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CPD • Dermatology doi: 10.1111/j.1365-2230.2007.02352.x

Cutaneous manifestations of tuberculosis

J. E. Lai-Cheong, A. Perez, V. Tang, A. Martinez,* V. Hill and H. du P. Menagé
Departments of Dermatology and *Pathology, University Hospital Lewisham, London, UK

Summary Cutaneous involvement is a rare manifestation of tuberculosis (TB). The correct

diagnosis is often significantly delayed because cutaneous TB is not routinely
considered in the differential diagnosis or because investigations fail to reveal the
presence of Mycobacterium tuberculosis. The clinical features of cutaneous TB are
diverse, and result from exogenous and endogenous spread of M. tuberculosis and from
immune-mediated mechanisms. The recognition of cutaneous TB is important, as the
diagnosis is frequently overlooked resulting in delayed treatment.

The early classification system of cutaneous TB was

Introduction
Tuberculosis (TB) is on the increase in the UK, partic-
ularly in areas of high population migration. This
problem is compounded by the emergence of both human
immunodeficiency virus (HIV) ⁄ acquired immunodefi-
ciency syndrome (AIDS) and multidrug-resistant TB.1–3
While pulmonary TB is the commonest manifestation of
primary inoculation with M. tuberculosis, cutaneous TB is
relatively rare, with a reported incidence of 1–4.4% of all
cases of TB.4,5 The development of cutaneous TB depends
on several factors, including the patient’s immune status,
route of inoculation and past sensitization with TB.
largely morphologically based; as knowledge about the
mechanism of infection became clearer, a change in the
classification of cutaneous TB became necessary.
Tappeiner and Wolff proposed that cutaneous TB could
be classified on the basis of the mode of inoculation
(exogenous vs. endogenous) and the immune status of
the patient.7 A third group of cutaneous TB, known as
the tuberculids, probably has an immunological basis.
Mode of inoculation
Endogenous inoculation

The endogenous inoculation of M. tuberculosis can occur

Pathogenesis and the spectrum of cutaneous
TB
Cutaneous TB is caused by M. tuberculosis, a Gram-
negative bacillus, although Mycobacterium bovis and the
bacille Calmette–Guerin (BCG) vaccination, an attenu-
ated form of M. bovis, are sometimes implicated.6
M. tuberculosis can be acquired by inhalation, ingestion
and inoculation, and eventually leads to a caseating
destructive granulomatous inflammation in the affected
organs. In the skin, in addition to granuloma formation,
TB can cause vasculitis and panniculitis.
Correspondence: Dr Joey E. Lai-Cheong, St John’s Institute of Dermatology,
Guy’s and St Thomas’ Hospital, London SE1 7EH, UK.
E-mail: joey.lai-cheong@kcl.ac.uk
Conflict of interest: none declared.
Accepted for publication 9 November 2006
by autoinoculation, via the lymphatic system, as well as
by haematogenous and contiguous spread, and causes
scrofuloderma, metastatic tuberculous abscesses, lupus
vulgaris (LV), miliary TB and orificial TB.
In scrofuloderma, an underlying tuberculous focus
such as an infected lymph node, testicle, joint or bone is
present. It is often associated with pulmonary TB,8 and
cervical gland infection seems to be the commonest
underlying focus, with the face and neck being the most
frequently affected sites.9 This leads to the formation of
cold abscesses in the overlying skin, which subsequently
breaks down, exuding a purulent discharge.10 Not
uncommonly, scrofuloderma secondary to bone and
joint involvement sometimes presents to the orthopaedic
surgeon.11 The clinical features of scrofuloderma
include ulcerated purplish plaques, which on healing
tend to leave retracted and puckered scars (Fig. 1). The

