key: cord-027679-89yt6fzo
authors: McLoud, Theresa C.; Boiselle, Phillip M.
title: Pulmonary Infections in the Normal Host
date: 2020-06-22
journal: Thoracic Radiology
DOI: 10.1016/b978-0-323-02790-8.00003-2
sha: 
doc_id: 27679
cord_uid: 89yt6fzo

nan

The computed tomography (CT) features of lobar pneumonia are similar to those seen on standard radiography ( Fig. 3-3 ). There is usually evidence of confluent opacification with air bronchograms. The air bronchograms are often more easily visualized with CT examination. Table 3 -2 summarizes the radiographic clues to the cause of pneumonia.

Bronchopneumonia (i.e., lobular pneumonia) results when organisms are deposited in the epithelium of peripheral airways (i.e., distal bronchi or bronchioles), resulting in epithelial ulcerations and formation of a peribronchiolar exudate. The inflammatory process spreads through the airway to involve the peribronchiolar alveoli, which become filled with edema and pus. Lobules may be affected in a patchy pattern initially, and further spread results in involvement of contiguous pulmonary lobules. Eventually, a confluent bronchopneumonia may resemble lobar pneumonia. Offending organisms that produce this type of pathologic response include S. aureus, gram-negative organisms, anaerobic bacteria, and L. pneumophila.

The radiographic appearance of bronchopneumonia pneumonia is most frequently that of multiple, ill-defined nodular opacities that are patchy but that may eventually become confluent and produce consolidation with airspace opacification (Fig. 3-4) . The opacification may be multifocal and involve several lobes, or it may be diffuse. As the disease progresses, segmental and lobar opacification develops, similar to the pattern of a lobar pneumonia. Early necrosis and cavitation can occur. The nodular opaci- ties of bronchopneumonia can be identified with facility on CT scans. The small nodules, usually less than 1 cm in diameter, represent peribronchiolar areas of consolidation or ground-glass opacity. They are called acinar or airspace nodules, but these nodules histologically are found in a peribronchiolar location. They are ill-defined and may be of homogenous soft tissue opacity and obscuring vessels, or they may be hazy and less dense so that adjacent vessels are clearly seen (i.e., ground-glass opacity). These nodules usually have a centrilobular location because of their proximity to small bronchioles.

This type of pneumonia is usually produced by viral organisms, which result in edema and mononuclear cell infiltration around the bronchi and bronchiolar walls and extend into the interstitium of the alveolar walls.

Bronchopneumonia or an acute interstitial pneumonia may be seen with viral infections . The early radiographic appearance is that of thickening of end-on bronchi and tram lines. However, this often evolves into a reticular pattern that may be seen extending outward from the hila.

Hematogenous spread to the lungs from bacterial infection may occur, although this is unusual. One of the most frequent manifestations is septic infarcts. They usually originate from right-sided tricuspid endocarditis or infected thrombi within major systemic veins. This phenomenon is seen in intravenous drug abusers and patients with longstanding indwelling central catheters.

Septic infarcts tend to be multiple and peripheral and to abut the pleural surface. They occur more frequently in the lower lobes. These nodules or wedge-shaped opacities may show evidence of cavitation ( Fig. 3-6) . CT often demonstrates a vessel connected to the area of infarction. On CT, the septic infarcts appear as wedge-shaped, peripheral opacities abutting the pleura. They may contain air bronchograms or rounded lucencies of air, sometimes referred to as pseudocavitation. True cavitation is common.

Occasionally, septic bacterial infection may result in diffuse massive seeding of the lungs with a miliary pattern (i.e., very small nodular pattern), although this is much more common with hematogenous dissemination of granulomatous infections.

Box 3-1 outlines the complications of pneumonia.

Necrosis of lung parenchyma with cavitation ( Fig. 3-7) may occur in pneumonia, particularly that produced by virulent bacteria, including S. aureus, streptococci, gram-negative bacilli, and anaerobic bacteria. If the inflammatory process is localized, a lung abscess will form. It is usually rounded and focal, and it appears to be a mass ( Fig. 3-8) . With liquefaction of the central inflammatory process, a communication may develop with the bronchus; air enters the abscess, forming a cavity, which often contains an air-fluid level.

