Cutaneous Manifestations of Tuberculosis

Cutaneous manifestations of tuberculosis
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Authors
Evangeline B Handog, MD
Maria Juliet E Macarayo, MD
Section Editor
Ted Rosen, MD
Deputy Editor
Abena O Ofori, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: Jun 29, 2015.
INTRODUCTION Tuberculosis (TB) is a mycobacterial infection that most frequently occurs due to infection with
Mycobacterium tuberculosis, an acid-fast bacillus. The high prevalence of TB worldwide (one-third of the world
population), its transmissible nature, and the significant morbidity and mortality associated with this infection account
for the status of TB as a major public health concern [1,2]. (See "Epidemiology of tuberculosis", section on 'Global
burden'.)
Cutaneous lesions are relatively uncommon manifestations of TB, occurring in only 1 to 2 percent of infected patients.
The clinical findings vary; inflammatory papules, verrucous plaques, suppurative nodules, chronic ulcers, or other
lesions may be seen. Factors such as the pathway of bacterial entry into the skin, the host's immune status, and the
presence or absence of host sensitization to M. tuberculosis influence the presentation of TB in the skin.
The cutaneous disorders associated with TB will be reviewed here. The epidemiology and microbiology of TB,
extracutaneous TB, and the general principles of the treatment of TB are reviewed separately. (See "Epidemiology of
tuberculosis" and "Natural history, microbiology, and pathogenesis of tuberculosis" and "Treatment of pulmonary
tuberculosis in HIV-uninfected patients".)
HISTORY Cutaneous TB was first documented in 1826, when Laennec reported his own "prosector's wart," a
lesion that likely represented tuberculosis verrucosa cutis, a variant of TB that results from direct entry of the organism
into the skin [3]. However, the causative organism of TB was unknown until Robert Koch discovered Mycobacterium
tuberculosis in 1882 [4]. Subsequently, the bacillus was detected in cutaneous lesions [5]. (See 'Clinical variants'
below.)
GENERAL PRINCIPLES Cutaneous TB is a relatively uncommon manifestation of TB, accounting for only 1 to 2
percent of all cases [6-9]. Similar to other forms of TB, a resurgence of cutaneous TB has been noted in parts of the
world where human immunodeficiency virus (HIV) infection and multidrug-resistant TB are prevalent [9-13]. (See
"Epidemiology of tuberculosis", section on 'Global burden'.)
Etiologic agents TB is defined as a disorder caused by mycobacteria in the Mycobacterium tuberculosis complex,
which includes M. tuberculosis, M. bovis, M. africanum, M. microti, M. canetti, M. caprae, and M. pinnipedii [14]. M.
tuberculosis, a slow-growing acid-fast bacillus, is the predominant causative organism of cutaneous TB. M. bovis and
the Bacille Calmette-Gurin (BCG) vaccine (a vaccine composed of attenuated M. bovis), have also been associated
with the development of cutaneous lesions [13,15,16]. (See "Natural history, microbiology, and pathogenesis of
tuberculosis", section on 'Microbiology' and "Mycobacterium bovis" and 'BCG vaccination reactions' below.)
Classification The multiple disorders classified as manifestations of TB differ not only according to the clinical
appearance of lesions, but also by the method of skin infection, the quantity of organisms in the skin, and predisposing
factors, such as a patient's age, immune competence, and TB sensitization status [10,17]. The method of infection is
the characteristic most often used to subdivide the disorders. Although most cases arise from contiguous spread or
hematogenous dissemination to the skin from an endogenous focus of infection, direct entry of M. tuberculosis into the
skin occasionally results in local infection [10,12]. (See 'Clinical variants' below.)
The classification of the variants of TB according to the mode of infection is as follows:
Inoculation from an exogenous source (see 'Exogenous inoculation' below)
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Primary inoculation TB
Tuberculosis verrucosa cutis
Endogenous spread by contiguous extension or autoinoculation (see 'Contiguous spread' below)
Scrofuloderma
Tuberculosis cutis orificialis
Lupus vulgaris
Hematogenous spread to the skin (see 'Hematogenous spread' below)
Lupus vulgaris
Acute miliary TB
Metastatic tuberculous abscess
The disorders that constitute cutaneous TB may also be divided according to the bacterial load in the skin [8].
Multibacillary forms (bacilli easily detectable in tissue or exudate) include primary inoculation TB, scrofuloderma,
tuberculosis cutis orificialis, acute miliary TB, and metastatic tuberculous abscess. The paucibacillary forms of
cutaneous TB include tuberculosis verrucosa cutis and lupus vulgaris.
The tuberculids are a separate category of TB-associated cutaneous disorders that likely represent hypersensitivity
reactions to mycobacterial antigens, rather than manifestations of local skin infection. The disorders included in the
category of tuberculids include papulonecrotic tuberculid, lichen scrofulosorum, and erythema induratum of Bazin. (See
'Tuberculids' below.)
Host factors As mentioned above, the likelihood for specific cutaneous manifestations of M. tuberculosis infection
varies based upon multiple host characteristics, such as age, sex, and health status [18-21]. As examples, primary
inoculation TB, scrofuloderma, and lichen scrofulosorum commonly affect children, and females are more likely than
males to develop lupus vulgaris and erythema induratum of Bazin. In addition, the presence of poor immunity against
M. tuberculosis is a risk factor for tuberculosis cutis orificialis, metastatic tuberculous abscess, and acute miliary TB
[4,10]. Higher levels of immunity against M. tuberculosis are linked with tuberculosis verrucosa cutis, lupus vulgaris,
and tuberculids [10]. (See 'Clinical variants' below.)
Histopathology A characteristic histopathologic finding in cutaneous TB is the tuberculoid granuloma, an
accumulation of epithelioid histiocytes and Langhans-type giant cells that demonstrates a variable degree of central
caseation necrosis and a peripheral rim composed of numerous lymphocytes (picture 1) [11,22]. Although tuberculoid
granulomas are a common finding in cutaneous TB, their detection does not confirm the presence of TB, and their
absence does not exclude the diagnosis. Leprosy, syphilis, granulomatous rosacea, leishmaniasis, deep fungal
infections, and other disorders may also present with tuberculoid granulomas [11,23,24].
The classic granulomas of sarcoidosis differ from tuberculoid granulomas. Compared with tuberculoid granulomas,
sarcoidal granulomas tend to be more circumscribed, exhibit fewer peripheral inflammatory cells (naked granulomas),
and are less likely to have central caseation necrosis (picture 2A-B). (See "Cutaneous manifestations of sarcoidosis",
section on 'Histopathology'.)
Diagnostic tests Similar to extracutaneous TB, multiple diagnostic studies are utilized for the evaluation of patients
with cutaneous TB. The conventional techniques include mycobacterial culture (the gold standard for diagnosis),
stained smears, lesional biopsies, and tuberculin skin testing. However, in paucibacillary variants, culture, smears, and
histopathology often fail to detect the presence of M. tuberculosis due to the relatively low number of organisms in
lesional tissue. Such tests also are not typically useful for the diagnosis of tuberculids, in which mycobacteria generally
are not detected in skin lesions. The tuberculin skin test can be positive in both multibacillary and paucibacillary forms
of cutaneous TB; however, a positive test only identifies individuals who have been sensitized to TB and does not
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confirm active TB infection.