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Cutaneous manifestations of tuberculosis J. E. Lai-Cheong et al.
Figure 1 Scrofuloderma, showing multiple retracted, puckered
and and hypertrophic scars present along the jawline and and
neck associated with cervical lymphadenopathy (arrow).
diagnosis is made by a combination of characteristic
clinical features, skin biopsy and tissue culture. Histo-
logically, a caseating granulomatous inflammation is
seen in the lower dermis.
Metastatic tuberculous abscesses (tuberculous gum-
mas) usually arise secondary to haematogenous spread
from a primary focus of infection, especially during a
period of decreased immunity. The abscesses are located
on the trunk and extremities (Fig. 2a,b). Insidious
bacteraemia without a primary infective source can also
lead to the development of metastatic abscesses.12,13 In
addition, tuberculous abscesses have been described in
patients with miliary TB14 and can also be found along
the course of the lymphatics, giving rise to a sporotrich-
oid pattern.15 Mycobacterial culture is frequently neg-
ative because this form of TB is paucibacillary. A strong
clinical suspicion and a good response to antitubercu-
lous medications confirm the diagnosis.
Lupus vulgaris is the commonest form of cutaneous
TB,16 and is acquired mainly through endogenous
inoculation (haematogenous, via lymphatics or contigu-
ous spread) and rarely by exogenous exposure such as
BCG vaccination.17 It is characterized by the presence of
well-demarcated, reddish-brown plaques in the facial and
cervical areas, which, if left untreated, may lead to
significant cosmetic disfigurement. In addition, malig-
nant transformation can arise within lupus vulgaris
(LV).18 The cutaneous lesions show the characteristic
apple-jelly appearance on diascopy. Histologically, tuber-
culous granulomas with areas of caseating necrosis can
be found in the upper dermis. Tissue culture may be
462 Journal compilation  2007 Blackwell Publishing Ltd • Clinical and Experimental Dermatology, 32, 461–466
(a)
(b)
Figure 2 (a, b) Metastatic tuberculous abscess: prominent ÔcoldÕ
nodule on the dorsum of the left hand with release of a purulent
discharge.
negative for M. tuberculosis because LV is associated with
a high degree of immunity.8
Miliary TB is a life-threatening form of TB resulting
from haematogenous dissemination of tubercles, usually
from a pulmonary source of TB. Cutaneous miliary TB is
rare but is re-emerging in patients with HIV and CD4
counts of < 100 cells ⁄ lL.19 Clinically, there are sheets
of discrete white-topped papules, and the patient is
systemically unwell with lethargy, weight loss and
pyrexia. In severe immunosuppression, the tuberculin
test can be negative, owing to anergy. Miliary TB is
often complicated by the presence of multidrug resistant
TB.8 Similarly, orificial TB, which affects the oral, nasal,
anal and sometimes vulval mucosa, occurs in individ-
uals with severely impaired cell-mediated immunity and
advanced TB in other organs such as the lungs and
gastrointestinal tract. Clinically, yellow papules are
found in the affected mucosal surfaces, and the lesions
respond poorly to treatment.10
Exogenous inoculation
Exogenous inoculation can give rise to a warty lesion on
the fingers called tuberculosis verrucosa cutis (TVC),
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particularly at trauma-prone sites in previously sensiti-
zed individuals on a background of moderate to high
immunity. In the past, certain professionals such as
anatomists and physicians were prone to this form of
cutaneous TB as a result of direct inoculation of the
tubercles through broken skin. In the tropics, TVC is
seen more often in children, caused by walking barefoot
on soil contaminated with tuberculous sputum.20 TVC
develops as a small papule surrounded by a purple
inflammatory halo and progresses into an asympto-
matic warty lesion. Other manifestations of exogenous
inoculation include tuberculous chancre and rarely LV.
Tuberculous chancre, also known as primary inocu-
lation TB, occurs as a result of trauma, often unre-
ported, to the skin, which facilitates the entry of
M. tuberculosis in previously non-sensitized patients.
Within a month, a nodular lesion develops, rapidly
