Abamectin resistance in strains of vegetable leafminer,Liriomyza sativae (Diptera: Agromyzidae) is linked to elevated glutathione S‐transferase activity

Abamectin resistance was selected in the vegetable leafminer, Liriomyza sativae (Blanchard) (Diptera: Agromyzidae) under laboratory conditions, and cross‐resistance patterns and possible resistance mechanisms in the abamectin‐resistant strains (AL‐R, AF‐R) were investigated. Compared with the susceptible strain (SS), strain AL‐R displayed 39‐fold resistance to abamectin after 20 selection cycles during 25 generations, and strain AF‐R exhibited 59‐fold resistance to abamectin after 16 selection cycles during 22 generations. No cross‐resistance to cyromazine was found in both abamectin‐resistant strains. However, we failed to select for cyromazine resistance in L. sativae under laboratory conditions by conducting 17 selection cycles during 22 generations. However, moderate levels of cross‐resistance to abamectin (6–9 fold) were observed in strains which received cyromazine treatments. Biochemical analysis showed that glutathione S‐transferase (GST) activity in both abamectin‐resistant strains (AL‐R, AF‐R) was significantly higher than in the susceptible strain (SS), suggesting metabolically driven resistance to abamectinin L. sativae. Recommendations of mixtures or rotation of cyromazine and abamectin should be considered carefully, as consecutive cyromazine treatments may select for low‐level cross‐resistance to abamectin.     

Cyromazine resistance in the house fly (Diptera: Muscidae): genetics and cross-resistance to diflubenzuron

Larvae of a house fly, Musca domestica L., strain collected in a chicken house near Pittsburg, Tex, after a control failure with the poultry feedthrough insecticide cyromazine showed 6.5-fold resistance to cyromazine and 10-fold resistance to diflubenzuron. Adults of the strain showed high levels of resistance to carbaryl, DDT, and diazinon; moderate resistance to cypermethrin and permethrin; and low resistance to dieldrin. In contrast, no resistance to cyromazine was observed in eight laboratory house fly strains with resistance to four groups of conventional insecticides. When the genetics of cyromazine resistance was investigated in crosses to susceptible strains with visible mutant markers, results indicated cyromazine resistance was incompletely dominant over susceptibility and the resistance gene was on chromosome V. The same or a closely linked gene conferred resistance to diflubenzuron. A strain containing only chromosome V from the original resistant strain was resistant to cyromazine and diflubenzuron, but not to other insecticides except for low level resistance to DDT and carbaryl. Resistance to the latter insecticides appeared to be due to a linked, but distinct, gene. Therefore, resistance to cyromazine and probably diflubenzuron appears to be genetically distinct from other types of insecticide resistance.     

桔小实蝇实验种群对敌百虫、高效氯氰菊酯和阿维菌素的抗性增长规律

桔小实蝇Bactrocera doralis (Hendel)是华南地区水果蔬菜上重要害虫,近年来暴发成灾,造成巨大的经济损失。使用化学杀虫剂是防治该虫的重要方法。在长期、频繁接触杀虫剂条件下该虫的抗药性产生、发展规律等问题值得深入研究。本文采用LC₅₀、LC_80-90两种剂量汰选成虫、幼虫,研究了桔小实蝇对敌百虫、高效氯氰菊酯和阿维菌素3种药剂的抗性增长规律。通过不接触药剂继代饲养获得了对3种杀虫剂的敏感品系,建立了毒力回归方程,明确了毒力敏感基线LC₅₀分别为1.6024 mg/L,3.0964 mg/L和0.6074 mg/L。不同药剂种类、不同汰选方式时桔小实蝇的抗药性发展速度是不同的。以成虫死亡率50%左右作为选择压力,桔小实蝇对敌百虫的抗性发展最快,汰选至14代抗性增长至84.6倍;其次是高效氯氰菊酯,抗性增长至27.1倍;而对阿维菌素的抗性仅上升至7.7倍 。在成虫和幼虫80%～90%死亡率左右的选择压力下,桔小实蝇对高效氯氰菊酯的抗性发展最快,汰选14代后抗性增长至125.4倍; 其次是敌百虫,抗性增大至49.9倍;对阿维菌素抗性增长相对较缓慢,11代后为17.9倍。在成虫80%～90%死亡率左右的选择压力下,汰选14代、14代、11代后桔小实蝇对高效氯氰菊酯、敌百虫、阿维菌素分别增大至58.7倍、37.6倍、11.9倍。对成虫、幼虫均进行汰选桔小实蝇抗药性发展更快。建立了不同汰选方式时桔小实蝇实验种群汰选代数与对3种杀虫剂的抗性程度之间的关系方程,其中高效氯氰菊酯、敌百虫处理符合韦布尔曲线模型,阿维菌素处理符合幂曲线方程。     

