Cuticular lipids of two resistant and a susceptible strain of houseflies

Patil, Vasant L.; Guthrie, F. E.

doi:10.1002/ps.2780100506

Cited by 13 publications

(4 citation statements)

References 22 publications

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“…Development of cuticle thickening, as also discovered in the PARRA strain (Lilly et al ), concentration of other resistance mechanisms in the integument (Zhu et al ) and up‐regulation of cuticle protein‐encoding contigs (Koganemaru et al ) may all also confer a degree of reduced susceptibility that could eventually lead to the development of neonicotinoid resistance. Such mechanisms can support the development of resistance by way of increasing the efficiency of metabolic detoxification (Sawicki ; Sawicki ; Patil and Guthrie ; Gunning et al ; Ahmad et al ; Mamidala et al ) or prolonging the onset of kdr ‐type derived knockdown (Plapp and Hoyer ; Scott ; Wood et al ).…”

Section: Discussionmentioning

confidence: 99%

Are Australian field‐collected strains of Cimex lectularius and Cimex hemipterus (Hemiptera: Cimicidae) resistant to deltamethrin and imidacloprid as revealed by topical assay?

et al. 2017

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Resistance profiling on Cimex lectularius and Cimex hemipterus in Australia has previously revealed the existence of resistance to pyrethroid insecticides and that multiple resistant mechanisms exist in field populations. To further investigate insecticide resistance in modern field populations of bed bugs, a program to collect and screen field specimens was initiated. Over 50 bed bug strains (a mixture that included both C. lectularius and C. hemipterus) have been collected from across Australian, with 35 subsequently colonised (31 C. lectularius and 4 C. hemipterus) for laboratory-based insecticide resistance testing. Bed bugs were exposed topically to pyrethroids at a discriminating dose of 2.5 g/L deltamethrin in acetone applied at a rate of 1 μL/bug and, for neonicotinoids, a dose of 0.1 g/L of imidacloprid applied at a rate of 1 μL/bug. Mortality was recorded 24 h post application. Twenty adult bed bugs of mixed sex and age in two replicates of 10 were used for the bioassays, plus controls. Results indicated a broad spread in the frequency of resistance against deltamethrin in C. lectularius, represented by a range of mortality values between 15 and 100%. Mortality was predominantly uniform with C. lectularius against imidacloprid at ≥95%, except for several recently collected strains that returned between 70 and 85%, indicating that a degree of tolerance may be developing in select strains. Three of four C. hemipterus strains returned mortality values at or below 10%, with the remainder recording 75% mortality, thereby indicating pyrethroid resistance is similarly advanced in this species. Normal susceptibility (≥95% mortality) was otherwise evident in all four C. hemipterus strains to imidacloprid. These findings complement concurrent research, which indicates that variable patterns of resistance are present across the country and around the world. The results have profound implications for product manufacturers and registration authorities in ensuring that a product is as effective at controlling bed bugs in the field as the laboratory. Key wordscommon bed bug, insecticide resistance, tropical bed bug.

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Section: Discussionmentioning

confidence: 99%

Are Australian field‐collected strains of Cimex lectularius and Cimex hemipterus (Hemiptera: Cimicidae) resistant to deltamethrin and imidacloprid as revealed by topical assay?

et al. 2017

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“…Reduced penetration in other insecticide-resistant insects has been known to be a resistance mechanism since it was first established in the 1960s with pyrethrin [ 19 ], organophosphates [ 20 – 22 ], carbamates [ 23 , 24 ], and organochlorines [ 25 – 28 ] . It can occur via multiple mechanisms, including enhanced expression of metabolic resistance mechanisms in the integument [ 18 ], the increased presence of binding proteins, lipids, and/or sclerotization that trap insecticides [ 29 , 30 ], a measurably thicker cuticle [ 31 , 32 ], or a combination of some or all of these mechanisms together [ 30 , 33 – 35 ]. Several of these mechanisms have been found in bed bugs with, to date, the exception of cuticle thickening.…”

