[CASE REPORT AND LITERATURE REVIEW]

Cutaneous Tuberculosis
A Practical Case Report and Review for the Dermatologist

AMYLYNNE FRANKEL, MD; CAROLIN PENROSE, MD; JASON EMER, MD

Mount Sinai School of Medicine, Department of Dermatology, New York, New York

ABSTRACT
Cutaneous tuberculosis occurs rarely, despite a high and increasing prevalence of tuberculosis worldwide.
Mycobacterium tuberculosis, Mycobacterrium bovis, and the Bacille Calmette-Gurin vaccine can cause tuberculosis
involving the skin. Cutaneous tuberculosis can be acquired exogenously or endogenously and present as a multitude of
differing clinical morphologies. Diagnosis of these lesions can be difficult, as they resemble many other dermatological
conditions that are often primarily considered. Further, microbiological confirmation is poor, despite scientific
advances, such as the more frequent use of polymerase chain reaction. The authors report a case that illustrates the
challenges faced by dermatologists when considering a diagnosis of cutaneous tuberculosis.
(J Clin Aesthetic Dermatol. 2009;2(10):1927.)

M
ycobacterium tuberculosis is a worldwide, lesion on her right buttock that began during her
problematic, communicable pathogen that has pregnancy four years prior. The lesion appeared as a large,
increasingly been regarded as a notable, serious reddish-brown, scaly plaque with well-defined borders and
infection in the United States. The underlying basis of this central atrophic changes covering the entire surface of the
recent epidemic is dependent on such factors as the right buttock (Figure 1). The lesion was tender and warm
association of tuberculosis (TB) with the human with notable expression to light touch of purulent material
immunodeficiency virus (HIV) epidemic, increased through multiple fissures along the periphery. The patient
immigration from endemic countries, and the transmission of reported no other symptoms, such as fever, chills, cough,
TB in crowded settings, such as healthcare facilities, prisons,
and homeless shelters.14 Most often TB is an airborne
transmissible disease with skin manifestations presenting as
a result of hematogenous spread or direct extension from a
latent or active foci of infection. However, primary
inoculation may occur as a direct introduction of the
mycobacterium into the skin or mucosa of a susceptible
individual by trauma or injury. Increased risk of acquiring
disease occurs with HIV infection, intravenous drug abuse,
diabetes mellitus, immunosuppressive therapy, malignancies,
end-stage renal disease, and infancy. Cutaneous tuberculosis
(CTB) is frequently elusive as it mimics a wide differential
diagnosis and also evades microbiological confirmation
despite recent advances in sophisticated techniques.5
Although rare, given its worldwide prevalence, it is important
for clinicians to recognize the many clinical variants of CTB
to prevent missed or delayed diagnoses.
FIGURE 1. Large, reddish-brown, scaly plaque covering the entire
CASE REPORT
surface of the right buttock
A 24-year-old Hispanic woman presented with a painful

DISCLOSURE: The authors report no relevant conflicts of interest.

ADDRESS CORRESPONDENCE TO: Jason Emer, MD, Mount Sinai School of Medicine, Department of Dermatology, 5 East 98th Street, 5th Floor,
New York, NY 10029; Phone: (212) 241-3288; Fax: (212) 876-8961; e-mail: [email protected].

19 [ October 2009 Volume 2 Number 10] 19

FIGURES 2 and 3. Histology demonstrating pseudoepitheliomatous hyperplasia and neutrophilic microabscesses in the epidermis and a mixed
neutrophilic and granulomatous infiltrate in the dermis (H&E, low and medium powers)