The walls of the cavity may be smooth, but more often, they are thick and irregular. Multiple, small cavities or microabscesses may develop in necrotizing pneumonia ( Fig. 3-9 ). They are recognized as multiple areas of lucency within a consolidated lobe or segment. A similar appearance may be produced by consolidation superimposed on areas of preexisting emphysema. If the necrosis is extensive, arteritis and vascular thrombosis may occur in an area of intense inflammation, causing ischemic necrosis and death of a portion of lung. This is a particular complication of Klebsiella pneumonia and other pneumonias producing lobar enlargement. The radiographic features include multiple areas of cavitation, often with air-fluid levels. Portions of dead lung may slough and form intracavitary masses. Coned-down view of the right lung demonstrates a fine reticulonodular pattern, which is more prominent centrally.

Pneumatoceles are usually associated with pneumonia caused by virulent organisms; the classic offender is S. aureus (Fig. 3-10) . They usually form subpleural collections of air, which result from alveolar rupture. Radiographically, they appear as single or multiple, cystic lesions with thin and smooth walls. They may show rapid change in size and location on serial radiographs.

Intrathoracic lymphadenopathy that can be recognized on standard radiographs is uncommon in most bacterial and viral infections; some notable exceptions include Mycobacterium tuberculosis, Pasteurella tularensis, and Yersinia pestis. Adenopathy may be associated with fungal infections or bacterial infections that are long-standing or virulent, as in lung abscesses. CT may show slightly enlarged nodes (>1 cm) in patients with common bacterial infections that are not visible on standard radiography.

Pleural effusion is a common complication of pneumonia, occurring in about 40% of cases ( Fig. 3-11 ). Most effusions are parapneumonic, but infection of the pleural space with empyema requiring drainage is an important but uncommon complication of some pneumonias. Empyemas can be recognized by the presence of gross pus within the pleural space, by a white blood cell count in the pleural fluid of greater than 15,000 cells/mm 3 , by the presence of bacteria within the pleural fluid, or by a pH less than 7.2. Chapter 18 provides more detail on the pleural complications of pneumonia.

Parenchymal necrosis in an underlying pneumonia may produce a fistula between the bronchus and the pleural space (i.e., bronchopleural fistula), and this results in an empyema with an air-fluid level. Further discussion of these entities can be found in Chapter 18.

Rapidly progressive and fulminant bacterial or viral pneumonia may result in the acute respiratory distress syndrome (ARDS). In the preantibiotic era, bronchiectasis was an extremely common complication of bacterial pneumonia, but the incidence of bronchiectasis has declined with the advent of antibiotics. Most pneumonias clear within 2 or 3 weeks, but in elderly patients, resolution may take 3 to 4 months. Necrotizing pneumonias also tend to resolve slowly. Recurrent pneumonias are frequently found in patients with predisposing factors such as chronic obstructive lung disease, bronchiectasis, alcoholism, and diabetes. Although recurrent or persistent pneumonia in the same location raises the possibility of an obstructing endobronchial lesion due to lung carcinoma, cancer accounts for less than 5% of such cases.

The most common gram-positive bacteria causing pneumonia include S. pneumoniae (pneumococcus), S. aureus, and Streptococcus pyogenes.

S. pneumoniae (Box 3-2) is responsible for one third to one half of community-acquired pneumonias in adults. These infections occur more frequently in the winter and early spring. Pneumococcal pneumonia occurs in healthy people, but it is much more common in alcoholic, debilitated, and other immunocompromised individuals.

The radiographic features include consolidation that is usually unilateral, although it may be bilateral, and it typically affects the lower lobes (see Fig. 3-1) . Although it is a lobar pneumonia, it is uncommon for the lobe to be completely consolidated. Cavitation is rare, and large pleural effusions are uncommon. When present, they suggest the development of empyema. Sometimes, especially in children, the pneumonia may have a rounded, masslike appearance ( Fig. 3-12) . This is called a round pneumonia; it results from centrifugal spread of the rapidly replicating bacteria by way of the pores of Kohn and canals of Lambert from a single primary focus in the lung. 

