International Journal of Infectious Diseases 32 (2015) 87–93

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International Journal of Infectious Diseases

journal homepage: www.elsevier.com/locate/ijid

Review

Imaging in tuberculosis
Evangelia Skoura a, Alimuddin Zumla b, Jamshed Bomanji a,*
a
Institute of Nuclear Medicine, University College Hospitals NHS Trust, London NW1 2BU, UK
b
Division of Infection and Immunity, Centre for Clinical Microbiology, University College London, and NIHR Biomedical Research Centre,
University College London Hospitals, London, UK

A R T I C L E I N F O S U M M A R Y

Article history: Early diagnosis of tuberculosis (TB) is necessary for effective treatment. In primary pulmonary TB, chest
Received 14 November 2014 radiography remains the mainstay for the diagnosis of parenchymal disease, while computed
Received in revised form 28 November 2014 tomography (CT) is more sensitive in detecting lymphadenopathy. In post-primary pulmonary TB, CT
Accepted 1 December 2014
is the method of choice to reveal early bronchogenic spread. Concerning characterization of the infection
Corresponding Editor: Eskild Petersen, as active or not, CT is more sensitive than radiography, and 18F-fluorodeoxyglucose positron emission
Aarhus, Denmark
tomography/CT (18F-FDG PET/CT) has yielded promising results that need further confirmation. The
diagnosis of extrapulmonary TB sometimes remains difficult. Magnetic resonance imaging (MRI) is the
Keywords: preferred modality in the diagnosis and assessment of tuberculous spondylitis, while 18F-FDG PET shows
Pulmonary tuberculosis superior image resolution compared with single-photon-emitting tracers. MRI is considered superior to
Extrapulmonary tuberculosis CT for the detection and assessment of central nervous system TB. Concerning abdominal TB, lymph
Computed tomography
nodes are best evaluated on CT, and there is no evidence that MRI offers added advantages in diagnosing
Positron emission tomography
hepatobiliary disease. As metabolic changes precede morphological ones, the application of 18F-FDG PET/
Fluorodeoxyglucose
Magnetic resonance imaging CT will likely play a major role in the assessment of the response to anti-TB treatment.
! 2015 The Authors. Published by Elsevier Ltd on behalf of International Society for Infectious Diseases.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-
nc-nd/4.0/).

improve the radiologist’s familiarity with the spectrum of imaging

1. Introduction
Tuberculosis (TB) remains a global emergency despite substan-
tial investment in health services over the past two decades.
Patients with sputum-negative pulmonary TB (PTB) and extra-
pulmonary TB (EPTB) are difficult to diagnose and may be missed
at all points of care. Diagnostic imaging is challenging because
signs of TB may mimic those of other diseases such as neoplasms or
sarcoidosis. Clinical signs and symptoms in affected adults can be
non-specific and a high level of pre-test clinical suspicion based on
history is fundamental in the diagnostic work-up. The global
impact of TB is extremely important, considering that an estimated
9.0 million people developed TB in 2013 and 1.5 million died from
the disease, according to the recent World Health Organization
(WHO) global tuberculosis report 2014.
Early diagnosis promotes effective treatment and leads to a
reduced onward transmission of TB. This article gives a review of
imaging patterns of chest TB as may be detected on conventional
radiography and computed tomography (CT). The main aim is to
* Corresponding author.
E-mail address: jamshed.bomanji@uclh.nhs.uk (J. Bomanji).
features of this disease in order to facilitate timely diagnosis.
Furthermore, we consider the emerging role of alternative
methods of imaging, such as magnetic resonance imaging (MRI),
which can be helpful and highly accurate for a better definition of
some of the signs of TB.
Although new imaging methods are now being used, conven-
tional radiography remains the initial modality for suspected PTB and
for mass screening purposes.1 CT and MRI are the modalities of choice
for the evaluation of specific body parts.1 Positron emission
tomography/computed tomography with the use of 18F-fluorodeox-
yglucose (18F-FDG PET/CT) is a non-invasive imaging method that
has been used widely for the differentiation of malignant from
benign lesions. However, 18F-FDG also accumulates in inflammatory
cells such as neutrophils, activated macrophages, and lymphocytes at
the site of inflammation or infection.2 Consequently, 18F-FDG uptake
is observed in PTB, in tuberculoma, and in other TB-related lesions.3,4
Using PET/CT, pulmonary and extrapulmonary TB involvement is
assessed simultaneously, with time- and cost-saving implications.
Although any organ of the body can be involved, the lung
remains the most commonly involved organ in TB. The imaging
appearances of TB are described below for both pulmonary and
extrapulmonary involvement.

