Symposium: dermatology

Infections and infestations

of the skin in children
Nevianna Tomson
Jane C Sterling

Abstract
Infections and infestations of the skin form a large proportion of skin dis-
eases in children, especially in the tropics, but also in temperate areas.
In many instances, superficial skin infections can be self-limiting as long
as there is no impairment of the immune system, but some infections
are chronic even when the immune responses are intact. In this review,
we will concentrate on primary skin infections and infestations that are
common in Europe, those potentially serious if not recognised and those
in which recent advances have altered approach to management.

Figure 1 Crusted impetigo on the cheek.

be acting as a reservoir of infection with Staphylococcus carriage

within the nose or flexures.
Staphylococcus aureus toxin-mediated disease
Bullous impetigo and staphylococcal scalded skin syndromes:
superficial infection with an exfoliative toxin-producing strain
of S. aureus will cause bullous impetigo, but if the infection is
systemic, for instance in the soft tissue or throat, staphylococcal
scalded skin syndrome (SSSS) may develop. The toxin responsible for epidermolysis cleaves the desmoglein 1 molecule,
resulting in a loss of adhesion between keratinocytes within the
superficial epidermis.1 The surface layers of the skin separate
and peel off leaving a moist but not haemorrhagic superficial
erosion.
In bullous impetigo, the eruption arises at the site of inoculation and presents first with mild discomfort or irritation, evolving
rapidly to fragile fluid- or pus-filled blisters that produce little
crusting when they rupture (Figure 2). SSSS occurs most commonly in children or the elderly. The child is usually unwell and
pyrexial, presenting with skin discomfort mostly starting in the
flexures. The affected skin is erythematous and the condition
rapidly develops to superficial epidermal loss. Hospitalisation for
close monitoring, parenteral antibiotic and general supportive
measures is advised. If the skin surface loss is extensive and very
painful, treatment in a burns unit may be considered.

Keywords bacteria; fungus; infection; infestation; paediatrics; skin; virus

Bacterial infections
Impetigo
Impetigo contagiosa is a common infection in children caused most
frequently by Staphylococcus aureus, or by Streptococcus pyogenes
or a combination of the two. It is a superficial infection producing discomfort and mild irritation, with the classical appearances
of inflammation with yellowish crusting and superficial erosion
(Figure 1). Clearance of the infection usually occurs within a few
days of taking either topical or, if more widespread, systemic antibiotic, but antimicrobial therapy should be accompanied by soaking and removal of the crusts, which otherwise harbour bacteria.
Topical antibiotics suitable for localised impetigo include mupirocin and fusidic acid, although the latter is showing increasing
resistance. Systemic treatment is with flucloxacillin, erythromycin
or a cephalosporin. Community-acquired infection may be with
methicillin-resistant S. aureus so therapy should always be preceded by culture of crusts or a swab from the eroded area.
Children affected by impetigo usually remain well, but the
onset of fever, malaise or lymphadenopathy may suggest that the
organism is Streptococcus and that systemic spread of the infection or local cellulitis is developing.
Recurrences of impetigo are not uncommon in children with
atopic eczema, who have a high carriage rate of bacteria on the
skin. In non-eczematous children, repeated episodes of impetigo
should prompt a search for another family member who may

Nevianna Tomson MB ChB MRCP is Specialist Registrar in Dermatology at

Addenbrookes Hospital, Cambridge, UK.
Jane C Sterling MA MB BChir PhD FRCP FHEA is Consultant Dermatologist and
Senior Lecturer at the Departments of Dermatology and Medicine,
Addenbrookes Hospital, University of Cambridge, UK.

PAEDIATRICS AND CHILD HEALTH 17:10

Figure 2 Bullous impetigo with flaccid blisters.

