Primary tuberculosis is said to occur when clinically manifest infection follows

the first exposure to the organism. Ultimately, the ability of MTb to cause
human infection is related to the organism's ability to survive dormant within
host macrophages for long periods of time, and to incite a T-cell-mediated,
delayed hypersensitivity response by the infected host. Under normal
circumstances, the host will sequester the MTb organism by forming
granulomas. Usually, these granulomas show caseous necrosis, a pattern
characteristically, but not exclusively, associated with tuberculous infection.
The initial infection site has been termed the Ghon focus. Shortly after the
infection occurs, organisms may spread through the lymphatics to hilar and
mediastinal lymph nodes. Both sites usually heal with fibrosis and calcification.
The combination of the lung parenchymal and lymph node MTb infection sites
has been termed the Ranke or Ghon complex (figure 1).

Organisms within the active Ghon focus often gain access to the bloodstream
and may disseminate to extrathoracic organs; but, usually, host defenses are
sufficient to prevent overt infection from developing in extrathoracic sites. It is
important to remember that, although the pulmonary, lymphatic, and
extrathoracic foci of infection are usually inactive at this point, organisms
remain viable and may serve as the nidus for reactivation of disease when
circumstances become favorable. Primary MTb infection in children is usually
asymptomatic, and may be detected only with the conversion of skin tests.
When symptoms occur, cough and fever are most common. In contrast, adults
with primary MTb infection are usually symptomatic, and may present with
weight loss, failure to thrive, fever, cough, and hemoptysis. Night sweats may
also occur.

Patients with primary MTb most often show no radiologic abnormalities. If

overt infection occurs, the pattern is usually one of air-space consolidation
(figure 2), often involving an entire lobe. The right lung is more commonly
affected than the left, although no definite zonal predominance is seen.
Cavitation in primary MTb is unusual, and miliary dissemination is similarly
uncommon.

Atelectasis is often encountered in children with primary MTb (figure 3), and
may be related to airway compression by enlarged lymph nodes. Less
commonly, rupture of an infected lymph node into an adjacent bronchus may
cause endobronchial dissemination of infection associated with atelectasis.
Adults with primary MTb uncommonly present with pulmonary atelectasis.

Radiographic abnormalities in primary MTb infections are often slow to

resolve, even with the institution of prompt treatment. Air-space opacities may
take more than 6 months to clear, and lymphadenopathy may take even longer
to resolve. Lymphadenopathy commonly occurs in children with primary MTb
infection. Usually hilar lymph nodes are involved, and mediastinal lymph
nodes, particularly in the right paratracheal region, may be enlarged, as well.
Unilateral lymphadenopathy is more often seen than is bilateral disease, and
occasionally lymph node enlargement may be the only radiographic finding
present. Lymphadenopathy is uncommon in adults with primary MTb, unless
they are immunocompromised (see later). Lymph nodes actively infected with
MTb quite commonly show central low attenuation, representing necrosis, on
contrast-enhanced CT. Pleural effusion may occur in patients with primary
MTb infection. Often, when tuberculosis is discovered as the cause of pleural
effusion, no parenchymal focus of disease is radiographically evident; this
pattern is considered characteristic of primary MTb pleural infection.
Usually such effusions are small and unilateral.

Progressive Primary Tuberculosis

Rarely, a parenchymal focus of primary MTb infection becomes rapidly
progressive. Extensive consolidation and cavitation develop, either at the site of
the initial pulmonary parenchymal focus of infection or in the apical and
posterior segments of the upper lobes. Thus, progressive primary MTb
infection may closely resembles postprimary MTb infection.

*Primary tuberculosis typically appears as air-space consolidation in the lower lobes,

hilar and mediastinal lymphadenopathy, pleural effusion, and miliary disease.
Postprimary tuberculosis appears most commonly as nodular and linear areas of increased
opacity or increased attenuation at the lung apex. Pleural effusion and miliary disease are
less common in postprimary tuberculosis

*In contrast to primary tuberculosis, in which fibrosis and healing are the rule, the
postprimary form of the disease tends to progress, with foci of inflammation and necrosis
enlarging to occupy greater portions of the lung parenchyma. During this process,
communication with airways is common. In addition to erosion into an airway, the
expanding infection may extend toward the periphery of the lung and rupture into the
pleural space, resulting in development of tuberculous empyema
*Tuberculoma and Thin-walled Cavity
Tuberculoma may be a manifestation of either primary or postprimary tuberculosis. In
postprimary tuberculosis, a tuberculoma is the main or only abnormality seen on chest
radiographs in approximately 5% of patients (14). It is a round or oval granuloma caused
by acid-fast bacilli with a wall lined by granulomatous inflammatory tissue or
encapsulated by connective tissue (1215). The central portion of the tuberculoma shows
caseation necrosis. A healed, filled-in cavity and a rounded-off, contracted, healing
tuberculous lesion are the reported possible mechanisms of tuberculoma formation.
Calcification is found in 20%30% of tuberculomas and is usually nodular and diffuse
(12) (Fig 1).

