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Current Pediatric Reviews
ISSN: 1573-3963
eISSN: 1875-6336
SCIENCE
BENTHAM
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Current Pediatric Reviews, 2024, 20, 137-149
137
REVIEW ARTICLE
Bed Bug Infestation: An Updated Review
Alexander K.C. Leung1,*, Joseph M. Lam2, Benjamin Barankin3, Kin Fon Leong4 and Kam Lun Hon5,6
1Department of Pediatrics, The University of Calgary, Alberta Children’s Hospital, Calgary, Alberta, Canada;
2Department of Pediatrics and Department of Dermatology and Skin Sciences, University of British Columbia, Vancou-
ver, British Columbia, Canada; 3Toronto Dermatology Centre, Toronto, Ontario, Canada; 4Pediatric Institute, Kuala
Lumpur General Hospital, Kuala Lumpur, Malaysia; 5Department of Paediatrics, The Chinese University of Hong
Kong; 6Department of Paediatrics and Adolescent Medicine, Hong Kong Children’s Hospital, Hong Kong, China
Abstract: In the past decade, there has been a global resurgence of bed bug infestations, especially
in developed countries. Proper awareness and identification of bed bug infestations are essential to
guide treatment and eradication. The purpose of this article is to familiarize physicians with bed bug
bites so that they can effectively diagnose, treat, and address questions about bed bug bites and in-
festations. Bed bug bites are often painless. Typical reactions include pruritic, erythematous macu-
lopapules occurring in clusters or in a linear or curvilinear distribution in exposed areas of the body.
A small red punctum may be visualized at the center of the bite mark. Lesions that appear three in a
row and papules on the upper eyelid associated with erythema and edema are highly suggestive of
bites from bed bugs. Exaggerated local reactions such as vesicles, urticarial wheals, urticarial per-
ilesional plaques, diffuse urticaria, bullae, and nodules may occur in previously sensitized individu-
als. Reactions to bed bug bites are self-limited. As such, treatment is mainly symptomatic. Topical
pramoxine and oral antihistamines can be used to alleviate pruritus. Topical corticosteroids can be
used for significant eruptions to control inflammation and pruritus, and to hasten resolution of the
lesions. Integrated pest management, an approach for the eradication of bed bugs, includes monitor-
ing devices (active monitors include the use of heat or carbon dioxide attractants and passive moni-
tors include the use of sticky pads for trapping), and judicious use of nonchemical and chemical
treatments known to be effective. Nonchemical interventions include keeping affected areas clean
and free of clutter, vacuuming, washing linens with hot water, caulking wall holes and cracks where
bugs can hide, proper disposal of highly infested items, and placement of bed bug traps/interceptors
at the base of beds and furniture. Chemical interventions involve the use of insecticides such as syn-
thetic pyrethroids, silicates, insect growth disruptors, carbamates, organophosphates, neonico-
tinoids, diethyl-meta-toluamide, chlorfenapyr, fipronil and plant essential oils. Insecticides should
be used with caution to prevent over-exposure and toxicity (in particular, cardiovascular and neuro-
logic toxicity), especially if there are young children around. It is important to note that multiple
mechanisms of insecticide resistance exist and as such, chemical treatment should only be under-
taken by trained professionals who understand the current literature on resistance. Both non-
chemical and chemical technologies should be combined for optimal results.
Bed bug infestations may cause diverse dermal reactions, stigmatization, poor self-esteem, emo-
tional stress, anxiety, significant adverse effect on quality of life, and substantial socioeconomic
burden to society. As such, their rapid detection and eradication are of paramount importance. Con-
sultation with a professional exterminator is recommended to fully eradicate an infestation.
A R T I C L E H I S T O R Y
Received: July 22, 2022
Revised: January 12, 2023
Accepted: January 20, 2023
DOI:
10.2174/1573396320666230406084801
Keywords: Cimex, papular urticaria, pruritic papules, pyrethroids, urticarial wheals, bed bug infestations.
1. INTRODUCTION
Bed bugs are hematophagous arthropods that can infest
human dwellings and inflict bites to humans [1]. In recent
years, there has been a global resurgence of bed bug infesta-
tions, especially in developed countries [2-6]. Physicians
*Address correspondence to this author at Department of Pediatrics, The
University of Calgary, Alberta Children’s Hospital, Calgary, Alberta, Cana-
da; Tel: (403) 230 3300; Fax: (403) 230 3322; E-mail: aleung@ucalgary.ca
should familiarize themselves with bed bug bites to effec-
tively diagnose, treat, and answer questions about bed bug
bites and infestations. A review of the topic is therefore in
order and is the purpose of the present article. This review
covers mainly literature published in the previous ten years.
