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Cutaneous manifestations of tuberculosis

Cutaneous manifestations of tuberculosis
Literature review current through: Jan 2024.
This topic last updated: Jul 14, 2023.

INTRODUCTION — Tuberculosis (TB) is a mycobacterial infection that most frequently occurs due to infection with Mycobacterium tuberculosis, an acid-fast bacillus. Although there has been progress in the delivery of TB care and a decline in TB-related deaths globally, TB still remains a major public health concern [1]. (See "Epidemiology of tuberculosis", section on 'Global burden'.)

Cutaneous involvement is a relatively uncommon manifestation of TB. The clinical findings vary and include papules, verrucous plaques, suppurative nodules, chronic ulcers, and other lesions. The pathway of bacterial entry into the skin, the host's immune status, and the presence or absence of prior host sensitization to M. tuberculosis influence the morphologic presentation of cutaneous TB.

The cutaneous disorders associated with TB will be reviewed here. These include:

Primary inoculation TB (picture 1)

TB verrucosa cutis (picture 2A-B)

Scrofuloderma (picture 3A-B)

TB cutis orificialis (picture 4)

Lupus vulgaris (picture 5)

Metastatic tuberculous abscesses (picture 6)

Acute miliary TB

Tuberculids (papulonecrotic tuberculid (picture 7A-B), lichen scrofulosorum (picture 8), erythema induratum of Bazin [EIB] (picture 9A-C))

General principles of TB are reviewed separately.

(See "Tuberculosis disease in children: Epidemiology, clinical manifestations, and diagnosis".)

(See "Epidemiology of tuberculosis".)

(See "Tuberculosis: Natural history, microbiology, and pathogenesis".)

(See "Pulmonary tuberculosis: Clinical manifestations and complications".)

HISTORY — Cutaneous TB was first documented in 1826, when Laennec reported his own "prosector's wart," a lesion that likely represented TB verrucosa cutis, a variant of TB that results from direct entry of the organism into the skin [2]. However, the causative organism of TB was unknown until the discovery of M. tuberculosis in 1882 [3]. Subsequently, the bacillus was detected in cutaneous lesions [4]. (See 'True cutaneous tuberculosis' below.)

EPIDEMIOLOGY — Cutaneous TB is a relatively uncommon manifestation of TB. According to World Health Organization (WHO) 2019 data, extrapulmonary TB constituted 15 percent of the seven million incident cases in 2018 [1]. Cutaneous lesions account for less than 2 percent of all extrapulmonary manifestations [5-7].

Similar to other forms of TB, a resurgence of cutaneous TB has been noted in parts of the world where HIV infection and multidrug-resistant TB are prevalent [8-10]. (See "Epidemiology of tuberculosis", section on 'Global burden'.)

ETIOLOGY — TB is defined as a disorder caused by mycobacteria in the M. tuberculosis complex, which includes M. tuberculosis, Mycobacterium bovis, Mycobacterium africanum, Mycobacterium microti, Mycobacterium canettii, Mycobacterium caprae, and Mycobacterium pinnipedii [11]. M. tuberculosis, a slow-growing, acid-fast bacillus, is the predominant causative organism of cutaneous TB. (See "Tuberculosis: Natural history, microbiology, and pathogenesis", section on 'Microbiology'.)

M. bovis and the Bacille Calmette-Guérin (BCG) vaccine (a vaccine composed of attenuated M. bovis) have also been associated with the development of cutaneous lesions [12-14]. (See "Mycobacterium bovis" and 'Bacille Calmette-Guérin vaccination reactions' below.)

CLASSIFICATION — Classification systems for cutaneous TB vary. Commonly, cutaneous TB is divided into two major groups: true cutaneous TB and tuberculids [10]. (See 'True cutaneous tuberculosis' below and 'Tuberculids' below.)

True cutaneous TB includes conditions in which cutaneous lesions are a direct manifestation of infection at the site of the skin lesions. In true cutaneous TB, mycobacteria can be identified in the sites of skin involvement using tests such as smears, in situ hybridization of pathology specimens, or cultures [10]. Detection may be more difficult in some forms of true cutaneous TB. (See 'Bacterial load' below.)

In contrast, tuberculids are considered to result from a hypersensitivity reaction to mycobacterial antigens. Mycobacteria typically are not detectable via smears, histopathologic techniques, or cultures from tuberculid lesions. (See 'Tuberculids' below.)

True cutaneous tuberculosis — The characteristic most often used to subdivide true cutaneous TB is the mode of infection. The quantity of organisms typically present in the skin (bacterial load) is another method of classification. (See 'Mode of infection' below and 'Bacterial load' below.)

Mode of infection — Most cases of true cutaneous TB arise from contiguous spread or hematogenous dissemination to the skin from an endogenous focus of infection. Direct entry of M. tuberculosis into the skin (ie, inoculation from an exogenous source) occasionally results in localized infection [15,16]. (See 'True cutaneous tuberculosis' below.)

Classification according to mode of infection:

Contiguous spread or autoinoculation (see 'Contiguous spread' below)

Scrofuloderma

TB cutis orificialis

Hematogenous spread to the skin (see 'Hematogenous spread' below)

Lupus vulgaris

Acute miliary TB

Metastatic tuberculous abscess

Inoculation from an exogenous source (see 'Exogenous inoculation' below)

Primary inoculation TB/TB chancre

TB verrucosa cutis

Bacterial load — True cutaneous TB may also be classified according to the bacterial load in the skin [17]:

Multibacillary forms (bacilli easily detectable in tissue or exudate):

Primary inoculation TB/TB chancre

Scrofuloderma

TB cutis orificialis

Acute miliary TB

Metastatic tuberculous abscess

Paucibacillary forms (bacilli hard to detect in tissue or exudate):

TB verrucosa cutis

Lupus vulgaris

Tuberculids — The tuberculids are TB-associated cutaneous disorders that represent hypersensitivity reactions to mycobacterial antigens, rather than manifestations of local skin infection. (See 'Tuberculids' below.)

