Association between sickle cell trait and low density parasitaemia in a P. falciparum malaria holoendemic region of Western Kenya

Abstract

Aims: The frequency of the mutant gene for sickle cell is widely distributed in the sub- Saharan Africa, the Middle East, and the Indian subcontinent. There is epidemiologic evidence that sickle cell trait confers a survival advantage against malaria and that the selection pressure due to malaria has resulted in high frequencies of the mutant gene in areas of high malaria transmission. We carried out a study to look at the relationship between sickle cell trait, age, haemoglobin level, and malaria parasite density. Methods: We carried out a cross-sectional study between the months of October and December, 2004 in Kombewa Division of Kisumu West District, a P. falciparum malaria Research Article International Journal of TROPICAL DISEASE & Health, 2(4): 231-240, 2012 232 holoendemic area with entomological inoculation rates estimated at 31.1 infective bites per person per year. We screened and quantified malaria parasitaemia in participants (age 0 to 45 years n = 342). Haemoglobin electrophoresis was performed on blood from all the participants. Results: In total, 402 participants were screened of which 342 were enrolled. Of these, 280(81.4%) had haemoglobin AA, 60(17.4%) had haemoglobin AS and 2(0.6%) had haemoglobin SS. Those with HbAA and HbAS were included for the analysis bringing the total number to 340 participants. For asymptomatic individuals in the community who displayed no signs of an acute or chronic illness and who were P. falciparum malaria parasite positive; the mean parasite density/L for HbAS of 4064.0 (95% CI 1858.0 – 6270.0) was significantly lower than that of HbAA 11,067.9 (95% CI 7616.0 – 14520.0) (P = 0.001). Conclusion: The sickle cell carrier status is high (17.4%) in this population and is protective against high density parasitaemia. It is suggested that any malaria intervention strategies should factor in the possibility of sickle cell trait as a confounder to the protective effect of the intervention.