First evidence of the A302S <i>Rdl</i> insecticide resistance mutation in populations of the bed bug, <i>Cimex lectularius</i> (Hemiptera: Cimicidae) in North America

Abstract

The common bed bug, Cimex lectularius (L.) (Hemiptera: Cimicidae), is a pervasive indoor pest with prominent medical, veterinary, and economic impacts. Bed bug infestations are controlled by a wide range of insecticides, including pyrethroids, neonicotinoids, pyrroles, and phenylpyrazoles; however, bed bugs have evolved resistance mechanisms to most of these insecticides. Mutations in the Rdl (resistance to dieldrin) gene, located in a subunit of the γ-amino butyric acid (GABA)-gated chloride channel, have been identified in several pest insects, including the German cockroach. These have been found to confer resistance to fipronil, a phenylpyrazole insecticide commonly used in urban environments, in addition to cyclodienes (eg dieldrin), a class of insecticides banned in most countries since the 1990s. While resistance to dieldrin and fipronil has been reported in bed bugs, both C. lectularius and the tropical bed bug, C. hemipterus, the occurrence of mutations in the Rdl gene has yet to be thoroughly investigated. In this study, we sequence a fragment of the Rdl gene commonly found to harbor cyclodiene and phenylpyrazole conferring mutations from 134 unique populations collected across the United States and Canada spanning a 14-yr period. Homozygous genotypes for the A302S mutation were found in 2 geographically distinct populations. This finding represents the first record of a non-synonymous Rdl mutation in bed bugs and identifies another mechanism by which insecticide resistance may be conferred in this species.