S c a b i e s It c h

Arnaud Jannic, MDa,b,*, Charlotte Bernigaud, MDa,b, Emilie Brenaut, MDc,d,

Olivier Chosidow, MD, PhDa,e

KEYWORDS

Itch
Pruritus
Scabies
Sarcoptes scabiei

KEY POINTS

Scabies is a parasitic infestation of the skin caused by Sarcoptes scabiei, a mite present worldwide
that affects 100 to 130 million people yearly.

Itch is nearly continuously present during a scabies infestation; it is intense, generalized, and more
intense at night time.

Secondary bacterial infections caused by scratching behavior can have dramatic long-term conse-
quences, especially in tropical areas.

Psychosocial complications of the itch in scabies are known to have a strong impact on quality of life.

The latest insights into host-mite interactions open ways to better understand the mechanisms of
itch in scabies.

The itch in scabies is usually controlled after the use of specific treatments but in certain conditions
it may persist up to 2-4 weeks.

WHAT IS SCABIES? different populations.6 Tropical regions with low

Scabies is one of the first human diseases for
which the cause was known in the 17th century.1
It is a contagious parasitic skin infestation caused
by a mite, Sarcoptes scabiei variety hominis.
Scabies is present worldwide.2 According to the
Global Burden of Diseases study, 100 to 130
million people are infected yearly,3 and scabies
is responsible for 0.21% of disability-adjusted
life-years from all of the 315 conditions studied,
a relevant burden (even if scabies-related impe-
tigo was not taken into account).4,5 Scabies prev-
alence ranged from 0.2% to 71.4% depending on
resources are the most affected regions.4 In
wealthier countries, scabies can occur in both
sexes, in all age and in all socioeconomic groups.
When it comes to low-resource life conditions,
children (mostly under the age of 2) and disad-
vantaged populations are at greater risk.6 In
both conditions, outbreaks may be frequent,
requiring considerable resources to be managed,
especially when they occur in collectives or in
institutions.2
The scabies mite is an obligate human para-
site. The female mite burrows into the epidermis

Disclosure Statement: C. Bernigaud reports receiving a research grant from MSD France; a research support
from Bioderma Laboratoire Dermatologique and Codexial Dermatologie; and a travel grant from Medicines
Development. O. Chosidow reports receiving drugs donated free of charge for research from Codexial Derma-
tologie and MSD France, lecture fees from Zambon Laboratoire, Codexial Dermatologie, and MSD France. No
other potential conflict of interest was reported.
a
Dermatology Department, AP-HP, Hôpital Henri Mondor, 51 avenue du Maréchal de Lattre de Tassigny,
94010 Créteil, France; b Research Group Dynamyc, Ecole nationale vé té rinaire d’Alfort, Maisons-Alfort, Uni-
versité Paris-Est Créteil, EA7380, Créteil, France; c Dermatology Department, University hospital of Brest, 2
avenue Foch, 29200, Brest, France; d Laboratory on Interactions Neurons-Keratinocytes (LINK), University of
derm.theclinics.com

Western Brittany, EA4685, 29238 Brest, France; e EpiDermE, Epidé miologie en Dermatologie et Evaluation
des Thé rapeutiques, Université Paris-Est Créteil, EA 7379, 9400 Créteil, France
* Corresponding author. Dermatology Department, AP-HP, Hôpital Henri Mondor, 51 avenue du Maréchal de
Lattre de Tassigny, 94010 Créteil, France.
E-mail address: arnaud.jannic@aphp.fr