2. ENTOMOLOGY
Bed bugs are obligate hematophagous ectoparasites that
belong to the phylum Arthropoda, the class Hexapoda (In-
1875-6336/24 $65.00+.00 © 2024 Be ntham Science Publishers
138 Current Pediatric Reviews, 2024, Vo l . 20, No. 2 Leung et al.
secta), the order Hemiptera, the family Cimicidae, and the
genus Cimex [1, 7]. Cimex lectularius (the common or tem-
perate bed bug) and Cimex hemipterus (the tropical bed bug)
are the two main species that feed primarily on humans [6,
8]. Cimex is derived from the Roman word for "bug" and
lectularius from the Latin word for "bed" or "couch" [9].
While humans are the preferred host, C. lectularius and C.
hemipterus can feed on other warm-blooded mammals and
birds [10-13]. The term “bed bug” is a misnomer as bed bugs
tend to hide not only in beds, but also in other indoor harbor-
ages that provide easy access to the human host. [14].
Adult bed bugs are reddish-brown, flat, oval-shaped,
wingless insects, typically 4 to 7 mm long, with females
slightly larger than males [7, 15, 16]. Latter instars and
adults are easily visible without magnification. Bed bugs are
usually brown in color and turn dull red or violaceous and
increase in size after feeding [7, 9]. They have a “buggy” or
"sickly sweet" odor [4, 17]. Bed bugs have 3 pairs of legs, a
pyramid-shaped head, a retroverted, slender and elongated
piercing-sucking labium (mouthparts), widely spaced com-
pound eyes, a pair of four-segmented antennae, a small sem-
icircular to triangular scutellum (dorsal sclerotic plate) be-
hind the pronotum (plate-like structures covering the dorsal
thorax), and an 11-segment abdomen (Fig. 1) [1, 18-20].
Short lateral hairs can be observed along the margins of the
upper thorax. Males have a pointed abdomen at the apex
while the females have a more rounded abdomen [4, 11].
The female has a ventral notch or paragenital sinus on the
posterior abdomen whereas the male has a paramere on only
one side of the posterior abdomen [20].
Fig. (1). Appearance of a bed bug on dermoscopy. (A higher reso-
lution / colour version of this figure is available in the electronic
copy of the article).
Adult females lay approximately 5 to 8 eggs per week for
approximately 18 weeks when conditions are favorable
(23oC, 90% relative humidity) and with unlimited access to
blood meals [4, 10]. The eggs are translucent or light cream-
colored, elongated, and approximately 1 mm in length and
half as wide [21]. They become progressively darker and
larger as they develop [4]. Eggs typically hatch in 4 to 10
days [17, 22]. Newly hatched nymphs are pale and translu-
cent [17]. Nymphs molt five times and mature into adults in
6 to 8 weeks [17, 23]. The female bed bug needs a blood
meal to develop eggs and each nymph needs a blood meal
before each molt [9].
The typical lifespan of bed bugs in temperate climates is
6 to 24 months [11, 17]. Bed bugs can survive 12 months
without feeding and up to 24 months in cooler environments
[17, 24]. However, males starved longer than 2 weeks will
cease to mate, and females starved longer than 2 months
produce fewer eggs than those starved for a much shorter
period of time [24, 25].
Bed bugs are unable to fly or jump [24]. It has been
shown that female bed bugs have more difficulty in climbing
smooth surfaces compared with their counterparts, presuma-
bly because of the larger weight gain by female bed bugs
after feeding [26]. Bed bugs are nocturnal, photophobic, live
in groups, respond to aggregation pheromones when condi-
tions are favorable and disperse when conditions are unfa-
vorable [20, 27]. Five volatile components (dimethyl disul-
fide, dimethyl trisulfide, 2-hexanone, (E)-2-hexanal, (E)-2-
octenal) and one less-volatile component (histamine) of bed
bug aggregation pheromones have been identified [28]. The
former five volatile components attract bed bugs to safe shel-
ters and the latter less-volatile component causes their ar-
restment upon contact [28].
During the day, bed bugs hide in surrounding habitat in
close proximity (usually within 2 meters) to where their
hosts sleep or rest [29, 30]. Bed bugs tend not to live on the
human body, and they return to their haborage after feeding
[10, 31]. They prefer to hide along seams in the mattresses,
in cracks and crevices of box springs and mattresses, uphol-
stered furniture, backsides of headboards, between wooden
floorboards, and behind loose pieces of wallpaper [20, 30,
32]. Bed bugs prefer black, blue, and red harborages more
than other colored harborages [33]. They tend to avoid
glossy or smooth surfaces [2]. Bed bugs can withstand tem-
peratures from 7°C to 45°C [6]. Exposure to a much higher
temperature, on the other hand, may reduce the feeding and
inhibit the development of bed bugs [34]. Bed bugs have
lipid-based physicochemical properties that protect them
against insecticides [35].