Newer techniques that have been developed for the evaluation of patients with suspected TB include interferon-gamma
release assays, which, like the tuberculin skin test, identify patients who have been exposed to M. tuberculosis, and
nucleic amplification tests (eg, polymerase chain reaction) that identify mycobacterial DNA in lesional tissue. The role
that these newer techniques should play in the diagnosis of cutaneous TB remains uncertain. (See "Diagnosis of
pulmonary tuberculosis in HIV-uninfected patients" and "Diagnosis of latent tuberculosis infection in HIV-infected
patients" and "Diagnosis of latent tuberculosis infection (tuberculosis screening) in HIV-uninfected adults" and
"Interferon-gamma release assays for diagnosis of latent tuberculosis infection".)
Mycobacterial culture Mycobacterial culture is the gold standard for determining the presence of active TB
infection. The procedure also provides the means to distinguish M. tuberculosis form nontuberculous
mycobacteria and allows for the determination of antibiotic sensitivity [6,10,25]. (See "Diagnosis of pulmonary
tuberculosis in HIV-uninfected patients", section on 'Diagnostic microbiology' and "Diagnosis of pulmonary
tuberculosis in HIV-uninfected patients", section on 'Culture'.)
Stained smear The examination for acid-fast bacilli on a stained smear is a more rapid diagnostic technique
than culture. The diagnostic yield of stained smears is highest for moist or exudative lesions that have a high
bacterial load such as primary inoculation TB, scrofuloderma, tuberculosis cutis orificialis, or metastatic
tuberculous abscess. The Ziehl-Neelsen acid-fast stain is the most commonly used stain for this purpose. (See
"Diagnosis of pulmonary tuberculosis in HIV-uninfected patients", section on 'Stained smears'.)
Skin biopsy The accessibility of skin lesions makes the obtainment of a tissue biopsy a relatively simple
procedure. The identification of tuberculoid granulomas, acid-fast bacilli, or other characteristic histopathologic
features of specific variants of cutaneous TB may be used to support the diagnosis. (See 'Histopathology'
above.)
Tuberculin skin test The tuberculin skin test identifies individuals sensitized to M. tuberculosis [6,25-27]. It has a
specificity of 63 percent and a sensitivity between 33 and 96 percent for cutaneous TB that becomes higher in
unvaccinated populations [15,28]. The Mantoux technique, the recommended method for performing tuberculin
skin testing, involves the intradermal injection of tuberculin antigen (purified protein derivative [PPD]) into the inner
surface of the forearm, followed by re-examination of the injection site 48 to 72 hours later (table 1). The test
becomes positive 2 to 10 weeks following infection [6]. Immunologically, the basis for the tuberculin skin test is a
delayed hypersensitivity reaction involving T cells [27,29,30]. (See "Diagnosis of latent tuberculosis infection
(tuberculosis screening) in HIV-uninfected adults", section on 'Tuberculin skin test' and "Latent tuberculosis
infection in children", section on 'Tuberculin skin test'.)
Reactivity to the tuberculin protein may be impaired in young infants, older adults, and patients with deficient
cellular immunity (table 2). In addition, the likelihood of a positive tuberculin skin test varies among the different
subtypes of cutaneous TB. (See 'Clinical variants' below.)
Interferon-gamma release assay Interferon-gamma release assays are serologic tests that assess for latent
TB infection via the measurement of interferon-gamma production from peripheral blood mononuclear cells after
exposure to antigens from M. tuberculosis [23,26]. A study evaluating an interferon-gamma release assay
(T-SPOT.TB) in patients with suspected cutaneous TB found a sensitivity of 92 percent and a specificity of 76
percent [31].
According to guidelines from the United States Centers for Disease Control, interferon-gamma release assays
are an acceptable alternative to tuberculin skin tests [32]. However, there may be indeterminate results in certain
patient groups (eg, age over 65 years, history of previous severe disease requiring ICU admission, malnourished
or lymphopenic states, increased C-reactive protein serum levels, or decreased total protein levels). The error
rate approaches zero for individuals below 35 years old devoid of these characteristics [15,28,33]. (See
"Interferon-gamma release assays for diagnosis of latent tuberculosis infection".)
Unlike the tuberculin skin test, the bacille Calmette-Gurin (BCG) vaccination does not influence the results of this
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test. However, prior infections with select environmental mycobacteria, such as M. marinum and M. kansasii,
may result in a false positive interferon-gamma release assay.
Polymerase chain reaction Polymerase chain reaction (PCR) testing for M. tuberculosis infection involves the
use of nucleic amplification for the detection of M. tuberculosis DNA in tissue specimens. The procedure can be
performed in a few hours and confirmation of results obtained within one to three days. Polymerase chain
reaction tests can differentiate between M. tuberculosis and other species of mycobacteria and can identify gene
mutations associated with drug resistance [25].
PCR appears to be the most useful in the multibacillary forms of cutaneous TB [34-37]. Although PCR may be
positive in paucibacillary disease when both cultures and histopathologic stains for the organism are negative, the
results of testing are inconsistent [35,38-42]. In addition, the availability of PCR in developing countries is limited
[35,39,43]. PCR is primarily used as an adjunct to clinicopathologic evaluation [23] and is not yet recommended
to replace diagnostic conventional culture [44]. (See "Diagnosis of pulmonary tuberculosis in HIV-uninfected
patients", section on 'Nucleic acid amplification'.)
Therapeutic trial A therapeutic trial of anti-TB medications may be used to confirm the diagnosis of TB in
difficult cases. In cutaneous TB, a response to multidrug therapy is usually evident within six weeks [43,45,46].
With the exception of tuberculids and some patients with minimal clinical activity prior to treatment, the diagnosis
should be reevaluated in patients who fail to improve within this period [45]. (See 'Treatment overview' below.)
Evaluation for extracutaneous involvement Patients with lesions consistent with variants of cutaneous TB that
result from the spread of the bacillus from endogenous foci of infection should be evaluated for the primary site of
infection [47]. The evaluation for extracutaneous TB is reviewed separately. (See "Diagnosis of pulmonary tuberculosis
in HIV-uninfected patients" and "Epidemiology, clinical manifestations, and diagnosis of tuberculosis in HIV-infected
patients" and "Tuberculosis disease in children", section on 'Diagnosis'.)
