AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Background

Tuberculosis is an infectious disease that has been known for centuries. Traditionally, the term tuberculosis has been used to indicate infections caused by Mycobacterium tuberculosis and Mycobacterium bovis; however, a multitude of causative mycobacteria are recognized.

Tuberculosis may involve multiple organs such as the lung, liver, spleen, kidney, brain, and bone. In endemic regions, the normal host immune response may be sufficient to contain the infection and prevent clinical presentation. Uncontrolled or uncontained infection may result in great morbidity and mortality.

For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center and Procedures Center . Also, see eMedicine's patient education articles Tuberculosis and Bronchoscopy.

Pathophysiology

Mycobacteria are non–spore-forming bacilli that are obligate aerobes. They are recognized microscopically by an intense staining with aniline dyes (notably carbol-fuchsin) and resistance to decoloration with acid washing; therefore, the term acid-fast bacilli is used to describe them. Unlike other bacteria, mycobacteria require enriched culture media and extended incubation (usually 2-8 wk). Therefore, bacteriologic recognition of a mycobacterial infection is a protracted process that may delay appropriate medical therapy. The advent of polymerase chain reaction (PCR) techniques has increased the rapidity with which tuberculous infection is diagnosed.

Tuberculous infection occurs as a consequence of the inhalation of bacillus-laden droplets expelled from an infected host. Given the stringent growth requirements of the organism, the development of an infection depends on prolonged exposure (on the order of weeks) to an individual with active pulmonary tuberculosis. Once the organism is inhaled, it travels via the airways to the pulmonary parenchyma, where it is deposited. Although the organism may be deposited in any lobe, a predilection for the lower lobes exists.

The organism is ingested by alveolar macrophages, which then attempt to phagocytize the bacilli. As a result of the natural defenses of the tubercle bacillus, alveolar macrophages may be unsuccessful in attempting to completely destroy the bacilli, which then lie dormant within the macrophage. As a consequence, bacilli often remain viable within the macrophages in immunocompetent individuals. Subsequently, bacilli may travel via the pulmonary lymphatics, or they may enter the vascular system and seed distant sites such as the liver, spleen, or bone marrow.

In most immunocompetent individuals, macrophages are successful in containing the bacilli, and the infection is self-limited and often subclinical. The contained infection in immunocompetent hosts is called primary tuberculosis. Primary tuberculosis is seen most often in children in endemic regions.^{1, 2} Since the advent of the AIDS era, adults may present with radiographic findings similar to those of primary tuberculosis.

In some patients, pulmonary macrophages are unable to contain the bacilli and are overwhelmed, leading to a clinically apparent infection. This is more common in patients who are immunocompromised, notably the population with HIV/AIDS.³ This form of tuberculosis is called progressive primary tuberculosis. Patients with progressive primary tuberculosis may present with pulmonary manifestations (often with miliary tuberculosis) or with manifestations of systemic or disseminated disease.

Postprimary (reactivation) tuberculosis is seen in patients in whom the initial infection was contained successfully by the pulmonary macrophages, with bacilli remaining viable within the macrophages. Infection results when the host's immune status (T cells) is compromised. This form may appear in the elderly population, for example.

Related eMedicine topics:
Mycobacterium Avium-Intracellulare
HIV Infection and AIDS

Related Medscape topics:
CME/CE Nontuberculous Mycobacteria
Resource Center HIV Pathogenesis
Resource Center HIV Transmission & Prevention

Frequency

United States

The incidence of tuberculosis markedly declined in the United States from the 1950s to the 1980s, largely as a result of improvements in public health programs, the development of effective chemotherapeutic agents, and improved living conditions. Subsequently, the incidence increased in 1985-1992, with an overall incidence of 10.5 cases per 100,000 population in 1992. The change has been attributed to the emergence of the HIV/AIDS epidemic during this decade. The incidence of tuberculosis again declined in the 1990s, with an incidence of 6.8 cases per 100,000 population in 1998.⁴

International

In 1997, the World Health Organization conducted a study to determine worldwide incidence and prevalence of tuberculosis.⁵ The total number of new cases in 1997 was estimated to be 7.96 million. This figure includes an estimated 3.52 million cases of infectious pulmonary tuberculosis. The death rate attributed to tuberculosis in 1997 was approximately 1.87 million.

