alexa Abstract | Chloroquine Resistance and Host Genetic Factors among Nigerian Children with Uncomplicated P.falciparum Infection

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Abstract

Chloroquine resistance and host genetic factors among Nigerian children with uncomplicated P.falciparum infection. Background: Chloroquine resistance is widespread. Host factors play a role in drug resistance. The study aims to determine the association between hosts red cell factors namely G6PD status, ABO blood group and haemoglobin genotype with Pfmdr1 mutations and treatment outcome. Methods: One hundred and twenty patients (aged 1-15years) with acute symptoms of P.falciparum malaria were treated with chloroquine (CQ). Blood sample was obtained for haematological parameters and analysis of parasite DNA. Nested PCR followed by restriction fragment length polymorphism (RFLP) at codon 86 of the Pfmdr1 gene was determined in the 120 isolates. Relationship between Pfmdr1 alleles, CQ resistance, G6PD deficient, sickle cell trait and parasite diversity was evaluated. Results: Seventy of the 120 patients enrolled into this study completed the 14-day follow-up, aged 7.8 ± 4.6 years, 62 (52%) were females with parasites geometric mean 21,861 (range 1000-354,667) asexual parasites per microlitre of blood. Thirtyseven of the 70 (53%) were cured while 47% failed chloroquine treatment; mean parasite clearance time (PCT) was 7.1 days, whereas the mean fever clearance time was 3.4 days. Mutation revealed wild type N86 (56), mutant type Y86 (50) and mixed genotype N86+Y86 (14). No significant correlation was found between Pfmdr1 mutations and in-vivo outcome (p=0.21). About 51% (36/70) of the in-vivo pre-treatment samples carried the Pfmdr1 Y86 mutation and its prevalence varied with age (p=0.017). The Pfmdr1Y86 mutation was detected in majority (19/33) of patients with clinical failure OR=1.711; 95% CI: 0.517-5.668; p=0.378 and was more in younger OR=1.200; 95% CI: 0.782-1.840 than in older children OR=0.818; 95% CI: 0.507-1.321. Conclusion: There is an association between Pfmdr1Y86 mutation and CQ treatment failure which tends to be stronger in younger children. These suggest the role of age and host immunity in modifying the relationship between molecular markers and resistance.

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Author(s): CM NnejiADA AdedapoPN OkorieOG Ademowo

Keywords

General Medicine, Heart Disease and Genetics

 
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