Platelet Hypersensitivity In Acute Malaria Infection (Plasmodium Falciparum) In Man

Abstract

We had earlier reported altered ADP-induced platelet aggregation in man during acute malaria infection. The present study sought to determine (i) whether the changes suggested platelet hypersensitivity to ADP and (ii) whether such changes occurred in vivo or in vitro.The aggregation response of platelets (as citrated PRP) to addition of ADP from thirty patients with acute malaria infection has been compared with that of 29 control i.e., non-infected subjects. The age range of the subjects in both groups varied from 2 to 70 years. These tests were performed before the patients took any drugs. With addition of l.0μM ADP to 1 ml of PRP, the mean aggregation amplitude (as % light transmission) obtained from 8 patients, 39.8±27.1% was significantly greater than that from 9 control subjects (5.2±6.7%; t = 3.51; P < 0.005). With higher ADP concentrations (2.4 - 5.0μM) similar response in 22 subjects (mean 89.1±14.9%) was also significantly greater than that in 20 controls (77.8±16.5%; t = 12.45; P < 0.02). These results suggest that during acute malaria infection in man, circulating platelets become hypersensitive to ADP in vitro. No instances of spontaneous aggregation were however observed in the patients.βTG was determined in 7 patients and 6 controls. The mean plasma βTG in the patients (208.3±15.6 ng/ml) was significantly higher than that in controls (59.2±15.7 ng/ml; t = 13.44; P <0.001). These latter results suggest that the platelets were probably activated in vivo to release the βTG. They further suggest that the hypersensitive changes noted earlier also probably occurred in vivo.It is suggested that acute malaria (P.falciparum) infection in man is probably another clinical condition associated with platelet hypersensitivity.

Human platelet inhibition ofToxoplasma gondiigrowth

“…The observation that T. gondii causes platelet activation is consistent and complementary to the studies of Yong et al [15]. Similar results on the activation of platelets by other protozoa such as P. falciparum have also been reported [19,[31][32][33]. In toxoplasmosis, transient parasitaemia is only observed in the acute and the reactivated phases [34,35].…”

A Study on Course of Infection and Haematological Changes in falciparum-Infected in Comparison with Artemisinin(s)-Treated Mice

“…Thrombocytopenia seems to be due mainly to a reduced platelet life span and splenic pooling. The reduced platelet life span may be caused by binding of malaria antigen onto platelets followed by antibody-mediated phagocytosis [29] or to platelet activation in vivo. Macrophage activation and hyperplasia especially in the spleen may also play a role [30].…”

Blood coagulation in falciparum malaria—a review

“…In the initial phase of infection, threshold for aggregation for platelets is considerably reduced and hyperaggregable platelets are generally seen (Essien and Ebhota 1981). One of the hypotheses for this activation was release of adenosine diphosphate from parasite-infected red cells (Inyang et al 1987a,b).…”