key: cord-0035383-e2h7trvz authors: Singh, Dinesh title: Imaging of Pulmonary Infections date: 2019-01-15 journal: Thoracic Imaging DOI: 10.1007/978-981-13-2544-1_6 sha: e77bc56a5ac4ffbb032182cac02e56a79c715a5d doc_id: 35383 cord_uid: e2h7trvz Pulmonary infections have always been a cause of high morbidity and mortality, particularly in the pediatric and geriatric population and in immunocompromised hosts [1]. Pulmonary infections have various etiologies and have variegated patterns on radiographs and computed tomography (CT). Imaging plays an important role in the initial diagnosis and follow-up of various lung infections. Radiographs can be normal or non-specific during the initial evaluation, and CT findings may be more definitive. CT not only helps with the diagnosis but can also aid in management by guiding the diagnostic and therapeutic procedure. The pulmonary infections spread by direct or indirect contact with the infected host, droplet transmission, or an airborne spread. In rare cases, some infections can also be transmitted by vectors, namely, insect or animal hosts, and rarely by direct invasion from nearby infected organs. Pulmonary infections may have typical imaging patterns and distribution based on the mode of spread. There are a number of well-described imaging patterns of alveolar infections. The localization and morphological features on imaging may help in the diagnosis of infection and identification of mode of infection and, in certain cases, the microorganism responsible for the infection. Pulmonary infections have always been a cause of high morbidity and mortality, particularly in the pediatric and geriatric population and in immunocompromised hosts [1] . Pulmonary infections have various etiologies and have variegated patterns on radiographs and computed tomography (CT). Imaging plays an important role in the initial diagnosis and follow-up of various lung infections. Radiographs can be normal or non-specific during the initial evaluation, and CT findings may be more definitive. CT not only helps with the diagnosis but can also aid in management by guiding the diagnostic and therapeutic procedure. The pulmonary infections spread by direct or indirect contact with the infected host, droplet transmission, or an airborne spread. In rare cases, some infections can also be transmitted by vectors, namely, insect or animal hosts, and rarely by direct invasion from nearby infected organs. Pulmonary infections may have typical imaging patterns and distribution based on the mode of spread. There are a number of well-described imaging patterns of alveolar infections. The localization and morphological features on imaging may help in the diagnosis of infection and identification of mode of infection and, in certain cases, the microorganism responsible for the infection. Patterns of Lung Infections Consolidation is a typical pattern of a lung infection on a radiograph of the chest, usually initiating as a small focus close to the fissures. Pneumonia can be caused by a variety of organisms like bacteria, bacteria-like organisms like Mycoplasma pneumonia, fungi, or even a number of viruses. Lobar pneumonia and bronchopneumonia are two distinct patterns of pulmonary infections (Figs. 6.1 and 6.2). Lobar pneumonia results in a homogenous opacity, limited by the fissures and without any associated volume loss. There may be the presence of "air bronchograms" that result from relative sparing of the bronchi, appearing as dark air-filled linear spaces within the exudate-filled alveoli. Lobar pneumonia usually has surrounding ground-glass opacities, better seen on computed tomography (CT), and can have associated complications like an abscess, pleural effusion, or empyema. The opacification of an entire lobe is uncommon nowadays due to early antibiotic treatment, which stops the progress of the infective process. Some cases of lobar pneumonia have typical imaging patterns (Table 6 .1) (Fig. 6. 3) [2, 3] . However, one should remember that consolidation is not diagnostic of infection and can also be seen in other conditions like pulmonary edema, hemorrhage, organizing pneumonia, vasculitis, and even malignancies. A unique pattern of lung infection, generally seen in children younger than 12 years of age, is called "round pneumonia" [4] . This pattern of infection is seen in children due to lack of development of interalveolar connections and collateral airways. Typically, occurring as a solitary lesion, these are usually due to bacterial infection, most commonly caused by Streptococcus pneumonia. Round pneumonia can be seen on a chest radiograph as rounded nodular opacity with illdefined margins, commonly involving the superior segments of the lower lobes. Associated