Abstract:The novel mutation I936F may be a kdr mutation but appeared to contribute less resistance to the pyrethroids than the V419L and L925I mutations. The detection of high frequencies of kdr mutations indicates that kdr-type resistance is widespread across Australia. Hence, there should be a reduced reliance on pyrethroid insecticides and an integrated management approach for the control of C. lectularius infestations.
“…Several studies showed that kdr -type resistance to DDT and pyrethroids results from a single or multiple point mutations (also known as kdr mutations) in coding sequences of VGSC in various insect pests (Fig. 2) [46, 150, 154, 155], including bed bugs [17, 54, 156, 157]. Yoon et al [156] first cloned and sequenced the coding gene of C. lectularius VGSC from both insecticide resistant and susceptible strains in the USA.…”
Section: Mechanisms Of Resistancementioning
confidence: 99%
“…One hundred percent of the tested C. lectularius collected from Paris, France [158] and Berlin, Germany [159] only contained L925I. Of C. lectularius collected from various locations in Australia (25 strains), 96% possessed L925I [55], while from Israel (12 strains), 100% had L925I, of which, a few specimens from both countries had additional V419L [54, 160]. Based on the various genotypes of V419L and L925I mutations of 110 field-collected strains of C. lectularius in the USA, Zhu et al [157] identified four haplotypes; haplotype A (without V419L and L925I mutations; 15.5% [17/110]), haplotype B (only L925I; 40.9% [45/110]), haplotype C (V419L and L925I; 40.9% [45/110]) and haplotype D (V419L; 2.7% [3/110]).Fig.…”
Section: Mechanisms Of Resistancementioning
confidence: 99%
“…However, with the worldwide resurgence of bed bugs over the last two decades, resistance to pyrethroids (Table 4) has been documented in many parts of the world for both C. lectularius [16, 30, 47–54] and C. hemipterus [12, 16, 17, 55, 56]. …”
The worldwide resurgence of bed bugs [both Cimex lectularius L. and Cimex hemipterus (F.)] over the past two decades is believed in large part to be due to the development of insecticide resistance. The transcriptomic and genomic studies since 2010, as well as morphological, biochemical and behavioral studies, have helped insecticide resistance research on bed bugs. Multiple resistance mechanisms, including penetration resistance through thickening or remodelling of the cuticle, metabolic resistance by increased activities of detoxification enzymes (e.g. cytochrome P450 monooxygenases and esterases), and knockdown resistance by kdr mutations, have been experimentally identified as conferring insecticide resistance in bed bugs. Other candidate resistance mechanisms, including behavioral resistance, some types of physiological resistance (e.g. increasing activities of esterases by point mutations, glutathione S-transferase, target site insensitivity including altered AChEs, GABA receptor insensitivity and altered nAChRs), symbiont-mediated resistance and other potential, yet undiscovered mechanisms may exist. This article reviews recent studies of resistance mechanisms and the genes governing insecticide resistance, potential candidate resistance mechanisms, and methods of monitoring insecticide resistance in bed bugs. This article provides an insight into the knowledge essential for the development of both insecticide resistance management (IRM) and integrated pest management (IPM) strategies for successful bed bug management.
