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Cutaneous Tuberculosis in Children

Gomathy Sethuraman, M.D.,* and Venkatesh Ramesh, M.D.


*Department of Dermatology, All India Institute of Medical Sciences, New Delhi, India, Department of
Dermatology, Safdarjung Hospital, New Delhi, India
Abstract: Cutaneous tuberculosis is a rare form of extrapulmonary
tuberculosis that accounts for 1% to 2% of cases. Childhood skin
tuberculosis represents 18% to 82% of all cutaneous tuberculosis cases.
Scrofuloderma andlupus vulgaris are the twomost common clinical forms in
children. An increase in the number of tuberculids, especially lichen
scrofulosorum, has been observed in the last several years. Cutaneous
tuberculosis in children can be severe and have a protracted course. Multi-
plicity of lesions and multifocal disseminated involvement in scrofuloderma
and lupus vulgaris is common. Scrofuloderma progressing to gummatous
lesions (scrofulous gumma) is mostly described in children. Morbidities and
deformities are more severe in children.
Tuberculosis in children remains a major health
problem worldwide, especially in developing countries.
Of the estimated 9 million annual tuberculosis cases,
approximately 1 million(11%) occur inchildrenyounger
than 15 years of age. The estimated annual risk of
tuberculosis in children living in developing countries is
2.5%. Pulmonary tuberculosis has been the most com-
monforminchildren, but there has beenasteadyincrease
in the number of cases of extrapulmonary tuberculosis,
especially tuberculous lymphadenitis. During the last
several years, extrapulmonary tuberculous infections
have outnumbered cases of pulmonary tuberculosis (1).
Cutaneous tuberculosis is a rare form of extrapul-
monary tuberculosis that accounts for approximately
1% to 2% of cases (2,3). The clinical presentation is
diverse. The spectrum of skin tuberculosis in children is
comparable with that in adults, but extensive and
disseminated involvement with several unusual variants
and systemic involvement are more common in children.
Delay in diagnosis and treatment can cause serious
morbidity and disability in children. In this review we
focus on the clinical spectrum, diagnosis, and treatment
of skin tuberculosis in children.
EPIDEMIOLOGY
Cutaneous tuberculosis is a chronic granulomatous dis-
ease caused by Mycobacteriumtuberculosis and rarely by
Mycobacterium bovis. Rarely children may develop skin
tuberculosis after Bacillus CalmetteGue rin (BCG)
vaccination. Most published studies in childhood skin
tuberculosis are fromdeveloping countries, and much of
the epidemiological data reects disease in southeast
Asia. In India, the reported prevalence of childhood skin
tuberculosis varies from18%to 54%(38). Pakistan has
recorded the highest prevalence of childhood skin
tuberculosis, with 82% of all skin tuberculosis being
reported in children. Sixty-nine (45.1%) cases were
Address correspondence to Gomathy Sethuraman, M.D.,
Department of Dermatology, All India Institute of Medical sci-
ences, New Delhi 110 029, India, or e-mail: kgsethu@yahoo.com
or aiimsgsr@gmail.com.
DOI: 10.1111/j.1525-1470.2012.01794.x
2012 Wiley Periodicals, Inc. 7
Pediatric Dermatology Vol. 30 No. 1 716, 2013
children younger than 10 years old and 57 (37.2%) were
age 10 to 20 years (9). In a hospital-based study of 26
cases over a period of 20 years in Tunisia, childhood
cases accounted for only 6% (10). In a 2-year study of
202 cases of skin tuberculosis in Ethiopia, the prevalence
of childhood tuberculosis was 24.3% (11).
Predisposing factors for cutaneous tuberculosis in-
clude poverty, malnutrition, poor living conditions, the
emergence of drug-resistant M. tuberculosis, and the
human immunodeciency virus (HIV). Cutaneous
tuberculosis is usually seen in children ages 1014 years,
although it can be seen in any age group, including
newborns and neonates. Sex distribution is variable in
dierent studies, but there does not appear to be a
signicant dierence in male-to-female ratio (12). The
two most common forms of childhood cutaneous
tuberculosis are lupus vulgaris and scrofuloderma (3,7
9). An increase in the number of tuberculids, especially
lichen scrofulosorum, has been observed in the last
several years (3,8).
PATHOGENESIS AND CLASSIFICATION
Cutaneous tuberculosis manifests in several clinical
forms. It may occur as a result of exogenous inoculation
of tuberculosis or endogenous spread of the organisms.
