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Open AccessArticle

Molecular detection of antimalarial drug resistance in Plasmodium vivax from returned travellers to NSW, Australia during 2008–2018

1
Marie Bashir Institute for Infectious Diseases and Biosecurity, The University of Sydney, Sydney, NSW 2006, Australia
2
Westmead Institute for Medical Research, Westmead, NSW 2145, Australia
3
Westmead Hospital (Research and Education Network), Westmead, NSW 2145, Australia
4
Department of Microbiology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla 90110, Thailand
5
School of Life Sciences, University of Technology Sydney, Ultimo, NSW 2007, Australia
6
Centre for Infectious Diseases and Microbiology Laboratory Services, NSW Health Pathology-ICPMR, Westmead Hospital, Westmead, NSW 2145, Australia
*
Author to whom correspondence should be addressed.
Pathogens 2020, 9(2), 101; https://doi.org/10.3390/pathogens9020101
Received: 23 October 2019 / Revised: 27 January 2020 / Accepted: 27 January 2020 / Published: 5 February 2020
(This article belongs to the Special Issue Addressing Plasmodium Vivax: from Control to Elimination )
To monitor drug resistance in Plasmodium vivax, a multidrug resistance 1 (Pvmdr1) gene and a putative transporter protein (Pvcrt-o) gene were used as molecular markers for chloroquine resistance. The biomarkers, the dihydrofolate reductase (Pvdhfr) gene and the dihydropteroate synthetase (Pvdhps) gene, were also used for the detection of resistance to sulphadoxine-pyrimethamine (SP); this drug is often accidentally used to treat P. vivax infections. Clinical blood samples (n = 120) were collected from patients who had been to one of eight malaria-endemic countries and diagnosed with P. vivax infection. The chloroquine resistance marker, the Pvmdr1 gene, showed F976:L1076 mutations and L1076 mutation. A K10 insertion in the Pvcrt-o gene was also found among the samples successfully sequenced. A combination of L/I57:R58:M61:T117 mutations in the Pvdhfr gene and G383:G553 mutations in the Pvdhps gene were also observed. Mutations found in these genes indicate that drug resistance is present in these eight countries. Whether or not countries are using chloroquine to treat P. vivax, there appears to be an increase in mutation numbers in resistance gene markers. The detected changes in mutation rates of these genes do suggest that there is still a trend towards increasing P. vivax resistance to chloroquine. The presence of the mutations associated with SP resistance indicates that P. vivax has had exposure to SP and this may be a consequence of either misdiagnosis or coinfections with P. falciparum in the past.
Keywords: plasmodium vivax; drug resistance; chloroquine; sulfadoxine-pyrimethamine plasmodium vivax; drug resistance; chloroquine; sulfadoxine-pyrimethamine
MDPI and ACS Style

Noisang, C.; Meyer, W.; Sawangjaroen, N.; Ellis, J.; Lee, R. Molecular detection of antimalarial drug resistance in Plasmodium vivax from returned travellers to NSW, Australia during 2008–2018. Pathogens 2020, 9, 101.

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