Imidacloprid is the most widely used neonicotinoid insecticide against house flies, which are major pests at animal production facilities worldwide. However, cases of both physiological and behavior resistance have been reported. Recently, physiological resistance to imidacloprid was found in the United States (California and Florida). However, no studies have been undertaken to characterize this resistance in house flies from the United States. Three imidacloprid selections of a strain originally collected from Florida increased the level of resistance, ultimately resulting in a strain that had 2300-fold resistance in females and 130-fold in males. Imidacloprid resistance was not overcome with piperonyl butoxide (PBO) suggesting that resistance is not due to detoxification by cytochrome P450s. Resistance was mapped to autosomes 3 and 4. There was⩾100-fold cross-resistance to acetamiprid and dinotefuran, but no cross-resistance to spinosad. The resistance in this imidacloprid selected population was unstable and declined over a period of several months. The significance of these results to management of imidacloprid resistance in the field, and potential mechanisms of resistance involved, are discussed.
Keywords: Genetic linkage; Musca domestica; Neonicotinoid resistance.
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