Interaction of Chemotherapy and the immune response in experimental malaria infections

Plasmodium chabaudl malaria Infections in CBA mice showed a characteristic and consistent pattern. Primary parasitaemias reached a peak of 30-50% but resolved within 3 weeks. Small recrudescences occurred at 4 and at 8 weeks and parasites were demonstrable up to 9 weeks by subinoculation of blood and other tissues. Infections in T-lymphocyte deprived mice were not fatal but the mice remained parasitaemic for at least 120 days. By contrast, P. berghel killed both intact and deprived mice; the survival time of the T-cell deprived mice was significantly longer. Treatment of P. chabaudl infections with chloroquine, quinine or pyrimethamine was generally more effective in intact than in T-cell deprived mice. Chloroquine and quinine treatment of P. berghel infections, however, was more effective in the deprived mice. None of the recrudescences of either P. berghel or P. chabaudl infections following treatment showed evidence of increased resistance to the drugs. Mice treated with cortisone acetate died of P. chabaudi infections and were not as effectively treated with quinine or chloroquine as infected controls. Induced protein energy malnutrition prolonged P. chabaudi parasitaemias but these were as readily treated as infections in controls on balanced diet. Suppression of P. chabaudi infections by subcurative chemotherapy gave rise to a strong immunity. Curative treatment given early in infections resulted in only partial immunity to challenge whereas treatment late in the infection gave a high degree of resistance to infection. Generalized immunodepression during P. chabaudi infection was related to the degree of parasitaemia. There was some increase in the rate of catabolism of immunoglobulins as a result of the infection. P. chabaudi infections were significantly suppressed in mice which had mature Schistosoma mansoni infections but acute or chronic infections did not influence development of the schistosomiasis.