The tuberculids include:

Papulonecrotic tuberculid

Lichen scrofulosorum

Erythema induratum of Bazin (EIB)

RISK FACTORS — The major risk factors for the development of TB are increased exposure to sources of infection and immunologic susceptibility of the host to infection. (See "Epidemiology of tuberculosis", section on 'Risk factors'.)

Host factors that appear to influence risk for specific cutaneous manifestations of TB include age, sex, and immune status [18-21]:

Age and sex – Primary inoculation TB, scrofuloderma, and lichen scrofulosorum commonly affect children, and lupus vulgaris affects adults. Erythema induratum of Bazin (EIB) occurs more frequently in females than in males.

Immune status – Poor immunity against M. tuberculosis is a risk factor for TB cutis orificialis, metastatic tuberculous abscess, and acute miliary TB [3,15]. Higher levels of immunity against M. tuberculosis are linked with TB verrucosa cutis, lupus vulgaris, and tuberculids [15]. (See 'True cutaneous tuberculosis' below.)

HISTOPATHOLOGY — The characteristic histopathologic finding in true 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 10A-B) [22,23].

Although tuberculoid granulomas are a common finding, their detection does not confirm the presence of TB, and their absence does not exclude the diagnosis. Leprosy, tertiary syphilis, granulomatous rosacea, leishmaniasis, deep fungal infections, and other disorders may also present with tuberculoid granulomas [23-25].

Tuberculoid granulomas should be distinguished from the classic granulomas of sarcoidosis. Compared with tuberculoid granulomas, sarcoidal granulomas tend to be more circumscribed, exhibit fewer peripheral inflammatory cells ("naked granulomas"), and are not likely to have central caseation necrosis (picture 11A-B). (See "Cutaneous manifestations of sarcoidosis", section on 'Histopathology'.)

DIAGNOSTIC APPROACH — Suspicion for cutaneous TB can arise from the recognition of suggestive clinical lesions during a physical examination or the detection of features supportive of cutaneous TB on a skin biopsy. Multiple tests are used to evaluate patients for cutaneous manifestations of TB. (See 'General approach' below and 'Specific tests' below and 'Challenging cases' below.)

General approach — The diagnosis of a cutaneous TB is typically made based upon the detection of consistent clinical, pathologic, and laboratory findings. Methods of detecting the causative mycobacteria include mycobacterial culture (the gold standard for diagnosis of true cutaneous TB), stained smears, and lesional biopsies. (See "Diagnosis of pulmonary tuberculosis in adults", section on 'Microbiologic testing'.)

Tests that evaluate for immunologic evidence of infection, such as tuberculin skin testing and interferon-gamma release assays, can be helpful for supporting a diagnosis, particularly when the results of pathologic and microbiologic assessments are negative or inconclusive. Additionally, nucleic acid amplification (NAA) tests to detect mycobacterial deoxyribonucleic acid (DNA) may play a role in diagnosis.

For patients who present with clinical features that raise suspicion for cutaneous TB, our typical initial approach includes:

Lesional skin biopsy for histopathologic examination

Acid-fast bacilli (AFB) smear from exudate or biopsy tissue

Mycobacterial culture from exudate or biopsy tissue

Testing for immunologic evidence of TB infection (tuberculin skin test or interferon-gamma release assay)

The expected results of these tests vary based upon the specific diagnosis. Culture, smears, and histopathology often fail to detect M. tuberculosis in paucibacillary variants of cutaneous TB due to the relatively low number of organisms in lesional tissue. Similarly, cultures and smears are not typically useful for the diagnosis of tuberculids, in which mycobacteria generally are not detected in skin lesions. (See 'True cutaneous tuberculosis' below and 'Tuberculids' below.)

NAA tests are primarily used as an adjunct to clinicopathologic and microbiologic evaluation for cutaneous TB [24]. Although NAA testing is an established diagnostic test for pulmonary TB, the role NAA testing should play in the diagnosis of cutaneous TB is being explored, particularly in cases in which detection of M. tuberculosis through other means is difficult [26-29]. (See 'Specific tests' below.)

In scenarios in which strong clinical suspicion for cutaneous TB remains despite an inability to confirm the diagnosis with histopathology or laboratory tests, a response to an empirical trial of anti-TB therapy can support the diagnosis. (See 'Challenging cases' below.)

Specific tests — Tests utilized in the diagnosis of cutaneous manifestations of TB are briefly reviewed below:

Detection of mycobacteria or tissue findings consistent with cutaneous manifestations of TB:

Mycobacterial culture – Mycobacterial culture remains the gold standard for determining the presence of active TB infection, providing the means to distinguish M. tuberculosis from nontuberculous mycobacteria and allowing the determination of antibiotic sensitivity [5,13,15,30-32]. A tissue biopsy of the skin lesion(s) is the recommended specimen for culture; discharge from draining lesions may be used as well [33].

