Introduction
Background
Tuberculosis (TB) has been around for millennia, and despite initial declines in its incidence during the middle of the 20th century, the disease has been reemerging across the world.1 The radiologic diagnosis of TB started only about a century ago, after Roentgen's discovery of x-rays.2 Fluoroscopy was used in the early part of the 20th century to detect cavitary TB, because experienced fluoroscopists could easily detect cavities. Over the years, improvements in technology, coupled with extensive investigation into the radiologic patterns of pulmonary TB, have resulted in diagnostic imaging being an essential adjunct to the clinical and microbiologic diagnosis of this disease. These events contributed to the routine practice of documenting cavitary disease and following up the disease on film.3,4
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Pathophysiology
TB results from infection by any of the TB complex mycobacteria, including Mycobacterium tuberculosis, M bovis, M africanum, M microti, and M canetti.5
TB can be divided into primary, progressive-primary, and postprimary forms on the basis of the natural history of the disease. Postprimary TB results from either reactivation of a latent primary infection or, less commonly, from the repeat infection of a previously sensitized host. The term "postprimary" is preferred to "reactivation" when referring to the clinical diagnosis because firmly distinguishing recurrence from an antecedent infection is impossible in most cases. Approximately 10% of all infected patients are likely to develop reactivation, and the risk is highest within the first 2 years or during periods of immunosuppression.6,7,8
The major determinants of the type and extent of TB disease are the patient's age and immune status, the virulence of the organism, and the mycobacterial load. Postprimary TB is typically a disease of adolescence and adulthood that results from reactivation of an initially contained infection by a TB complex mycobacterium. Pulmonary reactivation usually occurs in the apical and posterior segments of the upper lobes or in the superior segments of the lower lobes.4,9 This distribution may be related to the higher oxygen tension or the reduced perfusion and lymphatic clearance in these lung segments.4,9
Frequency
United States
Approximately 15 million people are infected with TB organisms.1,3,5 Although this number represents less than 10% of the population, it results in a large reservoir of people who are at risk for postprimary TB. The actual annual incidence of disease that is characterized by positive cavitary smear results is less than 0.1%.1,3,5
International
Worldwide, approximately 19-43% of the population is infected with TB. Although most are asymptomatic, the likelihood of reactivation is increasing because of human immunodeficiency virus (HIV) infection. Almost half of all patients coinfected with HIV and TB eventually have a reactivation of the disease. The annual incidence of active TB may approach 4% in certain populations.1,10
Mortality/Morbidity
Untreated postprimary TB has a mortality rate in excess of 50%. Antibiotic therapy can reduce this rate to less than 10%. Residual fibrosis, cavities, and/or bronchiectasis are complications of untreated postprimary TB disease.
Race
Increased susceptibility to TB, such as that found in Native Americans, results in progressive primary disease. Postprimary disease is typically seen in populations that have a high natural resistance to TB, which results in an initial containment of the infection. Within such groups, TB occurs disproportionately in the disadvantaged, the infirm, the elderly, and those who have coinfection with HIV. True racial or sex-based differences, however, are likely to be minor in postprimary TB disease.
Sex
When socioeconomic factors are considered, no clear propensity for either sex is observed.
Age
Postprimary TB is primarily a disease of adults, but patients range from adolescents and young adults in endemic areas to the middle-aged and elderly in areas of low prevalence. This distribution may be related to the age at which the initial infection is most likely to occur.
Anatomy
Postprimary TB starts as an expanding granuloma. Unchecked proliferation of the mycobacteria results in rapid necrosis because of preexisting hypersensitivity from the primary infection. Spontaneous arrest can occur, but the disease is usually progressive; this finding is in contrast to that of primary TB, in which the development of immunity in a naive host arrests the spread of disease (see Lung, Primary Tuberculosis). Erosion into adjacent anatomic structures results in further spread. The classic postprimary TB progression involves cavitation into a bronchus with endobronchial spread. Other patterns can cause erosion into the blood vessels, pleural space, or, rarely, the lymphatics.
Presentation
The classic clinical presentation of TB includes cough, fever, weight loss, night sweats, hemoptysis, and acid-fast bacilli in the sputum. None of these is universally present, and patients often present with minimal signs or symptoms. Isolated hemoptysis is neither sensitive nor specific for the diagnosis of TB.
Patients with postprimary cavitary TB are more infectious than those with miliary TB. Cavitation into a bronchus results in a high bacterial load in the sputum and, thus, higher infectivity.
