The course of Plasmodium berghei, P. chabaudi and P. yoelii infections in beta-thalassaemic mice.

In order to study the effects of acclimatization of Plasmodium in beta-thalassaemic mice, we used a mouse model of beta-thalassaemia (DBA/2J/beta-thal/beta-thal), similar to that observed in humans. We acclimatized 3 rodent malarias (P. berghei, P. chabaudi and P. yoelii) in DBA/2J and DBA/2J/beta-thal mice lines, by 4 intraperitoneal serial transfers. All 3 rodent malarias developed in red blood cells of beta-thalassaemic mice without losing their virulence. There was no delay in infection and peaks of parasitaemia were similar in beta-thalassaemic and normal mice. The mortality occurred earlier in beta-thalassaemic mice than in control mice for P. berghei and P. chabaudi. The difference was more pronounced for P. yoelii NS where normal mice did not die. These results could be explained by a failure of erythropoiesis in beta-thalassaemic mice, which are unable to compensate for the destruction 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 Heinz bodies. In conclusion, no effective protection against malaria was provided by the beta-thalassaemia in this mouse model.