Variation of Musca domestica L. acetylcholinesterase in Danish housefly populations

Anti-cholinesterase resistance is in many cases caused by modified acetylcholinesterase (MACE). A comparison was made of toxicological data and AChE activity gathered from 21 field populations and nine laboratory strains of houseflies, Musca domestica L., to elucidate the best way of generating data to provide advice for management strategies and gathering information for resistance risk assessment on the organophosphates azamethiphos and dimethoate and the carbamate methomyl, which have been the primary insecticides used against adult houseflies in Denmark. Cluster analysis was performed and > 2000 houseflies were assigned to one of three phenotypes based on total acetylcholinesterase activity as well as inhibition by azamethiphos, methomyl or omethoate. A cluster, i.e. a phenotype, with high total AChE activity and high sensitivity to azamethiphos and less sensitivity to inhibition by methomyl and omethoate was shown to be linked to methomyl resistance. It was not possible to define any clusters that could be linked to azamethiphos or dimethoate resistance. The five mutations V180L, G262A, G262V, F327Y and G365A causing anticholinesterase resistance in houseflies were all identified in the Danish housefly strains. The data are very heterogeneous, and a correlation of molecular genetic background and resistance of phenotypes is not obvious with the available data.     

The pyrethrins and related compounds part XL— structure-activity relationships of pyrethroidal esters with acyclic side chains in the alcohol component against resistant strains of housefly (Musca domestica)

Activities of a range of pyrethroidal esters, incorporating structural variations in all regions of the acid and alcohol components, have been measured against two fully characterised and homozygous resistant strains of Musca domestica (kdr and super-kdr). The results, limited in this paper to esters of alcohols with acyclic side chains, show the same level of uniform resistance as the kdr strain observed previously, across a range of acid and alcohol variations. Against the super-kdr strain, in contrast to the cyclic side chain set, resistance factors are barely higher than for the kdr strain. Against super-kdr flies, some dependence of resistance factor on the position of the side chain substituent was detected. Polyfluorobenzyl esters confer particularly low resistance factors.     

The pyrethrins and related compounds part XXXIX— structure-activity relationships of pyrethroidal esters with cyclic side chains in the alcohol component against resistant strains of housefly (Musca domestica)

Activities of a range of pyrethroidal esters, incorporating structural variations in all regions of the acid and alcohol components, have been measured against two fully characterised and homozygous resistant strains of Musca domestica L. (kdr and super-kdr). The results, limited in this paper to esters of alcohols with cyclic side chains, indicate uniform resistance to the kdr strain across the whole range of structural variations. Against the super-kdr strain, while variation in the acid component has little effect, the resistance factor is sensitive to the nature of the alcohol component, in particular on whether it contains an α-cyano substituent.     

Inheritance of beta-cypermethrin resistance in the housefly Musca domestica (Diptera: Muscidae)

BACKGROUND: Beta-cypermethrin, a synthetic pyrethroid insecticide, was applied frequently in the control of health pests including houseflies, Musca domestica L., in China. However, different levels of resistance to beta-cypermethrin were monitored in field strains of houseflies. A strain of M. domestica, 4420-fold resistant to beta-cypermethrin after continuous 25 generations of selection, was used in this paper to determine the mode of inheritance of pyrethroid resistance. RESULTS: The estimated realized heritability (h(2)) of beta-cypermethrin resistance was 0.30 in this resistant strain. Results of bioassays showed no significant difference in values of LD(50) and slope of log dose-probit lines between reciprocal progenies F(1) and F'(1), and yielded values of - 0.10 (F(1)) and - 0.11 (F'(1)) for the degree of dominance (D). Chi-square analysis from responses of self-bred and backcross progenies (F(2), BC(1) and BC(2) respectively) indicated that the null hypothesis, a single gene responsible for resistance, was accepted. The minimum number of independent segregation genes was 0.93 for F(1) by Lande's method. CONCLUSION: It was concluded that beta-cypermethrin resistance in the housefly was inherited as a single, major, autosomal and incompletely recessive factor. These results would provide the basic information for pest management programmes.     