Dermatol Clin - (2018) -–-

https://doi.org/10.1016/j.det.2018.02.009
0733-8635/18/Ó 2018 Elsevier Inc. All rights reserved.
2 Jannic et al
after mating and lays eggs that hatch into a
larvae, followed by a nymph that reaches adult-
hood in 10 to 14 days.1 Scabies clinical manifes-
tations are caused by the direct effect of the
infestation by the mite, and by the hypersensitiv-
ity caused by the mites, their saliva, and other
products. Besides an intense itch, classic clinical
signs are burrows, vesicles, or papulo-nodular
erythematous lesions localized on the finger
webs, the wrists, the axillae, the breasts, the
buttock, or the genitalia (Fig. 1). Atypical forms
such as profuse or crusted scabies in immuno-
compromised patients, or superinfected scabies
(impetigo) in children, can be seen among spe-
cific populations. Crusted scabies is a rare and
severe clinical form, with localized or generalized
hyperkeratotic lesions due to a huge mite prolif-
eration.7 Diagnosis is based on patient history
and physical examination. Direct identification
of mites, eggs, or feces by microscopy or dermo-
scopy in characteristic lesions is supportive. The
confirmation of the diagnosis can be challenging
in classic scabies, as only 5 to 15 adult mites live
simultaneously on the host, whereas hundreds,
thousands, or even millions live on the host in
profuse/crusted scabies. Superinfection of le-
sions with bacteria may occur as the mite burrow
provides an entry point for pathogens into the
skin. These bacteria can cause local infections
that can become invasive or lead to delayed
complications.8,9 The public health burden
caused by scabies, far beyond just a simple itchy
rash, was for a long time underappreciated.
Recently, a global initiative driven by the Interna-
tional Alliance for the Control of Scabies
(IACS, http://www.controlscabies.org), aiming to
enhance the agenda for scabies control,10
fostered the addition of scabies to the World
Health Organization list of neglected tropical
Fig. 1. Papulo-nodular erythematous lesions and
scratching lesions observed on the arms and the
abdomen of a patient with a confirmed diagnosis of
scabies.
diseases11 (http://www.who.int/neglected_diseases/
diseases/en/).
SCABIES ITCH: CLINICAL ASPECTS
Characteristics
Itch is the cardinal symptom of scabies and is
often used as a major criterion to diagnose
scabies.12 Scabies should be suspected when-
ever a patient is suffering from itch and should
be ruled out by a careful physical examination
and parasitology test if needed. Regardless of
the clinical type of scabies, having an history of
itch within the family members, relatives, or sex-
ual partners is a strong diagnosis criterion. Its
absence does not eliminate the diagnosis. Actu-
ally, in an article by Boralevi and colleagues,13 an
itch shared within the family was present in only
50% of the cases. The itch is described to be
more intense during the night; however, this
characteristic seems to not be highly specific,
and also described in other dermatoses such
as psoriasis or atopic dermatitis.14–17 There are
only a few clinical studies with a limited number
of patients included that aimed to characterize
the itch in scabies. The primary characteristics
are presented in Table 1.
Prevalence
In several prospective and retrospective
studies, the itch is reported to be affecting
more than 90% of classic scabies patients.18–21
In the pediatric population, Boralevi and col-
leagues13 described the clinical characteristics
of 323 patients with scabies (divided into 3
age groups: <2 years old, 2 to 15 years old,
and >15 years old). Overall, itching was present
in 94.5% of the patients, regardless of their
age. Looking into subgroups, the itch was
less frequent in pediatric cases compared with
adults, and increased with age: 90.3% before
2 years old and 95.4% in 2 to 15 years old.13
In infants, the itch can be expressed by
crying, discomfort, irritability or difficulty to eat,
making the symptom difficult to assess and
define.2 This may justify the potential underesti-
mation and lower frequency of itch in this
population.
In 1976, Mellanby made the observation that
“in man it is the active finger nails of the host
which keep down the parasite population.”29
This statement may explain the apparition of
hyperinfested crusts in anatomic regions that
lack cutaneous sensation, and indeed itch
sensation (eg, after spinal injury, stroke, leprosy,
or syringomyelia) in patients diagnosed with
crusted scabies.26–28 Historically, the itch was
 Scabies Itch 3

Table 1
Primary characteristics of the scabies itch according to the different clinical forms

