director, the Kenya Medical Research Institute.

Financial support: This work was supported by funds from the U.S. Department of Defense Military Infectious Disease Research Program, by a TDR grant from the World Health Organization, Multilateral Initiative on Malaria, and by NIH grant R01 HL 71502-01 to José A. Stoute. Erick Mibei is supported by a training grant 1 D43 TW006239-01 from the Fogarty International Center.

Disclaimer: The views of the authors do not purport to reflect the position of the Department of the Army or the Department of Defense. The U.S. Government has the right to retain a nonexclusive, royalty-free license in and to any copyright covering this paper.

Authors’ addresses: Erick Mibei, Walter Reed Project, PO Box 54, Kisumu, Kenya. Alloyce S. S. Orago, Department of Zoology, Kenyatta University, P.O. Box 43844, Nairobi, Kenya. José A. Stoute, Department of Cellular Injury, Walter Reed Army Institute of Research, 503 Robert Grant Ave., Silver Spring, MD 20910.

Reprint requests: José A. Stoute, Department of Cellular Injury, Walter Reed Army Institute of Research, 503 Robert Grant Ave., Silver Spring, MD 20910, Tel 301-319-9510, Fax 301-319-9133, E-mail: jose.stoute{at}us.army.mil.

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