3. PATHOPHYSIOLOGY
At night, bed bugs crawl to their host to feed, being at-
tracted to the host by body warmth, sweat, odor, and exhaled
carbon dioxide [36-42]. The peak feeding times occur be-
tween 1 and 5 am, usually while the victim is asleep or rest-
ing [4]. Each feeding typically lasts 3 to 12 minutes [15].
Usually, an adult bed bug sucks blood from the host every
2.5 to 4 days [43, 44]. During feeding, bed bugs grasp the
human skin with their forelegs [20]. The mouthparts which
are normally held close beneath the head and thorax, swing
down before feeding [13]. The bed bugs then pierce the skin
with their proboscis which is composed of two elongated
extremely fine needle-like stylets. The first stylet secretes
several substances including anesthetic compounds, vasodi-
lators (such as nitrophorin), anticoagulant factors (e.g., fac-
tor-X inhibitor), apyrase (e.g., adenosine triphosphate-
diphosphohydrolase) which is a platelet- activation and ag-
gregation inhibitor, and pharmacologically active substances
(e.g., hyaluronidase, proteases, kinins) [10, 23, 45, 46]. The
second stylet extracts blood either directly from the capillary
or from the extravasated blood from damaged tissue [17].
Bed bugs can increase in weight by 150 to 200% and length
Bed Bug Infestation Current Pediatric Reviews, 2024, Vol. 20, No. 2 139
by 30 to 50% after a feed [9, 47]. Cutaneous reactions such
as erythema and wheals are caused by the pharmacologically
active substances such as various proteins found in the saliva
of bed bugs [10, 48]. The type of reaction depends on the
immunocompetence and sensitivity of the individual [13].
Repeated exposure may sensitize the individual, leading to
more severe cutaneous or systemic hypersensitivity reactions
[23, 49].
4. EPIDEMIOLOGY
Both sexes are equally affected. Bed bugs are found in-
ternationally but are more prevalent in areas of lower socio-
economic status [50-52]. Cimex lectularius is most prevalent
in temperate climates whereas C. hemipterus is most preva-
lent in tropical regions within 30 degrees of the equator. In
recent years, both C. lectularius and C. hemipterus have
been found outside their traditional zones of infestation [51].
Wang et al. [53] examined bed bug prevalence in 2,372 low-
income apartments in four New Jersey cities using a combi-
nation of resident interviews, brief visual inspections, and
monitoring with Climbup Insect Interceptors. Infestation
rates ranged from 3.8% to 29.5%, with an overall infestation
rate of 12.3% [53]. Sheele et al. [54] surveyed 706 patients
in an emergency department in Cleveland, Ohio, about their
experiences with bed bugs. Of the 706 patients, 2% had a
current bed bug infestation, 37% had a history of bed bug
infestation, 15% currently knew someone with an active in-
festation, and 59% knew someone who had bed bug infesta-
tion within 5 years. It is estimated that 1 in 5 Americans ei-
ther has had a bed bug infestation in their home or knows
someone who has had a bed bug infestation [4]. Areas of
high occupant turnover, such as hotels (especially low budg-
et ones), motels, hostels, nursing homes, dormitories, low-
income, high-rise apartments, and shelters for the homeless
are more frequently affected [17, 29, 50, 55]. Bed bug infes-
tations are also common in refugee camps [22]. Other pre-
disposing factors include poverty, overcrowding, homeless-
ness, poor hygiene, and poor pest control [4, 17].
The recent resurgence in bed bugs especially in devel-
oped countries has been attributed to evolving resistance to
pesticides (e.g., pyrethroids, carbamates, organophosphates),
inadequate pest control programs, lack of public awareness,
more frequent travel (especially international travel), and
immigration [56-58]. Bed bugs are usually transported pas-
sively, mainly in luggage, book bags, clothing, and furniture
[2, 59, 60]. Less commonly, bed bugs may spread actively
from room to room in communities, such as through ventila-
tion ducts, power outlets, and electrical wiring [61]. Skin-to-
skin transfer of bed bugs is rare, owing to the nocturnal na-
ture of bedbugs and the fact that bedbugs tend to avoid mov-
ing hosts [10].
5. HISTOPATHOLOGY
Histologic examination of a classic lesion shows epider-
mal spongiosis, dermal edema, and perivascular eosinophilic
and lymphocytic infiltrates [4, 62]. Extravasated erythrocytes
may also be noted [21].
6. CLINICAL MANIFESTATIONS OF BED BUG
BITES
Typically, bed bug bites are painless [7, 63]. Clinically,
bites are distributed in exposed areas of the body which are
not covered by clothing, such as the arms, forearms, wrists,
legs, ankles, neck and face and are often noticed upon awak-
ening [16, 50, 64]. Bed bugs cannot bite through physical
barriers such as cloth or paper [21]. Local bite reactions de-
pend on the host's prior sensitivity. Approximately 50% of
individuals react to the first bite [62, 65].