Section: Introductionmentioning

confidence: 99%

Cuticle Thickening in a Pyrethroid-Resistant Strain of the Common Bed Bug, Cimex lectularius L. (Hemiptera: Cimicidae)

et al. 2016

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Thickening of the integument as a mechanism of resistance to insecticides is a well recognised phenomenon in the insect world and, in recent times, has been found in insects exhibiting pyrethroid-resistance. Resistance to pyrethroid insecticides in the common bed bug, Cimex lectularius L., is widespread and has been frequently inferred as a reason for the pest’s resurgence. Overexpression of cuticle depositing proteins has been demonstrated in pyrethroid-resistant bed bugs although, to date, no morphological analysis of the cuticle has been undertaken in order to confirm a phenotypic link. This paper describes examination of the cuticle thickness of a highly pyrethroid-resistant field strain collected in Sydney, Australia, in response to time-to-knockdown upon forced exposure to a pyrethroid insecticide. Mean cuticle thickness was positively correlated to time-to-knockdown, with significant differences observed between bugs knocked-down at 2 hours, 4 hours, and those still unaffected at 24 hours. Further analysis also demonstrated that the 24 hours survivors possessed a statistically significantly thicker cuticle when compared to a pyrethroid-susceptible strain of C. lectularius. This study demonstrates that cuticle thickening is present within a pyrethroid-resistant strain of C. lectularius and that, even within a stable resistant strain, cuticle thickness will vary according to time-to-knockdown upon exposure to an insecticide. This response should thus be considered in future studies on the cuticle of insecticide-resistant bed bugs and, potentially, other insects.

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“…The protein and lipid contents are greater in the cuticle of resistant larvae and, furthermore, the cuticle of the resistant larvae probably had a higher degree of sclerotization [57]. In M. domestica, two resistant strains, with reduced penetration as one of the resistance mechanisms, also showed increased cuticular lipid content; more total lipids, mono-glycerides, fatty acids, sterols and phospholipids were present in the resistant strains compared to a susceptible strain [58]. Reduced penetration has been documented as a resistance mechanism only at the level of the insect cuticle, but any biological membrane may serve as a barrier and thereby give resistance [59].…”

Section: Reduced Penetrationmentioning

confidence: 99%

Biochemical Insecticide Resistance in Tea Pests

Saha¹

2016

Insecticides Resistance

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Polyphagous insect herbivores encounter numerous toxins (xenobiotics) as they pass through their life cycle; some toxins are produced naturally by the host plants (allelochemicals) and others by humans (insecticides) to manage these insects having pest status. The host plants have evolved defensive mechanisms for protection from herbivory, including chemical repellents and toxins (secondary metabolites). Many classes of insect repellents and toxic substances, such as isoflavonoids, furanocoumarins, terpenoids, alkaloids and cyanogenic glycosides are synthesized in plants. The biosynthetic pathways leading to these allelochemicals are continually evolving to generate new secondary metabolites. Similarly, to control the herbivorous insect pests, numerous chemicals of synthetic origin are used continuously against them. In response, the attacking organisms also evolve mechanisms that enable them to resist the defensive chemicals of their hosts and those toxins of synthetic origin applied for their control. A variety of defence mechanisms, including enzymatic detoxification systems, physiological tolerance and behavioural avoidance, protect insect herbivores from these xenobiotic compounds. Insect pests have evolved the mechanisms to degrade metabolically (enzymatically) or otherwise circumvent the toxic effect of many types of chemicals that we have synthesized as modern insecticides. The extent to which insects can metabolize and thereby degrade these antibiotics or toxins is of considerable importance for their survival in hostile chemical environment. These mechanisms continue to evolve as insects attempt to colonize new plant species or encounter newer molecules of synthetic insecticides. Generally, three main enzymes, general esterases (GEs), glutathione Stransferases (GSTs) and cytochrome P450-mediated monooxygenases (CYPs), are involved in the process of metabolic detoxification of insecticides. During the past 70 years, following the discovery and extensive use of synthetic insecticides, resistance of insects to insecticides has registered the greatest increase and strongest impact. The evolution of resistance to insecticides is an example of evolutionary process. An insecticide is the selection pressure, which results in a very strong but differential fitness of the individual in a population having susceptible and resistant genotypes. The survival and subsequent reproduction of resistant individuals lead to a change in the frequency of alleles conferring resistance in the population over

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Cuticular lipids of two resistant and a susceptible strain of houseflies

Cited by 13 publications

References 22 publications

Are Australian field‐collected strains of Cimex lectularius and Cimex hemipterus (Hemiptera: Cimicidae) resistant to deltamethrin and imidacloprid as revealed by topical assay?

Are Australian field‐collected strains of Cimex lectularius and Cimex hemipterus (Hemiptera: Cimicidae) resistant to deltamethrin and imidacloprid as revealed by topical assay?

Cuticle Thickening in a Pyrethroid-Resistant Strain of the Common Bed Bug, Cimex lectularius L. (Hemiptera: Cimicidae)

Biochemical Insecticide Resistance in Tea Pests

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