Drug Resistance in the Malaria-Endemic World
The development of resistance to drugs poses one of the greatest threats to malaria control and results in increased malaria morbidity and mortality. Resistance to currently available antimalarial drugs has been confirmed in only two of the four human malaria parasite species, Plasmodium falciparum and P. vivax. It is unknown if P. malariae or P. ovale has developed resistance to any antimalarial drugs. P. knowlesi, a zoonotic monkey malaria that infects humans in forest fringe areas of Southeast Asia, is fully susceptible to chloroquine and other currently used drugs.
Drug-resistant P. falciparum
Chloroquine-resistant P. falciparum first developed independently in three to four areas in Southeast Asia, Oceania, and South America in the late 1950s and early 1960s. Since then, chloroquine resistance has spread to nearly all areas of the world where falciparum malaria is transmitted.
P. falciparum has also developed resistance to nearly all of the other currently available antimalarial drugs, such as sulfadoxine/pyrimethamine, mefloquine, halofantrine, and quinine. Although resistance to these drugs tends to be much less widespread geographically, in some areas of the world, the impact of multi-drug resistant malaria can be extensive. Most recently, resistance to the artemisinin and non-artemisinin components of artemisinin-based combination therapy has emerged in parts of Southeast Asia, impacting the efficacy of this vital antimalarial class.
Drug-resistant P. vivax
Chloroquine-resistant P. vivax malaria was first identified in 1989 among Australians living in or traveling to Papua New Guinea. P. vivax resistance to chloroquine has also now been identified in Southeast Asia, Ethiopia , and Madagascar.Isolated reports have suggested chloroquine-resistance P. vivax in other countries and regions, but further evaluation is needed. Vivax malaria parasites, particularly from Oceania, show greater resistance to chloroquine than P. vivax isolates from other regions of the world.