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Abstract
One of the fundamental steps toward malaria control is the use of antimalarial drugs. The success of antimalarial treatment can be affected by the presence of drug-resistant populations of Plasmodium falciparum. To assess resistance, we used molecular methods to examine 351 P. falciparum isolates collected from 4 sentinel sites in Mozambique for K13, pfmdr1, pfcrt, and pfdhps polymorphisms and for plasmepsin2 (pfpm2) and pfmdr1 copy numbers. We found multiple copies of pfpm2 in 1.1% of isolates. All isolates carried K13 wild-type alleles (3D7-like), except 4 novel polymorphisms (Leu619Leu, Phe656Ile, Val666Val, Gly690Gly). Prevalence of isolates with pfcrt mutant (K76T) allele was low (2.3%). Prevalence of isolates with pfdhps mutant alleles (A437G and K540E) was >80%, indicating persistence of sulfadoxine/pyrimethamine resistance; however, markers of artemisinin were absent, and markers of piperaquine resistance were low. Piperaquine resistance isolates may spread in Mozambique as dihydroartemisinin/piperaquine drug pressure increases.
Highlights
One of the fundamental steps toward malaria control is the use of antimalarial drugs
In 2002, chloroquine monotherapy was replaced with sulfadoxine/pyrimethamine/amodiaquine as the first line of treatment against uncomplicated malaria [33]; 2 years later, this combination was replaced with artesunate/sulfadoxine/pyrimethamine [33]
To determine whether parasites carrying these polymorphisms or gene amplifications exist in Mozambique, we conducted molecular surveillance targeting Kelch 13 (K13), pfmdr1, pfcrt, and pfdhps polymorphisms and pfpm2 and pfmdr1 copy numbers in field isolates collected from 4 sentinel sites
Summary
One of the fundamental steps toward malaria control is the use of antimalarial drugs. We used molecular methods to examine 351 P. falciparum isolates collected from 4 sentinel sites in Mozambique for K13, pfmdr, pfcrt, and pfdhps polymorphisms and for plasmepsin (pfpm2) and pfmdr copy numbers. A nonsynonymous polymorphism in the pfcrt gene was shown to be prevalent in the genetic background of K13 mutant artemisinin-resistant isolates [26]. Polymorphisms in pfdhfr and pfdhps genes, the quintuple mutant, including the pfdhfr substitutions N51I, C59R, and S108N, as well as the pfdhps substitutions A437G and K540E, have been associated with a failure of sulfadoxine/pyrimethamine treatment against uncomplicated P. falciparum malaria [27]. To determine whether parasites carrying these polymorphisms or gene amplifications exist in Mozambique, we conducted molecular surveillance targeting K13, pfmdr, pfcrt, and pfdhps polymorphisms and pfpm and pfmdr copy numbers in field isolates collected from 4 sentinel sites
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