Residual thin-walled cavities may be seen in both active and inactive disease. After
antituberculous chemotherapy, the tuberculous cavity may disappear; occasionally, the
wall becomes paper-thin and an air-filled cystic space remains (8). Serial imaging helps
determine the stability or activity of pulmonary disease. The wall of a chronic cavity
varies from 1 cm to less than 1 mm in thickness and may be smooth, sometimes
simulating an emphysematous bulla (Fig 2). It can be difficult to distinguish true cavities
from bullae, cysts, or pneumatoceles

Cicatrization and Destruction of the Lung

Cicatrization atelectasis is a common finding after postprimary tuberculosis. Up to 40%
of patients with postprimary tuberculosis have a marked fibrotic response, which
manifests as atelectasis of the upper lobe, retraction of the hilum, compensatory lower
lobe hyperinflation, and mediastinal shift toward the fibrotic lung. Tuberculosis is almost
always present in the opposite upper lobe (8,16). A nonspecific radiologic pattern of
fibrosis consisting of parenchymal bands, fibrotic nodules and cavities, or traction
bronchiectasis is occasionally encountered (Fig 3). Apical pleural thickening associated
with fibrosis may reveal proliferation of extrapleural fatty tissue and peripheral atelectasis
at CT

Aspergilloma
Approximately 25%55% of patients with aspergilloma have a history of chronic cavitary
tuberculosis. The prevalence of aspergilloma associated with chronic tuberculosis has
been reported to be 11% (8). Although aspergilloma may exist for years without
symptoms, hemoptysis is the most common clinical complication, with a prevalence of
50%90% (18). Aspergilloma is usually located within a cavity or ectatic bronchus and
consists of masses of fungal hyphae admixed with mucus and cellular debris (1821).

At radiography, a mobile, rounded mass surrounded by a crescentic air shadow is noted

inside a lung cavity (air-crescent sign) (Fig 6a). CT demonstrates a mobile fungus ball,
usually with air interspersed between the masses of mycelia (Fig 6b). Calcification of the
mycelial ball occurs in some cases (1821). Thickening of the walls of tuberculous
cavities or of the adjacent pleura is reported to be an early radiographic sign (8) (Fig 7).

Bronchogenic Carcinoma
Bronchogenic carcinoma and pulmonary tuberculosis often coexist, creating a difficult
diagnostic problem. Manifestations of carcinoma may be obscured or misinterpreted as
progression of tuberculosis. Tuberculosis may favor the development of bronchogenic
carcinoma by local mechanisms (scar cancer), or tuberculosis and carcinoma may be
coincidentally associated. In addition, carcinoma may lead to reactivation of tuberculosis,
both by eroding into an encapsulated focus and by decreasing the patients resistance (22
25). Therefore, any predominant or growing nodule should be suspicious for coexisting
lung cancer in patients with tuberculosis

Bronchiectasis
Bronchiectasis may develop as a result of tuberculous involvement of the bronchial wall
and subsequent fibrosis. Bronchiectasis is seen in 30%60% of patients with active
postprimary tuberculosis and in 71%86% of patients with inactive disease at high-
resolution CT (26,27). Although bronchiectasis in postprimary tuberculosis can be a result
of cicatricial bronchostenosis after local infection (Fig 3), more commonly it occurs by
destruction and fibrosis of the lung parenchyma with secondary bronchial dilatation
(traction bronchiectasis) (Fig 9). Bronchiectasis located in the apical and posterior
segments of the upper lobe is highly suggestive of a tuberculous origin (Figs 3, 10). When
multiple apical cavities are encountered, the possibility that cystic bronchiectasis is
present in addition to necrotic cavities must be considered (8,2628)

Tracheobronchial Stenosis
Tracheobronchial stenosis resulting from tuberculosis may be caused by granulomatous
changes in the tracheobronchial wall or by extrinsic pressure from enlarged peribronchial
lymph nodes. Endobronchial involvement occurs in approximately 2%4% of patients
with pulmonary tuberculosis (6). In tracheobronchial tuberculosis, the stenosis begins as
simple erythema and edema with lymphocytic infiltration of the submucosa followed by
tubercle formation. Extensive granulation tissue destroying and replacing the mucosa and
submucosa and subsequent fibrosis may result in tracheobronchial narrowing. The left
main bronchus is most frequently involved in fibrotic disease (2932).