Histopathology of the plaque showed pseudoepitheliomatous

hyperplasia and neutrophilic microabscesses in the
epidermis. The dermis contained a mixed neutrophilic and
granulomatous infiltrate (Figures 2 and 3). Acid-fast
bacillus (AFB) staining showed rare elongated acid-fast
structures suggestive of TB infection (Figure 4). Culture
from lesional tissue grew Mycobacterium tuberculosis
and serum QFT-G testing was positive. The patient was
referred to infectious disease to rule out active TB
infection. Sputum cultures were negative and a chest x-
ray showed no active pulmonary disease.
A diagnosis of CTB was made based on the patients
history, clinical picture, and diagnostic testing. Although
an explicit classification of CTB could not be specified,
lupus vulgaris (LV) and tuberculosis verrucosa cutis
(TVC) are two variants of CTB that have been shown to
occur in a previously sensitized individual, and her
diagnosis was assumed to be one of these two variants.
The patient was treated by infectious disease with
FIGURE 4. Staining showing elongated acid-fast structures multidrug TB therapy (pyrazinamide, rifampin,
ethambutol, and isoniazid) resulting in lesion clearance at
or fatigue. On physical examination, vital signs were within three months. Currently, the patient remains free of
normal limits, the skin demonstrated no other significant tuberculous disease.
changes, and the patient had no notable
lymphadenopathy. On history, the patient reported the DISCUSSION
skin lesion had progressively increased over the past four CTB describes dermatological manifestations of TB
years. She had been previously diagnosed with psoriasis involving the skin, which can be caused by
and was treated with multiple topical therapies, including Mycobacterium tuberculosis, Mycobacterium bovis,
salicylic acid and potent topical corticosteroids without and the BCG vaccination. These lesions can be acquired
any relief. Further, the patient reported having a similar exogenously or endogenously, although the former is
lesion (which was on her neck) as a child that was significantly less common. TB is one of the most common,
surgically removed in Mexico. She had been Bacille rampant infectious diseases in underdeveloped countries,
Calmette-Gurin (BCG)-vaccinated in the past. and the number of cases in industrialized countries has
Serum QuantiFERON-TB Gold (QFT-G; Cellestis increased in recent years as a result of the increased
Inc.,Valencia, California) testing was performed along with incidence of HIV infection and increasing multidrug
tissue cultures and skin biopsy with histological analysis. resistance.6 Although CTB is reported as less than one

20 [October 2009 Volume 2 Number 10]

 TABLE 1. Two differing classifications of
tuberculosis
CLASSIFICATION SYSTEM 1

EXOGENOUS

Tuberculous chancre, tuberculosis verrocosa cutis,

lupus vulgaris

ENDOGENOUS

Contiguous

Scrofuloderma, orificial tuberculosis

FIGURE 5. Primary inoculation TB or tuberculous chancre
Hematogenous Source = DermNetNZ.org

Acute miliary tuberculosis, metastatic

tuberculosis abscess (gummatous tuberculosis),
papulonecrotic tuberculid, lupus vulgaris

