Bossard R L, Hinkle N C, Rust M K
Department of Entomology, Kansas State University, Manhattan 66506, USA.
J Med Entomol. 1998 Jul;35(4):415-22. doi: 10.1093/jmedent/35.4.415.
Insecticide resistance often is blamed for failures of insecticides to control cat fleas, Ctenocephalides felis (Bouché). Yet the genetics and adaptive advantage of resistance traits remain unexamined. Lethal doses of insecticides that kill 50% of the population fluctuate 7-fold within a cat flea strain. Many reports of flea resistance may be attributable to variable mortality from effects of solvents, substrates, humidities, temperatures, colonization, and ages of fleas. Resistance ratios (ratios of lethal doses of a resistant to a susceptible strain) are < 690-fold in fleas; lower than many other arthropods. This, plus strain variability, hinders resistance detection. Relationships between resistance levels, control failures, and health threats are unclear. Insensitive acetylcholinesterase, knockdown recovery, glutathione transferase conjugation, and mixed function oxidase/cytochrome P450 are demonstrated resistance mechanisms in cat fleas. Ecological genetics of resistance in cat fleas probably involves flea transfer among hosts, host movements, refugia, founder effects, and mortality from abiotic factors. Understanding cat flea resistance requires population monitoring before, during, and after insecticide treatments using conventional and rapid molecular bioassays. Sustained insecticide release devices such as flea collars and long-lived insecticide residues for premises possibly contribute to the development of resistance. New systemic and topical insecticides, especially when given prophylactically, may act similarly. Eliminating insecticides prevents insecticide resistance but necessitates application of biorational tactics incorporating mechanical, environmental, and cultural controls. Using high temperatures, low humidities, host grooming and such tactics as decreasing doses, increasing action thresholds, rotating insecticides, and leaving spatial and temporal refugia may suppress cat flea resistance.
杀虫剂抗性常被认为是杀虫剂无法有效控制猫蚤（Ctenocephalides felis，布歇）的原因。然而，抗性性状的遗传学及适应性优势仍未得到研究。在一个猫蚤品系中，能杀死50%种群的杀虫剂致死剂量波动幅度达7倍。许多关于跳蚤抗性的报告可能归因于溶剂、底物、湿度、温度、定殖以及跳蚤年龄等因素导致的死亡率差异。跳蚤的抗性比率（抗性品系与敏感品系致死剂量之比）小于690倍；低于许多其他节肢动物。这一点，再加上品系变异性，阻碍了抗性检测。抗性水平、防治失败与健康威胁之间的关系尚不清楚。不敏感的乙酰胆碱酯酶、击倒恢复、谷胱甘肽转移酶结合以及混合功能氧化酶/细胞色素P450是已证实的猫蚤抗性机制。猫蚤抗性的生态遗传学可能涉及宿主间的跳蚤转移、宿主移动、避难所、奠基者效应以及非生物因素导致的死亡率。了解猫蚤抗性需要在杀虫剂处理前、处理期间和处理后使用传统和快速分子生物测定法进行种群监测。持续释放杀虫剂的装置，如跳蚤项圈和用于场所的长效杀虫剂残留，可能有助于抗性的发展。新型的全身和局部杀虫剂，尤其是预防性使用时，可能会有类似作用。消除杀虫剂可防止产生杀虫剂抗性，但需要采用结合机械、环境和文化控制的生物合理策略。利用高温、低湿度、宿主梳理以及降低剂量、提高作用阈值、轮换杀虫剂和设置空间和时间避难所等策略，可能会抑制猫蚤抗性。
