Carmona-Antoñanzas Greta, Bekaert Michaël, Humble Joseph L, Boyd Sally, Roy William, Bassett David I, Houston Ross D, Gharbi Karim, Bron James E, Sturm Armin
Institute of Aquaculture, Faculty of Natural Sciences, University of Stirling, Stirling, Scotland, United Kingdom.
The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, Scotland, United Kingdom.
PLoS One. 2017 Jul 12;12(7):e0180625. doi: 10.1371/journal.pone.0180625. eCollection 2017.
Parasitic infections by the salmon louse, Lepeophtheirus salmonis (Krøyer), cause huge economic damage in salmon farming in the northern hemisphere, with combined treatment costs and production losses in 2014 having been estimated at US$ 350 million for Norway (annual production 1.25 million tonnes). The control of L. salmonis relies significantly on medicinal treatments, supplemented by non-pharmacological approaches. However, efficacy losses have been reported for several delousing agents, including the pyrethroid deltamethrin. The aim of the present study was to analyse the genetic basis of deltamethrin resistance in L. salmonis. Deltamethrin median effective concentrations (EC50) were 0.28 μg L-1 in the drug susceptible L. salmonis strain IoA-00 and 40.1 μg L-1 in the pyrethroid resistant strain IoA-02. IoA-00 and IoA-02 were crossed to produce families spanning one parental and three filial generations (P0, F1-F3). In three families derived from P0 crosses between an IoA-00 sire and an IoA-02 dam, 98.8% of F2 parasites (n = 173) were resistant, i.e. remained unaffected after exposure to 2.0 μg L-1 deltamethrin. F3 parasites from these crosses showed a deltamethrin EC50 of 9.66 μg L-1. In two families of the inverse orientation at P0 (IoA-02 sire x IoA-00 dam), 16.7% of F2 parasites were resistant (n = 84), while the deltamethrin EC50 in F3 animals was 0.26 μg L-1. The results revealed a predominantly maternal inheritance of deltamethrin resistance. The 15,947-nt mitochondrial genome was sequenced and compared among six unrelated L. salmonis strains and parasites sampled from wild salmon in 2010. IoA-02 and three further deltamethrin resistant strains, established from isolates originating from different regions of Scotland, showed almost identical mitochondrial haplotypes. In contrast, the mitochondrial genome was variable among susceptible strains and L. salmonis from wild hosts. Deltamethrin caused toxicity and depletion of whole body ATP levels in IoA-00 but not IoA-02 parasites. The maternal inheritance of deltamethrin resistance and its association with mitochondrial haplotypes suggests that pyrethroid toxicity in L. salmonis may involve molecular targets encoded by mitochondrial genes.
鲑虱(Lepeophtheirus salmonis,克罗耶氏)引起的寄生虫感染给北半球的鲑鱼养殖造成了巨大经济损失,2014年挪威的治疗成本和生产损失总计估计达3.5亿美元(年产量125万吨)。鲑虱的控制在很大程度上依赖药物治疗,并辅以非药物方法。然而,已有报道称包括拟除虫菊酯溴氰菊酯在内的几种除虱剂的疗效有所下降。本研究的目的是分析鲑虱对溴氰菊酯抗性的遗传基础。在对溴氰菊酯敏感的鲑虱菌株IoA - 00中,溴氰菊酯的半数有效浓度(EC50)为0.28 μg/L,而在对拟除虫菊酯具有抗性的菌株IoA - 02中为40.1 μg/L。将IoA - 00和IoA - 02杂交,产生涵盖一个亲代和三个子代世代(P0、F1 - F3)的家系。在由IoA - 00父本与IoA - 02母本杂交产生的三个家系中,98.8%的F2代寄生虫(n = 173)具有抗性,即在暴露于2.0 μg/L溴氰菊酯后未受影响。这些杂交产生的F3代寄生虫的溴氰菊酯EC50为9.66 μg/L。在P0代反向杂交的两个家系(IoA - 02父本×IoA - 00母本)中,16.7%的F2代寄生虫具有抗性(n = 84),而F3代动物的溴氰菊酯EC50为0.26 μg/L。结果显示溴氰菊酯抗性主要呈母系遗传。对15,947个核苷酸的线粒体基因组进行了测序,并在六个无关的鲑虱菌株以及2010年从野生鲑鱼采集的寄生虫之间进行了比较。IoA - 02以及另外三个从苏格兰不同地区分离株建立的对溴氰菊酯具有抗性的菌株,显示出几乎相同的线粒体单倍型。相比之下,敏感菌株和来自野生宿主的鲑虱的线粒体基因组存在差异。溴氰菊酯对IoA - 00寄生虫造成毒性并使全身ATP水平降低,但对IoA - 02寄生虫则无此作用。溴氰菊酯抗性的母系遗传及其与线粒体单倍型的关联表明,鲑虱中拟除虫菊酯的毒性可能涉及线粒体基因编码的分子靶点。