Experimental infection with Plasmodium chabaudi in rats. Observations on adaptation and the immune responses to infection.

Plasmodium chabaudi was adapted to rats after some initial refractoriness. Progressive adaptation was indicated by shortening of the prepatent period and increases in peak parasitemia with successive passages. Rats infected with parasites of early passages resisted the infection, and even splenectomized rats quickly recovered. However, the parasites appeared to become more virulent with successive passages and after the 45th passage, all adult rats inoculated with the parasite died with severe hemolytic anemia. After adaptation, infections of the rat strain appeared to stimulate resistance in mice that was more effective against challenge with parasites of the homologous strain than it was against challenge with mouse strain parasites. Rats recovered from P. chabaudi were highly resistant to the homologous strain of P. chabaudi, but they were no more resistant to Babesia radhaini than were normal rats. However, when the rat strain was used to immunize mice, they were as resistant to B. rodhaini as they were to mouse strain P. chabaudi. Serologic studies made on rats with acute infection indicated that anemia was associated with antibody to erythrocytes as well as with high parasitemia. The soluble serum antigen (SA) associated with malarial and babesial infections was not present and its antibody was not detected in serum of recovered rats. However, antibody to SA was detected in blood mice that had recovered from rat strain P. chabaudi infection. Thus acquired resistance to B. rodhaini appeared to have been associated with elaboration of SA.