On CT scans, irregular luminal narrowing with wall thickening, enhancement, and

enlarged adjacent mediastinal nodes are common findings in the active stage of stenosis.
The CT findings include concentric narrowing of the lumen, uniform thickening of the
wall, and involvement of a long bronchial segment in the fibrotic stage (Fig 11a).
Multiplanar and three-dimensional images are helpful in understanding tracheobronchial
status, particularly for evaluation of focal stenosis of the airways and the longitudinal
extent of tracheobronchial lesions (32) (Fig 11b).

Lymph Node Calcification and Extranodal Extension

Tuberculous mediastinal lymphadenitis is a frequent manifestation of primary pulmonary
tuberculosis. Although enlarged nodes occur in 83%96% of pediatric cases, the
prevalence of lymphadenopathy decreases with increasing age (4042). Pubertal and
young adult women, the elderly, and patients with acquired immunodeficiency syndrome
are the most commonly affected among adult patients (43). Tuberculous mediastinal
lymphadenitis is caused by the formation of tuberculous caseating granulomas in lymph
nodes, which more commonly involves the right side. In the active stage, the nodes have
central low attenuation and peripheral rim enhancement at CT, which correspond to
caseation or liquefaction necrosis and granulation tissue with inflammatory
hypervascularity, respectively, at pathologic analysis. With treatment, the nodes change in
appearance, first becoming homogeneous and finally disappearing or resulting in a
residual mass composed of fibrotic tissue and calcifications without low-attenuation areas
(44,45) (Fig 16). Extranodal extension may occur into adjacent structures such as the
bronchus, pericardium, and esophagus (Figs 1721).

Esophagomediastinal Fistula
Esophageal involvement by tuberculosis is rare. The most common cause of esophageal
tuberculosis is secondary involvement from adjacent tuberculous lymphadenitis.
Esophageal involvement results in strictures due to granulomatous inflammatory tissue in
active disease and scar tissue after healing, tracheobronchial or mediastinal fistulas, and
traction diverticula (8,46). Presenting symptoms may include fever, cough, weight loss,
dysphagia, chest discomfort, or back pain. The preferential involvement of the subcarinal
region occurs mainly because of the anatomic proximity of the esophagus to diseased
lymph nodes (47). When tuberculous lymph nodes erode the adjacent esophageal or
bronchial wall, an esophagonodal or esophagobronchial fistula may be formed, which
manifests as a localized gaseous collection within the mediastinum (46,47) (Figs 19, 20).

Pericardial Tuberculosis
Tuberculous pericarditis is reported to complicate up to 1% of cases of tuberculosis (48).
Pericardial involvement is commonly caused by extranodal extension of tuberculous
lymphadenitis into the pericardium because of the close anatomic relationship between
the lymph nodes and the posterior pericardial sac. The pericardium can also be involved
in miliary spread of the disease (12). At CT, lymphadenopathy and pericardial thickening
with or without effusion may be seen (Fig 21).

Constrictive pericarditis occurs in about 10% of patients with tuberculous pericarditis. It

is characterized by fibrous or calcific constrictive thickening of the pericardium, which
prevents normal diastolic filling of the heart (49). CT shows pericardial thickening of
more than 3 mm with or without pericardial effusion. Secondary CT findings are
dilatation of the inferior vena cava secondary to right-sided heart failure and acute
angulation or sinus configuration of the interventricular septum, which may be related to
redundancy of the septum secondary to the restriction of expansion of the pericardium
(49). Visceral pericardial calcification may occur at the atrioventricular grooves, the
interventricular grooves, or especially the crux of the heart (49) (Fig

Fibrosing Mediastinitis
Fibrosing mediastinitis is uncommon and involves the presence of excessive fibrosis in
the mediastinum (50). Although tuberculosis is an important cause of chronic
mediastinitis, tuberculous mediastinitis is rare; the most common cause of mediastinitis is
histoplasmosis (51). Tuberculous mediastinitis progresses insidiously without significant
clinical symptoms and may result in mild symptoms, including cough and low-grade
fever, and symptoms due to compression of the superior vena cava, esophagus, and
tracheobronchial tree (52). The mediastinal granulomatous lymph nodes coalesce, and the
development of multiple tuberculous granulomas creates both reactive fibrous changes
and acute inflammatory changes in the mediastinum. The granulomas evolve into
fibrosing mediastinitis when reactive changes predominate (50).