enlarges and forms a painless ulcer.1 Tissue culture is
often positive for M. tuberculosis, and histologically, a
necrotizing inflammatory infiltrate with the presence of
tubercle bacilli is seen early in the course of the
infection. As the disease progresses, a granulomatous
inflammation is noted, with a concomitant reduction in
the number of bacilli.21
Immune-mediated mechanisms: the
tuberculids
The tuberculids are a group of cutaneous TB resulting
from a hypersensitivity reaction to an extracutaneous
source of M. tuberculosis, usually in individuals with high
(a)
Figure 3 (a) Erythema induratum of
Bazin: multiple erythematous purulent
nodules measuring 30–50 mm in diam-
eter, distributed on both lower limbs;
(b) after two months of antituberculous
treatment, the nodules have healed with
postinflammatory hyperpigmentation.
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Cutaneous manifestations of tuberculosis J. E. Lai-Cheong et al.
immunity. This leads to the destruction of the bacilli; it
then becomes difficult to demonstrate their presence.22
The various forms of tuberculids include erythema
induratum of Bazin (EIB), lichen scrofulosorum, papulo-
necrotic tuberculid, and a newly described form called
nodular tuberculid.23 All the tuberculids show a dra-
matic response to antituberculous chemotherapy.
EIB is characterized by the presence of multiple,
chronic, painful, indurated, often ulcerated nodules that
predominantly affect the lower limbs (Fig. 3a,b), usually
in women. This condition is associated with a strong
tuberculin hypersensitivity reaction, but clinically overt
TB is rare. The search for M. tuberculosis in EIB has
yielded conflicting results even with the use of
polymerase chain reaction (PCR). Ziehl–Nielsen stain
for acid-fast bacilli (AFB), tissue culture and PCR for M.
tuberculosis are often negative. A recent study carried
out in northwest Spain showed that about 10% of cases
of EIB were positive for M. tuberculosis by PCR.24 Other
organisms such as M. bovis25 and Mycobacterium
marinum may also be implicated.26 Histologically, EIB
is characterized by lobular panniculitis associated with
vasculitis (Fig. 4). The main differential diagnosis is
erythema nodosum (EN), which can be triggered by a
range of infectious and noninfectious agents, and can
occur in association with systemic diseases such as
sarcoidosis. Among the infectious agents, streptococcal
infection and primary TB are the commonest aetiologi-
cal factors. Several reports have suggested that EN is
seen only in primary tuberculous infection.27,28 Similar
to EIB, EN occurs more frequently in women, and may
(b)
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Figure 4 Erythema induratum of Bazin: a florid lobular pannic-
ulitis associated with a small vessel vasculitis is present, and gra-
nulomas with foci of central necrosis in the deep dermis and and
subcutis can be seen.
represent a hypersensitivity reaction to a variety of
antigens such as M. tuberculosis, and can therefore be
regarded as a tuberculid. However, it differs both
clinically and histologically from EIB. EN is character-
ized by the presence of tender indurated nonulcerative
nodules seen predominantly on the lower limbs. It may
be preceded by flu-like symptoms, and resolves sponta-
neously within 8 weeks. Histologically, EN is charac-
terized by a septal panniculitis without vasculitis.
Lichen scrofulosorum is a rare asymptomatic skin
eruption involving the trunk, and consists of groups of
skin-coloured papules, 1–2 mm in diameter, usually in
patients (mainly children) with high immunity. Plaques
and micropustules have also been described in this
condition.22 Tissue culture and PCR are usually negat-
ive for M. tuberculosis, but histologically, a perifollicular
granuloma formation in the papillary dermis with a
striking absence of caseation necrosis is found.
Nodular tuberculid is a newly described form of
tuberculid.23,29 The clinical feature is the appearance of
dusky-red nontender nodules on the shins. Histologi-
cally, a granulomatous inflammation is found at the
junction of the subcutaneous fat and the lower der-
mis.23,29 In papulonecrotic tuberculid, there is a sym-
metrical, asymptomatic eruption consisting of dusky-red