CLINICAL VARIANTS The clinical variants of cutaneous TB may be divided into infections acquired through
exogenous inoculation, infections that result from contiguous spread, infections related to hematogenous dissemination,
and the tuberculids. The tuberculids are thought to be hypersensitivity reactions to M. tuberculosis, and include
papulonecrotic tuberculid, lichen scrofulosorum, and erythema induratum of Bazin. (See 'Tuberculids' below.)
Exogenous inoculation Primary inoculation TB and tuberculosis verrucosa cutis represent the variants of
cutaneous TB that are acquired through the inoculation of the organism into the skin. Primary inoculation TB occurs in
individuals who have not previously been sensitized to M. tuberculosis, whereas tuberculosis verrucosa cutis develops
in individuals with prior exposure to the bacterium.
Primary inoculation tuberculosis Primary inoculation TB (also known as tuberculous chancre and primary
tuberculous complex) is a rare form of cutaneous TB that results from the direct entry of the organism into the skin or
mucosa of a nonsensitized individual. The disorder primarily occurs in children in endemic areas [4]. Minor trauma
resulting in a compromised skin barrier usually precedes the infection. Surgical procedures performed with unsterilized
equipment, tattoos, and piercing may also lead to lesion development [48,49].
Clinical features Primary inoculation TB becomes clinically evident within one month after inoculation.
Classically, the lesion begins as a nondescript red-brown papule or nodule that evolves into a painless, shallow
and undermined ulcer with a granulomatous base. Lesions are usually 1 cm or less in diameter, but occasionally
exceed 5 cm [4]. The face and extremities are the most common sites for lesion development.
Slowly progressive and painless regional lymphadenopathy frequently becomes apparent three to eight weeks
after the appearance of the skin lesion. Occasionally, lymph node involvement results in perforation of the skin
and the development of draining sinuses [4,34]. The combination of the cutaneous findings and lymphadenopathy
in primary inoculation TB are analogous to the Ghon complex of pulmonary TB infection [8]. (See "Natural history,
microbiology, and pathogenesis of tuberculosis", section on 'Primary disease'.)
Diagnosis Early primary inoculation TB is multibacillary, and acid-fast bacilli (AFB) are usually easily detected
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in smears taken from early lesions [11,50,51]. A positive culture confirms the diagnosis. As immunity develops,
the number of bacteria present in the lesions decreases [11].
Skin biopsies obtained early in the disease course reveal necrosis, neutrophilic infiltrates, and numerous acid-fast
bacilli [4]. In contrast, lesions that have been present for several weeks or longer demonstrate tuberculoid
granulomas with or without caseation necrosis, and few or no bacilli [50,52,53]. (See 'Histopathology' above.)
The tuberculin skin test is negative at the time of disease onset, but becomes positive with disease progression
and resolution [11,54].
Differential diagnosis The differential diagnosis of primary inoculation TB includes other infections that may
present with inflammatory nodules or ulcers, including deep fungal infections, nocardiosis, syphilis, leishmaniasis,
yaws, tularemia, bartonellosis, cat-scratch disease, and other mycobacterioses [6,11,51].
Disease course Left untreated, primary inoculation TB may persist for up to one year [4]. A scar typically
remains after resolution. Patients become sensitized to TB as a consequence of infection. (See 'Treatment
overview' below.)
A potential complication of primary inoculation TB is hematogenous spread of the bacillus leading to TB of other
organs or acute miliary disease [11]. Moreover, erythema nodosum occurs in approximately 10 percent of cases,
and occasionally lupus vulgaris or scrofuloderma develops at the site of a lesion [4]. (See "Clinical manifestations,
diagnosis, and treatment of extrapulmonary and miliary tuberculosis" and "Erythema nodosum".)
Tuberculosis verrucosa cutis Tuberculosis verrucosa cutis (TBVC, also known as prosector's wart, anatomic
tuberculosis, verruca necrogenica, and warty tuberculosis) is a form of cutaneous TB that occurs after direct
inoculation of the mycobacteria into the skin of a previously sensitized host with moderate to high immunity against the
bacillus [6,10,11,34]. Inoculation typically occurs from an exogenous source; rarely, inoculation may occur from the
patient's own sputum [15].
Children who play in contaminated areas and adults with occupational exposure to mycobacteria (eg, pathologists,
laboratory technicians, undertakers, butchers, and farmers) are at greatest risk for this infection [4,55]. TBVC is much
more common than the primary inoculation variant [4].
Clinical features In adults, TBVC most frequently develops on the acral extremities; the fingers and dorsum of
the hands are commonly affected [4,6,17,23,55,56]. The ankles or buttocks are frequent sites for lesion
occurrence in children [6].
The skin lesions are usually solitary and manifest as painless, violaceous or brown-red, indurated warty plaques
that range from 1 to 5 cm in diameter (picture 3). TBVC grows via peripheral extension; central clearing and
atrophy may or may not be present [6]. Although ulceration is uncommon, fissures that exude purulent drainage
or keratinous material may occur [4,15]. Other potential clinical findings include regional adenopathy in patients
with secondary bacterial infection and lymphostasis and elephantiasis of affected extremities in patients with
extensive and chronic involvement [15,17].
Diagnosis The histopathologic findings of TBVC include pseudoepitheliomatous hyperplasia, marked
hyperkeratosis, and microabscesses in the superficial dermis or the pseudoepitheliomatous rete pegs (picture 4).
An inflammatory infiltrate composed of epithelioid cells and giant cells is usually present in the upper and middle
dermis. Frank tuberculoid granulomas may or may not be evident [4,11,52,57].
Although a few acid-fast bacilli can be detected on careful histopathologic examination in some cases
[4,15,52,57], cultures taken from lesions of TBVC are often negative [6,11,34]. The tuberculin skin test is strongly
positive, indicative of the high level of immunity against the bacterium in affected patients [6,51].
Interferon-gamma release assay also may be useful for detecting evidence of tuberculosis in TBVC [58].
Differential diagnosis Other disorders to be considered in patients with lesions suggestive of TBVC include
diseases that may present with hyperkeratotic or verrucous plaques, including atypical mycobacterioses,
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blastomycosis, Majocchi's granuloma, chromoblastomycosis, tertiary syphilis, verrucous epidermal nevus,

