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.

Japanese encephalitis virus (JEV) and other arboviruses are demonstrating an emergence in the southern part of New Guinea Island. JE was previously unknown in this part of the world until 1995 when it was found in the Torres Strait, northern Australia. In this study 96 sera collected from residents of the Timika region of Irian Jaya were tested for antibodies to JEV and related arboviruses by epitope-specific blocking ELISA. Of the 9 sera deemed to be positive for JEV antibodies by ELISA, 5 were collected from persons indigenous to Timika, and who had not travelled to regions where JE is known to be active. This indicates that these individuals were infected with JEV in the Timika area and supports a recent report of a clinical case of JE in this region. Non-immune expatriates visiting or working in the Lowland areas of Irian Jaya and/or Papua New Guinea should consider immunization against JE. Precautions should always be taken to avoid being bitten by any mosquito both in the daytime and at night.

No abstract

Japanese encephalitis (JE) is one of the emerging infectious diseases now widespread in Asia, with recent extension into Torres Strait in northern Australia.1,2 In Indonesia, JE was not considered to be a serious clinical problem,3 although seroprevalence studies showed high prevalence of JE-neutralizing antibody in residents of Java, Kalimantan, Bali, with low prevalence in Sulawesi, Maluka and Irian Jaya.4 Confirmed clinical cases of JE have been rare in Indonesia and mainly have been reported in the west,3 and in tourists visiting Bali.5 No clinical cases of JE have been reported from Irian Jaya. This paper describes a clinical case of JE in a child from Irian Jaya and its confirmation by serology.

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.