Exogenous inoculation of organisms may produce an
asymptomatic papule, plaque, or nodule that can ulcer-
ate or eventually heal with scarring. Inoculation
tuberculosis may be associated with regional lymphade-
nopathy. Endogenous tuberculosis spreads tothe skinby
contiguous spread (scrofuloderma, oricial tuberculo-
sis), hematogenous spread (lupus vulgaris, tuberculous
gumma, and miliary tuberculosis), or lymphatic spread
(lupus vulgaris). Tuberculids are delayed-type hyper-
sensitivity reactions to M. tuberculosis (12).
A simple classication system of cutaneous
tuberculosis includes true primary and secondary skin
tuberculosis and tuberculids. True skin tuberculosis is
further divided into primary and secondary tuberculosis
depending on previous sensitization to the mycobacte-
rium (Table 1).
SCROFULODERMA
Scrofuloderma is the most common form of childhood
cutaneous tuberculosis in Africa and developing
countries (11). In India, scrofuloderma was reported in
36.5% of cases (7), while Bhutto et al reported it in
48% (33 69) of cases aecting children younger than
10 years in Pakistan (9). Scrofuloderma usually devel-
ops from the contiguous spread of infection from un-
derlying tuberculous focus, most often from the
cervical group of lymph nodes. Inguinal, axillary,
parasternal, preauricular, postauricular, occipital, sub-
mandibular, epitrochlear and supraclavicular are the
other groups of lymph nodes that can be involved.
Scrofuloderma can also develop from the tuberculous
focus in the bones, joints, testes, breasts. and lacrimal
glands (3,6,13).
Clinically scrofuloderma begins as asymptomatic
subcutaneous swellings that may persist for several
months. As the lesions grow, they softenandbreakdown
to form ulcers or discharging sinuses. Ulcers are usually
shallow and undermined and have bluish margins. In
children, the lesions can be multiple and sometimes
widespread (Fig. 1AD). Scrofuloderma may heal
spontaneously over a period of years. The typical cere-
briform or bridging scars are diagnostic of a healed
scrofuloderma (Fig. 2A,B) (7,12). Several unusual vari-
ants of scrofuloderma can occur in children, such as
multifocal involvement of cervical, axillary, and inguinal
lymph nodes; symmetrical scrofuloderma involving the
bilateral feet; and linear sporotrichoid lesions (7,1216).
Insevere cases, scrofuloderma canmanifest as scrofulous
gumma that is characterized by multiple swellings and
sinuses with irregular nger-like extensions involving
larger areas (Fig. 3). In one study scrofulous gummas
have been described in ve of 28 children with scrofulo-
derma (7). Scrofuloderma can be associated with an
underlying systemic tuberculous focus in up to 66% of
cases (3). In a study of skin tuberculosis in children,
pulmonary involvement was the most common focus
seen (45% [9 20] of cases) followed by bone (35%
[7 20]), lung and bone involvement (15% [3 20]), and
abdominal tuberculosis (5% [1 20]) (3).
A skin biopsy should be taken from the edge of the
sinus, whichwill showtuberculoidgranuloma along with
neutrophils, eosinophils, and necrosis. Organisms may
be identied in biopsies or cytologic smears (7,17). In
a study by Terranova et al (11) from Ethiopia, the
organisms were always identied in one or two samples
in cytology smears.
TABLE 1. Classication of Skin Tuberculosis in Children
Primary tuberculosis
Tuberculous chancre
Miliary tuberculosis
Secondary tuberculosis
Lupus vulgaris
Scrofuloderma
Tuberculosis verrucosa cutis
Tuberculous gumma (metastatic abscess)
Oricial tuberculosis
Tuberculids
Micropapularlichen scrofulosorum
Papularpapulonecrotic tuberculid
Nodularnodular tuberculid (erythema induratum)
8 Pediatric Dermatology Vol. 30 No. 1 January February 2013
LUPUS VULGARIS
Lupus vulgaris is the most common form of cutaneous
tuberculosis, seen in 41% (52 126) of aected children
and adolescents in Pakistan (9). It was seen in 68% of
the children in a study of Ramesh et al (7). In an Ethi-
opian study of skin tuberculosis, none of the children
had lupus vulgaris (11). Clinically, lupus vulgaris is a
slowly progressive form of cutaneous tuberculosis that
occurs in individuals with previous sensitization and
moderate immunity. The head and neck are the usual
sites of involvement in most individuals. In India, lupus
vulgaris in children commonly occurs on the lower
extremities and gluteal region as a result of inoculation
tuberculosis. The lesions are solitary but multifocal, and
multiple lesions can occur in children. It begins as slowly
progressing asymptomatic papules and plaques. The
plaque is the result of the coalescing microgranuloma-
tous papules that can be seen as soft, reddish-brown,
apple jelly nodules on diascopy. The lesions are
usually dry, but occasionally there may be thin sero-
sanguineous or purulent discharge and surface crusting
due to secondary bacterial infection. The enlarging
plaque shows an active peripheral margin with erythema
and inltration and central atrophy and scarring
(Fig. 4A,B). Sometimes there can be involution and
scarring in one area or corner of the lesion and pro-
gression in another area, resulting in a geographic or
A B
C D
Figure 1. Scrofuloderma: (A) subcutaneous abscess before rupturing; (BD) typical undermined ulcers with bluish margins.
