i n d i a n j o u r n a l o f t u b e r c u l o s i s x x x ( 2 0 1 8 ) 1 e6

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indian-journal-of-tuberculosis/

Review article

Breast tuberculosis

Richa Sinha a,*, Rahul b

a
Microbiology, PMCH, Patna, Bihar, India
b
Surgical Gastroenterology, SGPGI, Lucknow, U.P, India

article info abstract

Article history: Tuberculosis (TB) of breast is an uncommon entity even in endemic regions. Moreover, it is
Received 17 March 2018 seldom reported. It often presents in young lactating females as a painless breast lump and
Accepted 3 July 2018 confused with breast malignancy or pyogenic abscess. A high index of suspicion is
Available online xxx required. Fine needle aspiration cytology is important to direct the patient to further tests
pertaining to TB. New diagnostic modalities based on detection of nucleic acids have
Keywords: improved the accuracy and cut down the time to diagnosis. Anti-tubercular chemotherapy
Extrapulmonary tuberculosis remains the standard of care. Surgical intervention is seldom required.
Mastitis The fact that the disease being rare, having symptom overlap with commonly prevalent
Acid fast bacillus breast malignancy and potentially curable, it becomes important to analyze the presen-
Breast tuberculosis tation, available investigative modalities for early goal directed treatment.
© 2018 Tuberculosis Association of India. Published by Elsevier B.V. All rights reserved.

accounts for 15e20% of all cases. Eighteen percent of patients

1. Introduction
Tuberculosis (TB) is a major global health problem and a
leading cause of mortality due to infectious etiology, after
Human Immunodeficiency Virus (HIV). In 2014, approximately
9.6 million new TB cases were estimated worldwide by World
Health Organization (WHO). Twelve percent were HIV posi-
tive. The death toll due to the disease was 1.5 million globally
including 0.4 million among HIV-positive people. In the last
two decades, incidence and deaths due to TB have decreased
significantly due to socioeconomic improvement, progress in
therapy and improved health care.1
Lungs are the most common organ to be affected in TB.
Other systems that may be involved include lymph nodes,
central nervous system, bones/joints, genito-urinary tract,
abdomen and breast. Extrapulmonary Tuberculosis (EPTB)
have only extra-pulmonary disease.2
TB of breast is a rare entity, even in developing countries.
In 1829, Sir Astley Cooper cited the first case of breast TB
which he addressed as “Scrofulous swelling of bosom”.3 The
overall incidence of tuberculous mastitis is reported to be 0.1%
of all breast lesions. It constitutes 3e4.5% of all surgically
treated breast lesions in developing countries.4 A survey done
by Morgan in 1931, revealed 439 cases of tubercular mastitis
with the incidence between 0.5 and 1.04%.5 Klossner in 1944,
reported 50 cases of breast TB in women.6 Haagensen studied
approx 8000 breast specimens between 1938 and 1967, in
which he could find only 5 cases of breast TB.7
There are few reports on breast TB from India as it is often
misdiagnosed, under-reported and ill treated. The rarity of the
disease and overlap of features with breast carcinoma and

* Corresponding author.
E-mail address: dr.richa.sinha@gmail.com (R. Sinha).
https://doi.org/10.1016/j.ijtb.2018.07.003
0019-5707/© 2018 Tuberculosis Association of India. Published by Elsevier B.V. All rights reserved.

