Abstract

Infestations of the common bed bug (Cimex lectularius L.) have increased substantially in the United States in the past 10–15 years. The housing authority in Harrisonburg, Virginia, conducts heat-treatments after bed bugs are detected in a lower-income housing complex, by treating each infested unit at 60°C for 4–6 hours. However, a high frequency of recurrent infestations called into question the efficacy of this strategy. Genetic analysis using Bayesian clustering of polymorphic microsatellite loci from 123 bed bugs collected from 23 units from May 2012 to April 2013 in one building indicated that (a) 16/21 (73%) infestations were genetically similar, suggesting ineffective heat-treatments or reintroductions from within the building or from a common external source, followed by local spread of existing populations; and (b) up to 5 of the infestations represented new genotypes, indicating that 5 new populations were introduced into this building in one year, assuming they were not missed in earlier screens. There was little to no gene flow among the 8 genetic clusters identified in the building. Bed bugs in the U.S. often possess one or both point mutations in the voltage-gated sodium channel, termed knockdown resistance (kdr), from valine to leucine (V419L) and leucine to isoleucine (L925I) that confer target-site resistance against pyrethroid insecticides. We found that 48/121 (40%) bed bugs were homozygous for both kdr mutations (L419/I925), and a further 59% possessed at least one of the kdr mutations. We conclude that ineffective heat treatments, new introductions, reintroductions and local spread, and an exceptionally high frequency of pyrethroid resistance are responsible for chronic infestations in lower-income housing. Because heat treatments fail to protect from reintroductions, and pesticide use has not decreased the frequency of infestations, preventing new introductions and early detection are the most effective strategies to avoid bed bug infestations in multistory apartment buildings.

Highlights

  • The common bed bug, Cimex lectularius L., is an obligate, blood-feeding ectoparasitic insect that avidly feeds on humans

  • Explanations for this resurgence include increased international travel, changes in pest control practices for other urban pests, increased trade in secondhand furniture, and widespread bed bug resistance to commercially-available pesticides registered for use against this insect [8,9,10]

  • A survey revealed that 88% of bed bug populations collected from 17 states across the U.S possessed one or both of these knockdown resistance mutations, which conferred target-site resistance against deltamethrin and related pyrethroid insecticides [17]

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Summary

Introduction

The common bed bug, Cimex lectularius L., is an obligate, blood-feeding ectoparasitic insect that avidly feeds on humans. A survey revealed that 88% of bed bug populations collected from 17 states across the U.S possessed one or both of these knockdown resistance (kdr) mutations, which conferred target-site resistance against deltamethrin and related pyrethroid insecticides [17]. By genotyping bed bugs from multiple units over multiple collection events, we sought to determine whether bed bugs were escaping and hiding during the thermal treatment and returning to reinfest the same apartment and its neighbors, or if subsequent re-infestations represented new, unique introductions. We compared polymorphic microsatellite loci from bed bugs collected over a year from this building to determine if chronic reinfestations were the product of the same matriline that escaped the treatment and spread from unit to unit or if each infestation was a new introduction from elsewhere. Because we observed extensive pesticide use by tenants, and pyrethroid resistance is widespread in the U.S, we assessed the frequency of kdr mutations to infer the extent of pyrethroid resistance

Materials and Methods
Results and Discussion
Microsatellite Results and Cluster Analysis
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