S. aureus (Box 3-3) is a gram-positive coccus, and the spherical organisms occur in pairs and clusters. This pneumonia rarely develops in healthy adults, but it is sometimes a complication of viral infections and is much more common in infants and children. In infants, unilateral or bilat-eral consolidation involving the lower lungs is the most frequent radiographic presentation. Pneumatoceles, thinwalled cysts filled with air or partially filled with fluid, may develop and occasionally rupture into the pleural space, resulting in pneumothorax. In adults, the disease is usually bilateral and is preceded by an atypical pneumonia such as influenza. Cavitation is a common feature, and the cavities may be multiple, thick walled, and irregular ( Fig. 3-13 ). There is a high incidence of large pleural effusions, and empyema resulting from bronchopleural fistula is a common complication. Methicillin resistant staphylococcus aureus (MRSA) pneumonia usually occurs as a nosocomial infection in health care centers particularly in older, immunocompromised or intensive care unit patients.

Staphylococcal infection in the lungs may occur by way of the hematogenous route. This is usually the result of septic emboli, which arise in the central veins or as vegetations on cardiac valves, particularly in intravenous drug abusers and patients with indwelling intravenous catheters. The radiographic appearance is that of multiple nodular masses with or without cavitation, as previously described.

Streptococci (Box 3-4) are gram-positive cocci that occur in pairs and chains. The pneumonia occasionally occurs in epidemic proportions. This form of pneumonia is much less common than that caused by Staphylococcus or S. pneumoniae (pneumococcus).

The radiographic features include lower lobe consolidation, often occurring with a segmental distribution. Pleural effusions occur frequently, but localized empyema is unusual.

Pneumonias caused by gram-negative organisms usually are nosocomial pneumonias that affect hospitalized patients. These pneumonias tend to occur in patients maintained on artificial ventilators or in those who have intravenous catheters or a variety of other ancillary support systems. The incidence of gram-negative pneumonia acquired in the community is increasing, which may be related to the A B C 

Klebsiella pneumonia (Box 3-5) usually occurs in middle-aged or elderly patients, in those with underlying chronic lung disease, and in alcoholic individuals. Radiographic features consist of an upper lobe consolidation. Cavitation is common, and the lobar consolidation may lead to an expanded lobe with bulging interlobar fissures (see Fig. 3 -2). If necrosis is extensive, pulmonary gangrene may develop.

E. coli pneumonia (Box 3-6) may be caused by direct extension from the gastrointestinal or genitourinary tract across the diaphragm or result from bacteremia. As is true of most of the gram-negative pneumonias, it is frequently characterized by the development of necrosis and multiple cavities. The lower lobes are more frequently involved. 

P. aeruginosa pneumonia (Box 3-7) usually occurs in hospitalized patients, particularly those with debilitating disease (see Fig. 3 -9). Organisms that affect the lungs often result from contamination of suction and tracheostomy devices. Radiographic features include a lower lobe predilection. However, the consolidation may spread rapidly to affect both lungs. Pleural effusions are uncommon. Multiple, irregular nodules may develop and are usually associated with bacteremia. These nodules may cavitate.

H. influenzae pneumonia (Box 3-8) usually develops in patients with COPD. The appearance is typically that of a bronchopneumonia with homogeneous segmental opacities, usually in the lower lobes. Cavitation and pleural effusions are rare. Chemical pneumonitis and acute lung injury Diffuse consolidation resembling pulmonary edema Aspiration of particulate matter or foreign bodies may produce different clinical syndromes, depending on the size of the aspirated material and the level of airway obstruction. Large food particles or foreign bodies may be aspirated into the larynx and upper trachea, resulting in the so-called café coronary syndrome, which is caused by acute upper airway obstruction. These patients exhibit respiratory distress and aphonia.

Results of chest radiographs are usually normal for patients who have aspirated foreign bodies. If the foreign body is opaque, it may be visible in the airways. Air trapping may occur if the foreign body causes airway obstruction of one of the major bronchi. This can be demonstrated by inspiratory and expiratory radiographs, decubitus views, or chest fluoroscopy. Occasionally, complete obstruction of the bronchus results in atelectasis and, if the foreign body is unrecognized, in the development of distal pneumonitis or bronchiectasis.

Ninety percent of aspiration pneumonias and lung abscesses are caused by anaerobic organisms. The pathogens include Prevotella, Bacteroides, Fusobacterium, and Peptostreptococcus. Because of the presence of oxygen in the lung, the progression of anaerobic infection is slow, beginning in the dependent lung zones. If the patient is in a supine position when the aspiration occurs, the superior segments of the lower lobes are most commonly affected, with the right side affected more frequently than the left (Fig. 3-14) . Aspiration can also affect the posterior segments of both upper lobes. Chronic or recurrent aspiration, particularly in patients who are in the upright position, usually results in consolidation involving the basilar segments of the lower lobes. The middle lobe and lingula are uncommon sites for aspiration pneumonia. Aspiration is the most common cause of a primary lung abscess (see Fig. 3-8) .