Mortality/Morbidity

In immunocompetent patients in endemic regions, the primary infection is contained, and the patients remain asymptomatic. In some patients with relative immune compromise, primary infection may lead to fulminant pulmonary infection, with pulmonary necrosis leading to death. This is called progressive primary tuberculosis. Pulmonary manifestations of progressive pulmonary tuberculosis may be radiographically indistinguishable from manifestations of postprimary tuberculosis.

Postprimary tuberculosis is a significant cause of worldwide morbidity and mortality. Morbidity may result in any affected organ system. Pulmonary morbidity may result from a chronic cough, hemoptysis (which may be fatal), fibrosis, superinfection (eg, mycetoma), bronchial stenosis, repeated pulmonary infections from tuberculous bronchiectasis, or empyema.^{6, 7} Significant morbidity also may arise from chronic tuberculous osteomyelitis, chronic renal insufficiency, or neurologic changes related to central nervous system (CNS) tuberculosis.

Race

Tuberculosis is a worldwide infection. Endemic areas include India, Southeast Asia, and sub-Saharan Africa.

Sex

No sex predilection exists for tuberculosis.

Age

Infection may occur at any age and is most significant at the extremes of age. Primary tuberculosis is usually seen in young children in endemic regions. The incidence is increasing in individuals in nonendemic regions who are immunocompromised.

Anatomy

Tuberculosis is transmitted via the spread of bacilli in aerosolized droplets. Infected droplets pass from the nasopharynx into the tracheobronchial tree and continue to the lung. As a result of gravity, droplets tend to be deposited in the lower lobes; therefore, primary tuberculosis is more common in the lower lobes. The oxygen tension is higher in the upper lobes, where reactivation tuberculosis usually occurs.

The intrapulmonary lymphatics and blood vessels play an important role in the manifestations of tuberculosis. The lymphatics and vasculature lie within the interstitium of the lung, and they drain (veins and lymphatics) and supply (arteries) the adjacent region of lung. This anatomy accounts for ipsilateral lymphadenopathy because infected lymph is drained along the interstitium to the hilar and mediastinal lymph nodes. Venous drainage allows hematogenous dissemination of the infection.

Clinical Details

Primary tuberculosis is usually a self-limited infection seen in children in endemic regions. As many as 60% of children and 5% of adults with primary tuberculosis are asymptomatic. Patients with primary pulmonary tuberculosis may be minimally symptomatic, with minimal constitutional symptoms. Children may present with fever, malaise, weight loss, cough, and occasional hemoptysis.

Progressive primary tuberculosis occurs in the setting of acute infection in patients with minimal or marked immune compromise. Patients with progressive primary tuberculosis become acutely ill, and they may have extensive lung parenchymal opacities and cavitation. Hypoxia and death may occur.

Patients with postprimary tuberculosis often manifest disease within 2 years of the initial infection or many years later, often as a result of comorbid states: old age, malnutrition, and/or neoplasm. These patients experience indolent clinical symptoms that include lethargy, anorexia, weight loss, low-grade fever, cough, hoarseness, and hemoptysis.

Preferred Examination

Diagnosis is based on a combination of tuberculin skin testing (purified protein derivative testing), sputum cultures, and radiography. Bronchoscopy may be required to obtain specimens.

Patients with primary tuberculosis may not undergo imaging; however, if imaging is performed, a conventional chest radiograph may be sufficient for diagnosis in the appropriate clinical setting.

In patients with progressive primary or postprimary tuberculosis, computed tomography (CT) is often performed, in addition to chest radiography. Magnetic resonance imaging (MRI) may be used to evaluate complications of thoracic disease. Patients with postprimary tuberculosis may also undergo bronchoscopy to evaluate endobronchial disease and to obtain sputum specimens for microbacteriologic cultures.^{8, 9}

Limitations of Techniques

With the purified protein derivative skin test, false-positive results may be seen in individuals who have been inoculated with bacillus Calmette-Guérin vaccine. False-negative results may occur in patients who are anergic, such as patients with HIV infection and decreased CD4 counts. These patients require an anergy panel.