Lymphatic

Lupus vulgaris

CLASSIFICATION SYSTEM 2

MULTIBACILLARY

Tuberculous chancre, scrofuloderma, tuberculosis orificialis,

acute miliary tuberculosis, gummatous tuberculosis

PAUCIBACILLARY

Tuberculosis verrocosa cutis, lupus vulgaris, tuberculids FIGURE 6. Scofuloderma

Source = DermNetNZ.org

percent of all cases of TB, it is important for practitioners the Tappeiner and Wolff system included further
to consider this infection when faced with a suggestive distinction based on bacterial load. This system is
clinical picture.7 extremely similar to Ridley and Joplings description of
Early classification of CTB was based on lesion Mycobacterium leprae in Hansons disease. In the
morphology. As knowledge of the disease increased, it multibacillary forms, a plethora of mycobacteria can easily
became apparent that although lesions appeared clinically be identified on histological examination utilizing the
similar, their development, progression, and prognosis Ziehl-Neelsen staining (AFB) method and culture. In the
were different. Tappeiner and Wolff proposed the most paucibacillary forms, sparse bacilli are seen on histological
widely accepted classification based on the route of examination and culture isolation of mycobacteria is the
infection (Table 1).5,8 Exogenous inoculation occurs after exception rather than the rule.1
the direct inoculation of Mycobacterium tuberculosis
into the skin of a person who is susceptible to infection. MULTIBACILLARY FORMS
This leads to TVC, tuberculosis chancre, and some cases of Primary inoculation TB (tuberculous chancre) typically
LV. Endogenous infection occurs in patients who were follows a penetrating injury that results in the direct
previously infected either by lymphatic spread, introduction of mycobacterium into the skin or mucosa of
hematogenous spread, or contiguous extension. Lymphatic an individual with no previous TB infection. Within 2 to 4
spread is seen occasionally in LV. Hematogenous spread is weeks, an inflammatory papule develops at the inoculation
seen in acute miliary TB, metastatic TB abscess site and evolves into a firm, shallow, non-tender,
(gummatous TB), papulonecrotic tuberculid (PNT), and nonhealing, undermined ulcer with a granulomatous base
LV. Contiguous extension is seen in scrofuloderma and (Figure 5).3,5,9 Painless, regional lymphadenopathy is
orificial tuberculosis. frequently apparent around the time a tuberculin skin test
An additional classification system designed to enhance (TST) converts to positive.

21 [ October 2009 Volume 2 Number 10] 21

FIGURE 7. Miliary TB or disseminated TB FIGURE 8. Tuberculosis verrucosa cutis
Source = DermNetNZ.org Source = DermNetNZ.org

Scrofuloderma is the most common form of CTB in miliary TB has historically been extremely rare and well
children and historically was seen after consumption of known for its occurrence in children, it is an increasingly
milk contaminated with Mycobacterium bovis. It results serious infection in immunosuppressed patients, such as
as a direct extension from an underlying TB focus, such as those infected with HIV, on long-term oral corticosteroid
a regional lymph node or infected bone or joint, to the therapy, or on other immunosuppressive therapies for
overlying skin. Lesions present as firm, painless, organ transplant or inflammatory or autoimmune
subcutaneous, red-brown nodules overlying an infected conditions. Cutaneous skin lesions consist of small,
focus, which gradually enlarge and suppurate forming erythematous to violaceous papules or pustules with
ulcers and sinus tracts that drain watery, purulent, or hemorrhagic necrosis and umbilication affecting a
caseous material (Figure 6). Skin biopsy reveals substantial portion of the body (Figure 7). If healing
tuberculoid granuloma surrounding areas of wedge- occurs, lesions leave atrophic, depressed scars
shaped necrosis. Culture, smear, or biopsy will surrounded by a brownish, hyperpigmented halo. TST is
demonstrate the organisms and confirm the diagnosis in a typically negative because of anergy. Skin biopsy with
TST-positive individual.9 The ulcers may heal histological examination reveals numerous
spontaneously with scarring. microabscesses containing neutrophils and numerous
TB cutis orificialis (TBCO) affects individuals with mycobacterial organisms.3 Confirmation of the diagnosis
dramatically impaired cell-mediated immunity and requires cultures of sputum, blood, and skin lesions, as
advanced TB in other organs, such as the gastrointestinal well as diagnostic tests, such as bronchoscopy, chest x-ray,
tract and lungs. The oral, nasal, anal, and vulval regions or computed tomography of the chest. Prognosis is poor, as
become infected with Mycobacterium tuberculosis by affected individuals tend to be very ill at initial presentation
autoinoculation from active infectious sites that are (i.e., they have HIV, cancer, and/or are immunosuppressed).
draining.5 The red-yellow nodules break down and form Metastatic TB abscesses (TB gumma) can arise from
painful, soft, circular or irregularly shaped punched-out breakdown of an old healed tubercle that still contains live
ulcers with a pseudomembranous fibrinous base.5,6 TST organisms or from cell-mediated immune defense
may or may not be positive, although organisms are easily inhibition that reactivates.1,3 TB gumma is usually seen in
seen on skin biopsy in the deep dermis and ulcer walls.9 malnourished children and immunosuppressed adults.5
The presence of TBCO heralds a poor prognosis, as Single or multiple nontender, fluctuant nodules develop
patients tend to have severe internal organ disease prior to forming draining sinus abscesses unless surgically incised
skin manifestations. and drained. Nodules can occur at any location without
Miliary TB (disseminated TB) is characterized by a any specific predominance. Histological examination
wide dissemination of Mycobacterium tuberculosis into reveals massive skin necrosis with copious mycobacterial
the body and shows a distinctive pattern on chest x-ray of organisms. TST is variable.
multiple, tiny lesions (millet-sized) distributed throughout
the lung fields. Miliary TB may hematogenously infect any PAUCIBACILLARY FORMS
number of organs, including the lungs, liver, and spleen, in TVC occurs after direct inoculation of TB into the skin
patients with advanced TB disease. There is a systemic of people who were previously infected. It manifests as a
failure of the cell-mediated immune system that allows painless, solitary, purplish or brownish-red warty plaque
and facilitates the spread of infection resulting in rapid that may extend peripherally causing central atrophy or
deterioration and death.3 Certain events, infections, and form fissures that exude pus or keratinous material
medications that suppress the bodys cell-mediated (Figure 8).5,6 On physical examination, there is often
immune system can precipitate this infection. Although lymphadenopathy. Skin biopsy with histological