Generating susceptible strain and resistance status of field populations of Spodoptera exigua (Lepidoptera: Noctuidae) against some conventional and new chemistry insecticides in Pakistan

Two field populations of Spodoptera exigua (Hübner) (Lepidoptera: Noctuidae) from Dera Ghazi Khan (D. G. Khan) and Multan, Pakistan, were tested for resistance to the 10 most commonly used insecticides in Pakistan by using a standard leaf disc bioassay on the F1 progeny. For comparison, a susceptible strain was generated from the Multan strain, which displayed lower LC50 values for most of the insecticides, by either mass rearing without exposure to insecticides or single-pair crosses against selected insecticides. The single-pair crosses generated a more susceptible strain than mass rearing. The D. G. Khan field strain was highly resistant to cypermethrin, profenofos, spinosad, abamectin, and chlorpyrifos and moderately resistant to deltamethrin, indoxacarb, and methoxyfenozide compared with susceptible lab strain. The Multan strain was highly resistant to profenofos and indoxacarb. Both field populations were susceptible to emamectin benzoate and lufenuron. Rotating these two insecticides with others that show very low, low, or moderate levels of resistance and have different modes of action may be useful for the effective management of this pest.     

Effect of rotational use of insecticides on pyrethroids resistance in Helicoverpa armigera (Lep.: Noctuidae)

Abstract:  To investigate fluctuation in susceptibility to insecticides in the field, natural populations of Helicoverpa armigera were collected from the same field in the region of Multan, Pakistan in 2002 and 2003. The populations were examined against pyrethroids (viz. cypermethrin, esfenvalerate and fenpropathrin) and new insecticides (viz. spinosad, abamectin and indoxacarb). In 2002, the resistance ratio (RR) of cypermethrin and esfenvalerate was significantly higher than fenpropahrin compared with susceptible population. The susceptibility to cypermethrin, esfenvalerate and fenpropathrin increased significantly in 2003; however, the RR for cypermethrin was about half the RR (38) of esfenvalerate (101) and fenpropathrin (89). The toxicity of spinosad, abamectin and indoxacarb was identical in both years. In the field experiments, abamectin was more effective than other compounds tested whereas fenpropathrin, cypermethrin and esfenvalerate had similar toxicity. These results might have important implications in resistance management and suggest that the rotational use of spinosad, abamectin and indoxacarb could help to avoid the development of multiple resistant in H. armigera .     

南京地区小菜蛾的抗药性检测及初步分析

利用浸叶法对南京郊区小菜蛾Plutella xylostella的抗药性进行了监测,发现其对拟除虫菊酯类药剂的抗性较高,而对氟虫腈、辛硫磷、毒死蜱、多杀菌素和虫酰肼依然处于敏感阶段。利用抗性小菜蛾测试发现,氧化胡椒基丁醚（增效醚,简称PBO）对拟除虫菊酯具有显著的增效作用。室内敏感性恢复实验表明,在不接触药剂的条件下,小菜蛾对拟除虫菊酯的抗性迅速下降,繁殖10代以后,抗性维持在低抗水平。因此, 小菜蛾的抗药性治理,应充分利用不同药剂的轮换使用,避免单一使用某一品种,以延缓抗性的发展,同时可以利用PBO增强拟除虫菊酯的防治效果,保证这类药剂在小菜蛾防治中的作用。     

Insecticide resistance and cross-resistance in the house fly (Diptera: Muscidae)