A B
Figure 2. Scrofuloderma: (A) healing lesion; (B) typical scar of scrofuloderma.
Sethuraman and Ramesh: Skin Tuberculosis in Children 9
gyrate outline. Severe brosis, contractures of the joints,
and mutilation may occur in some children. Lupus
vulgaris may aect the oral, nasal, or genital mucosae as
an extension of the skin lesions (7).
Five clinical variants of lupus vulgaris have been de-
scribed in children: keratotic, hypertrophic, atrophic,
ulcerative, and plane forms. Of these, keratotic is the
most common formof lupus vulgaris (7). Bhutto et al (9)
reported nodular, papular, erythematous, and psoriasi-
form types. The other unusual clinical variants of lupus
vulgaris reported in children are kissing lupus vulgaris,
involving the gluteal cleft, and multifocal lesions,
involving the head and neck area, extremities, and
mucosae (7,12). Symmetrical lupus vulgaris (possiblydue
to exogenous inoculation of the organism) involving the
knees and ankles and with a sporotrichoid pattern due to
lymphatic spread have been described (16,18). Rarely
lupus vulgaris can develop in the vicinity of a scrofulo-
derma sinus as a result of autoinoculation tuberculosis
(7,12). The occurrence of lupus vulgaris after BCG vac-
cination has also been described (Fig. 5). Constitutional
symptoms are usuallyabsent. Systemic tuberculous focus
can be seen in the lymph nodes, lungs, and liver. In one
study, lymphadenopathy was described in 37 of 40 chil-
dren with lupus vulgaris, pulmonary involvement in 3
and paravertebral abscess in 1 (7). Biopsy fromthe active
margin shows tuberculoid granulomas with Langhans
giant cells. Epidermal hyperplasia is usually marked.
Necrosis is absent (17).
TUBERCULOSIS VERRUCOSA CUTIS
Tuberculosis verrucosa cutis is seen in 4.4% to 16% of
pediatric skin tuberculosis (3,9). Alarge number of cases
have been reported in Pakistan. Eight of 29 cases were
younger than 10 years, and 12 were ages 11 to 20 years
(9). It occurs as a result of exogenous inoculation
tuberculosis in previously sensitized individuals. In chil-
dren, the exposed parts of the lower extremities are
commonly aected due to the inoculation of M.
tuberculosis by unnoticed trauma. Typically a lesion is a
hyperkeratotic or verrucous plaque with an inamma-
tory areola. With progression of the lesion, the plaque
becomes larger and may involve the entire sole or foot.
The surface may show ssures or clefts with exudation
and crusting. Irregular extension of the lesions may lead
toa serpiginous outline withinvolutionat the center, and
it may resemble lupus vulgaris and hence is considered to
be the hypertrophic variant of lupus vulgaris. Anoma-
lous forms such as deeply destructive papillomatous and
sclerotic variants withdeformities of the limbs may occur
in children. Symmetrical bilateral tuberculosis verrucosa
cutis on the extremities have been described (14). Con-
stitutional symptoms are usually absent. Lymph nodes
maybe enlarged(7,12). Skinbiopsyshouldbe takenfrom
the least keratotic area and should be deep enough to
include the underlying indurated lesion. It shows epi-
thelioid cell granulomas admixed with lymphocytes and
plasma cells along with massive pseudoepitheliomatous
hyperplasia (17).
A B
Figure 4. Lupus vulgaris: (A) large erythematous and inltrated plaque with active margin and scarring in the center; (B)
erythematous plaque showing active lesion on one side and scarring on the other side of the lesion.
Figure 3. Scrofulous gumma.
10 Pediatric Dermatology Vol. 30 No. 1 January February 2013
TUBERCULOUS GUMMA
Tuberculous gumma represents 1.3% to 2% of skin
tuberculosis in children (4,8). It is otherwise known as
tuberculous metastatic abscess and is the result of
hematogenous dissemination of the organisms from a
primary focus during periods of lowered resistance. This
form has been infrequently reported in children with
malnutrition, immunosuppression, or lymphomas. It
can be considered to be the severe variant of scrofulo-
derma. It presents as several soft subcutaneous swellings
that break down to form ulcers or sinuses. Sometimes it
can present as multiple conuent swellings and sinuses
aecting contiguous groups of lymph nodes with nger-
like extensions radiating across the neck or chest wall (7).
