Multiple mechanisms associated with deltamethrin and imidacloprid resistance in field-collected common bed bug, Cimex lectularius L.

Abstract

Pyrethroids and neonicotinoids are commonly used to manage the common bed bug (Cimex lectularius L.) infestations. However, the effectiveness of these insecticides is often challenged due to insecticide resistance. We investigated the mechanisms of deltamethrin and imidacloprid resistance in eight C. lectularius strains collected from New Jersey, U.S. Piperonyl butoxide (PBO), S,S,S-tributyl phosphorotrithioate (DEF), and diethyl maleate (DEM) were topically applied on bed bugs before deltamethrin or imidacloprid treatments (deltamethrin: 115 ng per adult; imidacloprid: 67 ng per adult). The results showed that PBO and DEF had a greater synergistic effect with deltamethrin treatments than DEM based on the significantly increased 72 h mortality of Aberdeen, Bayonne 2015, Cotton, Irvington, and Irvington 624-5G strains. With imidacloprid alone, seven out of eight strains experienced 100 % mortality except for the Linden 2019 strain. The Linden 2019 strain had mean mortalities of 93, 97, and 47 % from imidacloprid after receiving PBO, DEF, and DEM, respectively. The activities of glutathione S-transferase and general esterase in all strains were enhanced compared to a susceptible strain. Molecular detection of voltage-gated sodium channel (VGSC) mutations revealed homozygous V419L and L925I resistance mutations in all strains at 20–100 % and 30–100 % frequency, respectively. The presence of both V419L and L925I was found in 20–100 % of the individuals from each resistant strain. The results indicate a combination of metabolic and target site insensitivity mechanisms confers resistance to deltamethrin and imidacloprid in C. lectularius.