Please cite this article in press as: Sinha R, Rahul, Breast tuberculosis, Indian Journal of Tuberculosis (2018), https://doi.org/10.1016/
j.ijtb.2018.07.003
2 i n d i a n j o u r n a l o f t u b e r c u l o s i s x x x ( 2 0 1 8 ) 1 e6
pyogenic breast abscess makes it important to understand the
pathophysiology, evaluation and management.
2. Routes of infection
TB is caused by acid fast bacilli (AFB), Mycobacterium tubercu-
losis. The breast tissue is remarkably resistant to Mycobac-
teria. It provides infertile environment for the survival and
multiplication of the bacilli, like skeletal muscles and spleen.8
The various modes by which breast may get involved are:
(i) haematogenous;
(ii) lymphatic;
(iii) spread from contiguous structures like infected rib,
costochondral cartilage, sternum, shoulder joint9;
(iv) direct inoculation through nipple skin abrasions or
through lactiferous ducts10; and
(v) ductal infection.11
3. Demography
Breast TB is common in young age (20e40 years), multiparous,
lactating females.12,13 This may be because of the fact that
female breast undergoes frequent changes during this period.
Increased blood supply, dilated ducts during lactation and
physiological stress of breast feeding are contributory factors.
Past history of suppurative mastitis and trauma to the breast
are also important risk factors.
4. Host factors
Several host's defense mechanisms come into play. Cell
mediated immunity (CMI) mainly confers protection against
M. tuberculosis. Humoral immunity has no defined role.
Two types of cells are responsible for the immunity:
i) Macrophages: directly phagocytose the TB bacilli,
ii) T-cells, mainly CD4 lymphocytes: induce protection through
the production of lymphokines.14 Immunocompromised
patients (uncontrolled diabetes, immune deficiency syn-
dromes, immunosuppressive therapy, anticancer treat-
ment) are at an increased risk of tubercular infection.
5. Pathogenesis
Infection by mycobacteria initiates a sequence of events. It
triggers the activation of macrophages in 2e8 weeks, which
engulf them. They form a barrier around the bacilli, preventing
dissemination. This macrophagocytic cell aggregate is called
as granuloma. Majority of the bacilli are killed or destroyed.
Few survive and multiply inside these cells, if host's immune
response is weak. They get released when the macrophages
die. Dead macrophages with or without bacilli, result in soft
and white cheese like material called “Casseation Necrosis”.
Please cite this article in press as: Sinha R, Rahul, Breast tuberculosis, Indian Journal of Tuberculosis (2018), https://doi.org/10.1016/
j.ijtb.2018.07.003
Breast TB can be primary or secondary.15,16 Raw and Mor-
gan, proposed the theory of secondary involvement of breast
from a tuberculous lesion elsewhere.17 Mckeown and Wil-
kinson later classified breast TB as primary when the breast
lesion was the only manifestation, and secondary when there
was an additional focus in the body.9
Faucial tonsils of suckling infants harboring mycobacte-
rium can directly transmit the infection to the lactiferous
ducts of the feeding mother. Milk stasis or milk over-
production, coupled with infection through traumatized
nipple can cause lactation mastitis. Transient breast
enlargement from maternal hormones in the postnatal period
also makes them vulnerable for infection.18
In duct ectasia (dilated ducts associated with inflamma-
tion), there occurs squamous metaplasia of lactiferous ducts.
This blocks the ductal opening, leading to their dilation. In the
presence of inflammation, ducts can rupture. Any infection in
this condition can result in an abscess.11
Secondary involvement of breast can occur through
lymphatic spread, haematogenous (miliary) dissemination, or
contiguous spread from the pleura or chest wall. The path of
disease spread from lungs to the breast tissue was traced via
the tracheobronchial, paratracheal and mediastinal
lymphatic trunk to the internal mammary nodes. Cooper in
his theory explained the secondary involvement of breast by
retrograde lymphatic extension from axillary nodes to the
breast tissue.3,19,20 This is the most common route of infec-
tion. The presence of ipsilateral axillary lymphadenitis in
more than 50% cases of tubercular mastitis further supports
the fact.8
6. Incubation period
The history of presenting symptoms in breast TB is usually
less than a year but varies from few months to several
years.8,20
7. Virulence factors
Virulence factors are defined as proteins or genes, which when
omitted lead to loss of pathogenicity of an organism without
affecting its multiplication or growth in standard conditions.