Biopsy shows massive necrosis and acid-fast bacilli.
Tubercle bacilli can usually be isolated fromthe pus (17).
PRIMARY TUBERCULOUS CHANCRE
Tuberculous chancre is extremely rare in children. It has
not been reported in any of the large series of childhood
tuberculosis (3,68,11). It occurs in previously nonsen-
sitized individuals. In children, the face and limbs are the
sites of predilection. The lesion develops at the site of
inoculation of the organism, which is usually introduced
at the site of minor trauma such as injections, ritual cir-
cumcision, ear piercing, and tattooing. The lesion begins
as an asymptomatic papule or nodule that ulcerates. The
ulcer is granulomatous and shallow, with undermined
bluish margins. Regional lymphadenopathy develops in
4 to 8 weeks and may break down to form a discharging
sinus. Any painless nonhealing ulcer with regional
lymphadenopathy in a child should arouse suspicion.
The clinical variants include granulomatous conjuncti-
vitis, gingivitis, paronychia, and dactylitis (4,12).
TUBERCULOSIS CUTIS ORIFICIALIS
Autoinoculation of the organisms in individuals with
abdominal or pulmonary tuberculosis causes tubercu-
losis cutis oricialis. The lesions most commonly occur in
the mouth or less commonly around the genital or anal
mucosae. It is rare in children. Bhutto et al (9) described
oricial tuberculosis in four patients younger than
20 years that involved the genital and anal mucosal
areas. It presents as a shallow granulomatous ulcer with
undermined bluish edges that is characteristically painful
(12).
ACUTE MILIARY TUBERCULOSIS
Hematogenous dissemination of M. tuberculosis causes
acute miliary tuberculosis. The cutaneous lesions are
nonspecic. It presents as widespread erythematous
papules, pustules, or vesicles. Aected individuals are
seriouslyill withsevereconstitutional symptoms. Internal
organs are usually aected, especially the lungs and
meninges. Tuberculin skin test is negative (12). Skin
biopsy shows acute inammatory cells with numerous
microabscesses. Theorganisms canbedemonstrated(17).
TUBERCULIDS
Tuberculids are delayed-type hypersensitivity reactions
to M. tuberculosis that occur in children with good
immune response. The diagnostic criteria include tuber-
culoid histology on skin biopsy, strongly positive Man-
toux reaction, absence of M. tuberculosis in the smear
and negative culture, and resolution of skin lesions with
antituberculous therapy. Lichen scrofulosorum (micro-
papular tuberculid), papulonecrotic tuberculid (papu-
lar), and erythema induratum (nodular tuberculid) are
considered to be tuberculids. Erythema nodosum is a
facultative tuberculid in which M. tuberculosis is one of
many causative factors. Although the smear and culture
are negative for M. tuberculosis, polymerase chain reac-
tion (PCR) techniques have identied mycobacterial
DNAin the lesional tissue of all types of tuberculids (12).
LICHEN SCROFULOSORUM
Lichen scrofulosorum is the most common tuberculid
reported in children (3,8). In a prospective study of 511
Figure 5. Lupus vulgaris occurring on a BCG scar.
Sethuraman and Ramesh: Skin Tuberculosis in Children 11
patients (children and adults) with cutaneous tubercu-
losis, lichen scrofulosorum was observed in 39 (7.6%)
(19). Of these, 84%were children. Lichen scrofulosorum
was the second most common type of tuberculosis, seen
in 23.5% (16 68) and 33% (34 103) of children in two
hospital-based studies (3,8). Lichen scrofulosorum is
mostly seen in association with M. tuberculosis and
rarely with Mycobacterium avium and Mycobacterium
szulgai infections. It has also been reported after BCG
vaccination (19).
The lesions of lichen scrofulosorum consist of
asymptomatic, pin headsize, skin-colored to erythem-
atous, lichenoid, rm, follicular and parafollicular pap-
ules (Figs. 6A,B and 7). Sometimes the tiny papules are
arranged in groups or in a discoid pattern. The papules
are at topped or spiny. Micropustules or central
adherent crusts may also be seen. The lesions are mostly
seen on the trunk and proximal extremities. Skin biopsy
fromthe lesion demonstrates epithelioid cell granulomas
around the follicles or sweat ducts (1923).
An underlying tuberculous focus can be seen in up to
73% of cases. Lymph node tuberculosis (especially cer-
vical, hilar, and mediastinal) may be present in 65% of
cases (20,22). The other foci can be the lungs or bone.
Recently, extensive and inammatory psoriasiform
lichenscrofulosorumwas describedina16-year-oldchild
who also had disseminated tuberculous focus in the
lungs, several groups of nodes, and the liver (20). Lichen
scrofulosorummay occur in association with other types
of cutaneous tuberculosis suchas scrofuloderma(Fig. 7),
lupus vulgaris, and erythema induratum (12,20).