22 [October 2009 Volume 2 Number 10]

examination reveals pseudocarcinomatous hyperplasia
with noncaseating tuberculous granulomata without
mycobacteria seen or cultured. Skin lesions may evolve
and persist for years, although spontaneous resolution can
also occur. These lesions respond to typical anti-TB
therapy of a combination of antibiotics given over months
to years.
LV is a chronic and progressive form of CTB that is
widely described as the most common form of CTB with a
multitude of presentations. Lesions occur in normal skin as
a result of direct extension from underlying deeper TB
focus, by lymphatic or hematogenous spread, after
primary inoculation, after BCG vaccination, or in scars of
old scrofuloderma.10 Lesions usually are small, solitary,
nodular, sharply defined, reddish-brown lesions with a FIGURE 9. Lupus vulgaris
gelatinous consistency (called apple-jelly nodules) on the Source = DermNetNZ.org
head and neck of individuals in Western countries while
those individuals in tropical and subtropical areas present and LS represent true hypersensitivity reactions rather
with lesions on the lower extremities or buttocks (Figure than the result of a local CTB infection. This is based on
9). Clinical variations exist and are defined as 1) classic the observation that these lesions have consistently failed
plaque or keratotic; 2) hypertrophic; 3) ulcerative; and 4) to either stain positive for or culture mycobacterial
vegetating. The plaque type begins as discrete, red-brown organisms. Although the organisms are absent,
papules that coalesce and form plaques with a slightly mycobacterial DNA have been detected in biopsy
elevated verrucas border and central atrophy. The specimens subjected to PCR. Furthermore, all
consistency of the plaque is soft and gelatinous and has a tuberculids exhibit granulomatous inflammation and
classic apple-jelly appearance on dermoscopic examination. some degree of necrosis and vasculitis suggesting that
Persistent lesions may damage underlying tissue and these lesions are a result of released mycobacterial
ulcerate causing severe disfigurement and an increased antigens in the setting of a concurrent or distant
risk of cancer formation. Skin biopsy with histological infection.
examination reveals tuberculous granulomas with few to LS is an eruption of multiple, small, grouped,
no bacilli. Confirmation by culture is rare, even though an asymptomatic, firm, perifollicular, lichenoid papules or
individuals TST is usually positive. plaques most often affecting children or young adults that
progresses and subsides within weeks to months without
TUBERCULIDS scarring.3 Skin biopsy with histological analysis shows
The relationship between tuberculids and TB superficial, perifollicular, epithelioid granulomas
continues to be debated. Tuberculids are generalized surrounding hair follicles and sweat glands without
exanthems in patients with a moderate or high degree of evidence of necrosis. Typically no AFB are visualized
immunity to TB due to previous infection. Patients are histologically, although TST is often very remarkable.
usually in good health and show 1) positive TST; 2) EIB is a TB-associated panniculitis that presents with
tuberculous involvement (usually inactive) of viscera or multiple, painful, recurring, ulcerated nodules that affect
lymph nodes; 3) negative staining and culture for the lower limbs of women (Figure 10).3,5 Pre-existing
pathogenic mycobacteria in affected tissue; and 4) skin vascular disease may predispose patients to lesions during
lesions that heal with remission or treatment of TB. exposure to cold weather. Lesions are chronic; slow to
Classification includes three types: 1) PNT; 2) erythema resolve, if at all; and result in atrophic hyperpigmented
induratum of Bazin (EIB); and 3) lichen scrofulosorum scarring after several months. Histology should show three
(LS). Tuberculids can be classified into two groups: true of four of the following elements: 1) septal panniculitis; 2)
tuberculids and facultative tuberculids. The former fat necrosis; 3) small or large vessel vasculitis; and 4)
classified because Mycobacterium tuberculosis plays a granulomas. Although patients show TB skin
major etiologic role and the latter because hypersensitivity, AFB are rarely identified. A 2005 study in
Mycobacterium tuberculosis is one of several possibly Spain demonstrated that about 10 percent of cases were
etiologic agents. All were once believed to be a positive for Mycobacterium tuberculosis using PCR
consequence of hypersensitivity to the presence of technique of identification.11 In a case series and literature
mycobacterial antigens within a host of previously review, Bayer-Garner et al found that organisms, such as
acquired immunity to TB; however, most are now Mycobacterium bovis and Mycobacterium marinum,
understood not to be uniquely caused by TB. PNT and LS may also be involved as the etiology of EIB, although no
are still widely accepted as true tuberculids and EIB as a identification was found during their investigation. They
facultative tuberculid. Whatever underlies the suggested that EIB has diverse etiologies with varying
pathophysiology, a consensus has been reached that PNT pathogeneses leading to similar histological changes, and