Concerns about mycobacterial culture, especially with the paucibacillary forms, are the potential for low mycobacterial yields and the slow growth rate of M. tuberculosis. Results may be delayed for one to several weeks, depending upon the culture method [29]. (See "Diagnosis of pulmonary tuberculosis in adults", section on 'Mycobacterial culture'.)

Acid-fast bacilli (AFB) smear – The examination for AFB 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, TB cutis orificialis, or metastatic tuberculous abscess. (See "Diagnosis of pulmonary tuberculosis in adults", section on 'Sputum AFB smear'.)

The specimen for an AFB smear is best derived from a tissue biopsy taken from the edge of an actual skin lesion. For cutaneous TB lesions from which exudates are easily obtained, exudate can also serve as a specimen.

Skin biopsy for histopathologic examination The accessibility of skin lesions makes the obtainment of a tissue biopsy a relatively simple procedure. Biopsies of cutaneous manifestations of TB can reveal tuberculoid granulomas, AFB, or other characteristic histopathologic features of specific variants. (See 'Histopathology' above and 'True cutaneous tuberculosis' below and 'Tuberculids' below.)

The preferred biopsy technique is an incisional biopsy at the edge of the representative lesion. A 3 to 5 mm punch biopsy tool may also be used to obtain a specimen [34].

Detection of immunologic evidence of M. tuberculosis infection:

Tuberculin skin test – The tuberculin skin test identifies individuals sensitized to M. tuberculosis [31,32,35,36]. The immunologic basis for the tuberculin skin test is a delayed hypersensitivity reaction involving T cells. (See "Use of the tuberculin skin test for diagnosis of tuberculosis infection (tuberculosis screening) in adults" and "Tuberculosis infection (latent tuberculosis) in children", section on 'Tuberculin skin test'.)

The Mantoux technique, the recommended method for performing tuberculin skin testing, involves the intradermal injection of 0.1 mL tuberculin antigen (purified protein derivative [PPD]) into the inner surface of the forearm, followed by re-examination of the injection site for induration (not erythema) 48 to 72 hours later (table 1). It has a specificity of 63 percent and a sensitivity between 33 and 96 percent for cutaneous TB that becomes higher in unvaccinated populations [12,37]. Reactivity to the tuberculin protein may be impaired in young infants, older adults, and patients with deficient cellular immunity (table 2).

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 [24,35]. 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 [38]. (See "Use of interferon-gamma release assays for diagnosis of tuberculosis infection (tuberculosis screening) in adults".)

Unlike the tuberculin skin test, the Bacille Calmette-Guérin (BCG) vaccination does not influence the results of this test. However, prior infections with select environmental mycobacteria, such as Mycobacterium marinum, Mycobacterium kansasii, and Mycobacterium szulgai, may result in a false-positive interferon-gamma release assay [39]. (See "Use of interferon-gamma release assays for diagnosis of tuberculosis infection (tuberculosis screening) in adults".)

Detection of M. tuberculosis DNA:

NAA tests – NAA tests for M. tuberculosis detect M. tuberculosis DNA in tissue specimens. These tests provide rapid results (within two hours), can differentiate between M. tuberculosis and other species of mycobacteria, and may identify gene mutations associated with drug resistance (including rpoB gene for rifampicin resistance) [32,40]. (See "Diagnosis of pulmonary tuberculosis in adults", section on 'NAA (probe-based) testing'.)

In the evaluation of cutaneous TB, NAA tests are primarily used as an adjunct to clinicopathologic and microbiologic evaluation [24]. The potential advantage of NAA testing is rapid detection of M. tuberculosis, especially when AFB staining and culture results are negative or when fresh tissue or exudate has not been collected for culture [41].

Sensitivity and specificity of NAA tests vary from 25 to 100 percent and 74 to 100 percent, respectively [29]. NAA tests may most likely be positive in the multibacillary forms of cutaneous TB [42-45]. Although NAA tests may be positive in paucibacillary disease when both cultures and histopathologic stains for the organism are negative, the results of testing are inconsistent [43,46-50]. In addition, the availability of NAA testing in resource-limited countries is another constraint [43,47,51].

Challenging cases — In difficult cases, a therapeutic trial of anti-TB medications may be used to confirm the diagnosis of cutaneous TB. For true cutaneous TB, a response to multidrug therapy is usually evident within six weeks [51-53]. Expectations for tuberculid responses to anti-TB therapy are reviewed below. (See 'Tuberculids' below.)

The diagnosis should be re-evaluated in patients who fail to improve within the expected period. Of note, improvement may be less easily detected in patients with minimal clinical activity prior to treatment [52]. (See 'Treatment overview' below.)

TRUE CUTANEOUS TUBERCULOSIS — The characteristics of the subtypes of true cutaneous TB, grouped according to mode of infection (exogenous inoculation, contiguous spread, or hematogenous spread), are reviewed below.

Exogenous inoculation — Primary inoculation TB and TB verrucosa cutis 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 TB verrucosa cutis develops in individuals with prior exposure to the bacterium. TB verrucosa cutis is much more common than the primary inoculation variant [3].

Primary inoculation tuberculosis — Primary inoculation TB is a rare multibacillary form of cutaneous TB that results from the direct entry of the organism into the skin or mucosa of a nonsensitized individual:

Alternative terms – Tuberculous chancre, primary tuberculous complex.

Risk factors – Primary inoculation TB primarily occurs in children in endemic areas [3] but has been reported in adults as well [54,55]. Minor trauma resulting in a compromised skin barrier usually precedes the infection. Surgical procedures performed with unsterilized equipment, tattoos, piercings, and acupuncture sites may also lead to lesion development [39,54,56,57].