hypertrophic lichen planus, lupus vulgaris, halogenoderma, benign keratoses, and verruca vulgaris [6,11,51].
Disease course Skin lesions may persist for years if left untreated, although spontaneous resolution can also
occur [10,11,34,51]. Patients typically improve with anti-TB therapy [34]. (See 'Treatment overview' below.)
Contiguous spread TB infection can be transmitted to the skin from adjacent structures. Scrofuloderma,
tuberculosis cutis orificialis, and lupus vulgaris can occur as a result of this process.
Scrofuloderma Scrofuloderma (also known as tuberculosis colliquativa cutis) is a form of cutaneous TB that
occurred much more frequently prior to the advent of effective therapies for TB. This disorder results from the direct
extension of the infection from a deep structure (eg, lymph node, bone, joint, or epididymis) into the overlying skin
[18,34,48]. Scrofuloderma may occur at any age, but most commonly develops in children, adolescents, and older
adult individuals [11,17,34,51].
In addition to M. tuberculosis infection, M. bovis infection related to the consumption of contaminated milk may lead to
scrofuloderma [59]. The occurrence of scrofuloderma following bacille Calmette-Gurin (BCG) vaccination has also
been reported [60]. Scrofuloderma has also been reported to occur in association with Hansen's disease [61] and
psoriasis [62]. (See "Mycobacterium bovis" and "BCG vaccination".)
Clinical features Early lesions of scrofuloderma are firm, painless, subcutaneous, red-brown nodules that
overly foci of tuberculous infection. The neck, axillae, and groin are often involved, with the cervical lymph nodes
as the most common source of infection [4,17]. The suppurative nodules gradually enlarge, and eventually form
ulcers and sinus tracts that drain watery, purulent, or caseous material (picture 5) [15,34]. Lesions may be single
or multiple. A linear arrangement can occur if the infection overlies multiple lymph nodes within a region [4].
Diagnosis The diagnosis of scrofuloderma is based upon the identification of the causative organism by
culture, smear, or skin biopsy [15]. Skin biopsy reveals tuberculoid granulomas surrounding areas of wedgeshaped necrosis [11,34,57]. Tuberculin skin testing is positive [11,50].
Differential diagnosis Scrofuloderma must be differentiated from other causes of suppurative nodules,
including atypical mycobacterioses, sporotrichosis, actinomycosis, coccidioidomycosis, lymphogranuloma
venereum, syphilis, severe forms of acne conglobata, and hidradenitis suppurativa [6,11,51]. In the neck,
scrofuloderma may mimic a dental sinus.
Disease course Spontaneous healing may occur, but it may be years before lesions are completely replaced
by scar tissue [15]. Scars may be depressed, retractable, adherent, hypertrophic, or keloidal [11,17,34,50,51].
Coexistence with an active pulmonary process is relatively common [17,51]. In addition, lupus vulgaris may
develop within or near sites of scrofuloderma [11]. (See 'Lupus vulgaris' below.)
Tuberculosis cutis orificialis Tuberculosis cutis orificialis (TBCO, also known as orificial tuberculosis and
tuberculosis ulcerosa cutis et mucosae) is a rare manifestation of TB that most frequently occurs among middle-aged
and older adults [51]. TBCO develops in individuals with both advanced TB of the gastrointestinal tract, lungs, or
genitourinary tract and dramatically impaired cell-mediated immunity [6,11,34]. The skin lesions result from the
autoinoculation of the mucocutaneous tissues near body orifices by the draining sites of visceral infection [15,23].
Clinical features TBCO occurs on the oral, nasal, or anogenital skin or mucosa [15,23]. Among patients with
oral involvement, the distal and lateral tongue are most frequently affected; lesions may also involve the palate,
lips, or other sites [11,15]. A typical lesion appears as a red-yellow nodule that rapidly breaks down to form a
painful, circular or irregularly shaped, "punched-out" and friable 1 to 3 cm ulcer with a pseudomembranous
fibrinous base (picture 6) [6,10,11,15,51]. Inflammation and edema are often present at the peripheral margins
[4].
Diagnosis The possibility of TBCO should be considered in patients with nonhealing periorificial ulcers and
signs or symptoms suggestive of advanced TB [50]. The detection of acid-fast bacilli in affected tissue via
culture, stained smear, or skin biopsy confirms the diagnosis. Histopathologic examination of skin biopsies
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demonstrates easily detectable bacilli in the ulcer walls and tuberculoid granulomas at the ulcer edge and in the
deep dermis [4,6,63]. Cutaneous necrosis and intense nonspecific cellular infiltrates are also present [6,11,51].
Tuberculin skin tests are often negative in patients with TBCO due to the associated impairment in host immunity.
Because TBCO occurs as a consequence of visceral infection, the focus of active extracutaneous TB must be
sought as part of the patient evaluation [17]. (See "Diagnosis of pulmonary tuberculosis in HIV-uninfected
patients" and "Tuberculosis disease in children", section on 'Diagnosis'.)
Differential diagnosis Other causes of persistent periorificial ulcers should be considered during the evaluation
of patients with suspected TBCO. Examples include aphthous ulcers, lymphogranuloma venereum, syphilis, and
cutaneous malignancies [4,11,51].
Disease course The presence of TBCO heralds a poor overall prognosis, as patients tend to have severe
internal organ disease prior to skin manifestations [11,34]. Without successful treatment of the TB infection, the
lesions progress and may eventually contribute to the development of fatal miliary TB [64]. Although resolution
within two months after the initiation of treatment has been reported [64-66], other cases may be recalcitrant to
treatment [15].
Lupus vulgaris Lupus vulgaris (also known as tuberculosis lupus) is a chronic and progressive form of
cutaneous TB that represents a reactivation of TB infection in people with moderate to high immunity against the
bacillus [4,10]. Lupus vulgaris may occur either as a result of direct extension from an underlying focus of infection or
via lymphatic or hematogenous spread. The development of lupus vulgaris has also been reported in patients with prior
scrofuloderma, and as a rare complication of BCG vaccination or primary inoculation TB [67-70].
This disorder is considered the most common form of cutaneous TB in Europe; scrofuloderma appears to be more
prevalent in some tropical regions [8,71,72]. Lupus vulgaris occurs in individuals of all ages. For unknown reasons,
females are two to three times more likely than males to be affected [11].
Although the most common causative organism is M. tuberculosis, there are reported cases caused by M. bovis, and
clinical presentation is no different than lupus vulgaris caused by M. tuberculosis. Persons at risk for M. bovis lupus
vulgaris are those residing in rural areas, in contact with cattle, and with exposure to infected milk products [73,74].
Clinical features The clinical findings of lupus vulgaris are variable. The classic plaque type of the disorder
begins as a collection of discrete, red-brown papules that subsequently coalesce to form an indolent,
asymptomatic plaque (picture 7). The plaque gradually grows peripherally to reach a size of 0.5 to 10 cm and
develops central clearing and atrophy. The borders may acquire a serpiginous or verrucous quality. Hypertrophic,
ulcerative, and vegetative forms of lupus vulgaris may also occur [15]. Secondarily infected lesions may exhibit a
seropurulent discharge and crusting.
The distribution of lesions is variable. In western countries, lesions often develop on the head and neck, while in
tropical and subtropical areas, lesions are commonly found on the lower extremities or buttocks [34,75].
Similar to other granulomatous disorders such as sarcoidosis and leprosy, diascopy (examination of the lesion under
compression with a glass slide) of non-hyperkeratotic areas of lupus vulgaris often reveals a yellow-brown color
referred to as an "apple jelly" appearance [4]. However, this finding can be difficult or impossible to appreciate in
patients with dark skin [15].
Diagnosis Lupus vulgaris is a paucibacillary form of cutaneous TB, and mycobacteria often cannot be detected
histopathologically or by culture [15]. Information that may be used to support the diagnosis includes consistent
clinical and histopathologic features and positive PCR test results [76]. Tuberculin skin testing is also often
positive.
Histopathologic examination reveals tuberculoid granulomas with discrete central caseation in the upper dermis
[34,50,51]. The epidermis may be atrophic or acanthotic with excessive hyperkeratosis or pseudoepitheliomatous
hyperplasia (picture 8) [6,11,57].