air bronchograms are usually confirmatory, thereby preventing delay in diagnosis. Bronchopneumonia usually results from inhalation and rarely from hematogenous spread of microorganisms and is initially limited in and around the airways. The early airways and peribronchial ground-glass densities spread and become confluent resulting in consolidation ( Fig. 6.2) . The involvement eventually spread to larger areas, involving the segment or the entire lobe. The most common causes of bronchopneumonia include Staphylococcus aureus, Pseudomonas aeruginosa, Haemophilus influenzae, Escherichia coli, some fungi, and anaerobes. The appearance of bronchopneumonia on radiograph depends upon the stage and may range from multifocal ground-glass opacities to consolidations. The opacities are usually asymmetric in distribution and may predominantly involve the lung bases. The pattern is better appreciated on computed tomography (CT) scans. Usual CT features include focal bronchial wall thickening, centrilobular nodularity, and multifocal opacities around the bronchioles, which can also be associated with tree-in-bud appearance [5] . With the progression of infection, the ground-glass opacities lead to confluent areas of consolida-tion, and in most of the cases, CT shows scattered foci of the combination of two opacities. The term "ground-glass opacification" describes lung opacity through which the bronchovascular markings are still visible. This is much better appreciated on CT scans and can be seen in a number of lung pathologies including interstitial Axial CT images show consolida-tion with "air bronchograms" in the left upper lobe and right lower lobe along with "crazy-paving" pattern in the right middle lobe (asterisk) pneumonia [6] . This is due to cellular infiltrate in the alveolar septa and the peribronchovascular interstitium with resultant peribronchial and interlobular septal thickening or due to partial filling of airspaces in the lungs by exudate or transudate [1] . Predominant ground-glass opacification is usually seen in atypical pneumonia caused by Mycoplasma pneumonia and viral infections, particularly the opportunistic infections in an immunocompromised host [7] . These include Pneumocystis jiroveci pneumonia (PJP), cytomegalovirus (CMV) pneumonia, and herpes simplex virus (HSV) pneumonia. There are many other causes for ground-glass opacities, in immunocompromised hosts (Table 6 .2). Lung nodules are less than 3 cm, round to oval opacities that appear well-defined when surrounded by the normally aerated lung. They have a wide range of differentials ranging from infections, occupational lung diseases, malignancies, and immunological disorders. Solitary nodules can be seen in infections like tuberculosis, histoplasmosis, and hydatid disease. Multiple lung nodules can have centrilobular, perilymphatic (around fissures, peribronchovascular and subpleural), or random distribution [8] . These are discussed in the chapter of imaging of nodular lung diseases. Nodules may demonstrate secondary changes like calcification and cavitation or can have surrounding ground-glass opacities. Cavitation is frequently seen in nosocomial infections and in immunocompromised hosts [9] . Some common causes of infective nodules include tuberculosis, nocardiosis, angioinvasive aspergillosis, cryptococcal infection, and atypical mycobacterial infection [1] . Miliary pattern, i.e., diffuse nodules less than 3 mm, can be seen in a number of infections. Septic pulmonary embolism should always be considered in cases of cavitary pulmonary nodules ( Fig. 6.4 ). This condition results from embolization of infectious particles in the lungs, which block the peripheral pulmonary artery divisions, resulting in infarction and necrosis of the lung parenchyma. Common sources of septic emboli include infectious tricuspid endocarditis (especially in intravenous drug abusers), peripheral thrombophlebitis, infected central line, and cardiac pacemaker [10] . Although not a reliable [11] . Ground-glass changes surrounding lung nodules can also be due to surrounding hemorrhage and have been described in viral infections, atypical mycobacterial infection, and candida infection [12, 13, 14] . Nodules with surrounding ground-glass changes and subpleural wedge-shaped opacities are highly suggestive of angioinvasive aspergillosis, in a context of severe neutropenia. Lung cavities are thick-walled, gas-filled areas within the lung usually in a mass, area of consolidation, or even within a nodule. Bacterial infections can result in cavities as a complication of pneumonia, also termed as cavitating pneumonia. Lung abscess is a lesion within the lung with a collection of pus, usually seen in elderly, malnourished, or