The global emergence and spread of malaria parasites resistant to antimalarial drugs is the major problem in malaria control. The genetic basis of the parasite's resistance to the antimalarial drug chloroquine (CQ) is well-documented, allowing for the analysis of field isolates of malaria parasites to address evolutionary questions concerning the origin and spread of CQ-resistance. Here, we present DNA sequence analyses of both the second exon of the
Plasmodium falciparum
CQ-resistance transporter (
pfcrt) gene and the 5' end of the
P. falciparum multidrug-resistance 1 (
pfmdr-1) gene in 40
P. falciparum field isolates collected from eight different localities of Odisha, India. First, we genotyped the samples for the
pfcrt K76T and
pfmdr-1 N86Y mutations in these two genes, which are the mutations primarily implicated in CQ-resistance. We further analyzed amino acid changes in codons 72-76 of the
pfcrt haplotypes. Interestingly, both the K76T and N86Y mutations were found to co-exist in 32 out of the total 40 isolates, which were of either the CVIET or SVMNT haplotype, while the remaining eight isolates were of the CVMNK haplotype. In total, eight nonsynonymous single nucleotide polymorphisms (SNPs) were observed, six in the
pfcrt gene and two in the
pfmdr-1 gene. One poorly studied SNP in the
pfcrt gene (A97T) was found at a high frequency in many
P. falciparum samples. Using population genetics to analyze these two gene fragments, we revealed comparatively higher nucleotide diversity in the
pfcrt gene than in the
pfmdr-1 gene. Furthermore, linkage disequilibrium was found to be tight between closely spaced SNPs of the
pfcrt gene. Finally, both the
pfcrt and the
pfmdr-1 genes were found to evolve under the standard neutral model of molecular evolution.