Unlike other pathogens, mycobacteria do not produce classical
virulence factors like toxins. Mycobacteria instead, have
evolved a mechanism to evade the hostile environment inside
immune cells. They can thrive in the host cells for a long period
and get activated in an immune deficient stage.
Under normal circumstances, pathogens are engulfed by
macrophages. They are contained in the phagosome, which
later fuses with lysosome to expose the bacilli to free radicals,
hydrolases and nitrogen molecules. This creates an acidic
environment around the bacteria and destroys it.21
Mycobacterium produces a protein called “exported re-
petitive protein” that prevents the phagosome-lysosome
fusion, thus extending the intra-cellular survival. It also pro-
duces cord factor (trehalose-6-6ˈ-dimycolate) which inhibits
the migration of leukocytes, causing chronic granuloma for-
mation. It serves as an immunologic adjuvant as well.
 i n d i a n j o u r n a l o f t u b e r c u l o s i s x x x ( 2 0 1 8 ) 1 e6
The peculiarity of mycobacteria is its lipid content i.e.
mycolic acids, waxes and phosphatides. Nearly 40% of dry cell
weight of mycobacteria is made up of the lipids in the cell
wall.22 Mycolic acid forms complex with muramyldipeptide
and promotes granuloma formation. Mycolic acid methyl
transferases (MAMTs) are responsible for methylation. This
causes minor structural changes in cell wall, important in
deciding the virulence of pathogenic mycbacteria.23 Phos-
pholipids also induce caseous necrosis. High concentration of
mycolic acid confers low permeability, thus reducing the
effectiveness of antibiotics.
Liporabinomannan, a cell wall glycolippid inhibits IFN-ɣ
mediated activation of macrophages and suppression of T-cell
proliferation. Protein antigens (CFP10 and ESAT-6) also add to
the virulence by illiciting T-lymphocytes response. These
proteins are also important in relation to the vaccination
against the mycobacteria.
Other factors are KatG gene (encodes catalase and peroxi-
dase enzymes), rpoV gene (main sigma factor initiating tran-
scription of several genes) and Erp gene (encodes proteins
required for multiplication of the bacteria).24
8. Clinical presentation
Breast TB is common in young females, primarily in the
reproductive age group.25,26 Males are rarely affected. Evi-
dence in literature is limited to isolated case reports. In a se-
ries of 52 patients with breast TB by Khanna et al, two were
male.20,27 Most common presentation is a breast lump with or
without axillary lymph nodes. In a study by Basarkod SL et al,
the most common symptom was breast lump, followed by
lump with a sinus and breast abscess.28 More like the breast
cancer, upper outer and the central quadrant of the breast are
most commonly affected. Symptoms that differentiate
mycobacterial infection from malignancy are presence of
constitutional symptoms (fever and pain).
9. Classification
Tewari et al classified mammary TB into 3 types based on the
presentation and management: Nodular variety, Disseminated
disease and Breast abscess.10,29 Original classification by
Mckeown et al included two additional varieties: Sclerosing
type and Mastitis obliterans.9 Both of them have been rarely
reported in last 2e3 decades. Sclerosing mastitis is character-
ized by extensive fibrosis. It lacks any evidence of suppuration.
It is common in old age and mimics scirrhotic carcinoma. The
breast becomes hard and the nipple gets retracted. Mastitis
obliterans presents with ductal infection, leading to prolifera-
tion and periductal fibrosis. This occludes the ducts and pro-
duces cystic dilatations, thus is also called as “cystic mastitis”.
Nodular variety of the disease affects young females. It is
the most common form of presentation, often painless and a
well defined breast lump to start with. In their series of 52
patients, Khanna et al documented the presence of a lump in
62% patients.20 Similarly, Khan et al reported a lump in 80% of
patients with breast TB.30 It is frequently confused with
fibroadenoma or malignancy. The lump is initially free from
Please cite this article in press as: Sinha R, Rahul, Breast tuberculosis, Indian Journal of Tuberculosis (2018), https://doi.org/10.1016/
j.ijtb.2018.07.003
3
the underlying chest wall, but may get tethered to the skin
with time, owing to the ongoing inflammation. Involvement of
the skin causes pain. Late in the course, if left untreated ulcers
may develop. It is important to note that unlike malignancy,
TB seldom involves the nipple areola complex.31 Subareolar
involvement has been documented in less than one fourth of
those affected.20,30,32 Ipsilateral axillary lymphadenitis is