immunocompromised patients. Chest radiograph usually shows lung ing consolidation (black arrow) in the right upper lobe with "bulging fissure" (white arrow). (c) Follow-up radiograph after treatment shows residual scarring in the right upper lung (black arrow). "Bulging fissure" is a characteristic but not specific sign of Klebsiella pneumonia opacity with or without an air-fluid level. CT with intravenous contrast is diagnostic, with a demonstration of thickwalled, rim-enhancing lesion, containing air-fluid level, within an area of consolidation ( Fig. 6 .5). Larger abscesses seldom respond to antibiotic treatment, usually need percutaneous or surgical drainage, and despite that have higher associated mortality rates. Pneumatoceles are air-filled cystic spaces within the lung sequel to pneumonia, trauma, or aspiration and are almost always asymptomatic. Pneumatoceles can be confused with abscesses; important differentiating features include smooth Ground-glass opacities in midzones and perihilar distribution, peripheral sparing, may be associated with reticular opacities, nodules, pneumatoceles, or even consolidation HSV pneumonia (immunocompromised and mechanically ventilated patients) Ground-glass opacities with mild bronchial dilatation and areas of consolidation CMV pneumonia (especially following stem cell or solid organ transplant, AIDS) Ground-glass opacities with lobar consolidation, miliary nodules, often with surrounding halo, irregular reticular opacities Pulmonary infections are frequently associated with a number of ancillary findings like pleural effusion, pleural thickening, empyema, mediastinal lymphadenopathy, or even bone destruction. Simple parapneumonic effusions without associated pleural thickening usually respond to medical treatment; however loculated effusions and empyema typically need percutaneous drainage. Lung infections can present with enlargement of the hilar and the mediastinal nodes. Contrast-enhanced CT can not only identify enlarged nodes but can also characterize internal appearance and guide biopsy. Tuberculosis is a granulomatous infection caused by Mycobacterium tuberculosis, a rod-shaped aerobic bacterium. It is a global health problem, common in developing Southeast Asian and African countries. Historically, pulmonary tuberculosis is classified into two subtypes: primary and post-primary tuberculosis. Primary tuberculosis patients have no previous exposure and, usually, develop active disease within 2 years of infection. Post-primary tuberculosis is also known as reactivated tuberculosis, seen in patients who have had a previous infection. It is more commonly endogenous reactivation rather than due to superinfection (exogenous). Clinical presentation of tuberculosis varies with age and the immune status of the patient, with a cough, lowgrade fever, anorexia, and loss of weight being the usual presenting complaints. There are no well-established criteria on imaging for the two subtypes of pulmonary tuberculosis. The role of imaging is to assess the disease burden, the presence of cavities, and complications of tuberculosis (Figs. 6.6, 6.7, 6.8, and 6.9). Primary tuberculosis occurs most commonly in children but is being seen with increasing frequency in adults. There are three main components of primary tuberculosis: parenchymal focus, lymphadenopathy, and pleural effusion ( Table 6 .3). The parenchymal focus is typically unilateral airspace consolidation due to bronchoalveolar caseous exudate. The parenchymal focus called "Ghon focus" usually resolves without any sequel on chest radiograph or less commonly heals by calcification or calcified granuloma [15, 16] . In a small number of cases, the infection progresses with enlargement of the parenchymal lesion and spread of infection along the lymphatics in the mediastinal lymph nodes. Majority of the cases of childhood primary tuberculosis in the endemic zones have dominant lymphadenopathy, a finding less commonly seen in adults. "Ranke complex" is suggestive of previous tuberculous infection and compromises of Ghon focus with calcification in the hilar node. Pleural involvement is seen in few cases, usually the same side as the parenchymal disease [17] . Historically, the cavities are considered as a hallmark of post-primary tuberculosis but are increasingly recognized in adults with primary tuberculosis. Post-primary tuberculosis usually involves the apical and posterior segments of the upper lobe and the superior segment of the lower lobe, explained by relatively poor lymphatic drainage and higher oxygen tension [18] (Table 6 .4). Most cases involve more than one segment, in many cases even showing bilateral disease. Cavitation may be present in almost up to 50% of cases