DOI:10.2214/AJR.07.3896
AJR 2008; 191:834-844
© American Roentgen Ray Society
Pulmonary Tuberculosis: Up-to-Date Imaging and Management
Yeon Joo Jeong1 and
Kyung Soo Lee2
1 Department of Diagnostic Radiology, Pusan National University Hospital, Pusan
National University School of Medicine and Medical Research Institute, Pusan,
Korea.
2 Department of Radiology and Center for Imaging Science, Samsung Medical
Center, Sungkyunkwan University School of Medicine, 50, Ilwon-Dong,
Kangnam-Ku, Seoul 135-710, Korea.
Received February 24, 2008;
accepted after revision April 11, 2008.
Supported by the SRC/ERC program of MOST/KOSEF (grant no.
R11-2002-103).
CME
This article is available for CME credit.
See
www.arrs.org
for more information.
Address correspondence to K. S. Lee
(kyungs.lee{at}samsung.com).
Abstract
OBJECTIVE. Pulmonary tuberculosis (TB) is a common worldwide
infection and a medical and social problem causing high mortality and
morbidity, especially in developing countries. The traditional imaging concept
of primary and reactivation TB has been recently challenged, and radiologic
features depend on the level of host immunity rather than the elapsed time
after the infection. We aimed to elaborate the new concept of the diagnosis
and treatment of pulmonary TB, to review the characteristic imaging findings
of various forms of pulmonary TB, and to assess the role of CT in the
diagnosis and management of pulmonary TB.
CONCLUSION. Fast and more accurate TB testing such as bacterial DNA
fingerprinting and whole-blood interferon-
assay has been
developed. Miliary or disseminated primary pattern or atypical manifestations
of pulmonary TB are common in patients with impaired immunity. CT plays an
important role in the detection of TB in patients in whom the chest radiograph
is normal or inconclusive, in the determination of disease activity, in the
detection of complication, and in the management of TB by providing a roadmap
for surgical treatment planning. PET scans using 18F-FDG or
11C-choline can sometimes help differentiate tuberculous granuloma
from lung malignancy.
Keywords: lung CT • lung disease • lung infection • tuberculosis • pulmonary
Introduction
Tuberculosis (TB) is an airborne infectious disease caused by
Mycobacterium tuberculosis and is a major cause of morbidity and
mortality, particularly in developing countries
[1–3].
In 2005, 8.8 million people developed active TB and 1.6 million died of the
disease [4]. Most cases occur
in Southeast Asia and Africa.
Patients with active pulmonary TB may be asymptomatic, have mild or
progressive dry cough, or present with multiple symptoms, including fever,
fatigue, weight loss, night sweats, and a cough that produces bloody sputum.
If TB is detected early and fully treated, people with the disease quickly
become noninfectious and eventually cured. However, multidrug-resistant (MDR)
and extensively drug-resistant TB, HIV-associated TB, and weak health systems
are major challenges. The World Health Organization is making an effort to
dramatically reduce the burden of TB and to halve TB deaths and prevalence by
2015, through its Stop TB Strategy and supporting the Global Plan to Stop TB
[5].
The prompt diagnosis of TB is essential for community public health
infection control measures as well as for ensuring the appropriate therapy for
infected patients. Unfortunately, acid-fast bacilli are found in the sputum in
a limited number of patients with active pulmonary TB
[6]. Therefore, the imaging
diagnosis would provide an appropriate therapy for infected patients before
the definitive diagnosis by the bacteriology. The aim of this article is to
elaborate new concepts in the diagnosis and treatment of pulmonary TB in the
21st century, to review the characteristic imaging findings of various forms
of pulmonary TB, and to assess the role of CT in the diagnosis and management
of pulmonary TB.
Development of Infection and Pathogenesis
M. tuberculosis is an aerobic, nonmotile, non-spore-forming rod
that is highly resistant to drying, acid, and alcohol. It is transmitted from
person to person via droplet nuclei containing the organism and is spread
mainly by coughing. A person with active but untreated TB infects
approximately 10–15 other people per year. The probability of
transmission from one person to another depends on the number of infectious
droplets expelled by a carrier, the duration of exposure, and the virulence of
the M. tuberculosis. The risk of developing active TB is greatest in
patients with altered host cellular immunity, including extremes of age,
malnutrition, cancer, immunosuppressive therapy, HIV infection, end-stage
renal disease, and diabetes.
