Prevalence of resistance markers of artemisinin, partner drugs, and sulfadoxine-pyrimethamine in Nanyumbu and Masasi Districts, Tanzania between 2020 and 2021.

Abstract

Regular monitoring of the emergence and spread of Plasmodium falciparum markers of resistance against artemisinin, partner drugs, sulfadoxine, and pyrimethamine is important for the treatment and prevention of malaria in Tanzania. Blood samples were collected from febrile and non-febrile children aged 3 to 59 months in Masasi and Nanyumbu Districts between 2020 and 2021. The samples were subjected to molecular analysis for markers of artemisinin, partner drugs, sulfadoxine, and pyrimethamine resistance, including Plasmodium falciparum kelch (Pfk) 13 gene, P. falciparum chloroquine resistance transporter gene (Pfcrt), P. falciparum multidrug resistance gene (Pfmdr) 1, P. falciparum dihydrofolate reductase (Pfdhfr), and P. falciparum dihydropteroate synthase (Pfdhps). A total of 531 blood samples were involved in the analysis. None of the P. falciparum isolates analyzed for Pfk13 carried any of the validated markers of artemisinin resistance. Pfcrt CVMNK wild-type haplotype occurred in 88.9% (271/305) of the parasites, and the mutant CVIET haplotype occurred only in 0.7% (2/305). Conversely, the majority of the parasites (24.2% [48/198]) were carrying Pfmdr1 NFD haplotype, followed by the wild-type haplotype NYD (19.1% (39/198), and the rest were mixed infections. Quintuple mutation IRNI-SGEAA occurred in 54.4% (62/114), and sextuple mutation IRNI-FAKGS occurred only in 0.9% (1/114) of the parasites. No parasite carried any of the validated markers of artemisinin resistance; however, the prevalence of Pfcrt and Pfmdr1 resistance markers against the partner drugs reached the saturation point. Sextuple Pfdhfr-Pfdhps mutations occurred only in one patient; therefore, SP remains efficacious for IPTp in the Districts.