Malaria Journal (Jan 2010)

Costs of insensitive acetylcholinesterase insecticide resistance for the malaria vector <it>Anopheles gambiae </it>homozygous for the G119S mutation

  • Noel Valérie,
  • Djogbénou Luc,
  • Agnew Philip

DOI
https://doi.org/10.1186/1475-2875-9-12
Journal volume & issue
Vol. 9, no. 1
p. 12

Abstract

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Abstract Background The G119S mutation responsible for insensitive acetylcholinesterase resistance to organophosphate and carbamate insecticides has recently been reported from natural populations of Anopheles gambiae in West Africa. These reports suggest there are costs of resistance associated with this mutation for An. gambiae, especially for homozygous individuals, and these costs could be influential in determining the frequency of carbamate resistance in these populations. Methods Life-history traits of the AcerKis and Kisumu strains of An. gambiae were compared following the manipulation of larval food availability in three separate experiments conducted in an insecticide-free laboratory environment. These two strains share the same genetic background, but differ in being homozygous for the presence or absence of the G119S mutation at the ace-1 locus, respectively. Results Pupae of the resistant strain were significantly more likely to die during pupation than those of the susceptible strain. Ages at pupation were significantly earlier for the resistant strain and their dry starved weights were significantly lighter; this difference in weight remained when the two strains were matched for ages at pupation. Conclusions The main cost of resistance found for An. gambiae mosquitoes homozygous for the G119S mutation was that they were significantly more likely to die during pupation than their susceptible counterparts, and they did so across a range of larval food conditions. Comparing the frequency of G119S in fourth instar larvae and adults emerging from the same populations would provide a way to test whether this cost of resistance is being expressed in natural populations of An. gambiae and influencing the dynamics of this resistance mutation.