Clinical features Primary inoculation TB becomes clinically evident within one month after inoculation. The classic 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 [3]. Significant crusting may occur.

Primary inoculation TB is generally located in the upper limbs, lower limbs, or the buttocks [39]. The hands may be the most frequent location [13,58]. Sporotrichoid presentations (ie, linear distribution of nodules along lymphatic vessels) have been reported (picture 1) [59].

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 [3,42]. The combination of the cutaneous findings and lymphadenopathy in primary inoculation TB are analogous to the Ghon complex of pulmonary TB infection [17,58]. (See "Pulmonary tuberculosis: Clinical manifestations and complications", section on 'Natural history'.)

Diagnosis – A diagnosis of primary inoculation TB can often be made through a smear or skin biopsy taken from an early lesion. Early primary inoculation TB is multibacillary, and acid-fast bacilli (AFB) are usually easily detected [23,60,61]. A positive culture confirms the diagnosis.

Skin biopsies obtained early in the disease course reveal necrosis, neutrophilic infiltrates, and numerous AFB [3]. 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 [60,62,63]. (See 'Histopathology' above.)

The tuberculin skin test is typically negative at the time of disease onset but later becomes positive [55,64].

Differential diagnosis – The differential diagnosis of primary inoculation TB includes other disorders that may present with inflammatory nodules or ulcers. Examples include abscesses, foreign body granulomas, sarcoidosis, and other nontuberculous mycobacterial infections.

Disease course Left untreated, primary inoculation TB may spontaneously regress or may persist for up to one year [3,39]. A scar typically remains after resolution, with calcification of the regional lymph nodes [39,58]. (See 'Treatment overview' below.)

Hematogenous spread of the bacillus leading to TB of other organs or acute miliary disease is a potential complication [23]. Erythema nodosum occurs in approximately 10 percent of cases [3]. Occasionally, lupus vulgaris, scrofuloderma, or TB verrucosa cutis develops at the site of a lesion [3,58]. (See "Clinical manifestations, diagnosis, and treatment of miliary tuberculosis" and "Erythema nodosum".)

Tuberculosis verrucosa cutis — TB verrucosa cutis is a paucibacillary 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 [15,23,31,42]. Inoculation typically occurs from an exogenous source; rarely, inoculation may occur from the patient's own sputum [12]:

Alternative terms – Prosector's wart, anatomic TB, verruca necrogenica, warty TB.

Risk factors – 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 [3,65].

Clinical features In adults, TB verrucosa cutis most frequently develops on the acral extremities; the fingers and dorsum of the hands are commonly affected [3,24,31,65-67]. The ankles or buttocks are frequent sites for lesion occurrence in children [31]. Rare lip involvement has been reported [68].

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 2A-B). TB verrucosa cutis grows via peripheral extension; central clearing and atrophy may or may not be present [31].

Although ulceration is uncommon, fissures that exude purulent drainage or keratinous material may occur [3,12]. 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 [12,66].

Diagnosis Correlation of the physical findings with a skin biopsy plus other evidence of TB infection, such as a positive tuberculin skin test or interferon-gamma release assay, is the primary method for diagnosing TB verrucosa cutis [69].

The histopathologic findings of TB verrucosa cutis include (picture 12) [3,23,62,70]:

Pseudoepitheliomatous hyperplasia

Marked hyperkeratosis

Microabscesses in the superficial dermis or the pseudoepitheliomatous rete pegs

Frequent presence of an inflammatory infiltrate composed of epithelioid cells and giant cells in the upper and middle dermis

Frank tuberculoid granulomas may or may not be evident [3,23,62,70].

The tuberculin skin test is typically strongly positive, indicative of the high level of immunity against the bacterium [31,61]. Although a few AFB can be detected on careful histopathologic examination in some cases, cultures taken from lesions of TB verrucosa cutis are often negative [31,42].

Differential diagnosis – The differential diagnosis of TB verrucosa cutis includes other diseases that may present with hyperkeratotic or verrucous plaques, including atypical mycobacterioses, blastomycosis, Majocchi's granuloma, chromoblastomycosis, tertiary syphilis, verrucous epidermal nevus, hypertrophic lichen planus, hyperkeratotic lupus vulgaris, halogenoderma, benign keratoses, prurigo nodularis, and verruca vulgaris [23,31,61].

Disease course Skin lesions may persist for years if left untreated, although spontaneous resolution can also occur [15,23,42,61]. Patients typically improve with anti-TB therapy [42]. (See 'Treatment overview' below.)

Contiguous spread — TB infection can be transmitted to the skin from adjacent structures. Scrofuloderma, TB cutis orificialis, and lupus vulgaris can occur as a result of this process.

Scrofuloderma — Scrofuloderma is a multibacillary 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 [18,42,56]:

Alternative term – TB colliquativa cutis.

Risk factors – Scrofuloderma may occur at any age but most commonly develops in children, adolescents, and older adult individuals [23,42,61,66].

In addition to M. tuberculosis infection, M. bovis infection related to the consumption of contaminated milk may lead to scrofuloderma [71]. The occurrence of scrofuloderma following Bacille Calmette-Guérin (BCG) vaccination has also been reported [72]. (See "Mycobacterium bovis" and "Prevention of tuberculosis: BCG immunization and nutritional supplementation".)

Scrofuloderma has also been reported to occur with other forms of cutaneous TB, such as TB verrucosa cutis [68,73,74].