of post-primary tuberculosis. The endobronchial spread of the disease occurs when the caseous necrosis liquefaction communicates with the bronchial tree, resulting in nodular lesions distant to the cavity. This results in classical "tree-in-bud" opacities on CT scan, compromising of tiny centrilobular nodules, and branching linear opacities [19] . Tuberculoma can be solitary or multiple, round, oval, or elongated nodules and appear hyperdense or demonstrate frank areas of peripheral calcification. Pleural disease and chest wall involvement are less common and seen only in a minority of the cases. Lung cavities and bronchiectasis are late complications of pulmonary tuberculosis, usually seen in the apical and posterior segments of the upper lobes. A characteristic CT feature of the tubercular cavity is its communication with the tracheobronchial tree. Secondary colonization of a tuberculous cavity by Aspergillus can result in the formation of a fungal ball. CT imaging demonstrates air surrounding an intracavitary mass, also known as the "air crescent sign" [20] . Tuberculosis can also extend into the trachea and the bronchial tree, leading to scarring and bronchostenosis [21] . The infection can spread from the pleural space to the soft tissues of the chest wall, resulting in chest wall abscess also known as "empyema necessitans" [22] . Rasmussen aneurysm is a pseudoaneurysm that arises within or adjacent to a tuberculous cavity. It is a rare complication and results due to the weakening of the inflamed wall of a pulmonary artery branch ( Fig. 6.10 ). Miliary tuberculosis can be seen in both primary and postprimary tuberculosis and is due to hematogenous dissemination of the infection. Chest radiographs can be unremarkable until advanced disease, where it can show small nodules extensively involving the lung fields. CT is diagnostic with 1-3 mm nodules with or without associated interlobular septal thickening, identifiable on high-resolution computed tomography (HRCT) (Fig. 6.11 ). Nontuberculous mycobacteria (NTM) infections were confirmed to be true human pathogens only by 1950 and were later shown to be very similar to post-primary tuberculosis by Christensen et al., in the 1970s [23] . Table 6 .5 (Figs. 6.12 and 6.13). Diagnosis of these infections is difficult as these organisms often colonize the airways and a positive culture is not diagnostic of an infection. Invasive measures like bronchoalveolar lavage and transbronchial biopsy are often needed for confirming the diagnosis. There can be a disseminated pattern of nontuberculous mycobacterial infection in patients who are immunocompro-mised [25] . MAC is the most common organism for atypical mycobacterial infection in AIDS (acquired immune deficiency syndrome). These infections usually occur with low CD4 counts of below 100 cells/mm 3 . The diagnosis is difficult on imaging as these infections coexist with a number of other opportunistic lung infections. The most common imaging feature is mediastinal lymphadenopathy, followed by airspace opacities, miliary lung nodules, and pleural effusion [26] . Nontuberculous mycobacterial infections can also be [27, 28] . Radiographic findings are limited to reticulonodular opacities, cavities, and lymphadenopathy. There are reported cases of hypersensitivity pneumonitis caused by inhalation of MAC, most commonly from hot tub exposure [29] . Pneumocystis jiroveci, Candida, and mucormycosis, while those in the immunocompetent include histoplasmosis, coccidioidomycosis, blastomycosis, and Paracoccidioides brasiliensis [30] . Infection typically occurs due to inhalation of the fungal spores, conidia, or reactivation of a latent infection. The incidence of fungal infections is increasing due to increased numbers of immunocompromised and susceptible patients (hematological and stem cell transplant procedures, solid organ transplant, critical care setup). Diagnosing these infections is challenging and imaging can aid in early diagnosis. Cryptococcus neoformans, the causative organism for cryptococcosis, is found in soil with avian or pigeon droppings [31] . The infection can occur in both immunocompetent and immunocompromised hosts; the incidence is much more in the latter [32] . Pulmonary cryptococcosis in immunocompetent hosts is usually asymptomatic. Disseminated disease is not uncommon in AIDS, with the involvement of the central nervous system, bones, and skin. Imaging features of pulmonary cryptococcosis are described in Table. 