Genetics, cross-resistance and mechanism of resistance to spinosad in a field strain of Musca domestica L. (Diptera: Muscidae)

Summary A Lab-selected field strain of Musca domestica developed 155-fold resistance to spinosad. The resistance was autosomal, incomplete dominant, and controlled by more than one gene. •A Lab-selected field strain of Musca domestica developed 155 fold resistance to spinosad with negative cross-res...

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Veröffentlicht in:Acta tropica 2014-02, Vol.130, p.148-154
Hauptverfasser: Khan, Hafiz Azhar Ali, Akram, Waseem, Shad, Sarfraz Ali
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Sprache:eng
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Zusammenfassung:Summary A Lab-selected field strain of Musca domestica developed 155-fold resistance to spinosad. The resistance was autosomal, incomplete dominant, and controlled by more than one gene. •A Lab-selected field strain of Musca domestica developed 155 fold resistance to spinosad with negative cross-resistance to imidacloprid.•The resistance was autosomal, incomplete dominant, and controlled by more than one gene.•Synergism studies with PBO and DEF revealed that metabolic detoxification was not responsible for resistance to spinosad. 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.
ISSN:0001-706X
1873-6254
DOI:10.1016/j.actatropica.2013.11.006