Concept: Masked hunter
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.
The global population of bed bugs (Cimex lectularius and Cimex hemipterus, family Cimicidae) has undergone a significant resurgence since the late 1990s. This is likely due to an increase in global travel, trade, and the number of insecticide-resistant bed bugs. The global bed bug population is estimated to be increasing by 100-500 % annually. The worldwide spread of bed bugs is concerning, because they are a significant socioeconomic burden and a major concern to public health. According to the United States Environmental Protection Agency, bed bugs are “a pest of significant health importance.” Additionally, 68 % of U.S. pest professionals reported that bed bugs are the most challenging pest to treat. Upwards of 45 disease pathogens have been reported in bed bugs. Recent studies report that bed bugs may be competent vectors for pathogens, such as Bartonella quintana and Trypanosoma cruzi. However, public health reports have thus far failed to produce evidence that major infectious disease outbreaks have been associated with bed bugs. Since many disease pathogens have previously been reported in bed bugs and the worldwide bed bug population is now drastically increasing, it stands to reason to wonder if bed bugs might transmit human pathogens. This review includes a literature search on recently published clinical and laboratory studies (1990-2016) investigating bed bugs as potential vectors of infectious disease, and reports the significant findings and limitations of the reviewed studies. To date, no published study has demonstrated a causal relationship between bed bugs and infectious disease transmission in humans. Also, we present and propose to expand on previous hypotheses as to why bed bugs do not transmit human pathogens. Bed bugs may contain “neutralizing factors” that attenuate pathogen virulence and, thereby, decrease the ability of bed bugs to transmit infectious disease.
Bed bugs (both Cimex hemipterus [F.] and Cimex lectularius L.) worldwide are highly resistant to the pyrethroids. An important resistance mechanism known as ‘knockdown resistance’ (kdr) is caused by genetic point mutations on the voltage-gated sodium channel (VGSC) gene. Previous studies have identified two point mutations (V419L and L925I) on the VGSC gene in C. lectularius that are responsible for kdr-type resistance. However, the kdr mutations in C. hemipterus have not been investigated.
Pyrethroid resistance in the Common bed bug, Cimex lectularius L. has been reported worldwide. An important resistant mechanism is via knockdown resistance (kdr) mutations, notably V419L and L925I. Information regarding this kdr-type resistant mechanism is unknown in Australia. This study aims to examine the status of kdr mutations in Australian C. lectularius strains.
The rapid increase of bed bug populations resistant to pyrethroids demands the development of novel control tactics. Products combining pyrethroids and neonicotinoids have become very popular for bed bug control in the United States, but there are concerns about evolution of resistance to these compounds. Laboratory assays were used to measure the toxicity of topical applications of four neonicotinoids to a susceptible population and three pyrethroid-resistant populations. Activity of esterases, glutathione S-transferases, and cytochrome P450s of all strains was also evaluated. High levels of resistance to four neonicotinoids, acetamiprid, imidacloprid, dinotefuran, and thiamethoxam, relative to the susceptible Fort Dix population, were detected in populations collected from human dwellings in Cincinnati and Michigan. Because activity of detoxifying enzymes was increased in these two populations, our results suggest that these enzymes have some involvement in neonicotinoid resistance, but other resistance mechanisms might be involved as well. Detection of high levels of resistance to neonicotinoids further limits the options for chemical control of bed bugs.
Insecticide resistance is a major impediment for effective control of Cimex lectularius L. Previous resistance detection studies with bed bugs have focused on certain pyrethroid, neonicotinoid, organochlorine, organophosphate, and carbamate insecticides. Within the pyrethroid class, resistance studies have mostly been limited to deltamethrin, lambda-cyhalothrin, and alpha- and beta-cyfluthrin. The goal of this study was to develop diagnostic concentration bioassays for assessing bed bug susceptibility levels to chlorfenapyr- and bifenthrin-containing products. First, glass vial and filter paper bioassay methods were compared for their utility in susceptibility monitoring. Statistical comparison of toxicity data between bioassays indicated that the vial assay was less confounded by assay susbtrate effects, required less insecticide, and was faster, especially for chlorfenapyr. Next, using vial diagnostic concentrations (LC99) for each insecticide, 10 laboratory-adapted field strains and the Harlan lab-susceptible strain were screened for susceptibility to chlorfenapyr and bifenthrin. The results of this study reveal recent bed bug susceptibility levels to certain chlorfenapyr- and bifenthrin-containing products. Reduced susceptibility was detected in three and five field strains to chlorfenapyr and bifenthrin, respectively. Detection of reduced susceptibility suggests that certain strains may be segregating toward greater chlorfenapyr and bifenthrin resistance. These results merit continuous resistance monitoring efforts to detect chlorfenapyr and bifenthrin susceptibility shifts. Additionally, to reduce insecticide selection pressures and delay resistance development, adoption of integrated bed bug control strategies that combine chemical and nonchemical methods is recommended.
