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Migrants from Java arrive in hyperendemic Papua, Indonesia lacking exposure to endemic malaria. We evaluated records of evacuation to hospital with a diagnosis of severe malaria from a transmigration village in northeastern Papua. During the first 30 months, 198 residents with severe disease were evacuated (7·5 evacuations/100 person-years). During this period the risk of evacuation for adults (>15 years of age) was 2·8. (95% CI=2·1–3·8; P16; 95% CI[ges ]2·0–129; P=0·0009), and diminished during the second 6 months (RR=9·4; 95% CI=2·7–32·8; PP=0·0004). During the next two 6-month intervals, the RR for adults was 1·6 and 1·5 (95% CI range 0·8–2·6; P

Chloroquine combined with primaquine was evaluated for therapy of uncomplicated malaria caused by Plasmodium falciparum in nonimmune Javanese migrants to northeastern Papua, Indonesia. Subjects were randomized to treatment with standard chloroquine therapy (25 mg/kg in 3 doses over the course of 48 hours) with 30 mg primaquine administered daily for 28 days (n = 25) or a placebo of primaquine (n = 28). The 14-day cumulative incidence of therapeutic failure was 56% with primaquine and 79% with placebo (odds ratio [OR], 0.35; 95% confidence interval [CI], 0.1-1.3; P = 0.08). Primaquine administered daily created a marginally significant improvement in therapeutic efficacy at day 14, but not at day 7 (20% versus 36%; OR, 0.2; 95% CI, 0.1-1.8; P = 0.2) or day 28 (82% versus 93%; OR, 0.31; 95% Cl, 0.04-2.1; P = 0.23). This report corroborates studies suggesting that therapeutic doses of primaquine exert no discernible effect on parasitemia by P. falciparum.

Chloroquine remains the first-line therapy for uncomplicated malaria in Indonesia. Among a series of trials of chloroquine for malaria on this archipelago conducted since 1990, we now report the highest risk of therapeutic failure yet observed. A clinical trial of standard chloroquine therapy for uncomplicated malaria at Arso PIR V in northeastern Indonesian Papua was conducted during 1995. We enrolled 104 non-immune subjects infected with Plasmodium falciparum (n = 55), P. vivax (n = 29), or P. falciparum plus P. vivax (n = 20) and administered supervised standard chloroquine therapy (10 + 10 + 5 mg/kg at 24-hour intervals). The 28-day cumulative incidence of therapeutic failure was 95% for P. falciparum, 84% for P. vivax, and 100% for mixed infections. Only one subject each for P. falciparum and P. vivax remained free of parasites at day 28. All recurrent parasitemias occurred with whole blood levels of chloroquine plus desethylchloroquine exceeding 100 ng/ml. These findings document almost complete failure of chloroquine against P. falciparum or P. vivax near the northeastern coast of Indonesian Papua.

Between January 1998 and December 2000, the Jayapura Provincial Public Hospital in northeastern Indonesian New Guinea (Papua) admitted 5,936 patients with a diagnosis of malaria. The microscopic diagnosis at admission was Plasmodium falciparum (3,976, 67%), Plasmodium vivax (1,135, 19%), Plasmodium malariae (8, < 1%), and mixed species infections (817, 14%). Approximately 9% (367) of patients were classified as having severe malaria (277 P. falciparum, 36 P. vivax, 53 mixed infections, and 1 P. malariae) and 88 died (79 P. falciparum/mixed infections and 9 P. vivax). Risk of fatal outcomes among severe malaria patients was indistinguishable between those with falciparum versus vivax malaria (OR = 0.89; P = 0.771). Compared with non-pregnant women, pregnant women showed no higher risk of severe malaria (P = 0.643) or death caused by severe malaria (P = 0.748). This study compares admissions per population (based on census data), parasitemia, morbidity, and mortality among children versus adults, pregnant versus non-pregnant women, and urban/suburban versus rural residents.

This report describes one of the few remaining foci of endemic malaria on the island of Java, the Kokap subdistrict, near the Southcentral coast. Kokap was hypoendemic in June 1994 with prevalence of parasitemia at 0.98% (n = 10,606 of 40,246 residents). Plasmodium vivax comprised 63% of infections and P. falciparum all others. The incidence of indigenous infection during 1993 was 48 cases/1,000 person-years (p-yr), and it was relatively uniform among age groups (38 to 53/1,000 p-yr). Nine deaths due to malaria had been recorded in the past three years (8.3 deaths per 100,000 p-yr); the case fatality rate was 0.17%. Subdistricts adjoining Kokap to the north, east, and south reported incidence rates of < 2 cases/1,000 p-yr. To the west, Purworejo District had a high case incidence (11 cases/1,000 p-yr) but other districts to the west did not (< 1.2 cases/1,000 p-yr). The highest case incidence village area within Kokap (169 cases/1,000 p-yr) bordered the district of Purworejo to the west. Endemic malaria in Kokap and Purworejo coincided with where steep hills and narrow valleys dominated the terrain.