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Dermoscopy of lupus vulgaris has revealed linear telangiectasias on a yellow to golden background and whitish
reticular streaks [77]. Though characteristic of lupus vulgaris, specificity may not be high and correlation with
other diagnostic procedures is still necessary.
Differential diagnosis Lupus vulgaris shares clinical features with multiple disorders [6,11,17,51]. Papular
lesions should be distinguished from colloid milia, acne, and rosacea. Plaques may resemble deep fungal
infections, leishmaniasis, late syphilis, discoid lupus, lymphocytoma cutis, tuberculoid leprosy, and pyodermatitis
vegetans.
Disease course If anti-TB therapy is not administered, lesions of lupus vulgaris persist. Over the course of
years, the plaques may grow to enormous sizes. In addition, ulceration and destruction of underlying tissues such
as the nose, ears, and lips, may occur, causing severe disfigurement [4,15]. (See 'Treatment overview' below.)
Squamous cell carcinoma occasionally develops in long-standing lesions [76,78-80]. The development of basal
cell carcinoma and other cutaneous malignancies has also been reported [80].
Hematogenous spread Hematogenous transmission of M. tuberculosis from a primary site of infection may lead to
metastatic tuberculous abscesses (tuberculous gumma), acute miliary TB, or lupus vulgaris.
Metastatic tuberculous abscesses (tuberculous gummas) Metastatic tuberculous abscesses (also known
as tuberculous gummas) usually arise as a consequence of hematogenous spread of the bacillus from a primary focus
of infection to the subcutaneous tissue during a state of reduced cell-mediated immunity [15]. These lesions typically
occur in malnourished children and immunosuppressed adults [6,15,17]. Immunocompetent adults are infrequently
affected; such patients tend to have few lesions [81].
Clinical features Patients with metastatic tuberculous abscesses present with single or multiple, non-tender,
fluctuant, subcutaneous nodules. The nodules eventually penetrate the skin, resulting in the formation of ulcers
and draining sinuses (picture 9) [4]. Lesions may occur at any skin site but frequently develop on the extremities
[17]. Associated regional adenopathy usually is not present [17].
Diagnosis The diagnosis of metastatic tuberculous abscess is based upon the results of cultures, smears, or
skin biopsies that demonstrate the presence of the bacillus. The histopathologic examination is characterized by
massive skin necrosis with numerous mycobacterial organisms and may also demonstrate tuberculoid
granulomas in the deep dermis [4,6,34]. The results of tuberculin skin testing are variable [34].
Differential diagnosis Metastatic tuberculous abscesses share clinical and histologic features with
scrofuloderma. However, scrofuloderma occurs as a result of contiguous extension of an infection from an
underlying tuberculous focus, rather than hematogenous dissemination [81]. (See 'Scrofuloderma' above.)
Disease course Metastatic tuberculous abscesses are a negative prognostic finding in malnourished and
immunosuppressed individuals. Although lesions in immunocompetent individuals may persist for years if
untreated, spontaneous resolution can eventually occur [4].
Acute miliary tuberculosis Acute miliary TB (also known as tuberculosis cutis miliaris disseminata) is a rare
form of TB that results from the hematogenous dissemination of mycobacteria from a primary focus of infection, such
as the lung. The disorder typically occurs in infants or individuals with impaired cell-mediated immunity, such as patients
with advanced acquired immune deficiency syndrome (AIDS) [15].
Most patients with acute miliary TB do not exhibit cutaneous lesions. When present, the cutaneous findings result from
bacteremia [13] and are nonspecific. Pinpoint red-blue or purpuric papules with overlying tiny vesicles that
subsequently become umbilicated and crusted are typically seen. Individual lesions heal over the course of one to four
weeks, and often resolve with hypopigmented depressed scars [15].
Skin biopsies can aid in the diagnosis of acute miliary TB in patients who present with cutaneous lesions. Numerous
acid-fast bacilli and abscesses are typically detected [15]. Granulomas may be present in older lesions [52]. The
tuberculin skin test is often negative due to associated anergy.
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Acute miliary tuberculosis is discussed in greater detail separately. (See "Clinical manifestations, diagnosis, and
treatment of extrapulmonary and miliary tuberculosis".)
Lupus vulgaris In addition to arising from contiguous spread, lupus vulgaris may also occur as a consequence
of hematogenous dissemination of M. tuberculosis. Lupus vulgaris is discussed above. (See 'Lupus vulgaris' above.)
Tuberculids The pathogenesis of the disorders classified as tuberculids is not fully understood, but they are
commonly considered to be cutaneous hypersensitivity eruptions to M. tuberculosis that occur in patients with a
moderate or high levels of immunity against the organism [4,15,34]. The three main tuberculid disorders are
papulonecrotic tuberculid, lichen scrofulosorum, and erythema induratum of Bazin.
The following findings support the designation of a condition as a tuberculid [4,6,34,50]:
Failure to detect M. tuberculosis in stains or cultures of affected tissue
Presence of detectable extracutaneous M. tuberculosis infection, a strongly positive tuberculin skin test, or a
positive interferon-gamma release assay [82] (these findings support a history of exposure to the bacillus)
Histopathologic evidence for granulomatous inflammation in skin lesions
Frequent resolution of skin lesions with anti-TB therapy
Although bacilli are usually not detectable in tuberculid lesions, DNA from M. tuberculosis has been detected, albeit
inconsistently, in tissue specimens from papulonecrotic tuberculid and erythema induratum of Bazin [83,84]. This finding
offers some support for a role for M. tuberculosis in the pathogenesis of tuberculids.
Papulonecrotic tuberculid Papulonecrotic tuberculid is the most common of the tuberculid disorders, first
established as a distinct entity by Pautrier in 1936 [85]. It is most frequently seen in children and young adults [86].
Papulonecrotic tuberculid may coexist with other tuberculids, lupus vulgaris, and scrofuloderma [85,87-93].
Clinical features Papulonecrotic tuberculid typically presents as a symmetric and recurring eruption of 2 to 8
mm, firm, dark red or violaceous papules that subsequently become pustular or necrotic (picture 10A-B). Lesions
most commonly occur on the face, ears, extensor extremities, and buttocks [6,10,11,17,51,85].
Fever and constitutional symptoms may precede the appearance of skin lesions [23,50] and associated
lymphadenitis is common [15].
Diagnosis The diagnosis of papulonecrotic tuberculid is suggested by the presence of consistent clinical and
histopathologic findings in a patient with risk factors for TB. Histopathologic examination often demonstrates
wedge-shaped necrosis in the upper dermis and epidermis and nonspecific or tuberculoid granulomatous
inflammation. Granulomatous vasculitis may also be present [6,11,86]. M. tuberculosis bacilli usually are not
detectable via microscopy or cultures.
In addition to the typical histopathologic findings, data that can support the diagnosis include a positive tuberculin
skin test, a detectable extracutaneous focus of TB infection, the detection of mycobacterial DNA in lesional tissue
[83,86,94], and a positive response to anti-TB therapy. An extracutaneous focus of tuberculosis (eg, cervical
lymph nodes, lungs, or other sites) is detectable in 38 to 75 percent of patients [95]. In a series of 12 patients
with papulonecrotic tuberculid, mycobacterial DNA was detected by PCR in 11 of 22 biopsy specimens [83].
Differential diagnosis The differential diagnosis of papulonecrotic tuberculid includes papular disorders that
may present with necrotic or excoriated papules. Examples include pityriasis lichenoides et varioliformis acuta
(PLEVA), prurigo, secondary syphilis, varicella, lymphomatoid papulosis, perforating disorders, leukocytoclastic
vasculitis, and Churg-Strauss syndrome [6,11,51].
Clinical course Although lesions may spontaneously resolve over the course of several weeks, leaving residual
pitted or varioliform scars, recurrence is common and if untreated, papulonecrotic tuberculid may persist for
years [6,11,23,50,95]. Patients typically improve within days to weeks of the initiation of anti-TB therapy [94,96].
(See 'Treatment overview' below.)
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Lichen scrofulosorum Lichen scrofulosorum is a rare tuberculid that most frequently occurs in children and
