[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: jason.emer@mssm.edu.

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)
FIGURE 4. Staining showing elongated acid-fast structures
or fatigue. On physical examination, vital signs were within
normal limits, the skin demonstrated no other significant
changes, and the patient had no notable
lymphadenopathy. On history, the patient reported the
skin lesion had progressively increased over the past four
years. She had been previously diagnosed with psoriasis
and was treated with multiple topical therapies, including
salicylic acid and potent topical corticosteroids without
any relief. Further, the patient reported having a similar
lesion (which was on her neck) as a child that was
surgically removed in Mexico. She had been Bacille
Calmette-Gurin (BCG)-vaccinated in the past.
Serum QuantiFERON-TB Gold (QFT-G; Cellestis
Inc.,Valencia, California) testing was performed along with
tissue cultures and skin biopsy with histological analysis.
20 [October 2009 Volume 2 Number 10]
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
multidrug TB therapy (pyrazinamide, rifampin,
ethambutol, and isoniazid) resulting in lesion clearance at
three months. Currently, the patient remains free of
tuberculous disease.
DISCUSSION
CTB describes dermatological manifestations of TB
involving the skin, which can be caused by
Mycobacterium tuberculosis, Mycobacterium bovis,
and the BCG vaccination. These lesions can be acquired
exogenously or endogenously, although the former is
significantly less common. TB is one of the most common,
rampant infectious diseases in underdeveloped countries,
and the number of cases in industrialized countries has
increased in recent years as a result of the increased
incidence of HIV infection and increasing multidrug
resistance.6 Although CTB is reported as less than one
 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
to consider this infection when faced with a suggestive
clinical picture.7
Early classification of CTB was based on lesion
morphology. As knowledge of the disease increased, it
became apparent that although lesions appeared clinically
similar, their development, progression, and prognosis
were different. Tappeiner and Wolff proposed the most
widely accepted classification based on the route of
infection (Table 1).5,8 Exogenous inoculation occurs after
the direct inoculation of Mycobacterium tuberculosis
into the skin of a person who is susceptible to infection.
This leads to TVC, tuberculosis chancre, and some cases of
LV. Endogenous infection occurs in patients who were
previously infected either by lymphatic spread,
hematogenous spread, or contiguous extension. Lymphatic
spread is seen occasionally in LV. Hematogenous spread is
seen in acute miliary TB, metastatic TB abscess
(gummatous TB), papulonecrotic tuberculid (PNT), and
LV. Contiguous extension is seen in scrofuloderma and
orificial tuberculosis.
An additional classification system designed to enhance
the Tappeiner and Wolff system included further
distinction based on bacterial load. This system is
extremely similar to Ridley and Joplings description of
Mycobacterium leprae in Hansons disease. In the
multibacillary forms, a plethora of mycobacteria can easily
be identified on histological examination utilizing the
Ziehl-Neelsen staining (AFB) method and culture. In the
paucibacillary forms, sparse bacilli are seen on histological
examination and culture isolation of mycobacteria is the
exception rather than the rule.1
MULTIBACILLARY FORMS
Primary inoculation TB (tuberculous chancre) typically
follows a penetrating injury that results in the direct
introduction of mycobacterium into the skin or mucosa of
an individual with no previous TB infection. Within 2 to 4
weeks, an inflammatory papule develops at the inoculation
site and evolves into a firm, shallow, non-tender,
nonhealing, undermined ulcer with a granulomatous base
(Figure 5).3,5,9 Painless, regional lymphadenopathy is
frequently apparent around the time a tuberculin skin test
(TST) converts to positive.

21 [ October 2009 Volume 2 Number 10] 21

FIGURE 7. Miliary TB or disseminated TB
Source = DermNetNZ.org
Scrofuloderma is the most common form of CTB in
children and historically was seen after consumption of
milk contaminated with Mycobacterium bovis. It results
as a direct extension from an underlying TB focus, such as
a regional lymph node or infected bone or joint, to the
overlying skin. Lesions present as firm, painless,
subcutaneous, red-brown nodules overlying an infected
focus, which gradually enlarge and suppurate forming
ulcers and sinus tracts that drain watery, purulent, or
caseous material (Figure 6). Skin biopsy reveals
tuberculoid granuloma surrounding areas of wedge-
shaped necrosis. Culture, smear, or biopsy will
demonstrate the organisms and confirm the diagnosis in a
TST-positive individual.9 The ulcers may heal
spontaneously with scarring.
