Pyrethroid resistance and cross‐resistance in the German cockroach,Blattella germanica (L)

A German cockroach (Blatella germanica (L)) strain, Apyr‐R, was collected from Opelika, Alabama after control failures with pyrethroid insecticides. Levels of resistance to permethrin and deltamethrin in Apyr‐R (97‐ and 480‐fold, respectively, compared with a susceptible strain, ACY) were partially or mostly suppressed by piperonyl butoxide (PBO) and S,S,S,‐tributylphosphorotrithioate (DEF), suggesting that P450 monooxygenases and hydrolases are involved in resistance to these two pyrethroids in Apyr‐R. However, incomplete suppression of pyrethroid resistance with PBO and DEF implies that one or more additional mechanisms are involved in resistance. Injection, compared with topical application, resulted in 43‐ and 48‐fold increases in toxicity of permethrin in ACY and Apyr‐R, respectively. Similarly, injection increased the toxicity of deltamethrin 27‐fold in ACY and 28‐fold in Apyr‐R. These data indicate that cuticular penetration is one of the obstacles for the effectiveness of pyrethroids against German cockroaches. However, injection did not change the levels of resistance to either permethrin or deltamethrin, suggesting that a decrease in the rate of cuticular penetration may not play an important role in pyrethroid resistance in Apyr‐R. Apyr‐R showed cross‐resistance to imidacloprid, with a resistance ratio of 10. PBO treatment resulted in no significant change in the toxicity of imidacloprid, implying that P450 monooxygenase‐mediated detoxication is not the mechanism responsible for cross‐resistance. Apyr‐R showed no cross‐resistance to spinosad, although spinosad had relatively low toxicity to German cockroaches compared with other insecticides tested in this study. This result further confirmed that the mode of action of spinosad to insects is unique. Fipronil, a relatively new insecticide, was highly toxic to German cockroaches, and the multi‐resistance mechanisms in Apyr‐R did not confer significant cross‐resistance to this compound. Thus, we propose that fipronil could be a valuable tool in integrated resistance management of German cockroaches. © 2001 Society of Chemical Industry     

Cross‐resistance study and biochemical mechanisms of thiamethoxam resistance in B‐biotype Bemisia tabaci (Hemiptera: Aleyrodidae)

BACKGROUND: B‐biotype Bemisia tabaci (Gennadius) has invaded China over the past two decades. To understand the risks and to determine possible mechanisms of resistance to thiamethoxam in B. tabaci, a resistant strain was selected in the laboratory. Cross‐resistance and the biochemical mechanisms of thiamethoxam resistance were investigated in the present study. RESULTS: A 66.3‐fold thiamethoxam‐resistant B. tabaci strain (TH‐R) was established after selection for 36 generations. Compared with the susceptible strain (TH‐S), the selected TH‐R strain showed obvious cross‐resistance to imidacloprid (47.3‐fold), acetamiprid (35.8‐fold), nitenpyram (9.99‐fold), abamectin (5.33‐fold) and carbosulfan (4.43‐fold). No cross‐resistance to fipronil, chlorpyrifos or deltamethrin was seen. Piperonyl butoxide (PBO) and triphenyl phosphate (TPP) exhibited significant synergism on thiamethoxam effects in the TH‐R strain (3.14‐ and 2.37‐fold respectively). However, diethyl maleate (DEM) did not act synergistically with thiamethoxam. Biochemical assays showed that cytochrome P450 monooxygenase activities increased 1.21‐ and 1.68‐fold respectively, and carboxylesterase activity increased 2.96‐fold in the TH‐R strain. However, no difference was observed for glutathione S‐transferase between the two strains. CONCLUSION: B‐biotype B. tabaci develops resistance to thiamethoxam. Cytochrome P450 monooxygenase and carboxylesterase appear to be responsible for the resistance. Reasonable resistance management that avoids the use of cross‐resistance insecticides may delay the development of resistance to thiamethoxam in this species. Copyright © 2009 Society of Chemical Industry     

Mutations in the mitochondrial cytochrome b of Tetranychus urticae Koch (Acari: Tetranychidae) confer cross‐resistance between bifenazate and acequinocyl

BACKGROUND: Resistance of Tetranychus urticae Koch to bifenazate was recently linked with mutations in the mitochondrial cytochrome b Q_o pocket, suggesting that bifenazate acts as a Q_o inhibitor (Q_oI). Since these mutations might cause cross‐resistance to the known acaricidal Q_oI acequinocyl and fluacrypyrim, resistance levels and inheritance patterns were investigated in several bifenazate‐susceptible and bifenazate‐resistant strains with different mutations in the cd1 and ef helices aligning the Q_o pocket. RESULTS: Cross‐resistance to acequinocyl in two bifenazate‐resistant strains was shown to be maternally inherited and caused by the combination of two specific mutations in the cytochrome b Q_o pocket. Although most investigated strains were resistant to fluacrypyrim, resistance was not inherited maternally, but as a monogenic autosomal highly dominant trait. As a consequence, there was no correlation between cytochrome b genotype and fluacrypyrim resistance. CONCLUSIONS: Although there is no absolute cross‐resistance between bifenazate, acequinocyl and fluacrypyrim, some bifenazate resistance mutations confer cross‐resistance to acequinocyl. In the light of resistance development and management, high prudence is called for when alternating bifenazate and acequinocyl in the same crop. Maternally inherited cross‐resistance between bifenazate and acequinocyl reinforces the likelihood of bifenazate acting as a mitochondrial complex III inhibitor at the Q_o site. Copyright © 2009 Society of Chemical Industry     

