PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Insecticide Resistance”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1995

Mosquito carboxylesterase Est alpha 2(1) (A2). Cloning and sequence of the full-length cDNA for a major insecticide resistance gene worldwide in the mosquito Culex quinquefasciatus.

Organophosphorus insecticide resistance in Culex mosquitoes is commonly caused by increased activity of one or more esterases. The commonest phenotype involves elevation of the esterases Est alpha 2 (A2) and Est beta 2 (B2). A cDNA encoding the Est alpha 2 esterase has now been isolated from a Sri Lankan insecticide-resistant mosquito (Culex quinquefasciatus, Say) expression library. In line with a recently suggested nomenclature system (Karunaratne, S. H. P. P. (1994) Characterization of Multiple Variants of Carboxylesterases Which Are Involved in Insecticide Resistance in the Mosquito Culex quinquefasciatus. Ph.D. thesis, University of London), as the first sequenced variant of this esterase, it is now referred to as Est alpha 2(1). The full-length cDNA of est alpha 2(1) codes for a 540-amino acid protein, which has high homology with other esterases and lipases and belongs to the serine or B-esterase enzyme family. The predicted secondary structure of Est alpha 2(1) is similar to the consensus secondary structure of proteins within the esterase/lipase family where the secondary and tertiary structures have been resolved. The level of identity (approximately 47% at the amino acid level) between the est alpha 2(1) and the various Culex est beta (B1 and B2) cDNA alleles that have been cloned and sequenced suggests that the two esterase loci are closely related and arose originally from duplication of a common ancestral gene. The lack of a distinct hydrophobic signal sequence for Est alpha 2(1) and two possible N-linked glycosylation sites, both situated close to the active site serine, suggest that it is a nonglycosylated protein that is not exported from the cell. Southern and dot blot analysis of genomic DNA from various insecticide-resistant and susceptible mosquito strains show that the est alpha 2(1) gene, like est beta 2(1), is amplified in resistant strains. The restriction fragment length polymorphism patterns, after probing Southern blots of EcoRI-digested genomic DNA with esta alpha 2(1) cDNA, show that the amplified and nonamplified est alpha alleles differ in the resistant and susceptible Sri Lankan mosquitoes.

Amino Acid Sequence↗
PubMed1993

Transposable elements as initiators of insecticide resistance.

Genetic change that leads to insecticide resistance is poorly understood for most resistance genes. Transposable elements have been shown to be powerful mutagenic agents in Drosophila melanogaster (Meigen), and they potentially can create genetic change leading to resistance in pest insect populations. Here the characteristic of transposable elements and the consequences of their movement in D. melanogaster and other insects are discussed, and reports of their involvement in insecticide resistance are examined. I conclude that transposable elements must be considered as mutagenic agents that can lead to resistance. Their involvement needs to be directly addressed in studies of resistant insects, particularly by investigators involved in cloning resistance genes.

Animals↗
PubMed2005

The Anopheles gambiae detoxification chip: a highly specific microarray to study metabolic-based insecticide resistance in malaria vectors.

Metabolic pathways play an important role in insecticide resistance, but the full spectra of the genes involved in resistance has not been established. We constructed a microarray containing unique fragments from 230 Anopheles gambiae genes putatively involved in insecticide metabolism [cytochrome P450s (P450s), GSTs, and carboxylesterases and redox genes, partners of the P450 oxidative metabolic complex, and various controls]. We used this detox chip to monitor the expression of the detoxifying genes in insecticide resistant and susceptible An. gambiae laboratory strains. Five genes were strongly up-regulated in the dichlorodiphenyltrichloroethane-resistant strain ZAN/U. These genes included the GST GSTE2, which has previously been implicated in dichlorodiphenyltrichloroethane resistance, two P450s, and two peroxidase genes. GSTE2 was also elevated in the pyrethroid-resistant RSP strain. In addition, the P450 CYP325A3, belonging to a class not previously associated with insecticide resistance, was expressed at statistically higher levels in this strain. The applications of this detox chip and its potential contribution to malaria vector insecticide resistance management programs are discussed.

Anopheles↗
PubMed2007

Lack of cross-resistance to indoxacarb in insecticide-resistant Spodoptera frugiperda (Lepidoptera: Noctuidae) and Plutella xylostella (Lepidoptera: Yponomeutidae).

