Polymorphisms inK13, pfcrt, pfmdr1, pfdhfr, andpfdhpsin parasites isolated from symptomatic malaria patients in Burkina Faso

Abstract

Background: The emergence of resistance to artemisinin derivatives in western Cambodia is threatening to revert the recent advances made toward global malaria control and elimination. Known resistance-mediating polymorphisms in the K13, pfcrt, pfmdr1, pfdhfr, and pfdhps genes are of greatest importance for monitoring the spread of antimalarial drug resistance. Methods: Samples for the present study were collected from 244 patients with uncomplicated malaria in health centers of Bobo-Dioulasso, Burkina Faso. Blood sample was collected on filter paper before the subject received any treatment. The parasite DNA was then extracted and amplified by Polymerase Chain Reaction (PCR) to evaluate the prevalence of polymorphism of pfcrtK76T, pfmdr1 (N86Y, Y184F), and pfdhps (A437G, K540E). The K13 gene polymorphism was analyzed by nested PCR followed by sequencing. Results: The overall results showed 2.26% (5/221) of K13 synonymous mutant alleles (two C469C, one Y493Y, one G496G, and one V589V), 24.78%, 19.58%, 68.75%, 60.9%, 53.7%, 63.8%, and 64.28%, respectively, for mutant pfcrt 76T, pfmdr1-86Y, pfmdr1-184F, pfdhfr51I, pfdhfr59R, pfdhfr108N, and pfdhps 437G. We did not report any mutation at codon 540 of pfdhps. Conclusion: These results provide baseline prevalence of known drug resistance polymorphisms and suggest that artemisinin combination therapies may retain good efficacy in the treatment of uncomplicated malaria in Burkina Faso.

Prevalence of Plasmodium falciparum Chloroquine Resistance Transporter (Pfcrt76T) Mutation Associated with Antimalarial Drug Resistance in Two Different Epidemiological Setting (Banfora and Saponé) in Burkina Faso Few Years after the Implementation of Artemisnine Based Combination Therapy (ACTs)

“…The overall significance of this study indicated a clear reduction of the chloroquine resistance parasite since the introduction of the ACTs in 2005 in Burkina Faso. This conforms with the results obtained by Some et al in 2016 as well as [17]. This re-affirmed the efficacy of the ACTs on the chloroquine-resistant parasite as described previously.…”

“…Our results corroborate with those obtained by MAHAMAT et al, in (2008), in Burkina Faso [16]. However, some literature reviews note that high parasite densities favour the appearance and selection of mutations under the influence of drug pressure [22]. This contradiction with ours could be explained by the fact that the test was carried by in vitro and giving only an overall response of the parasite population.…”

“…Indeed, the prevalence of Pfcrt 76T mutation before the introduction of CTAs was estimated at 60% in Burkina Faso [15]. With the studies conducted in 2008 and 2016, the overall results showed a prevalence of Pfcrt76T mutation at 50% [16]; 24.78% [17] respectively; This was a representative of a decline in…”

Genetic Polymorphisms of Pfcrt K76T and Pfmdr1 N86Y among Asymptomatic School Children in Forest Communities of Ekondo Titi Subdivision along the Cameroon-Nigeria Border Area

“…Compared with the high prevalence of the pfcrt T76 mutation, fewer samples had mutations in codon 86 of pfmdr1. The low prevalence of the pfmdr1 86Y mutant allele among P. falciparum isolates from Ekondo Titi, is in discordant with the findings of [36] in Yemen and [10] in Cameron. Moreover, [35] has shown that the parasites with the pfmdr1 86Y allele produce a higher number of gametocytes, which would gain the advantage in terms of transmission.…”

Resistance of <i>Plasmodium falciparum</i> to Sulfadoxine-Pyrimethamine (<i>Dhfr</i> and <i>Dhps</i>) and Artemisinin and Its Derivatives (K13): A Major Challenge for Malaria Elimination in West Africa

“…In the case of Sub-Saharan Africa, the data in the literature are controversial on the probable relationship between the presence of k13 mutants and resistance to artemisinin [4] [7]. On the other hand, cases of resistance to SP have already been demonstrated by several authors, while SP continues to be offered as an intermittent and preventive treatment against malaria [5] [8] [9] [10] [11]. In the current context of West Africa, the insufficiency of information and the divergence of the conclusions of most of the studies on the Plasmodium resistance genes to SP and to artemisinin contribute to disseminate uncertainties on the choice of certain molecules such as SP for intermittent preventive treatment (IPT) and the probable presence of mutations in the k13 gene associated with resistance to artemisinin [12].…”