No abstract

Drug resistance is an important problem hindering malaria elimination in tropical areas. Point mutations in Plasmodium falciparum dihydrofolate reductase (Pfdhfr) and dihydropteroate synthase (Pfdhps) genes confer resistance to antifolate drug, sulfadoxine-pyrimethamine (SP) while P. falciparum chloroquine-resistant transporter (Pfcrt) genes caused resistance to chloroquine (CQ). Decline in Pfdhfr/Pfdhps and Pfcrt mutations after withdrawal of SP and CQ has been reported. The aim of present study was to investigate the prevalence of Pfdhfr, Pfdhps, and Pfcrt mutation from 2 endemic areas of Thailand. All of 200 blood samples collected from western area (Thai-Myanmar) and southern area (Thai-Malaysian) contained multiple mutations in Pfdhfr and Pfdhps genes. The most prevalent haplotypes for Pfdhfr and Pfdhps were quadruple and double mutations, respectively. The quadruple and triple mutations of Pfdhfr and Pfdhps were common in western samples, whereas low frequency of triple and double mutations was found in southern samples, respectively. The Pfcrt 76T mutation was present in all samples examined. Malaria isolated from 2 different endemic regions of Thailand had high mutation rates in the Pfdhfr, Pfdhps, and Pfcrt genes. These findings highlighted the fixation of mutant alleles causing resistance of SP and CQ in this area. It is necessary to monitor the re-emergence of SP and CQ sensitive parasites in this area.

Plasmodium vivax is the most widespread parasite causing human malaria and the major cause of malaria in most of Asia and Latin America. Anemia is considered as major important markers of severity during the clinical course of severe Plasmodium vivax malaria. The hypnozoitocidal and schizonticidal anti-malarial drug for the radical cure of vivax malaria infection is primaquine. The main adverse effect of primaquine is hemolytic anemia in individual glucose-6-phosphate dehydrogenase (G6PD) deficiency. The objective of this study was to determine the prevalence of G6PD variants in malaria patients residing along Thai-Mynmar and Thai-Malaysian border. Total of one hundred and seventy-one blood samples with Plasmodium vivax identification were collected from Kanchanaburi and Ranong province (Thai-Mynmar), and Yala province (Thai-Malaysian). The G6PD deficiency variants were analyzed by polymerase chain reaction and restriction fragment length polymorphism (PCR/RFLP). Three specific primers of each G6PD deficiency variants mostly found in Thailand were investigated including Mahidol variants (487G>A), Chinese-4 variants (392G>T), and Viangchan variants (871G>A). Approximately five percent of isolates were identified as G6PD deficiency with Mahidol and Chinese 4 variant. According to Thai-myanmar border, 5.4% of Mahidol variant and 0.7% of Chinese 4 were found. Whereas, Thai-Malaysian border only one variant with 2.3% of were found. The coexistence might be related to high hemolytic risk in malaria patients leading to severity due to insufficient of G6PD enzyme in patients who live in different endemic area. No Viangchan variants was found. Dosage regimen of primaquine for treatment of Plasmodium vivax malaria in this population may need to be optimized, based on G6PD variants information. With this limited G6PD variants, other variation of G6PD should be required to obtain accurate genetic mapping of G6PD variants in malaria patients residing in malaria endemic areas along Thai-neighboring borders.