Fig. (2). Bed bug bites presenting as erythematous macules and
papules (papular urticaria). (A higher resolution / colour version of
this figure is available in the electronic copy of the article).
Fig. (3). Erythematous urticarial papules (papular urticaria) result-
ing from bed bug bites. (A higher resolution / colour version of this
figure is available in the electronic copy of the article).
Typical reactions include pruritic, erythematous macules
and papules, also known as papular urticaria (Figs. 2 and 3)
which are usually 2 to 5 mm in diameter [17, 66]. Bites typi-
cally occur in clusters or in a linear (Fig. 4) or curvilinear
distribution (Fig. 5) [67-69]. Lesions that appear three in a
row (Fig. 6), colloquially referred to as the "breakfast, lunch,
and dinner" sign, are highly suggestive of bed bug bites [67-
71]. A small red (hemorrhagic) punctum may be visualized
at the center of the bite mark [8, 16]. Some lesions may have
140 Current Pediatric Reviews, 2024, Vo l . 20, No. 2 Leung et al.
a central crust or erosion (Fig. 7). Most lesions resolve with-
in one week [16, 20]. Some authors have noted that papules
on the upper eyelid associated with erythema and edema (the
"eyelid sign") consistent with arthropod bites are highly sug-
gestive of bites from bed bugs [62, 72]. Exaggerated local
reactions such as vesicles, urticarial wheals (Fig. 8), urticari-
al perilesional plaques, diffuse urticaria, bullae (Fig. 9), and
nodules (may be hemorrhagic) may occur in previously sen-
sitized individuals and these lesions are usually pruritic [2, 7,
73-80]. If there are large numbers of bites, lesions can be
generalized [63]. Reactions can be immediate or delayed up
to 2 weeks after a bite [16]. At times, skin reactions are so
minor that they go undetected, and the only evidence of a
bed bug may just be a small punctum [18]. Rarely, systemic
reactions such as asthma and anaphylaxis may occur [73,
81].
Fig. (4). Bed bug bites presenting as erythematous papules in a
linear configuration. (A higher resolution / colour version of this
figure is available in the electronic copy of the article).
Fig. (5). Bed bug bites presenting as erythematous papules in a
curvilinear configuration. (A higher resolution / colour version of
this figure is available in the electronic copy of the article).
Fig. (6). Three lesions in a row, colloquially referred to as the
"breakfast, lunch, and dinner" sign. (A higher resolution / colour
version of this figure is available in the electronic copy of the arti-
cle).
Fig. (7). Central crusts noted in some of bed bug bite lesions. (A
higher resolution / colour version of this figure is available in the
electronic copy of the article).
Fig. (8). Bed bug bites resulting in urticarial wheals. (A higher
resolution / colour version of this figure is available in the electron-
ic copy of the article).
Bed Bug Infestation Current Pediatric Reviews, 2024, Vol. 20, No. 2 141
Fig. (9). A bullous eruption resulting from a bed bug bite. (A higher
resolution / colour version of this figure is available in the electron-
ic copy of the article).
7. DIAGNOSIS
The diagnosis is suggested by the history (recent travel to
infested areas, poor home environment, residence within
building with known bed bug infestation, concurrent infesta-
tion among cohabitants, use of previously owned furniture),
clinical findings of bites (tiny hemorrhagic punctum, pruritic
erythematous maculopapules and wheals in clusters or linear
pattern in exposed areas of the body), and findings of flecks
of blood on bed linen, dark brown insect fecal droplets, exo-
skeleton casts, and identification of bed bugs in cracks and
crevices of mattress seams, box springs, and upholstered
furniture [16, 30]. Dermoscopy is a useful tool to observe the
tiny hemorrhagic punctum (bite spots) in a background of
diffuse erythema [82-84]. With heavy infestation, a pungent
“sickly sweet” malodor may be detected. In the majority of
cases, the diagnosis can be confirmed by visual identification
of the bed bug.
From a public health perspective, use of a trained bed
bug-detection dog is gaining popularity [80, 85-87]. In one
study, the diagnostic accuracy was 96.3% with a positive
predictive value of 83.3% and a negative predictive value of
99.1% [85]. Lateral flow strip tests for detecting specific
proteins in biological samples can be used for the detection
of the bed bug specific proteins in the sample, thus allowing
the diagnosis of bed bug infestation to be made without the
expertise of an entomologist [88]. Proper identification of
bedbug infestation is essential to guide treatment and eradi-
cation.