TB infection begins when the mycobacteria reach the pulmonary alveoli,
where they invade and replicate within alveolar macrophages. Inhaled
mycobacteria are phagocytized by alveolar macrophages, which interact with T
lymphocytes, resulting in differentiation of macrophages into epithelioid
histiocytes [7]. Epithelioid
histiocytes and lymphocytes aggregate into small clusters, resulting in
granulomas. In the granuloma, CD4 T lymphocytes (effector T cell) secrete
cytokines, such as interferon-, which activate macrophages to destroy
the bacteria with which they are infected. CD8 T lymphocytes (cytotoxic T
cell) can also directly kill infected cells
[8]. Importantly, bacteria are
not always eliminated from the granuloma, but can become dormant, resulting in
a latent infection. Another feature of human TB granulomas is the development
of necrosis in the center of the tubercles.
The primary site of infection in the lungs is called the Ghon focus
[9]. It either enlarges as
disease progresses or, much more commonly, undergoes healing. Healing may
result in a visible scar that may be dense and contain foci of calcification.
During the early stage of infection, organisms commonly spread via lymphatic
channels to regional hilar and mediastinal lymph nodes and via the bloodstream
to more distant sites in the body. The combination of the Ghon focus and
affected lymph nodes is known as the Ranke complex. The initial infection is
usually clinically silent. In approximately 5% of infected individuals,
immunity is inadequate and clinically active disease develops within 1 year of
infection, a condition known as progressive primary infection
[10]. For most infected
individuals, however, TB remains clinically and microbiologically latent for
many years.
In approximately 5% of the infected population, endogenous reactivation of
latent infection develops many years after the initial infection (this has
also been called "postprimary TB")
[10]. The reactivation TB
tends to involve predominantly the apical and posterior segments of the upper
lobes and the superior segments of the lower lobes. This location is likely
due to a combination of relatively higher oxygen tension and impaired
lymphatic drainage in these regions
[11]. As distinct from primary
infection site, in which healing is the rule, reactivation TB tends to
progress. The main abnormalities are progressive extension of inflammation and
necrosis, frequently with development of communication with the airways and
cavity formation. The endobronchial spread of necrotic material from a cavity
may result in TB infection in the same or in other lobes. Hematogenous
dissemination may result in miliary TB.
Diagnosis
A definitive diagnosis of TB can only be made by culturing M.
tuberculosis organisms from a specimen taken from the patient. However,
TB can be a difficult disease to diagnose, mainly because of the difficulty in
culturing this slow-growing organism in the laboratory. A complete evaluation
for TB must include a medical history, a chest radiograph, a physical
examination, and microbiologic smears and cultures. It may also include a
tuberculin skin test and a serologic test.
The treatment of latent TB infection to prevent progression to active
disease has been an essential component of public health efforts to eliminate
TB [12]. Currently, latent
infection is diagnosed in a nonimmunized person by a tuberculin skin test
(TST), which yields a delayed-hypersensitivity-type response to purified
protein derivatives of M. tuberculosis. However, the TST, which has
been used for years for the diagnosis of latent TB infection, has many
limitations, including falsepositive test results in individuals who were
vaccinated with bacille Calmette-Guérin (BCG) and in individuals who
have infections not related to M. tuberculosis
[13,
14].
Discovery of the role of T lymphocytes and interferon- in the immune
process has led to the development of an in vitro assay for cell-mediated
immune reactivity to M. tuberculosis
[15]. Recently, this
whole-blood interferon- assay has been introduced for the diagnosis of
latent TB infection and has shown a higher diagnostic accuracy than the TST
[13,
16]. These new TB tests are
being developed with the hope of cheap, fast, and more accurate TB testing.
These new tests use polymerase chain reaction detection of bacterial DNA and
whole-blood interferon- assay
[17]. Individuals with a
positive TST or whole-blood interferon- assay, especially HIV-infected
persons or those who have chest radiographic or CT findings consistent with
TB, should be considered for treatment of a latent infection
[18].
New Concept of Radiologic Manifestations of Tuberculosis
Patients who develop disease after initial exposure are considered to have
primary TB, whereas patients who develop disease as a result of reactivation
of a previous focus of TB are considered to have reactivation TB.
Traditionally, it was believed that the clinical, pathologic, and radiologic
manifestations of reactivation TB were quite distinct from those of primary
TB. This concept has been recently challenged on the basis of DNA
fingerprinting.
DNA fingerprint pattern with restriction fragment length polymorphism
(RFLP) analysis of M. tuberculosis isolates can give clinicians an
insight into the transmission of TB
[19]. Isolates from patients
infected with epidemiologically unrelated strains of TB have different RFLP
patterns, whereas those from patients with epidemiologically linked strains
generally have identical RFLP patterns. Therefore, clustered cases of TB,
defined as those in which the isolates have identical or closely related
genotypes, have usually been transmitted recently. In contrast, cases in which
the isolates have distinctive genotypes generally are a reactivation of
infection acquired in the distant past
[20,
21].
