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BACKGROUND Neonicotinoid seed treatments suppress populations of pest insects efficiently and can enhance crop growth, but they may have negative effects on beneficial arthropods. We evaluated the effects of either imidacloprid or thiamethoxam on the abundances of a sucking pest, the cotton leafhopper (Amrasca devastans), and its arthropod predators under field conditions. We also evaluated the impact of seed treatment on transgenic cotton plant growth, with pests and natural enemies present or absent. RESULTS Imidacloprid and thiamethoxam reduced pest abundance, with greater effects when dosages were higher. Treatment at recommended doses delayed the pest in reaching the economic damage threshold by around 10–15 days (thiamethoxam) and 20 days (imidacloprid). Recommended doses also enhanced plant growth under all tested conditions; growth is affected directly as well as via pest suppression. Neonicotinoid applications reduced abundance of beneficial arthropods, with lower populations after higher doses, but negative effects of imidacloprid were not apparent unless the manufacturer‐recommended dose was exceeded. CONCLUSION Imidacloprid applied at the recommended dose of 5 g kg−1 seed is effective against A. devastans and appears to be safer than thiamethoxam for natural enemies, and also enhances plant growth directly. We caution, however, that possible sublethal negative effects on individual beneficial arthropods were not evaluated. © 2015 Society of Chemical Industry

BACKGROUNDImidacloprid, a neonicotinoid insecticide, is widely sprayed alone or mixed with other insecticides against Dysdercus koenigii, a potential pest of cotton in Pakistan. Recently, resistance to imidacloprid in field populations of D. koenigii has developed because of its overuse. Herein, we have investigated inheritance of imidacloprid resistance in D. koenigii and its cross‐resistance to other insecticides.RESULTSThe imidacloprid‐selected population had a 91 421‐fold increase in resistance to imidacloprid after six generations. Overlapping 95% fiducial limits of LC50s of the F1 (Imida‐Sel ♂ × Sus‐ST ♀) and F1† (Imida‐Sel ♀ × Sus‐ST ♂) suggested an autosomal and incomplete dominant resistance to imidacloprid (DLC = 0.84 for F1 and 0.86 for F1†). Reciprocal backcrosses of the F1 and F1† with Sus‐ST predicted a polygenic inheritance. Realized heritability of imidacloprid resistance was 0.38. When mean slope = 1.74 and h2 = 0.38, then 3–13 generations would be required for a ten‐fold increase in LC50s at 90–20% intensity of selection. Very high cross‐resistance to emamectin benzoate (143‐fold), deltamethrin (1675‐fold) and lambda‐cyhalothrin (140‐fold), and moderate cross‐resistance to acetamiprid (37‐fold) in the imidacloprid‐selected strain compared to the field population were observed.CONCLUSIONImidacloprid resistance developed very quickly under continuous selection pressure in the laboratory. These factors might lead to an increasing likelihood of resistance development in field populations, if imidacloprid is used continuously without insecticide rotation for prolonged periods. The present results would be supportive for better management of D. koenigii by devising an effective resistance management strategy. © 2020 Society of Chemical Industry