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The diagnosis of both of these conditions may be clinical but

should always include surface swabs for identification and antibiotic sensitivity testing of the infecting organism and, in the case
of SSSS, a search for the focus of infection. Histology of either the
blister roof or a full-thickness biopsy of an early lesion will show
acantholysis of the epidermis as well an epidermal split within
the subcorneal upper epidermis.
The treatment of these conditions will include appropriate
antibiotic therapy as well as local and supportive treatment.2 The
skin surface should be kept clean and dry, but dressings will be
more comfortable when the erosions are most marked. Systemic
antibiotic therapy will produce the best control of the infection,
but if localised, bullous impetigo may be managed with topical antibiotics alone. The organisms will usually be sensitive to
standard anti-staphylococcal antibiotics such as flucloxacillin,
erythromycin or a cephalosporin.

and has both a high morbidity and a high mortality (1020%)

rate.5,7
Other bacterial skin infections include mycobacterial infections such as tuberculosis, leprosy and atypical mycobacteria.
Their effect worldwide is great but cannot be included in this
review. Protozoan infections such as leishmaniasis also affect
a large number of children in the Mediterranean region, Asia
and South America, but these have again been omitted from this
review.

Viral infections
Herpes simplex
Infection with the herpes simplex virus may affect the skin or
mucous membranes. Two antigenic types have been distinguished, type I usually causing herpes of the mouth, lips and
non-genital skin, and type II predominantly affecting the genital
area. In primary infections, a prodrome of fever, malaise and
tender lymphadenopathy typically occurs 37 days following
exposure. In children, 60% of primary herpes simplex infections
present as gingivostomatitis with mouth ulceration, vesicles over
the lips, sore throat and fever.8 Dysphagia and drooling due to
oedema, pain and ulceration of the oropharyngeal membranes
are common. Primary infection may be subclinical, but recurrent
episodes present with lesions on the vermillion border of the
lip, perioral skin, nasal mucosa or cheek. Localised tenderness
and burning is followed by painful vesicles on an erythematous
base that progress to pustules which may ulcerate. Reactivation
may be precipitated by various factors including fever, ultraviolet light, trauma and the menses.912 Episodes are self-limiting
with lesions crusting over and healing in 26 weeks. Often no
treatment is required, although antiviral therapy with aciclovir,
famciclovir or valaciclovir is available.
Complications of herpetic skin infection include herpes keratitis, encephalitis and eczema herpeticum (Kaposis varicelliform
eruption). Infants and children with atopic dermatitis are susceptible to generalised herpes simplex virus infection due to the disrupted epidermal barrier. Widespread vesicles may occur on the
skin even when the dermatitis is inactive, and are accompanied
by fever and lassitude. Treatment with aciclovir is necessary.

Toxic shock syndrome: staphylococcal toxic shock syndrome

was originally described and recognised in association with menstruation and tampon use, although it is now recognised to occur
just as commonly as a non-menstrual infection. The strains of
S. aureus causing toxic shock may carry genes responsible for the
production of the leukotoxin PantonValentine leukocidin.3 The
same bacterial enterotoxin, TSS toxin-1, can also be the cause
of a severe illness with widespread eruption in neonates, when
the condition is termed neonatal toxic shock syndrome-like exanthematous disease. Streptococcal infection is also recognised to
produce a similar toxic shock-like syndrome.
Children affected by toxic shock syndrome may have an obvious site of primary infection, but this is frequently not apparent.
The first signs are usually of general malaise, high pyrexia and
shock with a diffuse macular pale erythematous eruption.2
Following appropriate treatment and recovery, desquamation
follows approximately 2 weeks later. If antibacterial treatment
and resuscitation are delayed, there may be a failure of other
organs and a mortality of 510%.4
Necrotising fasciitis
This soft tissue bacterial infection has previously been called
progressive bacterial synergistic gangrene, bacterial Meleneys
synergistic gangrene and Fourniers gangrene. More than one
organism is usually identified in the affected tissue and blood,
and these can include Staphylocccus aureus (including methicillinresistant strains), Streptococcus pyogenes, Klebsiella pneumoniae
and other bacteria such as Bacteroides species. The condition
often starts with a small skin infection such as a boil or surface
wound, evolving into localised cellulitis that then spreads rapidly.
A high pyrexia and marked general malaise develop, and areas
of purplish discoloration can be seen within the cellulitic area.
Predisposing factors include diabetes, malnutrition, pre-existing
superficial skin infection and intravenous cannulae.5
Recognition and treatment must be rapid. Intravenous delivery of antibiotic is essential to provide an adequate tissue dose.
This must be started before microbiological confirmation and
should be broad spectrum, including anti-staphylococcal and
anti-streptococcal activity as well as efficacy against Gramnegative organisms.6 Gangrenous tissue is removed surgically,
often on more than one occasion, and full supportive and analgesic care will be required. The condition can evolve very rapidly