8. DIFFERENTIAL DIAGNOSIS
Swallow bugs (Cimex vicarius) and bat bugs (Cimex ad-
junctus) may incidentally bite humans although humans are
not the preferred host [22]. These bugs may produce bites
similar to bed bug bites. Examination of the insect by an
entomologist can aid in the diagnosis. In general, swallow
bugs are smaller than bed bugs, are grayish in color, have
long, fine body hairs, and visible antennae. Swallow bugs
infest the nests of swallow birds. Bat bugs have longer lat-
eral hairs (longer than the diameter of the eye) on the upper
thorax than in the bedbugs (shorter than the diameter of the
eye) and they stay close to their bat hosts and only wander to
other hosts when abandoned [22].
Bed bug bites should be differentiated from scabies and
other arthropod bites. Scabies, an infestation of the skin
caused by the mite Sarcoptes scabiei var. hominis, is charac-
terized by burrows, an erythematous papular eruption, and
intense pruritus typically worse at night [89, 90]. Burrows
which are pathognomonic of the disease, appear as serpigi-
nous grayish, whitish, reddish, or brownish lines several mil-
limeters long in the upper epidermis usually in the intertrigi-
nous regions and the interdigital web spaces. Finding the
mite, ova, or scybala on microscopic examination of scrap-
ings taken from skin lesions confirms the diagnosis. The use
of dermoscopy in patients with scabies reveals a sinuous
burrow with a brown jet-shaped triangular structure (“delta
wing jet” or “mini triangle” sign) composed of the pigment-
ed head and anterior legs of the mite. Flea bites are charac-
terized by irregular groups of multiple erythematous pruritic
wheals with a central punctum on the lower legs (especially
ankles) and are more often seen in pet owners [6, 91]. Mos-
quito bites present as urticarial papules and wheals and occur
on exposed areas only. Tick bites present as an asymptomat-
ic papule which may evolve into an annular lesion at the site
of a tick bite (in exposed areas of the body) in the case of
Lyme disease [91]. Central clearing of the lesion as the le-
sion expands, gives rise to “bull's eye” or “target” appear-
ance [91]. Tick bites are more commonly seen in pet owners
and hikers especially during the spring and summer.
Other differential diagnoses include drug eruptions, food
allergies, urticaria, chickenpox, contact dermatitis, erythema
multiforme, dermatitis herpetiformis, pityriasis lichenoides
et varioliformis acuta, prurigo nodularis, lymphomatoid pap-
ulosis, Grover disease, Sweet syndrome, Gianotti-Crosti
syndrome, and delusional parasitosis [92-104]. The distinc-
tive features of each condition usually allow for a straight-
forward differentiation from bed bug bites.
9. COMPLICATIONS
Post-inflammatory pigmentary changes may occur but
are usually transient [62]. Scratching can lead to secondary
bacterial infection including impetigo, cellulitis, folliculitis,
ecthyma, and lymphangitis usually caused by Staphylococ-
cus aureus or group A streptococci [13]. Scratching may
lead to excoriation and may increase the severity of existing
skin conditions, such as atopic dermatitis and psoriasis. Itch-
ing may lead to sleep deprivation, reduced ability to concen-
trate, tiredness, and somnolence [105].
With heavy infestations, iron deficiency anemia may re-
sult from chronic blood loss [43, 106-108]. Otitis externa has
been reported as a result of bed bug infestation in the ear
canal [82]. Rarely, bed bug bites may result in anaphylaxis
especially in individuals with a history of atopy [22].
Bed bug infestation can also lead to social stigmatization,
poor self-esteem, anxiety, nervousness, psychological dis-
tress, nightmares, hypervigilance, flashbacks, avoidance be-
haviors, depression, and posttraumatic stress disorder [45,
109-112]. One case of suicide resulting from bed bug infes-
tation has been reported [113].
142 Current Pediatric Reviews, 2024, Vo l . 20, No. 2 Leung et al.
Bed bug bites can have a significant adverse effect on
quality of life [6]. Also, the economic burden in the eradica-
tion of bed bug infestation can be substantial [6]. Although
pathogens such as hepatitis B virus, hepatitis C virus, human
immunodeficiency virus, Leishmania parasites, Francisella
tularensis, Borrelia burgdorferi, Bartonella quintana,
Wolbachia, Rickettsia parkeri, and Trypanosoma cruzi have
been detected in bed bugs, thus far, there is insufficient evi-
dence that bed bugs are involved in the transmission of these
infectious diseases to humans [114-119].