Prevalence of the Characteristics of the Physical Psychosocial

Clinical Types Itch Itch Complications Complications
Classic scabies 90%–100%13,18–21
Generalized and
GAS and S aureus
Disturbed sleep
intense superinfections
Low work

Sparing the head18  Local (impetigo, attendance

More intense excoriations) or
Loss of work
during the invasive productivity,
night13,14,18,22,23 infections and overall

Described as  Acute or delayed performance
stinging, burning poststreptococcal
Social
or crawling14,22 complications stigmatization

Associated with
Eczematization
Feeling of
heat sensation, shame
sweating, and
Sexual life
pain22 impairment

Increased with
heat, sweating, and
stress22

Decreased with
cool environment,
concentration at
work, or having a
bath22
Scabies 90.3% in infants
Affects the face and
School
affecting <2 y13 the scalp13 absenteeism
infants and 95.4% in children
In infants, it may be
Lack of
children between 2 and assessed by discom- concentration
15 y13 fort or crying or memory

May be more
Fatigue
intense during
Loss of perfor-
daytime (20% of mance at school
the cases)13
Crusted scabies Described as less
Hyperkeratosic
Same complications
Severe
frequent24 but lesions can be that in classic outbreaks
present in up present only in scabies around a case
to 100% in anatomic regions
General infectious
case series25,26 that lack complications
cutaneous (deeper fissures)
sensation26–28 and comorbidities

Sepsis

Death

Abbreviations: GAS, Group A Streptococcus; S aureus, Staphylococcus aureus.

described to be inexistent or less intense in Complications of Itch in scabies

crusted scabies compared with classic scabies,
The main complication of scabies is related to
and would decrease with the duration of the
secondary bacterial skin infections. Impetigo is
infestation. However, in crusted scabies case se-
a common complication of itch in scabies, partic-
ries, up to 100% of patients suffered from itch-
ularly in children, and in patients living in over-
ing.25,26 It is likely that the itch in crusted
crowded conditions in the tropics (eg, Australian
scabies may be overlooked. The rationale for
Aboriginal communities, the Fijis, and the Solomon
the absence of itch in such population could
islands in the Pacific area where the conditions
be explained by the incapacity to scratch in pa-
were well studied).6,19,30–33 The itch in scabies
tients with neurologic disabilities, or to report
may cause severe scratching behavior and conse-
the associated feeling (eg, in patients with cogni-
quently excoriations of skin lesions that are a port
tive disorders).
4 Jannic et al
of entry of bacteria penetrating the skin.19 The
most common pathogens known to be involved
are group A Streptococcus (GAS) and Staphylo-
coccus aureus. Scratching lesions seem more
frequent in scabies than in any other pruritic skin
conditions.14 Superinfection of the skin can lead
to local or general infectious complications (cellu-
litis, abscesses, lymphadenopathy, bacteremia) or
poststreptococcal complications (acute glomeru-
lonephritis, acute rheumatic fever, or rheumatic
heart disease).8,9,34–37 Recent molecular studies
have characterized several classes of scabies
mite complement inhibitors that counteract the
Table 2
Hypotheses regarding possible mechanisms involved in scabies itch based on known host-mite
interactions
Pathophysiology of Scabies
Direct scabies mite actions
TLR pathway activation56
Proteases present in mite feces
Direct action on keratinocytes
Proteins homologous with house dust
mite antigens58
Immune response against scabies54
Complement system activation
Eosinophil dermal infiltrates
Mast cell activation
Histamine
TNF-a
Tryptase
Macrophage implication
Prostaglandins and leukotrienes
T cell dermal infiltrates
CD41 (classic scabies)
CD81 (crusted scabies)
Th1 response (classic scabies)
CD41 and CD81 T cells
IFN-g, TNF-a, IL-2
Th2 response (crusted scabies)
Nonprotective allergy-like response
B cell activation
IL-4, IL-5, IL-13, IL-31
IgE, IgG
Secondary bacterial superinfections
Staphylococcal superantigens
TLR activation
Persistent infestation in absence of
treatment
Abbreviations: Ig, Immunoglobulin; IL, interleukin; TLR, Toll-like receptor.
host complement pathways in the mite-infected
skin, helping GAS and staphylococcal bacteria to
grow mutually.38–43
In crusted scabies, infectious complications
seem to be more severe. This can be due to pa-
tient comorbidities (eg, immunosuppression) and
deeper excoriations causing invasive infections
leading to severe sepsis.26,44
Apart from infectious complications, eczemati-
zation of scabies lesions may appear, often
misleading the initial diagnosis25 or delaying treat-
ment efficacy.45 This misdiagnosis can lead to
incorrect prescriptions of topical steroids, initially
Possible Involvement in Scabies Itch
Activation of TLR 3, 4, and 7 expressed on primary sensory
neurons57
Activation of protease-activated receptor-223
Release of protease activating protease-activated
prurireceptors52
IgE-mediate allergic response: mast cell activation and
histamine release
Mast cell activation59
Expression of neurotrophins52: cutaneous nerve sprouting
and myelinization of nerves
Activation of histamine H1 and H4 prurireceptors49,50
Activation of protease-activated prurireceptor by tryptase50
Itch potentiation50
Activation of cytokine prurireceptors by IFN-g and IL-249
Increase involvement of eosinophils
Activation of cytokine prurireceptors by IL-3123,50
Mast cells activation by IgE
Expression of IL-31 mRNA in the skin52
Activation of TLR 3,4 and 7 expressed on primary sensory
neurons57
Peripheral sensitization of prurireceptors: decreased
threshold for activation, increased responsiveness, and
presence of ongoing activity60