23 [ October 2009 Volume 2 Number 10] 23

 percent and 98.5 percent, respectively.15,16 Mycobacterial
growth is better on an egg-based medium, but quicker on
agar medium. Liquid systems allow for rapid growth (13
weeks), while growth on solid media can take from 3 to 8
weeks. Two cases of EIB have been confirmed using
guinea pig inoculation.17 An AFB smear is useful if lesions
have a high bacterial load as seen in LS, miliary TB, and
TB gumma. With the advent of polymerase chain reaction
(PCR), even the smallest tissue sample can be analyzed
and amplified for mycobacterial DNA sequences,
confirming its presence. In the future, it is believed that
PCR will become more advanced to detect
Mycobacterium tuberculosis in all lesions. Currently,
PCR appears to be the most useful in multibacillary forms
of CTB.18,19 In one report of AFB-negative specimens, the
overall sensitivity of PCR was found to be 50 to 72
percent.20 Another source reported AFB-positive
respiratory specimens to have a sensitivity and specificity
of 95 and 98 percent, respectively.15 In a comparison study
of PCR and standard culture technique in pulmonary TB,
one group found the positive rate of PCR was 82 percent
compared to 16 percent in standard culture.21 Margall et al
detected Mycobacterium tuberculosis DNA in 77
percent of cases of various types of CTB.4 Although PCR
FIGURE 10. Erythema induratum of bazin or nodular vasculitis has shown to have high specificity and good positive
Source = DermNetNZ.org predictive value, it seems to work best as a confirmatory
test in patients with a high pre-test probability.22 In
the cases analyzed may not have had an infectious etiology multibacillary CTB, PCR has the highest likelihood of
(suggesting a facultative tuberculid picture).12 yield. Nonetheless, a combination of diagnostic tests is
needed when a case of CTB is suspected to confirm a
DIAGNOSIS diagnosis. In developing countries, PCR is not always
Diagnosis of CTB is complicated and requires a full readily available and therefore physicians must rely on a
work-up, including a detailed history and physical positive response to anti-TB drugs to confirm difficult
examination; careful consideration of clinical presentation; cases.18,20,23 It is essential to search for extracutaneous foci
TST; serum QFT-G (and possibly other laboratory testing); of TB by urine, blood, and sputum samples; x-ray or CT
skin biopsy with histological analysis and special staining scan of the chest; and bone scans. Often, there is a delay
methods for identification of AFB; and the use of other in the diagnosis because CTB is not always considered in
diagnostic tests, such as chest x-ray and sputum culture. the differential diagnosis of atypical or nonhealing skin
The QFT-G is an in-vitro diagnostic aid that measures a lesions (Table 2). It is imperative that physicians have a
component of cell-mediated immunity to Mycobacterium high index of suspicion in high-risk patients and in
tuberculosis and is based on the quantification of atypical presentations.
interferon-gamma released from sensitized lymphocyte.
QFT-G was approved in 2005 by the US Food and Drug TREATMENT
Administration for the diagnosis of both latent and active CTB treatment is the same as that for systemic TB and
TB infections. The antigens used in QFT-G are not shared consists of long, multidrug therapy (Table 3). First, the
by BCG vaccine strain or by nontuberculous chemotherapeutic treatment of TB is divided into two
