Chloroquine-Resistant Plasmodium vivax Malaria in Borneo.

Abstract

Chloroquine-resistant Plasmodium vivax infection has been reported from Myanmar (Burma),’ the island of Nias, Indonesia,‘ Papua New Guinea,”‘ and Irian Jaya (Indonesian New Guinea).’.” We describe a case of chloroquine-resistant I? vivux infection acquired in Sabah, Borneo. A 58-year-old Swedish man was admitted to our department in June 1993 with intermittent high fever, malaise, and headache. Nine days before adnlission, the patient had returned from a 4-week period of work within a forest research project outside Tawau in Sabah, Borneo. From the date of arrival in Borneo until admission, he had taken chloroquine (300 mg base weekly) as prophylaxis. On adniission, I? vivax trophozoites and gametocytes were found in thick and thin bloodfilms. Blood concentrations of chloroquine and desetylchloroquine, 2 days after the last dose, were 540 nmol/L and 170 nmol/L, respectively, in a sample. After treatment with mefloquine (total dose 1500 mg), the patient recovered uneventfully.To prevent further relapse, primaquine 22.5 mg base daily for 14 days was given. Nevertheless, during the following 6 months the patient experienced two relapses of I? vivux infection.The first was in September 1993; the patient fell ill when returning from a 6-day stay without malaria prophylaxis in an urban area ofKota Kmabalu in Sabah,Borneo.This was his only visit to an endemic area afier the initial hospitalization. I? vivux was again demonstrated, and treatment with quinine 700 mg t.i.d. for 1 day and thereafter 600 mg t.i.d. for 3 days was given, followed by primaquine 22.5 mg base per day for 14 days.The patient recovered and, on a follow-up in October 1993, no malaria plasmodies were found in blood smears. The second relapse occurred in January 1994. I! vivax rings, gametocytes, and trophozoites were again found in blood smears.The patient was only treated with mefloquine (total dose of 1500 mg) and recovered. Strong evidence indicates that the present I? vivux strain was chloroquine resistant. The patient developed symptomatic infection in spite of having putatively protective whole blood levels of chloroquine.’ Furthermore, despite two courses of primaquine treatment, he had two verified relapses of I? vivax infection.This implies that the strain probably also was resistant to primaquine, which is well-known in the area. Compliance was, however, not controlled by analyses of blood concentrations of priniaquine. Reinfection with I? vivax during the second brief visit to Borneo seems highly unlikely, as symptoms appeared within 6 days after arrival in Borneo and he stayed in an urban area with limited risk of malaria transmission. This is, to our knowledge, the first report of a chloroquine-resistant Z? vivax infection acquired in Borneo. Although the magnitude of the problem is not known, our report supports further geographical spread of chloroquine-resistant vivax strains in the region.