Abstract
Blood-feeding insects have evolved resistance to various insecticides (organochlorines, pyrethroids, carbamates, etc.) through gene mutations and increased metabolism. Bed bugs (Cimex lectularius) are hematophagous ectoparasites that are poised to become one of the major pests in households throughout the United States. Currently, C. lectularius has attained a high global impact status due to its sudden and rampant resurgence. Resistance to pesticides is one factor implicated in this phenomenon. Although much emphasis has been placed on target sensitivity, little to no knowledge is available on the role of key metabolic players (e.g., cytochrome P450s and glutathione S-transferases) towards pesticide resistance in C. lectularius. In this review, we discuss different modes of resistance (target sensitivity, penetration resistance, behavioral resistance, and metabolic resistance) with more emphasis on metabolic resistance.
Highlights
Bed bugs (Cimex lectularius) are nocturnal hematophagous ectoparasites that have a long-standing association (~300 BC) with man [1] and during evolution these ectoparasites may have switched hosts [2]
In this review of all four modes of resistance, we focus on the modus operandi of metabolic resistance in bed bugs
Zhu et al [15] further suggested that the widespread distribution of bed bugs across North America can be attributed to target-site sensitivity of the voltage-gated sodium channel α-subunit gene among the populations scanned
Summary
Bed bugs (Cimex lectularius) are nocturnal hematophagous ectoparasites that have a long-standing association (~300 BC) with man [1] and during evolution Stress, and insomnia are common responses to bed bug infestations [6]. There is no definitive evidence that bed bugs transmit blood-borne infectious diseases; these ectoparasites have become an important public health issue that affects all socioeconomic classes [7]. The repetitive use of insecticides with long-lasting residual, such as dichlorodiphenyltrichloroethane (DDT) (an organochlorine), organophosphates, and carbamates, drastically reduced the bed bug population [8]. Since the late 1990s, there has been a worldwide resurgence of bed bugs, in developed countries including Eastern Asia, Europe, Australia, and North America [9,10,11]. Gene structure, i.e., point mutations [18] and upregulation of metabolic genes [19]
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