young adults with nodal, pulmonary, skeletal, or intracranial TB [4,15,34,97,98]. Lichen scrofulosorum has also been
reported after BCG vaccination and in association with M. avium-intracellulare infection [99-102].
Clinical features Lichen scrofulosorum presents with crops of firm 1 to 5 mm, asymptomatic, grouped,
yellow-red to brown-red papules (picture 11). Lesions tend to be follicular or perifollicular, and are most often
found on the trunk [4,11,23,50,51,98,103].
Diagnosis Similar to papulonecrotic tuberculid, the diagnosis of lichen scrofulosorum is based upon a
consistent clinical picture in the context of concordant histopathologic findings and evidence for TB infection. The
tuberculin skin test is often strongly positive [11,34,98]. Mycobacterial cultures are negative [6,11].
Histopathologic examination reveals tuberculoid granulomas in the upper dermis as well as around hair follicles
and eccrine glands. Acid-fast bacilli are not detected [6,11,34,57].
Differential diagnosis Other papular disorders may present with lesions that resemble lichen scrofulosorum.
As examples, lichen planus, lichenoid secondary syphilis, papular eczema, lichen nitidus, and papular sarcoidosis
should be considered in the differential diagnosis [6,11,51].
Clinical course Without treatment, lesions spontaneously resolve without scarring after several months to
several years [15]. Anti-TB treatment usually leads to complete resolution within weeks [11]. (See 'Treatment
overview' below.)
Erythema induratum of Bazin The terms "erythema induratum of Bazin" (EIB) and "nodular vasculitis" are used
to refer to a granulomatous lobular panniculitis of the lower extremities that may develop in association with a variety of
disorders, particularly infections [84,104]. Bazin first described this entity in 1855, with the belief of TB as the origin.
Although the two terms are often used interchangeably to refer to this presentation, some authors have preferably
utilized the term EIB to refer to TB-associated lesions [84,105]. Young women and middle-aged women are most
commonly affected [104].
Clinical features EIB classically presents with the development of mildly tender, dull red, subcutaneous
nodules on the lower legs over the course of several weeks. The lesions are most commonly located on the
posterior aspects of the lower legs and may be up to several centimeters in diameter [84,104]. Break-down of
the nodules often occurs, leading to the formation of deep, draining ulcers (picture 12A-C).
Diagnosis The diagnosis of TB-associated EIB is made based upon recognition of the clinical features,
histopathologic findings, and evidence for M. tuberculosis infection (eg, history of TB, a detectable focus of
infection, a positive tuberculin skin test, or improvement with TB therapy) [16,84,106]. Mycobacterial DNA can be
detected by PCR in 14 to 77 percent of biopsy specimens [84]. Usefulness of interferon-gamma release assays
has been noted [107,108].
Since EIB is a form of panniculitis, a biopsy that obtains an adequate sample of the subcutaneous fat is essential for
histopathologic examination. An excisional wedge biopsy is the preferred procedure. The tissue specimen usually
reveals a lobular or mixed lobular and septal panniculitis; tuberculoid or poorly formed granulomas; a mixed
inflammatory infiltrate with neutrophils, lymphocytes, and plasma cells; and fat necrosis [52]. Vascular changes are
also usually present; in some cases, necrotizing vasculitis is seen. Acid-fast bacilli typically are not detected [4,34].
If an association with TB is not found in a patient with skin lesions consistent with this disorder, other potential causes
of the eruption should be investigated. Hepatitis C is another disorder that may be a triggering factor for nodular
vasculitis/EIB [84,109,110].
Differential diagnosis Similar to EIB, nodules due to erythema nodosum primarily occur on the lower legs.
However, in contrast to EIB, lesions of erythema nodosum are more likely to occur on the anterior legs and
demonstrate a septal panniculitis on histopathologic examination (see "Erythema nodosum"). Other disorders to
consider include polyarteritis nodosa, tertiary syphilis, and other panniculitides [6].
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Clinical course The course of EIB is chronic. Although individual lesions spontaneously resolve over the course
of several weeks to a few months, leaving scars and postinflammatory hyperpigmentation [104], recurrences
may occur every three to four months [84]. Treatment with anti-TB agents is recommended for patients with
evidence for TB-associated disease [84,104]. Other agents that have been used for the management of
EIB/nodular vasculitis include potassium iodide, nonsteroidal antiinflammatory agents, dapsone, colchicine,
antimalarials, tetracyclines, gold salts, and systemic glucocorticoids [84].
Other Nodular tuberculid is a more described tuberculid disorder that has been reported in several patients
[111,112]. Similar to EIB, patients present with nodules on the lower legs. However, in contrast to EIB, granulomatous
inflammation occurs at the junction of the dermis and subcutaneous fat, rather than primarily within the panniculus. In
addition, the lesions do not tend to ulcerate.
TREATMENT OVERVIEW The treatment of cutaneous TB is the same as that for systemic TB. The administration
of a course of multidrug therapy is the treatment of choice [6,10,23,34,50,113]. An initial bactericidal phase given for
eight weeks to induce a rapid reduction in the number of bacteria is followed by a longer treatment phase designed to
eradicate any remaining bacteria [4,15,114]. The choice of a specific regimen is influenced by patient comorbidities
and immune status, as well as mycobacterial resistance patterns. Every effort should be made to culture the organism
for sensitivity testing. Drug treatment regimens for TB are reviewed separately. (See "Treatment of pulmonary
tuberculosis in HIV-uninfected patients" and "Treatment of pulmonary tuberculosis in the HIV-infected patient" and
"Tuberculosis disease in children", section on 'Treatment'.)
The response to treatment of cutaneous lesions can be assessed clinically. In general, treatment should be continued
for at least two months following the complete resolution of skin lesions.
Surgical intervention is not routinely utilized for the management of cutaneous TB, but is sometimes employed as an
adjunct to pharmacologic therapy [11]. Surgical excision has been utilized to aid in the management of extensive or
recalcitrant scrofuloderma. In addition, surgical excision, cauterization, and cryosurgery have been performed to
hasten the resolution of small, early lesions of TBVC and lupus vulgaris. Reconstructive plastic surgery after treatment
can be beneficial for patients with destructive lesions of lupus vulgaris [11,23].
ASSOCIATED DISORDERS
BCG vaccination reactions The bacille Calmette-Gurin (BCG) vaccine is composed of a living attenuated strain
of M. bovis that is used in many parts of the world to enhance immunity to TB. Rarely, dermatologic complications of
BCG vaccination occur. Local tissue reactions, ulceration, abscess formation, scrofuloderma, lupus vulgaris, EIB,
papulonecrotic tuberculid, and lichen scrofulosorum-like lesions have been described [6,99,115]. (See "BCG
vaccination", section on 'Safety and adverse effects'.)
SUMMARY AND RECOMMENDATIONS
Tuberculosis (TB) is a mycobacterial infection that can affect multiple organ systems. M. tuberculosis, an
acid-fast bacillus, is the primary inciting organism of cutaneous TB. (See 'General principles' above.)
Cutaneous TB may result from direct entry of the mycobacterium into the skin or from local or hematogenous
spread of M. tuberculosis from an endogenous focus. The immune response of the host to M. tuberculosis is an
important factor in the development of cutaneous TB. (See 'General principles' above and 'Clinical variants'
above.)
A variety of diagnostic studies are used for the evaluation of patients with suspected cutaneous TB.
Mycobacterial cultures represent the gold standard for confirming active infection. Other studies that may be
utilized for patient evaluation include stained smears, histopathologic evaluation, tuberculin skin tests,
interferon-gamma release assays, and nucleic acid amplification tests. (See 'Diagnostic tests' above.)
The tuberculids are a group of cutaneous disorders that may reflect hypersensitivity reactions to M. tuberculosis
antigens. The three main subtypes of tuberculids are papulonecrotic tuberculid, lichen scrofulosorum, and
erythema induratum of Bazin. Organisms usually are not detectable in cultures, smears, or pathology specimens
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taken from tuberculid skin lesions. (See 'Tuberculids' above.)

