| The western flower thrips (WFT), Frankliniella occidentalis (Pergande), is one of the most destructive pests of vegetables, fruit and ornamental crops worldwide. The use of chemical insecticides has been the primary strategy for controlling WFT. Due to the frequent application of chemical insecticides against WFT and its short generation time, high female fecundity, and haplodiploid reproduction system, WFT has the potential of fast development of resistance. Insecticide resistance in WFT has been documented in a number of insecticide classes, including the organochlorines, organophosphates, carbamates, pyrethroids and spinosad. Abamectin, a natural fermentation product of the soil bacterium Streptomyces avermitilis, acts on the y-aminobutyric acid (GABA)-gated chloride channel and glutamate-gated chloride channel. Due to its distinctive mechanism of action, its environmental friendly nature and broad spectrum of activity against insects and mites, abamectin has been used on agronomic, fruit, vegetable and ornamental crops worldwide. In this paper, abamectin resistance was selected in the western flower thrips under the laboratory conditions, and resistance risk, cross-resistance patterns, resistance genetics, and possible resistance mechanisms of abamectin resistance in WFT were investigated. Furthermore, co-toxicity of abamectin with three insecticides against the western flower thrips was also studied.Abamectin resistance in WFT was selected using leaf dipping methods. After15cycles of selection during18generations, an abamectin-resistant strain of WFT was obtained, which exhibited45.66-fold resistance to abamectin compared with unselected parent strain. According to the realized resistance heritability (h2=0.1286) and assuming selection pressure being80%-90%, it requires10-13generations for WFT to development100-fold resistance to abamectin. These results suggested that WFT may have high resistance risk to abamectin. Studies on the resistance stability showed that the abamectin resistance ratio in the resistant strain significantly declined from45.66to6.94after8generations without exposure to the insecticide, suggesting abamectin resistance in WFT was not stable. Moderate and low levels of cross-resistance to chlorpyrifos (RR=11.38) and lambda-cyhalothrin (3.98) were observed in the ABA-R strain, but no significant cross-resistance was found to spinosad (2.01), acetamiprid (1.46) and chlorfenapyr (0.26).. Genetic crosses were carried out to study inheritance of resistance to abamectin in WFT. Reciprocal crosses of susceptible and resistant strain showed that the LC50values of abamectin in two F1populations were not different significantly (P>0.05), the degrees of dominance were0.26and0.13, respectively, suggesting that the resistance of WFT to abamectin was autosomal, incompletely dominant. Analysis of F1-backcross progeny and F2-masscross progeny showed significant deviation between the observed and the expected mortality, suggesting that abamectin resistance in WFT was probably controlled by polygenic gene locus. The synergistic effects of the oxidase inhibitor piperonyl butoxide (PBO), the esterase inhibitor S,S,S-tributyl phosphorotrithioate (DEF) and the glutathione S-transferase inhibitor diethyl maleate (DEM) with abamectin against the ABA-S and ABA-R strains were studied. A significant synergism was seen for PBO in the ABA-R strain (3-fold); however, there was a negligible effect in the ABA-S strain. No synergistic effect was seen for DEF and DEM in either the ABA-S or the ABA-R strain. Activities of cytochrome P450monooxygenases, esterases and glutathione S-transferases were measured in both strains. The cytochrome P450enzyme activity in the ABA-R strain was6.67-fold higher than that in ABA-S strain. Further analysis showed that the cytochrome P450enzyme activity correlated well with levels of resistance to abamectin in several tested generations (r2=0.8754) However, esterase activity using a-naphthyl acetate as substrate and the glutathione S-transferase activity towards CDNB and DCNB were not significantly different between the two strains.To select synergistic mixture of abamectin with other insecticides against WFT, the toxicity of abamectin, chlorpyrifos, imidacloprid and pymetrozine against the second instar larva of western flower thrips were tested in the laboratory by leaf dipping methods, and the optimal combination and mixture ratio of abamectin and other insecticides were determined by co-toxicity factor method and the co-toxicity coefficient method, respectively. The results showed that both the abamectin and chlorpyrifos had relatively high toxicity against the second instar nymphs of western flower thrips. Significant synergism was observed in the mixture of abamectin and chlorpyrifos, with the ratio of1:4and4:1showing the highest synergism, while the mixture of abamectin with pymetrozine and imidacloprid showed antagonism. |
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