As a result of the stringent growth requirements of the bacillus, culturing of the organisms is often a lengthy and difficult process. False-negative results may be seen if insufficient organisms are present in the specimen.

Conventional radiography is limited in its sensitivity and specificity. As many as 15% of patients with primary tuberculosis have normal chest radiographic findings. Clinical suspicion must remain high for prompt diagnosis in these individuals. Chest radiographic results are not specific for tuberculosis, and other entities must remain in the differential diagnosis,¹⁰

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

RADIOGRAPH

Section 4 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Primary tuberculosis

Pulmonary imaging findings in individuals with primary tuberculosis are nonspecific.^{11, 12, 13}

• Common findings include segmental or lobar airspace consolidation, ipsilateral hilar and mediastinal lymphadenopathy, and/or pleural effusion.
• Atelectasis may occur in primary pulmonary tuberculosis, often as a consequence of tuberculous airway involvement.
• Note that chest radiographic findings may be normal in as many as 15% of patients with primary pulmonary tuberculosis.
• Parenchymal consolidation may be observed.
  • Although consolidation may occur in any segment or lobe or in multiple segments or lobes, the disease has a predilection for the lower lobes, for the middle lobe and lingula, and for the anterior segments of the upper lobes.
  • Airspace consolidation tends to be homogeneous, with ill-defined margins. If the consolidation abuts a fissure, a well-defined margin may be identified.
  • Cavitation within parenchymal opacity is distinctly uncommon in primary infection. As the host immune response continues, healing begins.
  • Caseous necrosis occurs centrally within the lung parenchymal opacity, decreasing its size.
  • The lung opacity tends to become rounded with healing, and it continues to shrink until only a small nodule remains. Subsequently, the nodule may become calcified or ossified, resulting in a calcified granuloma. Note that although a granuloma may calcify, this does not necessarily reflect an absence of bacilli. The organisms may remain quiescent within this nodule, serving as a possible source for reactivation of disease.
• Lymphadenopathy is a common manifestation of primary pulmonary tuberculosis.
  • The presence of hilar and mediastinal lymphadenopathy may distinguish primary from postprimary tuberculosis, because lymphadenopathy is conspicuously absent in postprimary tuberculosis.
  • Lymphadenopathy without a parenchymal opacity may occur as the only manifestation of primary pulmonary tuberculosis. Most commonly, this is seen in the population with HIV infection.
  • As expected, adenopathy is most common in the ipsilateral hilar region. Hilar lymphadenopathy is seen in approximately 60% of children with primary tuberculosis, paratracheal adenopathy is seen in 40%, and subcarinal lymphadenopathy is seen in 80%.
  • In adults, lymphadenopathy is unusual in an immunocompetent host but it does occur, particularly in blacks and Asians. In adults with HIV infection, adenopathy is common.
  • The pattern of lymphadenopathy is indistinguishable from that of sarcoid or lymphoma.
  • Lymphadenopathy may be symptomatic if it secondarily involves the airways.
  • With an appropriate immune response or with adequate chemotherapy, enlarged necrotic lymph nodes may diminish in size and commonly calcify. The presence of calcified lymph node and a granuloma represents the Ranke complex.
• Airway involvement is frequently present in primary tuberculosis.
  • The airway may be involved in one of the following ways:
    • Airway compression by adjacent lymphadenopathy with resultant atelectasis
    • Mucosal infection with resultant ulceration and long-term stricture formation
    • Broncholithiasis, ie, extrinsic erosion of a bronchus by adjacent lymphadenopathy with extrusion of calcified material into the bronchus
    • Endobronchial spread of infection
    • Bronchiectasis
  • Atelectasis is most notable within the anterior segments of the upper lobes and the medial segment of the middle lobe. Atelectasis may resolve as lymphadenopathy regresses with host response. A sudden resolution of atelectasis may represent perforation of an infected lymph node into the airway, which relieves the bronchial obstruction.
  • A possible long-term sequela of infection is tracheobronchial stenosis. The airways may be involved by tuberculosis in a variety of ways, including direct mucosal involvement from infected sputum, direct extension from perforating lymphadenopathy or adjacent parenchymal infection, and hematogenous or lymphatic drainage.
  • The endobronchial spread of infection may be seen with tuberculous tracheobronchial disease. Bacilli from the infected airways disseminate into more distal bronchi and bronchioles and subsequently enter the alveoli, where they become deposited. The resultant radiographic appearance is one of small ill-defined acinar shadows and small nodules.
  • Endobronchial tuberculosis may lead to bronchiectasis, either from bronchial stenosis or secondary to traction from fibrosis. Bronchiectasis is more frequently seen in postprimary tuberculosis (see Postprimary tuberculosis below).
• Pleural involvement is uncommon in children with primary tuberculosis, occurring in approximately 10% of children. Pleural involvement is seen more frequently in adults with primary pulmonary tuberculosis, and it is even more frequently identified in postprimary tuberculosis.