A recent study based on genotyping M. tuberculosis isolates with
RFLP showed that the radiographic features are often similar in patients who
apparently have a primary disease and those who have a reactivation TB
[22,
23]. Therefore, time from
acquisition of infection to the development of clinical disease does not
reliably predict the radiographic appearance of TB. The only independent
predictor of radiographic appearance may be integrity of the host immune
response; namely, severely immunocompromised patients show a tendency to have
the primary form of TB, whereas immunocompetent patients tend to have the
reactivation form [22,
23]. Because this result is
preliminary and most published data are based on the traditional concept of
primary and reactivation disease, we follow the traditional outline in this
article.
Radiologic Manifestations in Immunocompetent Hosts
Primary Tuberculosis
The initial parenchymal focus of TB may enlarge and result in an area of
airspace consolidation or, more commonly, undergo healing by transformation of
the granulomatous tissue into mature fibrous tissue. Primary TB occurs most
commonly in children but is being seen with increasing frequency in adults
[24]. The most common
abnormality in children is lymph node enlargement, which is seen in
90–95% of cases [25,
26]. The lymphadenopathy is
usually unilateral and located in the hilum or the paratracheal region. On CT,
the enlarged nodes typically show central low attenuation, which represents
caseous necrosis, and peripheral rim enhancement, which represents the
vascular rim of the granulomatous inflammatory tissue
[27,
28] (Fig.
1A,
1B).
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Fig. 1A —Primary tuberculosis manifesting primarily as lymphadenopathy
in 26-year-old woman. Posteroanterior chest radiograph shows right hilar mass
(arrow). Note smaller nodule (arrowhead) in right upper lung
zone.
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Fig. 1B —Primary tuberculosis manifesting primarily as lymphadenopathy
in 26-year-old woman. Contrast-enhanced transverse CT scan (5.0-mm section
thickness) obtained at level of basal trunk using mediastinal window setting
shows enlarged right hilar and subcarinal lymph nodes (arrows),
central necrotic low attenuation, and peripheral rim enhancement.
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Airspace consolidation, related to parenchymal granulomatous inflammation
and usually unilateral, is evident radiographically in approximately 70% of
children with primary TB [26].
It shows no predilection for any particular lung zone
[26]. On CT, the parenchymal
consolidation in primary TB is most commonly dense and homogeneous but may
also be patchy, linear, nodular, or mass-like
[29] (Fig.
2A,
2B).
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Fig. 2B —Primary tuberculosis presenting with consolidation and
lymphadenopathy in 21-year-old woman. Contrast-enhanced transverse CT scan
(5.0-mm section thickness) obtained at level of right middle lobar bronchus
using mediastinal window setting shows airspace consolidation in right middle
lobe. Note enlarged right hilar and subcarinal lymph nodes (arrows).
Hilar node has necrotic low attenuation.
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Pleural effusion is usually unilateral and on the same side as the primary
focus of TB. The effusion may be large and occur in patients without evidence
of parenchymal disease on chest radiographs
[30].
Reactivation Tuberculosis
The most common radiographic manifestation of reactivation pulmonary TB is
focal or patchy heterogeneous consolidation involving the apical and posterior
segments of the upper lobes and the superior segments of the lower lobes
[29,
31]. Another common finding is
the presence of poorly defined nodules and linear opacities, which are seen in
approximately 25% of patients
[31]. Cavities, the radiologic
hallmark of reactivation TB, are evident radiographically in 20–45% of
patients
[29–31].
In approximately 5% of patients with reactivation TB, the main manifestation
is a tuberculoma, defined as a sharply marginated round or oval lesion
measuring 0.5–4.0 cm in diameter
[29,
31]. Histologically, the
central part of the tuberculoma consists of caseous material and the
periphery, of epithelioid histiocytes and multinucleated giant cells and a
variable amount of collagen. Satellite nodules around the tuberculoma may be
present in as many as 80% of cases
[32]. Because of active
glucose metabolism caused by active granulomatous inflammation, tuberculomas
sometimes have been reported to accumulate 18F-FDG and to cause PET
scans to be interpreted as false-positive for malignancy
[33]
(Fig. 3). Unlike
18F-FDG PET scans, 11C-choline PET scans can help
differentiate between lung cancer and tuberculoma
[34]. The standard uptake
value of tuberculoma is low in 11C-choline PET scans.
