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Imaging Manifestations of
Genitourinary Tuberculosis
Muhammad Naeem, MD
Maria Zulfiqar, MD
Mohammed Azfar Siddiqui, MD
Anup S. Shetty, MD
Adeel Haq, MD1
Cristian Varela, MD
Cary Siegel, MD
Christine O. Menias, MD
Abbreviations: IVU = intravenous urography,
TB = tuberculosis
RadioGraphics 2021; 41:1123–1143
https://doi.org/10.1148/rg.2021200154
Content Codes:
From the Mallinckrodt Institute of Radiology,
Washington University School of Medicine, 510
S Kingshighway Blvd, Campus Box 8131, St
Louis, MO 63110 (M.N., M.Z., A.S.S., C.S.);
Department of Radiology, Division of Body Im-
aging, University of Missouri Health System,
Columbia, Mo (M.A.S.); Department of Radiol-
ogy, Division of Body Imaging, Sindh Institute
of Urology and Transplantation, Civil Hospital,
Karachi, Pakistan (A.H.); Department of Imag-
ing, Division of Body Imaging, Clinica Davila,
Recoleta, Chile (C.V.); and Department of Ra-
diology, Division of Abdominal Imaging, Mayo
Clinic Arizona, Scottsdale, Ariz (C.O.M.). Re-
cipient of a Magna Cum Laude award for an ed-
ucation exhibit at the 2019 RSNA Annual Meet-
ing. Received June 9, 2020; revision requested
August 14 and received September 11; accepted
September 21. For this journal-based SA-CME
activity, the author C.O.M. has provided disclo-
sures (see end of article); the other authors, the
editor, and the reviewers have disclosed no rel-
evant relationships. Address correspondence
to M.N. (e-mail: mnaeem@wustl.edu).
1
Current address: Mallinckrodt Institute of Ra-
diology, Washington University School of Medi-
cine, St Louis, Mo.
©
RSNA, 2021
SA-CME LEARNING OBJECTIVES
After completing this journal-based SA-CME
activity, participants will be able to:
Describe the most common imaging
„ TB, is one of the major forms of extrapulmonary TB and accounts
manifestations of genitourinary TB.
List entities that can mimic various
„
organ-based forms of genitourinary TB.
Discuss the pathophysiologic mecha-
„
nisms of genitourinary TB.
See rsna.org/learning-center-rg.
An earlier incorrect version of this article
appeared online and in print. This article
was corrected on April 20, 2022.
1123
GENITOURINARY IMAGING
The genitourinary region is one of the most common sites of extra-
pulmonary tuberculosis (TB) involvement. The imaging features of
genitourinary TB are protean and can mimic other entities, includ-
ing malignancy, and pose a diagnostic dilemma. Hematogenous
seeding and lymphatic spread of mycobacteria from pulmonary,
tonsillar, and nodal TB are implicated in the pathogenesis of geni-
tourinary TB. In addition, contiguous extension from the urinary
tract and sexual transmission are described as sources of genital TB.
Genitourinary TB can be indolent and results in nonspecific signs
and symptoms; thus, imaging has a vital role in the working diag-
nosis for these cases. Classic uroradiologic signs of genitourinary
TB are primarily described from the era of intravenous urography
and conventional radiography. Now, CT, CT urography, MRI, and
US are used in the diagnosis and management. Familiarity with the
imaging features of genitourinary TB may help guide the diagnosis
and, in turn, lead to timely management. US has a vital role in the
evaluation of scrotal and female genital TB. MRI offers superior
soft-tissue contrast resolution and excellent depiction of anatomic
detail. The various imaging manifestations of genitourinary TB are
highlighted.
©
RSNA, 2021 • radiographics.rsna.org
Introduction
According to the Centers for Disease Control and Prevention
(CDC), 9025 new cases of tuberculosis (TB) were diagnosed in the
United States in 2018, with an estimated incidence of 2.8 cases per
100 000 people (1). Although the incidence of TB has decreased, this
infection remains one of the top 10 leading causes of death from a
single infectious agent worldwide, interestingly higher in rank than
the causes of death related to HIV and AIDS (2). Statistics on extra-
pulmonary TB vary owing to the lack of classic clinical and labora-
tory signs, which results in a delayed or no diagnosis.
According to the European Centre for Disease Prevention and
Control, one in five patients with TB has extrapulmonary TB, which
is defined as infection of an organ or organs in addition to or other
than the lungs (3). Genitourinary TB, also referred to as urogenital
for approximately 30%–40% of all extrapulmonary TB cases, second
in frequency only to nodal TB involvement (4). Two percent to 20%
of patients with pulmonary TB usually have concurrent genitouri-
nary TB, with a higher incidence in developing countries (4).
Chest radiography and induced sputum analysis for acid-fast
bacilli are mainstays in the diagnosis of pulmonary TB, but negative
results do not exclude extrapulmonary TB and pose a diagnostic
dilemma (4,5). Patients with genitourinary symptoms can undergo
urinalysis and urine culture testing. Analysis of urine sediment from
a 24-hour specimen for acid-fast bacilli testing yields positive results
1124  July-August 2021 radiographics.rsna.org
TEACHING POINTS
„ Combined with the clinical features of Addison disease, imag-
ing findings may aid in the diagnosis of adrenal TB, especially
when there is bilateral adrenal enlargement with peripheral
rimlike enhancement.
„ Peripheral lobar calcifications represent another pattern that
delineates end-stage kidney disease and are characteristic of
TB. With this pattern, lobar calcific rims usually outline the
periphery of distorted renal lobes as a sequela of papillary
necrosis.
„ Even in the absence of documented pulmonary TB, the pres-
ence of three or more imaging features, including papillary
necrosis, pelvi-infundibular strictures, cortical low-attenuating
lesions, parenchymal scarring, and calcifications, is highly
suggestive of renal TB. Similarly, nonuniform caliectasis with
urothelial thickening and a nondilated renal pelvis is a good
indicator of renal TB.
„ With TB, the calcifications are contiguous with the renal col-
lecting system, whereas with schistosomiasis, they are more
focal and more common in the urinary bladder. Also, ureteral
calcifications in TB are intraluminal and appear as a cast of
the ureter, whereas with schistosomiasis, calcifications are in-
tramural.
„ Multiple diverticular outpouchings similar to SIN may be seen.
However, SIN remains confined to the isthmus portion of the
tube, as compared with TB, which involves the entire tube.
This is an important imaging feature for distinguishing TB
from SIN.
in 80%–90% of cases of renal TB. In the pres-
ence of pyuria and/or hematuria without growth
of routine bacterial organisms, culture speci-
mens for acid-fast bacilli should be obtained.
Positive preliminary urine or tissue culture
results are reported within 12–24 hours. Nega-
tive cultures are reported after 6–8 weeks, with
a false-negative rate of 10%–20%. Even when
laboratory test results are positive, they do not
reveal the site and extent of disease, underlin-
ing the role of imaging that is essential not only
during the initial stages of workup but also for
follow-up of these patients (6).
The imaging diagnosis of genitourinary TB
may result in early initiation of therapy and po-
tentially lead to decreased morbidity, given that
confirmatory laboratory tests may take weeks to
yield a diagnosis. In this article, various imaging
manifestations of genitourinary TB are described,
with the goals of aiding the diagnostic radiologist
in pattern recognition and revealing TB as the
differential diagnosis in the appropriate clinical
context.
Pathologic Mechanism of
Genitourinary TB
A simplistic diagrammatic representation of
the pathologic mechanisms of genitourinary TB
is shown in Figure 1. Knowledge of the patho-
genesis of genitourinary TB is largely based on
animal models. Primary infection commonly
develops by way of inhalation of aerosols con-
taining Mycobacterium tuberculosis or ingestion
of Mycobacterium bovis in contaminated nonpas-
teurized milk and dairy products. The bacteria
then travel to the local-regional lymph nodes,
and the infection can then reach the genito-
urinary system by way of lymphatic spread. In
addition, the primary pulmonary or gastrointes-
tinal infection can spread via a hematogenous
route to the genitourinary system.
When the kidneys are seeded by mycobacte-
ria, granulomas form in the peritubular capillary
bed or in the cortex adjacent to the glomeruli
(5). The renal medulla is usually spared in the
initial phase (5). Renal tubercles are barely vis-
ible at first and later coalesce to form white and
yellow granulomas that preferentially involve the
upper and lower poles of the kidneys (7). These
granulomas are loosely formed in immunocom-
promised individuals, leading to more diffuse
renal involvement (5). The tubercular content
within the granulomas spills down the nephrons,
where it is entrapped in the narrow segments of
the loop of Henle, resulting in infection of the
renal papilla (7). The inflammatory response
incited by these granulomas results in chronic
tubulointerstitial nephritis, papillary necrosis,
and ulceration, followed by healing and fibrosis
that cause extensive caseous destruction and
deformation of the renal parenchyma (5).
The clinical manifestations of genitourinary
TB have an average latency period longer than
20 years. This explains why genitourinary TB is
extremely rare in children (5). If these granulo-
mas do not heal, they may rupture into the col-
lecting system and cause downstream infection
and spreading. It is interesting that TB of the
bladder also can develop by means of retrograde
spread from the testes or prostate in men, in ad-
dition to lymphatic and hematogenous spread.
Primary bladder TB can also be due to
administration of the bacillus Calmette-Guérin
vaccine for treatment of bladder cancer (7–9).
TB of the testes, epididymis, vas deferens, and
seminal vesicles occurs by means of hematog-
enous spread or retrograde spread from the
prostate via the lymphatics or capillaries. Infec-
tion of the female genital tract develops owing
to hematogenous or lymphatic spread from
primary or secondary pulmonary TB (5). In
addition, sexual transmission has been impli-
cated in some cases of genital TB (5). Although
solitary genitourinary TB is not contagious, the
medical personnel treating and imaging patients
with genitourinary TB and concomitant pul-
monary involvement should observe airborne
precautions.
RG  •  Volume 41  Number 4 Naeem et al  1125

Figure 1.  Pathophysiologic

mechanisms of genitourinary TB.
Inhalation of aerosols containing
Mycobacterium tuberculosis (1)
can result in pulmonary TB (2).
The second major route of pri-
mary TB is ingestion of Mycobacte-
rium bovis–infected products (3),
which can result in gut TB (4).
The triad of primary Ghon focus,
lymphangitis, and lymphadenitis
is known as the primary Ghon
complex (yellow outlines, 2 and
4). In addition, tonsilar TB (5)
can reach regional lymph nodes
and spread via the lymphatics.
The kidneys can be seeded via
lymphatic spread from either
these Ghon complexes or hema-
togenous spread. Seeding of the
glomeruli results in tuberculous
granuloma formation in the peri-
tubular capillary bed (6). The tu-
bercular content in the granulo-
mas spills down the nephrons (7),
where it is entrapped in the nar-
row segments of the loop of
Henle, resulting in infection of
the renal papilla and collecting
system TB (8). M tuberculosis de-
scends via urine (9) or through
hematogenous or lymphatic
spread, resulting in lower uri-
nary tract TB. The genital organs
are then involved via any route.
(Only male genitalia are shown
for simplification.) TB can also directly seed from the prostate to the ejaculatory ducts, seminal vesicles, vas deferentia, epididy-
mides, and testes in a retrograde fashion, unilaterally or bilaterally.