PAEDIATRICS AND CHILD HEALTH 17:10

Neonatal herpes: the incidence of neonatal herpes is rising, presently occurring in 1 in 20005000 deliveries.13 It usually develops
in the infants of mothers with active infection of the cervix, vulva
or perineum at the time of delivery. Women infected with their
first episode of genital herpes are much more likely to transmit
the infection to their neonate (3350%) than are women who
have recurrent herpes (3%).14 Localised or disseminated small
13 mm vesicles are present at birth or appear on the skin up
to 7 days after delivery and may progress to large, 1 cm bullous
lesions. Keratoconjunctivitis and chorioretinitis may occur. Disseminated infection presenting with encephalitis, liver or adrenal
involvement is associated with significant morbidity and mortality and has the worst prognosis. Elective caesarean section is
advisable in mothers with active genital herpes.
Varicella zoster (chickenpox)
Varicella typically affects children under the age of 10 years.
Spread is by droplets from the upper respiratory tract or contact
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Symposium: dermatology

from communal swimming pools and bathing facilities. The

incubation period is on average 4 months but may range between
1 and 20 months.

with infected vesicular fluid. Crops of lesions appear initially on

the trunk and spread to the face, scalp and limbs. Lesions begin as
faint erythematous macules that progress to oedematous papules
and then to vesicles within 2448 hours. Individual lesions develop
crusts that shed to leave shallow erosions. Crops of lesions appear
to reveal several stages of lesion at any one time. Lesions may
involve the mucous membranes of the conjunctiva, oral cavity
or nasal mucosa.9,15 Children are highly contagious from 2 days
before the onset of skin eruption to 5 or 6 days afterwards.
Healthy children need supportive treatment only, but 14%
require systemic antibiotics for secondary bacterial infection,
usually due to Staphylococcus aureus.8 In the immunocompromised child, severe generalised infection may develop, with
high fever, encephalitis, pneumonia, hepatitis or disseminated
intravascular coagulation requiring systemic antiviral therapy.
Reactivation of the latent varicella zoster viruses as herpes zoster is rare in childhood. It may be seen in immunocompromised
individuals or those who had a primary intrauterine infection or
acute varicella within the first year of life.16

Plane warts: these often persistent flesh-coloured, flat spots mainly

occur on the face, hands and limbs. They may be pigmented and
slightly raised. Lesions often occur in lines of trauma such as those
corresponding to scratching (the Koebner phenomenon).
Common warts: these discrete flesh-coloured papules have
a rough surface and may occur anywhere on the skin, but are
particularly common on the hands and feet.
Plantar warts: plantar warts (verrucas) can penetrate deeply
into the soles of feet due to body-weight pressure. They may
be painful and impair walking. Thrombosed capillaries are often
seen as black specks on their surface, which aids with differentiation from simple corns.
Mosaic warts: mosaic warts are particularly resistant to treatment and present as plaques of roughened skin on the soles and
palms that are usually asymptomatic.

Hand, foot and mouth

Hand, foot and mouth disease is caused by a coxsackievirus, usually strain A16 that enters through the buccal mucosa and small
intestine. Following 57 days of incubation, which may be accompanied by a mild prodrome of systemic disturbance, yellow vesicles
surrounded by erythema appear over the hands and feet. In the
mouth, vesicles easily rupture, leading to painful erosions. Lesions
differ from those of herpangia by being more anterior and erythematous.17 Diagnosis is made on clinical signs and may be confirmed
serologically with specific enteroviral IgM. Electron microscopy of
vesicular fluid, saliva or stool may be positive for enteroviruses.
Symptoms usually last for 7 days, and treatment is supportive.

