Multiple mechanisms of deltamethrin resistance in the common bed bug (Cimex lectularius) populations and the efficacy of insecticide synergists

One of the factors contributing to the bed bug resurgence is resistance to different insecticides. Two of the known mechanisms of insecticide resistance include increased metabolic detoxification and decreased sensitivity on target site (kdr-type mutation). Eight bed bug (Cimex lectularius) populations collected in New Jersey have been reported with high resistance to deltamethrin. In this study, the detoxification activities of these resistant populations were evaluated. The results showed that the mean enzyme activities were enhanced in various levels among the resistant populations. Compared to a laboratory strain, monogeneses (P450s) increased from 1.5 to 15.0-folds; the 1-naphthol increased from 1.1 to 4.4-folds; the 2-naphthol increased from 1.2 to 4.0-folds; and the glutathione S-transferase increased from 1.1 to 2.9-folds. Kdr-type mutation including V419L and L925I points were also examined. Only 20% of “Cotton” and “Irvington” populations did not have mutation at V419L and L925I. Seven populations had at least one mutated point. Over 80% of the tested insects in the seven populations exhibit mutation at both points. To test the efficacy of insecticide synergists, piperonyl butoxide, S,S,S,-tributyl phosphorotrithioate, and diethyl maleate were applied to bed bugs prior to deltamethrin treatment. The mortality of most populations cannot reach 77% even after 72 h. The results indicate the kdr-type mutation may be the main mechanism of deltamethrin resistance in bed bug populations. A strong need of management program on resistant bed bug is urgent.