Classic Signs of Genitourinary TB lence of up to 6% in cases of active pulmonary

The majority of the classic signs of genitouri-
nary TB described in the radiology literature are
based on conventional radiography and intra-
venous urography (IVU) findings, which are
summarized in the Table. These signs have been
helpful in raising suspicion for genitourinary
TB and guiding the initiation of antimicrobial
therapy before definitive confirmation. They
have also been quite helpful in the era predating
the routine use of microbiologic tests such as
culture analysis (7,10). IVU and radiography are
no longer used; instead, CT depiction of these
classic signs is provided in some instances.
Organ-based Imaging Manifestations
of Genitourinary TB
The schematic representation in Figure 2 sum-
marizes the imaging features of genitourinary TB.
These features are described in further detail,
with imaging examples, in the following organ-
categorized sections.
Adrenal Glands
The adrenal gland is the most common endo-
crine site of extrapulmonary TB, with a preva-
TB seen at autopsy (11). Adrenal involvement is
almost always bilateral, and this can lead to Addi-
son disease. The adrenal glands are the fifth most
common site of extrapulmonary TB, following
the liver, spleen, kidneys, and bones. If greater
than 90% or more of the glands is destroyed,
then a life-threatening addisonian crisis ensues.
When Thomas Addison described his first series
of patients in 1855, all of the cases were attribut-
able to TB; however, in a more recent large study
(11), one-third of the cases of Addison disease
were due to TB, compared with 70% of the cases
in past series.
On radiographs, adrenal TB has no specific
imaging feature. Adrenal calcifications can be
seen with both treated and untreated TB. Nearly
half of cases of untreated TB can manifest as
adrenal calcifications (12). The CT appearance
depends on the chronicity, as well as the treat-
ment status of the patient. Masslike enlargement
is seen in 50%–65% of cases, and adreniform
hyperplasia is seen in 35%–50% of cases. One-
third of cases involve heterogeneous enhance-
ment of the adrenal glands (Fig 3). The classic
pattern of peripheral rimlike enhancement
1126  July-August 2021 radiographics.rsna.org

Imaging Manifestations and Associated Classic Signs of Genitourinary TB

Affected Organ Imaging Findings† Associated Imaging Signs

Adrenal glands Bilateral involvement …
Calcifications in ~50% of cases
Masslike gland enlargement in 50%–65% of cases
Peripheral rim enhancement in ~50% of cases
Kidneys Parenchyma: “Putty” kidney
  Hypoenhancing granulomas “Ball-on-tee” sign
  Striated nephrogram Phantom calyx
  Abscess and tuberculomas “Daisy-flower” kidney
 Autonephrectomy
Pelvicalyceal system:
  Papillary necrosis
  Focal calyceal blunting and dilatation
  Infundibular and/or pelvic stenosis
  Peripheral urothelial calcifications
Ureters Distal third is most common site “Sawtooth” appearance
Ureteral thickening with calcifications Kerr kink
Mucosal tuberculomas “Pipe stem” ureter
Mucosal ulcerations Beaded or “corkscrew”
Sharp angulation at UPJ ureter
Strictures and scarring
Urinary bladder Diffuse or focal wall thickening with calcifications “Thimble” bladder
Mucosal ulcerations and trabeculations
Contracted fibrotic bladder
Urethra Affects more men than women “Watering can” perineum
Long-segment strictures
Fistulas to perineum
Prostate Can mimic cancer “Watermelon” prostate
Solitary or multiple nodules or masses
Fluid density at CT
Nodular type: low T2 signal intensity at MRI, with diffusion restric-
tion and DCE
Diffuse type: low streaky lesions in the peripheral zone at T2-
weighted MRI
Testes and epi- At US: diffuse or focal enlargement and heterogeneity with hy- …
didymides poechoic appearance; rarely, miliary pattern of involvement
At MRI: T2-hypointense lesions with variable calcifications
Vas deferens Enlarged and heterogeneous …
and/or sper- Focal or diffuse involvement
matic cord Little or no detectable flow at Doppler US
Seminal vesicles Acute phase: enlarged with or without abscess, wall and septal …
thickening with calcifications
Chronic phase: atrophy and calcifications
Fallopian tubes Beaded appearance; interstitial salpingitis can appear like SIN at HSG …
Dilated tube with fluid or abscess
Wall thickening with nodular calcifications at CT and MRI
Uterus and At HSG: Asherman syndrome “Gloved-finger” uterus
cervix T-shaped uterus, pseudounicornuate appearance, Netter syndrome
At CT and MRI: thickened endometrium, enlarged heterogeneous-
ly enhancing cervix, may show calcifications during chronic stage
Ovaries Tubo-ovarian mass or abscess …
May not respect fascial planes
Vagina and vulva Enhancing nodule or mass that may mimic malignancy …
†
DCE = dynamic contrast enhancement, HSG = hysterosalpingography, SIN = salpingitis isthmica nodosa, UPJ =
uteropelvic junction.
RG  •  Volume 41  Number 4 Naeem et al  1127

Figure 2.  Diagrammatic representation of various morphologic features that can help in diagnosing tuberculous disease of the ad-
renal glands, kidneys, ureters, and urinary bladder. A = acute adrenalitis (adrenal gland enlargement), B = adrenal gland calcifications
(diffuse and focal), C = urothelial thickening, D = “moth-eaten” calyx, E = papillary necrosis, F = calyceal blunting, G = papillitis (deep
calyceal cup), H = infundibular stenosis, I = pyelonephritis, J = cortical abscess rupturing into the perinephric space and into the col-
lecting system, K = lobar calcification/putty kidney, L = miliary tuberculosis, M = cortical scarring, N = hiked-up pelvis (Kerr kink), O =
stricturing and beading of ureters, P = granulation and intravesical septa causing ureterovesical obstruction, Q = thimble bladder, R =
urethral stricture. (Created with BioRender.com.)

usually is seen in half of affected patients and is

Figure 3.  Adrenal TB in an 18-year-old woman with Addison
disease and known pulmonary TB (miliary pattern). The 21-hy-
droxylase antibodies were negative. The patient’s very-long-
chain fatty acid levels were not elevated; hence, adrenoleu-
kodystrophy was ruled out. Her blood cultures were negative
for fungal organisms, including Blastomyces dermatitidis and
Histoplasma capsulatum, and her HIV test result was negative.
Axial abdominal CT image with intravenous contrast material
reveals right adrenal gland atrophy and coarse calcifications
(white arrow), representing chronic tuberculous involvement.
Masslike enlargement of the left adrenal gland with hypoen-
hancement (black arrow) is compatible with acute left tuber-
culous adrenalitis.
more commonly seen with TB than with cen-
trally necrotic adrenal tumors (13).
The MRI appearance of adrenal TB is based
on the different pathologic stages of the infec-
tion. Caseous necrosis and active granulomatous
inflammation manifest as masslike enlargement
and demonstrate a hypo- to isointense signal on
T1-weighted MR images, with hyperintensity on
T2-weighted MR images. Similar to the en-
hancement pattern at CT, the contrast enhance-
ment pattern at MRI is rimlike in the presence
of caseous necrosis and homogeneous in the ab-
sence of necrosis. In the chronic stage, fibrosis,
calcification, and atrophy are present. Thus, the
gland is hypointense on T1- and T2-weighted
MR images, with no corresponding contrast
enhancement (14).
At fluorine 18 fluorodeoxyglucose (FDG)
PET/CT, the adrenal glands demonstrate in-
creased FDG uptake that is often an incidental
finding. The pattern of FDG uptake could be
homogeneous or heterogeneous, and findings
1128  July-August 2021 radiographics.rsna.org

Figure 4.  Patterns of renal pa-

renchymal TB in three patients.
(a) Pseudotumoral pattern of re-
nal parenchymal TB in a 47-year-
old woman with pulmonary TB
and flank pain. Axial arterial phase
abdominal CT image shows a hy-
poenhancing mass (arrow) along
the anterior aspect of the right
kidney. There is no perinephric fat
stranding. The findings are suspi-
cious for renal cell carcinoma. The
mass was biopsied and deemed
to be a pseudotumoral type of re-
nal TB at histopathologic analysis.
(b) Pyelonephritis pattern of renal
parenchymal TB in a 35-year-old
man with HIV infection and flank pain. Coronal contrast-enhanced
CT image shows an enlarged left kidney with a roughly wedge-
shaped area of hypoenhancement and a poorly defined interface
(arrow) between the involved and uninvolved renal parenchyma,
indicating pyelonephritis. No perinephric fat stranding is seen.
This patient had sterile pyuria, and urine cultures grew M tuber-
culosis. (c) Abscess pattern of renal parenchymal TB in a 35-year-
old woman with a fever, night sweats, and a history of renal TB.
Axial contrast-enhanced CT image obtained owing to a persistent
fever and pyuria at urinalysis shows intermediate attenuation in
the lesion, with minimal peripheral enhancement and a fuzzy in-
terface with the parenchyma (solid arrow). There is no perinephric
fat stranding. There is evidence of prior renal TB, with right-sided
autonephrectomy (dashed arrow). Fine-needle aspiration results
confirmed the presence of a tuberculous abscess.