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Fig. 3 —Tuberculous granulomas in 58-year-old man. 18F-FDG
PET/CT scan shows increased FDG uptake in nodules—well-defined
predominant nodule (arrow) and surrounding smaller satellite nodules
(arrowheads)—in right upper lobe with maximum standard uptake
value of 6.1.
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Hilar or mediastinal lymphadenopathy is uncommon in reactivation TB, being
seen in approximately 5–10% of patients
[30,
31]. Pleural effusion,
typically unilateral, occurs in 15–20% of patients
[35].
The most common CT findings of reactivation pulmonary TB are centrilobular
small nodules, branching linear and nodular opacities (tree-in-bud sign),
patchy or lobular areas of consolidation, and cavitation
[24,
36,
37]. The centrilobular small
nodules and tree-in-bud sign reflect the presence of endobronchial spread and
are due to the presence of caseous necrosis and granulomatous inflammation
filling and surrounding terminal and respiratory bronchioles and alveolar
ducts [36,
38] (Fig.
4A,
4B,
4C,
4D,
4E). These tree-in-bud signs
are considered a reliable marker of the activity of the process
[6]. Cavitation is also a sign
of an active disease process and usually heals as a linear or fibrotic
lesion.
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Fig. 4B —Reactivation tuberculosis in 55-year-old man. High-resolution
CT scans (1.0-mm section thickness) obtained at levels of aortic arch
(B) and proximal ascending aorta (C) show consolidation and
acinus-sized nodules containing several cavities in both upper lobes. Note
branching nodular and linear opacities (tree-in-bud signs) (arrows)
and centrilobular small nodules (arrowheads, C) in both
lungs.
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Fig. 4C —Reactivation tuberculosis in 55-year-old man. High-resolution
CT scans (1.0-mm section thickness) obtained at levels of aortic arch
(B) and proximal ascending aorta (C) show consolidation and
acinus-sized nodules containing several cavities in both upper lobes. Note
branching nodular and linear opacities (tree-in-bud signs) (arrows)
and centrilobular small nodules (arrowheads, C) in both
lungs.
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Fig. 4D —Reactivation tuberculosis in 55-year-old man. Photograph of
gross specimen obtained at lobectomy from different patient shows multiple
foci of nodules and consolidation that are distinctly white, consistent with
caseous necrosis. Most have nodular appearance and some appear to be branching
(arrows), suggestive of airway-centered nature of lesions.
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Fig. 4E —Reactivation tuberculosis in 55-year-old man. Photomicrograph
of surgical specimen discloses multiple granulomas, each related to small
membranous bronchiole (arrows). Some granulomas show central caseous
necrosis (arrowhead). (H and E, x40)
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Although it is usually accompanied by parenchymal abnormalities, pleural
effusion may be the sole imaging manifestation of TB. In this particular
situation, the determination of pleural fluid adenosine deaminase (ADA) level
(elevated in TB pleurisy) can be helpful for the characterization of the
pleural fluid; the ADA assay has a sensitivity of 92% (95% CI, 90–93%)
and a specificity of 90% (89–91%) for diagnosing TB pleurisy
[39]. New subpleural lung
nodules may develop during medication for TB pleural effusion. It should not
be regarded as treatment failure. These paradoxical subpleural nodules will
eventually show improvement with continued medication
[40].
Miliary Tuberculosis
Miliary TB refers to widespread dissemination of TB by hematogenous spread.
It occurs in 2–6% of primary TB and also occurs somewhat more frequently
in reactivation TB [41]. In
the latter situation, miliary TB may be seen in association with typical
parenchymal changes or may be the only pulmonary abnormality. Each focus of
miliary infection results in local granulomas that, when well developed,
consist of a region of central necrosis surrounded by a relatively
well-delimited rim of epithelioid histiocytes and fibrous tissue.
The characteristic radiographic and high-resolution CT findings consist of
innumerable, 1- to 3-mm diameter nodules randomly distributed throughout both
lungs
[41–44]
(Fig. 5A,
5B). Thickening of
interlobular septa and fine intralobular networks are frequently evident
[37]. Diffuse or localized
ground-glass opacity is sometimes seen, which may herald acute respiratory
distress syndrome
[43–45]
(Fig. 6A,
6B,
6C).
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Fig. 5B —Miliary tuberculosis in 70-year-old man. High-resolution CT
image (1.0-mm section thickness) at level of right upper lobar bronchus shows
uniform-sized small nodules randomly distributed throughout both lungs. Note
subpleural and subfissural nodules (arrows).