mycobacterium. According to the Centers for Disease phases: 1) an intensive or bactericidal phase, designed to
Control and Prevention guidelines of 2005, QFT-G can be rapidly reduce the total body burden of Mycobacterium
used in place of the TST as it has increased specificity, lack tuberculosis; and 2) a continuation or sterilizing phase.
of cross-reactivity to BCG, and convenience for both The most commonly used drugs are isoniazid, rifampin,
patient and provider.13 Concordance rates between TST pyrazinamide, and either ethambutol or streptomycin.3,5,24
and QFT-G range from 60 to 90 percent. The cost After eight weeks of therapy, the patients are considered
effectiveness of QFT-G test still needs to be studied.14 no longer infectious, but still require longer term
Mycobacterial culture remains the most reliable treatment for eradication. The continuation or sterilizing
method to determine the presence of mycobacteria and phase is designed to execute the remaining bacteria that
their sensitivities, but the yield is often low and often resist the initial intensive or bactericidal phase. It is not
takes many weeks.2,9,16 Culture sensitivity is much lower clear why some of the bacteria resist the initial treatment,
than specificity, with sources ranging from 80 to 85 but the first-line drugs are typically highly effective. If the

24 [October 2009 Volume 2 Number 10]

patient responded positively to
TABLE 2. The differential diagnoses of various forms
isoniazid and rifampin, both are
continued either daily or two or three of cutaneous tuberculosis
times weekly for the second phase. PRIMARY INOCULATION TUBERCULOSIS (TUBERCULOUS CHANCRE)
Surgical intervention may be
considered for the treatment of LV, Infectious Etiologies
TVC, and LS in recalcitrant cases.5,6
Blastomycosis, histoplasmosis, coccidioidomycosis, sporotrichosis, tularemia, cat
Several considerations must be
scratch disease
made prior to multidrug therapy in
order to tailor the treatment to an Infiltrative or Autoimmune Etiologies
individual patient. Considerations
include 1) overall general health Pyoderma gangrenosum, cutaneous pseudolymphoma, sarcoidosis, discoid lupus
condition, including the immunity erythematosus, squamous cell carcinoma
level of the patient; 2) the type of
cutaneous involvement; 3) the stage SCROFULODERMA
of the disease; and 4) patient
Sporotrichosis, coccidioidomycosis, actinomycosis, chronic bacterial osteomyelitis,
compliance with the duration of hidradenitis suppurativa, severe acne conglobata
treatment and possible medication
side effects. Adherence with TUBERCULOSIS CUTIS ORIFICIALIS
treatment is especially important as
improper use of anti-TB therapy can Aphthous ulcers, herpes lesions, syphilitic chancre, lymphogranuloma venereum,
contribute to unwanted treatment cutaneous malignancy, amoebiasis, paracoccidioidomycosis
side effects and the development of
drug resistance that further facilities METASTATIC TUBERCULOSIS ABSCESSES (TB GUMMA)
the spread of disease. Directly
Syphilitic gumma, leishmaniasis, deep fungal infections
observed treatment involves observed
therapy by personnel from the public
TUBERCULOSIS VERRUCOSA CUTIS
health department to help increase
patient adherence and control an Verrucose leishmaniasis, blastomycosis, chromoblastomycosis, sporotrichosis, verrucose
infection that is a public health tertiary syphilis, mycobacterium marinum, hypertrophic lichen planus, squamous cell
concern. carcinoma, psoriasis