Two field strains of the fall armyworm, Spodoptera frugiperda (JE Smith), collected from corn in north Florida showed high resistance to carbaryl (626- and 1159-fold) and moderate resistance to parathion-methyl (30- and 39-fold) as compared with a laboratory susceptible strain. A field strain of the diamondback moth, Plutella xylostella (L.) collected from cabbage in north Florida and selected for 20 generations with permethrin showed high resistance to permethrin (987-fold) as compared with a susceptible strain. However, in all instances, no cross-resistance to indoxacarb, a novel oxidiazine insecticide, was observed in these two species. Biochemical studies revealed that, in S. frugiperda, activities of detoxification enzymes (microsomal oxidase, glutathione S-transferase and general esterase) were significantly higher in the field strains than in the susceptible strain, indicating that these detoxification enzymes were not actively involved in the resistance to indoxacarb. The lack of cross-resistance between indoxacarb and permethrin in P. xylostella further supports the notion that the mode of action of these insecticides on the insect sodium channel is different.

Animals↗
PubMed2006

High Wolbachia density correlates with cost of infection for insecticide resistant Culex pipiens mosquitoes.

In the mosquito Culex pipiens, insecticide resistance genes alter many life-history traits and incur a fitness cost. Resistance to organophosphate insecticides involves two loci, with each locus coding for a different mechanism of resistance (degradation vs. insensitivity to insecticides). The density of intracellular Wolbachia bacteria has been found to be higher in resistant mosquitoes, regardless of the mechanism involved. To discriminate between costs of resistance due to resistance genes from those associated with elevated Wolbachia densities, we compared strains of mosquito sharing the same genetic background but differing in their resistance alleles and Wolbachia infection status. Life-history traits measured included strength of insecticide resistance, larval mortality, adult female size, fecundity, predation avoidance, mating competition, and strength of cytoplasmic incompatibility (CI). We found that: (1) when Wolbachia are removed, insecticide resistance genes still affect some life-history traits; (2) Wolbachia are capable of modifying the cost of resistance; (3) the cost of Wolbachia infections increases with their density; (4) different interactions occurred depending on the resistance alleles involved; and (5) high densities of Wolbachia do not increase the strength of CI or maternal transmission efficiency relative to low Wolbachia densities. Insecticide resistance genes generated variation in the costs of Wolbachia infections and provided an interesting opportunity to study how these costs evolve, a process generally operating when Wolbachia colonizes a new host.

Animals↗
PubMed2005

Modelling the interactions between phenology and insecticide resistance genes in the codling moth Cydia pomonella.

In the codling moth Cydia pomonella (L), insecticide resistance genes have been associated with pleiotropic effects affecting phenology. In this paper, we investigated whether an increase in the frequency of insecticide resistance in field populations of C pomonella was likely to entail significant divergences in the temporal occurrence of both susceptible and insecticide-resistant individuals. For this purpose, we built a phenological model that provided suitable predictions of the distinct and diverging seasonal evolutions of populations of a susceptible and two insecticide-resistant (at two and three loci) homozygous genotypes of C pomonella. Model simulations for each genotype were further compared with pheromone trap catches recorded in a field insecticide-treated population over an 8-year period (from 1992 to 2000), which reflected the progressive annual increase in the frequency of resistance in southeastern France. We found a significant delay in field adult emergence relative to those predicted by the homozygous susceptible model, and the magnitude of such a delay was positively correlated with increasing frequencies of insecticide resistance in the sampled field population of C pomonella. Adult emergence predicted in the theoretical population that was homozygous for resistance at two loci converged with those recorded in the field during the investigated 8-year period. This suggested that the pleiotropic effects of resistance were likely to result in a significant phenological segregation of insecticide-resistant alleles in the field. The results of this study emphasized the potential for pest populations exposed to chemical selection to evolve qualitatively with respect to phenology. This may raise critical questions regarding the use of phenological modelling as a forecasting tool for appropriate resistance management strategies that would take into account the diverging seasonal evolutions of both insecticide resistance and susceptibility.

Animals↗
PubMed1998

Mosquito carboxylesterases: a review of the molecular biology and biochemistry of a major insecticide resistance mechanism.