Cross‐resistance,mode of inheritance and stability of resistance to emamectin in Spodoptera litura (Lepidoptera: Noctuidae)

BACKGROUND: Spodoptera litura (F.) is a cosmopolitan pest that has developed resistance to several insecticides. The aim of the present study was to establish whether an emamectin‐selected (Ema‐SEL) population could render cross‐resistance to other insecticides, and to investigate the genetics of resistance. RESULTS: Bioassays at G₁ gave resistance ratios (RRs) of 80‐, 2980‐, 3050‐ and 2800‐fold for emamectin, abamectin, indoxacarb and acetamiprid, respectively, compared with a laboratory susceptible population Lab‐PK. After three rounds of selection, resistance to emamectin in Ema‐SEL increased significantly, with RRs of 730‐fold and 13‐fold compared with the Lab‐PK and unselected (UNSEL) population respectively. Further studies revealed that three generations were required for a tenfold increase in resistance to emamectin. Resistance to abamectin, indoxacarb, acetamiprid and emamectin in UNSEL declined significantly compared with the field population at G₁. Furthermore, selection with emamectin reduced resistance to abamectin, indoxacarb and acetamiprid on a par with UNSEL. Crosses between Ema‐SEL and Lab‐PK indicated autosomal and incomplete dominance of resistance. A direct test of a monogenic model and Land's method suggested that resistance to emamectin was controlled by more than one locus. CONCLUSION: Instability of resistance and lack of cross‐resistance to other insecticides suggest that insecticides with different modes of action should be recommended to reduce emamectin selection pressure. Copyright © 2010 Society of Chemical Industry     

Cross‐resistance,inheritance and biochemical mechanisms of imidacloprid resistance in B‐biotype Bemisia tabaci

BACKGROUND: The B‐type Bemisia tabaci (Gennadius) has become established in many regions in China, and neonicotinoids are extensively used to control this pest. Imidacloprid resistance in a laboratory‐selected strain of B‐type B. tabaci was characterised in order to provide the basis for recommending resistance management tactics. RESULTS: The NJ‐Imi strain of B‐type B. tabaci was selected from the NJ strain with imidacloprid for 30 generations. The NJ‐Imi strain exhibited 490‐fold resistance to imidacloprid, high levels of cross‐resistance to three other neonicotinoids, low levels of cross‐resistance to monosultap, cartap and spinosad, but no cross‐resistance to abamectin and cypermethrin. Imidacloprid resistance in the NJ‐Imi strain was autosomal and semi‐dominant. It is shown that enhanced detoxification mediated by cytochrome‐P450‐dependent monooxygenases contributes to imidacloprid resistance to some extent in the NJ‐Imi strain. Results from synergist bioassays and cross‐resistance patterns indicated that target‐site insensitivity may be involved in imidacloprid resistance in the NJ‐Imi strain of B. tabaci. CONCLUSION: Although oxidative detoxification mediated by P450 monooxygenases is involved in imidacloprid resistance in the NJ‐Imi strain of B‐type B. tabaci, target‐site modification as an additional resistance mechanism cannot be ruled out. Considering the high risk of cross‐resistance, neonicotinoids should be regarded as a single group when implementing an insecticide rotation scheme in B. tabaci control. Copyright © 2009 Society of Chemical Industry     

小菜蛾对丁烯氟虫腈的抗性遗传力及风险评估

采用丁烯氟虫腈对小菜蛾敏感品系进行室内抗性筛选,饲养15代,汰选13代,平均成活率为35.12%,获得抗性品系(R),与敏感品系(S)比较,抗性指数为90.27倍。应用域性状分析法,研究小菜蛾对丁烯氟虫腈的抗性现实遗传力,并对不同杀死率下抗性发展速率进行预测。结果表明,连续筛选前7代(F₀~F₆),小菜蛾对丁烯氟虫腈的抗性现实遗传力为0.2332;不连续筛选后6代(F₇~F₁₄,8代中有2代未筛选),现实遗传力为0.0203。整个13代筛选期间,现实遗传力为0.2206。假设遗传力为室内筛选估算值的一半、死亡率为50%~90%,预计小菜蛾对丁烯氟虫腈抗性增长10倍,需要约22.8~10.3代。     

Efficacy of various pyrethroid structures against a highly metabolically resistant isogenic strain of Helicoverpa armigera (Lepidoptera: Noctuidae) from China

BACKGROUND: Resistance to pyrethroids and other types of insecticides in Helicoverpa armigera (Hübner) has been documented in many countries. The isolation of specific resistance mechanisms in isogenic strains is an optimal approach to investigate cross-resistance pattern, and to validate resistance breaking pyrethroids. In this study an isogenic metabolic resistance CMR strain was successfully isolated from a field pyrethroid-resistant population of H. armigera. With this strain, cross-resistance among 19 pyrethroid insecticides with varying chemical structures was analysed. RESULTS: Resistance to pyrethroids in the CMR strain was likely to be due to enhanced oxidative metabolism. The most significant cross-resistance in the CMR strain was between pyrethroids such as fenvalerate, tau-fluvalinate and flumethrin characterised by having both phenoxybenzyl and aromatic acid moieties. Substitution of the phenoxybenzyl group with a polyfluorobenzyl group, as in tefluthrin, benfluthrin and transfluthrin, overcame most of this resistance. CONCLUSION: The findings in this study support the assertion that it is possible to find pyrethroids that are active against resistant populations. Such pyrethroids could be considered as possible partners or resistance breaking pyrethroids in a pyrethroid resistance management programme for H. armigera in China and in other Asian countries where the oxidative metabolism resistance is a dominant mechanism.