Elucidating the spatial dynamic and core constituents of the microbial communities found in association with arthropod hosts is of crucial importance for insects that may vector human or agricultural pathogens. The hematophagous Cimex lectularius (Hemiptera: Cimicidae), known as the human bed bug, has made a recent resurgence in North America, as well as worldwide, potentially owing to increased travel, climate change and resistance to insecticides. A comprehensive survey of the bed bug microbiome has not been performed to date, nor has an assessment of the spatial dynamics of its microbiome. Here we present a survey of internal and external bed bug microbial communities by amplifying the V4-V6 hypervariable region of the 16S rDNA gene region followed by 454 Titanium sequencing using 31 individuals from eight distinct collection locations obtained from residences in Cincinnati, OH. Across all samples, 97% of the microbial community is made up of two dominant OTUs, previously identified as the α-proteobacterium Wolbachia and an unnamed γ-proteobacterium from the Enterobacteriaceae. Microbial communities varied among host locations for measures of community diversity and exhibited structure according to collection location. This broad survey represents the most in-depth assessment, to date, of the microbes that associate with bed bugs.
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.
The climbing abilities of two bed bug species, Cimex lectularius L. and Cimex hemipterus (F.), were determined by evaluating their escape rates from smooth surface pitfall traps using four commercial bed bug monitors (Verifi Bed Bug Detector, ClimbUp Insect Interceptor, BlackOut Bed Bug Detector, and SenSci Volcano Bed Bug Detector). All detectors were used in the absence of lures or attractants. Unlike C. lectularius, adult C. hemipterus were able to escape from all traps. On the other hand, no or a low number nymphs of both species escaped, depending on the evaluated traps. Examination of the vertical friction force of adults of both species revealed a higher vertical friction force in C. hemipterus than in C. lectularius. Scanning electron microscope micrograph observation on the tibial pad of adult bed bugs of C. hemipterus showed the presence of a greater number of tenent hairs on the tibial pad than on that of adult C. lectularius. No tibial pad was found on the fourth and fifth instars of both species. Near the base of the hollow tenent hairs is a glandular epithelium that is better developed in adult C. hemipterus than in adult C. lectularius. This study highlights significant morphological differences between C. lectularius and C. hemipterus, which may have implications in the monitoring and management of bed bug infestations.
Insecticide sprays and dusts are used for controlling bed bugs, Cimex lectularius L. In natural environments, bed bugs have daily access to hosts after they are exposed to insecticides. The established laboratory insecticide bioassay protocols do not provide feeding after insecticide treatments, which can result in inflated mortality compared with what would be encountered in the field. We evaluated the effect of posttreatment feeding on mortality of bed bugs treated with different insecticides. None of the insecticides tested had a significant effect on the amount of blood consumed and percent feeding. The effect of posttreatment feeding on bed bug mortality varied among different insecticides. Feeding significantly reduced mortality in bed bugs exposed to deltamethrin spray, an essential oil mixture (Bed Bug Fix) spray, and diatomaceous earth dust. Feeding increased the mean survival time for bed bugs treated with chlorfenapyr spray and a spray containing an essential oil mixture (Ecoraider), but did not affect the final mortality. First instars hatched from eggs treated with chlorfenapyr liquid spray had reduced feeding compared with nymphs hatched from nontreated eggs. Those nymphs hatched from eggs treated with chlorfenapyr liquid spray and successfully fed had reduced mortality and a higher mean survival time than those without feeding. We conclude that the availability of a bloodmeal after insecticide exposure has a significant effect on bed bug mortality. Protocols for insecticide efficacy testing should consider offering a bloodmeal to the treated bed bugs within 1 to 3 d after treatment.