TB cutis orificialis (TBCO) affects individuals with
dramatically impaired cell-mediated immunity and
advanced TB in other organs, such as the gastrointestinal
tract and lungs. The oral, nasal, anal, and vulval regions
become infected with Mycobacterium tuberculosis by
autoinoculation from active infectious sites that are
draining.5 The red-yellow nodules break down and form
painful, soft, circular or irregularly shaped punched-out
ulcers with a pseudomembranous fibrinous base.5,6 TST
may or may not be positive, although organisms are easily
seen on skin biopsy in the deep dermis and ulcer walls.9
The presence of TBCO heralds a poor prognosis, as
patients tend to have severe internal organ disease prior to
skin manifestations.
Miliary TB (disseminated TB) is characterized by a
wide dissemination of Mycobacterium tuberculosis into
the body and shows a distinctive pattern on chest x-ray of
multiple, tiny lesions (millet-sized) distributed throughout
the lung fields. Miliary TB may hematogenously infect any
number of organs, including the lungs, liver, and spleen, in
patients with advanced TB disease. There is a systemic
failure of the cell-mediated immune system that allows
and facilitates the spread of infection resulting in rapid
deterioration and death.3 Certain events, infections, and
medications that suppress the bodys cell-mediated
immune system can precipitate this infection. Although
22 [October 2009 Volume 2 Number 10]
FIGURE 8. Tuberculosis verrucosa cutis
Source = DermNetNZ.org
miliary TB has historically been extremely rare and well
known for its occurrence in children, it is an increasingly
serious infection in immunosuppressed patients, such as
those infected with HIV, on long-term oral corticosteroid
therapy, or on other immunosuppressive therapies for
organ transplant or inflammatory or autoimmune
conditions. Cutaneous skin lesions consist of small,
erythematous to violaceous papules or pustules with
hemorrhagic necrosis and umbilication affecting a
substantial portion of the body (Figure 7). If healing
occurs, lesions leave atrophic, depressed scars
surrounded by a brownish, hyperpigmented halo. TST is
typically negative because of anergy. Skin biopsy with
histological examination reveals numerous
microabscesses containing neutrophils and numerous
mycobacterial organisms.3 Confirmation of the diagnosis
requires cultures of sputum, blood, and skin lesions, as
well as diagnostic tests, such as bronchoscopy, chest x-ray,
or computed tomography of the chest. Prognosis is poor, as
affected individuals tend to be very ill at initial presentation
(i.e., they have HIV, cancer, and/or are immunosuppressed).
Metastatic TB abscesses (TB gumma) can arise from
breakdown of an old healed tubercle that still contains live
organisms or from cell-mediated immune defense
inhibition that reactivates.1,3 TB gumma is usually seen in
malnourished children and immunosuppressed adults.5
Single or multiple nontender, fluctuant nodules develop
forming draining sinus abscesses unless surgically incised
and drained. Nodules can occur at any location without
any specific predominance. Histological examination
reveals massive skin necrosis with copious mycobacterial
organisms. TST is variable.
PAUCIBACILLARY FORMS
TVC occurs after direct inoculation of TB into the skin
of people who were previously infected. It manifests as a
painless, solitary, purplish or brownish-red warty plaque
that may extend peripherally causing central atrophy or
form fissures that exude pus or keratinous material
(Figure 8).5,6 On physical examination, there is often
lymphadenopathy. Skin biopsy with histological
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
gelatinous consistency (called apple-jelly nodules) on the
head and neck of individuals in Western countries while
those individuals in tropical and subtropical areas present
with lesions on the lower extremities or buttocks (Figure
9). Clinical variations exist and are defined as 1) classic
plaque or keratotic; 2) hypertrophic; 3) ulcerative; and 4)
vegetating. The plaque type begins as discrete, red-brown
papules that coalesce and form plaques with a slightly
elevated verrucas border and central atrophy. The
consistency of the plaque is soft and gelatinous and has a
classic apple-jelly appearance on dermoscopic examination.
Persistent lesions may damage underlying tissue and
ulcerate causing severe disfigurement and an increased
risk of cancer formation. Skin biopsy with histological
examination reveals tuberculous granulomas with few to
no bacilli. Confirmation by culture is rare, even though an
individuals TST is usually positive.
TUBERCULIDS
The relationship between tuberculids and TB
continues to be debated. Tuberculids are generalized
exanthems in patients with a moderate or high degree of
immunity to TB due to previous infection. Patients are
usually in good health and show 1) positive TST; 2)
tuberculous involvement (usually inactive) of viscera or
lymph nodes; 3) negative staining and culture for
pathogenic mycobacteria in affected tissue; and 4) skin
lesions that heal with remission or treatment of TB.
