Abstract
BackgroundDengue suppression often relies on control of the mosquito vector, Aedes aegypti, through applications of insecticides of which the pyrethroid group has played a dominant role. Insecticide resistance is prevalent in Ae. aegypti around the world, and the resulting reduction of insecticide efficacy is likely to exacerbate the impact of dengue. Dengue has been a public health problem in Saudi Arabia, particularly in Jeddah, since its discovery there in the 1990s, and insecticide use for vector control is widespread throughout the city. An alternative approach to insecticide use, based on blocking dengue transmission in mosquitoes by the endosymbiont Wolbachia, is being trialed in Jeddah following the success of this approach in Australia and Malaysia. Knowledge of insecticide resistance status of mosquito populations in Jeddah is a prerequisite for establishing a Wolbachia-based dengue control program as releases of Wolbachia mosquitoes succeed when resistance status of the release population is similar to that of the wild population.MethodsWHO resistance bioassays of mosquitoes with deltamethrin, permethrin and DDT were used in conjunction with TaqMan® SNP Genotyping Assays to characterize mutation profiles of Ae. aegypti.ResultsScreening of the voltage-sensitive sodium channel (Vssc), the pyrethroid target site, revealed mutations at codons 989, 1016 and 1534 in Ae. aegypti from two districts of Jeddah. The triple mutant homozygote (1016G/1534C/989P) was confirmed from Al Safa and Al Rawabi. Bioassays with pyrethroids (Type I and II) and DDT showed that mosquitoes were resistant to each of these compounds based on WHO definitions. An association between Vssc mutations and resistance was established for the Type II pyrethroid, deltamethrin, with one genotype (989P/1016G/1534F) conferring a survival advantage over two others (989S/1016V/1534C and the triple heterozygote). An indication of synergism of Type I pyrethroid activity with piperonyl butoxide suggests that detoxification by cytochrome P450s accounts for some of the pyrethroid resistance response in Ae. aegypti populations from Jeddah.ConclusionsThe results provide a baseline for monitoring and management of resistance as well as knowledge of Vssc genotype frequencies required in Wolbachia release populations to ensure homogeneity with the target field population. Vssc mutation haplotypes observed show some similarity with those from Ae. aegypti in southeast Asia and the Indo-Pacific, but the presence of the triple mutant haplotype in three genotypes indicates that the species in this region may have a unique population history.Graphical
Highlights
Dengue suppression often relies on control of the mosquito vector, Aedes aegypti, through applica‐ tions of insecticides of which the pyrethroid group has played a dominant role
The results provide a baseline for monitoring and management of resistance as well as knowledge of Voltage-sensitive sodium channel (Vssc) genotype frequencies required in Wolbachia release populations to ensure homogeneity with the target field population
Vssc mutation haplotypes observed show some similarity with those from Ae. aegypti in southeast Asia and the Indo-Pacific, but the presence of the triple mutant haplotype in three genotypes indicates that the species in this region may have a unique population history
Summary
Dengue suppression often relies on control of the mosquito vector, Aedes aegypti, through applica‐ tions of insecticides of which the pyrethroid group has played a dominant role. Dengue has been a public health problem in Saudi Arabia, in Jeddah, since its discovery there in the 1990s, and insecticide use for vector control is widespread throughout the city. Voltage-sensitive sodium channel (Vssc) mutations at codons 1016 and 1534 occur in Ae. aegypti within the pyrethroid receptor sites in Domains II (S6) and III (S6) of the protein molecule [2]. A third mutation, S989P, which is often in perfect linkage with V1016G, is not known to reduce the sensitivity of the sodium channel [2], but confers some additive pyrethroid resistance in the homozygous state in combination with 1016G [3]. Direct links between these mutations and resistance phenotypes in this locality are still unclear
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