are nonspecific, mimicking those of other disease

processes (13–15). In situations in which the
diagnosis of adrenal TB is not clear, percutaneous
sampling of the adrenal lesions may be necessary.
Owing to the high location of the adrenal glands
in the abdomen, CT-guided biopsy is often
performed. In addition to obtaining samples for
histopathologic analysis, one should take care
in obtaining additional samples, saving them in
sterile saline for acid-fast bacilli cultures.
Combined with the clinical features of Ad-
dison disease, imaging findings may aid in the
diagnosis of adrenal TB, especially when there
is bilateral adrenal enlargement with peripheral
rimlike enhancement.
Renal Parenchyma and Collecting System
Renal TB is the most frequent form of genito-
urinary TB, and it may be seen concomitantly in
10% of cases involving active lung TB (7). Almost
half of patients with renal TB have some imag-
ing evidence of prior pulmonary TB. Renal TB
can be divided into that with renal parenchymal
involvement and that with pelvicalyceal system
involvement.
Renal Parenchyma.—The earliest parenchymal
changes seen at imaging are tiny granulomas,
which are best evaluated during the corticome-
dullary and nephrogenic phases of CT urography
(8,16). Parenchymal granulomas are hypoat-
tenuating, with minimal to no enhancement on
contrast-enhanced CT images. Larger granu-
lomas are masslike, and most of them enhance
peripherally. These lesions can mimic renal cell
carcinoma and often are confirmed to be TB
granuloma at biopsy only; hence, the description
of these lesions as demonstrating a pseudotu-
moral pattern (Fig 4a) (17,18). Renal TB paren-
chymal lesions can sometimes manifest as cystic
masses with internal septa, mimicking Bosniak
IIF and III lesions (19).
Active inflammation leads to parenchymal
edema and hypoperfusion due to vasoconstric-
tion, which manifest on CT images as geographic
areas of parenchymal hypoattenuation that mimic
acute pyelonephritis (Fig 4b). In the absence
of pulmonary involvement or known history of
TB, this pattern can be confused with that of
acute focal nephritis or a solid renal neoplasm
(20). Complications include the formation of
an abscess, which can rupture into the perirenal
space; CT is excellent at delineating the extent of
this rupture. Acute tuberculous renal abscesses
are usually 10–40 HU in attenuation with mild, if
any, peripheral enhancement (Fig 4c) (8).
A chronic abscess can mimic a cyst or a cystic
renal neoplasm. In contrast to a classic bacte-
RG  •  Volume 41  Number 4 Naeem et al  1129
Figure 5.  Renal TB in a 46-year-old man. Conven-
tional abdominal radiograph shows the lobar pat-
tern of ground-glass calcifications (arrows) in the left
kidney, with central areas of relatively low attenua-
tion representing caseous necrosis.
Figure 6. Peripheral lobar calcifications in a
39-year-old man with renal TB. Axial contrast-en-
hanced CT image shows lobar calcific rims (arrow)
outlining the periphery of distorted renal lobes. This
is an end-stage disease appearance and pathogno-
monic for renal TB.
rial abscess, with which parenchymal edema can
provide a hint to the diagnosis, with a tubercular
abscess, the edema is usually mild (8). However,
a fuzzy interface between the parenchyma and the
abscess, calcifications, perirenal stranding, thick-
ening of pararenal fascia, and a clinical history of
fever may guide the diagnosis of TB in an endemic
region (21).
Renal parenchymal involvement by tubercu-
lous infection heals by means of fibrosis or scar-
ring, which can lead to focal cortical thinning or
absence of the renal cortex and associated focal
caliectasis. Calcifications can also develop with
healing and vary in appearance, from punctate
foci of calcifications to complete replacement of
the renal parenchyma during the autonephrec-
tomy stage, which is also referred to as putty kid-
ney (Fig 5). At imaging, putty kidney appears as
a faint area of uniform calcification that is greater
than 1 cm in diameter (7,8). The calcifications
are homogeneous with a ground-glass appear-
ance, representing calcified caseous necrosis, and
they characteristically manifest in a lobar pattern.
The renal lobe is the segment of the parenchyma
that comprises a renal pyramid and an overly-
ing cortex. On average, there are 7–18 lobes in
one kidney (10). The attenuation values of these
calcifications range from 50 HU to 120 HU at
noncontrast CT (7,8).
Peripheral lobar calcifications represent another
pattern that delineates end-stage kidney disease
and are characteristic of TB. With this pattern,
lobar calcific rims usually outline the periphery
of distorted renal lobes as a sequela of papillary
necrosis (Fig 6). A focal globular pattern of calcifi-
cation of the entire renal lobe, when seen, is often
a sequela of a granulomatous mass (22). Lobar
calcification, in which a densely calcified rim out-
lines the periphery of the distorted renal lobes, is
considered to be characteristic of renal TB (8).
Pelvicalyceal System.—Collecting system in-
volvement in the earliest stages of disease usually
manifests as papillary necrosis or minor calyceal
deformity. Papillary necrosis is more common
and occurs owing to ischemic necrosis of the
renal papillae from inflammation (7). In addition
to TB, there are many other causes of papillary
necrosis (10). Once the papilla is necrotic, it can
be absorbed or sloughed off in urine, or calcify.
Papillary sloughing leaves a cavity that communi-
cates with the collecting system.
CT urography has surpassed IVU in the
diagnosis of papillary necrosis, whereby excreted
contrast material outlines the necrotic papilla,
with various described appearances. These ap-
pearances include (a) central excavation with a
ball-on-tee appearance, (b) forniceal excavation,
(c) a lobster claw appearance, (d) a signet ring
appearance, and (e) a sloughed papilla with a
clubbed calyx (Fig 7a, 7b) (10). Calyceal blunt-
ing due to mucosal edema is usually considered
the earliest sign of calyceal TB at IVU; however,
this finding may be extremely subtle.
With progression of TB, the calyceal margins
become fuzzy and irregular owing to erosion,
resulting in the so-called “moth-eaten” calyx
sign (Fig 7c) (7,8,10). At histopathologic analy-
sis, this appearance is due to papillary necrosis
that results in further cavitation in the medulla,
which eventually communicates with the collect-
ing system (10). A phantom calyx refers to the
nonvisualization of one or more calyces, which
1130  July-August 2021 radiographics.rsna.org

Figure 7.  (a) Renal papillary ne-

crosis secondary to TB in a 48-year-
old woman from Pakistan. IVU im-
age with overlay shows bilateral cal-
yceal blunting and dilatation, and a
small round focus of extracalyceal
contrast opacification, resembling a
golf ball on a tee (arrow), in the re-
gion of the papilla. (b) Renal TB in a
62-year-old man. Maximum inten-
sity projection CT urogram shows
bilateral infundibular stenosis and
papillary necrosis (arrows). (Fig 7a
and 7b courtesy of Marya Hameed,
MBBS, Karachi, Pakistan.) (c) IVU
image in a 44-year-old man shows
irregular paracalyceal contrast ma-
terial pooling in the renal medulla
of the left upper renal pole. The
pooling contrast material commu-
nicates with the upper renal polar
calyces, resulting in the so-called
moth-eaten calyx sign (inset, ar-
row). (d) IVU image in a 30-year-
old man shows complete stricturing
of an inferior infundibulum (solid
white arrow) causing failed con-
trast material excretion and non-
visualization of the involved calyx,
or a phantom calyx. Also note the
moth-eaten appearance (dashed ar-
row) and blunting (black arrow) of
the upper group of calyces.

