Submicroscopic infection and G6PD deficiency in malaria patients
Plasmodium vivax malaria is a neglected tropical disease, despite being more geographically widespread than any other form of malaria. Glucose-6-phosphate dehydrogenase (G6PD) is a cytosolic enzyme with a vital role for the integrity and functioning of red blood cells. Lower activity of G6PD enzyme can lead to acute hemolytic anemia especially after exposure to oxidative stressors like primaquine. Primaquine is an antimalaria drug for radical cure of P. vivax and blocking transmission of P. falciparum. It is important to identify G6PD deficient individuals and administer primaquine with special care due to its hemolytic side effects. This research aims to investigate the prevalence of G6PD deficiency in malaria patients from Bonga town in Southwestern Ethiopia. The level of G6PD activity was measured by careSTARTTM POC biosensor. The overall median activity was calculated for females and males to determine if G6PD levels were normal, intermediate, or deficient. Further, portion of the G6PD gene was amplified and sequenced to examine the association between G6PD phenotype and genotype. Of the 271 subjects who were tested for G6PD phenotype, 19 out of 297 (7%) of individuals had a low level of G6PD enzyme, 38 (14%) had intermediate enzyme activity, and 214 (78.9%) had normal levels. No significant correlation observed between G6PD enzyme levels and odds of being infected by P. vivax. No mutations were observed in A376G, G202A, and C563T but three novel non-synonymous mutations in exon 2 among G6PD deficient individuals. Findings of this study have important implications to using primaquine for malaria treatment. Presented at the 2022 UNC Charlotte Undergraduate Research Conference.