A house fly strain, ALHF, was collected from a poultry farm in Alabama after a control failure with permethrin, and further selected in the laboratory with permethrin for five generations. The level of resistance to permethrin in ALHF was increased rapidly from an initial 260-fold to 1,800-fold after selection. Incomplete suppression of permethrin resistance by piperonyl butoxide (PBO) and S,S,S,-tributylphosphorotrithioate (DEF) reveals that P450 monooxygenase- and hydrolase-mediated detoxication, and one or more additional mechanisms are involved in resistance to permethrin. The ALHF strain showed a great ability to develop resistance or cross-resistance to different insecticides within and outside the pyrethroid group including some relatively new insecticides. Resistance to beta-cypermethrin, cypermethrin, deltamethrin, and propoxur (2,400-4,200-, 10,000-, and > 290-fold, respectively, compared with a susceptible strain, aabys) in ALHF house flies was partially or mostly suppressed by PBO and DEF, indicating that P450 monooxygenases and hydrolases are involved in resistance to these insecticides. Partial reduction in resistance with PBO and DEF implies that multiresistance mechanisms are responsible for resistance. Fifteen- and more than fourfold resistance and cross-resistance to chlorpyrifos and imidacloprid, respectively, were not effected by PBO or DEF, indicating that P450 monooxygenases and hydrolases are not involved in resistance to these two insecticides. Forty-nine-fold cross-resistance to fipronil was mostly suppressed by PBO and DEF, revealing that monooxygenases are a major mechanism of cross-resistance to fipronil. Multiresistance mechanisms in the ALHF house fly strain, however, do not confer cross-resistance to spinosad, a novel insecticide derived from the bacterium Saccharopolyspora spinosa. Thus, we propose that spinosad be used as a potential insecticide against house fly pests, especially resistant flies.     

Putative polymerase chain reaction markers for insecticide resistance in the leafminer Liriomyza trifolii (Diptera: Agromyzidae) to cyromazine and abamectin

In this study, random amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) was used to identify polymorphic genomic DNA that would discriminate among cyromazine-resistant, abamectin-resistant, and susceptible Liriomyza trifolii (Burgess) (Diptera: Agromyzidae) leafminers. Using a reference strain that was susceptible to both cyromazine and abamectin, and a cyromazine-resistant strain and an abamectin-resistant strain, 400 oligonucleotides were assayed using RAPD-PCR. We found that two oligonucleotides, B10 and G16, amplified unique bands in the cyromazine-resistant strain but not in the reference or abamectin-resistant strains. Three oligonucleotides, K04, J13, and I02, showed polymorphisms unique to the abamectin-resistant strain but not in the reference or cyromazine-resistant strain. Leaf dip bioassays and RAPD-PCR were performed on two additional reference strains, seven strains from commercial ornamental production greenhouses, and one field strain. The two reference strains were negative for the resistance-correlated oligonucleotides. Of the seven strains from ornamental greenhouses, leaf dip bioassays showed that five had some level of resistance to both abamectin and cyromazine, whereas two were susceptible. The field strain was susceptible to both cyromazine and abamectin. In RAPD-DNA analyses, the five strains with abamectin resistance were positive for the three abamectin resistance-correlated oligonucleotides K04, J13, and I02. In the cases of cyromazine resistance, the five strains with cyromazine resistance were positive for the two cyromazine resistance-correlated oligonucleotides B10 and G16. The field strain and two greenhouse strains that were susceptible in leaf dip bioassays were negative for all three abamectin resistance-correlated oligonucleotides. The field strain and one greenhouse strain were negative for the two cyromazine resistance-correlated oligonucleotides; however, one greenhouse strain that was susceptible to cyromazine in leaf dip bioassay tested positive for one of the cyromazine resistance-correlated oligonucleotides. This method can be used to quickly identify cyromazine resistance, abamectin resistance, or both in leafminers, enabling a grower to choose an effective insecticide for leafminer control in a timely manner.     

Molecular mechanisms conferring asymmetrical cross-resistance between tebufenozide and abamectin in Plutella xylostella