Clinical features – Early lesions of scrofuloderma are firm, painless, subcutaneous, red-brown nodules that overly foci of tuberculous infection (picture 3B). The neck, axillae, and groin are often involved, with the cervical lymph nodes as the most common source of infection [3,66].

The suppurative nodules gradually enlarge and eventually form ulcers and sinus tracts that drain watery, purulent, or caseous material (picture 3A) [12,42]. Lesions may be single or multiple. A linear arrangement can occur if the infection overlies multiple lymph nodes within a region [3].

Diagnosis The diagnosis of scrofuloderma is based upon the identification of the causative organism by culture, smear, or skin biopsy [12]. Skin biopsy reveals tuberculoid granulomas surrounding areas of wedge-shaped necrosis [42,70].

Tuberculin skin testing is typically positive, exhibiting a pronounced skin reaction [23,60].

Differential diagnosis The differential diagnosis includes other causes of suppurative nodules, such as atypical mycobacterioses, sporotrichosis, actinomycosis, nocardiosis, paracoccidioidomycosis, coccidioidomycosis, lymphogranuloma venereum, syphilitic gumma, severe forms of acne conglobata, and hidradenitis suppurativa [23,31,58,61]. In the neck, scrofuloderma may mimic a dental sinus. Detection of M. tuberculosis distinguishes scrofuloderma.

Disease course Spontaneous healing may occur, but it may be years before lesions are completely replaced by scar tissue [12]. Scars may be depressed, retractable, adherent, hypertrophic, or keloidal [42,60,61,66]. The characteristic scars can lead to the recognition of patients with a prior history of scrofuloderma.

Coexistence with an active pulmonary process is relatively common [61,66]. In addition, lupus vulgaris may develop within or near sites of scrofuloderma [23]. (See 'Lupus vulgaris' below.)

Tuberculosis cutis orificialis — TB cutis orificialis is a rare multibacillary manifestation of TB that typically occurs in the setting of advanced extracutaneous TB and immunodeficiency:

Alternative terms – Orificial TB, TB ulcerosa cutis et mucosae.

Risk factors – TB cutis orificialis develops in individuals with both advanced TB of the gastrointestinal tract, lungs, or genitourinary tract and dramatically impaired cell-mediated immunity [13,23,31,42]. The skin lesions result from the autoinoculation of the mucocutaneous tissues near body orifices by the draining sites of visceral infection [12,24]. TB cutis orificialis most frequently occurs in middle-aged and older adults [61].

Clinical features TB cutis orificialis occurs on the oral, nasal, or anogenital skin or mucosa [12,24]. The most frequent oral sites are the distal and lateral tongue; lesions may also involve the palate, lips, or other sites [12,23,75].

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 (picture 4) [12,15,31,61]. Ulcers have a pseudomembranous, fibrinous base. Inflammation and edema are often present at the peripheral margins [3].

Diagnosis The possibility of TB cutis orificialis should be considered in patients with nonhealing, periorificial ulcers and signs or symptoms suggestive of advanced TB [60]. The detection of AFB in affected tissue via culture, stained smear, or skin biopsy confirms the diagnosis.

Histopathologic examination of skin biopsies demonstrates [3,31,61,76]:

Easily detectable bacilli in the ulcer walls

Tuberculoid granulomas at the ulcer edge and in the deep dermis

Cutaneous necrosis

Intense nonspecific cellular infiltrates

Tuberculin skin tests are often negative in patients with TB cutis orificialis due to the associated impairment in host immunity.

Because TB cutis orificialis occurs as a consequence of visceral infection, the focus of active extracutaneous TB must be sought as part of the patient evaluation [66]. (See "Tuberculosis disease in children: Epidemiology, clinical manifestations, and diagnosis", section on 'Diagnosis' and "Diagnosis of pulmonary tuberculosis in adults".)

Differential diagnosis Other causes of persistent, periorificial ulcers should be considered during the evaluation of patients with suspected TB cutis orificialis. Examples include aphthous ulcers, lymphogranuloma venereum, syphilis, South American blastomycosis, mucocutaneous leishmaniasis, and cutaneous malignancies, such as squamous cell carcinoma [3,23,61].

Disease course – The presence of TB cutis orificialis heralds a poor overall prognosis, as patients tend to have severe internal organ disease prior to skin manifestations [23,42]. Without successful treatment of the TB infection, the lesions progress and may eventually contribute to the development of fatal miliary TB [77]. Although resolution within two months after the initiation of treatment has been reported [77-79], other cases may be recalcitrant to treatment [12].

Lupus vulgaris — Lupus vulgaris is a chronic and progressive paucibacillary form of cutaneous TB that represents a reactivation of TB infection in people with moderate to high immunity against the bacillus [3,15]. Lupus vulgaris may occasionally occur as a result of direct extension from an underlying focus of infection or via lymphatic or hematogenous spread:

Alternative term – TB lupus.

Risk factors – Lupus vulgaris is considered the most common form of cutaneous TB in Europe and some areas of India [21,41,50,80-83]. In contrast, scrofuloderma appears to be more prevalent in some tropical regions [17,84,85].

Lupus vulgaris occurs in individuals of all ages. For unknown reasons, females are two to three times more likely than males to be affected [23].

The development of lupus vulgaris has also been reported in patients with prior TB verrucosa cutis, scrofuloderma, and as a rare complication of BCG vaccination or primary inoculation TB [39,86-90].

Although the most common causative organism is M. tuberculosis, there are reported cases caused by M. bovis, and clinical presentation is similar to 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 [91,92].