http://dx.doi.org/10.1016/j.ijid.2014.12.007
1201-9712/! 2015 The Authors. Published by Elsevier Ltd on behalf of International Society for Infectious Diseases. This is an open access article under the CC BY-NC-ND
license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
88 E. Skoura et al. / International Journal of Infectious Diseases 32 (2015) 87–93
2. Pulmonary tuberculosis
Classically, PTB can be divided into a primary and a post-
primary pattern, each presenting with characteristic radiological
features. In practice, however, it is very difficult to draw distinct
lines between these radiographic patterns, and there is consider-
able overlap in the radiological manifestations.5
2.1. Primary tuberculosis
Primary TB is due to first-time exposure to Mycobacterium
tuberculosis. At radiology, primary PTB manifests as four main
entities – parenchymal disease, lymphadenopathy, pleural effu-
sion, and miliary disease – or any combination thereof.1
Chest radiography continues to be the mainstay of diagnosis.
Typically, parenchymal disease manifests as consolidation in any
lobe, with predominance in the lower and middle lobes.6 In these
cases, the bacterial infections are much more likely to be the cause
of such radiological features and hence the findings are non-
specific, although primary infection should be suspected in
individuals at risk of exposure to TB. Multilobar consolidation
can be seen in almost 25% of cases.1 In approximately two-thirds of
cases, the parenchymal lesion resolves without sequelae on
conventional radiography.6 In the remainder, a radiological scar
persists that can be calcified in up to 15%, while persistent mass-
like opacities called tuberculomas are seen in approximately 9% of
cases.6 Frequently, the only radiological evidence suggestive of
previous TB is the so-called Ranke complex: the combination of a
parenchymal scar, calcified or not (Ghon lesion), and calcified hilar
and/or paratracheal lymph nodes.5 Destruction and fibrosis of the
lung parenchyma result in the formation of traction bronchiectasis
within the fibrotic region.5
The most common abnormality in children is lymph node
enlargement, which is seen in 90–95% of cases; by comparison, in
adults the percentage reaches up to 43%.7 Right paratracheal and
hilar lymph nodes are the most common sites of nodal involve-
ment, although involvement is bilateral in about a third of cases. CT
is more sensitive than plain radiography in detecting tuberculous
lymphadenopathy. It reveals nodes often measuring more than
2 cm, with a very characteristic, but not pathognomonic, ‘rim sign’
that consists of a low-density centre, representing caseous
necrosis, surrounded by a peripheral enhancing rim due to
granulomatous inflammatory tissue.8,9
In contrast to lymphadenopathy, the prevalence of radiographi-
cally detectable parenchymal involvement is significantly lower in
children up to 3 years old (51%) than in older children, among whom
the prevalence is similar to the reported percentage in adults
(80%).7,8 Also, evolution to cavitary disease is rare in children.5
18
Figure 1. Arrows indicate a mildly F-FDG avid right lower lobe nodule measuring 1.5 cm (SUVmax 2). The differential diagnosis for this nodule would include cancer or
tuberculosis.
Concerning the role of 18F-FDG PET/CT, two distinct patterns of
PTB have been described: (1) the lung pattern, related to a
restricted and slight hypermetabolic infection, with 18F-FDG
uptake in areas of lung consolidation ! cavitation surrounded by
micronodules and mild uptake within lymph nodes, and (2) the
lymphatic pattern, related to a systemic and intense infection, with
more enlarged and 18F-FDG-avid hilar and mediastinal lymph
nodes.10
A limitation to the use of 18F-FDG PET/CT for the assessment of a
single pulmonary nodule, especially in endemic areas, is the
inability to distinguish tubercular from malignant lesions
(Figure 1).11 Studies investigating the diagnostic value of dual
time-point 18F-FDG PET/CT imaging have shown limited promise,
but further investigations in larger series of patients are
warranted.12,13
2.2. Post-primary tuberculosis
Post-primary PTB is one of the many terms (including
reactivation, secondary, or adulthood) applied to the form of TB
that develops and progresses under the influence of acquired
immunity.5 The most common radiographic manifestation of post-
primary PTB is focal or patchy heterogeneous, poorly defined
consolidation involving the apical and posterior segments of the
upper lobes and the superior segments of the lower lobes
(Figure 2).14,15 In the majority of cases, more than one pulmonary
segment is involved.6 Cavitation, the radiological hallmark of PTB,
is radiographically evident in 20–45% of patients (Figure 3), while
air-fluid levels in the cavity occur in 10% of cases.14,15 Cavitation
may progress to endobronchial spread and results in a typical ‘tree-
in-bud’ distribution of nodules in addition to cavitation; this is
considered a reliable marker of active TB.16 High-resolution CT is
the method of choice to reveal early bronchogenic spread, with 2-
to 4-mm centrilobular nodules and sharply marginated linear
branching opacities around terminal and respiratory bronchioles
(tree-in-bud sign).16 The tree-in-bud sign is the constellation of
small centrilobular nodules and concomitant branching opacities,
which mimics the branching pattern of a budding tree.17 The
centrilobular nodules are peripheral, spare the subpleural lung,
and denote the inflammatory lesions in the bronchioles and
peribronchial alveoli.16,17 Hilar or mediastinal lymphadenopathy
is uncommon in post-primary PTB, seen in only 5–10% of patients
(Figure 4).18,19
Although pulmonary tuberculomas are most often the result of
healed primary PTB, a pulmonary tuberculoma is the main or only
abnormality on chest radiographs in approximately 5% of patients
with reactivation.20 The CT scan shows a round or oval granuloma,
measuring from 0.4 to 5 cm in diameter, with a wall lined by
 E. Skoura et al. / International Journal of Infectious Diseases 32 (2015) 87–93 89

Figure 2. Trans-axial CT section showing a patchy, heterogeneous, poorly defined consolidation with cavitating lesion in the upper lobe of the right lung.

