| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 842 | 94 | 13 |
| Full Text Views | 31 | 4 | 0 |
| PDF Downloads | 35 | 5 | 0 |
%20CFA%20Deadline%20Proof%201.png)
Human Cerebral Malaria
Masamichi Aikawa
Masamichi Aikawa
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106
Search for other papers by Masamichi Aikawa in
Current site
Google Scholar
PubMed
Search for other papers by Masamichi Aikawa in
Current site
Google Scholar
PubMed
Possible factors contributing to the development of cerebral malaria were discussed based on pathological changes in Burmese patients who died of cerebral malaria. Blockage of cerebral capillaries by Plasmodium falciparum infected erythrocytes appeared to be the principal cause of cerebral malaria. From electron microscopic results, it was concluded that knobs on infected erythrocytes acted as focal junctions which mediated adhesion to endothelial cells. The knobs are, therefore, important contributors to the blockage of the capillary lumen and ensuing pathological changes in cerebral tissues. Host cell molecules such as OKM5 and thrombospondin may function as endothelial cell surface receptors for the attachment of knobs of P. falciparum infected erythrocytes. Immunological events might also play a role in the pathogenesis of cerebral malaria. This was suggested by the presence of IgG, IgM, P. falciparum antigens, and knob proteins in the cerebral capillaries of the people with cerebral malaria. It will be important to assess the candidate malaria vaccines now in development not only for their efficacy in reducing parasitemia but for effects they may have on the sequestration of infected erythrocytes in the brain.
Author Notes
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 842 | 94 | 13 |
| Full Text Views | 31 | 4 | 0 |
| PDF Downloads | 35 | 5 | 0 |