Abstract
The salt marsh mosquito Ochlerotatus detritus Haliday, 1833 (Diptera: Culicidae) is locally abundant in some areas of the UK, can be a pernicious summer nuisance biter and is one of eleven British mosquitoes considered as a potential bridge vector of West Nile Virus. WHO bioassays of insecticide susceptibility were performed on O. detritus from Parkgate Marshes, Little Neston, Wirral, UK using three insecticides, the pyrethroid permethrin, the carbamate bendiocarb and the organophosphate fenitrothion. O. detritus were fully susceptible to permethrin and fenitrothion but exhibited strong resistance to bendiocarb (66% of females alive following 1–hr exposure; LT50 of 116 minutes). Sequencing of the known resistance-causing mutations in the acetylcholinesterase target site of carbamate/organophosphates, and of pyrethroids, the voltage-gated sodium channel, revealed no known target-site mutations indicating the carbamate resistance is not target-site mediated. Pre-exposure to the synergist piperonyl butoxide recovered full bendiocarb susceptibility further implicating metabolic resistance. We show that UK mosquitoes have the potential to develop resistance to insecticides and suggest that the carbamate resistance detected could be a result of exposure to agricultural insecticides.
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