Anogenital warts: anogenital warts in children are usually

caused by autoinoculation and are rarely secondary to sexual
abuse. Vertical infection to the newborn may occur following
delivery through an infected birth canal.
Warts involute spontaneously, and in children virtually all
warts disappear within 3 years.19 Although treatment is rarely
needed, children or their parents often request treatment due to
cosmetic concern or pain caused by the warts. Topical preparations containing salicylic acid or glutaraldehyde are often tried
first. Cryotherapy is painful and often better applied with a cotton bud rather than a cryospray in children. However, freezing
should be maintained for 5 seconds to be effective and this is
rarely possible in young children. Treatment should be repeated
at 24-weekly intervals. The response to treatment declines with
increasing duration of the wart.

Molluscum contagiosum
Infection with this pox virus occurs following contact with an
infected individual or contaminated object, for example swimming pools. Infection is more common in patients with disorders
of T-cell function, particularly atopic dermatitis, congenital immunodeficiency lymphoproliferative disorders and HIV infection.
Following an incubation period of up to 6 months, asymptomatic
flesh-coloured papules with a central depression (umbilication)
appear on the skin, predominantly on the face and neck. Whereas
in adults lesions on the genitals or lower abdomen are almost
invariably contracted during sexual activity, in children molluscum
are seen quite commonly on the genital, perineal and surrounding
skin and do not indicate abuse unless there are other suspicious
features. Individual lesions often become inflamed or eczematous
shortly before resolving spontaneously after about 2 months.
As lesions remain a source of infection, many parents press for
treatment. Cryotherapy may be used, although this may lead to
some scarring. Mild irritation with a diluted phenol or a salicylic
acid paint may speed clearance.18

Epidermodysplasia verruciformis: this rare autosomal recessive (occasionally autosomal dominant) disorder presents with
numerous rapidly growing warts in childhood. It usually results
from defective cell-mediated immunity with a reduction in Tcell numbers and function. Dysplasia and malignancy may occur,
and sunlight may act as a co-carcinogen as actinic keratosis,
Bowens disease and squamous cell carcinomas tend to occur on
sun-exposed skin.

Fungal infections
There are three common superficial fungal infections of childhood: dermatophytoses, tinea versicolor and candidiasis.
Tinea infections
Dermatophytoses or tineas are a group of superficial mycoses
caused by fungi that parasitize keratin-rich structures such as
the outer layer of the epidermis (stratum corneum), hair and
nails. The source of infection may be the geophylic dermatophytes found in soil (Trichophyton solum, Microsporum gypseum

Viral warts
Warts caused by human papillomavirus are a common infection
in children and adolescents, the highest incidence being between
the ages of 12 and 16 years. Spread is facilitated by local trauma,
and thus warts are typically found on the hands and feet. The
virus is usually contracted from other infected individuals or

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and Trichophyton mentagrophytes), zoophilic dermatophytes

that live on animals such as cats and dogs (Microsporum canis)
or androphilic dermatophytes from other parasitizes humans
(Trichophyton tonsurans, Trichophyton rubrum and Trichophyton floccosum).17 Species of dermatophyte are capable of producing several clinical manifestations in different parts of the body
and hence are divided into clinical forms according to regions of
the body they commonly affect. Scalp ringworm (tinea capitis)
is common in childhood but infections elsewhere are rare and
therefore not covered by this review.