inflammatory granulomatous tissue or encapsulated by connective
tissue.21 Tuberculomas can cavitate, while calcification is found in
20–30% of them.21 In 80% of cases, satellite lesions are observed in
the immediate vicinity of the main lesion.5 Because of increased
glucose metabolism caused by active granulomatous inflammation,
tuberculomas may accumulate 18F-FDG.22 Maximum standardized
uptake values (SUVmax) tend not to be significantly different for
tuberculous and malignant lesions.23,24 One study has suggested
that unlike 18F-FDG PET, the 11C-choline PET scan can help to
differentiate between lung cancer and tuberculoma, because
tuberculoma shows low tracer uptake on 11C-choline PET scan.25
2.3. Radiological patterns in primary and/or post-primary PTB
Miliary pulmonary disease affects between 1% and 7% of
patients with all forms of TB.6 It is usually seen in the elderly,
infants, and immunocompromised persons.6 Initially, standard
radiographs are normal in 25–40% of cases.26 CT can demonstrate
miliary disease before it becomes radiographically apparent, and
its characteristic findings consist of innumerable 1- to 3-mm-
diameter nodules randomly distributed throughout both lungs,
often associated with intra- and interlobular septal thickening.14,27
The nodules usually resolve within 2–6 months with treatment,
without scarring or calcification; however, they may coalesce to
form focal or diffuse consolidation.6
A pleural effusion is seen in approximately one-fourth of
patients with primary PTB and in 18% of post-primary PTB.26
Although, usually observed in association with parenchymal
and/or nodal disease, pleural effusion has been reported to be the
only radiographic finding indicative of primary PTB in approxi-
mately 5% of adult cases.26 Pleural effusion is usually unilateral and
on the same side as the primary focus of PTB, while complications
such as effusion, empyema, and bronchopleural fistula are rare.6 The
CT scan of patients with post-primary pleural effusion typically
shows smooth thickening of visceral and parietal pleura.28
Ultrasonography often demonstrates a complex septated effusion.6
Fibrothorax with diffuse pleural thickening, but without pleural
effusion on CT, suggests inactivity.29 The 18F-FDG PET/CT scan may
demonstrate diffusely intense 18F-FDG uptake in thickened pleura
that can be confused with pleural mesothelioma.30
2.4. Differentiation between active and inactive TB
TB makes its presence felt on imaging long after the resolution
of disease. Sometimes a question that needs to be answered is
whether the infection is active or not. Active disease is in general
characterized by the presence of centrilobular nodules, tree-in-bud
pattern, thick-walled cavities, consolidation, miliary nodules,
pleural effusions, or necrotic lymphadenopathy.1 Resolution to
thin-walled smooth cavities, fibrosis, and parenchymal, nodal, or
pleural calcifications often denotes inactive disease.1
Chest radiographs may be normal or show only mild or non-
specific findings in patients with active disease.26 The diagnosis of
PTB with radiography is initially correct in only 49% of all cases:
34% for primary and 59% for post-primary PTB.26 On the other
hand, CT can correctly diagnose 91% of cases of PTB and correctly

