THE COURSE OF PLASMODIUM-BERGHEI, P-CHABAUDI AND P-YOELII INFECTIONS IN BETA-THALASSEMIC MICE

In order to study the effects of acclimatization of Plasmodium in beta -thalassaemic mice, me used a mouse model of beta-thalassaemia (DBA/2J /beta-thal/beta-thal), similar to that observed in humans. We acclimat ized 3 rodent malarias (P. berghei, P. chabaudi and P. yoelii) in DBA/ 2J and DBA/2J/beta-thal/beta-thal mice lines, by 4 intraperitoneal ser ial transfers. All 3 rodent malarias developed in red blood cells of b eta-thalassaemic mice without losing their virulence. There was no del ay in infection and peaks of parasitaemia were similar in beta-thalass aemic and normal mice. The mortality occurred earlier in beta-thalassa emic mice than in control mice for P. berghei P. chabaudi. This differ ence was more pronounced for P. yoelii NS where normal mice did not di e. These results could be explained by a failure of erythropoiesis in beta-thalassaemic mice, which are unable to compensate for the destruc tion of red blood cells by the parasites, and the mice died of anaemia . Ultrastructural examination of the rodent malaria parasites in beta- thalassaemic RBC showed a normal development even in the presence of H einz bodies. In conclusion, no effective protection against malaria wa s provided by the beta-thalassaemia in this mouse model.