The possible involvement of platelets in the pathogenesis of malaria was examined by monitoring the changes in platelet function (bleeding time [BT] and thrombin time [TT]) concomitantly with changes in packed cell volume (PCV) and erythrocyte infection rate (EIR) in Plasmodium yoelii nigeriensis infection in mice. In untreated plasmodium-infected mice, there was a progressive reduction (day 1–7) in BT from 120.0 ± 12.6 s to 77.5 ± 5.9 s (p < 0.005), a reduction in TT from 26. 8 ± 1.2 s to 17.8 ± 1.2 s (p < 0.005), an increase in EIR from 0 to 64.6 ± 6.3% and a reduction in PCV from 44.9 ± 1.9% to 21.5 ± 3.9% (p < 0.001). Mortality on day 9 was 100%. Antiplatelet serum treatment of plasmodium-infected mice protected against malaria and there was a blunting of the malaria-induced changes in platelet function, EIR and PCV. The values obtained in these rats were significantly higher than those of the untreated malarious mice. The respective values obtained on day 1 were comparable to those of control mice. Data obtained on day 7 were: BT, 106.4 ± 7.4 s (p < 0.05), TT, 22.7 ± 1.1 s(p < 0.05), EIR, 45.7 ± 3.2% (p < 0.01) and PCV, 39.5 ± 2.0% (p < 0.01). Mortality on day 9 of infection was 60%. The protection by antiserum was not due to its thrombocytopenic response as busulphan-induced thrombocytopenia did not have the same effect. These results suggest that platelets play an important role in malaria infection as well as in the attendant coagulopathic complications.

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