Figure 3. Left panel: CT image showing a 1.6 " 1.2-cm cavitating lesion (arrow) in the upper lobe of the right lung. Right panel: this lesion shows mild 18F-FDG uptake on the
PET scan (small arrow) (SUVmax 2.2). Bottom left panel: Fused 18F-FDG PET/CT image showing the same cavitating avid lesion (arrow).
90 E. Skoura et al. / International Journal of Infectious Diseases 32 (2015) 87–93
Figure 4. Left panel: Multiple intensity projection image showing 18F-FDG uptake in the mediastinal and bilateral hilar lymph nodes (arrows). Right panel: Multiple fused
trans-axial section 18F-FDG PET/CT images showing hilar and mediastinal lymph nodes (arrows).
characterize 80% of patients with active disease and 89% with
inactive disease.31
CT is more sensitive than radiography in the detection and
characterization of both parenchymal disease and mediastinal
lymphadenopathy.9,32 In a study that compared the two methods,
high-resolution CT showed cavities in 58% of patients with active
PTB, whereas chest radiographs in only 22%.32 The diagnosis of active
PTB was based on positive acid-fast bacilli in sputum and changes on
serial radiographs obtained during treatment.32 CT may also show
pleural disease that is not evident on chest radiography and be
helpful in the evaluation of pleural complications.33
CT features predictive of highly infectious/active PTB include
the following:34 (1) consolidation involving the apex or the
posterior segment of the right upper lobe or the apico-posterior
segment of the left upper lobe, (2) consolidation involving the
superior segment of the right or left lower lobe, (3) a cavity lesion,
(4) clusters of nodules, and (5) absence of centrilobular nodules.
High-resolution CT is better than chest radiography in predicting
active PTB, with a sensitivity of 96% versus 48%.35
It has been reported that 18F-FDG PET is able to differentiate
active PTB from old or inactive disease, as active tuberculoma has
significantly higher SUVmax values compared with inactive
tuberculoma.3 When a SUVmax of 1.05 (at 60 min) was used as
the cut-off, the sensitivity and specificity were 100% and 100%,
respectively.3 A recent study concluded that 18F-FDG PET/CT has
the potential to become a tool for monitoring the treatment
response in selected cases of EPTB or multidrug resistance.36 An
interesting study of patients with radiographic lesions suggestive
of old healed TB aimed to gather information on the metabolic
status of TB lesions using 18F-FDG PET/CT imaging.37 The authors
showed that patients with old healed TB lesions with a higher
SUVmax may be at higher risk of active TB.37 Further investigation is
needed to confirm these results.
3. Extrapulmonary tuberculosis
Despite recent advances in imaging, the diagnosis of extra-
pulmonary involvement sometimes remains difficult.38 The
imaging of some frequent extrapulmonary sites of TB is reviewed
below.
3.1. Musculoskeletal tuberculosis
Approximately 50% of cases of skeletal TB involve the spine.6
Spondylodiscitis, also known as Pott’s disease, is the most
common form.39 The infection begins in subchondral bone and
spreads slowly to the intervertebral disk space and the adjacent
vertebral bodies, commonly in the lower dorsal and upper lumbar
spine.40 Failure to identify and treat these areas of involvement at
an early stage may lead to serious complications such as vertebral
collapse, spinal compression, and spinal deformity.38 Plain
radiography is normal early in the disease.1 The first sign may
be demineralization of the endplates with resorption and loss of
dense margins. As the disease progresses, radiography will show
progressive vertebral collapse with anterior wedging and gibbus
formation.1 MRI is the preferred imaging modality in the
diagnosis and assessment of tuberculous spondylitis.41,42 Be-
cause of the often multifocal nature of spinal TB, the MRI imaging
of the entire spinal column could be more effective in the early
diagnosis of the disease.43 In cases of spinal TB, the spinal cord is
susceptible to myelopathy secondary to compression from an
epidural abscess.6 The collapsed vertebra along with the
epidural collection/abscess is also best evaluated on MRI.6 After
antibiotic administration is initiated, repeat imaging is advised at
approximately 4-week intervals or at any time if neurological
deterioration occurs.44
As tubercular lesions demonstrate high 18F-FDG uptake, 18F-
FDG PET/CT is a promising technique for the diagnosis of spinal
infection (Figures 5 and 6).45–48 An interesting finding was that
63.6% of patients with spinal TB had clinically occult non-
contiguous multifocal skeletal involvement at the time of
whole-body 18F-FDG PET/CT scan.49
Besides the spine, any part of the musculoskeletal system can
become involved, but the large joints of the lower limbs are most
commonly affected. Imaging findings in musculoskeletal TB are
often non-specific. MRI is the most sensitive modality for early
diagnosis and complete delineation of the disease.1
 E. Skoura et al. / International Journal of Infectious Diseases 32 (2015) 87–93 91

Figure 5. CT (left panel) and 18F-FDG PET/CT fused images (right panel): trans-axial and sagittal sections. Moderate to intense 18F-FDG uptake is seen in a paravertebral soft
tissue mass lesion extending from the level of T7–T10 vertebrae with associated lytic sclerotic changes in T7–T9 vertebrae and collapse of the T8 vertebra (arrows). The lesion
infiltrates into the spinal canal at the level of the T8 vertebra and involves the spinal cord (small arrow). The lesion is seen to extend along the left costal margin, with faint 18F-
FDG uptake and foci of calcification, likely representing a cold abscess (courtesy of Prof. B.R. Mittal).