Based on the confirmation of asymmetrical cross-resistance between abamectin and tebufenozide in Plutella xylostella, the present work proved that the cytochrome P450 monooxygenase plays a decisive role in cross-resistance, and the expression of various cytochrome P450 (CYP450) genes in different strains was surveyed to elucidate the molecular basis of the underlying mechanisms. Enzyme analysis showed the activity of cytochrome P450 monooxygenase was notable enhanced in the strains resistant to both tebufenozide (3.07-fold) and abamectin (3.37-fold), suggesting that the enhancement of cytochrome P450 monooxygenase is the main detoxification mechanism responsible for the cross-resistance. CYP4M7 (64.58-fold) and CYP6K1 (41.97-fold) had extremely high expression levels in the Teb-R strain, selected using tebufenozide, which was highly resistant to tebufenozide (RR 185.5) and moderately cross-resistant to abamectin (RR 41.0). When this strain was subjected to further selection using abamectin, the resultant Aba-R strain showed a higher expression of CYP6K1 (60.32-fold). However, the expression of CYP4M7 was reduced (10.62-fold). Correspondingly, the Aba-R strain became more resistant to abamectin (RR 593.8) and less resistant to tebufenozide (RR 28.0). Therefore, we concluded that the over expression of CYP4M7 was the main cause for tebufenozide resistance, and that CYP6K1 mainly conferred abamectin resistance. The asymmetrical cross-resistance occurred because tebufenozide selection not only enhanced the expression of CYP4M7, but also that of CYP6K1. This is the first report on the molecular mechanism of asymmetrical cross-resistance between insecticides.     

Cross-resistance and biochemical mechanisms of abamectin resistance in the B-type Bemisia tabaci

Abstract:  To understand the risk of resistance and the possible mechanisms of resistance to abamectin in B-type Bemisia tabaci (Gennadius) better, a resistant strain of B. tabaci was selected in the laboratory and cross-resistance pattern and resistance mechanisms to abamectin were investigated. The NJ-Abm strain of B. tabaci was derived from a field population (NJ) collected in Nanjing, China in 2002 with 18 generations of selection with abamectin in the laboratory. Compared with the unselected NJ strain, the selected NJ-Abm strain developed 14.5-fold resistance to abamectin and showed significant cross-resistance to emamectin benzoate (4.4-fold) and imidacloprid (3.4-fold), but no cross-resistance to fipronil. The oxidase inhibitor piperonyl butoxide (PBO) and glutathione S -transferase inhibitor diethyl maleate (DEM) produced significant synergism on abamectin in the NJ-Abm strain (with synergistic ratios of 3.9- and 4.1-fold respectively); however, the esterase inhibitor triphenyl phosphate (TPP) did not act synergistically with abamectin. Biochemical analysis confirmed that P450 monooxygenase activity and glutathione S -transferase activity of the NJ-Abm strain were elevated to 2.1- and 2.0-fold, respectively, compared with that of the NJ strain. This indicated that enhanced metabolism mediated by P450 monooxygenase and glutathione S -transferase is likely to be involved in abamectin resistance and cross-resistance to imidacloprid and emamectin benzoate in the NJ-Abm strain.     

斜纹夜蛾抗药性监测及茚虫威对其解毒代谢酶的影响

【目的】斜纹夜蛾Spodoptera litura (Fabricius)是主要的农业害虫之一。本研究旨在明确该害虫在湖南省5个主要蔬菜种植区的抗药性水平,并探讨该害虫对茚虫威的抗性与解毒代谢酶活性之间的关系,为斜纹夜蛾有效防控及抗性治理提供依据。【方法】采用浸叶法测定了2014-2016年湖南5地斜纹夜蛾田间种群对10种杀虫剂的抗性水平;将斜纹夜蛾敏感种群3龄幼虫在死亡率40%~70%的选择压下用茚虫威进行汰选,比较了斜纹夜蛾敏感种群和抗茚虫威种群的羧酸酯酶、谷胱甘肽S-转移酶和多功能氧化酶对硝基苯甲醚O-脱甲基活性。【结果】湖南5地斜纹夜蛾田间种群对有机磷类杀虫剂产生了26.9~220.2倍的抗性,对氨基甲酸酯类杀虫剂产生了68.3~890.8倍的抗性,对拟除虫菊酯类杀虫剂产生了21.0~267.2倍的抗性,对相对较新型杀虫剂（甲维盐、阿维菌素、茚虫威和溴虫腈）产生了5.2~53.4倍的抗性。经茚虫威汰选后第14代[抗性倍数(resistance ratio, RR)=26.43]斜纹夜蛾羧酸酯酶、谷胱甘肽S-转移酶和对硝基苯甲醚O-脱甲基酶活性分别上升2.86, 1.01和1.83倍。【结论】斜纹夜蛾对多种药剂产生了不同水平的抗性,斜纹夜蛾幼虫羧酸酯酶和对硝基苯甲醚O-脱甲基活性增强可能是斜纹夜蛾对茚虫威的抗性上升的重要因素。     

