Molecular surveillance of the Plasmodium falciparum Pfmdr1 N86Y mutation linked to antimalarial drug resistance in Mbouda, Cameroon

Malaria, mainly caused by Plasmodium falciparum, remains a major health concern in Cameroon due to the emergence of drug-resistant parasite strains. The Plasmodium falciparum multidrug resistance 1 (Pfmdr1) gene, particularly the N86Y mutation, is a key marker associated with reduced susceptibility to several antimalarial drugs. This study investigated the prevalence of the Pfmdr1-N86Y mutation in isolates from patients attending three health facilities in the Mbouda Health District to support improved malaria control strategies in the area. The study was conducted among patients attending three healthcare facilities in Mbouda. Three hundred and two (302) patients were recruited across these three centers and diagnosed by both rapid diagnostic test (RDT) and thick blood smear (TBS). positive samples were spotted on whatman paper. Plasmodial DNA was extracted using the chelex- 100 method. The Pfmdr1 gene was then amplified by nested PCR, visualized on a 1.3% agarose gel, and analyzed by restriction fragment length polymorphism (RFLP) using the AflIII restriction enzyme. Statistical analysis was performed with a significance threshold of 5% (p < 0.05) using SPSS software version 26, particularly employing Chi-square tests. The prevalence of Plasmodium falciparum infection was 28.8%, with the highest burden among males, children aged 0–5 years, and adults over 35 years. Insecticide use was identified as a significant protective factor, and parasite density was higher among males and young children. The Pfmdr1 gene was detected in 95% of isolates. Analysis of the Pfmdr1-N86Y mutation revealed that 94% of alleles were wild-type (N86), 1% were mixed (N86/Y86), and no mutant alleles (Y86) were observed and 5% tested negative for this gene, which may be due to poor DNA quality, often denatured, or poor extraction, or other reasons. This study indicates that, the Pfmdr1 gene exhibited a frequency 95%. These results therefore highlight the importance of other types of Pfmdr1 mutations and would be necessary for the evaluation of Pfmdr1 mutations associated with parasite resistance to antimalarial drugs. Measures should be taken to delay the evolution of these mutations by changing treatment policy in the affected area if these mutations are nevertheless very high.