Clinical features The clinical findings of lupus vulgaris vary. The classic plaque presentation begins as a collection of discrete, red-brown papules that subsequently coalesce to form an indolent, asymptomatic plaque (picture 5). 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 [5,12,13,58]. Secondarily infected lesions may exhibit a seropurulent discharge and crusting.

In Western countries, lupus vulgaris often develops on the head and neck, while in tropical and subtropical areas, lesions are commonly found on the lower extremities or buttocks [42,93]. A multifocal distribution may also occur [68,94].

Similar to other granulomatous disorders, such as sarcoidosis and leprosy, diascopy (examination of the lesion under compression with a glass slide) of nonhyperkeratotic areas of lupus vulgaris often reveals a yellow-brown color referred to as an "apple jelly" appearance [3]. However, this finding can be difficult or impossible to appreciate in patients with darkly pigmented skin [12].

Diagnosis Lupus vulgaris is a paucibacillary form of cutaneous TB, and mycobacteria often cannot be detected histopathologically or by culture [12]. Information that may be used to support the diagnosis includes consistent clinical and histopathologic features and positive nucleic acid amplification (NAA) test results [23,95]. Tuberculin skin testing is also often positive.

Histopathologic examination reveals tuberculoid granulomas with discrete, central caseation in the upper dermis [42,60,61]. The epidermis may be atrophic or acanthotic with excessive hyperkeratosis or pseudoepitheliomatous hyperplasia (picture 13) [23,31,70].

Dermatoscopy of lupus vulgaris has revealed well-focused, linear-branching telangiectasias on a diffuse or localized, structureless, yellow to orange background and whitish, reticular streaks (picture 14) [96,97]. Though characteristic of lupus vulgaris, specificity may not be high since this finding may also be seen in cutaneous sarcoidosis.

Differential diagnosis Lupus vulgaris shares clinical features with multiple disorders [10]. Papular lesions should be distinguished from sarcoidosis, colloid milia, acne, and rosacea. Plaques may resemble deep fungal infections, leishmaniasis, late syphilis, yaws, discoid lupus, lymphocytoma cutis, tuberculoid leprosy, pyodermatitis vegetans, and psoriasis.

Disease course – If untreated, lesions of lupus vulgaris persist and may grow to enormous sizes over the course of years. Ulceration and destruction of underlying tissues, such as the nose, ears, and lips, may occur, causing severe disfigurement [3,12]. (See 'Treatment overview' below.)

Squamous cell carcinoma occasionally develops in long-standing lesions [90,95,98-100]. Rarely, basal cell carcinoma has occurred in sites of long-standing lupus vulgaris [101,102].

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 — Metastatic tuberculous abscesses, a multibacillary form of cutaneous TB, 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 [12]:

Alternative term – Tuberculous gumma.

Risk factors – Metastatic tuberculous abscesses typically occur in malnourished children and immunosuppressed adults [12,31,66]. Immunocompetent adults are infrequently affected; such patients tend to have few lesions [103].

Clinical features Patients with metastatic tuberculous abscesses present with single or multiple nontender, fluctuant, subcutaneous nodules. The nodules eventually penetrate the skin, resulting in the formation of ulcers and draining sinuses (picture 6) [3,16].

Lesions may occur at any skin site but frequently develop on the extremities [66]. Associated regional adenopathy usually is not present [66].

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 [3,31,42].

The results of tuberculin skin testing are variable [42].

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 [103]. (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 [3].

Acute miliary tuberculosis — Acute miliary TB is a rare, multibacillary form of TB that results from the hematogenous dissemination of mycobacteria from a primary focus of infection, such as the lung:

Alternative term – TB cutis miliaris disseminata.

Risk factors – The disorder typically occurs in infants or individuals with impaired cell-mediated immunity, such as patients with advanced AIDS [12,39].

Clinical features – Most patients with acute miliary TB do not exhibit cutaneous lesions. When present, the cutaneous findings result from bacteremia and are nonspecific [13]. Pinpoint, red-blue or purpuric papules with overlying, tiny vesicles that subsequently become umbilicated and crusted are typically seen. Patients are usually systemically ill, unlike many of the other forms of cutaneous TB.

Individual lesions heal over the course of one to four weeks and often resolve with hypopigmented, depressed scars [12]. A cellulitis-like appearance is a rare manifestation of acute miliary TB [104].

Diagnosis – Skin biopsies can aid in the diagnosis of acute miliary TB in patients who present with cutaneous lesions. Numerous AFB and abscesses are typically detected [12]. Granulomas may be present in older lesions [62]. The tuberculin skin test is often negative due to associated anergy.

Acute miliary TB is discussed in greater detail separately. (See "Clinical manifestations, diagnosis, and treatment of 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 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 level of immunity against the organism [3,12,42]. The three main tuberculid disorders are papulonecrotic tuberculid, lichen scrofulosorum, and erythema induratum of Bazin (EIB).

The following characteristics are consistent with tuberculids [3,31,42,58,60]:

Failure to detect M. tuberculosis in stains or cultures of affected tissue

Presence of active or healed extracutaneous M. tuberculosis infection, a strongly positive tuberculin skin test, or a positive interferon-gamma release assay [105] (these findings support a history of exposure to the bacillus)

Histopathologic evidence for granulomatous inflammation in skin lesions

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 EIB [106,107]. This finding offers some support for a role of 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 [108]. Papulonecrotic tuberculid may coexist with other tuberculids, lupus vulgaris, and scrofuloderma [108-115]:

Risk factors – Papulonecrotic tuberculid is most frequently seen in children and young adults [116].

