Chloroquineresistant

Chloroquineresistant refers to the reduced susceptibility of malaria parasites to the antimalarial drug chloroquine, resulting in diminished clinical or parasitological effectiveness. The resistance phenotype is mainly described in Plasmodium falciparum, with variable occurrence in P. vivax and other species.

In P. falciparum, the best characterized mechanism involves mutations in the pfcrt gene, particularly the K76T substitution, which alters drug transport and reduces chloroquine accumulation in the parasite’s digestive vacuole. Additional mutations in pfmdr1 and changes in gene copy number can modulate the level of sensitivity and influence treatment outcomes. In P. vivax, resistance is associated with polymorphisms in pvcrt-o and pvmdr1, though the molecular basis is less well defined and research is ongoing.

Historically, chloroquine resistance was first detected in the late 1950s–1960s in Southeast Asia and the Pacific and subsequently spread to many regions, including Africa. The spread of resistance led to major changes in malaria treatment policies and public health strategies, with many countries adopting artemisinin-based combination therapies (ACTs) as first-line treatment for falciparum malaria.

Current implications include reduced use of chloroquine for falciparum malaria in areas where resistance is established, and continued use in settings where the parasite is still susceptible or for non-falciparum malaria as appropriate. Ongoing surveillance, therapeutic efficacy studies, and the development of new antimalarial agents remain essential to managing resistance and maintaining effective malaria control.