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Resistance to Avermectins in the House Fly, Musca domestica

Jeffrey G. Scott

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Abstract

Resistance to abamectin (avermectin B 1a ) has been studied in the house fly, Musca domestica . Cross-resistance was first detected in 1986 and appeared due to decreased penetration and a piperonyl butoxide suppressible factor (i.e. monooxygenase-mediated metabolism). Selection with abamectin resulted in a strain, called AVER, with >60,000-fold resistance by topical application. However, the level of resistance varied between technical and formulated material as well as by the method of bioassay. Resistance in the AVER strain is recessive, autosomal and appears to be due to decreased cuticular penetration and target site insensitivity. Insensitivity of the nervous system was associated with a small decrease in the number of binding sites per mg protein in non-neural tissue in the house fly thorax. The impact of resistance on the future use of abamectin is discussed.

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What this paper is about

Resistance to abamectin (avermectin B 1a ) has been studied in the house fly, Musca domestica . Cross-resistance was first detected in 1986 and appeared due to decreased penetration and a piperonyl butoxide suppressible factor (i.e. monooxygenase-mediated metabolism). Selection with abamectin resulted in a strain, called AVER, with >60,000-fold resistance by topical application. However, the level of resistance varied between technical and formulated material as well as by the method of bioassay. Resistance in the AVER strain is recessive, autosomal and appears to be due to decreased cuticular penetration and target site insensitivity. Insensitivity of the nervous system was associated with a small decrease in the number of binding sites per mg protein in non-neural tissue in the house fly thorax. The impact of resistance on the future use of abamectin is discussed.

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Available abstract

Resistance to abamectin (avermectin B 1a ) has been studied in the house fly, Musca domestica . Cross-resistance was first detected in 1986 and appeared due to decreased penetration and a piperonyl butoxide suppressible factor (i.e. monooxygenase-mediated metabolism). Selection with abamectin resulted in a strain, called AVER, with >60,000-fold resistance by topical application. However, the level of resistance varied between technical and formulated material as well as by the method of bioassay. Resistance in the AVER strain is recessive, autosomal and appears to be due to decreased cuticular penetration and target site insensitivity. Insensitivity of the nervous system was associated with a small decrease in the number of binding sites per mg protein in non-neural tissue in the house fly thorax. The impact of resistance on the future use of abamectin is discussed.

Key concepts: Abamectin, Musca, Piperonyl butoxide, Avermectin, Biology, Toxicology, Bioassay, Cross-resistance

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