PAPULONECROTIC TUBERCULIDS
Papulonecrotic tuberculids represent 4% of pediatric
skin tuberculosis (8). The lesions consist of asymptom-
atic symmetrical eruptions of necrotizing papulonodular
lesions that heal with varioliform atrophic scars. The
acral extremities andearlobes are the sites of predilection,
but localized lesions can occur on the face and buttocks.
Isolated childhood vulval papulonecrotic tuberculid
(genital tuberculid) has been described (24). Papulone-
crotic tuberculids inchildrenhave beenreportedtooccur
with active pulmonary and lymph node tuberculosis.
Phlyctenular conjunctivitis is also often associated in
children. In a series of eight children with papulonecrotic
tuberculid, associated pulmonary tuberculosis was
present in seven, hepatomegaly in four, lymphadenopa-
thy in three, phlyctenular conjunctivitis in three, and
splenomegaly in two (25). Skin biopsy reveals wedge-
shaped necrosis of the epidermis, upper dermis, and
adjacent follicle along with underlying epithelioid cell
granulomas (25).
A B
Figure 6. (A, B) Lichen scrofulosorum.
Figure 7. Lichen scrofulosorum with scrofuloderma on the
neck.
12 Pediatric Dermatology Vol. 30 No. 1 January February 2013
ERYTHEMA INDURATUM
Erythema induratum is rare in children. It has not been
reported in any of the larger published series (3,68), but
several cases have been reported from South Africa (26).
It represents a nodular panniculitis related to M. tuber-
culosis. Clinically it manifests as dull red or bluish red
nodules onthe posterior aspect of the legs. It canbe single
or multiple and can be 1 cm or larger in diameter.
Ulceration may occur. Skin biopsy shows a granuloma-
tous panniculitis with necrosis and vasculitis (small or
medium vessel). It is frequently associated with pulmo-
nary tuberculosis (26).
SPOROTRICHOID SKIN TUBERCULOSIS IN
CHILDREN
Sporotrichoid lesions refer to conditions that mimic the
chronic granulomatous infection of the skin and
subcutaneous tissue caused by Sporothrix schenckii (27).
Typically the lesions have a linear (lymphatic) arrange-
ment as a result of lymphatic spreadof the infectionfrom
a primary entry focus in the skin. In countries where
tuberculosis is endemic, M. tuberculosis rarely manifests
inthis sporotrichoidform. Mostly it has been reported in
children from developing countries. Recently it has also
been reported in children from Canada and Hungary
(27,28). This sporotrichoidformhas beenreportedin3%
of cases (Fig. 8) (16). Scrofuloderma and lupus vulgaris
canpresent inthis form. Sometimes, cord-like thickening
of the lymphatics between the lesions may occur, as in
cases of sporotrichosis, but regional lymphadenopathy
and ulceration is more often seen in tuberculosis. Agood
lymphatic drainage system in children and the physical
activities that predispose them to trauma may be
responsible for this rare sporotrichoid pattern of
tuberculosis (16).
The terms inverse sporotrichoid and segmental
sporotrichoid lesions refer totheoccurrenceof linear skin
lesions in the proximal lower extremities caused by retro-
grade lymphatic spread of the organismfromthe inguinal
lymph nodes. Tuberculosis verrucosa cutis and gumma
have been reported in this inverse form in India (12).
BCG AND SKIN TUBERCULOSIS
BCGvaccine is a live attenuatedbovine strainof tubercle
bacilli. Meta-analysis of BCG vaccination trials suggests
that BCG vaccine prevents approximately 50% of pul-
monary tuberculosis in adults and children and 50% to
80%of severe tuberculosis (disseminatedandmeningeal)
cases (29). Several studies have shown that BCG vacci-
nation does not appear to prevent skin tuberculosis. No
dierence was found in the clinical presentation of skin
tuberculosis between BCG vaccinated and unvaccinated
children (7). Paradoxically, children may develop lupus
vulgaris, scrofuloderma, tuberculids, and erythema
nodosum at the site of BCG vaccination (12).
HIV AND SKIN TUBERCULOSIS IN CHILDREN
Concomitant HIVinfection has been described in 24.5%
(n = 12) of 49 pediatric skin tuberculosis cases in Ethi-
opia. All 12 children presented with scrofuloderma (11).
HIV coinfection has not been described in any of the
childhood series published from India (3,7,8).
DIAGNOSIS
Diagnosis is usually based on the typical clinical
appearance of the lesion along with other supportive
laboratory tests. Askin biopsy is usually performed in all
cases of cutaneous tuberculosis for histopathology and
culture (30). Clinicopathologic correlation is seen in
approximately 80% of cases. The criterion standard for
diagnosis is isolation of the organism in the biopsy.