10. MANAGEMENT OF BED BUG BITES
Reactions to bed bug bites are self-limited and usually
spontaneously resolve within one to two weeks [22]. As
such, treatment is mainly symptomatic. Patients should be
advised to maintain good dermal hygiene and to avoid
scratching the lesions to reduce local reactions and to prevent
secondary bacterial infection. Topical pramoxine and oral
antihistamines (e.g., diphenhydramine, hydroxyzine, lorata-
dine, desloratadine, cetirizine, bilastine, rupatadine) can be
used to alleviate pruritus and can help with urticarial reac-
tions [23, 47, 120]. Topical corticosteroids can also be used,
if the eruption is significant enough, to control inflammation
and pruritus, and to hasten resolution of lesions [23]. In gen-
eral, the least potent corticosteroid that can control symp-
toms should be used. Oral corticosteroids should be consid-
ered for severe or diffuse bullous lesions [73]. Secondary
bacterial infection can be treated with topical antibiotics
(e.g., mupirocin, fusidic acid) and, in severe cases, with sys-
temic antibiotics [17, 23]. Severe systemic reactions such as
anaphylaxis may require treatment with intramuscular epi-
nephrine, oral antihistamines, and oral corticosteroids [17,
20, 47]. Psychologic support should be offered if needed,
especially for individuals with severe anxiety or secondary
delusional parasitosis [22].
A recent study on 20 children with recurrent papular urti-
caria due to bed bugs unresponsive to multiple treatments
(such as oral antihistamines, topical corticosteroids, eradica-
tion of bed bugs through application of insecticides in their
homes) treated with subcutaneous specific immunotherapy
(using whole body bed bug extract) showed significant im-
provement of papular urticaria [121]. The authors of the
study suggested that immunotherapy has a protective effect
against subsequent reactions to exposure to bed bugs by in-
creasing IgG4 [121]. Further studies are necessary to con-
firm or refute the above findings.
11. ERADICATION OF INFESTATION
Bed bugs are difficult to eradicate because they breed
quickly and are quite elusive [14]. In addition to the infested
rooms, the adjoining areas should be inspected and treated
meticulously. For eradication of bed bugs, integrated pest
management (IPM) may be an effective approach. The IPM
includes monitoring devices (active monitors include the use
of heat or carbon dioxide attractants and passive monitors
include the use of sticky pads for trapping), canine detection,
and judicious use of nonchemical and chemical treatments
known to be effective [122-124]. It has been shown that
blood deprivation combined with heat stress increases the
rate of eradication [125, 126]. Eradication of bed bug infesta-
tion requires the expertise of a professional exterminator
[14]. Patients should refrain from initiating control measures
themselves. Confirmation of live bed bugs two weeks after
appropriate treatment indicates continued infestation [78].
11.1. Non-chemical Interventions
Generally, nonchemical interventions have a more im-
mediate effect in reducing the number of bed bugs and are
less hazardous than chemical interventions [4]. Nonchemical
interventions include keeping affected areas clean and free of
clutter, vacuuming, use of equipment to heat room to a lethal
temperature (60°C) for bed bugs, steam treatment of furni-
ture, washing linens with hot water, placing infested items
into a freezer (temperature -17°C for at least two hours),
caulking wall holes and cracks where bugs can hide, mattress
encasements, proper disposal of highly infested items (sealed
in plastic), and placement of bed bug traps/interceptors (e.g.,
the “pitfall” style) at the base of beds and furniture [127-
132]. Most traps use heat or semiochemicals (e.g., carbon
dioxide, kairomones) to attract bed bugs.
11.2. Chemical Interventions
Chemical interventions involve the use of insecticides
such as synthetic pyrethroids (e.g., permethrin, cyperperme-
thrin, alpha-cyfluthrin, beta-cyfluthrin, deltamethrin, lamb-
da-cyhalothrin, bifenthrin), natural pyrethrins, silicates
(mostly diatomaceous earth dust [DED]), insect growth dis-
ruptors, formerly termed insect growth regulators, (e.g.,
lufenuron, novaluron, hydropene, methoprene, pyriproxy-
fen), carbamates (e.g., propoxur, carbaryl, bendiocarb, me-
toxadiazone), organophosphates (e.g., malathion, dichlorvos
[2,2-dichlorovinyl dimethyl phosphate] [DDVP], diazinon,
fenitrothion, trichlorfon, propetamphos, pirimiphos-methyl),
neonicotinoids (e.g., acetamiprid, clothianidin, fenthion, di-
notefuran, imidacloprid, nitenpyram, thiocloprid, thiameth-
oxam), diethyl-meta-toluamide (DEET), chlorfenapyr,
fipronil and plant essential oils [2, 62, 133, 134]. Application
of residual insecticides remains the primary choice for eradi-
cating bed bug infestations [133]. Insecticides can be applied
to cracks in furniture, seams and buttons of mattresses, walls,
and floors to eliminate bed bug infestation.