Insecticide resistance in house flies from caged‐layer poultry facilities

The frequency of resistance of eight strains of house flies, Musca domestica L., collected from caged‐layer poultry facilities across New York state, to nine insecticides (dimethoate, tetrachlorvinphos, permethrin, cyfluthrin, pyrethrins, methomyl, fipronil, spinosad and cyromazine) was measured relative to a laboratory susceptible strain. Percentage survival was evaluated at five diagnostic concentrations: susceptible strain LC₉₉, 3 × LC₉₉, 10 × LC₉₉, 30 × LC₉₉ and 100 × LC₉₉. The highest levels of resistance were noted for tetrachlorvinphos, permethrin and cyfluthrin. There was substantial variation in the levels of resistance to the different insecticides from one facility to another, independent of their geographical location. There was very little cross‐resistance detected in these populations to either fipronil or spinosad. Overall, there was a good correlation between insecticide use histories and the levels of resistance. The apparent isolation of fly populations within poultry facilities suggests that there are good opportunities for the implementation of successful resistance management strategies at these facilities. Differences between these results and those of a resistance survey on New York dairy farms in 1987 are discussed. © 2000 Society of Chemical Industry     

Low expression of nicotinic acetylcholine receptor subunit Mdα2 in neonicotinoid‐resistant strains of Musca domestica L.

BACKGROUND: Neonicotinoid action as well as resistance involves interaction with nicotinic acetylcholine receptors (nAChRs). In the housefly, neonicotinoid resistance also involves cytochrome P450, as indicated by bioassay with synergist as well as altered expression. In bioassay, synergism was only partial and indicated possible target‐site resistance. The nAChR α2 subunit is important in neonicotinoid toxicity to insects, and gene expression of the Mdα2 subunit was investigated in field populations and laboratory strains of neonicotinoid‐resistant and insecticide‐susceptible houseflies, Musca domestica L. The genomic sequence covering exon III–VII of Mdα2 was analysed for mutations. RESULTS: Gene expression profiling of Mdα2 revealed notable differences between neonicotinoid‐resistant and insecticide‐susceptible houseflies. On average, the neonicotinoid‐resistant field population 766b and the imidacloprid selected strain 791imi had 60% lower copy numbers of Mdα2 compared with the susceptible reference strain. Sequencing of exon III–VII of the Mdα2, encoding acetylcholine binding‐site regions and three out of four transmembrane domains, did not reveal any mutations explaining the increased neonicotinoid tolerance in the strains examined. CONCLUSION: Previous discoveries and the results of this study suggest that the neonicotinoid resistance mechanism in Danish houseflies involves both cytochrome P450 monooxygenase‐mediated detoxification and reduced expression of the nAChR subunit α2. Copyright © 2010 Society of Chemical Industry     

Thiamethoxam acts as a target‐site synergist of spinosad in resistant strains of Frankliniella occidentalis

BACKGROUND: Previous studies have suggested that the resistance mechanism towards spinosad in Frankliniella occidentalis (Pergande) is an altered target site. Like the neonicotinoids, the spinosyns act on nicotinic acetylcholine receptors (nAChRs) in insects, but at a distinct site. The changes in nAChRs related to spinosad resistance in thrips might involve interaction with neonicotinoids. In this study, the efficacy of spinosad and neonicotinoids, alone and in combination, was evaluated in susceptible and spinosad‐resistant thrips strains. RESULTS: The neonicotinoids tested were imidacloprid, thiacloprid, acetamiprid, thiamethoxam and clothianidin. No cross‐resistance was shown between spinosad and any of the neonicotinoids. However, an increased toxicity was observed when a mixture of spinosad with thiamethoxam or clothianidin was tested. No synergism was found in the susceptible strains. The more spinosad‐resistant the thrips strain, the stronger was the synergism. CONCLUSION: Data suggest that spinosad and thiamethoxam may interact at the nAChRs in spinosad‐resistant thrips, facilitating enhanced insecticidal action. Copyright © 2012 Society of Chemical Industry     