Culture positivity varies from 5% to 55% (3,5,31). With
improved culture techniques, such as use of Kirchners
liquid medium for preserving the biopsy specimens until
they are processed, use of multiple culture media, andthe
BACTEC system of culture, isolation will be better (5).
The utility of PCRis controversial andhas givenvariable
results in dierent studies. Hence the treatment decision
shouldnot be basedprimarily onPCRresults (32). Other
investigations include ne-needle aspiration cytology of
A B
Figure 8. Sporotrichoid skin tuberculosis.
Sethuraman and Ramesh: Skin Tuberculosis in Children 13
the lymph nodes or biopsy and organ-specic imaging
techniques. All childrenpresenting withskintuberculosis
should be evaluated for an underlying systemic focus of
tuberculosis, especially the lungs, bones, central nervous
system, and gastrointestinal tract, particularly in tuber-
culosis-endemic countries.
Screening tests include the Mantoux and Quantiferon
TB Gold tests (QFT G). The Mantoux tuberculin skin
test is performed using intradermal (on the forearm)
injection of ve tuberculinunits, whichequals 0.0001 mg
of puried protein derivative of M. tuberculosis. The
reading is taken after 48 to 72 hours. Induration of
10 mm or more is considered signicant and indicates
only infection (Fig. 9) and not necessarily disease. In
developing countries where tuberculosis is endemic, the
Mantoux test is of low accuracy in the diagnosis of
doubtful cases of skin tuberculosis (33). QFT G quanti-
es the release of interferon gamma by blood monocytes
upon stimulation with highly specic M. tuberculosis
antigens (1). The sensitivity of QFTGis similar tothat of
the Mantoux test. The Centers for Disease Control and
Prevention has indicated that QFT G can be used in all
circumstances in which the Mantoux test is recom-
mended, including patient contact investigation, evalua-
tion of recent immigrants, and surveillance programs (1).
Sometimes clinical morphology and laboratory eval-
uation may not favor the diagnosis of skin tuberculosis.
The clinician may not be able to exclude the diagnosis of
cutaneous tuberculosis. In such circumstances, a thera-
peutic trial of antituberculous therapy for 6 weeks is
recommended as a diagnostic tool. Signicant response
at the end of the trial period suggests cutaneous tuber-
culosis. Childrenwhohave not respondedby 6 weeks are
unlikely to do so with continuous treatment, and the
diagnosis should be reassessed (34,35).
TREATMENT
The standard regimenfor skin tuberculosis consists of an
initial 2 months of intensive-phase therapy with four
drugs (ethambutol [E], isoniazid [H], rifampicin [R],
pyrazinamide [Z]) followed by 4 months of maintenance
therapy with two drugs (HR) (2 EHRZ 4 HR). Pro-
phylactic pyridoxine (1025 mg day) shouldbe addedto
the regimen to prevent isoniazid-related neuropathy.
Patients with an underlying focus in the bone or other
organs or HIV infection may need a longer period of
antitubercular therapy. The World Health Organization
(WHO) has implemented Directly Observed Treatment,
Short course strategy (DOTS). According to DOTS
guidelines, all newly diagnosedpatients are treatedunder
supervision with EHRZ three times per week for
2 months, followed by HR three times per week for
4 months (36).
DRUG RESISTANCE IN SKIN TUBERCULOSIS
The WHO denes a multidrug-resistant strain as resis-
tant to at least isoniazid and rifampicin and an exten-
sively drug-resistant strain as resistant to isoniazid and
rifampicin along with any uoroquinolone and at least
one of the three second-line injectable drugs (amikacin,
capreomycin, and kanamycin). There are no studies on
drug resistance patterns, particularly in children. A few
case reports of drug resistance in children have been
published (37,38). Aggarwal et al (31) (Delhi, India), in
their comparison study of the radiometric BACTEC
460 TB culture system and Lo wenstein-Jensen medium
for the isolation of mycobacteria in cutaneous tubercu-
losis and their drug susceptibility pattern, observed drug
resistance in46.2%of isolates. Drugsusceptibilitytesting
demonstrated resistance to at least one drug in 12 iso-
lates, with 6 having multidrug resistance (31).