usually indicates a disease process that has oblit-
erated the collecting system (Fig 7d) (10).
Focal or diffuse caliectasis is usually a direct
result of pelvic and infundibular strictures (7,8).
Uneven caliectasis along with urothelial thicken-
ing is a useful diagnostic clue to renal TB (8).
Infundibular stricturing is a characteristic feature
and leads to focal hydrocalyx (Fig 8a, 8b) (23).
Involvement of a major calyx causes dilatation of
the minor calyces, which can be filled with urine
(0–10 HU), caseous necrotic tissue (10–30 HU),
putty-like calcifications (50–120 HU), and/or cal-
culi (>120 HU) (Fig 8c, 8d) (22). When the renal
pelvis and ureteropelvic junction are involved,
hydronephrosis becomes severe and, when associ-
ated with renal parenchymal atrophy, can mimic
a cystic renal neoplasm. However, the dilated ca-
lyces can be followed into a collapsed renal pelvis
in cases of pelvicalyceal TB (Fig 9) (8).
Transitional cell carcinoma usually manifests
with focal and frondlike enhancing papillary pro-
jections that differentiate it from TB. A virtually
absent renal pelvis due to chronic fibrosis may
cause an appearance known as daisy-flower kid-
ney (Fig 10a, 10b), which may be difficult to dif-
ferentiate from the bear-paw kidney appearance
in xanthogranulomatous pyelonephritis (XGP)
(8) (Fig 10c). Findings that favor TB rather than
XGP include peripheral or parenchymal calcifica-
tions as opposed to staghorn calculi, which are
seen in 90% of cases of XGP. Patients with renal
TB usually have preserved renal function until
the autonephrectomy stage (7).
Even in the absence of documented pulmo-
nary TB, the presence of three or more imaging
features, including papillary necrosis, pelvi-infun-
dibular strictures, cortical low-attenuating lesions,
parenchymal scarring, and calcifications, is highly
suggestive of renal TB. Similarly, nonuniform cali-
ectasis with urothelial thickening and a nondilated
renal pelvis is a good indicator of renal TB (18,22).
Renal TB has a propensity to extend into the
psoas sheath, perirenal and pararenal spaces
(resulting in cold abscesses), sinus tracts, and
fistulas and can also be seen in conjunction with
tuberculous spondylitis (Pott disease) (Fig 11)
(5,7,8). Extension to other viscera in the abdo-
men also has been described, with kidney-to–ali-
mentary tract fistulas being the most common.
Other fistulous communications to the skin,
solid viscera, and bronchi also may be seen (8).
Ureter, Bladder, and Urethra
Ureters.—Antegrade urinary transit of renal TB
granuloma from the pelvicalyceal system can seed
RG  •  Volume 41  Number 4 Naeem et al  1131
Figure 9.  Renal TB in a 38-year-old man. Coronal T2-weighted
half-Fourier acquisition single-shot turbo spin-echo MR image
shows bilateral nonuniform calyceal dilatation (arrows) second-
ary to multifocal infundibular strictures (not shown), represent-
ing progressive-stage TB. The dilated collecting system can
mimic a multiseptated cystic lesion. Knowledge of the patient’s
history of TB and comparison with prior imaging findings are
helpful in making the correct diagnosis.
the ureters, bladder, and urethra. With regard
to the ureters, ureteral TB develops concomi-
tantly with renal TB in 50% of cases, and to our
knowledge, isolated ureteric TB without renal TB
has never been described (5). The distal third of
the ureter, followed by the ureteropelvic junc-
tion, is the most common site of involvement
(7). Imaging findings include ureteral thickening
and enhancement, with periureteral stranding
similar to that with infectious ureteritis. How-
ever, tuberculous ureteritis may cause discrete
filling defects from either mucosal tuberculomas
Figure 8.  (a, b) Infundibular ste-
nosis and hydrocalyx in a 35-year-
old woman with renal TB. Coronal
abdominal CT images with intra-
venous contrast material show
urothelial thickening and enhance-
ment with luminal narrowing of
the infundibulum (arrow in a) and
calyceal dilatation, consistent with
infundibular stenosis related to urine
culture–positive TB; there is little
to no excreted contrast material in
the affected calyces (arrow in b).
(c, d) Collecting system involvement
in a 55-year-old woman with tuber-
cular spondylitis (Pott disease). IVU
image (c) shows mild beading of the
proximal ureter (white arrow) with
no calyceal involvement. There is also
evidence of Pott spine (black arrow).
The patient partially completed treat-
ment. Coronal contrast-enhanced
abdominal CT image (d) obtained 1
year later shows a progressive form
of collecting system TB with multifo-
cal caliectasis (solid white arrow) as-
sociated with infundibular strictures
(black arrow) and coarse calcification
in a dilated calyx (dashed arrow). This
calcification may be seen as the “sig-
net ring” sign at contrast-enhanced
urography (not shown).
or concomitant renal papillary necrosis with
sloughed papillae (23,24). Mucosal ulceration of
the ureter causes ragged irregularity of the lumen
with a dilated caliber, resulting in a sawtooth
appearance (10). Scarring in the adjacent tissues
due to chronic inflammation leads to a sharp
kink at the ureteropelvic junction, also called the
Kerr kink (Fig 12) (7). Later, the ureter may heal
as a straight and rigid tube, referred to as a pipe
stem ureter. Healing results in scarring, with a
so-called beaded or corkscrew ureter (7,8,10).
Fibrosis of the distal ureter (Fig 13a) can retract
the intravesical portion of the ureter, causing a
so-called “golf hole” ureteric orifice at cystos-
copy (23).
TB commonly has long-segment involvement
of the ureter, often with periureteric fat strand-
ing during the early phase of infection. Tran-
sitional cell cancer usually manifests as focal,
often asymmetric wall thickening of the ureter
without fat stranding. Calcifications (Fig 13b)
can manifest with TB and need to be differenti-
ated from schistosomiasis. With TB, the calcifi-
cations are contiguous with the renal collecting
system, whereas with schistosomiasis, they are
more focal and more common in the urinary
bladder. Also, ureteral calcifications in TB are
intraluminal and appear as a cast of the ureter,
whereas with schistosomiasis, calcifications are
intramural (25).
1132  July-August 2021 radiographics.rsna.org

Figure 10.  Renal TB. (a, b) Pelvic stenosis in a 67-year-old woman with lung and renal TB. Coronal maximum intensity projection
CT urogram (a) shows bilateral renal pelvic strictures (solid arrows) and additional areas of left infundibular stenosis with left superior
calyx calcifications (dashed arrow). There is also right hydronephrosis from a distal ureteral stricture (not shown). Follow-up retro-
grade pyelography image with overlay (b) shows a daisy-flower pattern of opacification (arrow) in the right collecting system that
is due to the severe pelvic stricture. (c) Renal TB in a 47-year-old woman. Coronal abdominal CT image with intravenous contrast
material shows global thinning of the renal parenchyma, with a multilocular cystic appearance of the left kidney due to assimilation
of the calyces into the renal parenchyma that resulted from communication of the tuberculous cavities and dilated calyces without
pelvic dilatation (arrow), in keeping with the daisy-flower pattern of findings secondary to TB. Unlike with xanthogranulomatous
pyelonephritis, with renal TB, there is no staghorn calculus.

Figure 11.  Tuberculous abscesses in the right psoas muscle and abdominal wall musculature in a 41-year-old man with a fever and
back pain. (a) Axial T2-weighted MR image of the lumbar spine shows osseous destruction and phlegmon, representing discitis and
osteomyelitis of the lumbar spine (dashed arrow), and an epidural abscess (arrowhead). There is also myositis and an abscess in the
right psoas muscle (*). In the left kidney, there is irregularity of the calyceal margins (solid arrow) with dilatation. (b) Axial abdominal
CT image with intravenous contrast material shows an enlarged left kidney with calyceal irregularity and dilatation (white arrow)
and smooth urothelial enhancement (arrowhead). The right psoas abscess is multiloculated with enhancing septa (*). There is an
additional abscess in the right abdominal wall musculature (black arrow). This pattern of findings is consistent with multifocal TB,
the presence of which was proven by means of CT-guided percutaneous drainage of the psoas abscess, with the obtained fluid and
urinary cultures positive for M tuberculosis.

Urinary Bladder.—Bladder TB is divided into appears as irregular mucosal masslike thicken-

four stages to guide the treatment strategy: Stage
1 involves tubercle-infiltrative bladder TB; stage
2, erosive-ulcerous bladder TB; stage 3, intersti-
tial cystitis; and stage 4, contracted bladder to full
obliteration (5). Immunocompromised individu-
als have been shown to have a lower incidence
of contracted bladder, probably because of the
lack of an intense granulomatous inflammatory
response (26).
Bladder TB in its initial stages results in cysti-
tis with mucosal inflammation and edema, which
ing, trabeculation, and mucosal edema of the
bladder wall (Fig 14) (5). Chronic inflammation
with progressive fibrosis can lead to scarring at
the ureterovesical junction, resulting in upstream
hydroureteronephrosis (5). Trigone fibrosis can
cause a widened and fixed ureterovesical junc-
tion that results in vesicoureteral reflux. Long-
standing inflammation also leads to a fibrotic and
thick-walled contracted bladder with reduced
capacity (ie, thimble bladder), akin to a thimble
(a small hard pitted cup worn on the finger for
RG  •  Volume 41  Number 4 Naeem et al  1133

Figure 13.  Ureteral TB in two patients. (a) Retrograde pyelogram in a 49-year-old

man with urinary TB shows a long-segment distal ureteral tubercular stricture (bracket).
(b) Coronal abdominal CT image with intravenous contrast material in a 27-year-old
woman shows a severe progressive form of calyceal and ureteral TB, as evidenced by
multifocal areas of stricturing in the right pelvicalyceal system (black arrow) and ureter
Figure 12.  Kerr kink ureter in a (white arrow), with associated dystrophic calcifications.
45-year-old woman with urinary
TB. Coronal CT image of the ab-
domen with intravenous contrast
material shows sharp angulation edema. When thickening is asymmetric, nodu-
at the ureteropelvic junction (out- lar, or masslike, residual or recurrent urothelial
lined in yellow), consistent with carcinoma should be suspected and needs to be
Kerr kink. The ureter (arrow) is di-
excluded by means of direct visualization and/or
lated, with tapering to the level of
the ureterovesical junction owing tissue sampling (9).
to a ureterovesical junction stric-
ture secondary to TB. Urethra.—Despite the constant exposure to My-
cobacterium bacilli in cases of genitourinary TB,
urethral involvement is exceedingly rare in both
sexes. When present, concomitant renal TB is
seen in 4.5% of cases (29). Urethral TB is more
common in men, as the urethra is a shared con-
duit for semen and urine; hence, the potential for
both genital and urinary TB to affect the urethra,
most commonly the prostatic urethra (5,30).
Acute urethritis with associated genital TB
can be seen as mucosal ulceration at endoscopy.
Imaging may reveal concomitant prostatitis
(5); however, strictures are rarely seen in the
acute setting, and urethrography findings are
usually normal at this stage. Chronic TB can
manifest with urethral strictures (usually long
Figure 14.  Urinary bladder TB in a 41-year-old woman whose
segment) with multiple associated fistulas into
urine cultures were positive for M tuberculosis. Axial CT image
of the pelvis with intravenous contrast material shows a thick- the perineum and surrounding regions that are
walled urinary bladder (white arrow), a partly calcified tuber- outlined by contrast material on fluoroscopic
culous abscess (black arrow) in the left sciatic notch, and locu- images (watering can perineum).These fistulas
lated peritonitis (*).
are best evaluated with voiding cystourethrog-
raphy and retrograde urethrography (Fig 16)
protection that pushes the needle in sewing) (Fig (5,30). This appearance is classically described
15) (27). Bladder wall calcifications are rare, in association with chronic gonorrheal infection.
but chronic cystitis can lead to seminal vesicle However, any chronic inflammation or traumatic
calcifications (28). Untreated bladder TB can condition, including genital TB, schistosomiasis,
result in fistulas and sinus tracts (5,28). Bacillus balanitis xerotica obliterans, fungal infections,
Calmette-Guérin–related cystitis causes circum- and chronic bacterial infections such as actino-
ferential thickening of the urinary bladder wall mycosis and lymphogranuloma venereum, can
with mucosal hyperenhancement and submucosal result in this appearance (31,32).
1134  July-August 2021 radiographics.rsna.org

Figure 15.  Thimble bladder in a 27-year-

old man with urinary TB. (a) Axial contrast-
enhanced CT image shows an irregular
small-capacity urinary bladder (arrow)
from extreme fibrosis and contracture of
the bladder walls, resulting in a tiny blad-
der resembling a thimble. (b) Coronal
contrast-enhanced CT image also shows
hydroureteronephrosis of the left kidney
(arrow) due to tuberculous fibrosis of the
left ureteral orifice (not shown), indicating
obstruction.