commonly associated with the nodular type of TB. The nodes
increase in size and later become matted.33
In disseminated type of disease: sinus and casseation are
common. It is commonly associated with immunosuppresion
e retroviral infection or immunotherapy for cancers. In a
study conducted by Khan et al sinuses were associated with
breast lump in two third and with breast abscess in one third
of the patients.30 Tubercular breast abscess is common in
young females. Peaud'orange of the skin over the lesion is a
frequent feature.31 It is often misinterpretated as a pyogenic
abscess or malignancy. The definitive diagnosis is based on
tissue biopsy, demonstration of caseating epitheloid granu-
loma and mycobacterial culture.
10. Differential diagnosis
Breast lump being the commonest presentation, it is often
confused with breast tumor. In late phases, when the disease
presents as a breast ulcer, it resembles a fungating tumor. A
patient with a fluctuating abscess may be confused with
traumatic fat necrosis, plasma cell mastitis, periareolar ab-
scess or chronic pyogenic abscess. A patient presenting with
multiple breast sinuses mimic common fungal infections like
actinomycosis and blastomycosis.29
11. Laboratory diagnosis
Breast TB is often misdiagnosed and patients are subjected to
an array of investigations. A high index of suspicion is needed
based on clinical examination. Definitive diagnosis of TB
mandates demonstration of bacilli by microbiological, cytopa-
thological or histopathological evaluation. These tests are often
invasive with low sensitivity. Moreover, even when adequate
tissue is procured, the pathological findings may be suggestive
of a “granulomatous infection” which encompasses a wide
range of differential diagnoses. Other tests which may be
helpful for the diagnosis of mycobacterial infection are:
(i) Mantoux test e Tuberculin test was described by Koch
in 1890. Modified technique of intradermal injection of
the antigen was developed by Charles Montoux in 1912.
Purified protein derivative (PPD) is the most commonly
used tuberculin, extracted from the cultures of M.
tuberculosis. PPD-RT (Research Tubercuin) 23 standard-
ized with Tween 80 (a detergent which when added to
tuberculin prevents its adsorption on plastic/glass sur-
face) is supplied in 1 or 2 TU strengths in India. It is
developed by BCG (Bacillus Calmette-Gue
rin) laboratory
in Chennai. Five TU of the tuberculin is injected intra-
dermally with a 26/28 gauge needle on the volar surface
of the left forearm. A wheal (skin elevation) of 6e10 mm
4 i n d i a n j o u r n a l o f t u b e r c u l o s i s x x x ( 2 0 1 8 ) 1 e6
indicates correct technique. The patient is advised to
keep the area clean and uncovered. The result is inter-
preted 48e72 hours later in good light. It is based on the
size of induration, determined by inspection and
palpation. The diameter of induration is measured in
millimeters perpendicular to the long axis of the fore-
arm. Peripheral erythema is not included in the mea-
surement.34,35 In immunocompetent patients with risk
factors (endemic region, chronic malnutrition or end
stage organ disease, mycobacteriology laboratory
workers), 10 mm induration is significant.36 In devel-
oping countries like India, where TB is highly endemic,
tuberculin skin test is difficult to interpret. The speci-
ficity and positive predictive value is poor.36 Area of
induration does not correlate with the disease activity,
but it does vary according to the medical risk factors. In
immunosuppressed patients (HIV positive, post-
transplant, chemotherapy), induration of even 5 mm
is considered a positive test. False-positive test can be
seen in individuals with previous Bacille Calmettee
Guerin (BCG) vaccination or sensitization to non tuber-
culous mycobacteria. A negative result should imply
that exposure to mycobacteria has never occurred, but
false-negative results are also common (immunocom-
promised patients, wrong technique of tuberculin in-
jection, elderly patients, overwhelming disease or
recent live virus vaccination). Moreover, this test re-
quires multiple visits, thus the compliance remains
poor. Technically, intradermal injection and interpre-
tation of final result is difficult. Therefore, multiple new
tests with better standardization using blood or serum
have evolved and replaced Tuberculin test. It is of little
or no diagnostic value for breast TB and stands obsolete
in present scenario.37
(ii) Interferon Gamma Release Assay (IGRA): It is a new
diagnostic test which detects Interferon gamma (IFN-g)
response produced by T lymphocytes after stimulation
by specific antigens [early secretary antigen target 6
