You are in: eMedicine Specialties > Radiology > CHEST Lung, Postprimary TuberculosisArticle Last Updated: Sep 20, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 9
  Author: Anjali Agrawal, MBBS, Assistant Professor of Radiology, Voluntary Staff, Department of Radiology, Baylor College of Medicine Anjali Agrawal is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America Coauthor(s): Anurag Agrawal, MBBS, Clinical Instructor, Department of Medicine, Section of Pulmonary and Critical Care Medicine, Baylor College of Medicine Editors: Judith K Amorosa, MD, FACR, Clinical Professor and Program Director, Department of Radiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School; Consulting Staff, Department of Radiology, Robert Wood Johnson University Hospital; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; John D Newell, Jr, MD, FACR, FCCP, FASER, Co-Director of Thoracic Imaging, UCDHSC; Director of Lung Imaging Center, Professor of Radiology and Professor of Medicine, Department of Radiology, University of Colorado Health Sciences Center, National Jewish Medical and Research Center; Univ. Colorado Hospital; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center Author and Editor Disclosure Synonyms and related 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 INTRODUCTIONSection 2 of 9
  BackgroundTuberculosis (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 For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center. Also, see eMedicine's patient education article Tuberculosis. PathophysiologyTB 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 FrequencyUnited StatesApproximately 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 InternationalWorldwide, 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/MorbidityUntreated 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. RaceIncreased 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. SexWhen socioeconomic factors are considered, no clear propensity for either sex is observed. AgePostprimary 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. AnatomyPostprimary 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. Clinical DetailsThe 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 ExaminationIn 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 TechniquesNo 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. DIFFERENTIALSSection 3 of 9
Blastomycosis, Thoracic Coccidioidomycosis, Thoracic Histoplasmosis, Thoracic Lung, Nontuberculous Mycobacterial Infections Sarcoidosis, Thoracic Silicosis and Coal Worker Pneumoconiosis Other Problems to Be ConsideredLung, Primary Tuberculosis (In immunocompromised patients, postprimary TB may mimic primary TB.) RADIOGRAPHSection 4 of 9
FindingsPulmonary 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 segments—namely, the apical or posterior segments of the upper lobe or the superior segment of a lower lobe—anterior or basal segments may be involved in as many as 75% of cases (see Images 1-2). 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 (see Image5). TB and lung cancer coexist in as many as 5% of cases, but whether TB independently increases the likelihood of cancer remains unclear. Degree of ConfidenceTB cannot be confidently diagnosed on the basis of chest radiographic findings alone because the imaging results can often be normal in primary TB. Normal findings are unusual in postprimary lung disease, but they cannot be used to exclude extrapulmonary TB. However, the combined positive predictive value is high for the typical symptoms of the disease and the finding of cavitary upper-lobe infiltrates on chest radiographs. False Positives/NegativesSarcoidosis, granulomatous fungal infections, Nocardia infections, and atypical mycobacterioses are the most common mimickers of pulmonary TB. CT SCANSection 5 of 9
FindingsBecause typical postprimary TB is readily seen on conventional chest radiographs, the major utility of CT scanning is for assessment of the extent and nature of the disease. As mentioned above in Radiograph, Findings, CT scanning is more sensitive than chest radiography in depicting cavitation. The associated complications of postprimary TB, such as the erosion of vessels, rupture into the pleural space, and miliary and bronchogenic spread, are also better defined with CT scanning than with radiography.12, 13, 14 A tree-in-bud pattern of 5- to 10-mm centrilobular nodules has been associated with endobronchial spread on high-resolution CT (HRCT) scans, which helps in identifying active disease. Also, postprimary TB disease in immunocompromised patients may not be seen on chest radiographs. Mediastinal adenopathy, subtle pleural changes, and miliary lung parenchymal involvement are best detected with CT scanning. Most cases of TB in patients with HIV infection or other immunosuppressive diseases are secondary to reactivation of a latent infection. However, a hypersensitive response or the absence of adequate immunity results in disease that behaves like primary TB. Miliary spread with systemic dissemination is more common in these immunocompromised individuals than in the healthy population. In these patients, radiographic findings are atypical, and the images often show diffuse dissemination, with striking lymphadenopathy and/or pleural effusions (see Image 8). Parenchymal involvement can range from consolidation to the absence of any lung opacities. In the developed world, cavitation is uncommon in HIV-infected patients who have TB. In endemic areas, a more typical response, including upper-lobe disease and cavitation, is frequently seen in affected patients. This variance may be related to differences in the immune status of the patients. In summary, diagnostic imaging is useful in differentiating postprimary TB disease from primary disease, but the distinctions are blurred in cases of immunocompromised patients. Although the findings of currently active TB can often be differentiated from previous scarring on radiologic images, the possibility of latent or temporarily quiescent infection exists, and healed or inactive TB should not be diagnosed without adequate clinical information and/or the finding of calcified lesions. Radiographic follow-up is recommended in all cases of TB because it provides valuable information regarding the extent of the disease and its progression. Degree of ConfidenceAlthough no single radiologic feature is diagnostic of postprimary TB, a combination of upper-lobe opacities with a dominant cavitary process increases confidence in the diagnosis of TB. A tree-in-bud pattern is associated with endobronchial spread and suggests active disease. False Positives/NegativesRegarding false-positive findings, nontuberculous mycobacterial (NTM) infections can mimic all radiologic findings that are associated with postprimary TB. Typically, these findings are seen in elderly men with chronic obstructive pulmonary disease (COPD); in such patients, NTM infections should always be considered. Fungal infections, particularly histoplasmosis, may also result in similar findings. Cavitary lung disease that resembles TB has also been reported in cases of pyogenic infections, sarcoidosis, vasculitis, parasitic infections, bronchiolitis obliterans and organizing pneumonia (BOOP), and malignancies. Regarding false-negative findings, postprimary TB resembles primary TB in immunocompromised patients, and it can be radiologically misclassified. CT scan and/or HRCT scan results are unlikely to be completely normal in postprimary TB. NUCLEAR MEDICINESection 6 of 9
FindingsPositron emission tomography (PET) scans may be positive in cases of active TB. Positive results are usually found when malignancy is suspected during the workup of a lung abnormality. INTERVENTIONSection 7 of 9
In the absence of adequate drug therapy, the disease is often fatal. Currently, TB can be effectively treated by using antibiotics alone; other modalities of treatment are of only historical interest. Primary resistance to anti-TB therapy (ATT) is still uncommon in most parts of the world. Posttreatment hemoptysis is usually secondary to bronchiectasis or aspergilloma. Ectatic vessels or aneurysms are other considerations to keep in mind. MULTIMEDIASection 8 of 9
REFERENCESSection 9 of 9
Lung, Postprimary Tuberculosis excerpt Article Last Updated: Sep 20, 2007 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