ESTMATION OF REALIZED HERITABILITY OF RESISTANCE TO FENPROPATHRIN, ABAMECTIN, PYRIDABEN AND THEIR MIXTURES IN ACARICIDE-SELECTED STRAINS OF TETRANYCHUS CINNABARINUS (BOIDUVAL)

Abstract Threshold trait analysis was used to estimate realized heritability (h²) of resistance to five acaricides (three single acaricide and two mixtures) and resistance risk in Tetranychus cinnabarinus (Boiduval). Tetranychus cinnabarinus collected from the field of Beibei, Chongqing reared more than 60 generations under pesticide free conditions and considered susceptible. Successively selected for about 30 generations, the strain had a 65.55-, 5.82-, 1.23-, 5.20- and 1.42-fold increase in resistance to fenpropathrin, abamectin, pyridaben, pyridaben-abamectin (pyridaben: abamectin = 7.4:0.1, m/m) and fenpropathrin-abamectin (fenpropathrin: abamectin = 8.9:0.1, m/m), respectively. The realized heritability of resistance to fenpropathrin, abamectin, pyridaben, pyridaben-abamectin (pyridaben: abamectin = 7.4:0.1, m/m) and fenpropathrin-abamectin (fenpropathrin: abamectin = 8.9:0.1, m/m) is 0.2167, 0.0967, 0.0130, 0.0800 and 0.0172, respectively. Under the selected condition, a 10-fold increase in resistance would be expected 15 generations for fenpropathrin, 34 generations for abamectin, 333 generations for pyridaben, 42 generations for pyridaben-abamectin (pyridaben: abamectin = 7.4:0.1, m/m) and 200 generations for fenpropathrin-abametcin (fenpropathrin: abamectin = 8.9:0.1, m/m). The highest resistance risk of the five acaricides in Tetranychus cinnabarinus was fenpropathrin, then abamection, pyridaben-abamectin (pyridaben: abamectin = 7.4: 0.1, m/m), fenpropathrin- abamectin (fenpropathrin: abamectin = 8.9:0.1, m/m) and that to pyridaben was the lowest. The mixture of pyridaben and abamectin is not useful in delaying development of resistance in the pest to the two single acaricide while the mixture of fenpropathrin and abamectin could do it.     

Field Evolved Resistance in Helicoverpa armigera (Lepidoptera: Noctuidae) to Bacillus thuringiensis Toxin Cry1Ac in Pakistan

Helicoverpa armigera (Hübner) is one of the most destructive pests of several field and vegetable crops, with indiscriminate use of insecticides contributing to multiple instances of resistance. In the present study we assessed whether H. armigera had developed resistance to Bt cotton and compared the results with several conventional insecticides. Furthermore, the genetics of resistance was also investigated to determine the inheritance to Cry1Ac resistance. To investigate the development of resistance to Bt cotton, and selected foliar insecticides, H. armigera populations were sampled in 2010 and 2011 in several cotton production regions in Pakistan. The resistance ratios (RR) for Cry1Ac, chlorpyrifos, profenofos, cypermethrin, spinosad, indoxacarb, abamectin and deltamethrin were 580-fold, 320-, 1110-, 1950-, 200-, 380, 690, and 40-fold, respectively, compared with the laboratory susceptible (Lab-PK) population. Selection of the field collected population with Cry1Ac in 2010 for five generations increased RR to 5440-fold. The selection also increased RR for deltamethrin, chlorpyrifos, profenofos, cypermethrin, spinosad, indoxacarb, abamectin to 125-folds, 650-, 2840-, 9830-, 370-, 3090-, 1330-fold. The estimated LC_50s for reciprocal crosses were 105 µg/ml (Cry1Ac-SEL female × Lab-PK male) and 81 g µg/ml (Lab-PK female × Cry1Ac-SEL male) suggesting that the resistance to Cry1Ac was autosomal; the degree of dominance (D_LC) was 0.60 and 0.57 respectively. Mixing of enzyme inhibitors significantly decreased resistance to Cry1Ac suggesting that the resistance to Cry1Ac and other insecticides tested in the present study was primarily metabolic. Resistance to Cry1Ac was probably due to a single but unstable factor suggesting that crop rotation with non-Bt cotton or other crops could reduce the selection pressure for H. armigera and improve the sustainability of Bt cotton.     

