TRAFFICKING OF PLASMODIUM-CHABAUDI ADAMI-INFECTED ERYTHROCYTES WITHINTHE MOUSE SPLEEN

Plasmodium chabaudi adami causes a nonlethal infection in mice. We fou nd that crisis, the time of rapidly dropping parasitemia, was abrogate d by splenectomy, indicating the role of spleen in parasite killing. T he factors that mediate spleen-dependent immunity are not known. An ea rlier study in Plasmodium berghei-infected rats showed an association between increased clearance of heat-treated erythrocytes and the onset of crisis [Wyler, D. J., Quinn, T. C. & Chen, L.-T. (1982) J. Clin. I nvest. 67, 1400-1404]. To determine the potential effects of different vascular beds in parasite killing, we studied the distribution of par asitized erythrocytes and bacteria in the spleens of P. chabaudi adami -infected mice during precrisis (a period of rising parasitemia) and d uring crisis. After intravenous injection, bacteria were localized pre dominantly in the marginal zone. In contrast, parasitized erythrocytes were found in the red pulp. We also found that during precrisis, a ti me of no immunity, the uptake of radiolabeled infected erythrocytes by the spleen was increased, not decreased. These data imply that no cha nge occurs in the flow of parasitized erythrocytes through the spleen during the transition to an immune state (crisis). Our observations su ggest that immune effector mechanisms, not circulatory changes, accoun t for spleen-dependent parasite killing during a P. chabaudi adami inf ection in mice.