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Pathophysiology of Malaria
Hematologic Observations in Human and Animal Studies
- Requests for reprints should be addressed to Col. Paul E. Teschan, MC, Director, Division of Medicine, Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington, D. C. 20012
SUMMARY
Clinical malaria does not occur without hemolysis and parasitemia of circulating erythrocytes. Different metabolic requirements of various malarial strains cause species specificity and alter morbidity. Hemolysis does not seem to be caused by antibodies or hypersplenism. It is postulated that hemolysis is caused by loss of negative charge from the surface of red blood cells because the parasite usurps essential metabolic functions of the infected erythrocyte. Hemolysis in excess of the number of observed parasitized erythrocytes may be caused by splenic pitting of parasites from infected red blood cells and the return of damaged spherocytes with a shortened survival to the circulation.
The demonstration of accelerated intravascular coagulation in malaria provides an explanation for the occurrence of both thrombosis and hemorrhage in multiple body organs. Heparin therapy seems to improve the morbidity and mortality of malaria and decrease parasitemia.
Article and Author Information
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From the Division of Medicine, Walter Reed Army Institute of Research, Washington, D. C.
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- Received August 12, 1968.
- Accepted August 30, 1968.
