An Australian expatriate on regular weekly antimalarial prophylaxis with chloroquine base and Maloprim developed symptomatic Plasmodium vivax infection which failed to respond adequately to 600 mg of chloroquine base. More ominously, a resident of the Highlands region of Papua New Guinea contracted vivax malaria which failed to be cleared by 2400 mg chloroquine base administered over 4 d. Both patients had achieved appropriate blood and plasma concentrations of chloroquine after treatment. Chloroquine-resistant P. vivax is now a clinical fact in Papua New Guinea.

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Bancroftian filariasis is highly endemic in the Ok Tedi region of Papua New Guinea, with a reported mean rate of 39% before the implementation of a single-dose diethylcarbamazine (DEC) treatment programme in 1986. This was followed by a 72% decline in the rate of detectable microfilaraemia and a 40% reduction in pre- and post-treatment splenomegaly. No significant difference was observed when spleen enlargement was compared to the presence of patent malaria. A significant difference in splenomegaly was observed between DEC-treated villagers and their untreated counterparts. Significant differences were reported in the rate of detectable microfilariae of Wuchereria bancrofti, but not of malaria, between the two groups. The number of DEC administrations and the period of time since the first treatment played a significant role immunologically. Significant differences were observed in immunoglobulin (Ig) M and IgG levels and in the extent of splenomegaly between DEC-treated and untreated areas. Filarial infection associated with malaria resulted in higher spleen rates and size. W. bancrofti is a major contributor to splenomegaly in the Ok Tedi region, and splenomegaly associated with bancroftian filariasis can be reduced or controlled by low, well-spaced doses of DEC.

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Halofantrine was administered as prophylaxis for malaria to mine workers returning from endemic areas of Papua New Guinea. The men were randomly assigned to receive 500 mg of halofantrine daily for 3 days (n = 195) or 6 days (n = 150) or a total dose of 1,500 mg of chloroquine over 3 days (n = 55). None of the men receiving halofantrine developed falciparum malaria during the subsequent 28 days, whereas three men receiving chloroquine did develop this disease (P < .02). The administration of halofantrine after departure from an endemic area is one strategy for the prevention of falciparum malaria after short-term exposure.