Abstract

The house fly, Musca domestica L., is a cosmopolitan insect with the ability to develop resistance to insecticides used for their management. In the present study, we investigated the genetics of spinosad resistance, and cross-resistance potential to other insecticides by selecting a field strain with a commercial spinosad formulation. Bioassays with the field strain, before selection with spinosad, gave resistance ratios (RRs) of 4, 5, 66, 21 and 5 fold for spinosad, indoxacarb, abamectin, imidacloprid and deltamethrin, respectively, in comparison to a laboratory susceptible (Lab-susceptible) strain. After continuous selection of the field strain (Spin-SEL) with spinosad, the RR was increased up to 155 fold; however, the resistance was unstable (RR decreased 1.43 fold) when this strain was not exposed to spinosad for five generations. The Spin-SEL strain did not show cross-resistance to abamectin, indoxacarb or deltamethrin, but showed negative cross-resistance to imidacloprid. Crosses between the Spin-SEL and Lab-susceptible strains revealed an autosomal and incomplete dominant mode of resistance to spinosad. A direct test using a monogenic inheritance model based on Chi-square analysis revealed that the resistance was governed by more than one gene. Moreover, the resistance was neither overcome with the insecticide synergist piperonyl butoxide nor with S,S,S-tributylphosphorotrithioate. Lack of cross-resistance and instability of resistance suggest that rotation with spinosad could be an effective resistance management strategy.

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