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Fig. 6A —Miliary tuberculosis presenting as acute respiratory distress
syndrome in 47-year-old man. Posteroanterior chest radiograph shows
innumerable millet-sized nodular opacities and ground-glass opacities in both
lungs.
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Fig. 6B —Miliary tuberculosis presenting as acute respiratory distress
syndrome in 47-year-old man. High-resolution CT image (1.0-mm section
thickness) obtained at ventricular level shows randomly distributed small
nodules and extensive bilateral ground-glass opacity. Note interlobular septal
(arrows) and intralobular interstitial thickenings in both lungs.
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Fig. 6C —Miliary tuberculosis presenting as acute respiratory distress
syndrome in 47-year-old man. Photomicrograph of pathologic specimen obtained
with transbronchial lung biopsy discloses granuloma (arrows) in
alveolar wall. Diffuse alveolar wall thickening and intraalveolar fibrin
deposition (not shown) suggesting early stage of diffuse alveolar damage were
also observed. (H and E, x400)
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Airway Tuberculosis
The most common cause of inflammatory stricture of the bronchus is TB.
Tracheobronchial TB has been reported in 10–20% of all patients with
pulmonary TB [24,
46]. The principal CT findings
of airway TB are circumferential wall thickening and luminal narrowing, with
involvement of a long segment of the bronchi
[46,
47]. In active disease, the
airways are irregularly narrowed in their lumina and have thick walls, whereas
in fibrotic disease, the airways are smoothly narrowed and have thin walls
[46,
47]. The left main bronchus is
involved more frequently in fibrotic disease, whereas both main bronchi are
equally involved in active disease
[46] (Fig.
7A,
7B,
7C).
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Fig. 7A —Actively caseating bronchial tuberculosis in 42-year-old
woman. Contrast-enhanced transverse CT scans (5.0-mm section thickness) using
mediastinal window setting obtained at levels of thoracic inlet (A) and
main bronchi (B) show luminal narrowing of trachea and proximal left
main bronchus and irregular wall thickening. Note lymph nodes
(arrows, A) in mediastinum.
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Fig. 7B —Actively caseating bronchial tuberculosis in 42-year-old
woman. Contrast-enhanced transverse CT scans (5.0-mm section thickness) using
mediastinal window setting obtained at levels of thoracic inlet (A) and
main bronchi (B) show luminal narrowing of trachea and proximal left
main bronchus and irregular wall thickening. Note lymph nodes
(arrows, A) in mediastinum.
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Fig. 7C —Actively caseating bronchial tuberculosis in 42-year-old
woman. Bronchoscopy shows narrowed left main bronchial lumen with its mucosa
swollen and covered diffusely with whitish cheeselike substance
(arrow).
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Radiologic Manifestations in Immunocompromised Hosts
Impaired host immunity has been regarded as a predisposing factor in TB.
Known risk factors for development of active TB include conditions that are
associated with defects in cell-mediated immunity, such as HIV infection;
malnutrition; drug and alcohol abuse; malignancy; end-stage renal disease;
diabetes mellitus; and corticosteroid or other immunosuppressive therapy
[48]. Infliximab and
etanercept (used in the treatment of Crohn's disease and rheumatoid arthritis)
are human antibodies against tumor necrosis factor-
(TNF-),
which is involved in the host defense against TB—killing of M.
tuberculosis by macrophage, granuloma formation, or apoptosis and
prevention of dissemination of infection to other sites. Active TB may develop
soon after the initiation of treatment with such drugs. Therefore, before
prescribing these drugs, assessment of TB infection risk factors and a TST or
interferon- assay are strongly recommended to determine the patient's
latent TB infection status and the risk of active disease
[49,
50].
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Fig. 8A —Paradoxical worsening of tuberculous lymphadenitis associated
with immune reconstitution inflammatory syndrome in 40-year-old woman with
AIDS. Contrast-enhanced transverse CT scan (5.0-mm section thickness) using
mediastinal window setting obtained at level of aortic arch just before highly
active antiretroviral therapy, shows multiple enlarged lymph nodes
(arrows) with central necrotic low attenuation in prevascular and
right paratracheal areas. Patient's HIV RNA viral load and CD4 counts were
more than 1 million copies/mL and 35 cells/µL, respectively.
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Fig. 8B —Paradoxical worsening of tuberculous lymphadenitis associated
with immune reconstitution inflammatory syndrome in 40-year-old woman with
AIDS. Follow-up CT image obtained 3 months after A shows increased
extent of necrotic lymph nodes (arrows). Patient's HIV RNA viral load
and CD4 counts at this time were 433 copies/mL and 142 cells/µL,
respectively.