UJ1 COBA DEC-GARAM UNTUK PEMBERANTASAN FILARIASIS DI JAMBI, KALIMANTAN SELATAN DAN SULAWESI TENGAH

Telah dilakukan evaluasi obat-obat antimalaria in-vitro dan in-vivo untuk menentukan pola resistensi dan memanfaatkan data ini untuk melakukan sistem pengamatan yang efektif. Semua penelitian pengobatan dan pencegahan malaria di lapangan dan rumah sakit dalam kurun waktu 1981 - 1995 ditelaah. Pertama kali kasus resistensi P. falciparum terhadap klorokuin ditemukan di Kalimantan Timur pada tahun 1973, dan telah menyebar ke seluruh (27) propinsi Indonesia dengan derajat RI - RIIL Pada saat ini, resistensi Riil telah didapatkan di 20 propinsi, sedangkan pada tahun 1981-1985 hanya di 4 propinsi. Kasus malaria vivaks resisten klorokuin dilaporkan pertama kali dari Sumatera Utara (P. Nias) pada tahun 1991, dan kemudian ditemukan di Irian Jaya (41%), Sumatera Utara (13%), Nusa Tenggara Timur (8%), Sulawesi Utara (2%) dan Jakarta (laporan kasus yang didapatkan dari transfusi darah). Malaria falsiparum yang tercatat resisten sulfadoksin-pirimetamin didapatkan di 11 propinsi dengan derajat RI - RII. P. falciparum resisten in-vitro juga didapatkan terhadap kina (6 propinsi), meflokuin (5 propinsi) dan amodiakuin (4 propinsi). Beberapa obat antimalaria baru (meflokuin, halofantrin dan derivat artemisinin) telah diteliti dan ternyata efektif untuk pengobatan malaria tanpa komplikasi. Penelitian pencegahan menunjukkan angka pencegahan untuk klorokuin 41-92%, sulfadoksin- pirimetamin 98%, primakuin 89-92%, doksisiklin 99% dan meflokuin 100 %. Efek samping obat-obat antimalaria tersebut umumnya ringan. Di Indonesia, penyebaran malaria falsiparum resisten klorokuin R1II dan malaria falsiparum resisten multidrug merupakan masalah kesehatan masyarakat yang serius dan tantangan dalam pengobatan. Demikian pula kehadiran malaria vivaks resisten klorokuin menimbulkan masalah baru yang lain. Oleh sebab itu obat-obat antimalaria yang didistribusikan sebaiknya dikemas per paket untuk dosis obat pengobatan yang lengkap dengan keterangan cara minum obat yang jelas. Dengan demikian dapat dicegah pemberian dosis pengobatan yang tidak cukup dan berkembangnya resistensi obat. Selama obat antimalaria baru belum tersedia di Indonesia, perlu dilakukan penelitian perbaikan efikasi obat antimalaria yang sudah ada. Obat pencegahan alternatif yang aman dan efektif untuk anak-anak, ibu hamil dan menyusui juga perlu diteliti.

Telah dilakukan penelitian tentang produksi gametosit dari P. falciparum secara in-vivo di Batang, Jawa Tengah. Hasil penelitian ini menunjukkan bahwa jumlah rata-rata gametosit sebelum diobati de­ngan Fansidar adalah 75 per ml darah, dan jumlah rata-rata pada hari 7 sesudah diobati adalah 654 per ml darah. Hal ini berarti bahwa perbandingan jumlah rata-rata sesudah : sebelum pengobatan adalah 8,7 : 1. Gametosit yang terbentuk sesudah pengobatan ini ternyata infektif untuk nyamuk Anopheles aconitus yang digigitkan pada volunteer, dan menghasilkan sporosoit pada hari 15—16 sesudah di-in-feksikan. Hasil tersebut menunjukkan bahwa pengobatan menggunakan Fansidar saja, akan dapat me­ningkatkan transmisi malaria falciparum.

Background Accurate information about the burden of malaria infection at the district or provincial level is required both to plan and assess local malaria control efforts. Although many studies of malaria epidemiology, immunology, and drug resistance have been conducted at many sites in Indonesia, there is little published literature describing malaria prevalence at the district, provincial, or national level. Methods Two stage cluster sampling malaria prevalence surveys were conducted in the wet season and dry season across West Sumba, Nusa Tenggara Province, Indonesia. Results Eight thousand eight hundred seventy samples were collected from 45 sub-villages in the surveys. The overall prevalence of malaria infection in the West Sumba District was 6.83% (95% CI, 4.40, 9.26) in the wet season and 4.95% (95% CI, 3.01, 6.90) in the dry. In the wet season Plasmodium falciparum accounted for 70% of infections; in the dry season P. falciparum and Plasmodium vivax were present in equal proportion. Malaria prevalence varied substantially across the district; prevalences in individual sub-villages ranged from 0–34%. The greatest malaria prevalence was in children and teenagers; the geometric mean parasitaemia in infected individuals decreased with age. Malaria infection was clearly associated with decreased haemoglobin concentration in children under 10 years of age, but it is not clear whether this association is causal. Conclusion Malaria is hypoendemic to mesoendemic in West Sumba, Indonesia. The age distribution of parasitaemia suggests that transmission has been stable enough to induce some clinical immunity. These prevalence data will aid the design of future malaria control efforts and will serve as a baseline against which the results of current and future control efforts can be assessed.

