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Immunity to falciparum malaria was compared in two populations from malarious areas of southern Sudan and Flores, Indonesia. In Sudan, splenomegaly in adults was rare and anti-plasmodium indirect fluorescent antibody (IFA) titers were low to moderate, 1:1,280 being the modal titer. Sudanese serum was profoundly inhibitory to cultured Plasmodium falciparum, reducing incorporation of radiolabeled hypoxanthine by 63-93% and severely retarding intraerythrocytic parasite development, resulting in moribund crisis-form parasites and virtually no healthy schizonts. In Flores, 64% of the serum donors had splenomegaly greater than or equal to Hackett spleen grade 4 or 5, and the modal IFA titer was 1:10,240. Sera from Indonesia did not retard intraerythrocytic parasite development, but inhibited merozoite erythrocyte invasion 22-87%. Anti-merozoite activity did not correlate with IFA titers. The differences in principal modes of anti-parasitic activity suggest that immunity to malaria in Sudan is based on cell-mediated immune mechanisms associated with crisis forms, merozoite neutralization being of secondary importance. In contrast, malaria immunity in Flores appears to be principally based on anti-merozoite antibody, which does not cause crisis forms and allows for development of reduced numbers of healthy schizonts. This less efficient mechanism may lead to a continuous low-grade parasitemia, which could explain the high specific malaria antibody titers and adult splenomegaly in Flores as compared to Sudan. This latter approach to immunity, being less efficient than the former, apparently results in chronic malaria infections with associated high Ig titers and splenomegaly.