朱砂叶螨对甲氰菊酯、阿维菌素,哒螨灵及其混剂抗性遗传力的分析(英文)

采用域性状分析法 ,估算了朱砂叶螨对 5种杀螨剂 (3种单剂和 2种混剂 )的抗性现实遗传力 ,并对 5种药剂的抗性风险进行了评估。把采自重庆北碚田间的朱砂叶螨种群 ,在室内不施药情况下饲养 6 0余代 ,以此作为抗性筛选的敏感品系。分别单一连续汰选近 30代 ,朱砂叶螨对甲氰菊酯、阿维菌素、哒螨灵、哒螨 -阿维 (哒螨灵 :阿维菌素 =7 4 :0 1,m m)和甲氰 -阿维 (甲氰菊酯 :阿维菌素 =8 9:0 1,m m)的抗性分别达 6 5 5 5、5 82、1 2 3、5 2 0和 1 4 2 倍 ;抗性现实遗传力分别为 0 2 16 7、0 0 96 7、0 0 130、0 0 80 0和 0 0 172。在实验室选择条件下 ,预计抗性增长 10倍时 ,甲氰菊酯、阿维菌素、哒螨灵、哒螨 -阿维 (哒螨灵 :阿维菌素 =7 4 :0 1,m m)和甲氰 -阿维 (甲氰菊酯 :阿维菌素 =8 9:0 1,m m)分别需要 15、34、333、4 2和 2 0 0代。甲氰菊酯抗性风险较高 ,其次是阿维菌素、哒螨 -阿维 (哒螨灵 :阿维菌素 =7 4 :0 1,m m)、甲氰 阿维 (甲氰菊酯 :阿维菌素 =8 9:0 1,m m) ,哒螨灵抗性风险较低。混剂哒螨 阿维 (哒螨灵 :阿维菌素 =7 4 :0 1,m m)不能延缓朱砂叶螨对两单剂哒螨灵和阿维菌素的抗性发展 ,而混剂甲氰 阿维 (甲氰菊酯 :阿维菌素 =8 9:0 1,m m)却能有效延缓朱砂叶螨对两单剂     

Genetic, biochemical, and physiological characterization of spinosad resistance in Plutella xylostella (Lepidoptera: Plutellidae)

Bioassays (at generation G2) with a newly collected field population (designated MN) of Plutella xylostella (L.) (Lepidoptera: Plutellidae) from Multan, Pakistan, indicated resistance to spinosad, indoxacarb, deltamethrin, abamectin, and acetamiprid. At G2 the field-derived population was divided into two subpopulations, one was selected (G2 to G11) with spinosad (Spino-SEL), whereas the second was left unselected (UNSEL). A significant reduction in the resistance ratio for each compound was observed in UNSEL at G12, indicating that the observed resistance to each insecticide was unstable. For Spino-SEL, bioassays at G12 found that selection with spinosad gave a resistance ratio of 283 compared with MN at G2. The resistance to indoxacarb and acetamiprid in the Spino-SEL population increased to 13- and 67-fold, respectively, compared with MN at G2. The toxicity of deltamethrin to Spino-SEL was similar to its toxicity to the MN population at G2. This suggests that spinosad selection maintained the otherwise unstable resistance to the compound. In contrast, resistance to abamectin decreased significantly from G2 to G12 in Spino-SEL. Logit regression analysis of F1 reciprocal crosses between Spino-SEL and the susceptible Lab-UK indicated that resistance to spinosad was inherited as an autosomal, incompletely recessive trait. The spinosad resistance allele significantly delays the developmental time, reduced pupal weight, number of eggs laid, and number of eggs hatched compared with Lab-UK. Further analysis suggests Spino-SEL exhibited a significantly lower intrinsic rate of population increase (r(m)) to all other populations tested.     