The radiographic findings include mediastinal widening or a localized mass. CT findings

include a mediastinal or hilar mass, calcification in the mass, tracheobronchial narrowing,
pulmonary vessel encasement, superior vena cava obstruction, and pulmonary infiltrates
(Fig 23). Pulmonary lesions in fibrosing mediastinitis may be caused by bronchial
obstruction with subsequent obstructive pneumonia or atelectasis or by obstruction of
major pulmonary veins with resultant pulmonary infarction (50,52).

Chronic Tuberculous Empyema and Fibrothorax

Pleural infection is usually caused by rupture of a subpleural caseous focus into the
pleural space; less commonly, it is caused by hematogenous dissemination and
contamination by adjacent infected lymph nodes. Tuberculous pleurisy progresses to
become chronic tuberculous empyema, which may be defined as persistent, grossly
purulent pleural fluid containing tubercle bacilli (5357). However, it may be difficult to
culture the bacilli in chronic empyema.

In chronic tuberculous empyema, CT scans show a focal fluid collection with pleural
thickening and calcification and with or without extrapleural fat proliferation (Fig 24).
Fibrothorax with diffuse pleural thickening but without effusion on CT scans suggests
inactivity (Fig 24) (5557). Chyliform or pseudochylous pleural effusion is a high-lipid
nonchylous effusion and is most commonly caused by tuberculous empyema. The
diseased pleura may result in an abnormally slow transfer of cholesterol and other lipids,
originating from degenerated red and white blood cells, out of the pleural space and lead
to accumulation of cholesterol in the pleural fluid (58,59). CT shows a fat-fluid or fat-
calcium level (Fig 25).

Bronchopleural Fistula
Bronchopleural fistula associated with tuberculosis usually follows trauma or a surgical
procedure but can also occur spontaneously, presumably due to an open pathway between
bronchus and pleura established by tuberculosis. High mortality can result from both the
acute and chronic phases. The former occurs because of toxicity, spread of disease, and
tension pneumothorax; the latter progresses to repeat small seedings and massive
aspiration of empyema fluid (60). The diagnosis is based on an increasing amount of
sputum production, air in the pleural space, a changing air-fluid level, and contralateral
spread of pneumonic infiltration. CT can demonstrate the sites of communication between
the pleural space and either one or more airways or the lung parenchyma in patients with
bronchopleural fistula (61) (Fig 26).

Pneumothorax
Pneumothorax secondary to tuberculosis often heralds severe and extensive pulmonary
involvement by the infectious process and the onset of bronchopleural fistula and
empyema. It occurs in approximately 5% of patients with postprimary tuberculosis,
usually in severe cavitary disease (Fig 27) but rarely in miliary tuberculosis (Fig 28). The
pathogenesis involves pleural caseous infiltrates that undergo liquefaction, resulting in
pleural necrosis and rupture. If any apical abnormality is seen after reexpansion of a
spontaneous pneumothorax, active tuberculosis should be considered. In some cases, the
lung will seal and reexpand over a long period in response to chemotherapy. However,
tube drainage is the treatment of choice (62,63).

*Pulmonary TB, especially postprimary disease, nearly always causes abnormalities

on chest radiographs. Typically, the disease is parenchymal without nodal enlargement,
and it manifests as cavitary lesions. Upper-lobe involvement with cavitation and the
absence of lymphadenopathy are helpful in distinguishing postprimary TB from primary
TB. In addition to the usually involved pulmonary segmentsnamely, the apical or
posterior segments of the upper lobe or the superior segment of a lower lobeanterior or
basal segments may be involved in as many as 75% of cases

Cavitation is a distinguishing feature of postprimary TB; this finding is seen on chest

radiographs in about half of the cases and is discernible on chest CT scans in most cases
(see Image 2). Typical cavities are thick walled and irregular. Air-fluid levels are
uncommon and usually indicate superinfection; however, in 9% of cases, air-fluid
levels can be seen in other circumstances. The persistence of cavitation without healing is
unusual and should be investigated to exclude mycetomas, particularly in patients with
persisting hemoptysis (see Image 3). Cavitation can lead to endobronchial spread to the
remaining lung (see Image 4) or rupture into the pleural space, where it can cause an
empyema or bronchopleural fistula. Cavitation can also cause pseudoaneurysms of the
pulmonary artery, which are called Rasmussen aneurysms