the tongue, soft and hard palate, and buccal and gingival mucosae, which may be painful.
The diagnosis is confirmed on removal of part of the oral
plaque with a cotton bud and examination under the microscope
or by fungal culture. Nystatin oral suspension four times daily for
12 weeks is usually effective. Nystatin or clotrimazole tablets
may be used in older children.
Tinea versicolor/pityriasis versicolor
This common superficial skin infection in adolescents, caused
by the yeast forms of the lipophilic fungus Malassezia furfur,
rarely affects prepubertal children.25 It presents with multiple
asymptomatic, oval, scaly macules distributed mainly over the
sebum-rich skin on the upper trunk and proximal arms, occasionally extending to the face and neck. Lesions may be hypo- or
hyperpigmented depending on the patients complexion and sun
exposure. It may be difficult to distinguish pityriasis versicolor
from vitiligo, pityriasis alba, postinflammatory hypo- or hyperpigmentation, pityriasis rosea or tinea corporis. Examination
under Woods light usually reveals a golden yellow fluorescence,
and some lesions not obvious to the naked eye.25 Microscopy and
culture of skin scrapings from the affected area will confirm the
diagnosis, although it must be remembered that Malassezia is
part of the normal skin flora.
The condition responds readily to treatment, but recurrences
are common. Topical preparations are preferred in younger children. Selenium sulphide 2.5% shampoo applied for 10 minutes
daily over 12 weeks and/or ketoconazole 2% shampoo as a
single application or used daily for 3 days can be effective. Topical antifungal creams are usually impractical due to the large
surface area affected. In recurrent or persistent infections, oral
antifungal agents may be used.

Tinea capitis
Tinea capitis is a fungal infection of the skin and hair of the
scalp that primarily affects prepubertal children between the ages
of 3 and 7 years.4,20 Infection is usually due to T. tonsurans or
M. canis.9,2124 Boys are affected more commonly than girls, perhaps due to the shorter hair allowing easier access for infecting
fungal spores.25 Transmission of infection occurs via infected
skin scales and hairs shed from the infected human or animal
host, or through the use of contaminated combs, hairbrushes and
other hairdressing equipment. The short incubation period of
13 weeks is followed by a varied presentation dependent on
the infecting fungus and the host response.
Signs may be localised to one or more areas, or affect the scalp
in a diffuse manner. Alopecia is present with a variable degree
of erythema or scaling. Scalp pustules may also be present.20
The degree of inflammation is generally larger when zoophilic
fungi are the cause. A vigorous host immune response to the
dermatophyte may produce a boggy, tender plaque with pustules
and a purulent discharge and overlying alopecia (kerion). Unless
treated promptly, this may result in permanent scarring alopecia
due to the severe inflammatory response. An ultraviolet lamp
with a maximal emission at 365 nm (Woods lamp) can be used
to confirm infection with Microsporum species with bright green
fluorescence of infected hairs, in contrast to Trichophyton species
that show no fluorescence at all. Diagnosis is ideally confirmed
by the microscopic observation of fungal elements in specimens
of infected skin, hair obtained by scalp scrapings or hair plucked
from the affected site. Fungal culture of the specimens will confirm the infecting agent.
The only agent licensed for treating tinea capitis is griseofulvin 1020 mg/kg per day for a minimum of 6 weeks, although
treatment is usually necessary for 23 months.9,22,2529 Although
unlicensed in children, terbinafine 3 mg/kg per day for 24
weeks is also effective against T. tonsurans, but less efficacious
against M. canis.26,27,29 Topical antifungal agents cannot reach
the hyphae within the hair shaft and are ineffective for treatment, but ketoconazole 2% shampoo may be used twice weekly
to reduce infectivity.

Infestations
Head lice
Head lice infestation with Pediculus humanus capitis is a worldwide problem during childhood. The incidence is highest (215%)
in primary school-aged children and is influenced by fashion and
population density.30,31 Transfer of lice from person to person
is mainly though head-to-head contact, and it is believed that
transmission between children can be minimised by keeping
hair short or tied back. Recent evidence has shown that the lice
can survive away from the warmth of the body in bedding or
headwear for some hours and can also spread through fomite
transmission during hair drying and brushing, and by fabric that
has been in contact with the affected hair, such as hats, scarves
or bedding. Washing potentially infested fabric should be carried
out with either a wash or a drying cycle of 50 C or more.32 After
laying, the egg develops to a fertile adult in 9 days, living for
5 weeks. The female can lay an average of five eggs per day,
which hatch after 57 days.
Two main groups of insecticides, the organophosphates and
the pyrethroids, have useful effects against head lice, although
resistance against both is increasing. Both types of agent have
been shown to have increasing resistance,33 especially permethrin, which in one study was shown to be as high as 50%. Malathion 0.5% lotion left on the hair overnight produces a 4080%
clearance, killing both live lice and eggs. A shorter application