Insecticides should be used with caution to prevent over-
exposure and toxicity (in particular, cardiovascular and neu-
rologic toxicity), especially if there are young children or
pets around [135, 136]. One may want to note that DEET
may modify the feeding behavior of bed bugs, in the sense
that bed bugs exposed to DEET may take multiple blood
meals instead of a single blood meal [13]. Also, extensive
use of insecticides has resulted in resistance in bed bug
populations.
By far, pyrethroids are the most commonly used insecti-
cide for bed bug control [4]. Presumably, pyrethroids work
by blocking sodium channel repolarization of the neuron of
bed bugs through cell membrane channels with resultant
Bed Bug Infestation Current Pediatric Reviews, 2024, Vol. 20, No. 2 143
paralysis and eventual death [137-139]. Resistance to pyre-
throids is increasing and is a growing global concern [140-
148]. An important resistance mechanism against pyre-
throids is resistance of target site caused by point mutations
in voltage-gated sodium channel (VGSC) gene that results in
substitutions of the amino acid sequence of the VGSC pro-
tein (also known as knockdown resistance) [141-151]. Other
resistance mechanisms include increased activities of detoxi-
cation enzymes (such as hydrolytic esterases and microsomal
oxidases) and cuticle thickening as a result of overexpression
of cuticle depositing protein [152-154]. The addition of pip-
eronyl butoxide may increase the efficacy of permethrin by
overcoming the resistance mechanisms of some strains of
bed bugs [4]. Natural pyrethrins have been found to be less
effective.
Silicates work by absorbing lipids on the waxy surface of
the epicuticle of the bed bug [4]. Bed bugs exposed to sili-
cates can no longer maintain moisture and may die of dehy-
dration [4]. Silicates are available in an aerosol or dust for-
mulation. Several studies have shown dust-based formula-
tions provide longer residual protection than aerosols and are
therefore more efficacious [155, 156]. The advantages of
using silicates are very low mammalian toxicity, long shelf-
life, long residual life, and low possibility of resistance [4].
The main disadvantage is that silicates are slow acting and
may take up to 6 days to achieve 100% mortality in bed bugs
[4].
There are two main kinds of insect growth disruptors,
namely, chitin synthesis inhibitors (e.g., lufenuron, novalu-
ron) and juvenile hormone analogs, also known as juvenile
hormone mimics (e.g., hydropene, methoprene, pyriproxy-
fen) [157]. Chitin synthesis inhibitors interfere with the for-
mation of chitin. Juvenile hormone analogs work by disrupt-
ing the metamorphosis of nymphal stages of bed bugs, par-
ticularly at juvenile stages [4, 158]. Nymphs so treated tend
to die during subsequent molts [4]. Female nymphs are more
susceptible than male nymphs [158]. Although insect growth
disruptors are slower acting than neurotoxic insecticides,
they have a favorable safety profile, including low mamma-
lian toxicity [153].
Carbamate insecticides are N-methyl carbamates derived
from carbamic acid that cause reversible carbamylation of
acetylcholinesterase at neuromuscular junctions and neuronal
synapses [159, 160]. The resultant elevated acetylcholine
may lead to increased neurotransmitter signalling, hyperpo-
larization, paralysis of nerves and muscles, and ultimate
death of bed bugs [160]. An amino acid substitution muta-
tion F348Y at an acyl-binding site of the paralogous acetyl-
cholinesterase gene accounts for carbamate resistance in bed
bugs [161].
Organophosphate insecticides work by causing irreversi-
ble inhibition of acetylcholinesterase at neuromuscular junc-
tions and neuronal synapses [161]. In many countries, or-
ganophosphate insecticides are no longer available except in
impregnated strips [4]. DDVP, a volatile organophosphate
often formulated into resin strips, can be used for fumigation
of infested items which are placed into sealed plastic bags
with the strips [4, 162]. The efficacy can be increased with
the use of heat and air circulation which will increase the
volatility of DDVP [4, 162]. Substitution mutation of F348Y
of acetylcholinesterase gene contributes to organophosphate
resistance in bed bugs [161]. Penetration resistance through
remodelling or thickening may also contribute to resistance
to organophosphate insecticides [133, 152].
Neonicotinoids act selectively on the nicotinic acetylcho-
line receptors in the central nervous system of bed bugs,
leading to depolarization and continuous firing in post-
synaptic neurons, resulting in spastic paralysis and ultimate
death of bed bugs [163]. Although neonicotinoids are less
efficacious than some pyrethroids, they are efficacious
against some pyrethroid-resistant bed bugs [4, 164]. Com-
mercial formulations that contain a combination of a neon-
icotinoid and a pyrethroid are more efficacious in the treat-
ment of bed bug infestation than either neonicotinoid or py-
rethroid alone [165, 166].