Classification includes three types: 1) PNT; 2) erythema
induratum of Bazin (EIB); and 3) lichen scrofulosorum
(LS). Tuberculids can be classified into two groups: true
tuberculids and facultative tuberculids. The former
classified because Mycobacterium tuberculosis plays a
major etiologic role and the latter because
Mycobacterium tuberculosis is one of several possibly
etiologic agents. All were once believed to be a
consequence of hypersensitivity to the presence of
mycobacterial antigens within a host of previously
acquired immunity to TB; however, most are now
understood not to be uniquely caused by TB. PNT and LS
are still widely accepted as true tuberculids and EIB as a
facultative tuberculid. Whatever underlies the
pathophysiology, a consensus has been reached that PNT
23 [ October 2009 Volume 2 Number 10]
FIGURE 9. Lupus vulgaris
Source = DermNetNZ.org
and LS represent true hypersensitivity reactions rather
than the result of a local CTB infection. This is based on
the observation that these lesions have consistently failed
to either stain positive for or culture mycobacterial
organisms. Although the organisms are absent,
mycobacterial DNA have been detected in biopsy
specimens subjected to PCR. Furthermore, all
tuberculids exhibit granulomatous inflammation and
some degree of necrosis and vasculitis suggesting that
these lesions are a result of released mycobacterial
antigens in the setting of a concurrent or distant
infection.
LS is an eruption of multiple, small, grouped,
asymptomatic, firm, perifollicular, lichenoid papules or
plaques most often affecting children or young adults that
progresses and subsides within weeks to months without
scarring.3 Skin biopsy with histological analysis shows
superficial, perifollicular, epithelioid granulomas
surrounding hair follicles and sweat glands without
evidence of necrosis. Typically no AFB are visualized
histologically, although TST is often very remarkable.
EIB is a TB-associated panniculitis that presents with
multiple, painful, recurring, ulcerated nodules that affect
the lower limbs of women (Figure 10).3,5 Pre-existing
vascular disease may predispose patients to lesions during
exposure to cold weather. Lesions are chronic; slow to
resolve, if at all; and result in atrophic hyperpigmented
scarring after several months. Histology should show three
of four of the following elements: 1) septal panniculitis; 2)
fat necrosis; 3) small or large vessel vasculitis; and 4)
granulomas. Although patients show TB skin
hypersensitivity, AFB are rarely identified. A 2005 study in
Spain demonstrated that about 10 percent of cases were
positive for Mycobacterium tuberculosis using PCR
technique of identification.11 In a case series and literature
review, Bayer-Garner et al found that organisms, such as
Mycobacterium bovis and Mycobacterium marinum,
may also be involved as the etiology of EIB, although no
identification was found during their investigation. They
suggested that EIB has diverse etiologies with varying
pathogeneses leading to similar histological changes, and
23

FIGURE 10. Erythema induratum of bazin or nodular vasculitis
Source = DermNetNZ.org
the cases analyzed may not have had an infectious etiology
(suggesting a facultative tuberculid picture).12
DIAGNOSIS
Diagnosis of CTB is complicated and requires a full
work-up, including a detailed history and physical
examination; careful consideration of clinical presentation;
TST; serum QFT-G (and possibly other laboratory testing);
skin biopsy with histological analysis and special staining
methods for identification of AFB; and the use of other
diagnostic tests, such as chest x-ray and sputum culture.
The QFT-G is an in-vitro diagnostic aid that measures a
component of cell-mediated immunity to Mycobacterium
tuberculosis and is based on the quantification of
interferon-gamma released from sensitized lymphocyte.
QFT-G was approved in 2005 by the US Food and Drug
Administration for the diagnosis of both latent and active
TB infections. The antigens used in QFT-G are not shared
by BCG vaccine strain or by nontuberculous
mycobacterium. According to the Centers for Disease
Control and Prevention guidelines of 2005, QFT-G can be
used in place of the TST as it has increased specificity, lack
of cross-reactivity to BCG, and convenience for both
patient and provider.13 Concordance rates between TST
and QFT-G range from 60 to 90 percent. The cost
effectiveness of QFT-G test still needs to be studied.14
Mycobacterial culture remains the most reliable
method to determine the presence of mycobacteria and
their sensitivities, but the yield is often low and often
takes many weeks.2,9,16 Culture sensitivity is much lower
than specificity, with sources ranging from 80 to 85
24 [October 2009 Volume 2 Number 10]
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
has shown to have high specificity and good positive
predictive value, it seems to work best as a confirmatory
test in patients with a high pre-test probability.22 In
multibacillary CTB, PCR has the highest likelihood of
yield. Nonetheless, a combination of diagnostic tests is
needed when a case of CTB is suspected to confirm a
diagnosis. In developing countries, PCR is not always
readily available and therefore physicians must rely on a
positive response to anti-TB drugs to confirm difficult
cases.18,20,23 It is essential to search for extracutaneous foci
of TB by urine, blood, and sputum samples; x-ray or CT
scan of the chest; and bone scans. Often, there is a delay
in the diagnosis because CTB is not always considered in
the differential diagnosis of atypical or nonhealing skin
lesions (Table 2). It is imperative that physicians have a
high index of suspicion in high-risk patients and in
atypical presentations.