6.6. Candidiasis is most commonly caused by Candida albicans, and lung infection is usually seen in immunocompromised patients, usually associated with widespread disease involving multiple organs. The imaging features of pulmonary candida infection are described in Table 6 .7. Mexico. Chest radiographs in the acute stage are usually unremarkable, sometimes showing areas of consolidation and bulky hilum (node enlargement). Solitary or multiple nodules with cavities can be seen in the chronic stage of the infection, better assessed on CT scans, the nodules more commonly involving the lung bases [33] (Fig. 6.14) . Cavities can be with thin ("grape-skin") or thick walls [34] . Disseminated disease in immunocompromised hosts usually shows diffuse reticulonodular or miliary pattern. Pulmonary blastomycosis is caused by Blastomyces dermatitidis, usually seen as necrotizing granulomas, especially suppurative type [30] . Imaging findings include patchy or confluent airspace consolidation, which may show associated cavitation. The other imaging feature is nodules or masses (Fig. 6.15 ). Disseminated infection results in a miliary pattern of involvement. Aspergillosis is usually caused by Aspergillus fumigatus, a fungus of the Aspergillus species. The lung infection is only seen when there is hypersensitivity or in patients with reduced immunity. Pulmonary aspergillosis is a term collectively used for a number of recognized forms of lung disease (Table 6 .8), each having distinct clinical and imaging features (Figs. 6.16, 6.17, 6.18, and 6.19). Aspergilloma and allergic bronchopulmonary aspergillosis (ABPA) are the noninvasive forms of the disease. Chronic necrotizing aspergillosis (CNA) is the locally invasive form, seen in immunocompromised patients and those with the chronic pulmonary disease. Invasive aspergillosis is a grave disease, affecting immunocompromised and critically ill patients or those with chronic obstructive pulmonary disease [35] . Aspergilloma is also known as "fungal ball" and is most commonly seen in a tuberculous cavity (Fig. 6.16 ). It can also be seen in other cavity-forming conditions or less commonly in cystic bronchiectasis [2] . ABPA is a type of eosinophilic lung disease, usually seen in patients with long-standing asthma, cystic fibrosis, or Kartagener's syndrome. The disease has various clinical stages from acute stage to end-stage fibrosis, patients usually presenting with asthma-like presentation with a recurrent lung infection. Imaging features are included in the major diagnostic criteria of ABPA. Invasive aspergillosis is the commonest fungal infection involving the lungs [30] , typically seen in immunocompromised patients with neutropenia. Angioinvasive aspergillosis is seen in severely immunocompromised patients (graft-versus-host disease following bone marrow transplant, late stages of AIDS, long-term corticosteroids, prolonged severe neutropenia). Clinical features are not reliable and early imaging is the key to identifying the pulmonary lesions. The diagnosis is confirmed only by histopathology evaluation. Mortality rates due to invasive aspergillosis can be as high as up to 70% [30] . Chronic aspergillosis is seen in patients with background chronic lung disease or diabetes and can present in cavitary or fibrosing forms [36, 37] . There is dilatation of the esophagus (black arrow) commonly seen in these patients Intracavitary usually mobile soft-tissue mass with surrounding crescent of air. Rarely, soft tissue obliterates the surrounding air crescent. There may be reactive pleural thickening Allergic bronchopulmonary aspergillosis (ABPA) • Chest radiograph: Consolidation, atelectasis, mucoid impaction hyperinflated lungs, tubular or ring opacities, volume loss • HRCT: Fleeting ground-glass opacities or consolidation Bronchiectasis (central, upper lobe, cystic), mucous plugging (bronchocele formation: "finger in glove" sign), areas of atelectasis, bronchial wall thickening, mosaic attenuation, areas of air trapping Semi-invasive or subacute invasive or chronic necrotizing aspergillosis (CNA) • Early: Upper zone opacity • Late: Similar to aspergilloma (air crescent sign), multiple cavities, surrounding infiltrates, expanding cavity, adjacent pleural thickening Airway invasive or bronchopneumonic aspergillosis (less common invasive form) Tracheobronchial wall thickening Bronchiolitis: centrilobular nodules with "tree-in-bud" opacities Bronchopneumonia (peribronchial consolidation) Angioinvasive aspergillosis (most aggressive form, life-threatening) • Chest radiograph: Peripheral nodules or masses • CT: Nodules or masses with surrounding ground-glass opacities ("halo sign"), cavitation Certain cases show central ground-glass opacity with surrounding higher-density consolidation ("reverse halo" sign) Peripheral wedge-shaped consolidation (areas of infarction) "Air crescent" sign in the recovery phase Chronic pulmonary aspergillosis Histoplasmosis is caused by Histoplasma