Molecular characterisation of malaria and glucose-6-phosphate dehydrogenase deficiency in conflict-affected zones of central and eastern Sudan

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Abstract

Background Malaria causes high morbidity and mortality in Sudan. Conflict and displacement have disrupted control efforts, likely increasing disease transmission. This study explored malaria epidemiology, parasite distribution, hematological changes, and the distribution of Glucose-6-Phosphate Dehydrogenase (G6PD) genotypes in conflict-affected zones hosting internally displaced populations (IDPs). Methods This cross-sectional study was conducted between 2023 and 2024, enrolling 717 patients with clinical symptoms suggestive of malaria in Kosti (Central Sudan, n = 252) and Kassala (Eastern Sudan, n = 465). Malaria infection was confirmed by light microscopy and species-specific real-time PCR targeting the 18S rRNA gene. Hematological indices were analyzed on automated analyzers, and PCR-RFLP was used to determine G6PD genotypes. Results PCR-confirmed malaria prevalence was 62.6% in Kassala and 52% in Kosti. P. vivax and P. falciparum were co-endemic in Kassala (66.2% and 46.2%), with 12.4% mixed infections and 24% sub-microscopic P. vivax infections. P. falciparum was most common in Kosti (97.7%). P. vivax infections often were afebrile (74%) and associated with thrombocytopenia (p = 0.001). Significant regional variation in G6PD genotypes was found (p < 0.001): the A- variant was detected in males from Kosti (7.4%) but not in males from Kassala. Kosti females showed a female-specific deficiency: 15.8% of males carried the A variant, while 8.3%, 2.5%, and 1.3% of females were heterozygous for A⁻ , homozygous for A , and homozygous or compound for A⁻ , respectively. In Kassala, 2.7% of males had the A variant, and 1.6% and 3% of females were BA⁻ and AA , respectively. Malaria prevalence did not vary significantly between IDPs and residents. Conclusions This study found a high prevalence of P. vivax in eastern Sudan, with co-endemicity of P. falciparum and a significant number of sub-microscopic infections. It revealed regional heterogeneity in G6PD deficiency, with the A⁻ variant only found among males from Kosti, central Sudan. Notably, this study adds to the scarce molecular data on G6PD deficiency in Sudan by documenting the presence of the G6PD A⁻ allele and the A⁻A⁻ genotype, confirming the sub-Saharan African A⁻ allele in the population.

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