Escholarship UC Item 55d3f43c
Escholarship UC Item 55d3f43c
Escholarship UC Item 55d3f43c
Title
An evolving presentation of cutaneous tuberculosis
Permalink
https://escholarship.org/uc/item/55d3f43c
Journal
Dermatology Online Journal, 26(8)
Authors
Brown, Ashley E
Ibraheim, Marina K
Petersen, Erik
et al.
Publication Date
2020
DOI
10.5070/D3268049889
Copyright Information
Copyright 2020 by the author(s).This work is made available under the terms of a Creative
Commons Attribution-NonCommercial-NoDerivatives License, available at
https://creativecommons.org/licenses/by-nc-nd/4.0/
Peer reviewed
Introduction
Cutaneous tuberculosis (CTB) is an uncommon
manifestation of tuberculosis (TB). Although TB is
becoming increasingly common in the United States
with 9,029 cases reported in 2017, CTB is reported in
1-2% of infections [1-3]. CTB has many different
morphologies including tuberculous chancre,
tuberculosis verrucosa cutis (TVC), lupus vulgaris
(LV), scrofuloderma, and metastatic tuberculous
abscess [4]. The varied clinical presentation of CTB
can make the diagnosis difficult. Furthermore, tissue Figure 1. Clustered violaceous papules on right wrist.
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Case Discussion
Diagnosing cutaneous tuberculosis can prove
challenging to clinicians as it causes a range of skin
morphologies that cannot easily be confirmed by
acid-fast testing for mycobacteria. Additionally, the
Figure 3. Swelling and erythema of the wrist. diagnosis itself is rare, reported in less than 1-2% of
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TB infections [2,3]. These morphologies include Metastatic tuberculous abscess is typically the result
tuberculous chancre, TVC, LV, scrofuloderma, and of hematogenous spread from a primary focus
metastatic tuberculous abscess [4]. Mode of during periods of lowered resistance such as in an
transmission partially dictates the morphologic type immunocompromised state [3].These nodules do
that manifests. This is worth considering in the not demonstrate predilection for any particular
context of the patient case presented above. The anatomic location. Inverse sporotrichoid spread of
case presented above exhibits an especially difficult abscesses, as seen in this patient, has been reported
situation as it does not adhere to one single CTB previously [8]. Abscesses begin as single or multiple
variant. During the initial visit, the papule form most nodules that form draining sinus abscesses unless
closely fit with TVC morphologically. However, it surgically incised and drained [4]. Histology shows
most likely represents LV mimicking TVC given the suppurative granulomata with nonspecific infiltrates
mode of transmission. As the infection progressed it and necrosis [3]. Pus drained from the abscess
assumed the morphology of metastatic tuberculous usually demonstrates mycobacteria. Given the
abscess. Although there have been a handful of pathophysiology of LV and metastatic tuberculous
cases reporting two concurrent manifestations of abscess both rely on hematogenous spread, the
CTB this is the first case to the author’s knowledge to progression of this patient’s clinical cutaneous
shift manifestations during the disease course [5,6]. findings could represent evolution of TB infection
Tuberculosis verrucosa cutis lesions result from from a superficial-to-deep infection originating from
exogenous inoculation of TB directly into the skin of the pulmonary lesions.
a susceptible individual [5]. These lesions present as Detection of mycobacteria within the suspected
slowly growing, asymptomatic violaceous or lesion can aid in determining the variant of CTB. The
brownish red plaques [4]. Histology shows multibacillary forms (TB chancre, scrofuloderma, TB
noncaseating granulomas without mycobacteria orificialis, military TB, metastatic TB abscess, and
being detected via acid-fast bacilli or culture [3]. some forms of LV) are more likely to be acid-fast
Acid-fast bacilli staining and mycobacterial culture bacilli positive whereas the paucibacillary forms (TVC
are often negative [7]. Although our patient’s original and acral forms of LV) are usually acid-fast bacilli
lesion morphologically resembled TVC, given the negative [4]. The presence of paucibacillary forms
lack of exogenous inoculation it is more consistent renders CTB a difficult diagnosis to clinch. As a
with LV. Neither TVC nor LV is known to produce an consequence, the differential diagnosis list widens
abscess. As a result, the later variant more closely
matched metastatic tuberculous abscess, also
known as TB gumma.
Lupus vulgaris lesions are sharply emarginated red
brown papules that have a gelatinous consistency,
giving them the description “apple jelly nodules.”
These lesions slowly change via peripheral extension
and central atrophy into large plaques. Lupus
vulgaris may arise as a result of direct inoculation in
a sensitive individual or hematogenous spread from
a primary infection. Histology shows noncaseating
granulomas and mononuclear cell infiltrate [3]. Acid-
fast bacilli staining and mycobacterial culture are
often negative [4]. Lupus vulgaris can manifest in a
sporotrichoid form, with lesions having a linear Figure 5. Re-biopsy exhibiting fibrous tissue with chronic
pattern along lymphatics spreading from a primary lymphohistiocytic inflammation, focal necrosis, and foreign body
focus. giant cells. H&E, 10x.
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considerably in this context, as CTB to appear similar used. The maintenance phase maintains sterility by
to a host of other diseases with cutaneous utilizing rifampin and isoniazid over the course of
manifestations. Diseases such as leishmaniasis, two months; ethambutol may be used in place if
leprosy, actinomyces, and deep fungal infection isoniazid if resistance is suspected. Two percent
must be considered in this setting [3]. The diagnosis lactic acid and local anesthesia may be applied if
of CTB requires a thorough history and physical lesions manifest near orifices. Surgery can be utilized
examination. A high degree of suspicion should be but it is typically reserved for treatment of LV, TVC,
entertained for immunocompromised or high-risk and scrofuloderma [10].
patients with atypical lesions. Additional tests that
could aid diagnosis are PCR for mycobacterium, Cutaneous TB, if caused by atypical mycobacteria,
tuberculin skin test, and serum QuantiFERON-TB cannot be treated by anti-TB drugs. For this reason,
gold testing. QuantiFERON-TB gold exposes the treatment proves to be difficult. Treatment must be
patient’s serum to Mycobacterium proteins and tailored to the exact organism but can involve
quantifies interferon production by the patient’s doxycycline, minocycline, amikacin, ciprofloxacin, or
white blood cells, which indicates infection by the trimethoprim-sulfamethoxazole depending on the
pathogen [4]. In our case, a rheumatologist who had organism [10].
seen the patient one year before presentation to
dermatology had ordered QuantiFERON-TB gold
testing; however, the test was not completed. Conclusion
Treatment for cutaneous TB is the same as treatment This case was challenging to diagnose owing to its
for pulmonary or systemic TB with a multi-drug presentation which was complicated by the evolving
approach that typically utilizes rifampin, isoniazid, clinical manifestations of CTB. This case shows CTB
pyrazinamide, and either ethambutol or can have fluid morphology that can confuse or delay
streptomycin [9]. The treatment scheme is divided the diagnosis if clinical suspicion is not high.
into two phases: the intensive phase and the
maintenance phase. The intensive phase lasts eight
weeks and is bactericidal; during this time, rifampin, Potential conflicts of interest
isoniazid, pyrazinamide, and streptomycin can be The authors declare no conflicts of interests.
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