CONCLUSION LUPUS VULGARIS

Tuberculosis is a serious infection Sarcoidosis, discoid lupus, deep fungal infections, lupoid leishmaniasis, basal cell
that affects many people worldwide, carcinoma, pyoderma gangrenosum
with a recent increasing prevalence
LICHEN SCROFULOSORUM
especially in high-risk patients, such
as those from endemic countries, in Keratosis pilaris, lichen spinulosus, lichen nitidus, lichenoid sarcoidosis, pityriasis rubra
an immunocompromised state, with a pilaris
history of previous tuberculosis ERYTHEMA INDURATUM OF BAZIN
infection, and/or with multiple
comorbidities. Although the incidence Nodular vasculitis, erythema nodosum
of CTB is rare, it should be considered
in patients presenting with atypical
skin lesions suggestive of an underlying infectious etiology. REFERENCES
It is imperative that physicians have a high index of 1. Bravo FG, Gotuzzo E. Cutaneous tuberculosis. Clin
suspicion in order to quickly and effectively diagnose and Dermatol. 2007;25(2):173180.
treat these substantially morbid skin conditions. This case 2. Faria MC, Gegundez MI, Piqu E, et al. Cutaneous
report demonstrates the importance of a proper history tuberculosis: a clinical, histopathologic, and bacteriologic
and physical examination as well as diligent laboratory and study. J Am Acad Dermatol. 1995;33(3):433440.
diagnostic testing in determining the etiology of a 3. MacGregor RR. Cutaneous tuberculosis. Clin Dermatol.
suspicious and treatment-resistant skin lesion. Prompt 1995;13(3):245255.
consideration leads to a swift diagnosis and proper 4. Bhutto AM, Solangi A, Khaskhely NM, et al. Clinical and
treatment resulting in high patient satisfaction. epidemiological observations of cutaneous tuberculosis in
Larkana, Pakistan. Int J Dermatol. 2002;41(3):159165.
ACKNOWLEDGMENT 5. Barbagallo J, Tager P, Ingleton R, et al. Cutaneous
The authors would like to thank Brian Marciniak for his tuberculosis: diagnosis and treatment. Am J Clin
help in editing this paper. Dermatol. 2002;3(5):319328.

25 [ October 2009 Volume 2 Number 10] 25

TABLE 3. First-line medications for cutaneous tuberculosis

MEDICATION ADULT DOSING CHILDREN DOSING

5mg/kg daily, max 300mg 1015mg/kg daily

Isoniazid
15mg/kg TIW, max 900mg 2030mg/kg intermittently

10mg/kg daily, max 600mg

Rifampin 1020mg/kg daily or BIW
10mg/kg TIW, max 600mg

2025mg/kg daily, max 2g 1530mg/kg daily

Pyrazinamide
3040mg/kg TIW, max 3g 4050mg/kg BIW

1520mg/kg daily, max 1600mg

1520mg/kg daily
Ethambutol 2535mg/kg TIW, max 2400mg
50mg/kg BIW
4050mg/kg BIW, max 4000mg