“…Several studies showed that kdr -type resistance to DDT and pyrethroids results from a single or multiple point mutations (also known as kdr mutations) in coding sequences of VGSC in various insect pests (Fig. 2) [46, 150, 154, 155], including bed bugs [17, 54, 156, 157]. Yoon et al [156] first cloned and sequenced the coding gene of C. lectularius VGSC from both insecticide resistant and susceptible strains in the USA.…”
Section: Mechanisms Of Resistancementioning
confidence: 99%
“…One hundred percent of the tested C. lectularius collected from Paris, France [158] and Berlin, Germany [159] only contained L925I. Of C. lectularius collected from various locations in Australia (25 strains), 96% possessed L925I [55], while from Israel (12 strains), 100% had L925I, of which, a few specimens from both countries had additional V419L [54, 160]. Based on the various genotypes of V419L and L925I mutations of 110 field-collected strains of C. lectularius in the USA, Zhu et al [157] identified four haplotypes; haplotype A (without V419L and L925I mutations; 15.5% [17/110]), haplotype B (only L925I; 40.9% [45/110]), haplotype C (V419L and L925I; 40.9% [45/110]) and haplotype D (V419L; 2.7% [3/110]).Fig.…”
Section: Mechanisms Of Resistancementioning
confidence: 99%
“…However, with the worldwide resurgence of bed bugs over the last two decades, resistance to pyrethroids (Table 4) has been documented in many parts of the world for both C. lectularius [16, 30, 47–54] and C. hemipterus [12, 16, 17, 55, 56]. …”
The worldwide resurgence of bed bugs [both Cimex lectularius L. and Cimex hemipterus (F.)] over the past two decades is believed in large part to be due to the development of insecticide resistance. The transcriptomic and genomic studies since 2010, as well as morphological, biochemical and behavioral studies, have helped insecticide resistance research on bed bugs. Multiple resistance mechanisms, including penetration resistance through thickening or remodelling of the cuticle, metabolic resistance by increased activities of detoxification enzymes (e.g. cytochrome P450 monooxygenases and esterases), and knockdown resistance by kdr mutations, have been experimentally identified as conferring insecticide resistance in bed bugs. Other candidate resistance mechanisms, including behavioral resistance, some types of physiological resistance (e.g. increasing activities of esterases by point mutations, glutathione S-transferase, target site insensitivity including altered AChEs, GABA receptor insensitivity and altered nAChRs), symbiont-mediated resistance and other potential, yet undiscovered mechanisms may exist. This article reviews recent studies of resistance mechanisms and the genes governing insecticide resistance, potential candidate resistance mechanisms, and methods of monitoring insecticide resistance in bed bugs. This article provides an insight into the knowledge essential for the development of both insecticide resistance management (IRM) and integrated pest management (IPM) strategies for successful bed bug management.
“…This strain has been extensively profiled for potential mechanisms conferring pyrethroid resistance, and has been found to possess haplotype B (homogeneous L925I) kdr -type resistance [13], hydrolytic esterase-derived metabolic detoxification [52], and cuticle thickening [50]. Exposure to a d-allethrin based rapid resistance field assay elicits no statistically significant levels of knockdown when compared to an untreated control [53].…”
Section: Methodsmentioning
confidence: 99%
“…Key amongst these has been a response to the growing global evidence that most field bed bug populations have developed resistance to multiple insecticide groups [5,6,7,8,9,10] and, in particular, that they have become highly resistant to pyrethroid insecticides [11,12,13,14,15,16,17,18,19,20,21,22,23]. Despite this, and due to a general scarcity of alternative control options [24], when faced with a bed bug infestation both pest management professionals (PMPs) and residents of infested properties continue to apply insecticides in attempts to achieve control [24,25,26,27,28].…”
Insecticide resistance in bed bugs (Cimex lectularius and Cimex hemipterus) has become widespread, which has necessitated the development of new IPM (Integrated Pest Management) strategies and products for the eradication of infestations. Two promising options are the diatomaceous earth and silica gel-based desiccant dusts, both of which induce dehydration and eventual death upon bed bugs exposed to these products. However, the impact of underlying mechanisms that confer resistance to insecticides, such as cuticle thickening, on the performance of these dusts has yet to be determined. In the present study, two desiccant dusts, CimeXa Insecticide Dust (silica gel) and Bed Bug Killer Powder (diatomaceous earth) were evaluated against two strains of C. lectularius; one highly pyrethroid-resistant and one insecticide-susceptible. Label-rate doses of both products produced 100% mortality in both strains, albeit over dissimilar time-frames (3–4 days with CimeXa vs. 14 days with Bed Bug Killer). Sub-label rate exposure to CimeXa indicated that the pyrethroid-resistant strain possessed a degree of tolerance to this product, surviving 50% longer than the susceptible strain. This is the first study to suggest that mechanisms conferring resistance to pyrethroids, such as cuticular thickening, may have potential secondary impacts on non-synthetic insecticides, including desiccant dusts, which target the bed bug’s cuticle.
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