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Fig. 9A —Pulmonary tuberculosis with lymphadenopathy and
extrapulmonary involvement in 42-year-old man with AIDS. His CD4 count was 64
cells/µL. Posteroanterior chest radiograph shows multiple small nodular
opacities in both lungs, especially in upper lung zones.
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Fig. 9B —Pulmonary tuberculosis with lymphadenopathy and
extrapulmonary involvement in 42-year-old man with AIDS. His CD4 count was 64
cells/µL. High-resolution CT scan (1.0-mm section thickness) obtained at
level of aortic arch shows randomly distributed small nodules and interlobular
septal thickenings in both lungs.
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Fig. 9C —Pulmonary tuberculosis with lymphadenopathy and
extrapulmonary involvement in 42-year-old man with AIDS. His CD4 count was 64
cells/µL. Contrast-enhanced transverse CT scans (5.0-mm section thickness)
using mediastinal window setting obtained at levels of mandible (C) and
thoracic inlet (D) show enlarged lymph nodes (arrows), central
necrotic low attenuation, and peripheral rim enhancement in right neck and
left axilla.
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Fig. 9D —Pulmonary tuberculosis with lymphadenopathy and
extrapulmonary involvement in 42-year-old man with AIDS. His CD4 count was 64
cells/µL. Contrast-enhanced transverse CT scans (5.0-mm section thickness)
using mediastinal window setting obtained at levels of mandible (C) and
thoracic inlet (D) show enlarged lymph nodes (arrows), central
necrotic low attenuation, and peripheral rim enhancement in right neck and
left axilla.
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TB is a major cause of death among people living with HIV infection or
AIDS. In 2005, the World Health Organization (WHO) estimated that 12% of HIV
deaths globally were due to TB and that there were 630,000 new coinfections
with TB and HIV [51]. Immune
restoration induced by highly active anti-retroviral therapy (HAART) in
developed countries has considerably improved the outcome of HIV-positive
patients and reduced the prevalence of opportunistic infection and TB in these
patients. However, HIV-associated TB still continues to occur in countries
where HAART is widely used
[52]. Furthermore, HAART may
result in paradoxical worsening or TB manifestations in patients with immune
reconstitution inflammatory syndrome
[53,
54] (Fig.
8A,
8B).
The radiographic manifestations of HIV-associated pulmonary TB are thought
to be dependent on the level of immunosuppression at the time of overt disease
[55–57].
On CT, HIV-seropositive patients with a CD4 T lymphocyte count <
200/mm3 have a higher prevalence of mediastinal or hilar
lymphadenopathy, a lower prevalence of cavitation, and often extrapulmonary
involvement as compared with HIV-seropositive patients with a CD4 T lymphocyte
count equal to or 
200/mm3
[58] (Figs.
9A,
9B,
9C,
9D and
10A,
10B,
10C). Miliary or disseminated
disease has also been reported to be associated with severe immunosuppression
[58] (Fig.
9A,
9B,
9C,
9D).
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Fig. 10A —Pulmonary tuberculosis in 51-year-old man with AIDS. His CD4
count was 4 cells/µL. Posteroanterior chest radiograph shows multifocal
masslike airspace consolidation in bilateral upper lung zones.
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Fig. 10B —Pulmonary tuberculosis in 51-year-old man with AIDS. His CD4
count was 4 cells/µL. High-resolution CT scans (1.0-mm section thickness)
obtained at levels of left innominate vein (B) and azygos arch
(C) show masslike airspace consolidation with air bronchograms,
centrilobular small nodules (arrows, C), and ground-glass
opacity in both upper lobes.
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Fig. 10C —Pulmonary tuberculosis in 51-year-old man with AIDS. His CD4
count was 4 cells/µL. High-resolution CT scans (1.0-mm section thickness)
obtained at levels of left innominate vein (B) and azygos arch
(C) show masslike airspace consolidation with air bronchograms,
centrilobular small nodules (arrows, C), and ground-glass
opacity in both upper lobes.
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Fig. 11A —Multidrug-resistant tuberculosis in 36-yearold man.
Posteroanterior chest radiograph shows multiple small nodules, patchy
consolidation containing several cavities, and linear opacities in both lungs.
Note decreased volume in right lung and apical pleural thickening.
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Fig. 11B —Multidrug-resistant tuberculosis in 36-yearold man.
High-resolution CT scan (1.0-mm section thickness) obtained at level of left
basal trunk shows consolidation containing several cavities in right middle
lobe and right lower lobe. Note small cavitary nodule and centrilobular
nodules in left upper lobe.