The major mechanism of organophosphorus insecticide resistance in Culex mosquitoes involves the elevation of one or more esterases. The general mechanism underlying this resistance is the amplification of the structural genes. This review covers the classification of the mosquito esterases in the context of classical esterase nomenclature. The function of the amplified esterases and the structure of the amplified DNA on which they occur are also described. Implications of information on the esterase amplicons are discussed in relation to the evolution and migration of insecticide resistance in Culex.

Animals↗
PubMed1996

Changes in the methylation of amplified esterase DNA during loss and reselection of insecticide resistance in peach-potato aphids, Myzus persicae.

Insecticide resistance in peach-potato aphids, Myzus persicae, results from the amplification of genes encoding an esterase that hydrolyses and sequesters insecticides. Resistance is normally stable, but highly resistant aphid clones sometimes lose resistance when insecticidal selection pressure is removed. This loss of resistance, termed reversion, arises from a loss of elevated esterase enzyme through transcriptional control, i.e. without loss of the amplified esterase DNA sequences. We have shown that loss of the elevated enzyme occurred simultaneously with loss of methylation at CCGG sites in the amplified DNA sequences. During reselection of resistance in these revertant clones, enzyme levels increased, but there was no corresponding return of methylation to DNA sequences. Thus, although DNA methylation is closely correlated with expression of the amplified esterase genes during reversion, it may not be a factor in the reverse process.

Animals↗
PubMed1998

Cytochrome P450 purification and immunological detection in an insecticide resistant strain of German cockroach (Blattella germanica, L.).

A German cockroach strain, Munsyana (MA) had 80-fold resistance to the pyrethroid insecticide cypermethrin, 4.5-fold greater total cytochrome P450 content and 2.5-fold greater cytochrome P450-mediated N-demethylation of 4-chloro-N-methylaniline compared to the susceptible Johnson Wax (JWax) strain. Immobilized artificial membrane high performance liquid chromatography (IAM-HPLC) of microsomal proteins from the MA strain enriched cytochrome P450 greater than 70-fold. Following purification, a single protein band of M(r) = 49,000 (P450 MA), was detected by silver-staining SDS PAGE gels. Antiserum to the purified protein from the MA strain (anti-P450 MA) was produced in mice. Anti-P450 MA inhibited cytochrome P450-mediated N-demethylation by 4-fold in both MA and JWax strains. In Western blots of microsomal proteins, anti-P450 MA differentiated single MA and JWax individuals by recognizing and M(r) 49,000 protein band in only the MA strain. In JWax cockroaches, the M(r) 49,000 band was only detectable in Western analysis following induction with pentamethylbenzene (PMB). PMB induction also increases N-demethylation 2.6 and 8.0-fold in the MA and JWax strains, respectively. These results are consistent with the hypothesis that insecticide resistance in the MA strain is due to over-expression of a cytochrome P450.

Animals↗
PubMed2000

Larval susceptibility of an insecticide-resistant western corn rootworm (Coleoptera: Chrysomelidae) population to soil insecticides: laboratory bioassays, assays of detoxification enzymes, and field performance.

Soil insecticides were evaluated in laboratory and field studies against larvae of an insecticide resistant population (Phelps County, NE) of western corn rootworm, Diabrotica virgifera virgifera LeConte. Insecticide toxicity was evaluated by topical application of technical insecticides to 3rd instars from Saunders County, NE (susceptible) and Phelps County populations. Resistance ratios (LD50 Phelps County/LD50 Saunders County) for the insecticides methyl parathion, tefluthrin, carbofuran, terbufos, and chlorpyrifos were 28.0, 9.3, 8.7, 2.6 and 1.3, respectively. Biochemical investigation of suspected enzymatic resistance mechanisms in 3rd instars identified significant elevation of esterase activity (alpha and beta naphthyl acetate hydrolysis [3.8- and 3.9-fold]). Examination of 3rd instar esterases by native PAGE identified increased intensity of several isoenzymes in the resistant population. Assays of cytochrome P450 activity (4-CNMA demethylation and aldrin epoxidation) did not identify elevated activity in resistant 3rd instars. Granular soil insecticides were applied at planting to corn, Zea mays L., in replicated field trials in 1997 and 1998 at the same Phelps County site as the source of resistant rootworms for the laboratory studies. In 1997, planting time applications of Counter 20CR, Counter 15 G (terbufos), and Lorsban 15 G (chlorpyrifos) resulted in the lowest root injury ratings (1-6 Iowa scale); 2.50, 2.55, 2.65, respectively (untreated check root rating of 4.55). In 1998, all insecticides performed similarly against a lower rootworm density (untreated check root rating of 3.72). These studies suggest that resistance previously documented in adults also is present in 3rd instars, esterases are possibly involved as resistance mechanisms, and resistance to methyl parathion in adults is also evident in larvae, but does not confer cross-resistance in larvae to all organophosphate insecticides.