Male Genital Tract

The true incidence of genital TB is not known,
as most patients are asymptomatic. It has been
estimated that genital TB accounts for 9% of all
cases of extrapulmonary TB (33). Male genital
TB can involve the prostate, seminal vesicles,
vas deferens–spermatic cord, testes, epididy-
mis, penis, and scrotum. Isolated male genital
involvement by TB is exceedingly rare and usu-
ally due to spread from renal or pulmonary TB,
or both (34). An autopsy series from 1949 that
included 5424 autopsies of men who had geni-
tourinary TB revealed that almost all of these
patients with cavitary renal lesions and half of
these patients with caseous renal necrosis had
genital tract involvement (29). Apart from the
sexual transmission in cases of genital TB, penile
TB has been reported in association with ritual
circumcision (35). The age range at which male
genital TB peaks is between 30 and 50 years.
The clinical manifestations can vary and can
mimic those of sexually transmitted infections
such as syphilis and gonorrhea. The imaging
findings of genital TB in each male genital organ
are described in the following sections:
Prostate.—The prostate is involved in 6.6% of
cases of genitourinary TB (34,35). Prostatic TB
can be asymptomatic and incidentally detected
in a transurethral resection specimen or pros-
tate biopsy sample, as the imaging findings can
mimic cancer (36). In individuals with HIV
infection, prostatic TB can manifest as large ab-
scesses (Fig 17) (37). In symptomatic individu-
als, urethral discharge, painful ejaculation with
or without hematospermia, perineal bogginess
or pain, dysuria, and infertility are some of the
symptoms reported at presentation.
At digital rectal examination, the prostate
may be enlarged, firm, and tender, particularly
Figure 16.  Watering-can penis-perineum in a 29-year-old
man with penile TB. Retrograde urethrography image shows
a long-segment urethral stricture (dashed bracket) with innu-
merable urethrocutaneous-urethroperineal fistulas (arrows),
causing the appearance of a watering-can penis-perineum.
during the acute phase of disease. The nodular
prostate contour may be mistaken for prostate
cancer; however, the gland is typically neither
enlarged nor tender in chronic TB cases (36,37).
In rare cases, prostatic TB may manifest with
autoprostatectomy and perineal fistulas (38).
The serum prostate-specific antigen level can be
mildly elevated during the inflammatory phase,
but it normalizes during the chronic phase, with
resolution of inflammation (39).
Prostatic abscesses are treated with anti-TB
chemotherapy and require drainage, which can
be performed through the rectum or perineum
with US guidance. Transrectal US is the pre-
ferred sonographic window owing to its capability
to depict the detailed anatomy of the prostate and
adjacent organs. Transrectal US also aids in de-
tailed evaluation of the most commonly affected
posterior and lateral lobes of the prostate gland
(40). Sonographic features include solitary or
multiple hypoechoic nodules or masses that can
mimic prostate cancer (41). At CT, these nodules
RG  •  Volume 41  Number 4 Naeem et al  1135

Figure 17.  Prostatic TB abscess in a 35-year-old man with HIV

infection who was being treated for renal TB and presented
with deep pelvic pain and a fever. Axial CT image of the pelvis
with contrast material shows a rim-enhancing fluid collection
(arrow) in the prostate, representing an abscess. The abscess
was drained, and fluid cultures grew M tuberculosis.

Figure 18.  Prostate TB in a 66-year-old man with an elevated prostate-specific antigen level (6 ng/mL) and, per his medical report,
high-grade prostatic intraepithelial neoplasia at recent biopsy. (a) Axial T2-weighted MR image shows the diffuse-type morphol-
ogy with a hypointense T2 signal involving nearly the entire prostate. Although the classic watermelon sign is not seen, the right
peripheral zone shows streaky areas of T2 hypointensity (arrow). (b, c) Corresponding apparent diffusion coefficient map (b) and
axial dynamic contrast-enhanced T1-weighted fat-saturated MR image (c) show marked restricted diffusion (average apparent diffu-
sion coefficient, 0.428 3 10−3 mm2/sec) (arrow in b) and intense contrast enhancement (arrow in c), mimicking a Prostate Imaging
Reporting and Data System (PI-RADS) category 5 lesion. Urinary cultures were positive for M tuberculosis.

are fluid-density collections with internal septa
and surrounding enhancing rims (40).
The MRI appearance of prostatic TB is
categorized into nodular and diffuse morpholo-
gies (36). With the nodular type, the caseous
granulomas demonstrate characteristically low
T2 signal intensity, with restricted diffusion and
moderate enhancement with dynamic contrast-
enhanced MRI sequences. With the diffuse
type, streaky lesions with low T2 signal intensity
are seen in the peripheral zone, creating the
so-called watermelon appearance. Of note, the
signal intensity of these lesions is lower than the
signal intensity of the normal background pe-
ripheral zone and slightly higher than that of the
granulomas seen in nodular form (Fig 18) (36).
Testes and Epididymides.—Usually, the epididy-
mis is involved initially, and if left untreated or
undertreated, the infection can spread to the tes-
tes. Isolated testicular TB is rare and can simulate
malignancy or infarct (42). The clinical presenta-
tion is a painless or slightly painful scrotal mass.
US is the imaging modality of choice for
evaluation of the scrotum (43). Three gray-scale
appearances of epididymal TB are described:
(a) a diffusely enlarged, heterogeneously hy-
poechoic epididymis; (b) a diffusely enlarged,
homogeneously hypoechoic epididymis; and
(c) a nodular enlarged, heterogeneously hy-
poechoic epididymis (43). TB preferentially
involves the tail of the epididymis (44). An
enlarged heterogeneous epididymis with pre-
dominant tail involvement may be helpful for
differentiating tuberculous from nontubercu-
lous epididymitis in endemic areas (43,44). The
heterogeneity is probably secondary to various
pathologic stages of granuloma formation, in-
cluding caseous necrosis and fibrosis (42,43). At
Doppler US, the central area is usually hypovas-
cular, indicating caseous necrosis, with sur-
rounding hyperemia indicating a peripheral rim
of granuloma formation with small vessels (Fig
19) (45,46). Differentiating acute tuberculous
epididymitis from routine bacterial epididymitis
is often challenging (46).
1136  July-August 2021 radiographics.rsna.org

Figure 19.  Tuberculous epididymo-orchitis in a

56-year-old man who presented with a history of
left (LT) testicular swelling and drainage of several
months’ duration. Color Doppler US image of both
testes shows innumerable hypoechoic lesions (black
arrows) throughout the left testis and a few hy-
poechoic lesions (arrowhead) in the right (RT) testis.
A sinus tract (yellow arrow) is seen in the left scro-
tum. Multiple enlarged iliac chain lymph nodes also
were seen (not shown). Fine-needle aspiration of the
testicular lesions and lymph node was performed,
and cultures were positive for M tuberculosis.

Figure 20.  M tuberculosis in a 44-year-old man with HIV infection who presented with a fever and
scrotal swelling of a few months’ duration. (a) Coronal T2-weighted MR image shows innumerable cystic
lesions replacing both testes. Some of these lesions are intensely T2 hyperintense (*), probably indicating
a more acute form of tuberculous orchitis, while others show heterogeneous hyperintensity (dashed ar-
row). Also note the chronic left epididymitis (solid arrow). (b) Axial contrast-enhanced T1-weighted MR
image shows no enhancement of the cystic lesions (black arrow) but enhancement of the surrounding
tissues (white arrow). Aspirate samples from a few of these lesions grew M tuberculosis.

Testicular involvement occurs as a late stage associated intrascrotal extratesticular calcifications,