3.2. Central nervous system (CNS) tuberculosis 3.3. Abdominal tuberculosis

TB of the CNS is a highly devastating form of the disease. Various
forms of involvement of the CNS are observed: parenchymal,
meningeal, calvarial, spinal, or any combination thereof.1 MRI is
generally considered superior to CT in detecting and assessing CNS
TB.50 Parenchymal involvement is most frequently seen in the form of
a tuberculoma, which may be single or multiple. In the paediatric age
group it is seen more frequently in the cerebellum, whereas in adults
it has a predilection for the cerebral hemispheres and basal ganglion.
The appearance of a tuberculoma varies on MRI depending on its
stage of maturation.50,51 A non-caseating granuloma is hyperintense
on T2 and hypointense on T1 and shows solid enhancement, while a
solid caseating granuloma is usually hypointense on both T1 and T2
images. On CT, tuberculomas appear as round or lobulated soft tissue
masses with varying attenuation and homogeneous or ring
enhancement.1 Miliary TB is often associated with TB meningitis
and presents as small (<2 mm) foci of hyperintensity on T2
acquisitions, while after gadolinium administration, T1 images show
numerous, round, small, homogeneous, enhancing lesions.50 Con-
trast-enhanced MRI is also superior to CT for the evaluation of
meningitis and its complications, including hydrocephalus.1
Abdominal lymphadenopathy is the most common manifesta-
tion of abdominal TB, seen in 55–66% of patients, and may or may
not be associated with other abdominal organ involvement.52
Abdominal lymph nodes are best evaluated on CT, which reveals
enlarged nodes with hypoattenuating centres and hyperattenuat-
ing enhancing rims.52,53 On MRI, the appearance is typically
hypointense on T1 images, whereas on T2 images the signal is
generally hyperintense or with peripheral low-intensity signal.1
Hepatic TB can be classified into local, miliary TB, or
tuberculomas.54 Miliary TB is the most common form of liver TB
and is a part of generalized disease; innumerable small nodules are
found on the liver which may or may not be seen on CT, but on
ultrasound usually present as bright liver or spleen patterns in the
form of a diffuse increase in echogenicity.54
Calcification in the hepatic region on plain radiography may
occasionally be seen in local hepatic TB.54 On CT, liver tuberculoma
appears as a non-enhancing, central, low-density lesion with a
slightly enhancing peripheral rim, while liver calcifications can
also be demonstrated. MRI offers no added advantage in
diagnosing hepatobiliary TB.55
92 E. Skoura et al. / International Journal of Infectious Diseases 32 (2015) 87–93
Figure 6. Multiple intensity projection image (left panel) and fused trans-axial section 18F-FDG PET/CT images (right panel) showing 18F-FDG uptake in multiple lymph nodes
(SUVmax 6.8) (porta hepatis, portacaval, para-aortic, retroperitoneal, bilateral internal iliac, left external iliac, and left inguinal (arrows)) and heterogeneous 18F-FDG uptake in
the grossly enlarged spleen (SUVmax 10.2) (arrow) and in bones (T8 vertebra coupled with paravertebral soft tissue uptake (SUVmax 17.6), L3 vertebral body anteriorly (SUVmax
11.6), and the right sacral alae (SUVmax 6.7) (arrows)) (courtesy of Dr A. Alshammari).
Few reports are available on 18F-FDG PET/CT imaging in
abdominal TB, showing that the appearance of abdominal TB is
non-specific and varied (Figure 6).56–58
4. Assessment of treatment response
This is potentially the most important clinical application of 18F-
FDG PET/CT in TB. During anti-TB treatment, some bacillus-negative
tuberculomas do not decrease in size and may even increase, making
it difficult for the physician to decide whether or not to modify
treatment. In these cases, 18F-FDG PET/CT imaging may help, as the
changes in glycolytic activity within the inflammatory lesion,
measured by 18F-FDG uptake, correlate well with the clinical
markers of response.49 Several studies have confirmed the value of
18
F-FDG PET/CT in the follow-up and evaluation of the treatment
response, especially in patients with extrapulmonary involvement
and when drug resistance is prevalent.57,59–63 In pulmonary and
extrapulmonary TB, a decrease of approximately one-third in
SUVmax has been reported after 1 month of anti-TB treatment when
there is a good response.60 Initial data has shown that SUVmax (both
early and delayed) of involved lymph nodes and the number of
involved lymph node basins are significantly higher in non-
responders than in responders.64 These findings warrant further
confirmation in larger cohorts of patients.
After 4 months of anti-TB treatment 18F-FDG PET/CT can also
evaluate the treatment response in patients with high sensitivity and
specificity, using the value of 4.5 as the SUVmax cut-off.62