improving the itch but finally leading to an aggra-
vation of the infestation such as profuse or crusted
scabies, or further complications.25
In scabies, itch-associated sleep disturbances
are common in up to 90% of patients according
to several studies,13,19,46 with a high correlation
between the level of itch and disturbed sleep.32
The absence of sleep results in deleterious
effects on health, functionality, and emotional
well-being.23
Overall, patients with scabies present an
altered quality of life assessed by standardized
questionnaire (modified Dermatology Quality of
Life Index).18,46,47 Worth and colleagues46 have
demonstrated that the degree of impairment
increased in parallel with the itch severity.
The psychosocial and economic burden caused
by the scabies itch through the lack of sleep,
school absenteeism, or loss of work productivity
and performance is considerable and leads to an
exacerbation of poverty in affected populations.48
PATHOPHYSIOLOGY
There are no specific data available aiming to
describe the pathophysiology of itch in scabies,
and the molecular pathways linking scabies and
itch are still poorly understood. However, consid-
erable progress has been made in understanding
mechanisms involving the itch in general.23,49–53
These mechanisms, including different prurirecep-
tors and itch mediators, are described by Ethan A.
Lerner in “Pathophysiology of Chronic Itch,” in this
issue.
Table 3
Currently available treatments for scabies
Agents Dose
Oral treatment
Ivermectin 200 mg/kg of body
weight per os
Topical treatment
Permethrin 5% cream
Benzyl benzoate 10% or 25% lotion
Malathion 0.5% aqueous lotion
Ivermectin 1% lotion
Sulfur 6%–33% cream,
ointment or lotion
Synergized pyrethrins Foam preparation
Lindane 1% cream or lotion
Abbreviations: CDC, Centers for Disease Control and Prevention; EADV, European Academy of Dermatology and Venere-
ology; EU, European Union; FDA, US Food and Drug Administration.
Scabies Itch 5
The main immune response steps resulting in
scabies mite infestation have been described in
recent reviews.54,55 Briefly, the innate immune
system is primarily involved via the complement
system, which can be partially inhibited by pro-
teins produced by the mite. Mast cells, activated
by the complement system or immunoglobulin
E (IgE), and eosinophils are important effectors of
the immune response. The T cell-mediated
response is different in classic scabies or crusted
scabies. In classic scabies, Th1 response is
predominant, whereas in crusted scabies it is a
nonprotective allergy-like Th2 response. CD81 T
cells are major constituents of T cell dermal infil-
trates in crusted scabies and may be responsible
for keratinocyte apoptosis, leading to epidermal
hyperproliferation. Indeed, several hypotheses
have been formulated on how all these mecha-
nisms may lead to the itch sensation in scabies
and are presented in Table 2.
The establishment of a surrogate experimental
porcine model for scabies has facilitated moni-
toring the itch during the infestation and after treat-
ment.61 It might be a helpful tool in the future to
determine new insights into the pathogenesis
and the mechanisms underlying itch in scabies.
TREATMENT
Treatment of Scabies
Scabies itch is generally controlled after specific
scabies treatment, but can be persistent in the
case of other associated causes. The current
available agents for scabies are summarized in
Notes