Given the plethora of manifestations of cutaneous tuberculosis, a high index of suspicion is of utmost importance
in making the correct diagnosis.
Systemic treatment with multidrug therapy is the cornerstone of treatment of cutaneous TB. (See 'Treatment
overview' above.)
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96. Jordaan HF, Van Niekerk DJ, Louw M. Papulonecrotic tuberculid. A clinical, histopathological, and
immunohistochemical study of 15 patients. Am J Dermatopathol 1994; 16:474.
97. Singal A, Bhattacharya SN. Lichen scrofulosorum: a prospective study of 39 patients. Int J Dermatol 2005;
44:489.
98. Kumar M, Satija T, Khanna D. Lichen scrofulosorum: An important diagnostic marker of underlying tuberculosis.
Ann Pediatr Child Health 2014; 2:1019.
99. Park YM, Kang H, Cho SH, Cho BK. Lichen scrofulosorum-like eruption localized to multipuncture BCG
vaccination site. J Am Acad Dermatol 1999; 41:262.
100. Tobita R, Sumikawa Y, Imaoka K, et al. Lichen scrofulosorum caused by pulmonary Mycobacterium avium
complex (MAC) infection. Eur J Dermatol 2011; 21:619.
101. Komatsu H, Terunuma A, Tabata N, Tagami H. Mycobacterium avium infection of the skin associated with lichen
scrofulosorum: report of three cases. Br J Dermatol 1999; 141:554.
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102. Jacobsen G, Samolitis NJ, Harris RM. Lichenoid eruption in a patient with AIDS--lichen scrofulosorum (LS)
tuberculid with underlying MAC infection. Arch Dermatol 2006; 142:385.
103. Sehgal VN, Srivastava G, Khurana VK, et al. An appraisal of epidemiologic, clinical, bacteriologic,
histopathologic, and immunologic parameters in cutaneous tuberculosis. Int J Dermatol 1987; 26:521.
104. Gilchrist H, Patterson JW. Erythema nodosum and erythema induratum (nodular vasculitis): diagnosis and
management. Dermatol Ther 2010; 23:320.
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107. Vera-Kellet C, Peters L, Elwood K, Dutz JP. Usefulness of Interferon- release assays in the diagnosis of
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108. Sim JH, Whang KU. Application of the QuantiFERON-TB Gold test in erythema induratum. J Dermatolog Treat
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Topic 15866 Version 6.0
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GRAPHICS
Tuberculoid granuloma
Tuberculoid granuloma. Epitheliod histiocytes, multinucleated giant