Other authors have aimed to monitor the metabolic changes in
spinal TB during the course of therapy.49 The mean changes in
SUVmax at various time points – from baseline to 6, 12, and
18 months, from 6 to 12 months, from 6 to 18 months, and from 12 to
18 months – were calculated and found to be highly significant (p-
value <0.001).49 18F-FDG PET/CT also shows encouraging results for
the prognosis and detection of residual disease in patients with
spinal infection, particularly when MRI is unconvincing in distin-
guishing between degenerative changes and infection.65
5. Tuberculosis in HIV patients
The diagnosis of active PTB is a major challenge, especially
in individuals with severe immunosuppression, such as those
co-infected with HIV. Such patients characteristically demon-
strate an atypical radiographic pattern, for example middle and
lower lung involvement, absence of cavity formation, presence
of lymphadenopathy and pleural effusions, or a miliary pattern.38
The radiographic appearance of HIV-associated PTB has been
found to be dependent on the level of immunosuppression at the
time of overt disease.66 Radiological manifestations in patients
with a CD4 T-lymphocyte count of <200/mm3 show a higher
incidence of mediastinal or hilar lymph node enlargement, a lower
prevalence of cavitation, and often extrapulmonary involvement
compared with HIV patients with a CD4 T-lymphocyte count of
#200/mm3.66 A study performed to determine the CT spectrum of
PTB in HIV patients showed nodular opacities (in 78.5% of cases),
consolidation (46.4%), lymphadenopathy (35.7%), pleural effusion
(35.7%), ground glass opacity (21.4%), and cavitation (21.4%).67
Other authors have reported that features of post-primary PTB are
patchy consolidation with involvement at unusual sites.68 Cavita-
tion is less common at lower CD4 counts. Patients with severe
immunosuppression have an increased incidence of miliary
pulmonary disease, with diffuse, randomly distributed nodules
on CT.69 Mediastinal and hilar lymphadenopathy occurs in 75–77%
of cases and is more commonly seen in HIV-positive than in HIV-
negative patients.68 Extrapulmonary localizations are frequent in
HIV-infected patients and may involve brain, pericardium,
gastrointestinal tract, peritoneum, and genitourinary tract.70
Currently there are no data to support the use of 18F-FDG PET/
CT in this patient group.
Funding: None.
Ethical approval: Ethical approval was not required.
Conflict of interest: All authors have no competing interests to
declare.
References
1. Bomanji JB, Gupta N, Gulati P, Das CJ. Imaging in tuberculosis. In: Kaufmann SH,
Rubin E, Zumla A, editors. Clinical tuberculosis. New York: Cold Spring Harbor
Laboratory Press; 2014.
2. Jones HA, Clark RJ, Rhodes CG, Schofield JB, Krausz T, Haslett C. In vivo
measurement of neutrophil activity in experimental lung inflammation. Am J
Respir Crit Care Med 1994;149:1635–9.
3. Kim IJ, Lee JS, Kim SJ, Kim YK, Jeong YJ, Jun S, et al. Double-phase 18F-FDG PET-
CT for determination of pulmonary tuberculoma activity. Eur J Nucl Med Mol
Imaging 2008;35:808–14.
 E. Skoura et al. / International Journal of Infectious Diseases 32 (2015) 87–93
4. Hahm CR, Park HY, Jeon K, Um SW, Suh GY, Chung MP, et al. Solitary pulmonary
nodules caused by Mycobacterium tuberculosis and Mycobacterium avium
complex. Lung 2010;188:25–31.
5. Van Dyck P, Vanhoenacker FM, Van den Brande P, De Schepper AM. Imaging of
pulmonary tuberculosis. Eur Radiol 2003;13:1771–85.
6. Burrill J, Williams CJ, Bain G, Conder G, Hine AL, Misra RR. Tuberculosis: a
radiologic review. Radiographics 2007;27:1255–7.
7. Leung AN, Muller NL, Pineda PR, FitzGerald JM. Primary tuberculosis in child-
hood: radiographic manifestations. Radiology 1992;182:87–91.
8. Pombo F, Rodriguez E, Mato J, Perez-Fontan J, Rivera E, Valvuena L. Patterns of
contrast enhancement of tuberculous lymph nodes demonstrated by computed
tomography. Clin Radiol 1992;46:13–7.
9. Kim WS, Moon WK, Kim IO, Lee HJ, Im JG, Yeon KM, et al. Pulmonary tubercu-
losis in children: CT evaluation. Am J Roentgenol 1997;168:1005–9.
10. Soussan M, Brillet PY, Mekinian A, Khafagy A, Nicolas P, Vessieres A, Brauner M.
Patterns of pulmonary tuberculosis on FDG-PET/CT. Eur J Radiol 2012;81:2872–6.
11. Li Y, Su M, Li F, Kuang A, Tian R. The value of (18)F-FDG-PET/CT in the
differential diagnosis of solitary pulmonary nodules in areas with a high
incidence of tuberculosis. Ann Nucl Med 2011;25:804–11.
12. Yen RF, Chen KC, Lee JM, Chang YC, Wang J, Cheng MF, et al. 18F-FDG PET for the
lymph node staging of non-small cell lung cancer in a tuberculosis-endemic
country: is dual time point imaging worth the effort? Eur J Nucl Med Mol Imaging
2008;35:1305–15.
13. Razak HR, Geso M, Abdul Rahim N, Nordin AJ. Imaging characteristics of
