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Am. J. Trop. Med. Hyg., 43(2_Part_2), 1990, pp. 30-37
Copyright © 1990 by The American Society of Tropical Medicine and Hygiene

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The Pathology of Human Cerebral Malaria

Masamichi Aikawa, Motohiro Iseki, John W. Barnwell, Diane Taylor, Maung Maung Oo AND Russell J. Howard
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio; New York University Medical Center, New York, New York; Georgetown University, Washington, DC; Yangon, Myanmar; DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, California

Blockage of the cerebral microvasculature by Plasmodium falciparum-infected erythrocytes appears to be the principal cause of human cerebral malaria. Knobs which appear on the membrane of the infected erythrocytes adhere to the endothelium, causing the obstruction of cerebral microvessels. Protein molecules such as CD36, thrombospondin, and intercellular adhesion molecule-1, which are present on the membrane of endothelial cells, may act as receptors for the attachment of knobs of P. falciparum-infected erythrocytes. Each of these candidate host molecules for infected-cell recognition and attachment are expressed in microvessels of the human brain. The presence of HRP1 and HRP2 in the cerebral microvessels of cerebral malaria patients may indicate the involvement of knob proteins in the pathogenesis of cerebral malaria. Owl monkeys infected with P. falciparum do not develop cerebral malaria. There is no blockage of cerebral microvessels by infected erythrocytes and knob proteins are absent. These findings support the contention that cerebral microvessel blockage and the presence of knob proteins are the probable causes of cerebral malaria.






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Copyright © 1990 by the American Society of Tropical Medicine and Hygiene.