Abstract
BackgroundGlucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked genetic disorder that results in impaired enzyme activity. Although G6PD deficiency is globally distributed it is more prevalent in malaria-endemic countries. Several mutations have been identified in the G6PD gene, which alter enzyme activity. The G6PD genotype predominantly found in sub-Saharan Africa is the G6PDB (G6PD376A) with (G6PD376G) and G6PDA- (G6PD376G/202A, G6PD376G/542T, G6PD376G/680T and G6PD376G/968C) occurring at lower frequencies.AimThe aim of this study was to identify the prevalence of G6PD deficiency and asymptomatic Plasmodium falciparum carriage in children living in southern Ghana and determine whether G6PD deficiency influences asymptomatic carriage of P. falciparum parasites.MethodsBlood samples were obtained once a month from 170 healthy Ghanaian school children aged between 5 and 12 years from Basic schools in two communities Obom and Abura with similar rainfall patterns and malaria peak seasons. G6PD enzyme activity was assessed using the qualitative G6PD RDT kit (AccessBIO). G6PD genotyping and asymptomatic parasite carriage was determined by PCR followed by restriction fragment length polymorphism (RFLP) of DNA extracted from dried blood spots.ResultsThe only sub-Saharan G6PD A- allele detected was the A376G/G202A found in 12.4 % (21/170), of the children and distributed as 4.1 % (7/170) A-, 1.8 % (3/170) A-/A- homozygous deficient males and females and 6.5 % (11/170) A/A- and B/A- heterozygous deficient females. Phenotypically, 10.6 % (15/142) of the children were G6PD deficient. The asymptomatic carriage of P. falciparum by PCR was 50, 29.4, 38.2 and 38.8 % over the months of February through May 2015, respectively, and 28.8, 22.4, 25.9 and 5.9 % by microscopy during the same periods.ConclusionsG6PD deficiency was significantly associated with a lowered risk of PCR-estimated asymptomatic P. falciparum carriage in children during the off peak malaria season in Southern Ghana.Electronic supplementary materialThe online version of this article (doi:10.1186/s12936-016-1440-1) contains supplementary material, which is available to authorized users.
Highlights
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked genetic disorder that results in impaired enzyme activity
Fifty-four percent (92/170) of the children were female (Table 1), the ratio was slightly increased to 56 % (80/142) in the subset used for the G6PD phenotype analysis
In order to identify any possible influence of G6PD deficiency on asymptomatic malaria carriage, this study was conducted over the off peak malaria season, from February through to May 2015, when symptomatic P. falciparum carriage is low
Summary
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked genetic disorder that results in impaired enzyme activity. G6PD deficiency (G6PDd) is one of the most common human genetic enzyme defects [2], affecting over 400 million people This enzymopathy is globally distributed, it is more prevalent in the tropics and. Amoah et al Malar J (2016) 15:388 sub-tropics, especially in malaria-prone countries [3] This X-linked genetic condition is characterized by reduced G6PD enzyme activity, which can remain asymptomatic. Glucose-6-phosphate dehydrogenase (G6PD) and a number of other human genetic traits including sickle cell anaemia and related haemoglobinopathies are predominantly found in populations living in malaria endemic countries and have been suggested to provide the host protection from severe forms of malaria [5,6,7,8] and asymptomatic malaria [9]. A number of genetic traits that protect the host against severe forms of malaria have recently been found to promote the development of the sexual transmissible stages of the parasite, and individuals with these traits serve as reservoirs for malaria transmission [10] or alter the acquisition of anti-parasite antibodies [11]
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