CHANGES IN PLATELET SURVIVAL AND SIALIC ACID CONCENTRATION IN PLASMODIUM BERGEI INFECTED RATS

Reduced circulating platelet count sometimes to thrombocytopenic levels in man and normally severe thrombocytopenia in animals are well known features of acute Plasmodium falciparum or experimental P. bergei infections in these respective organisms. Suggested mechanism(s), disseminated intravascular coagulation or immune mediated mechanism, thought to be involved in these observations are disputed. Shortened platelet survival has been reported in man.

We now present data on platelet survival and total platelet sialic acid concentration in P. bergei-infected Wistar rats. A total of 52 rats were used. For the platelet survival studies each of the 8 suckling test animals was infected by intraperi-toneal route with mouse-passaged P. bergei 4-5 days before inaction of Cr-labelled homologous rat platelets (50 μCi Na⁵¹ CrC₄/rat) the platelets being obtained from adult Wistarrats. Blood samples were then collected 2 hr after the injection (zero hr sample) and subsequently at 17.0, 42.5 and 66 hr s.Platelet recovery and survival curves were determined on these samples. It was found dat fewer platelets (as % recovery) were obtained from each infected rat sample compared with control, the difference was significant in the 42.5 and 66 hr samples: 7.9 ± 8.1 (test) vs 41.4 ± 15.2% (C) for 42.5 hr and 2.8 ±4.1 (t) vs 26.8 ± 6.2% (C) for the 66 hr samples (p < 0.005 for each). For sialic acid determinations, 40 suckling Wistar rats (30 test, 10 control) were treated as for survival studies.At identical periods, blood was collected, washed platelets obtained, lysed and protein and total sialic acid determined by Lowry (1951) and Aminoff (1961) methods respectively. Total sialic acid of 7.02 ± 4.21 nM/mg protein at 42.5 hrs and 4.8 ± 2.14 at 66 hrs were significantly less than control value of 11.43 nm/mg protein and also showed a negative correlation (r = -0.95) with % parasitaemia.

It is concluded that P. bergei infection causes a reduction in total platelet sialic acid with resultant significant shortening of the platelet life span.