Candidiasis
Newborn infants are physiologically susceptible to candidal infections that mainly present as oral thrush or nappy rash candidiasis
but may occur as intertrigo, vulvovaginitis, angular cheilitis or
nail fold involvement (paronychia). Oral Candida infection in
newborn infants is usually derived from the infected maternal
vagina during birth.17 It may also be acquired from the skin of the
mothers breast or hands, or from inadequately sterilised feeding
bottles or pacifiers. It presents with adherent white patches over

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time of only 30 minutes appears to have a similar efficacy but

with reduced absorption into the skin.34 Permethrin 1% lotion
left overnight in hair is easy to use and safe in children but less
effective than other remedies.
Carbaryl is also a useful insecticide and is not absorbed into
skin, but concerns about possible carcinogenicity have led to
restrictions on its use. Ivermectin applied topically also shows
an insecticidal effect.35 Plant insecticides have also been shown
to confer superior insecticidal effects both on eggs and live lice
when combined with other agents.35 Neem oil prepared as a
shampoo36 is reported to be effective, although shampoo applications of other agents have often proved to have a lower cure
rate than lotions.
The most popular method of mechanically removing lice is
via wet combing, using hair conditioner to facilitate the combing combined with a narrow toothed comb (nit comb) to catch
the larger lice and remove them from the hair. To be effective,
this needs to be repeated regularly every 3 or 4 days for at least
2 weeks as it will only catch the larger lice and have no effect on
eggs or young lice.
In comparison with insecticidal methods, some studies have
found bug-busting to be as effective, although others have found
it to be less so.37,38 It is more difficult in children with long hair,
and as the process takes about 1530 minutes it can often be
impossible to do properly, especially in large families where
more than one child will often need treatment.
Methods to heat the hair have also shown some use,39 with
eggs being more susceptible than live lice to a 30-minute treatment with a warm-to-hot hairdryer.
The newest method for lice clearance is by suffocation of the
insects. This can be achieved by applying soft paraffin (very
messy), conditioner that is then allowed to dry in situ (timeconsuming)40 or a silicone-based lotion that has a very low
surface tension, which allows it to flow into the breathing apparatus of the live lice.41 To be effective, any of these methods is
best repeated twice weekly for at least 2 weeks to kill lice after
hatching. Although initially thought to be a useful means of head
lice control, there is some doubt about the ability of suffocation
methods to kill lice as they can survive by immobilisation for
several hours.
Head lice can act as agents for the transmission of other
diseases such as bartonella.42

adult female, once transmitted to a new host, will burrow into

the epidermis, where 1020 eggs (or even up to 50 eggs) are
laid per day. The eggs hatch after 34 days and develop into the
adult mite, which lives for 46 weeks. After 24 weeks, the host
immune response produces a reactive dermatitis that leads to
scratching and skin damage.
In infants, all areas of skin can show signs of infestation. Adult
palm and sole skin may be too thick for the mites to penetrate,
but the soles of infants and toddlers frequently show burrows
(Figure 3). The face and scalp can also be infested. In chronic
infection, a steady state of mite load is usually reached, and itching and subsequent scratching can keep mite numbers down.
In individuals who are immunosuppressed or unable to scratch,
including neonates, mite numbers can rise hugely, leading to
crusted scabies in which a hyperkeratotic dermatitis harbours
very a large number of mites.
Insecticides will kill adult scabies mites, although not all are
ovicidal. Permethrin 5% cream is safe and well tolerated by children.45 Left on overnight, the treatment is bathed off the following morning, and all bed linen and clothes are washed. All
members of the household should be treated at the same time.
To increase the cure rate, the treatment can be repeated a week
later.
Malathion, available in an aqueous or alcohol base, can be
applied to the full surface of the skin, although the alcohol-based
preparation is best not used in flexures and around the eyes and
genitalia, or if the skin is eroded. There are concerns over the
toxicity of malathion and also 1% lindane, which is now rarely
used. Other therapies suitable for use in children include sulphur
610% ointment (an 8090% cure rate), 10% crotamiton (with a
lower cure rate than other topical agents)46 and benzyl benzoate
10% lotion, although this preparation stings on application.
Oral ivermectin (200 g/kg as a single dose repeated after 14
days) has been found to be very effective in the treatment of
scabies47 but is probably best reserved for situations in which
topical therapies are difficult to use or mite resistance is suspected. Topical ivermectin also appears promising, and a trial
using 400 g/kg applied as a 1% solution on two occasions a
week apart has reported excellent cure rates.48
Crusted scabies is rarely cleared with topical scabicides alone.
Removal of the hyperkeratotic layers of the epidermis from the
skin, including the subungual areas, is essential to remove areas

