Knowlesi Malaria in Monkeys IIa

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Abstract
During Stage II of knowlesi malaria, parasitized erythrocytes are coated with a sticky opsonizing material which permits spleen, bone marrow and liver phagocytes to ingest them selectively. During parasite segmentation, when the parasite count rises to between 50 and 300 parasites per 1000 red cells, a second precipitate forms around all blood cells, changing blood to pasty Stage HI sludge. This sludge resists passage through arterioles; flow rates sharply decrease; stagnant anoxia of endothelium ensues, permitting rapid plasma loss through venule walls, decreased venous return, and death. Controls Forty untreated monkeys died thus: all died within 12, most within 6 hours. Experiments: High heparin dosage (two monkeys) prevented formation of opsonins and sludge, and permitted development of high parasite counts in fluid, rapidly-flowing blood. Animals with some 1000 to 1800 parasites per 1000 erythrocytes lived an additional 12 hours or more after the parasite count was above 500. Death did not occur until parasites consumed almost all hemoglobin. Thus, Stage III sludge is lethal; it kills quicker than possible, but undemonstrated, parasite toxins. This study permits a new approach to experimental subdivision and analysis of mechanisms of disease: 1. Recognize the lethal mechanism in an untreated disease. 2Minimize or neutralize it, simultaneously maximising the etiology. 3Identify and evaluate the next lethal mechanism to appear. 4. Neutralize both lethal factors and maximize etiology. 5. Recognize next lethal factor. 6. Neutralize all three lethal factors, etc.

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