Antimalarial drug resistance has threatened global malaria control since chloroquine (CQ)-resistant emerged in Asia in the 1950s. Understanding the impacts of changing antimalarial drug policy on resistance is critical for resistance management. isolates were collected from 2003 to 2015 in western Kenya and analyzed for genetic markers associated with resistance to CQ (), sulfadoxine-pyrimethamine (SP) (/), and artemether-lumefantrine (AL) (/) antimalarials. In addition, household antimalarial drug use surveys were administered. 76T prevalence decreased from 76% to 6% from 2003 to 2015. / quintuple mutants decreased from 70% in 2003 to 14% in 2008, but increased to near fixation by 2015. SP "super resistant" alleles 581G and 613S/T were not detected in the 2015 samples that were assessed. The N86-184F-D1246 haplotype associated with decreased lumefantrine susceptibility increased significantly from 4% in 2005 to 51% in 2015. No mutations that have been previously associated with artemisinin resistance were detected in the study populations. The increase in / quintuple mutants that associates with SP resistance may have resulted from the increased usage of SP for intermittent preventative therapy in pregnancy (IPTp) and for malaria treatment in the community. Prevalent / mutations call for careful monitoring of SP resistance and effectiveness of the current IPTp program in Kenya. In addition, the commonly occurring N86-184F-D1246 haplotype associated with increased lumefantrine tolerance calls for surveillance of AL efficacy in Kenya, as well as consideration for a rotating artemisinin-combination therapy regimen.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5930917 | PMC |
http://dx.doi.org/10.4269/ajtmh.17-0763 | DOI Listing |
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