Postprimary tuberculosis

The findings of reactivation tuberculosis typically become radiographically apparent within 2 years of the initial infection.¹⁴ Pleural effusions develop if the infection remains untreated. Tuberculous empyema is a much less common finding.

• Postprimary tuberculosis may have any of a number of parenchymal manifestations including the following:
  • Patchy or confluent airspace opacities are opacities that involve the apical and posterior segments of the upper lobes and the superior segments of the lower lobes.
  • In postprimary tuberculosis, cavitary disease is secondary to caseous necrosis within the opacity.¹⁵ The debris from the lesion is expelled via the tracheobronchial tree with which the cavity is in communication. The cavities, similar to airspace opacities in reactivation tuberculosis, are commonly within the upper lung zones. The cavities demonstrate a thick outer wall with a smooth inner contour. Air-fluid levels may be present. Superinfection by Aspergillus organisms may occur, leading to a mycetoma.
  • Tuberculomas are rounded discrete nodules that are known to harbor bacilli. They may be present in primary or postprimary tuberculosis and radiographically appear as discrete nodules, typically within the upper lobes. Tuberculomas may calcify. Satellite lesions (ie, small discrete nodules in the vicinity of the tuberculoma) are present in as many as 90% of patients.
  • Endobronchial spread of infection with acinar opacities occurs as a consequence of infected material passing into the tracheobronchial tree from an infected portion of the lung. The organisms pass via the airways into previously uninvolved portions of the lung. The radiographic appearance is one of widespread ill-defined acinar shadows. Foci may become confluent and mimic bacterial pneumonia. Spread from the upper lobes to the lower lobes is common and called the upstairs-downstairs pattern.
  • Pulmonary miliary tuberculosis is a consequence of hematogenous spread of organisms to the pulmonary parenchyma. Radiographically, miliary spread can be recognized by circumscribed nodules less than 1-2 mm in diameter located diffusely throughout both lungs.
• In contrast to primary tuberculosis, lymphadenopathy is notably absent in patients with postprimary tuberculosis, with the exception of patients with HIV/AIDS infection.
• Airway involvement in postprimary tuberculosis may be observed.
  • Tracheobronchial stenosis may not be directly visualized on conventional chest radiographs. Airway stenosis may result in atelectasis in the segments of the lung supplied by that bronchus.
  • Bronchiectasis may be visualized on radiographs as dilated air-containing structures, with a tram-track appearance representing the parallel walls of the dilated airway. Dilated bronchi may be irregular in caliber and varicoid in appearance or may be cystic. Traction bronchiectasis may occur as well, as a consequence of fibrosis.
• Pleural involvement is seen more commonly in postprimary tuberculosis than in primary infection.
• • Pleural effusions may occur and may progress to empyema. An empyema may require emergent surgical intervention because the infection is maintained within a closed space and because it may result in rapid destruction of surrounding structures (eg, lung parenchyma, osseous structures of the thorax).
  • If infection extends from the pleural space to involve the chest wall, it is called empyema necessitans.
  • Osseous destruction and, possibly, air within subcutaneous tissues may be identified radiographically, or the empyema may present as a palpable soft-tissue mass.

Related Medscape topics:
CME Radiological Imaging in Pneumonia: Recent Innovations

Degree of Confidence

The imaging features of primary tuberculosis are nonspecific, and they may mimic those of other infectious processes. A finding that differentiates primary tuberculosis from other infectious processes is lymphadenopathy, which is typically absent in bacterial pneumonia.

