Abstract

This investigation was conducted to elucidate the roles of the spleen in Plasmodium berghei and Babesia rodhaini infections of intact, splenectomized, and parabiotic rats. In addition, the function of splenectomy in altering the host-specific resistance of the rat to infection with P. gallinaceum was studied. Removal of the spleen resulted in delay of about a week before the peak of parasitemia, anemic crisis, erythrophagocytosis, and the appearance of agglutinins occurred. Splenectomized rats infected with P. berghei invariably died, while splenectomized rats infected with B. rodhaini all survived; other parameters of these two infections in splenectomized rats were very similar to each other. In parabiotic rats, the single spleen was able to moderate the course of the disease in the conjoined pair for nearly 2 weeks but was not able to overcome the deteriorating influence of the splenectomized animal, since both eventually died. Ordinarily regarded as highly host specific for avian species, P. gallinaceum successfully parasitized splenectomized rats; erythrocytic and probably, exoerythocytic stages, were observed. The morphologic features of the parasite were somewhat changed in the rat. Filaments attached to the parasite were observed and photographed. When parasitized rat blood was inoculated into chickens, the morphologic features of the organism returned to normal, but the peak of parasitemia was delayed in all and lowered in many chickens. Parasites were observed in the peripheral blood of rats between 3 and 13 days postinjection (DPI) and in the liver and bone marrow of rats up to 18 DPI. Results demonstrated the importance of the spleen in both general and specific-host resistance.

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