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Unusual or atypical manifestations of pulmonary TB are common in patients
with impaired host immunity. In cases of active pulmonary TB, diabetic and
immunocompromised patients have a higher prevalence of multiple cavities in a
tuberculous lesion and of nonsegmental distribution than do patients without
underlying disease [48]. The
incidence of TB in patients with idiopathic pulmonary fibrosis (IPF) is more
than four times higher than that of the general population. Atypical
manifestations such as subpleural nodules or a lobar or segmental airspace
consolidation are common in patients with IPF, which may mimic lung cancer or
bacterial pneumonia [59].
Pulmonary TB in patients with systemic lupus erythematosus (SLE) has a higher
incidence and prevalence because of abnormal function of alveolar macrophages
and exposure to corticosteroid and cytotoxic drugs. TB in patients with SLE
tends to show radiologic findings of miliary dissemination, diffuse
consolidation, or primary TB
[60].
Radiologic Manifestations of Multidrug-Resistant Tuberculosis
Anti-TB drug resistance is a major public health problem that threatens the
success of global TB control. The major concerns of drug resistance are fear
regarding the spread of drug-resistant organisms and the ineffectiveness of
chemotherapy in patients infected with the resistant organisms. In addition,
MDR TB is a fatal disease because of the high mortality rate, depending on the
underlying diseases, particularly in HIV-infected patients
[61,
62].
Imaging findings of MDR TB do not basically differ from those of
drug-sensitive TB. However, multiple cavities and findings of chronicity, such
as bronchiectasis and calcified granulomas, are more common in patients with
MDR TB [63,
64] (Fig.
11A,
11B). A strong correlation
seems to exist between the radiologic features of MDR TB and the mode of
acquisition of drug-resistance. Patients with primary drug resistance, who
develop MDR TB without a history of anti-TB chemotherapy or a therapy history
of less than 1 month, were found to present with noncavitary consolidation,
pleural effusion, and a primary tuberculosis pattern of disease
[65]. On the other hand, those
who acquired MDR TB with a chemotherapy history of longer than 1 month often
show cavitary consolidations and in general show a reactivation pattern of the
disease.
Extensively-drug-resistant TB is defined as TB that has evolved resistance
to rifampin and isoniazid, as well as to any member of the quinolone family
and at least one of the following second-line TB treatments: kanamycin,
capreomycin, or amikacin [66].
Extensively-drug-resistant TB is associated with a much higher mortality rate
than MDR TB because of a reduced number of effective treatment options. The
epidemiology and imaging findings of extensively-drug-resistant TB have not
been well studied, but it is believed that the spread of
extensively-drug-resistant TB is closely associated with a high prevalence of
HIV and poor infection control
[67]. There has been no report
on radiologic findings of extensively-drug-resistant pulmonary TB; but in our
experience, the disease manifests an advanced pattern of primary TB (extensive
consolidation with or without lymphadenopathy) in AIDS patients and an
advanced pattern of MDR TB (multiple cavitary lesions in consolidative or
nodular lesions) in non-AIDS patients.
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Fig. 12A —Rasmussen aneurysm in chronic destructive pulmonary
tuberculosis in 62-year-old man. Contrast-enhanced transverse CT scan (2.5-mm
section thickness) obtained at level of main bronchi using mediastinal window
setting shows cavitary consolidation with air-crescent sign (low-attenuation
lesion and surrounding air) (arrow) in left upper lobe.
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Fig. 12B —Rasmussen aneurysm in chronic destructive pulmonary
tuberculosis in 62-year-old man. CT scan obtained 15 mm inferior to A
shows contrast-enhancing round vascular structure (arrow) in
consolidative lesion.
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Complications and Sequelae of Tuberculosis
A variety of thoracic sequelae and complications from pulmonary TB may
occur and may involve the lungs, airways, vessels, mediastinum, pleura, or
chest wall [47,
68–71]
(Appendix 1, Figs. 12A,
12B,
12C and
13A,
13B).
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Fig. 13A —Pleural and chest wall tuberculosis in 74-year-old man.
Posteroanterior chest radiograph shows loculated pleural fluid and pleural
calcification in right hemithorax. Soft-tissue bulging opacity is also
observed in right lower lateral chest wall (arrowheads). Note right
upper lobe volume loss, calcifications, and cavity.
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Fig. 13B —Pleural and chest wall tuberculosis in 74-year-old man.