Scabies
Infection with the mite Sarcoptes scabiei occurs throughout the
world but is especially common in poor communities with a high
population density and shared accommodation.43 The infestation
is characterised by intense itching, often worst at night, with
a papular excoriated rash most obvious on the hands, wrists,
and genitalia. The hallmark of scabies, the burrow, is usually
best seen in the fingerwebs, on the sides of the hands or on the
elbows or sides of the feet, where the use of the dermatoscope
can make it easier to visualise the 35 mm burrow with a darker
spot of the mite at the deeper end.
Transmission of the mite from person to person is most likely
within households in which close contact such as bed-sharing
permits the mites to move directly from skin to skin. Although
the mites are thin-shelled, they can survive away from the
warmth and humidity of the hosts body for about a day.44 An

Figure 3 Scabies. Papules and burrows on the sole of an infant.

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where the mites can persist. Preparations containing salicylic

acid can help to hasten the removal of thickened skin, but care
must be taken in young children owing to the potential risk of its
absorption.

21 Aly R. Ecology, epidemiology and diagnosis of tinea capitis. Pediatr

Infect Dis J 1999; 18(2): 1805.
22 Friedlander S. Tinea capitis: past, present and future. Curr Probl
Dermatol 2000; 12: 126.
23 Tack DA, Fleishcer Jr A, McMichael A, et al. The epidemic of tinea
capitis disproportionately affects school-aged African Americans.
Pediatr Dermatol 1999; 16(1): 75.
24 Hubbard TW. The predictive value of symptoms in diagnosing
childhood tinea capitis. Arch Pediatr Adolesc Med 1999; 153(11):
11503.
25 Clayton Y, Moore M. Superficial fungal infections.
In: Harper J, Oranje A, Prose N, eds. Textbook of Pediatric
Dermatology, 2nd edn. Oxford: Blackwell Publishing, 2006,
p. 542569.
26 Friedlander SF. The evolving role of itraconazole, fluconazole and
terbinafine in the treatment of tinea capitis. Pediatr Infect Dis J
1999; 18(2): 20510.
27 Bennett ML, Fleischer AB, Loveless JW, et al. Oral griseofulvin
remains the treatment of choice for tinea capitis in children.
Pediatr Dermatol 2000; 17(4): 3049.
28 Gupta AK, Hofstader SL, Adam P, et al. Tinea capitis: an overview
with emphasis on management. Pediatr Dermatol 1999; 16(3):
17189.
29 Krafchik B, Pelletier J. An open study of tinea capitis in 50 children
treated with a 2-week course of oral terbinafine. J Am Acad
Dermatol 1999; 41(1): 603.
30 Harris J, Crawshaw JG, Millership S. Incidence and prevalence of
head lice in a district health authority area. Commun Dis Public
Health 2003; 6(3): 2469.
31 Counahan M, Andrews R, Buttner P, et al. Head lice prevalence in
primary schools in Victoria, Australia. J Paediatr Child Health 2004;
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32 Izri A, Chosidow O. Efficacy of machine laundering to eradicate head
lice: recommendations to decontaminate washable clothes, linens,
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33 Kristensen M, Knorr M, Rasmussen AM, et al. Survey of permethrin
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34 Brand RM, Charron AR, Brand RE. Decreasing malathion application
time for lice treatment reduces transdermal absorption. Int J Pharm
2005; 301(12): 4853.
35 Burkhart CG, Burkhart CN. Head lice therapies revisited. Dermatol
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