TREATMENT
CTB treatment is the same as that for systemic TB and
consists of long, multidrug therapy (Table 3). First, the
chemotherapeutic treatment of TB is divided into two
phases: 1) an intensive or bactericidal phase, designed to
rapidly reduce the total body burden of Mycobacterium
tuberculosis; and 2) a continuation or sterilizing phase.
The most commonly used drugs are isoniazid, rifampin,
pyrazinamide, and either ethambutol or streptomycin.3,5,24
After eight weeks of therapy, the patients are considered
no longer infectious, but still require longer term
treatment for eradication. The continuation or sterilizing
phase is designed to execute the remaining bacteria that
resist the initial intensive or bactericidal phase. It is not
clear why some of the bacteria resist the initial treatment,
but the first-line drugs are typically highly effective. If the
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
5mg/kg daily, max 300mg
Isoniazid
15mg/kg TIW, max 900mg
10mg/kg daily, max 600mg
Rifampin
10mg/kg TIW, max 600mg
2025mg/kg daily, max 2g
Pyrazinamide
3040mg/kg TIW, max 3g
1520mg/kg daily, max 1600mg
Ethambutol 2535mg/kg TIW, max 2400mg
4050mg/kg BIW, max 4000mg
MEDICATION COMMON ADVERSE REACTIONS
Paresthesias and/or peripheral neu-
Isoniazid ropathy, elevated liver transaminases,
nausea and vomiting
Nausea and vomiting; anorexia;
abdominal pain; diarrhea; orange
and/or red-colored bodily fluids; flu-
Rifampin
like symptoms (fever, malaise,
headache, myalgias, arthralgias); ele-
vated liver transaminases
Malaise, joint pain, rash, urticaria,
photosensitivity, nausea, vomiting,
Pyrazinamide
anorexia, hyperuricemia, gout,
elevated liver transaminases
Blurred or changed vision, blindness,
flu-like symptoms (fever, malaise,
Ethambutol headache, myalgias, arthralgias),
nausea, vomiting, anorexia, elevated
liver transaminases, rash, pruritis
* 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]
CHILDREN DOSING
1015mg/kg daily
2030mg/kg intermittently
1020mg/kg daily or BIW
1530mg/kg daily
4050mg/kg BIW
1520mg/kg daily
50mg/kg BIW
COMMENTS MONITORING
Adjunctive pyridoxine (vitamin B6) 2550mg CMP at baseline; LFTs every month
daily if patient is >35 years old, has a his-
Can follow with liver function tests or tory of hepatic disease or alcohol or
discontinue medication if causes hepatotoxicity IV drug abuse, females in postpar-
Take medication on empty stomach or at tum period; option opthalmological
bedtime exam at baseline
Take medication on empty stomach or at
bedtime
Reassurance
CBC, CMP at baseline; LFTs if hepat-
Give antipyretics, nonsteroidal
ic impairment every 24 weeks
anti-inflammatory medications, rest
Can follow with liver function tests or
discontinue medication if causes hepatotoxicity
Give aspirin or nonsteroidal anti-inflammatory
Oral antihistamines, topical corticosteroids,
emollients, sun protection
Take medication at bedtime or treat with
CMP and uric acid at baseline, then
antinausea medications
periodically
Can follow with uric acid levels and treat with
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
anti-inflammatory medications, rest
CMP, CBC, optional ophthalmological
Take medication at bedtime or treat with
examination at baseline,
antinausea medications
then periodically
Can follow with liver function tests or
discontinue medication if causes hepatotoxicity
Oral antihistamines, topical corticosteroids,
emollients
6. Handog EB, Gabriel TG, Pineda RT. Management of
cutaneous tuberculosis. Dermatol Ther. 2008;21(3):
154161.
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