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In regions of coendemicity for Plasmodium falciparum and Plasmodium vivax where mefloquine is used to treat P. falciparum infection, drug pressure mediated by increased copy numbers of the multidrug resistance 1 gene (pvmdr1) may select for mefloquine-resistant P. vivax Surveillance is not undertaken routinely owing in part to methodological challenges in detection of gene amplification. Using genomic data on 88 P. vivax samples from western Thailand, we identified pvmdr1 amplification in 17 isolates, all exhibiting tandem copies of a 37.6-kilobase pair region with identical breakpoints. A novel breakpoint-specific polymerase chain reaction assay was designed to detect the amplification. The assay demonstrated high sensitivity, identifying amplifications in 13 additional, polyclonal infections. Application to 132 further samples identified the common breakpoint in all years tested (2003-2015), with a decline in prevalence after 2012 corresponding to local discontinuation of mefloquine regimens. Assessment of the structure of pvmdr1 amplification in other geographic regions will yield information about the population-specificity of the breakpoints and underlying amplification mechanisms.

Original publication

DOI

10.1093/infdis/jiw323

Type

Journal article

Journal

The Journal of infectious diseases

Publication Date

10/2016

Volume

214

Pages

1235 - 1242

Addresses

Global and Tropical Health Division, Menzies School of Health Research, Charles Darwin University, Australia.

Keywords

Humans, Plasmodium falciparum, Plasmodium vivax, Malaria, Falciparum, Malaria, Vivax, Mefloquine, Membrane Transport Proteins, Multidrug Resistance-Associated Proteins, Protozoan Proteins, DNA, Protozoan, Antimalarials, Genomics, Drug Resistance, Multiple, Genotype, Gene Dosage, Thailand