MEDICATION COMMON ADVERSE REACTIONS COMMENTS MONITORING

Adjunctive pyridoxine (vitamin B6) 2550mg CMP at baseline; LFTs every month
daily if patient is >35 years old, has a his-
Paresthesias and/or peripheral neu-
Can follow with liver function tests or tory of hepatic disease or alcohol or
Isoniazid ropathy, elevated liver transaminases,
discontinue medication if causes hepatotoxicity IV drug abuse, females in postpar-
nausea and vomiting
Take medication on empty stomach or at tum period; option opthalmological
bedtime exam at baseline

Take medication on empty stomach or at

Nausea and vomiting; anorexia;
bedtime
abdominal pain; diarrhea; orange
Reassurance
and/or red-colored bodily fluids; flu- CBC, CMP at baseline; LFTs if hepat-
Rifampin Give antipyretics, nonsteroidal
like symptoms (fever, malaise, ic impairment every 24 weeks
anti-inflammatory medications, rest
headache, myalgias, arthralgias); ele-
Can follow with liver function tests or
vated liver transaminases
discontinue medication if causes hepatotoxicity

Give aspirin or nonsteroidal anti-inflammatory

Oral antihistamines, topical corticosteroids,
emollients, sun protection
Malaise, joint pain, rash, urticaria,
Take medication at bedtime or treat with
photosensitivity, nausea, vomiting, CMP and uric acid at baseline, then
Pyrazinamide antinausea medications
anorexia, hyperuricemia, gout, periodically
Can follow with uric acid levels and treat with
elevated liver transaminases
appropriate agents or discontinue medication
Can follow with liver function tests or
discontinue medication if causes hepatotoxicity

Optional ophthalmological examination;

discontinuation of medication if necessary
Give antipyretics, nonsteroidal
Blurred or changed vision, blindness,
anti-inflammatory medications, rest
flu-like symptoms (fever, malaise, CMP, CBC, optional ophthalmological
Take medication at bedtime or treat with
Ethambutol headache, myalgias, arthralgias), examination at baseline,
antinausea medications
nausea, vomiting, anorexia, elevated then periodically
Can follow with liver function tests or
liver transaminases, rash, pruritis
discontinue medication if causes hepatotoxicity
Oral antihistamines, topical corticosteroids,
emollients

* TIW = three times weekly; BIW = three times weekly; CMP = complete metabolic panel; LFT = liver function tests; CBC = complete blood count

26 [October 2009 Volume 2 Number 10]

6. Handog EB, Gabriel TG, Pineda RT. Management of September 1999. Am J Respir Crit Care Med. 2000;161(4
cutaneous tuberculosis. Dermatol Ther. 2008;21(3): Pt 1):13761395.
154161. 16. API Consensus Expert Committee. API TB Consensus
7. Rai VM, Shenoi SD, Gowrinath. Tuberculous gluteal abscess Guidelines 2006: Management of pulmonary tuberculosis,
coexisting with scrofuloderma and tubercular lymphadenitis. extra-pulmonary tuberculosis and tuberculosis in special
Dermatol Online J. 2005;11(3):14. situations. J Assoc Physicians India. 2006;54:219234.
8. Lai-Chong JE, Perez A, Tang V, et al. Cutaneous 17. Schneider JW, Jordaan HF, Geiger DH, et al. Erythema
manifestations of tuberculosis. Clin Exp Dermatol. induratum of Bazin. A clinicopathological study of 20 cases
2007;32(4):461466. and detection of Mycobacterium tuberculosis DNA in skin
9. Brown FS, Anderson RH, Burnett JW. Cutaneous lesions by polymerase chain reaction. Am J
tuberculosis. J Am Acad Dermatol. 1982;6(1):101106. Dermatopathol. 1995;17(4):350356.
10. Marcoval J, Servitje O, Moreno A, et al. Lupus vulgaris. 18. Tan SH, Tan BH, Goh CL, et al. Detection of
Clinical, histopathologic, and bacteriologic study of 10 Mycobacterium tuberculosis DNA using polymerase chain
cases. J Am Acad Dermatol. 1992;26(3 Pt 2):404407. reaction in cutaneous tuberculosis and tuberculids. Int J
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