Evolution of the Pfcrt and Pfmdr1 Markers and Revert of Chloroquine Sensitive Plasmodium falciparum in a Seasonal Malaria Chemoprevention Setting in Cameroon
Author(s): Ngum Lesley Ngum, Innocent M Ali, Palmer Masumbe Netongo, Akindeh M Nji, Jean Paul Kengne Chedjou, Randolph Ngwafor, Pacome Valery tchuenkam kom Aristid M Ekollo, Peter Thelma Ngwa Niba, Mbu’u Mbanwi Cyrille, Calvino Tah Fomboh, Nana William Dorian and Wilfred F Mbacham
Plasmodium falciparum, the cause of the most lethal malaria in humans, which still remains a threat to global health, with children and pregnant women being the most affected. This burden is highly pronounced in areas were malaria transmission is seasonal. The emergence of drug-resistance poses a major obstacle to the control of malaria. However predicting decreased or increased sensitivity to anti-malarial and fixation of multidrug resistance genotypes is vital in the fight against malaria. In other to assess how drug policies can impact this burden in a seasonal malaria chemoprevention setting in Cameroon, we investigated molecular changes in Pfcrt and Pfmdr1 genes in pre and post seasonal malaria chemoprevention in Cameroon. To assess the evolution of these markers, finger-prick whole blood samples were collected on 3MM Whatman filter paper from over 405 children that were diagnosed positive for malaria. DNA was extracted from and dry blood spot and genotyped. Chi square test was used to test for significance in the distribution of the markers within the two time points or periods. Out of the 405 samples from different patients that were genotyped for Pfcrt and Pfmdr1. The proportion of pfcrt genotypes stood at 33.3% wild-types, 51.9% mutants and 14.2% mixed infection. That of Pfmdr1 stood at 25.3% wild-type, 63.5% mutants and 11.2% mixed infections. Pearson’s chi square/Fischer’s exact test revealed that the frequencies of the SNPs of the pfcrt and Pfmdr1 gene were significantly associated with their distribution within the two time points (pv ≤ 0.000001).