The mechanism of chloroquine (CQ) resistance in Plasmodium falciparum is not clearly understood.
This study has shown that high variation in the prevalence of T76 mutations of P. falciparum is linked with the level of CQ stocking and usage within study area.
Mutations in the chloroquine resistance transporter (PfCRT) are the primary determinant of chloroquine (CQ) resistance in the malaria parasite Plasmodium falciparum.
Drug resistant strains of the malaria parasite, Plasmodium falciparum, have rendered chloroquine ineffective throughout much of the world.
CQ withdrawal in Tanzania has resulted into >90% recovery of susceptibility in ten years of withdrawal.
In vitro CQ-resistance estimated in this study, estimated by the DELI test, was very similar to that observed in clinical trials, suggesting that in vitro procedures developed by capable local laboratories are useful in the surveillance of CQ-resistance in the Amazon; concurrent Amazon P. vivax strains with both CQ and MQ resistance may be common; and a non-synonymous mutation at pvdhps codon 382 (S[rightwards arrow]C) was associated to in vitro susceptibility to CQ, needing further studies to be confirmed.
We describe here the results of antimalarial therapeutic efficacy studies conducted in Cambodia from 2008 to 2010.
We report the discovery of new potent inhibitors of the growth of Plasmodium falciparum chloroquine (CQ)-resistant W2 strain.
The emergence of highly chloroquine (CQ) resistant P. vivax in Southeast Asia has created an urgent need for an improved understanding of the mechanisms of drug resistance in these parasites, the development of robust tools for defining the spread of resistance, and the discovery of new antimalarial agents.
The emergence and spread of Plasmodium falciparum with resistance to chloroquine (CQ), the safest and cheapest anti-malarial drug, coupled with the increasing cost of alternative drugs especially in developing countries have necessitated the urgent need to tap the potential of plants for novel anti-malarials.