The predisposing factors for drug resistance include
HIV infection, high disease burden, and the endemicity
of tuberculosis. Drugresistance is suspectedwhenthere is
a lack of good response to antituberculous therapy,
deteriorationof the lesion, andappearance of newlesions
in the vicinity of the existing lesion or at a distant site
while on therapy. Drug resistance has been reported in
scrofuloderma, lupus vulgaris, and tuberculosis verru-
cosa cutis (37,38). It is dicult to document drug resis-
tance in skin tuberculosis because the classical methods
of proving drug resistance often fail, but using modied
collection techniques for the samples, inoculation into
multiple media, and the BACTEC system may improve
the identication of resistant isolates. Another test that
appears promising is the line probe assay, which has the
ability to detect rifampicin and isoniazid resistance. This
Figure 9. Strongly positive Mantoux reaction.
14 Pediatric Dermatology Vol. 30 No. 1 January February 2013
test has beenusedfor sputumspecimens. Its usage inskin
tuberculosis needs to be evaluated (37,38).
Children with multidrug-resistant skin tuberculosis
should be treated using second-line drugs (Table 2). The
treatment regime consists of ve or six drugs, including
an injectable and a uoroquinolone, that should be
administered for 6 months followed by four oral drugs
for the next 18 months. Children should be monitored
carefully because the second-line drugs are toxic and
weak (37,38).
In conclusion, childhood skin tuberculosis continues
to be a health problem in tropical countries. The mani-
festations can be varied. Diagnosis primarily depends on
clinical grounds. Early diagnosis and initiation of anti-
tuberculous therapy is crucial because any delay in
treatment can lead to severe deformities. Because extra-
cutaneous tuberculosis infections are common in chil-
dren, systemic screening, especially of the lungs, bones,
and central nervous system, should be done. Health
education, awareness of the many unusual variants of
skin tuberculosis, intensied tuberculosis control pro-
grams, and eective DOTS are important and integral
components of the management of skin tuberculosis in
children.
REFERENCES
1. Mukherjee A, Lodha R, Kabra SK. Changing trends in
childhood tuberculosis. Indian J Pediatr 2011;78:328333.
2. Zouhair K, Akhdari N, Nejjam F et al. Cutaneous
tuberculosis in Morocco. Int J Infect Dis 2007;11:209212.
3. Pandhi D, Reddy BS, Chowdhary S et al. Cutaneous
tuberculosis inIndianchildren: the importance of screening
for involvement of internal organs. J Eur Acad Dermatol
Venereol 2004;18:546551.
4. Kumar B, Muralidhar S. Cutaneous tuberculosis: a twenty
year prospective study. Int J Tuberc Lung Dis 1999;3:494
500.
5. Umapathy KC, Begum R, Ravichandran G et al. Com-
prehensive ndings on clinical, bacteriological, histopath-
ological and therapeutic aspects of cutaneous tuberculosis.
Trop Med Int Health 2006;11:15211528.
6. Kumar B, Rai R, Kaur I et al. Childhood cutaneous
tuberculosis: astudyover 25 years fromnorthernIndia. Int
J Dermatol 2001;40:2632.
7. Ramesh V, Misra RS, Beena KR et al. A study of
cutaneous tuberculosis in children. Pediatr Dermatol
1999;16:264269.
8. Vashisht P, Sahoo B, Khurana N et al. Cutaneous tuber-
culosis in children and adolescents: a clinicohistological
study. J Eur Acad Dermatol Venereol 2007;21:4047.
9. Bhutto AM, Solangi A, Khaskhely NM et al. Clinical and
epidemiological observations of cutaneous tuberculosis in
Larkana, Pakistan. Int J Dermatol 2002;41:159165.
10. Mlika RB, Tounsi J, Fenniche S et al. Childhood cutane-
ous tuberculosis: a 20-year retrospective study in Tunis.
Dermatol Online J 2006;12:11.
11. Terranova M, Padovese V, Fornari U et al. Clinical and
epidemiological study of cutaneous tuberculosis in north-
ern Ethiopia. Dermatology 2008;217:8993.
12. Sethuraman G, Ramesh V, Ramam M et al. Skin
tuberculosis in children: learning from India. Dermatol
Clin 2008;26:285294.
13. Singal A, Pandhi D, Agrawal SK. Multifocal scrofuloder-
ma with disseminated tuberculosis in a severely malnour-
ished child. Pediatr Dermatol 2005;22:440443.
14. Sethuraman G, Kaur J, Nag HL et al. Symmetrical
scrofuloderma with tuberculosis verrucosa cutis. Clin
Exp Dermatol 2006;31:475477.
15. Kaur S, Thami GP, Kanwar AJ et al. Scrofuloderma, with
multiple organ involvement in a 5-year-old child. Pediatr
Dermatol 2001;18:328331.
16. Ramesh V. Sporotrichoid tuberculosis. Clin ExpDermatol
2007;32:680682.
17. Lucas S. Bacterial diseases. In: Elder DE, ed. Levers
histopathology of the skin. Philadelphia: Lippincott Wil-
liams & Wilkins, 2005:561565.
