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Decreased cuticular penetration has been documented as a mechanism of resistance in several insects, yet this mechanism remains poorly understood. Levels of resistance conferred, effects of the physicochemical properties on the manifestation of resistance and the effects of different routes of exposure are largely unknown. We recently selected a strain (FlurR) of house fly that was >11,000-fold resistance to fluralaner, and decreased cuticular penetration was one of the mechanisms of resistance (Norris et al., 2023). We sought to isolate the decreased penetration mechanism from FlurR into the background of the susceptible aabys strain, and to characterize the protection it conferred to fluralaner and other insecticides. We successfully isolated the decreased penetration mechanism and found that it conferred 7.1-fold resistance to fluralaner, and 1.4- to 4.9-fold cross-resistance to five other insecticides by topical application. Neither mass, metabolic lability, vapor pressure, nor logP explained the differences in the resistance ratios. The mechanism also conferred cross resistance by residual and feeding exposure, although at reduced levels compared to topical application. Remaining data gaps in our understanding of this mechanism are discussed., (Copyright © 2024. Published by Elsevier Inc.)

Insecticides are commonly employed in vineyards to control vinegar flies and limit sour rot disease. Widespread resistance to available insecticides is having a negative impact on managing Drosophila melanogaster populations, rendering control of sour rot more difficult. An insecticide registered for use in vineyards to which resistance is not yet widespread (at least in New York and Missouri) is spinetoram. Spinetoram targets the nicotinic acetylcholine receptor α6, and mutations in α6 have been associated with resistance in some insects. Our goals were to select for a spinetoram resistant strain of D. melanogaster (starting with field collected populations), characterize the resistance, and identify the mutation responsible. After five selections a strain (SpinR) with >190-fold resistance was obtained. Resistance could not be overcome by insecticide synergists, suggesting an altered target site was involved. We cloned and sequenced the α6 allele from the spinetoram resistant strain and identified a mutation causing a glycine to alanine change at amino acid 301 (equivalent position to the G275E mutation found in some spinosad/spinetoram resistant insects). This mutation was found at low levels in field populations, but increased with each selection until it became homozygous in SpinR. We discuss how the identification of the spinetoram resistance mutation can be used for resistance management., (Copyright © 2023 Elsevier Inc. All rights reserved.)

House flies, Musca domestica (L), are the mechanical vector of >100 human and animal pathogens, including those that are antibiotic-resistant. Given that house flies are associated closely with human and livestock activity, they present medical and veterinary health concerns. Although there are numerous strategies for control of house fly populations, chemical control has been favored in many facilities. Products with pyrethroid active ingredients have been used predominantly for >35 years in space sprays. As a result, strong selection for pyrethroid resistance has led to reduced control of many populations. Reliance on a limited number of insecticides for decades has created fly control problems necessitating the discovery and formulation of new control chemistries. Fluralaner is a relatively new insecticide and acaricide (first reported in 2010), belonging to the isoxazoline class. These insecticides target the glutamate- and gamma-aminobutyric acid-gated (GABA) chloride channels, which is a different mode of action from other insecticides used against house flies. Although is it not currently registered for house fly control in the United States, previous work has shown that fluralaner is highly toxic to house flies and that there was limited cross-resistance found in laboratory strains having high levels of resistance to other insecticides. Herein, we characterized the time and age dependency of fluralaner toxicity, detected cross-resistance in populations from across the United States, and selected a highly resistant (>11,000-fold) house fly strain. We found that the fluralaner LD 50 of 18-24 h old flies was 2-fold higher than for 5-6 d old flies. This appears to be due to more rapid penetration of fluralaner into the 5-6 d old flies. Fluralaner resistance was inherited as an intermediate to incompletely dominant trait and was mapped to chromosomes 5 and 3. Resistance could be suppressed to 7-fold with piperonyl butoxide, suggesting that cytochrome P450 (CYP)-mediated detoxification was a major mechanism of resistance. Decreased penetration was also demonstrated as a mechanism of resistance. The utility of fluralaner for house fly control is discussed., (Copyright © 2023 Elsevier Inc. All rights reserved.)