A frightening resurgence of bed bug infestations has occurred over the last 10 years in the U.S. and current chemical methods have been inadequate for controlling this pest due to widespread insecticide resistance. Little is known about the mechanisms of resistance present in U.S. bed bug populations, making it extremely difficult to develop intelligent strategies for their control. We have identified bed bugs collected in Richmond, VA which exhibit both kdr-type (L925I) and metabolic resistance to pyrethroid insecticides. Using LD50 bioassays, we determined that resistance ratios for Richmond strain bed bugs were ∼5200-fold to the insecticide deltamethrin. To identify metabolic genes potentially involved in the detoxification of pyrethroids, we performed deep-sequencing of the adult bed bug transcriptome, obtaining more than 2.5 million reads on the 454 titanium platform. Following assembly, analysis of newly identified gene transcripts in both Harlan (susceptible) and Richmond (resistant) bed bugs revealed several candidate cytochrome P450 and carboxylesterase genes which were significantly over-expressed in the resistant strain, consistent with the idea of increased metabolic resistance. These data will accelerate efforts to understand the biochemical basis for insecticide resistance in bed bugs, and provide molecular markers to assist in the surveillance of metabolic resistance.
Commercial gel formulations, including two new formulations of indoxacarb (0.6% AI; RG2V3 and DPX411), were evaluated for efficacy against a bait strain of German cockroaches (Saginaw strain). Bait consumption and subsequent mortality of the Saginaw cockroaches were compared with that of the VPI, susceptible strain. Both cockroach strains were exposed to formulations in choice tests where dry dog food was the alternative food resource. Feeding indices were calculated for each formulation. Feeding indices were positive for all products offered to the VPI susceptible strain. Negative feeding indices were calculated for MaxForce FC (0.01% fipronil), MaxForce (2.15% hydramethylnon) and Avert Formula 3 (0.05% abamectin B1) when these baits were offered to the averse Saginaw strain. However, feeding indices for the indoxacarb formulations were positive, indicating that the averse cockroaches preferred both of the indoxacarb baits to dog food. Mortality due to exposure was also significantly different between the susceptible and averse strains. In bioassays evaluating the VPI strain, all of the baits produced 100% mortality within the 7 d test period. The indoxacarb RG2V3 formulation produced the most rapid results with 100% mortality recorded within 24h. In bioassays evaluating the averse strain, mortality was dependent on the formulation offered. After 7d only 5% mortality was recorded for the Saginaw cockroaches exposed to fipronil bait. Hydramethylnon produced < 50% mortality during the same period. Mortality in the abamectin and indoxacarb DPX411 bioassays was 75% and 88.8%, respectively, in 7 d. However, the greatest efficacy for control of averse cockroaches was observed in bioassays evaluating indoxacarb RG2V3, where 100% mortality was achieved within 3 d.
Two strains of the common bed bug, Cimex lectularius L., eggs and first instars collected from pyrethroid-resistant adults were evaluated for insecticide resistance and compared to a susceptible strain. Dose-response bioassays were conducted using two insecticide formulations (Temprid: imidacloprid/β-cyfluthrin, and Transport: acetamiprid/ bifenthrin). The lethal concentration (LC50) for the two resistant egg strains exposed to imidacloprid/β-cyfluthrin ranged from 3 to 5-fold higher than susceptible strain eggs. Resistant strain eggs dipped into formulations of acetamiprid/bifenthrin had LC50 values which were significantly greater (39 to 1,080-fold) than susceptible strain eggs. Similar to eggs, resistant strain first instars exposed to residual applications of imidacloprid/β-cyfluthrin had LC50 values ranging from 121 to 493-fold greater than susceptible strain first instars. When resistant strain first instars were treated with acetamiprid/bifenthrin, they had LC50 values that were 99 to >1,900-fold greater than susceptible strain first instars. To determine differences between egg and first instar resistance, stage resistance ratios (SRR) were compared between the two stages. There was little difference between the egg and first instar stages, indicated by small SRR values ranging from 1.1 to 10.0. This study suggests that insecticide resistance is expressed early during bed bug development.