Postprimary tuberculosis may be recognized more readily with the presence of fibrocavitary disease and a history of prior tuberculosis exposure or infection. Radiologic findings of postprimary tuberculosis are highly suggestive of, but not pathognomonic for, the disease. Inactive disease cannot be established without prior radiographs, regardless of the pattern.

False Positives/Negatives

As many as 15% of conventional chest radiographs may be normal in primary tuberculosis.

In the immunocompromised population, lymphadenopathy occasionally may occur in isolation, and it may not be detected on conventional radiographs. Additional imaging with CT is often required because CT is more sensitive in depicting lymphadenopathy.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Primary tuberculosis¹⁶

• CT helps confirm the presence of an ill-defined parenchymal infiltrate, as well as lymphadenopathy.¹⁷
• CT scans may demonstrate enlarged lymph nodes typically measuring more than 2 cm. Lymph nodes demonstrate central hypoattenuation with peripheral rim enhancement with the administration of contrast material. This appearance reflects central necrosis within the node.
• CT is the examination of choice for evaluating lymphadenopathy and involvement of the tracheobronchial tree. Lymphadenopathy causing bronchial compression can be identified on CT scans, and airway compromise can be monitored during chemotherapy.
• Broncholiths may be identified in rare cases.
• Morphologically, the stenoses in active disease are areas of irregular luminal narrowing with circumferential wall thickening.
• Associated mediastinitis and even mediastinal abscesses may be present.
• In patients who are severely affected, segmentectomy or lobectomy may be required to treat the symptoms.
• Small pleural effusions are detected more readily on CT scans than on other images. Contrast enhancement may be useful in identifying evolution into an empyema.

Postprimary tuberculosis

CT scans may be helpful in evaluating parenchymal involvement, satellite lesions, bronchogenic spread of infection, and miliary disease.

• Cavitation is best demonstrated on CT scans. The outer wall of the cavity tends to be thick walled and irregular, whereas the inner wall tends to be smooth. An air-fluid level may be identified. The connection of the cavity to the airway may be visualized. Complications of cavitary disease may become apparent with mycetoma formation, which appears as an intraluminal collection of material with a crescent of surrounding air. Changes in patient positioning demonstrate a change in the position of the mycetoma relative to the cavity.
• Tuberculomas can be identified on CT scans as rounded nodules that usually have surrounding associated satellite lesions.
• The bronchogenic spread of tuberculosis is recognized on CT scans by the presence of acinar shadows and nodules of varying sizes in a peribronchial distribution. The lesions are seen throughout both lungs.
• Miliary tuberculosis is characterized by randomly distributed tiny nodules (1-2 mm), which tend to be smooth and well marginated.
  • Calcification is notably absent; this observation may aid in differentiating tuberculosis from metastatic diseases such as thyroid carcinoma.
  • CT scans may aid in the evaluation of uncommon complications of miliary tuberculosis, eg, acute respiratory distress syndrome (ARDS) and pulmonary hemorrhage resulting from disseminated intravascular coagulopathy. Both ARDS and pulmonary hemorrhage may manifest as alveolar filling in a background of miliary nodules.

Airway involvement

CT is the examination of choice for evaluating the tracheobronchial tree.

• Lymphadenopathy is a feature of primary infection; however, calcified lymph nodes may cause persistent extrinsic compression on the bronchi.
• Bronchial stenosis is more common in postprimary disease than in primary tuberculosis. In fibrocavitary tuberculosis, the proximal bronchi are more typically involved than the peripheral airways. Variable areas of stenosis are demonstrated. Wall thickening tends to be less marked than in primary tuberculosis.
• Bronchiectasis is a well-known sequela of postprimary disease. Bronchiectasis tends to occur in the upper lobes and often manifests as traction bronchiectasis on the basis of fibrotic disease with subsequent traction on the airways. Recurrent infections and hemoptysis may result from traction bronchiectasis.