extrapulmonary tuberculosis lesions on dual time point imaging (DTPI) of
FDG PET/CT. J Med Imaging Radiat Oncol 2011;55:556–62.
14. Leung AN. Pulmonary tuberculosis: the essentials. Radiology 1999;210:307–22.
15. Krysl J, Korzeniewska-Kosela M, Muller NL, FitzGerald JM. Radiologic features
of pulmonary tuberculosis: an assessment of 188 cases. Can Assoc Radiol J
1994;45:101–7.
16. Lee KS, Im JG. CT in adults with tuberculosis of the chest: characteristic findings
and role in management. AJR Am J Roentgenol 1995;164:1361–7.
17. Verma N, Chung JH, Mohammed TL. Tree-in-bud sign. J Thorac Imaging
2012;27:W27.
18. Curvo-Semedo L, Teixeira L, Caseiro-Alves F. Tuberculosis of the chest. Eur J
Radiol 2005;55:158–72.
19. Rodriguez E, Soler R, Juffé A, Salgado L. CT and MR findings in a calcified
myocardial tuberculoma of the left ventricle. J Comput Assist Tomogr
2001;25:577–9.
20. Sochocky S. Tuberculoma of the lung. Am Rev Tuberc 1958;78:403–10.
21. Lee KS, Song KS, Lim TH, Kim PN, Kim IY, Lee BH. Adult-onset pulmonary
tuberculosis: findings on chest radiographs and CT scans. Am J Roentgenol
1993;160:753–8.
22. Goo JM, Im JG, Do KH, Yeo JS, Seo JB, Kim HY, et al. Pulmonary tuberculoma
evaluated by means of FDG PET: findings in 10 cases. Radiology 2000;216:
117–21.
23. Sathekge MM, Maes A, Pottel H, Stoltz A, van de Wiele C. Dual time-point FDG
PET-CT for differentiating benign from malignant solitary pulmonary nodules
in a TB endemic area. S Afr Med J 2010;100:598–601.
24. Chen CJ, Lee BF, Yao WJ, Cheng L, Wu PS, Chu CL, et al. Dual-phase 18F-FDG PET
in the diagnosis of pulmonary nodules with an initial standard uptake value less
than 2.5. AJR Am J Roentgenol 2008;191:475–9.
25. Hara T, Kosaka N, Suzuki T, Kudo K, Niino H. Uptake rates of 18F-fluorodeox-
yglucose and 11C-choline in lung cancer and pulmonary tuberculosis: a posi-
tron emission tomography study. Chest 2003;124:893–901.
26. Jeong YJ, Lee KS. Pulmonary tuberculosis: up-to-date imaging and manage-
ment. AJR Am J Roentgenol 2008;191:834–44.
27. Kwong JS, Carignan S, Kang EY, Muller NL, FitzGerald JM. Miliary tuberculosis:
diagnostic accuracy of chest radiography. Chest 1996;110:339–42.
28. Yilmaz MU, Kumcuoglu Z, Utkaner G, Yalniz O, Erkmen G. CT findings of
tuberculous pleurisy. Int J Tuberc Lung Dis 1998;2:164–7.
29. Kim Y, Song KS, Goo JM, Lee JS, Lee KS, Lim TH. Thoracic sequelae and
complications of tuberculosis. Radiographics 2001;21:839–58.
30. Yeh CL, Chen LK, Chen SW, Chen YK. Abnormal FDG PET imaging in tuberculosis
appearing like mesothelioma: anatomic delineation by CT can aid in differential
diagnosis. Clin Nucl Med 2009;34:815–7.
31. Lee KS, Hwang JW, Chung MP, Kim H, Kwon OJ. Utility of CT in the evaluation of
pulmonary tuberculosis in patients without AIDS. Chest 1996;110:977–84.
32. Im JG, Itoh H, Shim YS, Lee JH, Ahn J, Han MC, et al. Pulmonary tuberculosis: CT
findings—early active disease and sequential change with antituberculous
therapy. Radiology 1993;186:653–60.
33. Hulnick DH, Naidich DP, McCauley DI. Pleural tuberculosis evaluated by
computed tomography. Radiology 1983;149:759–65.
34. Yeh JJ, Chen SC, Teng WB, Chou CH, Hsieh SP, Lee TL, et al. Identifying the most
infectious lesions in pulmonary tuberculosis by high-resolution multi-detector
computed tomography. Eur Radiol 2010;20:2135–45.
35. Raniga S, Parikh N, Arora A. Is HRCT reliable in determining disease activity in
pulmonary tuberculosis. Indian J Radiol Imaging 2006;16:221–8.
36. Heysell SK, Thomas TA, Sifri CD, Rehm PK, Houpt ER. 18-Fluorodeoxyglucose
positron emission tomography for tuberculosis diagnosis and management: a
case series. BMC Pulm Med 2013;13:14.
37. Jeong YJ, Paeng JC, Nam HY, Lee JS, Lee SM, Yoo CG, et al. (18)F-FDG positron-
emission tomography/computed tomography findings of radiographic lesions
suggesting old healed tuberculosis. J Korean Med Sci 2014;29:386–91.
38. Vorster M, Sathekge MM, Bomanji J. Advances in imaging of tuberculosis: the
role of 18F-FDG PET and PET/CT. Curr Opin Pulm Med 2014;20:287–93.
93
39. Martini M, Ouahes M. Bone and joint tuberculosis: a review of 652 cases.
Orthopedics 1988;11:861–6.
40. Weaver P, Lifeso R. The radiological diagnosis of tuberculosis of the adult spine.
Skeletal Radiol 1984;12:178–86.
41. Hoffman EB, Crosier JH, Cremin BJ. Imaging in children with spinal tuberculosis:
a comparison of radiography, computed tomography and magnetic resonance
imaging. J Bone Joint Surg Br 1993;75:233–9.
42. Modic MT, Feiglin DH, Piraino DW, Boumphrey F, Weinstein MA, Duchesneau
PM, et al. Vertebral osteomyelitis: assessment using MR. Radiology 1985;157:
157–66.
43. Akman S, Sirvanci M, Talu U, Gogus A, Hamzaoglu A. Magnetic resonance
imaging of tuberculous spondylitis. Orthopedics 2003;26:69–73.