(ESAT-6) and culture filtrate protein 10 (CFP-10)] enco-
ded by a genomic segment unique to M. tuberculosis.
This is absent in most of the other mycobacteria as well
as BCG. The absence of cross reactivity increases its
specificity, when compared to Tuberculin Test. Addi-
tional advantage over Mantoux is that the results
appear within 24 hours. However, this test is not widely
available and carries little significance in the endemic
regions as it does not help to differentiate between
latent and active infection.13,38
(iii) Imaging: Breast TB, especially granulomatous mastitis
and the nodular variant, resembles other benign and
malignant breast lesions. All lumps or swellings in the
breast should be approached by “Triple Assessment”
technique [Physical Examination, Radiological Assess-
ment (Ultrasonography, Mammography) and Cytology
or histology]. Imaging modalities are not specific for TB
breast. Mammography is unreliable, particularly in
young women due to high tissue density. It may help to
rule out other common breast lesions like fibroadenoma
(popcorn calcification). Common mammographic find-
ings are non-specific like skin thickening and coarse
Please cite this article in press as: Sinha R, Rahul, Breast tuberculosis, Indian Journal of Tuberculosis (2018), https://doi.org/10.1016/
j.ijtb.2018.07.003
stromal texture with or without an ill defined breast
mass. A dense sinus tract seen on mammogram con-
necting an ill defined breast mass to the skin is strongly
suggestive of tuberculous breast abscess. Chest radio-
graphs are also useful in evaluation. They can demon-
strate active pulmonary disease or document any old
healed lesion. Ultrasonography is useful in dis-
tinguishing cystic from solid lesions. Tubercular breast
abscess is better characterized by ultrasound. Guided
needle aspiration from breast tissue or the axillary
nodes increases the accuracy of cytology.13,39
(iv) Fine needle aspiration cytology (FNAC): Aspiration
cytology from the breast lump or axillary nodes is a
definitive method to establish the diagnosis. The yield of
FNAC in detecting AFB is around 25%. Microscopically,
mycobacteria appear as beaded red to pink colored rods
against blue background when stained with Ziehl-
Neelsen method. The limitation of microscopy is that
the sample must contain 5000e50,000 AFB/ml for the
smear to be positive.40 It can also be helpful in deciding
the course of treatment. In the presence of inflammatory
aspirate, it is important to subject the material for cul-
ture.41 Accuracy of FNAC in establishing the diagnosis is
73%e100%.20,40 Casseating granuloma is the histopatho-
logical hallmark of TB. It is not necessary to document the
presence of AFB before initiating anti-tubercular therapy,
especially in endemic regions. However, in cases of
diagnostic dilemma, an excision biopsy should be done. It
has a higher yield when sarcoidosis, fungal infection or
coexisting malignancy is suspected.42
(v) Mycobacterial culture: This remains the gold standard
for diagnosis of TB. However, the time required and
frequent negative results in pauci-bacillary specimens
are important limitations. The sample is inoculated in LJ
(Lowenstein-Jensen) culture bottle and incubated aero-
bically at 35e37  C in 5e10% CO2 in the dark upto 8
weeks. It is periodically observed and any suspicious
growth is confirmed by smear preparation. During the
last two decades, several rapid techniques for early
detection of mycobacterial growth (5e14 days as
compared to 2e8 weeks with conventional methods)
have been introduced. Bactec can detect as low as 100
bacilli per ml of the contaminated fluid.43
(vi) Molecular methods: A major breakthrough in the diag-
nosis of EPTB has been achieved by the introduction of
Nucleic Acid Amplification tests (NAAT) such as PCR
which detects nucleotide sequences unique to M.
tuberculosis directly in the specimens and gives results
within few hours.
a) Polymerase chain reaction (PCR): It is a complex pro-
cess, which includes shock treatment (acute change in
temperature) to break the cell wall of bacteria, chem-
ical lysis followed by DNA purification. This technique
depends on the quality of the DNA extracted. The M.
tuberculosis complex detection is based on the ampli-
fication of pathogen's DNA specific region (IS6110) as it
is present in multiple copies in its genome. It is
detected by agarose-gel electrophoresis. PCR not only
confers high sensitivity, but is effective even in pau-
cibacilary samples (can detect 10 bacilli per ml).43 It
 i n d i a n j o u r n a l o f t u b e r c u l o s i s x x x ( 2 0 1 8 ) 1 e6
can be helpful in monitoring the response to anti-
