Target site mutations and metabolic detoxification of insecticides in continental populations of Cimex lectularius and Cimex hemipterus (Hemiptera: Cimicidae).

Abstract

In recent decades, the common and the tropical bed bugs have experienced a resurgence in many parts of the world. The evolution of insecticide resistance in bed bug populations is considered a significant factor contributing to this resurgence. We analyzed samples of Cimex lectularius L. and Cimex hemipterus (F.) from Europe (Spain 41, Switzerland 2, the Czech Republic 1), Asia (Hong Kong 34), North America (USA 14, Mexico 3), and South America (Colombia 3) to assess the prevalence and mechanisms of insecticide resistance. We identified specimens morphologically and barcoded them by sequencing the mitochondrial Cytochrome c oxidase subunit I (COI) and the 16S ribosomal RNA (16S rRNA) genes. Additionally, we screened segments of the voltage-gated sodium channel (VGSC) and the nicotinic acetylcholine receptor (nAChR) genes for point mutations associated with insecticide resistance and measured the activity of detoxifying enzymes. All samples from North America and Europe were identified as C. lectularius, whereas specimens from Hong Kong were C. hemipterus. Out of 64 C. lectularius samples tested for knockdown resistance (kdr) mutations, 90.6% contained at least 1 known mutation. All 35 C. hemipterus samples exhibited kdr mutations. A new mutation was identified in the pyrethroid target site in both common (F1524C) and tropical (F1450C) bed bugs. No resistance-associated mutations in the nAChR gene were found. Several populations that exhibited kdr mutations also showed elevated activity of detoxifying enzymes. The high frequency of kdr-associated mutations in bed bug populations from Spain and Hong Kong limits the efficacy of pyrethroids for their control.