Clinical features Papulonecrotic tuberculid typically presents as an asymptomatic, symmetric, and recurring eruption of 2 to 8 mm, firm, dark red or violaceous papules that subsequently become pustular or necrotic (picture 7A-B). Lesions most commonly occur on the face, ears, extensor extremities, and buttocks [15,23,31,61,66,108].

Fever and constitutional symptoms may precede the appearance of skin lesions [24,60], and associated lymphadenitis is common [12].

Diagnosis The presence of consistent clinical and histopathologic findings and evidence for TB infection supports the diagnosis of papulonecrotic tuberculid.

Histopathologic examination often demonstrates wedge-shaped necrosis in the upper dermis and epidermis and nonspecific or tuberculoid granulomatous inflammation. Vascular involvement is a cardinal feature seen as obliterative or granulomatous vasculitis [23,31,116]. M. tuberculosis bacilli are not usually detectable via microscopy or cultures.

In addition to the typical histopathologic findings, data that can support the diagnosis include a positive tuberculin skin test or interferon-gamma release assay, a detectable extracutaneous focus of TB infection, the detection of mycobacterial DNA in lesional tissue [106,116,117], and a positive response to anti-TB therapy. An extracutaneous focus of TB (eg, cervical lymph nodes, lungs, or other sites) is detectable in 38 to 75 percent of patients [118]. In a series of 12 patients with papulonecrotic tuberculid, mycobacterial DNA was detected by polymerase chain reaction (PCR) in 11 of 22 biopsy specimens [106].

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 eosinophilic granulomatosis with polyangiitis [10,23,31,39,61].

Clinical course Lesions may spontaneously resolve over the course of several weeks, leaving residual, pitted or varioliform scars. However, recurrence is common, and if untreated, papulonecrotic tuberculid may persist for years [24,31,60,118].

Patients typically improve within days to weeks of the initiation of anti-TB therapy [117,119]. (See 'Treatment overview' below.)

Lichen scrofulosorum — Lichen scrofulosorum is a rare tuberculid:

Risk factors – Lichen scrofulosorum most frequently occurs in children and young adults with nodal, pulmonary, skeletal, or intracranial TB [3,12,42,120,121]. Lichen scrofulosorum has also been reported after Bacille Calmette-Guérin (BCG) vaccination and in association with Mycobacterium avium-intracellulare infection [122-125].

Clinical features Lichen scrofulosorum presents with crops of firm, 1 to 5 mm, asymptomatic, grouped, yellow-red to brown-red papules (picture 8). Lesions tend to be follicular or perifollicular and are most often found on the trunk [3,23,24,60,61,121,126].

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 [42,121]. A positive interferon-gamma release assay can also support the presence of a tuberculous focus.

Histopathologic examination reveals tuberculoid granulomas in the upper dermis as well as around hair follicles and eccrine glands. Acid-fast bacilli (AFB) are not detected [23,31,42,70].

Differential diagnosis Other papular disorders may present with lesions that resemble lichen scrofulosorum. As examples, lichen planus, lichenoid secondary syphilis, papular eczema, lichen nitidus, lichen spinulosus, pityriasis rubra pilaris, and papular sarcoidosis should be considered in the differential diagnosis [10,23,31,39,61].

Clinical course – Without treatment, lesions spontaneously resolve without scarring after several months to several years [12]. Anti-TB treatment usually leads to complete resolution within weeks [23]. (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 [107,127]. Bazin first described this entity in 1855, with the belief of TB as the origin. (See "Erythema induratum (nodular vasculitis)".)

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 [107,128]:

Risk factors – Young women and middle-aged women are most commonly affected [127].

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 symmetrically distributed and most commonly located on the posterior aspects of the lower legs and may be up to several centimeters in diameter [107,127]. Breakdown of the nodules often occurs, leading to the formation of deep, draining ulcers (picture 9A-C).

Associated findings may include erythrocyanosis, chronic venous insufficiency, livedo reticularis, and lower limb edema. Sclerosis may ensue [39].

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 interferon-gamma release assay, or improvement with TB therapy) [14,107,129-131]. Mycobacterial DNA can be detected by PCR in 14 to 77 percent of biopsy specimens [107].

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 [62]:

Lobular or mixed lobular and septal panniculitis

Tuberculoid or poorly formed granulomas

Mixed inflammatory infiltrate with neutrophils, lymphocytes, and plasma cells

Fat necrosis

Vascular changes are also usually present; in some cases, necrotizing vasculitis is seen. AFB are not typically detected [3,42].

If an association with TB is not found in a patient with skin lesions consistent with this disorder, other potential causes should be investigated. (See "Erythema induratum (nodular vasculitis)", section on 'Associated disorders' and "Erythema induratum (nodular vasculitis)", section on 'Additional studies'.).

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, do not ulcerate, and demonstrate a septal panniculitis on histopathologic examination. (See "Erythema nodosum".)

Other disorders to consider include polyarteritis nodosa, subcutaneous sarcoidosis, tertiary syphilis, and other panniculitides [31,132,133]. (See "Erythema induratum (nodular vasculitis)", section on 'Differential diagnosis'.)

Clinical course Although individual lesions spontaneously resolve over the course of several weeks to a few months, leaving scars and postinflammatory hyperpigmentation [127], recurrences may occur every three to four months [107]. Lymphedema or elephantiasis nostra may develop with frequent recurrences [132].