18. Sethuraman G, Thappa DM, Kurvilla S. Symmetrical
reinfection lupus vulgaris. Pediatr Dermatol 1999;16:488
490.
19. Singhal A, Bhattacharya SN. Lichen scrofulosorum: a
prospective study of 39 patients. Int J Dermatol 2005;44:
489493.
20. Kumar U, Sethuraman G, Verma P et al. Psoriasiform
type of lichen scrofulosorum: clue to disseminated tuber-
culosis. Pediatr Dermatol 2010;28:532534.
21. Torrelo A, Valverde E, Mediero IG et al. Lichen scrofu-
losorum. Pediatr Dermatol 2000;17:373376.
22. Thami GP, Kaur S, Kanwar AJ et al. Lichen scrofuloso-
rum: a rare manifestation of a common disease. Pediatr
Dermatol 2002;19:122126.
23. Beena KR, Ramesh V, Mukherjee A. Lichen scrofuloso-
ruma series of eight cases. Dermatology 2000;201:272
274.
24. Pandhi D, Mehta A, Singal A. Genital tuberculid in a
female child: a new entity (childhood vulval tuberculid).
Pediatr Dermatol 2007;24:573575.
25. Jordaan HF, Schneider JW, Schaaf HS et al. Papulone-
crotictuberculidinchildren: a report of eight patients. AmJ
Dermatopathol 1996;18:172185.
26. Jordaan HF, Schneider JW, Abdulla EA. Nodular tuber-
culid: a report of four patients. Pediatr Dermatol 2000;
17:183188.
TABLE 2. Antituberculous Drugs
Drug Dosage per day
First-line drugs
Isoniazid 46 mg kg
Rifampicin 812 mg kg
Pyrazinamide 2030 mg kg
Ethambutol 1520 mg kg
Second-line drugs
Amikacin 15 mg kg
Kanamycin 1530 mg kg
Streptomycin 1218 mg kg (1 g)
Ciprooxacin 5001000 mg
Ooxacin 400 mg
Levooxacin 500 mg
Gatioxacin 400 mg
Sethuraman and Ramesh: Skin Tuberculosis in Children 15
27. Pau WS, Al Saar H, Weinstein M et al. Sporotrichoid-
like tuberculosis. Pediatr Infect Dis J 2009;28:11351136.
28. Remenyik E, Nagy B, Kiss M et al. Sporotrichoid
cutaneous Mycobacterium tuberculosis infection in a child.
Acta Derm Venereol 2005;85:375376.
29. Starke JR, Munoz FM. Tuberculosis (Mycobacterium
tuberculosis). In: Kliegman RM, BehrmanRE, JensonHB,
Stanton BF, eds. Nelson textbook of pediatrics. Philadel-
phia: Saunders, 2008:1253.
30. Ramesh V, Misra RS, Jain RK. Secondary tuberculosis of
the skin. Clinical features and problems in laboratory
diagnosis. Int J Dermatol 1987;26:578581.
31. Aggarwal P, Singal A, Bhattacharya SNet al. Comparison
of the radiometric BACTEC 460 TB culture system and
Lo wenstein-Jensen medium for the isolation of mycobac-
teria in cutaneous tuberculosis and their drug susceptibility
pattern. Int J Dermatol 2008;47:681687.
32. Arora SK, Kumar B, Sehgal S. Development of a
polymerase chain reaction dot-blotting system for
detecting cutaneous tuberculosis. Br J Dermatol 2000;142:
7276.
33. Ramam M, Malhotra A, Tejasvi T et al. How useful is the
Mantoux test in the diagnosis of doubtful cases of
cutaneous tuberculosis? Int J Dermatol 2011;50:1379
1382.
34. Ramam M, Mittal R, Ramesh V. How soon does
cutaneous tuberculosis respond to treatment? Implications
for a therapeutic test of diagnosis. Int J Dermatol 2005;
44:121124.
35. Ramam M, Tejasvi T, Manchanda Y et al. What is the
appropriate duration of a therapeutic trial in cutaneous
tuberculosis? Further observations. Indian J Dermatol
Venereol Leprol 2007;73:243246.
36. World Health Organization. Treatment of tuberculosis
guidelines (WHO HTM TB 2009.420). Geneva: World
Health Organization, 2010.
37. Ramesh V, Muralidhar S, Kumar J et al. Isolation of drug
resistant tubercle bacilli in cutaneous tuberculosis. Pediatr
Dermatol 2001;18:393395.
38. Ramesh V, Sen MK, Nair D et al. Cutaneous tuberculosis
caused by multidrug resistant tubercle bacilli: report of
three cases. Int J Dermatol 2011;50:300303.
16 Pediatric Dermatology Vol. 30 No. 1 January February 2013

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