Cross-resistance potential of fipronil in Musca domestica

The toxicity of fipronil to insecticide-susceptible houseflies and the cross-resistance potential of fipronil were determined for six insecticide-resistant laboratory housefly strains by topical application and feeding bioassay. The insecticide-resistant strains represented different levels and patterns of resistance to pyrethroids, organophosphates, carbamates and organochlorines. Five strains were almost susceptible to fipronil in feeding bioassay with resistance factors at LC50 between 0.36 and 3.0. Four of these strains were almost susceptible to topically applied fipronil (resistance factors at LD50 were 0.55, 0.83, 3.3 and 2.5, respectively), whereas one strain was 13-fold resistant to topically applied fipronil. A highly gamma-HCH-resistant strain, 17e, was 430-fold resistant to fipronil in topical application bioassay and 23-fold resistant in feeding bioassay at LD50/LC50. We also tested the toxicity of fipronil in a feeding bioassay and gamma-HCH in topical application bioassay on thirteen housefly field populations. Eleven of the field populations had resistance factors for fipronil ranging from 0.98 to 2.4 at LC50, whereas two populations were 4.0- and 4.6-fold resistant to fipronil. The resistance level to gamma-HCH at LD50 in the field populations ranged from 1.8- to 8.1-fold. The two strains showing fipronil resistance were 3.4- and 8.1-fold resistant to gamma-HCH. Fipronil and gamma-HCH toxicities were positively correlated in the field populations. Biochemical assays of esterase, glutathione S-transferase and cytochrome P450 monooxygenase indicated that the low fipronil resistance observed in laboratory and field strains could be caused by elevated detoxification or be due to a target-site resistance mechanism with cross-resistance to gamma-HCH.     

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.     

Spinosad resistance in female Musca domestica L. from a field-derived population

BACKGROUND: Bait-formulated spinosad is currently being introduced for housefly (Musca domestica L.) control around the world. Spinosad resistance was evaluated in a multiresistant field population and strains derived from this by selection with insecticides. Constitutive and spinosad-induced expression levels of three cytochrome P450 genes, CYP6A1, CYP6D1 and CYP6D3, previously reported to be involved in insecticide resistance, were examined. RESULTS: In 2004 a baseline for spinosad toxicity of Danish houseflies where all field populations were considered to be susceptible was established. In the present study, females of a multiresistant field population 791a were, however, 27-fold spinosad resistant at LC₅₀, whereas 791a male houseflies were susceptible. Strain 791a was selected with spinosad, thiamethoxam, fipronil and imidacloprid, resulting in four strains with individual characteristics. Selection of 791a with spinosad did not alter spinosad resistance in either males or females, but counterselected against resistance to the insecticides thiamethoxam and imidacloprid targeting nicotinic acetylcholine receptors. A synergist study with piperonyl butoxide, as well as gene expression studies of CYP6A1, CYP6D1 and CYP6D3, indicated a partial involvement of cytochrome P450 genes in spinosad resistance. CONCLUSION: This study reports female-linked spinosad resistance in Danish houseflies. Negative cross-resistance was observed between spinosad and neonicotinoids in one multiresistant housefly strain. Spinosad resistance involved alterations of cytochrome P450 gene expression. Copyright © 2011 Society of Chemical Industry     

北京地区家蝇乙酰胆碱酯酶不敏感基因表现型的检测

在1998～1999年对北京地区室外家蝇种群乙酰胆碱酯酶 (ACh E)的不敏感基因表现型进行了检测。以敏感品系为标准 ,海淀区 (A)、海淀区 (B)、丰台区、朝阳区家蝇种群具有的对敌敌畏不敏感基因表现型频率分别为 11%、34%、56%和24% ;对灭多威不敏感基因表现型频率为4%、4%、8%和20 %。ACh E对敌敌畏和灭多威的不敏感基因表现型 ,北京地区家蝇可分成4种 :1)对敌敌畏和灭多威均敏感型 ;2 )对敌敌畏不敏感 ,对灭多威敏感型 ;3)对敌敌畏敏感 ,对灭多威不敏感型 ;4 )对敌敌畏和灭多威均不敏感型。目前 ,在北京地区以对敌敌畏和灭多威均敏感的 ACh E表现型为主 ,其次为第二种类型 ,第三和第四种类型的频率不高。     

Binding activity of substituted benzyl derivatives of chloronicotinyl insecticides to housefly‐head membranes,and its relationship to insecticidal activity against the housefly Musca domestica

Variously substituted benzyl derivatives of chloronicotinyl insecticides were synthesized with a wide range of substituents including halogens, NO₂, CN, CF₃ and small alkyl and alkoxy groups at the ortho, meta and para positions, as well as multiple‐substituted benzyl analogues. Their binding activity to the α‐bungarotoxin binding site in housefly (Musca domestica) head membrane preparations was measured. Among the compounds tested, the activity of the meta‐CN derivative was the highest, being 20–100 times higher than those of imidacloprid, acetamiprid and nitenpyram. The synergized insecticidal activity against houseflies was also measured for selected compounds with the metabolic inhibitor, NIA16388 (propargyl propyl phenylphosphonate). For the nitromethylene analogues, including both benzyl and pyridylmethyl analogues, higher binding activity usually resulted in higher insecticidal activity. © 2000 Society of Chemical Industry