of tuberculous epididymitis, and isolated orchi-
tis occurs by way of hematogenous infection. If
urine cultures are negative, US-guided fine-nee-
dle aspiration for cytologic analysis and culture
analysis of testicular lesions can be performed.
Anti-TB chemotherapy is the mainstay of treat-
ment. Rarely, orchiectomy is required for both
diagnosis and treatment.
Although the US findings of tuberculous
orchitis are well documented in the literature,
descriptions of the MRI features are confined
to a few case reports (45–50). On gray-scale US
images, four patterns of testicular TB have been
described: (a) a diffusely enlarged heterogeneously
hypoechoic testis; (b) a diffusely enlarged homoge-
neously hypoechoic testis; (c) a nodular enlarged
heterogeneous hypoechoic testis; and (d) a miliary
pattern comprising numerous tiny hypoechoic tes-
ticular nodules (43,45). Testicular TB and epididy-
mal TB can be present with or without an associ-
ated hydrocele, associated scrotal skin thickening,
an associated scrotal abscess, and/or associated
scrotal sinus tracts (Fig 19).
In adults, normal testes appear hyperin-
tense on T2-weighted MR images and hypo- to
isointense on T1-weighted images. The testis
is surrounded by the T1- and T2-hypointense
tunica albuginea. The epididymis is isointense
on T1-weighted images but hypointense on
T2-weighted images. Both the testicles and the
epididymis homogeneously enhance after con-
trast material administration (51). Testicular TB
has been shown to have variable appearances
at MRI (Fig 20). In case reports, epididymal
involvement has been seen in approximately half
of the cases. The lesions are hypointense on T2-
weighted images, with variable appearances on
T1-weighted images. Most lesions demonstrate
heterogeneous hyperintensity on T1-weighted
images. The low signal intensity on T2-weighted
images is usually related to fibrosis. Lesions with
more acute orchitis (and no fibrosis) dem-
RG  •  Volume 41  Number 4 Naeem et al  1137
Figure 21.  Tuberculous epididymitis and funiculitis in a 39-year-old man. (a) Gray-scale US image shows a diffusely enlarged and
heterogeneous spermatic cord with internal debris (arrow). (b) Color Doppler US image shows decreased blood flow (yellow outline),
indicating funiculitis.
onstrate T2 hyperintensity. Variable contrast
enhancement at MRI, ranging from no enhance-
ment to homogeneously enhancing lesions, has
been described (45–50). Fluorine 18 fluorode-
oxyglucose uptake, including uptake in normal
healthy testes, can be seen on PET/CT images,
but no specific findings have been described
(52).
Vas Deferens and Spermatic Cord.—The vas
deferens, also known as the ductus deferens,
originates from the caudal end of the epididymis
and transports sperm from the epididymis to the
ejaculatory duct. The lumen is relatively narrow
in this thick-walled tube, which is about 30 cm
long and has three segments: the scrotal, supra-
scrotal, and prepubic segments (53,54). On US
images, the normal vas deferens is an anechoic
or very hypoechoic noncompressible tubular
structure with no internal detectable blood flow
(54). The ductus deferens is itself a part of the
spermatic cord, which, in addition to the ductus
deferens, has adventitial tissue that courses from
the inguinal ring to each testicle. Tuberculous
infections of the vas deferens and spermatic
cord are referred to as vasitis and funiculitis, re-
spectively. However, these terms are often used
interchangeably.
There is enlargement of the vas deferens with
a heterogeneous hypoechoic duct. The involve-
ment can be focal with little or no detectable flow
at color Doppler US (55). On the other hand,
nontuberculous acute vasitis is usually more dif-
fuse, with increased vascularity, at color Doppler
US (53). Tuberculous funiculitis is extremely
rare and in the majority of cases manifests as a
painless groin mass. Unilateral involvement is
much more common than bilateral involvement
(56,57). The imaging features are usually similar
to those of vasitis, and focal involvement with
tuberculous granuloma can mimic a mass with
central caseous material (Fig 21).
Seminal Vesicles.—Tuberculous infection of
the seminal vesicles is usually due to contigu-
ous spread from adjacent organs and is rarely
a primary site of origin. Tuberculous infection
causes destruction of convolutions in the seminal
vesicles, with abscess formation. This can further
lead to fibrosis and calcifications. An infected
patient may have infertility due to azoospermia or
have hemospermia and decreased ejaculatory vol-
ume. Physical examination will reveal an enlarged
seminal vesicle (58).
Vesiculography was once the diagnostic
method of choice for the diagnosis of tubercu-
lous infection; however, it has essentially been
rendered obsolete owing to newer imaging mo-
dalities. Radiographs may show seminal vesicle
calcifications, which are nonspecific and can
be seen with other conditions such as diabetes
mellitus (59). During the acute phase, TB can
mimic bacterial seminal vesiculitis. Chronic bac-
terial seminal vesiculitis is sufficiently rare such
that TB or schistosomiasis should be considered
in cases that occur in endemic regions. Diffuse
wall and septal thickening with enhancement
is often seen on CT and MR images. During
the acute to subacute phase, cystic dilatation of
the seminal vesicle may be seen, and as fibrosis
ensues, the seminal vesicles become atrophied
and hypointense on T1- and T2-weighted MR
images. CT may show internal hypoattenuation
with surrounding hypervascularity, or complica-
tions such as abscess with cavitation and caseous
necrosis. Burned-out TB lesions will eventually
show calcifications (60,61) (Fig 22).
Penis.—Penile TB is exceedingly rare, even in
TB-endemic regions, and comprises less than
1% of cases of genital TB. Penile TB can involve
the penile skin, glans penis, or cavernous bodies.
Circumcision, sexual contact, and contact with
infected fomites are some of the reported modes
of transmission.
1138  July-August 2021 radiographics.rsna.org
Superficial ulceration, nodules, and masses are
some of the manifestations of penile TB. Cavern-
ous involvement is rare but can cause erectile
dysfunction when it is present. Inguinal lymph-
adenopathy can be palpable at physical examina-
tion (35).
Imaging is rarely required to diagnose penile
TB. However, if the results of biopsy and cul-
ture of the ulcer are positive for TB, then body
CT should be performed to evaluate for other
more common sites of TB such as the lungs and
kidneys (35,62).
Female Genital Tuberculosis
Approximately 1% of infertile women between
the ages of 20 and 40 years in the United States
have genital TB. Female genital TB can result
in infertility, menstrual irregularities, pelvic
pain, and abnormal vaginal discharge. In post-
menopausal women, it can manifest as bleeding,
resembling endometrial malignancy (63).
Fallopian Tubes.—The fallopian tubes are in-
volved in more than 90% of women with female
genital TB, and both tubes are nearly always
involved (64,65). Although only one tube may
appear to be infected, there are usually micro-
scopic lesions in the contralateral tube. The
ampullary region of the tube, followed by the
fimbria, shows the earliest changes; the isthmus
and interstitial portion may remain free of infec-
tion (65). The tubal involvement can manifest
as endosalpingitis, exosalpingitis, and interstitial
salpingitis and may have an appearance similar
to that of salpingitis isthmica nodosa (SIN) (64).
The acute phase of tuberculous salpingitis is
exudative; hydrosalpinx or pyosalpinx may form,
but few adhesions are present. In contrast, the
productive-adhesive form is most commonly seen
during surgery, at which the tubes are thickened,
nodular, and densely adherent to the surrounding
organs. Eventually, calcification and fibrosis may
occur owing to healing (65).
Hysterosalpingography (HSG) is contrain-
dicated in the presence of recent acute pelvic
infection and can result in exacerbation of
subclinical tubal TB and cause peritonitis (64).
However, HSG may be inadvertently performed
during the course of evaluating infertility. The
early imaging appearance is nonspecific, with
tubal occlusion, an irregular contour, or hydro-
salpinx. The fallopian tubes often have ragged
outlines with multiple strictures, causing a
beaded appearance (64,66). Multiple diverticu-
lar outpouchings similar to SIN may be seen
(66). However, SIN remains confined to the
isthmus portion of the tube, as compared with
TB, which involves the entire tube. This is an
Figure 22.  Tuberculous seminal vesiculitis in a 50-year-old
man who presented with a fever of unknown cause and ab-
dominal pain. Axial pelvic CT image with intravenous con-
trast material shows a thickened, enhancing, enlarged right
seminal vesicle (arrow) representing seminal vesiculitis. Note
the associated small calcified granuloma (arrowhead). Urine
culture grew M tuberculosis.
important imaging feature for distinguishing TB
from SIN (Fig 23a).
Various specific patterns indicative of ad-
vanced disease have been described. These
patterns include cotton wool plug, cobblestone
tube, pipe stem tube, golf club tube, beaded tube,
leopard skin tube, tobacco pouch, and Maltese
cross-appearance of tubes (66–68). TB should
be strongly suspected in the presence of syn-
echiae, multifocal strictures, or occlusions in the
ampullary region along with calcifications in the
adnexa and lymph nodes. (48). Adhesions in the
peritubal region may appear as rigid tubes with a
straight spill, peritubal halo, or corkscrew ap-
pearance (66). Fistulous tracts with other pelvic
organs may be identified (65).
On US images, the fallopian tubes may appear
to be dilated, with thickened walls. Clear fluid
in the tube represents hydrosalpinx, while the
presence of debris suggests pyosalpinx (Fig 23b)
(66). In addition, US images may show loculated
ascites, tubo-ovarian masses, and uterine involve-
ment. CT and MRI also may depict hydrosalpinx
or pyosalpinx, tubo-ovarian abscesses, ascites,
peritoneal deposits, lymphadenopathy, and/or
lesions in other abdominal viscera (69,70). PET/
CT may show nonspecific uptake in the tubo-
ovarian masses (71).
Although more commonly described in the
setting of gonorrhea or chlamydia infection, Fitz-
Hugh and Curtis syndrome or perihepatitis also
can occur, as a result of peritoneal extension of
TB from infected fallopian tubes or as a sequela
of peritoneal TB or disseminated disease. There
is usually a history of right upper quadrant pain.
At CT, thickening and hyperenhancement of the
hepatic capsule are seen (Fig 24). TB-associated
Fitz-Hugh and Curtis syndrome can be en-
RG  •  Volume 41  Number 4 Naeem et al  1139

Figure 23.  Tuberculous salpingitis in a 38-year-old woman with a history of ectopic pregnancy and prior
TB. (a) Hysterosalpingogram shows tubal occlusion with beading and dilatation of the tubes by entrapped
secretions (arrow) involving the entirety of the tube. (b) Gray-scale US image of the pelvis shows a hydro-
salpinx (arrow) with thick beaded tubes (arrowheads). The patient underwent laparoscopy, which revealed
widespread adhesions in the pelvis. Cultures from fallopian tube biopsy specimens grew M tuberculosis.

Figure 24.  Fitz-Hugh and Curtis syndrome in a 36-year-old woman with low pelvic and right upper quadrant abdominal
pain, as well as night sweats and a low-grade fever. (a) Axial pelvic CT image with intravenous contrast material shows locu-
lated nondependent anterior ascites (*) and bilateral tubo-ovarian abscesses (arrows). (b) Axial CT image of the abdomen
shows low-attenuation thickening at the hepatic capsule (arrows), with scalloping of the underlying hepatic parenchyma.
Vaginal cultures were positive for M tuberculosis. These findings are consistent with tuberculous pelvic inflammatory disease
complicated by Fitz-Hugh and Curtis syndrome. (Case courtesy of Marya Hameed, MBBS, Karachi, Pakistan.)

countered for the first time during laparotomy
performed for ectopic pregnancy, chronic pelvic
pain, or bowel obstruction, especially in endemic
regions (72).
Uterus.—The uterus is affected in 50%–80%
of patients with female genital TB (48,64). The
infection generally is localized to the endome-
trium and rarely extends into the myometrium,
probably owing to the cyclic menstrual shedding.
Initially, the endometrium has an unremarkable
appearance, with a normal size and shape of the
uterus (65). Later, ulcerative, granular, or fun-
gating lesions form, and in advanced cases, the
endometrial cavity may be obliterated owing to
intrauterine synechiae manifesting as Asherman
syndrome (Fig 25) (73).
HSG may reveal nonspecific findings such as
synechia formation, a truncated and deformed
uterine cavity, and venous and/or lymphatic
intravasation (66,68). Certain specific features
that suggest the diagnosis of female genital TB
include collar stud abscess, a T-shaped uterus,
and a pseudounicornuate uterus (33,66,67).
Extensive destruction and synechia formation
may result in complete narrowing of the entire
uterine cavity, or Netter syndrome, creating a
gloved-finger appearance on hysterosalpingo-
grams (33). US, CT, and MRI findings may
vary from normal to an abnormally thinned or
thickened endometrium. The endometrium may
appear heterogeneous owing to the presence
of intrauterine adhesions, fibrosis, or calcifica-
tion (Fig 26) (64,66). Sometimes the appear-
ance may resemble that of carcinoma, and the
extrauterine findings described with tubal TB
might prompt the radiologist to suggest female
genital TB.
1140  July-August 2021 radiographics.rsna.org

Figure 25.  Tuberculous endometritis in a 32-year-old woman who was undergoing molecular targeted therapy for
myelofibrosis complicated by disseminated TB and pelvic inflammatory disease. (a) Sagittal abdominal CT image with
intravenous contrast material shows a markedly enlarged uterus (*) with multiple irregular strands in the endometrial
cavity, representing endometritis. Endometrial biopsy specimens were positive for M tuberculosis. (b) Axial abdominal
CT image with intravenous contrast material shows additional sites of TB, with multiple enlarged retroperitoneal lymph
nodes (arrows). The patient was treated with isoniazid and rifampin.

