Genetics of chloroquine resistance in malaria parasites

Abstract

THE resistance of the malaria parasite of man, Plasmodium falciparum, to treatment with chloroquine is a growing problem, especially in South-east Asia and South America¹. It is not known whether the emergence of resistance is attributable to the selection of resistant mutants under drug pressure, to the spread of naturally resistant forms in the parasite population or to adaptation to the drug by previously sensitive parasites. In malaria parasites of rodents, it has been shown that resistance to the antifolate drug pyrimethamine arises by mutation² and that the genetic factors involved can undergo recombination with other markers in crosses between resistant and sensitive parasite lines³. Resistance to chloroquine in rodent plasmodia seems to take several forms. P. yoelii isolates are innately resistant to the drug⁴, whereas P. berghei and P. vinckei are sensitive. Stable chloroquine resistance has been produced in P. vinckei by drug selection in the laboratory⁵ but resistance developed in this way in P. berghei is usually unstable in the absence of the drug⁶.