Animals↗
PubMed1998

Review of insecticide resistance in cat fleas (Siphonaptera: Pulicidae).

Insecticide resistance often is blamed for failures of insecticides to control cat fleas, Ctenocephalides felis (Bouché). Yet the genetics and adaptive advantage of resistance traits remain unexamined. Lethal doses of insecticides that kill 50% of the population fluctuate 7-fold within a cat flea strain. Many reports of flea resistance may be attributable to variable mortality from effects of solvents, substrates, humidities, temperatures, colonization, and ages of fleas. Resistance ratios (ratios of lethal doses of a resistant to a susceptible strain) are < 690-fold in fleas; lower than many other arthropods. This, plus strain variability, hinders resistance detection. Relationships between resistance levels, control failures, and health threats are unclear. Insensitive acetylcholinesterase, knockdown recovery, glutathione transferase conjugation, and mixed function oxidase/cytochrome P450 are demonstrated resistance mechanisms in cat fleas. Ecological genetics of resistance in cat fleas probably involves flea transfer among hosts, host movements, refugia, founder effects, and mortality from abiotic factors. Understanding cat flea resistance requires population monitoring before, during, and after insecticide treatments using conventional and rapid molecular bioassays. Sustained insecticide release devices such as flea collars and long-lived insecticide residues for premises possibly contribute to the development of resistance. New systemic and topical insecticides, especially when given prophylactically, may act similarly. Eliminating insecticides prevents insecticide resistance but necessitates application of biorational tactics incorporating mechanical, environmental, and cultural controls. Using high temperatures, low humidities, host grooming and such tactics as decreasing doses, increasing action thresholds, rotating insecticides, and leaving spatial and temporal refugia may suppress cat flea resistance.

Animals↗
PubMed2025

Coordinated regulation of glutathione S-transferases confers metabolic flexibility in multi-insecticide-resistant Frankliniella occidentalis (Pergande).

INTRODUCTION: The evolution of multi-insecticide resistance in insect pests threatens global food security. Although glutathione S-transferases (GSTs) are implicated in detoxification, the coordinated mechanism by which specific gene subfamilies interact to confer broad-spectrum resistance remains inadequately characterized. OBJECTIVE: To dissect the functional allocation and cooperation of GST subfamilies in multi-insecticide-resistant strains of Frankliniella occidentalis. METHODS: We integrated comparative genomics (20 GST genes cloned), transcriptomics (qRT-PCR), RNAi-mediated silencing, molecular docking (AutoDock Vina), and in vitro metabolism assays (UPLC-MS/MS) across susceptible and resistant thrips strains. RESULTS: The two resistant strains (NIL-R and FS-R) exhibited moderate to high resistance to five insecticides (chlorfenapyr, emamectin benzoate, spinetoram, spinosad, and thiamethoxam), accompanied by significantly elevated GSTs activity. Phylogenetic analysis indicates that GSTs include 10 conserved delta and 7 diverse sigma members. The sigma subfamily has undergone a marked expansion due to gene duplication. Delta (FoGSTd1, d4, and d9) and sigma (FoGSTs1, s2, and s6) genes were significantly up-regulated in the resistant strains. RNAi showed specialized functional allocation among GSTs: delta GSTs mediated resistance to spinosad and chlorfenapyr, sigma GSTs were responsible for thiamethoxam resistance, and notably, cooperation between these subfamilies contributed to resistance against emamectin benzoate and spinetoram. Molecular docking and in vitro metabolism assays of FoGSTd9 and FoGSTs1 proteins further supported the functional allocation and cooperative roles of GST subfamilies. CONCLUSION: Our results indicate that F. occidentalis may coordinate GST subfamilies to achieve metabolic flexibility in response to multi-insecticide pressure. This survival strategy, mediated by mechanistic functional allocation and cooperative interactions among subfamilies, may contribute to energy conservation and reduced adaptive costs. Disruption of this coordinated mechanism represents a potential approach for overcoming resistance in agricultural pest populations.