Figure 26.  Tuberculous endometritis in a 29-year-old woman with disseminated TB and a bicornuate uterus.
(a) Axial T1-weighted contrast-enhanced MR image shows a bicornuate uterus (arrows). The endometrial cavity of
horn 2 is filled with fluid and debris (with fluid-fluid levels) (black *) and demonstrates heterogeneous myometrial
enhancement (white *). (b) Sagittal T2-weighted MR image shows a diffusely heterogeneous and thickened myome-
trium (dashed arrow) with prominent endometrial glands (solid arrow), as well as the dilated endometrial cavity of
horn 2 (*). Endometrial biopsy cultures were positive for M tuberculosis.

Ovaries.—The ovaries are affected in 20%–30%
of patients with female TB, and the involve-
ment is usually bilateral (33,64). Subtle involve-
ment may not always be apparent at imaging or
laparoscopy. The ovary may be surrounded by
adhesions forming a tubo-ovarian mass, which
is frequently adherent to the omentum and/or
intestines (66). The other form of involvement
is oophoritis, in which the infection starts in the
stroma of the ovary. This is relatively rare and
presumably has a hematogenous source (66).
US, CT, and MRI enable simultaneous evalu-
ation of tubo-ovarian masses and extrapelvic
findings (Fig 27). A tubo-ovarian abscess that
extends into the extraperitoneal compartment,
suggesting a tubercular cause, has been de-
scribed (20).
Cervix.—The cervix is involved in 5%–15% of
cases of female genital TB. This involvement
usually is due to TB of the fallopian tubes and
endometrium, but rarely it is sexually transmit-
ted from a male partner with genital TB (33,64).
Gross forms of cervical TB include those involv-
ing ulcerative, polypoidal, and miliary patterns
(64). Hysterosalpingography may reveal cervical
distortion, with an irregular endocervical canal
and feathery diverticular outpouchings. However,
cervical TB may resemble carcinoma, both grossly
and at imaging, necessitating tissue sampling (33).
RG  •  Volume 41  Number 4 Naeem et al  1141

Figure 27.  Tubo-ovarian abscess in a 40-year-old woman with a history of ectopic pregnancy.
(a) Gray-scale US image of the pelvis shows a dilated fallopian tube with a thick wall and intraluminal
debris (*), representing pyosalpinx. (b) Color Doppler US image shows the fallopian tube (*) to be
inseparable from a complex tubo-ovarian abscess (arrow). The fallopian tube wall and periphery of the
necrotic ovary are hyperemic (arrowhead). The abscess was laparoscopically drained, and the cultures
grew M tuberculosis.

Vagina and Vulva.—TB with involvement of eu/en/publications-data/what-extrapulmonary-tb. Published