Pleural involvement

• Empyema is visualized on contrast-enhanced CT scans with enhancement of the parietal and visceral pleurae. They may demonstrate enhancing septa within the pleural fluid collections. The pleural fluid collections are characterized by low attenuation; however, they do not have attenuation values consistent with simple fluid. Empyemas demonstrate the so-called split pleura sign. This sign consists of the pleural fluid collection tracking between the abnormally enhancing parietal and visceral pleura.
• Spontaneous pneumothorax is an uncommon complication of disease, may be secondary to peripherally located lesions.
• Involvement of the pericardium and spine may be demonstrated on CT images.

Degree of Confidence

CT is sensitive in the identification of pulmonary parenchymal and pleural disease. The pattern of disease and distribution of nodules is delineated clearly by using modern CT techniques. Lymphadenopathy may be diagnosed with a high degree of confidence, even without the use of intravenous contrast material.

Pericardial disease can be imaged with CT or MRI, although calcification related to prior tuberculous pericarditis is more readily apparent on CT images.

False Positives/Negatives

Osseous involvement is well delineated on CT scans; however, MRI is often necessary to evaluate the disk and the spinal canal.

MRI

Section 6 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

MRI is of limited value in the evaluation of patients with pulmonary tuberculosis. MRI is occasionally helpful in evaluating the complications of tuberculosis, such as the extent of thoracic wall involvement with empyema.

ULTRASOUND

Section 7 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Typically, ultrasonography is not useful in imaging pulmonary disease. Ultrasonography may be used for thoracentesis guidance or to evaluate the pericardium for secondary tuberculous involvement.

NUCLEAR MEDICINE

Section 8 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Typically, nuclear medicine studies are not used in the imaging of tuberculosis.

ANGIOGRAPHY

Section 9 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Angiography is not used in the diagnosis of pulmonary tuberculosis. Angiographic techniques such as bronchial arteriography and embolization in patients with hemoptysis may be used to treat the complications of cavitary pulmonary tuberculosis.

INTERVENTION

Section 10 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Interventional radiologists may be consulted to perform diagnostic and therapeutic bronchial artery studies.

Interventional radiologic techniques may be used to confirm the diagnosis with percutaneous lymph node aspiration or biopsy to obtain material for culture, cytologic, or histologic studies.

A radiologist may perform stent placement with fluoroscopic and/or CT guidance in collaboration with the bronchoscopist.

Radiologists often obtain fluid for evaluation by performing ultrasonography- or CT-guided thoracentesis.

Medical/Legal Pitfalls

• Medical pitfalls include delays in diagnosing active tuberculosis.
• Delay in diagnosis may result in a delay in isolation and treatment of patients with public health consequences.
• Populations at particular risk for failure of disease recognition and adequate treatment include individuals who are incarcerated, homeless, elderly, or underprivileged.
• • Given the overcrowded conditions in many shelters and prisons, the risk of widespread infection is increased.
  • Transient individuals who become infected in the setting of incarceration or temporary shelter stays are at increased risk of suboptimal diagnosis and treatment, as well as partial treatment, resulting in development of multidrug-resistant strains of tuberculosis.

Related Medscape topic:
Resource Center Medical Malpractice and Legal Issues.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  Case 1. Young male patient with fever and cough has a focal opacity in the left lower lobe that looks like a pneumonia. This is a case of primary tuberculosis in an adult.
	View Full Size Image
Media type:  X-RAY

Media file 2:  Case 2. Posteroanterior chest radiograph in a young patient shows a right upper lobe and right lower lobe consolidation and a small pleural effusion on the right side.
	View Full Size Image
Media type:  X-RAY

Media file 3:  Case 2. CT scan obtained with the pulmonary window setting demonstrates consolidation in the right upper lobe, ground-glass opacities in the right lower lobe, and a pleural effusion on the right side. This patient has extensive tuberculous pneumonia and is immunocompromised.
	View Full Size Image
Media type:  CT

Media file 4:  Case 3. A middle-aged man presents with a cough and fever lasting several weeks. Posteroanterior chest radiograph shows a prominent paratracheal area on the right, lymphadenopathy, a cavitary opacity in the right upper lobe, and a focal consolidation in the middle lung zone on the right.
	View Full Size Image
Media type:  X-RAY

Media file 5:  Case 3. CT scan obtained with the pulmonary window setting in the right upper lobe shows an irregular, thick-walled cavity with some increased markings around it. A nearby nodule is also shown.
	View Full Size Image
Media type:  CT

