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 less than 0.005), a reduction in TT from 26.8 +/- 1.2 s to 17.8 +/- 1.2 s (p less than 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 less than 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 less than 0.05), TT, 22.7 +/- 1.1 s (p less than 0.05), EIR, 45.7 +/- 3.2% (p less than 0.01) and PCV, 39.5 +/- 2.0% (p less than 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.