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Chloroquine pressure was applied over a 22 month period on a somewhat isolated, malarious rubber estate by examination of residents at 4-week intervals and treatment of parasitaemias with chloroquine. During this time the monthly attack rate for P. falciparum rose four-fold to an average of nearly 18% per month, while that of P. vivax remained relatively constant at about 8%. Eight in vivo chloroquine resistance studies, which allowed both detection of late recrudescing R-I resistance and estimation of the risk of reinfection, showed an apparent rise in the drug resistance rate, from 12% to 20% prior to the study to the range of 40-50%. Virtually all resistance encountered was R-I in nature. There was no convincing evidence of chloroquine resistance among 148 tested P. vivax infections.

A cohort of 62 persons living in a malaria-endemic area was examined by serology and by blood film 14 times over a 56-week period. Serologic responses (indirect hemagglutination test) of the group as a whole reflected the malaria transmission as determined by blood slide examination. The serologic responses of individuals showed titer changes that were not always consistent with blood slide results. The use of chloroquine may have modified the host's immune response.

The indirect hemagglutination test was used to measure malaria antibody levels in residents of an endemic area of Malaysia. Blood specimens were collected at 4-week intervals for a year. Seropositivity rates increased with age and number of episodes of malaria in young children. Although antibody levels were variable, titers tended to rise with parasitemia and fall in the absence of detected parasites. In general, the serologic indices tended to reflect the parasitologic findings.