tubercular treatment. When combined with myco-
bacterial culture, it can improve the accuracy of
detection of mycobacterial infection as well as reduce
the time to diagnosis.44
b) RT PCR: The mRNA-based reverse transcriptase-PCR
(RT-PCR) is a rapid method to differentiate viable and
nonviable M. tuberculosis. It has also been used for the
diagnosis of EPTB as well as monitor drug resistance.
c) Fluorescence in-situ hybridization(FISH): Oligonu-
cleotide probe labeled with fluorophore is used. It is
detected by direct fluorescent microscopy and is able
to differentiate M. tuberculosis from other mycobac-
teria from a single smear (prepared directly from the
specimen or the culture). Studies have documented
that FISH is more sensitive than PCR in detecting
mycobacteria.45
d) Xpert MTB/RIF: It was initially developed for the
evaluation of sputum samples. Recently, its impor-
tance in nonrespiratory samples has been success-
fully documented. It can detect both MTB (M.
tuberculosis bacilli) and rifampicin resistance (a sur-
rogate marker for Multi Drug Resistant strains). The
assay uses 3 specific primers and 5 unique molecular
probes to ensure a high degree of specificity. The
target is the rpoB gene, which plays a critical role in
identification of mutations associated with rifam-
picin resistance. Results become available within
two hours. It requires no instrumentation other than
the GeneXpert System. The sensitivity and specificity
of Xpert test for EPTB is 81% and 99% respectively.46
e) Immuno-PCR: It is a novel ultrasensitive assay to
detect protein antigens. Combining the versatility of
ELISA and sensitivity of NAA by PCR increases the
accuracy by at least 103e104 times of an analogous
ELISA. It has been proposed to detect M. tuberculosis-
specific RD1 and RD2 antigens [ESAT-6 (Rv3875), CFP-
10 (Rv3874), CFP-21 (Rv1984c) and MPT-64 (Rv1980c)]
and their antibodies in biological specimens of both
pulmonary and EPTB.47 It improves the accuracy as
well as cuts down the time of diagnosis. The only
deterrent to its use is the cost and necessary
infrastructure.
12. Treatment
Anti tubercular chemotherapy (ATC) remains the cornerstone
for treatment of breast tunerculosis.48 Six month ATC
including 2 months of intensive therapy entails excellent
clinical response (>90% success rates).25 Drugs used in the
intensive phase include: ethambutol 800mg, pyrazinamide
1500mg, rifampicin 450mg and isoniazid 300mg). This is fol-
lowed by a continuation phase of four months with two drugs
(isoniazid and rifampicin).2 At some centers, 9 month therapy
is followed (includes 7 months of continuation phase), with no
or little clinical benefit.
Few reports have highlighted the development of resis-
tance to the first line drugs. Such patients respond well to the
Please cite this article in press as: Sinha R, Rahul, Breast tuberculosis, Indian Journal of Tuberculosis (2018), https://doi.org/10.1016/
j.ijtb.2018.07.003
5
addition of second line drugs like Ofloxacin, Kanamycin,
Ethionamide and Para-amino salicylic acid (PAS).41
Surgical intervention is required in 15e40 percent cases. It
may be imperative in patients not responding to chemo-
therapy alone, or with widespread disease.20 Breast conser-
vation remains the goal of management.
Incidence of tubercular breast abscess has shown an up-
surge recently, owing to the rise in retroviral infection and
immunosuppressive therapy after transplant.49 This form of
the disease may require repeated aspiration or anti-gravity
drainage in combination with ATC. Adequate drainage pre-
vents the formation of fistulae and sinuses.42 Fortunately, the
classical presentation of breast abscess with multiple sinuses
and fistula is uncommon. Residual tracts after completion of
chemotherapy are taken care of by excision with minimum
tissue loss. Dissection of ipsilateral axillary nodes is at times
required for unresponsive ulcerated tender nodes.
Simple mastectomy as a management tool is seldom
required. Khanna R et al reported the necessity of mastectomy
in 4% of patients. Indications of radical surgery remain limited
to extensive disease with painful ulcers and complete
destruction of the gland.20
13. Conclusion
Breast TB is a diagnostic dilemma. Lactating young females
are at an increased risk, especially in developing countries
endemic for TB. Availability of accurate investigative modal-
ities and curative treatment entails a high index of suspicion
for early and timely diagnosis.
Appendix A. Supplementary data
Supplementary data related to this article can be found at
https://doi.org/10.1016/j.ijtb.2018.07.003.
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