Animals↗
PubMed1991

Insecticide resistance: can it be avoided?

The genetic background related to resistance against insecticides has abundantly been demonstrated during the last decades, hence slowing down the development of resistance has to be adapted accordingly. Currently, assays are designed to monitor the mechanisms of resistance in individual insects. Remarks on the interpretation of results obtained with the available bioassays are given together with some recommendations to control resistance.

Animals↗
PubMed1998

[The effect of insecticide resistance on the demographic parameters of 3 strains of Culex quinquefasciatus (Diptera: Culicidae) under laboratory conditions].

The life tables of 3 strains of Culex quinquefasciatus were studied under laboratory conditions: Slab, susceptible to reference; Old Havana, treated with cypermethrin until its fourth generation; and Cotorro, from the field. It was found that the different levels of resistance to organophosphate insecticides and pyrethroids present in the Cotorro and Old Havana strains did not influence either on the duration of the period of development of the immature stages or in the sexual proportion of the emerged adults, but they had a favorable and directly proportional effect on the survival and longevity of the adults. However, they exerted a negative and inversely proportional influence on the reproduction and population growth of these strains. Useful data for the use and management of insecticides within the strategies of control of Culex quinquefasciatus, an important vector of lymphatic filariasis, are provided.

Animals↗
PubMed1996

Unconventional organization of amplified esterase B gene in insecticide-resistant mosquitoes of the Culex pipiens complex.

The amplified esterase B gene responsible for resistance to organophosphorus insecticides in Culex mosquitoes is shown to form a DNA "puff" in salivary gland polytene chromosomes. This "puff" is absent in susceptible mosquitoes lacking the amplified gene, and unlike all puffs known today, it is neither related to development nor involved in protein synthesis. The "puff" therefore corresponds to a special arrangement of the very large number of copies (possibly up to 250,000) of the 25-30-kb DNA fragment encompassing the esterase B structural gene in polytene chromosomes. In addition, the amplified and nonamplified esterase B gene(s) were found to be localized on chromosome 2L, and flanked by identical banding patterns, indicating the absence of an important chromosome rearrangement before, during, or after gene amplification.

Animals↗
PubMed2000

Insecticide resistance studies on Blattella germanica (Dictyoptera:Blattellidae) from Cuba.

We studied the levels of resistance to seven insecticides: malathion, chlorpyrifos, pirimiphos-methyl, propoxur, cypermethrin, deltamethrin, and lambda-cyhalothrin in nine strains of Blattella germanica (Linnaeus, 1717) collected from sites in Santiago de Cuba and Havana City. The strains from Santiago de Cuba, generally had high levels of resistance to malathion, cypermethrin, deltamethrin, and lambda-cyhalothrin, but only low levels of resistance to pirimiphos-methyl, chlorpyrifos, and propoxur. In the strains from Havana City we found a moderate resistance to the organophosphate insecticides, resistance to the pyrethroids (except for three strains that showed susceptibility to lambda-cyhalothrin), and susceptibility to the carbamate insecticide (propoxur).

Animals↗
PubMed1994

The peach-potato aphid Myzus persicae and the tobacco aphid Myzus nicotianae have the same esterase-based mechanisms of insecticide resistance.

Biochemical and molecular studies have established that in the peach-potato aphid, Myzus persicae, insecticide resistance is conferred by amplification of genes encoding the insecticide-detoxifying esterases E4 or FE4. Here we report that two insecticide-resistant clones of the closely related tobacco aphid Myzus nicotianae have elevated esterases indistinguishable from E4 and FE4 and amplified esterase DNA sequences, and flanking regions, with identical restriction maps to the M. persicae genes. Furthermore, the DNA sequences of c. 630 bp fragments of the E4 and FE4 genes of M. persicae are different from each other but identical to the fragment from corresponding M. nicotianae clones. The existence of apparently identical insecticide resistance genes in the two species can be best explained by the selection of the amplified genes in M. persicae, transfer to hybrids of M. persicae and M. nicotianae by sexual reproduction and subsequent spread through M. nicotianae populations.

Animals↗