Only oral treatment available

Used in mass population treatment63

Standard regimen for the CDC and EADV64

Standard regimen for the CDC and EADV

Standard regimen for the EADV

Low level of evidence

Neurotoxicity: no longer distributed in the EU and
warning for use by the FDA
6 Jannic et al

Table 4
Main causes of persistent itch after treatment. In case of delusions of parasitosis, experienced
dermatologists may also ensure its management

Cause Management Prevention

Cutaneous irritation
Overtreatment
Severe eczematous scabies
Contact dermatitis
Treatment failure
Low compliance
Resistance
Relapse
Delusions of parasitosis
Nonscabietic origin
From Chosidow O. Scabies and Pediculosis. Lancet 2000;355;9206;822; Reprinted with permission from Elsevier
(The Lancet).
Intensive emollients, with or
without mild topical steroids
Topical steroids
Further scabicide application
Change scabicide
Further scabicide application (eg,
of scalp, new treatment of all
contacts at the same time)
Psychiatric referral
Treatment of the underlying
cause
Limiting quantity prescribed
Nonirritant scabicide
Nonallergic scabicide
Good instructions and evaluation
of comprehension
Head-to-toe application,
treatment of all contacts at the
same time

Table 3. Both topical treatments and oral iver-
mectin have to be repeated 7 to 15 days apart.
Clothing, bedding, and towels should be decon-
taminated, and the patient’s close contacts should
be checked and receive full treatment systemati-
cally. In many therapeutic studies, the reduction
of the itch has helped assessing treatment effi-
cacy. All recommended scabies treatments have
shown equivalent efficiency on the itch even if
permethrin has shown a faster efficacy than oral
ivermectin.62
Other Measures
Nonspecific medications may help reducing the
itch in scabies. The use of emollients to restore
the skin barrier impaired by the infestation should
be widely used, especially in cases with important
skin irritation caused by the infestation or the treat-
ment. Antihistamines may help, mainly sedative
antihistamines that help patients to sleep, even if
histamine is not considered as the main mediator
implicated in scabies itch.
Causes of Persistent Itch After Treatment
The itch may persist up to 2 to 4 weeks after an
efficient treatment.2 After this period, different
causes should be investigated and are explored
in Table 4.
Patients suffering from delusional parasitosis
are frequently incriminating scabies,65 but clinical
aspects of this condition are distinct from scabies.
This condition is described by Jason Reichenberg
and Anna Buteaus’ article, “Psychogenic Pruritus
and Its Management,” in this issue.
SUMMARY
Although itch is the cardinal symptom of
scabies, causing severe somatic and psychoso-
cial complications, its pathophysiological mech-
anisms remain underappreciated and poorly
understood. Better knowledge on how the
infestation with scabies mites leads to the itch
feeling may help to manage it better and pro-
pose more specific/targeted treatment in the
near future.
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