papules on the extensor surfaces of the limbs. The
papules may evolve into ulcers and involute to produce
pitted scars.8 In contrast to nodular tuberculid and EIB,
the granulomatous inflammation is seen in the upper
dermis and epidermis.
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Investigations and treatment of cutaneous
TB
There is often a significant delay in the diagnosis of
cutaneous TB because it is not always considered in the
differential diagnosis of nonhealing or atypical skin
lesions. In addition, the demonstration of M. tuberculosis
or AFB in tissue culture and smear, respectively, can be
formidably difficult because some forms of cutaneous TB
are paucibacillary. A diagnosis of cutaneous TB is
suspected on the basis of clinical history and examina-
tion and on typical histological findings. It is confirmed,
however, by the presence of M. tuberculosis in either
tissue culture from skin biopsy, histological smear or
PCR.8 Another diagnostic tool that has been reported
but not often used is a trial of antituberculous treatment
for a period of 6 weeks in the management of difficult
cases.30
It is imperative to search for an extracutaneous focus
of infection by means of a chest X-ray, sputum smears
and culture, and early-morning urine samples. Further
investigations such as computed tomography (e.g.
adrenal glands and kidneys) and bone scans can also
be considered. Anti-tuberculous chemotherapy is usu-
ally given for a period of 8 weeks in the form of
quadruple therapy (isoniazid, rifampicin, pyrazinamide
and ethambutol) followed by a continuation phase
consisting of isoniazid and rifampicin twice weekly for
16 weeks. Directly observed therapy given three times
weekly may also be an option, particularly in poorly
compliant patients. In localized areas of scrofuloderma
and TVC, surgical excision may be used.7
Following a diagnosis of cutaneous TB, individuals
who have been in close and prolonged contact with
the index case should be contact-traced and screened
for exposure to TB using a Mantoux test. A chest X-ray
and sputum analysis may also be offered. In England,
Wales and Northern Ireland, it is a statutory require-
ment for the diagnosing clinician to notify the local
consultant in communicable disease control (CCDC) of
all clinically diagnosed cases of TB, whether or not
microbiologically confirmed. Later, if the clinical diag-
nosis proves incorrect, this information should also be
given to the CCDC.
Conclusion
Cutaneous TB has a number of protean manifestations
resulting from exogenous inoculation, endogenous
spread and immune-mediated mechanisms. The recog-
nition of cutaneous TB is important because the
diagnosis is easily missed, leading to considerable delay
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in treatment. Cutaneous TB is still a relatively rare
entity in the developed world. However, in an era of
high population migration and the emergence of HIV
and AIDS, it is becoming increasingly prevalent, and
hence requires early recognition.
Learning points
• The incidence of tuberculosis (TB) in the UK is
rising, owing to the emergence of HIV and AIDS
and to mass immigration from developing coun-
tries.
• While pulmonary TB is common, cutaneous TB
is rare, with an incidence range of 1–4.4%.
• Endogenous and exogenous inoculation and
immune-mediated mechanisms are important in
the pathophysiology of cutaneous TB.
• Endogenous inoculation gives rise to scrofulo-
derma, miliary TB, metastatic abscesses, orificial
TB and lupus vulgaris.
• Tuberculosis verrucosa cutis and tuberculous
chancre develop as a result of exogenous inocula-
tion.
• The tuberculids are a group of cutaneous TB
that develops as a result of a hypersensitivity
reaction to tuberculous antigen. They comprise
erythema induratum of Bazin, lichen scrofuloso-
rum, papulonecrotic tuberculid and a newly des-
cribed entity called nodular tuberculid.
• A high index of suspicion is required for reach-
ing a diagnosis of cutaneous TB as Ziehl–Nielsen
stain, mycobacterial culture and PCR for myco-
bacterial TB may all be negative.
• TB is a notifiable disease. The consultant in
communicable disease control must be informed
once a clinical diagnosis of TB is made.
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