capsulatum, typically resulting in granulomatous inflammation, necrosis, and fibrosis, thereby resembling tuberculosis [30] . Acute histoplasmosis is often difficult to identify on chest radiograph, and CT evaluation is needed to identify the abnormalities. In some cases, the infection can extend to the mediastinal structures, resulting in fibrosing mediastinitis. Chronic histoplasmosis is a rare disease, typically seen in patients with background chronic obstructive pulmonary disease. Imaging findings in chronic histoplasmosis include patchy consolidation (upper lobe predominance), upper lobe cavitation, calcified hilar and mediastinal nodes, and rarely broncholithiasis ( Table 6 .9). Nocardiosis is mostly commonly caused by Nocardia asteroides or Nocardia brasiliensis and can result in pulmonary or systemic infection. Nocardia asteroides is usually responsible for the pulmonary disease, causing severe opportunistic infection in immunocompromised patients with non-specific imaging findings (Fig. 6 .20) (Table. 6.10). Pneumocystis jiroveci pneumonia is caused by a yeastlike organism and was previously known as Pneumocystis carinii [38] . The infection is seen in AIDS (CD4 counts of below 100 cells/mm 3 ), patients with hematological cancers, solid organ transplant recipients, and bone marrow transplant patients. Dyspnea and nonproductive cough are the usual presenting symptoms. The typical radiological features are listed in Table 6 .11 (Figs. 6.21, 6.22, and 6.23). Atypical imaging features can be seen in patients on prophylactic treatment. These features include consolidation, small nodules with tree-in-bud opacities, cavitating nodules, enlarged lymph nodes, and pleural effusion. Diagnosis is confirmed by identifying the organisms in bronchoalveolar lavage, in sputum, or by monoclonal antibody testing. Gallium-67 lung scintigraphy test has Angioinvasive aspergillosis in a 42-year-old man presenting with neutropenic fever following chemotherapy for acute myeloid leukemia. (a, b) Axial CT images show right lower lobe nodule with "halo" sign been shown to be highly sensitive for PCJ infection, and a negative test result virtually excludes this infection. Various RNA and DNA viruses can cause clinically important pulmonary infections, in both immunocompetent and immunocompromised hosts. Clinical presentations of most of these infections are similar, and the diagnosis is heavily reliant on the background picture, risk factors, and exposures [7] . Imaging is useful in identifying the pattern and extent of the disease, assessing response on follow-up and for diagnostic procedures. Chest radiographs are unremarkable or may demonstrate non-specific changes, like patchy ground-glass opacities, consolidations, effusion, or nod- Axial CT images (b, c) show multiple ground-glass density nodules ules. Although imaging features in bacterial and viral pulmonary infections show considerable overlap, CT may be useful by demonstrating few main patterns of disease (Table 6 .12) [39] . Some viral infections are more common with midzone and hilar predominance. There is no pleural effusion or lymphadenopathy in specific scenarios with a particular imaging pattern. Ground-glass opacities, multiple nodules, or "interstitial pneumonia" pattern in a patient with hematopoietic stem cell transplant is most commonly seen in cytomegalovirus infection. Aspiration pneumonia results from the passage of material from the oropharynx in the tracheobronchial tree instead of esophagus. Central nervous system diseases, drug overdose, alcohol intoxication, esophageal motility disorders, and anesthesia are some common predisposing risk factors for aspiration pneumonia [40] . It can be classified as acute and chronic aspiration pneumonitis, based on the time course. Mendelson syndrome is a form of acute chemical pneumonitis due to aspiration of acidic gastric content during general anesthesia usually for obstetric procedures. Imaging features are similar to noncardiogenic pulmonary edema. When aspiration occurs in a recumbent patient, the changes are seen involving the posterior segment of the upper lobes and the superior segment or posterior basal segments of lower lobes (Figs. 6.1, 6.24, 6.25, 6.26, and 6.27) ( Table 6. thickening, ground-glass changes, and peribronchial involvement sparing the subpleural lung. There is no pleural effusion or mediastinal lymphadenopathy basal, lingula, and middle lobe involvement can be seen in otherwise ambulatory patients. Chronic/recurrent aspiration pneumonitis usually appears as small and large airways disease but may mimic fibrotic lung disease or even a lung mass. Lung abscess or empyema can be seen in complicated cases. 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