ABSTRACTMalaria control is hindered by the evolution and spread of resistance to antimalarials, necessitating multiple changes to drug policies over time. A comprehensive antimalarial drug resistance surveillance program is vital for detecting the potential emergence of resistance to antimalarials, including current artemisinin-based combination therapies. An antimalarial drug resistance surveillance study involving 203Plasmodium falciparummalaria-positive children was conducted in western Kenya between 2010 and 2013. Specimens from enrolled children were analyzedin vitrofor sensitivity to chloroquine (CQ), amodiaquine (AQ), mefloquine (MQ), lumefantrine, and artemisinin derivatives (artesunate and dihydroartemisinin) and for drug resistance allele polymorphisms inP. falciparum crt(Pfcrt),Pfmdr-1, and the K13 propeller domain (K13). We observed a significant increase in the proportion of samples with thePfcrtwild-type (CVMNK) genotype, from 61.2% in 2010 to 93.0% in 2013 (P< 0.0001), and higher proportions of parasites with elevated sensitivity to CQin vitro. The majority of isolates harbored the wild-type N allele inPfmdr-1codon 86 (93.5%), with only 7 (3.50%) samples with the N86Ymutant allele (the mutant nucleotide is underlined). Likewise, most isolates harbored the wild-typePfmdr-1D1246 allele (79.8%), with only 12 (6.38%) specimens with the D1246Ymutant allele and 26 (13.8%) with mixed alleles. All the samples had a single copy of thePfmdr-1gene (mean of 0.907 ± 0.141 copies). None of the sequenced parasites had mutations in K13. Our results suggest that artemisinin is likely to remain highly efficacious and that CQ sensitivity appears to be on the rise in western Kenya.
Antimalarial Drug Sensitivity Profile of Western Kenya Plasmodium falciparum Field Isolates Determined by a SYBR Green I in vitro Assay and Molecular Analysis
