Abstract
BackgroundInsecticide resistance threatens malaria control in sub-Saharan Africa. Knockdown resistance to pyrethroids and organochlorines in Anopheles gambiae sensu lato (s.l.) is commonly caused by mutations in the gene encoding a voltage-gated sodium channel which is the target site for the insecticide. The study aimed to examine risk factors for knockdown resistance in An. gambiae s.l. and its relationship with malaria infection in children in rural Gambia. Point mutations at the Vgsc-1014 locus, were measured in An. gambiae s.l. during a 2-year trial. Cross-sectional surveys were conducted at the end of the transmission season to measure malaria infection in children aged 6 months–14 years.ResultsWhilst few Anopheles arabiensis and Anopheles coluzzii had Vgsc-1014 mutations, the proportion of An. gambiae sensu stricto (s.s.) mosquitoes homozygous for the Vgsc-1014F mutation increased from 64.8 to 90.9% during the study. The Vgsc-1014S or 1014F mutation was 80% higher in 2011 compared to 2010, and 27% higher in the villages with indoor residual spraying compared to those without. An increase in the proportion of An. gambiae s.l. mosquitoes with homozygous Vgsc-1014F mutations and an increase in the proportion of An. gambiae s.s. in a cluster were each associated with increased childhood malaria infection. Homozygous Vgsc-1014F mutations were, however, most common in An. gambiae s.s. and almost reached saturation during the study meaning that the two variables were colinear.ConclusionsAs a result of colinearity between homozygous Vgsc-1014F mutations and An. gambiae s.s., it was not possible to determine whether insecticide resistance or species composition increased the risk of childhood malaria infection.
Highlights
Insecticide resistance threatens malaria control in sub-Saharan Africa
Spatial autocorrelation was found in species distributions with peak autocorrelation operating between 9 and 14 km depending on the species and year
The literature suggests the distribution of species is likely to be due to differential larval habitats, this result may be because An. gambiae s.s. has less flexible host choice behaviours than An. arabiensis [32,33,34] and so contributes a larger proportion of the mosquito catch further away from the river
Summary
Insecticide resistance threatens malaria control in sub-Saharan Africa. Knockdown resistance to pyrethroids and organochlorines in Anopheles gambiae sensu lato (s.l.) is commonly caused by mutations in the gene encoding a voltage-gated sodium channel which is the target site for the insecticide. Cross-sectional surveys were conducted at the end of the transmission season to measure malaria infection in children aged 6 months–14 years. Three different point mutations in the voltage-gated sodium channel gene confer knockdown resistance (kdr) to pyrethroids and organochlorines such as dichlorodiphenyltrichloroethane (DDT) in Anopheles gambiae s.l. Tests performed during a cluster-randomised controlled trial in the URR which compared the efficacy of LLINs versus LLINs and IRS with DDT against malaria in children found complete susceptibility of An. gambiae s.l. to DDT and permethrin in 2010 and some loss of susceptibility the following year [9]. Malaria has been declining in The Gambia since 2000 [12, 13], there is continued moderately high seasonal transmission in the URR despite high vector control coverage [14]
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