Department of Entomology, Cornell University, Ithaca, NY, USA.
Department of Medical Entomology, National Institute of Infectious Diseases, Tokyo, Japan.
Pest Manag Sci. 2018 Mar;74(3):737-745. doi: 10.1002/ps.4771. Epub 2017 Dec 8.
Aedes aegypti is a vector of several important human pathogens. Control efforts rely primarily on pyrethroid insecticides for adult mosquito control, especially during disease outbreaks. A. aegypti has developed resistance nearly everywhere it occurs and insecticides are used. An important mechanism of resistance is due to mutations in the voltage-sensitive sodium channel (Vssc) gene. Two mutations, in particular, S989P + V1016G, commonly occur together in parts of Asia.
We have created a strain (KDR:ROCK) that contains the Vssc mutations S989P + V1016G as the only mechanism of pyrethroid resistance within the genetic background of Rockefeller (ROCK), a susceptible lab strain. We created KDR:ROCK by crossing the pyrethroid-resistant strain Singapore with ROCK followed by four backcrosses with ROCK and Vssc S989P + V1016G genotype selections. We determined the levels of resistance conferred to 17 structurally diverse pyrethroids, the organochloride DDT, and oxadiazines (VSSC blockers) indoxacarb (proinsecticide) and DCJW (the active metabolite of indoxacarb). Levels of resistance to the pyrethroids were variable, ranging from 21- to 107-fold, but no clear pattern between resistance and chemical structure was observed. Resistance is inherited as an incompletely recessive trait. KDR:ROCK had a > 2000-fold resistance to DDT, 37.5-fold cross-resistance to indoxacarb and 13.4-fold cross-resistance to DCJW.
Etofenprox (and DDT) should be avoided in areas where Vssc mutations S989P + V1016G exist at high frequencies. We found that pyrethroid structure cannot be used to predict the level of resistance conferred by kdr. These results provide useful information for resistance management and for better understanding pyrethroid interactions with VSSC. © 2017 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
埃及伊蚊是几种重要人类病原体的传播媒介。控制工作主要依赖于拟除虫菊酯类杀虫剂来控制成蚊,特别是在疾病爆发期间。埃及伊蚊几乎在所有出现的地方都产生了抗药性,并且杀虫剂也在使用。抗性的一个重要机制是由于电压敏感钠通道(Vssc)基因的突变。特别是 S989P + V1016G 这两个突变,在亚洲部分地区经常同时发生。
我们创建了一个品系(KDR:ROCK),该品系仅含有 Vssc 突变 S989P + V1016G,作为罗克韦尔(ROCK)遗传背景内对拟除虫菊酯类杀虫剂产生抗性的唯一机制,ROCK 是一种敏感的实验室品系。我们通过将抗药性的新加坡品系与 ROCK 杂交,然后与 ROCK 进行四次回交,并对 Vssc S989P + V1016G 基因型进行选择,从而创建了 KDR:ROCK。我们确定了 17 种结构不同的拟除虫菊酯、有机氯滴滴涕、恶二嗪(VSSC 阻滞剂)茚虫威(原杀虫剂)和 DCJW(茚虫威的活性代谢物)赋予的抗药性水平。对拟除虫菊酯的抗药性水平各不相同,范围从 21 倍到 107 倍,但未观察到抗药性与化学结构之间的明显关系。抗性是一种不完全隐性性状遗传。KDR:ROCK 对滴滴涕的抗性超过 2000 倍,对茚虫威的交叉抗性为 37.5 倍,对 DCJW 的交叉抗性为 13.4 倍。
在 S989P + V1016G 突变高频存在的地区,应避免使用乙硫苯威(和滴滴涕)。我们发现,拟除虫菊酯结构不能用于预测 kdr 赋予的抗性水平。这些结果为抗性管理提供了有用的信息,并有助于更好地了解拟除虫菊酯与 VSSC 的相互作用。©2017 作者。害虫管理科学由 John Wiley & Sons Ltd 代表化学工业协会出版。