
Effect of Drug Pressure on Promoting the Emergence of Antimalarial-Resistant Parasites among Pregnant Women in Ghana
Author(s) -
Bernard Tornyigah,
Romain Coppée,
Pascal Houzé,
Kwadwo Asamoah Kusi,
Bright Adu,
Isabella A. Quakyi,
Nathaniel Coleman,
Atikatou Mama,
Philippe Deloron,
Abraham K. Anang,
Jérôme Clain,
Rachida Tahar,
Michael F. Ofori,
Nicaise Tuikue Ndam
Publication year - 2020
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.02029-19
Subject(s) - artemisinin , drug resistance , sulfadoxine/pyrimethamine , malaria , plasmodium falciparum , sulfadoxine , pyrimethamine , biology , chloroquine , pharmacology , haplotype , drug , medicine , virology , traditional medicine , immunology , genetics , genotype , gene
The continuous spread of antimalarial drug resistance is a threat to current chemotherapy efficacy. Therefore, characterizing the genetic diversity of drug resistance markers is needed to follow treatment effectiveness and further update control strategies. Here, we genotyped Plasmodium falciparum resistance gene markers associated with sulfadoxine-pyrimethamine (SP) and artemisinin-based combination therapy (ACT) in isolates from pregnant women in Ghana. The prevalence of the septuple IRN I- A/FG K GS/T pfdhfr / pfdhps haplotypes, including the pfdhps A581G and A613S/T mutations, was high at delivery among post-SP treatment isolates (18.2%) compared to those of first antenatal care (before initiation of intermittent preventive treatment of malaria in pregnancy with sulfadoxine-pyrimethamine [IPTp-SP]; 6.1%; P = 0.03). Regarding the pfk13 marker gene, two nonsynonymous mutations (N458D and A481C) were detected at positions previously related to artemisinin resistance in isolates from Southeast Asia. These mutations were predicted in silico to alter the stability of the pfk13 propeller-encoding domain. Overall, these findings highlight the need for intensified monitoring and surveillance of additional mutations associated with increased SP resistance as well as emergence of resistance against artemisinin derivatives.