Diethyl-meta-toluamide (DEET), a synthetic chemical
repellent, works by blocking the neuronal responses within
the olfactory receptor neurons or odorant receptors of bed
bugs to specific human odors [167]. In addition, DEET may
function as a stimulus that triggers avoidance behavior of
bed bugs in response to human odors [167]. The product
provides a high level of repellency against bed bugs [168,
169]. Pyrethroid resistance is associated with a decreased
DEET repellency [170].
Chlorfenapyr is a pro-insecticide derived from a class of
microbially produced compounds known as halogenated
pyrroles. The pro-insecticide is converted to an active toxic
metabolite (AC-303268) by cytochrome P450 monooxygen-
ases of the insect [171, 172]. AC-303268 disrupts oxidative
phosphorylation in the mitochondria, preventing the for-
mation of adenosine triphosphate (ATP), which is vital for
the survival of the insect [171, 172]. The product is available
in aerosol and liquid spray formulations. Although chlorfe-
napyr is slow acting and does not cause quick knockdown, it
has a long residual life and activity (up to 4 months) [164,
171, 173]. Chlorfenapyr is a nonrepellent and is effective
against all bed bugs strains including multiple insecticide-
resistant bed bugs [134, 172, 174]. The insecticide is particu-
larly effective against first-instar nymphs [175]. Studies have
shown that bloodmeal feeding increases the survival time of
bed bugs exposed to topical application and fresh or aged
residual deposits of chlorfenapyr [176, 177]. Chlorfenapyr
has a relatively low toxicity to humans [164, 178] and re-
sistance of bed bugs to chlorfenapyr is low [164].
Fipronil, a phenylpyrazole, works by blocking the ligand-
gated ion channel of the gamma aminobutyric acid (GABA)
receptor and glutamate-gated chloride channels of the bed
bug. This causes hyperexcitation of nerves and muscles with
eventual death of the insect. Fipronil, available as a spray
and powder, is highly effective against bed bugs [164, 179].
Synergism with piperonyl butoxide increases the susceptibil-
ity of bed bugs to fipronil [163].
Many essential oils from plants (such as coconut oil,
clove oil, tea tree oil, peppermint oil, lemongrass oil) have
144 Current Pediatric Reviews, 2024, Vo l . 20, No. 2 Leung et al.
insect repellent effects and insecticidal activities [180, 181].
Plant-derived essential oils have a favorable safety profile
and have been used for the control of bed bug infestations
[182-186].
12. PREVENTION
While awaiting eradication of bed bugs, it is reasonable
to apply permethrin 5% cream or 40% DEET before going to
bed to prevent bed bug bites [9].
Avoidance is the best means in the prevention of bed bug
bites. Individuals should carefully inspect unfamiliar sleep-
ing areas such as hotel rooms for bed bugs or their fecal
droplets prior to use, with particular attention to mattress
seams, crevices in box springs, and behind headboards [18,
20, 187]. Items purchased at second-hand stores or at garage
sales should be carefully inspected for bed bugs before these
items are brought into homes. Improving sanitation and in-
creasing public health education, along with improved pest
control strategies, can improve the control of bed bug popu-
lations [80].
13. PROGNOSIS
The overall prognosis is excellent as the local reactions
usually resolve within one to two weeks assuming bed bugs
have been eradicated from the sleeping areas of the patients
[20, 23].
CONCLUSION
In recent years, there has been a global resurgence of bed
bug infestations. As the infestations may cause diverse der-
mal reactions, stigmatization, emotional stress, significant
adverse effect on quality of life, and substantial socioeco-
nomic burden to society, their rapid detection and eradication
are of paramount importance. Consultation with a profes-
sional exterminator is recommended to fully eradicate the
infestation.
AUTHORS’ CONTRIBUTIONS
Professor Alexander K.C. Leung is the principal author.
Dr. Joseph M. Lam, Dr Benjamin Barankin, Dr Kin Fon
Leong and Professor Kam Lun Hon are coauthors. All the
authors contributed to drafting and revising the manuscript
and approved the final version submitted for publication.
LIST OF ABBREVIATIONS
ATP
=
Adenosine Triphosphate
C.
=
Cimex
DDVP
=
2,2-Dichlorovinyl Dimethyl Phosphate
DED
=
Diatomaceous Earth Dust
DEET
=
Diethyl-meta-toluamide
GABA
=
Gamma Aminobutyric Acid
IPM
=
Integrated Pest Management
MALDI-
TOF MS
=
Matrix-Assisted Laser Desorption/Ioniza-
tion Time
-of-
Flight Mass Spectrometry
VGSC
=
Voltage-gated Sodium Channel
CONSENT FOR PUBLICATION
Not applicable.
FUNDING
None.
CONFLICT OF INTEREST
Professor Alexander K.C. Leung is a section editor of
Current Pediatric Reviews.
ACKNOWLEDGEMENTS
Declared none.
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