Media file 6:  Case 3. CT scan obtained with pulmonary window setting in the right middle lobe shows a focal area of consolidation with what may be tiny nodules. This patient has primary progressive tuberculosis with radiographic manifestations of mediastinal adenopathy, cavitary process, and endobronchial spread that occurs over a short period. He had a history of alcohol abuse.
	View Full Size Image
Media type:  CT

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

1. Kim WS, Moon WK, Kim IO, et al. Pulmonary tuberculosis in children: evaluation with CT. AJR Am J Roentgenol. Apr 1997;168(4):1005-9. [Medline].
2. Kim KI, Lee JW, Park JH, et al. Pulmonary tuberculosis in five young infants with nursery exposure: clinical, radiographic and CT findings. Pediatr Radiol. Nov 1998;28(11):836-40. [Medline].
3. Speert DP. Bacterial infections of the lung in normal and immunodeficient patients. Novartis Found Symp. 2006;279:42-51; disussion 51-5, 216-9. [Medline].
4. Friedman LN, ed. The epidemiology of tuberculosis in the U.S. In: Tuberculosis: Current Concepts and Treatment. 2nd ed. Boca Raton: CRC Press;2001:1-13.
5. Dye C, Scheele S, Dolin P, et al. Consensus statement. Global burden of tuberculosis: estimated incidence, prevalence, and mortality by country. WHO Global Surveillance and Monitoring Project. JAMA. Aug 18 1999;282(7):677-86. [Medline].
6. Tunçözgür B, Isik AF, Nacak I, Akar E, Elbeyli L. Dilemma on the treatment of haemoptysis: an analysis of 249 patients. Acta Chir Belg. Jun 2007;107(3):302-6. [Medline].
7. Choe KO, Jeong HJ, Sohn HY. Tuberculous bronchial stenosis: CT findings in 28 cases. AJR Am J Roentgenol. Nov 1990;155(5):971-6. [Medline].
8. Kim Y, Lee KS, Yoon JH, et al. Tuberculosis of the trachea and main bronchi: CT findings in 17 patients. AJR Am J Roentgenol. Apr 1997;168(4):1051-6. [Medline].
9. Nyman RS, Brismar J, Hugosson C, et al. Imaging of tuberculosis--experience from 503 patients. I. Tuberculosis of the chest. Acta Radiol. Jul 1996;37(4):482-8. [Medline].
10. Reed JC. Chest Radiology: Plain Film Patterns and Differential Diagnoses. 4th ed. St Louis: Mosby-Year Book;1997:190-1, 284-5, 421-2.
11. Freudlich IM, Bragg DG. Granulomatous infections of the lung. In: A Radiologic Approach to Diseases of the Chest. Philadelphia: Williams & Wilkins;1992:263-87.
12. Harisinghani MG, McLoud TC, Shepard JA, et al. Tuberculosis from head to toe. Radiographics. Mar-Apr 2000;20(2):449-70; quiz 528-9, 532. [Medline].
13. Lee KS, Song KS, Lim TH, et al. Adult-onset pulmonary tuberculosis: findings on chest radiographs and CT scans. AJR Am J Roentgenol. Apr 1993;160(4):753-8. [Medline].
14. Linh NN, Marks GB, Crawford AB. Radiographic predictors of subsequent reactivation of tuberculosis. Int J Tuberc Lung Dis. Oct 2007;11(10):1136-42. [Medline].
15. Lee KM, Choe KH, Kim SJ. Clinical investigation of cavitary tuberculosis and tuberculous pneumonia. Korean J Intern Med. Dec 2006;21(4):230-5. [Medline].
16. Primack SL, Logan PM, Hartman TE, et al. Pulmonary tuberculosis and Mycobacterium avium-intracellulare: a comparison of CT findings. Radiology. Feb 1995;194(2):413-7. [Medline].
17. Eisenhuber E, Mostbeck G, Bankier A, Stadler A, Rumetshofer R. [Radiologic diagnosis of lung tuberculosis]. Radiologe. May 2007;47(5):393-400. [Medline].

Article Last Updated: Feb 27, 2008