the vagina and vulva is the rarest form of female
genital TB, accounting for 1%–2% of cases (33).
The disease may begin as a nodule, which may
progress to a hypertrophic ulcer or warty growth.
Discharging perineal sinuses and vesicovaginal
and rectovaginal fistulas rarely form with ad-
vanced disease (73,74). The imaging and gross
appearances are nonspecific and may simulate
those of malignancy such that tissue sampling
and demonstration of granuloma histopathologic
features are required to make the diagnosis (64).
Conclusion
Genitourinary TB poses a diagnostic challenge
owing to its insidious and nonspecific clinical
presentation. However, knowledge of the imag-
ing findings of genitourinary TB may aid the
diagnostic radiologist in suggesting TB in the
differential diagnosis, facilitating appropriate and
timely clinical management.
Disclosures of Conflicts of Interest.—C.O.M. Activities related
to the present article: Editor of RadioGraphics (not involved in
the handling of this article). Activities not related to the present
article: disclosed no relevant relationships. Other activities: dis-
closed no relevant relationships.
References
1. Centers for Disease Control and Prevention. Tuberculosis
(TB): data and statistics. Centers for Disease Control and
Prevention website. https://www.cdc.gov/tb/statistics/de-
fault.htm. Published September 6, 2019. Accessed March
6, 2020.
2. World Health Organization. Tuberculosis. World Health
Organization website. https://www.who.int/news-room/
fact-sheets/detail/tuberculosis. Published March 3, 2020.
Accessed March 29, 2020.
3. European Centre for Disease Control and Prevention.
What is extrapulmonary TB? European Centre for Disease
Control and Prevention website. https://www.ecdc.europa.
March 24, 2013. Accessed March 27, 2020.
4. Figueiredo AA, Lucon AM, Junior RF, Srougi M. Epide-
miology of urogenital tuberculosis worldwide. Int J Urol
2008;15(9):827–832.
5. Muneer A, Macrae B, Krishnamoorthy S, Zumla A. Uro-
genital tuberculosis : epidemiology, pathogenesis and clinical
features. Nat Rev Urol 2019;16(10):573–598.
6. Ghaleb K, Afifi M, El-Gohary M. Assessment of diagnostic
techniques of urinary tuberculosis. Mediterr J Hematol Infect
Dis 2013;5(1):e2013034.
7. Merchant S, Bharati A, Merchant N. Tuberculosis
of the genitourinary system: urinary tract tuberculo-
sis—renal tuberculosis, part I. Indian J Radiol Imaging
2013;23(1):46–63.
8. Merchant S, Bharati A, Merchant N. Tuberculosis of the
genitourinary system: urinary tract tuberculosis—renal tuber-
culosis, part II. Indian J Radiol Imaging 2013;23(1):64–77.
9. Green DB, Kawashima A, Menias CO, et al. Complications
of intravesical BCG immunotherapy for bladder cancer.
RadioGraphics 2019;39(1):80–94.
10. Dyer RB, Chen MY, Zagoria RJ. Classic signs in uroradiol-
ogy. RadioGraphics 2004;24(suppl 1):S247–S280.
11. Lam KY, Lo CY. A critical examination of adrenal tubercu-
losis and a 28-year autopsy experience of active tuberculosis.
Clin Endocrinol (Oxf) 2001;54(5):633–639.
12. Zulfiqar M, Shetty A, Tsai R, Gagnon MH, Balfe DM,
Mellnick VM. Diagnostic approach to benign and malignant
calcifications in the abdomen and pelvis. RadioGraphics
2020;40(3):731–753.
13. Gambhir S, Ravina M, Rangan K, et al. Imaging in extra-
pulmonary tuberculosis. Int J Infect Dis 2017;56:237–247.
14. Zhang XC, Yang ZG, Li Y, et al. Addison’s disease due
to adrenal tuberculosis: MRI features. Abdom Imaging
2008;33(6):689–694.
15. Dong A, Cui Y, Wang Y, Zuo C, Bai Y. (18)F-FDG
PET/CT of adrenal lesions. AJR Am J Roentgenol
2014;203(2):245–252.
16. Gaudiano C, Tadolini M, Busato F, et al. Multidetector
CT urography in urogenital tuberculosis: use of reformatted
images for the assessment of the radiological findings—a
pictorial essay. Abdom Radiol (NY) 2017;42(9):2314–2324.
17. Li Y, Yang ZG, Guo YK, et al. Distribution and charac-
teristics of hematogenous disseminated tuberculosis within
the abdomen on contrast-enhanced CT. Abdom Imaging
2007;32(4):484–488.
18. Wang LJ, Wu CF, Wong YC, Chuang CK, Chu SH,
Chen CJ. Imaging findings of urinary tuberculosis on ex-
1142  July-August 2021 radiographics.rsna.org
cretory urography and computerized tomography. J Urol
2003;169(2):524–528.
19. Gurski J, Baker KC. An unusual presentation: renal tuber-
culosis. ScientificWorldJournal 2008;8:1254–1255.
20. Engin G, Acunas B, Acunas G, Tunaci M. Imaging of ex-
trapulmonary tuberculosis. RadioGraphics 2000;20(2):471–
488; quiz 529–530, 532.
21. Israel GM, Bosniak MA. Pitfalls in renal mass evaluation and
how to avoid them. RadioGraphics 2008;28(5):1325–1338.
22. Gibson MS, Puckett ML, Shelly ME. Renal tuberculosis.
RadioGraphics 2004;24(1):251–256.
23. Roylance J, Penry B, Davies R, Roberts M. Radiology in
the management of urinary tract tuberculosis. Br J Urol
1970;42(6):679–687.
24. Potenta SE, D’Agostino R, Sternberg KM, Tatsumi K,
Perusse K. CT urography for evaluation of the ureter.
RadioGraphics 2015;35(3):709–726.
25. Prakash J, Goel A, Sankhwar S, Singh BP. Extensive
renal and ureteral calcification due to tuberculosis: rare
images for an uncommon condition. BMJ Case Rep
2013;2013:bcr2012008508.
26. Figueiredo AA, Lucon AM, Júnior RF, Ikejiri DS, Nahas
WC, Srougi M. Urogenital tuberculosis in immunocom-
promised patients. Int Urol Nephrol 2009;41(2):327–333.
https://doi.org/10.1007/s11255-008-9436-6.
27. Mariappan K, Indiran V. Thimble bladder. Abdom Radiol
(NY) 2019;44(7):2669–2670.
28. Wong-You-Cheong JJ, Woodward PJ, Manning MA, Davis
CJ. From the archives of the AFIP: inflammatory and non-
neoplastic bladder masses—radiologic-pathologic correla-
tion. RadioGraphics 2006;26(6):1847–1868.
29. Figueiredo AA, Lucon AM. Urogenital tuberculosis: update
and review of 8961 cases from the world literature. Rev Urol
2008;10(3):207–217.
30. Gupta N, Mandal AK, Singh SK. Tuberculosis of the prostate
and urethra: a review. Indian J Urol 2008;24(3):388–391.
31. Segovis CM, Dyer RB. The “watering can perineum.”
Abdom Radiol (NY) 2016;41(6):1214.
32. Prakash G, Singh V, Sinha RJ, Babu S, Jhanwar A, Mehrotra
CN. Primary tuberculosis of urethra presenting as stricture
urethra and watering can perineum: a rarity. Urol Ann
2016;8(4):493–495.
33. Grace GA, Devaleenal DB, Natrajan M. Genital tubercu-
losis in females. Indian J Med Res 2017;145(4):425–436.
34. Kulchavenya E, Khomyakov V. Male genital tuberculosis
in Siberians. World J Urol 2006;24(1):74–78.
35. Venyo AK. Tuberculosis of the penis: a review of the litera-
ture. Scientifica (Cairo) 2015;2015:601624.
36. Cheng Y, Huang L, Zhang X, Ji Q, Shen W. Multiparamet-
ric magnetic resonance imaging characteristics of prostate
tuberculosis. Korean J Radiol 2015;16(4):846–852.
37. Trauzzi SJ, Kay CJ, Kaufman DG, Lowe FC. Management of
prostatic abscess in patients with human immunodeficiency
syndrome. Urology 1994;43(5):629–633.
38. Hemal AK, Aron M, Nair M, Wadhwa SN. ‘Autopros-
tatectomy’: an unusual manifestation in genitourinary
tuberculosis. Br J Urol 1998;82(1):140–141.
39. Speights VO Jr, Brawn PN. Serum prostate specific antigen
levels in non-specific granulomatous prostatitis. Br J Urol
1996;77(3):408–410.
40. Thornhill BA, Morehouse HT, Coleman P, Hoffman-Tretin
JC. Prostatic abscess: CT and sonographic findings. AJR
Am J Roentgenol 1987;148(5):899–900.
41. Bude R, Bree RL, Adler RS, Jafri SZ. Transrectal ultrasound
appearance of granulomatous prostatitis. J Ultrasound Med
1990;9(12):677–680.
42. Nepal P, Ojili V, Songmen S, Kaur N, Olsavsky T, Nagar
A. “The Great Masquerader”: sonographic pictorial review
of testicular tuberculosis and its mimics. J Clin Imaging
Sci 2019;9:27.
43. Muttarak M, Peh WC, Lojanapiwat B, Chaiwun B.
Tuberculous epididymitis and epididymo-orchitis: sono-
graphic appearances. AJR Am J Roentgenol 2001;176(6):
1459–1466.
44. Kim SH, Pollack HM, Cho KS, Pollack MS, Han MC.
Tuberculous epididymitis and epididymo-orchitis: sono-
graphic findings. J Urol 1993;150(1):81–84.
45. Okada H, Gotoh A, Kamidono S. Multiple hypoechoic lesions
in bilateral testes. Urology 2003;61(4):833–834.
46. Park KW, Park BK, Kim CK, Lee HM, Oh YL. Chronic
tuberculous epididymo-orchitis manifesting as a non-tender
scrotal swelling: magnetic resonance imaging-histological
correlation. Urology 2008;71(4):755.e5–755.e7.
47. Liu HY, Fu YT, Wu CJ, Sun GH. Tuberculous epididy-
mitis: a case report and literature review. Asian J Androl
2005;7(3):329–332.
48. Jung YY, Kim JK, Cho KS. Genitourinary tuberculosis:
comprehensive cross-sectional imaging. AJR Am J Roentgenol
2005;184(1):143–150.
49. Tsili AC, Tsampoulas C, Giannakis D, et al. Case report:
tuberculous epididymo-orchitis—MRI findings. Br J Radiol
2008;81(966):e166–e169.
50. Michaelides M, Sotiriadis C, Konstantinou D, Pervana S,
Tsitouridis I. Tuberculous orchitis US and MRI findings:
correlation with histopathological findings. Hippokratia
2010;14(4):297–299.
51. Parker RA 3rd, Menias CO, Quazi R, et al. MR imaging of the
penis and scrotum. RadioGraphics 2015;35(4): 1033–1050.
52. Ran P, Liang X, Zhang Y, Sun P, Dong A. FDG PET/CT
in a case of bilateral tuberculous epididymo-orchitis. Clin
Nucl Med 2019;44(9):757–760.
53. Yang DM, Kim HC, Lee HL, Lim JW, Kim GY. So-
nographic findings of acute vasitis. J Ultrasound Med
2010;29(12):1711–1715.
54. Middleton WD, Dahiya N, Naughton CK, Teefey SA, Siegel
CA. High-resolution sonography of the normal extrapelvic vas
deferens. J Ultrasound Med 2009;28(7):839–846.
55. Yang DM, Kim HC, Kim SW, Lee HL, Min GE, Lim SJ.
Sonographic findings of tuberculous vasitis. J Ultrasound
Med 2014;33(5):913–916.
56. Yamasaki S, Sugita O, Tanimura M, Morioka M. Tubercu-
loma arising in the inguinal portion of the spermatic cord: a
case report. Int J Urol 1996;3(6):514–517.
57. Sharma S. Spermatic cord tuberculosis: the great masquer-
ader. Int J Mycobacteriol 2019;8(2):196–198.
58. Wise GJ, Shteynshlyuger A. An update on lower urinary tract
tuberculosis. Curr Urol Rep 2008;9(4):305–313.
59. Stasinou T, Bourdoumis A, Owegie P, Kachrilas S, Buchholz
N, Masood J. Calcification of the vas deferens and seminal
vesicles: a review. Can J Urol 2015;22(1):7594–7598.
60. Kim B, Kawashima A, Ryu JA, Takahashi N, Hartman RP,
King BF Jr. Imaging of the seminal vesicle and vas deferens.
RadioGraphics 2009;29(4):1105–1121.
61. Reddy MN, Verma S. Lesions of the seminal vesicles and
their MRI characteristics. J Clin Imaging Sci 2014;4:61.
62. Singal A, Pandhi D, Kataria V, Arora VK. Tuberculosis of
the glans penis: an important differential diagnosis of genital
ulcer disease. Int J STD AIDS 2017;28(14):1453–1455.
63. Sharma JB. Current diagnosis and management of female geni-
tal tuberculosis. J Obstet Gynaecol India 2015;65(6):362–371.
64. Sharma JB, Sharma E, Sharma S, Dharmendra S. Fe-
male genital tuberculosis: revisited. Indian J Med Res
2018;148(suppl):S71–S83.
65. Varma TR. Tuberculosis of the female genital tract. The
Global Library of Women’s Medicine website. https://
www.glowm.com/section_view/heading/tuberculosis-of-
the-female-genital-tract/item/34. Published October 2008.
Accessed April 29, 2020.
66. Shah HU, Sannananja B, Baheti AD, Udare AS, Badhe
PV. Hysterosalpingography and ultrasonography find-
ings of female genital tuberculosis. Diagn Interv Radiol
2015;21(1):10–15.
67. Ahmadi F, Zafarani F, Shahrzad GS. Hysterosalpingographic
appearances of female genital tract tuberculosis. II. Uterus.
Int J Fertil Steril 2014;8(1):13–20.
68. Sharma JB, Pushparaj M, Roy KK, et al. Hysterosalpingo-
graphic findings in infertile women with genital tuberculosis.
Int J Gynaecol Obstet 2008;101(2):150–155.
69. Sharma JB, Karmakar D, Hari S, et al. Magnetic resonance
imaging findings among women with tubercular tubo-ovarian
masses. Int J Gynaecol Obstet 2011;113(1):76–80.
70. Bankier AA, Fleischmann D, Wiesmayr MN, et al. Update:
abdominal tuberculosis—unusual findings on CT. Clin Radiol
1995;50(4):223–228.
RG  •  Volume 41  Number 4 Naeem et al  1143

71. Sharma JB, Karmakar D, Kumar R, et al. Comparison of
PET/CT with other imaging modalities in women with genital
tuberculosis. Int J Gynaecol Obstet 2012;118(2):123–128.
72. Coremans L, de Clerck F. Fitz-Hugh-Curtis syndrome as-
sociated with tuberculous salpingitis and peritonitis: a case
presentation and review of literature. BMC Gastroenterol
2018;18(1):42.
73. Sharma JB, Roy KK, Pushparaj M, et al. Genital tuberculosis:
an important cause of Asherman’s syndrome in India. Arch
Gynecol Obstet 2008;277(1):37–41.
74. Wong A, Dhingra S, Surabhi VR. AIRP best cases in
radiologic-pathologic correlation: genitourinary tuberculosis.
RadioGraphics 2012;32(3):839–844.

TM
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E134

Erratum
July-August 2022 • Volume 42 • Number 4

Originally published in:

https://doi.org/10.1148/rg.2021200154
Imaging Manifestations of Genitourinary Tuberculosis
Muhammad Naeem, Maria Zulfiqar, Mohammed Azfar Siddiqui, Anup S. Shetty, Adeel Haq, Cristian Va-
rela, Cary Siegel, Christine O. Menias
Erratum in:
https://doi.org/10.1148/rg.229007
On page 1129 of the print issue, right column, the first sentence of the last paragraph should read as follows: Focal
or diffuse caliectasis is usually a direct result of pelvic and infundibular strictures (7,8).
The image shown in Figure 10b is a follow-up retrograde pyelography image.
The published Figure 2 was adapted from a previously published figure in reference 7 and has been replaced online
with the new Figure 2 and its legend shown below. This replacement does not change the meaning of the figure in
any way.

Figure 2.  Diagrammatic representation of various morphologic features that can help in diagnosing tuberculous disease of the
adrenal glands, kidneys, ureters, and urinary bladder. A = acute adrenalitis (adrenal gland enlargement), B = adrenal gland calcifica-
tions (diffuse and focal), C = urothelial thickening, D = “moth-eaten” calyx, E = papillary necrosis, F = calyceal blunting, G = papillitis
(deep calyceal cup), H = infundibular stenosis, I = pyelonephritis, J = cortical abscess rupturing into the perinephric space and into
the collecting system, K = lobar calcification/putty kidney, L = miliary tuberculosis, M = cortical scarring, N = hiked-up pelvis (Kerr
kink), O = stricturing and beading of ureters, P = granulation and intravesical septa causing ureterovesical obstruction, Q = thimble
bladder, R = urethral stricture. (Created with BioRender.com.)