EIB typically responds to anti-TB medical therapy [107,127]. Other agents that have been used for the management of EIB/nodular vasculitis are reviewed separately. (See "Erythema induratum (nodular vasculitis)", section on 'Treatment'.)

Other — Nodular tuberculid is a tuberculid disorder that has been reported in several patients [134,135]. 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.

MANAGEMENT — The management of patients with cutaneous manifestations of TB includes assessment for other sites of active TB infection and the initiation of anti-TB therapy.

Evaluation for extracutaneous involvement — A diagnosis of a cutaneous manifestation of TB should prompt an assessment for extracutaneous TB infection, as the presence of active extracutaneous TB is common. This generally includes at least a review of systems, physical examination, and chest radiograph. Additional evaluation is guided by these findings. (See "Tuberculosis infection (latent tuberculosis) in adults: Approach to diagnosis (screening)", section on 'Excluding TB disease' and "Diagnosis of pulmonary tuberculosis in adults" and "Tuberculosis infection (latent tuberculosis) in children", section on 'Excluding TB disease' and "Tuberculosis disease in children: Epidemiology, clinical manifestations, and diagnosis", section on 'Diagnosis'.)

Treatment overview — The general approach to treatment of cutaneous TB is the same as the approach to systemic TB, consisting of a course of systemic, multidrug anti-TB therapy [15,24,31,39,42,60,136]. Occasionally, surgical procedures are performed as an adjunct to systemic therapy. Special considerations for the treatment of erythema induratum of Bazin (EIB) are reviewed separately (see "Erythema induratum (nodular vasculitis)", section on 'Treatment'):

Systemic therapy – In general, systemic anti-TB therapy consists of an initial bactericidal phase to induce a rapid reduction in the number of bacteria and is followed by a longer treatment phase designed to eradicate any remaining bacteria [3,12,137]. The choice of a specific regimen is influenced by patient comorbidities and immune status, as well as local mycobacterial resistance patterns. Drug treatment regimens for TB are reviewed separately. (See "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults without HIV infection" and "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults with HIV infection: Initiation of therapy" and "Tuberculosis disease in children: Treatment and prevention".)

Every effort should be made to culture the organism for sensitivity testing to identify patients requiring an alternative approach to therapy.

The response to treatment of cutaneous lesions can be assessed through physical examination. In general, treatment should be continued for at least two months following the complete resolution of skin lesions.

As with pulmonary TB, patients with cutaneous TB are at risk for paradoxical worsening of cutaneous TB in association with the development of the immune reconstitution inflammatory syndrome (IRIS) after the initiation of antiretroviral therapy. The features, management, and prevention of IRIS are discussed in detail separately. (See "Immune reconstitution inflammatory syndrome", section on 'Tuberculosis' and "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults with HIV infection: Initiation of therapy", section on 'Preventing IRIS'.)

Surgery – Surgical intervention is not routinely utilized for the management of cutaneous TB but is sometimes employed as an adjunct to pharmacologic therapy [138].

Surgical excision has been utilized 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 TB verrucosa cutis and lupus vulgaris.

Reconstructive plastic surgery after treatment can be beneficial for patients with destructive lesions of lupus vulgaris [24,138].

Other – The efficacy and safety of topical isoniazid, an experimental drug, for cutaneous TB is under investigation [139,140].

ASSOCIATED DISORDERS

Bacille Calmette-Guérin vaccination reactions — The Bacille Calmette-Guérin (BCG) vaccine is composed of a live, 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, and suppurated lymphadenitis are most common [13,30], but scrofuloderma, lupus vulgaris, erythema induratum of Bazin (EIB), papulonecrotic tuberculid, and lichen scrofulosorum-like lesions have been described [23,31,122,141].

The time frame from vaccination to the development of skin lesions ranges from several months to years. The clinical presentation depends upon the patient's inherent susceptibility, virulence of bacillus, inoculum size, and technique [142]. (See "Prevention of tuberculosis: BCG immunization and nutritional supplementation", section on 'Safety and adverse effects'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Diagnosis and treatment of tuberculosis".)

SUMMARY AND RECOMMENDATIONS

Etiology – Tuberculosis (TB) is a mycobacterial infection that can affect multiple organ systems. Mycobacterium tuberculosis, an acid-fast bacillus, is the primary inciting organism of cutaneous manifestations of TB. (See 'Etiology' above.)

Classification – Cutaneous manifestations of TB are commonly divided into two groups: true cutaneous TB and tuberculids. (See 'Classification' above.)

True cutaneous tuberculosis – True cutaneous TB includes conditions in which cutaneous lesions are a direct manifestation of infection at the site of the skin lesions. True 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 'True cutaneous tuberculosis' above.)

Tuberculids – 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 (EIB). Organisms are not usually detectable in cultures, smears, or pathology specimens taken from tuberculid skin lesions. (See 'Tuberculids' above.)

Diagnosis – A variety of diagnostic studies are used for the evaluation of patients with suspected cutaneous manifestations of 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 (NAA) tests. (See 'Diagnostic approach' above.)

Given the plethora of cutaneous manifestations of TB, a high index of suspicion is of utmost importance in making the correct diagnosis. (See 'True cutaneous tuberculosis' above and 'Tuberculids' above.)

Treatment – Systemic treatment with multidrug therapy is the cornerstone of treatment of cutaneous manifestations of TB. (See 'Treatment overview' above.)

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Topic 15866 Version 15.0

References

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