Rabia Saeed1, Naeem Abbas2. 1. Entomology Section, Central Cotton Research Institute, Multan, Pakistan. 2. Department of Plant Protection, College of Food and Agriculture Sciences, King Saud University, Riyadh, Saudi Arabia.
Abstract
BACKGROUND: Imidacloprid, 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. RESULTS: The 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. CONCLUSION: Imidacloprid 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.
BACKGROUND:Imidacloprid, 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. RESULTS: The 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. CONCLUSION:Imidacloprid 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.