Contrast-enhanced transverse CT scan (5.0-mm section thickness) obtained at
level of porta hepatis using mediastinal window setting shows pleural fluid
collection and visceral pleural calcification (arrow) in right
hemithorax, suggesting chronic tuberculous empyema. Lentiform chest wall
lesion (arrowhead) showing central low attenuation, consistent with
focal tuberculous chest wall abscess, is also seen.
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The radiologic manifestations of acute respiratory distress syndrome
secondary to TB include extensive bilateral areas of ground-glass opacity or
consolidation superimposed on findings of miliary or endobronchial spread of
TB. Multiple cystic lesions may develop in patients recovering from acute
respiratory distress syndrome or in patients with extensive consolidation due
to TB [71]. The cystic lesions
may resemble pneumatoceles or bullae, which may resolve over several months or
persist [71].
Rasmussen aneurysm is a pseudoaneurysm that results from weakening of the
pulmonary artery wall by adjacent cavitary TB (Fig.
12A,
12B,
12C). Empyema necessitatis
(Fig. 13A,
13B) results from leakage of
tuberculous empyema through the parietal pleura and discharge of its contents
into the subcutaneous tissues of the chest wall or, less commonly, into the
pericardium, vertebral column, or esophagus
[69].
CT in Tuberculosis
Chest radiographs play a major role in the screening, diagnosis, and
response to treatment of patients with TB. However, the radiographs may be
normal or show only mild or nonspecific findings in patients with active
disease [30]. Common causes of
a missed diagnosis of TB are failure to recognize hilar and mediastinal
lymphadenopathy as a manifestation of primary disease in adults, overlooking
of mild parenchymal abnormalities in patients with reactivation disease, and
failure to recognize that an upper lobe nodule or mass surrounded by small
nodular opacities or scarring may represent TB
[30].
CT is more sensitive than chest radiography in the detection and
characterization of both subtle localized or disseminated parenchymal disease
and mediastinal lymphadenopathy
[37,
42,
72,
73]. The radiographic
diagnosis of TB is initially correct in only 49% of all cases—34% for
the diagnosis of primary TB and 59% for the diagnosis of reactivation TB
[30]. With CT, the diagnosis
of pulmonary TB is correct in 91% of patients and TB is correctly excluded in
76% of patients [74]. CT and
high-resolution CT are particularly helpful in the detection of small foci of
cavitation in areas of confluent pneumonia and in areas of dense nodularity
and scarring [37]. In one
study of 41 patients with active TB
[37], high-resolution CT
showed cavities in 58%, whereas chest radiographs showed cavities in only
22%.
In addition to the diagnosis of TB, high-resolution CT is useful in
determining disease activity. A tentative diagnosis of active TB on CT could
be based on the pattern of parenchymal abnormalities and the presence of
cavitation or evidence of endobronchial spread, such as the presence of
centrilobular nodules or a tree-in-bud pattern. In the series by Lee et al.
[74], 80% of patients with
active disease and 89% of those with inactive disease were correctly
differentiated on high-resolution CT.
CT is also helpful in the evaluation of pleural complications, including
tuberculous effusion, empyema, and bronchopleural fistula, and may show
pleural disease that is not evident on chest radiography
[75].
In addition to its major role in the diagnosis of TB, CT plays an important
role in the management of TB, especially in complicated or MDR TB. MDR TB
often shows multiple cavities, which lead to the expectoration of a large
number of bacilli and endobronchial spread to previously unaffected areas of
the lung. Limited drug penetration into the cavities that harbor large numbers
of mycobacteria is believed to contribute to the drug resistance. Therefore,
surgery may be an adjuvant treatment for MDR TB, although present-day TB
treatment relies on chemotherapy
[76]. CT can locate the site
of cavitation and the extent of active disease and therefore can be a roadmap
for the planning of surgical treatment.
Conclusion
Although the slow reduction of the incidence of TB has been seen in
developed countries, TB is still a major challenge among infectious diseases,
even in the 21st century. Fast and accurate TB testing, such as bacterial DNA
analysis and whole-blood interferon- assay, has been developed for
detecting latent infection. The traditional imaging concept of primary and
reactivation TB has recently been challenged on the basis of DNA
fingerprinting, and radiologic features depend on the level of host immunity
rather than the elapsed time after the infection. PET scans using
18F-FDG or 11C-choline can sometimes help differentiate
a tuberculous nodule from lung malignancy. CT is an effective diagnostic
method when chest radiographs are normal or inconclusive, and it provides
valuable information for the diagnosis and management of TB.
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B. J. Marais, S. K. Parker, S. Verver, A. van Rie, and R. M. Warren
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Y. J. Jeong, W.-J. Koh, and K. S. Lee
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Abstract
Introduction