44. Gabrielli A, Layon AJ, Yu M. Chapter 73: Neurological infections. In: Civetta,
Taylor, and Kirby’s (Eds) manual of critical care 2012, Lippincott Williams &
Wilkins; Philadelphia.
45. Lee IS, Lee JS, Kim SJ, Jun S, Suh KT. Fluorine-18-fluorodeoxyglucose positron
emission tomography/computed tomography imaging in pyogenic and tu-
berculous spondylitis: preliminary study. J Comput Assist Tomogr 2009;33:
587–92.
46. Gratz S, Dörner J, Fischer U, Behr TM, Béhé M, Altenvoerde G, et al. 18F-FDG
hybrid PET in patients with suspected spondylitis. Eur J Nucl Med Mol Imaging
2002;29:516–24.
47. Rivas-Garcia A, Sarria-Estrada S, Torrents-Odin C, Casas-Gomila L, Franquet E.
Imaging findings of Pott’s disease. Eur Spine J 2013;22(Suppl 4):567–78.
48. Kim SJ, Lee JS, Suh KT, Kim IJ, Kim YK. Differentiation of tuberculous and
pyogenic spondylitis using double phase F-18 FDG PET. Open Med Imaging J
2008;2:1–6.
49. Dureja S, Sen IB, Acharya S. Potential role of F18 FDG PET-CT as an imaging
biomarker for the noninvasive evaluation in uncomplicated skeletal tubercu-
losis: a prospective clinical observational study. Eur Spine J 2014 [Epub ahead of
print].
50. Trivedi R, Saksena S, Gupta RK. Magnetic resonance imaging in central nervous
system tuberculosis. Indian J Radiol Imaging 2009;19:256–65.
51. Celso L, da Cruz Jr H, Domingues RC. Intracranial infections. In: Atlas SW,
editor. Magnetic resonance imaging of the brain and spine. 4th ed., Philadelphia:
Lippincott Williams & Wilkins; 2009. p. 929–1026.
52. Leder RA, Low VH. Tuberculosis of the abdomen. Radiol Clin North Am
1995;33:691–705.
53. Denton T, Hossain J. A radiological study of abdominal tuberculosis in a Saudi
population, with special reference to ultrasound and computed tomography.
Clin Radiol 1993;47:409–14.
54. Chaudhary P. Hepatobiliary tuberculosis. Ann Gastroenterol 2014;27:207–11.
55. Reed DH, Nash AF, Valabhji P. Radiological diagnosis and management of a
solitary tuberculous hepatic abscess. Br J Radiol 1990;63:902–4.
56. Takalkar AM, Bruno GL, Reddy M, Lilien DL. Intense FDG activity in peritoneal
tuberculosis mimics peritoneal carcinomatosis. Clin Nucl Med 2007;32:244–6.
57. Tian G, Xiao Y, Chen B, Xia J, Guan H, Deng Q. FDG PET/CT for therapeutic
response monitoring in multi-site non-respiratory tuberculosis. Acta Radiol
2010;51:1002–6.
58. Jeffry L, Kerrou K, Camatte S, Lelievre L, Metzger U, Robin F, et al. Peritoneal
tuberculosis revealed by carcinomatosis on CT scan and uptake at FDG-PET.
BJOG 2003;110:1129–31.
59. Park IN, Ryu JS, Shim TS. Evaluation of therapeutic response of tuberculoma
using F-18 FDG positron emission tomography. Clin Nucl Med 2008;33:1–3.
60. Martinez V, Castilla-Lievre MA, Guillet-Caruba C, Grenier G, Fior R, Desarnaud S,
et al. (18)F-FDG PET/CT in tuberculosis: an early non-invasive marker of
therapeutic response. Int J Tuberc Lung Dis 2012;16:1180–5.
61. Park YH, Yu CM, Kim ES, Jung JO, Seo HS, Lee JH, et al. Monitoring therapeutic
response in a case of extrapulmonary tuberculosis by serial F-18 FDG PET/CT.
Nucl Med Mol Imaging 2012;46:69–72.
62. Sathekge M, Maes A, D’Asseler Y, Vorster M, Gongxeka H, Van de Wiele C.
Tuberculous lymphadenitis: FDG PET and CT findings in responsive and non-
responsive disease. Eur J Nucl Med Mol Imaging 2012;39:1184–90.
63. Hofmeyr A, Lau WF, Slavin MA. Mycobacterium tuberculosis infection in
patients with cancer, the role of 18-fluorodeoxyglucose positron emission
tomography for diagnosis and monitoring treatment response. Tuberculosis
(Edinb) 2007;87:459–63.
64. Sathekge M, Maes A, Kgomo M, Stoltz A, Van de Wiele C. Use of 18F-FDG PET to
predict response to first-line tuberculostatics in HIV-associated tuberculosis. J
Nucl Med 2011;52:880–5.
65. Kim SJ, Kim IJ, Suh KT, Kim YK, Lee JS. Prediction of residual disease of spine
infection using F-18 FDG PET/CT. Spine (Phila Pa 1976) 2009;34:2424–30.
66. Leung AN, Brauner MW, Gamsu G, Mlika-Cabanne N, Ben Romdhane H, Carette
MF, et al. Pulmonary tuberculosis: comparison of CT findings in HIV-seroposi-
tive and HIV-seronegative patients. Radiology 1996;198:687–91.
67. Atwal SS, Puranik S, Madhav RK, Ksv A, Sharma BB, Garga UC. High resolution
computed tomography lung spectrum in symptomatic adult HIV-positive
patients in South-East Asian nation. J Clin Diagn Res 2014;8:RC12–6.
68. Feng F, Yu-xin S, Gan-lin X, Ying Z, Hong-zhou Lu, Zhi-yong Z. Computed
tomography in predicting smear-negative pulmonary tuberculosis in AIDS
patients. Chin Med J 2013;126:3228–33.
69. Allen CM, Al-Jahdali HH, Irion KL, Ghanem SA, Gouda A, Khan AN. Imaging lung
manifestations of HIV/AIDS. Ann Thorac Med 2010;5:201–16.
70. Raviglione MC, Narain JP, Kochi A. HIV-associated tuberculosis in developing
countries: clinical features, diagnosis, and treatment. Bull World Health Organ
1992;70:515–26.