Multiplicity of Plasmodium falciparum infection in asymptomatic children in Senegal: relation to transmission, age and erythrocyte variants

Abstract Background Individuals living in malaria endemic areas generally harbour multiple parasite strains. Multiplicity of infection (MOI) can be an indicator of immune status. However, whether this is good or bad for the development of immunity to malaria, is still a matter of debate. This study...

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Bibliographic Details
Published in:Malaria Journal
Main Authors: Anchang Judith, Garcia André, Troye-Blomberg Marita, Vafa Manijeh, Migot-Nabias Florence
Format: Article in Journal/Newspaper
Language:English
Published: BMC 2008
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Online Access:https://doi.org/10.1186/1475-2875-7-17
https://doaj.org/article/7c35e184278643cdbbd9c87f20a4b415
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Summary:Abstract Background Individuals living in malaria endemic areas generally harbour multiple parasite strains. Multiplicity of infection (MOI) can be an indicator of immune status. However, whether this is good or bad for the development of immunity to malaria, is still a matter of debate. This study aimed to examine the MOI in asymptomatic children between two and ten years of age and to relate it to erythrocyte variants, clinical attacks, transmission levels and other parasitological indexes. Methods Study took place in Niakhar area in Senegal, where malaria is mesoendemic and seasonal. Three hundred and seventy two asymptomatic children were included. Sickle-cell trait, G6PD deficiency (A- and Santamaria) and α + -thalassaemia (-α 3.7 type) were determined using PCR. Multiplicity of Plasmodium falciparum infection, i.e. number of concurrent clones, was defined by PCR-based genotyping of the merozoite surface protein-2 ( msp2 ), before and at the end of the malaria transmission season. The χ 2 -test, ANOVA, multivariate linear regression and logistic regression statistical tests were used for data analysis. Results MOI was significantly higher at the end of transmission season. The majority of PCR positive subjects had multiple infections at both time points (64% before and 87% after the transmission season). MOI did not increase in α-thalassaemic and G6PD mutated children. The ABO system and HbAS did not affect MOI at any time points. No association between MOI and clinical attack was observed. MOI did not vary over age at any time points. There was a significant correlation between MOI and parasite density, as the higher parasite counts increases the probability of having multiple infections. Conclusion Taken together our data revealed that α-thalassaemia may have a role in protection against certain parasite strains. The protection against the increase in MOI after the transmission season conferred by G6PD deficiency is probably due to clearance of the malaria parasite at early stages of infection. The ABO ...