AI Article Synopsis
- The study focuses on the brown dog tick, a common parasite for dogs and humans, which has developed resistance to pesticides due to poor pest management practices.
- Researchers established a specific concentration (0.51%) of etofenprox to effectively screen for resistance in tick populations across different regions, including Asia, Africa, Europe, North America, and the Caribbean.
- Findings indicate that while metabolic resistance is likely the main cause of pesticide resistance, a sodium channel mutation also contributes to the ticks' tolerance to etofenprox.
Article Abstract
Background: The brown dog tick, Rhipicephalus sanguineus sensu lato (Latreille; Acari: Ixodidae), is a peridomestic ectoparasite of dogs and occasionally humans. In some populations, lack of integrated pest management practices and overuse of pesticides has resulted in high levels of resistance to multiple active ingredients. In this study, we established the etofenprox discriminating concentration (DC) and three additional screening concentrations to evaluate resistance status. Using mortality results, cross-resistance was investigated in brown dog tick populations from five geographically disparate regions, including Asia, Africa, Europe, North America, and the Caribbean, following exposure to the DC for both etofenprox and permethrin separately. Subsequently, using both larval packet tests and molecular methods, etofenprox resistance was investigated.
Results: The etofenprox DC was set at 0.51%, which allows for the rapid screening of peridomestic brown dog tick populations for resistance to this active ingredient. Cross-tolerance to two sodium channel-inhibiting pesticides, permethrin and etofenprox, was observed in one population.
Conclusion: Our study has provided a single etofenprox concentration that can be used in larval packet tests to determine resistance status in collected peridomestic brown dog ticks, which is particularly important when a single to a few engorged adult ticks are provided for evaluation. Although metabolic resistance is presumed to be the primary resistance mechanism, a sodium channel mutation also confers tolerance to etofenprox at the DC. © 2019 Society of Chemical Industry.
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