Preferred Examination
In nonendemic areas, the initial evaluation of all suspected cases of TB should include tuberculin and sputum testing in conjunction with chest radiography. The value of tuberculin testing is unclear in endemic areas or in countries in which bacille Calmette-Guérin (BCG) vaccination is prevalent. Newer diagnostic tests such as QuantiFERON-TB Gold and enzyme-linked immunospot (ELISpot) may be superior to tuberculin testing, especially in vaccinated individuals.10
Limitations of Techniques
No radiologic study shows findings that are specific for TB. A cavitary process that is demonstrated on chest radiographs or computed tomography (CT) scans in the apical and posterior segments of the upper pulmonary lobe or in the superior segments of the lower lobes is likely to be TB; however, differential considerations include other diseases, including histoplasmosis and other fungal infections, bacterial abscesses, and necrotic neoplasms, especially lung neoplasms.11
In immunocompromised patients, postprimary TB may mimic primary TB, and the condition can appear with pleural effusion, lymphadenopathy, or miliary spread. The usual pattern of cavitary upper-lobe disease is less common in immunocompromised hosts than in immunocompetent hosts.
Differential Diagnoses
Blastomycosis, Thoracic
Coccidioidomycosis, Thoracic
Histoplasmosis, Thoracic
Lung, Nontuberculous Mycobacterial
Infections
Sarcoidosis, Thoracic
Silicosis and Coal Worker Pneumoconiosis
Other Problems to Be Considered
Lung, Primary Tuberculosis (In immunocompromised patients, postprimary TB may mimic primary TB.)
More on Lung, Postprimary Tuberculosis |
Overview: Lung, Postprimary Tuberculosis |
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References
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Dunlap NE, Bass J, Fujiwara P, et al. Diagnostic standards and classification of tuberculosis in adults and children. Ad-hoc committee of the Scientific Assembly on Microbiology, Tuberculosis, and Pulmonary Infections. Am J Respir Crit Care Med. Apr 2000;161 (4 pt 1):1376-95. [Medline]. [Full Text].
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Essentials of Radiology [CD-ROM]. Moraga, Calif: Medical Interactive; 1999. Amorosa JK.
Goo JM, Im JG. CT of tuberculosis and nontuberculous mycobacterial infections. Radiol Clin North Am. Jan 2002;40(1):73-87, viii. [Medline].
Poey C, Verhaegen F, Giron J, et al. High resolution chest CT in tuberculosis: evolutive patterns and signs of activity. J Comput Assist Tomogr. Jul-Aug 1997;21(4):601-7. [Medline].
Campbell IA, Bah-Sow O. Pulmonary tuberculosis: diagnosis and treatment. BMJ. May 20 2006;332(7551):1194-7. [Medline]. [Full Text].
Division of Tuberculosis Elimination, National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention. TB guidelines. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/tb/pubs/mmwr/Maj_guide/List_date.htm. Accessed September 19, 2007.
Fujita J, Higa F, Tateyama M. Radiological findings of mycobacterial diseases. J Infect Chemother. Feb 2007;13(1):8-17. [Medline].
Griffith-Richards SB, Goussard P, Andronikou S, et al. Cavitating pulmonary tuberculosis in children: correlating radiology with pathogenesis. Pediatr Radiol. Aug 2007;37(8):798-804. [Medline].
Kim WS, Choi JI, Cheon JE, et al. Pulmonary tuberculosis in infants: radiographic and CT findings. AJR Am J Roentgenol. Oct 2006;187(4):1024-33. [Medline].
Kobashi Y, Obase Y, Fukuda M, et al. Clinical reevaluation of the QuantiFERON TB-2G test as a diagnostic method for differentiating active tuberculosis from nontuberculous mycobacteriosis. Clin Infect Dis. Dec 15 2006;43(12):1540-6. [Medline].
Koh WJ, Yu CM, Suh GY, et al. Pulmonary TB and NTM lung disease: comparison of characteristics in patients with AFB smear-positive sputum. Int J Tuberc Lung Dis. Sep 2006;10(9):1001-7. [Medline].
Washington L, Palacio D. Imaging of bacterial pulmonary infection in the immunocompetent patient. Semin Roentgenol. Apr 2007;42(2):122-45. [Medline].
Further Reading
Keywords
reactivation tuberculosis/TB, postprimary TB, primary tuberculosis/TB, progressive-primary tuberculosis/TB, Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium africanum, Mycobacterium microti, Mycobacterium canetti, M tuberculosis, M bovis, M africanum, M microti, M canetti
Overview: Lung, Postprimary Tuberculosis