Department of Entomology, Plant Pathology and Weed Science, New Mexico State University, Las Cruces, NM.
J Econ Entomol. 2019 Mar 21;112(2):786-791. doi: 10.1093/jee/toy376.
The common bed bug, Cimex lectularius L. (Hemiptera: Cimicidae), is an obligate hematophagous insect that has resurged worldwide since the early 2000s. Bed bug control is largely based on the widespread, intensive application of pyrethroid-based insecticide formulations, resulting in the emergence of insecticide-resistant bed bug populations. Insecticide resistance is frequently linked to metabolic detoxification enzymes such as cytochrome monooxygenase (P450s), esterases, glutathione S-tranferase, and carboxylesterase. Therefore, one way to overcome insecticide resistance could be the formulation of insecticides with synergists that counteract metabolic resistance. To test this hypothesis, we evaluated the impact of four synergists-piperonyl butoxide (PBO), diethyl maleate (DEM), S,S,S-tributyl phosphorotrithioate (DEF), and triphenyl phosphate (TPP)-on deltamethrin efficacy in two pyrethroid-resistant bed bug strains. A statistically significant difference in synergism ratios (SR) of a highly resistant field-derived strain (Jersey City, resistance ratio [RR] = 20,000) was noted when any of the four synergists (PBO SR = 20.5; DEM SR = 11.7; DEF SR = 102.3; and TPP SR = 9.7) were used with deltamethrin. In a less deltamethrin-resistant strain, Cincinnati (RR = 3,333), pretreatment with PBO and DEM significantly synergized deltamethrin (PBO SR = 158.8; DEM = 58.8), whereas application of DEF and TPP had no synergistic effect. The synergism data collected strongly suggest that detoxification enzymes play a significant role in the metabolic mechanisms that mediate deltamethrin resistance in bed bugs. The development and use of safe metabolic synergists that suppress detoxification enzymes offers an interesting avenue for the management of insecticide-resistant field populations.
常见的臭虫,Cimex lectularius L.(半翅目:臭虫科),是一种专性吸血昆虫,自 21 世纪初以来在全球范围内再次出现。臭虫的控制主要基于广泛的、密集的拟除虫菊酯类杀虫剂制剂的应用,导致抗药性臭虫种群的出现。杀虫剂抗性通常与代谢解毒酶如细胞色素单加氧酶(P450s)、酯酶、谷胱甘肽 S-转移酶和羧酸酯酶有关。因此,克服杀虫剂抗性的一种方法可能是使用增效剂来对抗代谢抗性的杀虫剂配方。为了验证这一假设,我们评估了四种增效剂-胡椒基丁醚(PBO)、马来酸二乙酯(DEM)、S,S,S-三丁基膦酸三硫酯(DEF)和磷酸三苯酯(TPP)-对两种拟除虫菊酯类抗性臭虫品系中溴氰菊酯效果的影响。当任何一种增效剂(PBO 的增效比 [SR] = 20.5;马来酸二乙酯的 SR = 11.7;DEF 的 SR = 102.3;TPP 的 SR = 9.7)与溴氰菊酯一起使用时,都观察到高度抗药性田间分离株(泽西城,抗性比 [RR] = 20000)的增效比存在统计学显著差异。在一种抗溴氰菊酯性较低的品系辛辛那提(RR = 3333)中,PBO 和 DEM 的预处理显著增效溴氰菊酯(PBO 的 SR = 158.8;马来酸二乙酯的 SR = 58.8),而 DEF 和 TPP 的应用则没有增效作用。收集到的增效数据强烈表明,解毒酶在介导臭虫对溴氰菊酯的代谢抗性的代谢机制中起着重要作用。开发和使用安全的代谢增效剂来抑制解毒酶为管理田间抗药性种群提供了一个有趣的途径。