cells, and a dense lymphocytic infiltrate are present.
Courtesy of Dr. Ma. Flordeliz Abad-Casintahan.
Graphic 74597 Version 2.0
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Cutaneous sarcoidosis - histopathology
This histologic specimen from a nodular lesion demonstrates a

granulomatous infiltrate throughout the dermis. Circumscribed "naked,"
epithelioid granulomas are present.
Courtesy of Shane A Meehan, MD.
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Cutaneous sarcoidosis - histopathology
Large aggregates of histiocytes forming tight, well-demarcated

granulomas are present in the dermis. The granulomas lack any signs of
caseating necrosis and are surrounded by a small number of
lymphocytes.
Courtesy of Shane A Meehan, MD.
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Interpretation of tuberculin skin test

Tuberculin
skin test
reaction
size (mm)
5
Situation in which reaction is considered positive*
HIV infection
Close contact of active contagious case
Abnormal chest radiograph with fibrotic changes consistent with old TB
Immunosuppressed patients: TNF-alpha inhibitors, chemotherapy, organ
transplantation, glucocorticoid treatment (equivalent of 15 mg/day prednisone for
1 month)
10
Persons with clinical conditions that increase the risk of reactivation, including
silicosis , chronic renal failure requiring dialysis , diabetes mellitus, some
malignancies (leukemias, lymphomas, carcinoma of the head, neck, or lung),
underweight (10 percent ideal body weight), jejunoileal bypass, injection drug
users
Children less than 4 years of age
Foreign born from countries with incidence >25/100,000
Residents and employees in high-risk settings, such as prisons, jails, healthcare
facilities, mycobacteriology labs, and homeless shelters
15
Healthy individuals age 4 years and older with low likelihood of true TB infection
TB: tuberculosis; TNF: tumor necrosis factor; TST: tuberculin skin test.
* The goal of testing for latent tuberculosis infection is to identify individuals who are at increased risk for
the development of tuberculosis and therefore would benefit from treatment of latent TB infection. Only
those who would benefit from treatment should be tested, so a decision to test presupposes a decision to
treat if the test is positive (refer to text).
The United States Centers for Disease Control and Prevention (CDC) recommends a 10 mm induration
definition for patients with silicosis or chronic renal failure. However, population-based studies demonstrate
that the relative risk for development of active tuberculosis in this category is high (10x that of healthy
individuals). For this reason, many favor a lower threshold for a positive test (5 mm).
The CDC indicates that only those foreign-born individuals who immigrated within the past 5 years should
be tested (regardless of age), although others do not favor this practice since most recently arrived foreign
born with positive TST have old (not recent) infection.
Persons with a low likelihood of true TB infection should not be tested routinely unless they are entering a
high-risk setting such as starting employment at a healthcare facility. A threshold of 15 mm is used in the
United States, and is appropriate for healthy individuals with low likelihood of true TB infection and high
likelihood of exposure to nontuberculous mycobacteria (eg, southern United States). However, Canadian
guidelines use a threshold of 10 mm for healthy individuals given the lower likelihood of exposure to
nontuberculous mycobacteria. (Refer to the topic on Epidemiology of nontuberculous mycobacterial
infections.).
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Potential causes of false-negative tuberculin tests

Technical (potentially correctable)
Tuberculin material:
Improper storage (exposure to light or heat)
Contamination, improper dilution, or chemical denaturation
Administration:
Injection of too little tuberculin or too deeply (should be intradermal)
Administration more than 20 minutes after drawing up into the syringe
Reading:
Inexperienced or biased reader
Error in recording
Biologic (not correctable)

Infections:
Active tuberculosis (especially if advanced)
Other bacterial infection (typhoid fever, brucellosis, typhus, leprosy, pertussis)
HIV infection (especially if CD4 count <200)
Other viral infection (measles, mumps, varicella)
Fungal infection (South American blastomycosis)
Recent live-virus vaccination (measles, mumps, polio)

Immunosuppressive drugs (corticosteroids, tumor necrosis factor inhibitors, and others)
Metabolic disease (chronic renal failure, severe malnutrition, stress [surgery, burns])
Diseases of lymphoid organs (lymphoma, chronic lymphocytic leukemia, sarcoidosis)
Age (infants <6 months, older adults)
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A violaceous plaque with a verrucous surface is present on the knee.

Scars are evident at the periphery of the plaque.
Courtesy of the Research Institute for Tropical Medicine, Philippines.
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This specimen from a lesion of tuberculosis verrucosa cutis demonstrates

epidermal acanthosis, intraepidermal abscess formation, and
a lichenoid lymphohistiocytic infiltrate in the dermis (A). A multinucleated giant
cell is visible at higher magnification (B).
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Scrofuloderma
A draining, ulcerated nodule is present on the flank.

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Tuberculosis cutis orificialis
Multiple nodules are present on the perianal skin.

Reproduced with permission from: Dr. M Ramam, New Delhi.
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Lupus vulgaris
Papular lesion of lupus vulgaris.

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Lupus vulgaris
Hyperkeratosis, pseudoepitheliomatous hyperplasia, and tuberculoid

granulomas are evident in this specimen from a lesion of lupus vulgaris.
Courtesy of Dr. Ma. Flordeliz Abad-Casintahan.
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Metastatic tuberculous abscesses (tuberculous

gummas)
Multiple ulcers are present on the back of this patient with metastatic
tuberculous abscesses, also known as tuberculous gummas.
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Papulonecrotic tuberculid
A symmetrical eruption of erythematous to violaceous papules is present

on the legs of this patient with papulonecrotic tuberculid.
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Papulonecrotic tuberculid
A purulent ulcer is present on the penis in this patient with

papulonecrotic tuberculid.
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Lichen scrofulosorum
Multiple follicular lichenoid papules are present on the trunk.

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Erythema induratum of Bazin
An ulcerated nodule and multiple scars are present on the lower legs of
this patient with erythema induratum of Bazin.
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Erythema induratum (nodular vasculitis)
Multiple nodules are present on the posterior lower legs.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.
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Erythema induratum (nodular vasculitis)
Multiple nodules are present on the posterior lower legs.

Reproduced with permission from: www.visualdx.com. Copyright Logical
Images, Inc.
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Disclosures
Disclosures: Evangeline B Handog, MD Nothing to disclose. Maria Juliet E Macarayo, MD Nothing to disclose. Ted Rosen, MD
Consultant/Advisory Boards: Anacor [Onychmycosis (Tavaborole)]; Valeant [Onychmycosis (Efinaconazole)]; Leo [Actinic keratosis]. Abena O
Ofori, MD Nothing to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a
multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
17/08/2015 07:58 p.m.

Cutaneous Manifestations of Tuberculosis

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Cutaneous Manifestations of Tuberculosis

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Cutaneous manifestations of tuberculosis

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