Stability of spinosad resistance in Frankliniella occidentalis (Pergande) under laboratory conditions

The stability of spinosad resistance in western flower thrips (WFT), Frankliniella occidentalis (Pergande), populations with differing initial frequencies of resistance was studied in laboratory conditions. The stability of resistance was assessed in bimonthly residual bioassays in five populations with initial frequencies of 100, 75, 50, 25 and 0% of resistant individuals. There were no consistent changes in susceptibility of the susceptible strain after eight months without insecticide pressure. In the resistant strain, very highly resistant to spinosad (RF50>23,000-fold), resistance was maintained up to eight months without further exposure to spinosad. In the absence of any immigration of susceptible genes into the population, resistance was stable. In the case of the population with different initial frequency of resistant thrips, spinosad resistance declined significantly two months later in the absence of selection pressure. With successive generations, these strains did not change significantly in sensitivity. Spinosad resistance in F. occidentalis declined significantly in the absence of selection pressure and the presence of susceptible WFT. These results suggest that spinosad resistance probably is unstable under field conditions, primarily due to the immigration of susceptible WFT. Factors influencing stability or reversion of spinosad resistance are discussed.     

甜菜夜蛾抗药性研究现状

就有关甜菜夜蛾Spodoptera exigua(Hbner)对常用杀虫剂的抗药性现状作综述。甜菜夜蛾对拟除虫菊酯类、有机磷类、氨基甲酸酯类杀虫剂已产生了较高水平的抗药性,其中山东泰安抗性种群对氯氟氰菊酯的抗性高达2445.5倍;对多杀菌素等生物杀虫剂产生了中低水平的抗性;对昆虫生长调节剂如虫酰肼的敏感性也有所降低,但昆虫生长调节剂依然是比较理想的防治药剂。对交互抗性及抗性治理也作了阐述。     

Organophosphorus resistance in Aphis gossypii (Hemiptera: Aphididae) on chrysanthemum in the UK

The FAO standard dip-test was used to test resistance of glasshouse populations of Aphis gossypii from chrysanthemums to the organophosphorus insecticides heptenophos and diazinon. Compared with a susceptible population collected in 1981, resistance factors to diazinon of up to 538 were found in populations collected after 1984. Resistance to heptenophos was less than that to diazinon but some populations collected after 1984 were 34 times as resistant as the susceptible strain. Possible reasons for the sudden increase in resistance in A. gossypii and current prospects for control of resistant populations are discussed.     

Genetics and fitness costs of cyromazine resistance in the house fly (Diptera: Muscidae)

The genetic basis of cyromazine resistance was investigated in the house fly, Musca domestica L. The ED-R strain, which was collected in Mississippi and selected further in the laboratory, was 116.5-fold resistant compared with the laboratory susceptible strain, OR-S. The SEL strain, which was created by crossing ED-R with OR-S followed by three cycles of reselection and backcrossing to OR-S, was 84.7-fold resistant relative to the susceptible strain. Mortality data from reciprocal crosses of resistant and susceptible flies indicated that resistance was autosomal and not influenced by maternal effects. The relative position of probit lines from the parental strains and reciprocal crosses showed that resistance was expressed as an incompletely dominant trait with D = 0.30 and 0.32 for ED-R and SEL, respectively. To determine the number of genes involved, models of one, two, three, four, and five loci were used to compare observed and expected mortality of F1ED-R x susceptible backcross. Resistance was best described by a polygenic model of three loci when equal and additive effects of loci were assumed. Another approach, which was based on phenotypic variances, showed that nE, or the minimum number of freely segregating genetic factors for ED-R, equaled 3.07. ED-R showed greater reductions in fitness compared with SEL independent of the presence or absence of sublethal concentrations of cyromazine. These data suggested that reduced fitness was not due to deleterious pleiotropic effects of the resistance genes themselves but arose from other loci in the ED-R genotype.     

Genetics of spinosad resistance in Frankliniella occidentalis (Thysanoptera: Thripidae)

The genetic basis of spinosad resistance was investigated in the western flower thrips, Frankliniella occidentalis (Pergande) (Thysanoptera: Thripidae). The resistant strain, selected in the laboratory for spinosad resistance from a pool of thrips populations collected in Almeria (southeastern Spain), showed a very high resistance to spinosad (356,547-fold based on LC50 values) compared with the laboratory susceptible strain. Mortality data from reciprocal crosses of resistant and susceptible thrips indicated that resistance was autosomal and not influenced by maternal effects. Analysis of probit lines from the parental strains and reciprocal crosses showed that resistance was expressed as an almost completely recessive trait. To determine the number of genes involved, a direct test of monogenic inheritance based on the backcrosses suggested that resistance to spinosad was probably controlled by one locus. Another approach, which was based on phenotypic variances, showed that nE, or the minimum number of freely segregating genetic factors for the resistant strain, equaled 0.59.