Date of this Version
Published in Antimicrobial Agents and Chemotherapy (November 2004) 48:11, p. 4075-4083. DOI: 10.1128/AAC.48.11.4075–4083.2004
Emerging resistance to chloroquine (CQ) by Plasmodium vivax threatens the health of the hundreds of millions of people routinely exposed to the risk of infection with this organism. CQ has been the first-line therapy for vivax malaria since 1946 (32, 115). Plasmodium falciparum developed resistance to CQ in the 1950s (110), and today it occurs globally (91). Resistance by P. vivax was unknown until 1989, when Australians repatriated from Papua New Guinea failed routine treatment (94). Subsequent reports affirmed that finding, and CQ-resistant P. vivax (CRPV) was reported from Indonesia (8, 35, 99, 100, 111). Reports from Myanmar (76, 82) and India (56, 107) followed. CRPV appeared in travelers from Guyana, South America (88). However, studies in Thailand (38, 72, 103), the Philippines (10), and Vietnam (105) revealed only CQ-sensitive P. vivax. Surveys in Indonesia revealed a low frequency of CRPV in the west (~10%) (15, 16, 49, 50, 51, 53, 75) and a higher risk in the east (~45%) (9, 18, 52, 81, 102, 106). This minireview summarizes the present state of knowledge of CRPV as a scientific, clinical, and public health problem. It examines the genesis of CQ therapy for P. vivax and the laboratory and clinical data underpinning the diagnosis of CRPV. The available data showing the global distribution of CRPV are listed. Finally, the clinical data on alternative therapies against CRPV are reviewed.