Between January 1998 and December 2000, the Jayapura Provincial Public Hospital in northeastern Indonesian New Guinea (Papua) admitted 5,936 patients with a diagnosis of malaria. The microscopic diagnosis at admission was Plasmodium falciparum (3,976, 67%), Plasmodium vivax (1,135, 19%), Plasmodium malariae (8,1%), and mixed species infections (817, 14%). Approximately 9% (367) of patients were classified as having severe malaria (277 P. falciparum, 36 P. vivax, 53 mixed infections, and 1 P. malariae) and 88 died (79 P. falciparum/mixed infections and 9 P. vivax). Risk of fatal outcomes among severe malaria patients was indistinguishable between those with falciparum versus vivax malaria (OR = 0.89; P = 0.771). Compared with non-pregnant women, pregnant women showed no higher risk of severe malaria (P = 0.643) or death caused by severe malaria (P = 0.748). This study compares admissions per population (based on census data), parasitemia, morbidity, and mortality among children versus adults, pregnant versus non-pregnant women, and urban/suburban versus rural residents.

Onset of clinical immunity to Plasmodium falciparum occurred among Javanese migrants to Indonesian Papua. Surveillance of the 243 migrants investigated began on the day of their arrival in Indonesian Papua and continued for 33 months. Asexual parasitaemia without fever constituted objective evidence of clinical immunity. Compared with first infection the odds ratio (OR) for not having fever at the fourth infection within 24 months was 3.2 [95% confidence interval (CI)=1.03–10.2; P=0.02]. The corresponding OR with fewer infections within 24 months was not distinguishable from 1.0. The level of the fourth parasitaemia within 24 months (N=58) was classified as ‘high’ or ‘low’ in relation to the median count at first infection (840 parasites/ml; N=187). Fourth parasitaemias that were low —but not those that were high (OR=1.8; CI=0.6–5.4; P=0.35)— were associated with dramatic protection from fever (OR=31; CI=3.5–1348; P=0.0001). Among the adult subjects the risk of fever with low parasitaemia was significantly higher at the first infection than at the fourth (OR=12.6; CI=1.7–530; P=0.005) indicating the development of clinical immunity. A similar but less marked pattern appeared among the children investigated (OR=6.5; CI=0.8–285; P=0.06). (authors)

Chloroquine remains the first-line therapy for uncomplicated malaria in Indonesia. Among a series of trials of chloroquine for malaria on this archipelago conducted since 1990, we now report the highest risk of therapeutic failure yet observed. A clinical trial of standard chloroquine therapy for uncomplicated malaria at Arso PIR V in northeastern Indonesian Papua was conducted during 1995. We enrolled 104 non-immune subjects infected with Plasmodium falciparum (n = 55), P. vivax (n = 29), or P. falciparum plus P. vivax (n = 20) and administered supervised standard chloroquine therapy (10 + 10 + 5 mg/kg at 24-hour intervals). The 28-day cumulative incidence of therapeutic failure was 95% for P. falciparum, 84% for P. vivax, and 100% for mixed infections. Only one subject each for P. falciparum and P. vivax remained free of parasites at day 28. All recurrent parasitemias occurred with whole blood levels of chloroquine plus desethylchloroquine exceeding 100 ng/ml. These findings document almost complete failure of chloroquine against P. falciparum or P. vivax near the northeastern coast of Indonesian Papua.

Background Drug resistant malaria poses an increasing public health problem in Indonesia, especially eastern Indonesia, where malaria is highly endemic. Widespread chloroquine (CQ) resistance and increasing sulphadoxine-pyrimethamine (SP) resistance prompted Indonesia to adopt artemisinin-based combination therapy (ACT) as first-line therapy in 2004. To help develop a suitable malaria control programme in the district of West Sumba, the seasonal distribution of alleles known to be associated with resistance to CQ and SP among Plasmodium falciparum isolates from the region was investigated. Methods Plasmodium falciparum isolates were collected during malariometric surveys in the wet and dry seasons in 2007 using two-stage cluster sampling. Analysis of pfcrt, pfmdr1, pfmdr1 gene copy number, dhfr, and dhps genes were done using protocols described previously. Results and Discussion The 76T allele of the pfcrt gene is nearing fixation in this population. Pfmdr1 mutant alleles occurred in 72.8% and 53.3%, predominantly as 1042D and 86Y alleles that are mutually exclusive. The prevalence of amplified pfmdr1 was found 41.9% and 42.8% of isolates in the wet and dry seasons, respectively. The frequency of dhfr mutant alleles was much lower, either as a single 108N mutation or paired with 59R. The 437G allele was the only mutant dhps allele detected and it was only found during dry season. Conclusion The findings demonstrate a slighly higher distribution of drug-resistant alleles during the wet season and support the policy of replacing CQ with ACT in this area, but suggest that SP might still be effective either alone or in combination with other anti-malarials.