“…Based on the aforementioned observations, it is reasonable therefore, to adduce that malaria parasites could grow better in the RBCs of G6PD non-deficient individuals than in the RBCs of the G6PD deficient ones, which could result to the high parasite density observed in nondeficient subjects. Our result, therefore, favours the malaria / G6PD deficiency hypothesis, which affirmed that G6PD deficiency, are contributing factors to malarial resistance (Usanga & Luzzatto, 1985). The result is also supported by the observation that more cohort G6PD non-deficient subjects, particularly children below 5 years of age were admitted in the hospital for the treatment of severe malaria than cohort G6PD deficient subjects during which severe malaria associated with symptoms including cerebral malaria, seizure, severe headache, vomiting, diarrhoea and respiratory distress, were evident.…”