A primary lung abscess refers to a focal, walled-off area of anaerobic pneumonia with central liquefaction necrosis. It is most commonly identified in the superior segments of either lower lobe. Lung abscesses have a fairly thick wall and may or may not have an air-fluid level. A rounded, masslike lesion may precede the development of cavitation.

Occasionally, aspiration of nontoxic material that contains insufficient bacteria to produce an infection or insufficient volume to produce atelectasis may occur. The radiographic appearance usually consists of basilar patchy opacities resembling atelectasis, and these areas clear within several days. Mendelson's syndrome is a specific form of aspiration that results from the aspiration of gastric acid. This event produces a chemical pneumonitis and acute lung injury. The radiographic manifestations of gastric aspiration are similar to those of noncardiogenic pulmonary edema. The distribution is usually diffuse.

Atypical pneumonia syndrome (Box 3-10) describes pneumonias that do not respond to usual empiric antimicrobial therapy or do not have clinical features distinctive from the usual bacterial pathogens responsible for communityacquired pneumonias. Originally, these atypical pneumonias were thought to be caused by viruses. However, other treatable organisms have emerged as important causes of atypical pneumonia, including M. pneumoniae, L. pneumophila, and Chlamydia. These nonviral, atypical pneumonias are for the most part readily treatable with antibiotics.

Most patients with atypical pneumonia present with a nonspecific syndrome consisting of fever, usually without shaking chills, and nonproductive cough, headache, myalgias, and some degree of dyspnea. This contrasts with the classic presentation of bacterial pneumonia, which is characterized by abrupt onset with fever, shaking chills, and purulent sputum, often with chest pain. Patients with the latter signs and symptoms usually have a bacterial pneumonia attributable to pneumococci, group A streptococci, Klebsiella, S. aureus, or H. influenzae. Many of the atypical pneumonias are associated with extrapulmonary manifestations. For example, diarrhea is a prominent part of Legionella and Mycoplasma infection.

M. pneumoniae (Box 3-11) accounts for approximately 20% of all cases of pneumonia. It usually occurs during the winter months in enclosed populations, such as students in college dormitories. The incubation period is 2 to 3 weeks, and the onset is often insidious, with low-grade fever and nonproductive cough. Extrapulmonary manifestations may include otitis, nonexudative pharyngitis, and diarrhea.

The radiographic features are usually those of a fairly diffuse, interstitial, fine reticulonodular pattern. This may evolve to patchy airspace consolidation, particularly in the lower lobes ( Fig. 3-15 ). Hilar adenopathy is seen in approximately 20% to 40% of patients. The radiographic appearance is very similar to that of many viral infections. The diagnosis is made by serologic evaluation.

The first outbreak of Legionnaires' disease was recognized in Philadelphia at a Legionnaires' convention (Box 3-12).

Clinical features include acute febrile illness without pneumonia; systemic disease with primarily pulmonary manifestations; a peak incidence in patients older than 60 years; a predisposition in smokers and those with alcoholic liver disease; high fever, shaking chills, and cough with small amounts of mucoid sputum; pleuritic chest pain; watery diarrhea in about one half of patients; and headache. The organism is spread by airborne transmission, usually through moist air exhaust or cooling towers.

The radiographic features of Legionnaires' disease often consist of segmental opacification and consolidation, particularly of an upper lobe. Rapid development of coalescence with complete consolidation of an involved lobe and rapid extension to adjacent lobes are common features ( Fig. 3-16 ). Parenchymal changes are extensive, but pleural effusions are uncommon. The diagnosis of Legionnaires' disease is usually made by serology using indirect fluorescent antibody. Direct identification of the organism may be confirmed by direct fluorescent antibody (DFA) techniques using properly collected specimens.

Chlamydia, a long recognized cause of pneumonia in neonates, is an increasingly frequent cause of communityacquired atypical pneumonia in adult patients (Box 3-13). It is caused by the TWAR agent (Chlamydia pneumoniae). Chlamydia pneumonia may occur in compromised and noncompromised adults as an atypical pneumonia. The disease is characterized by fever and nonproductive cough. It is often preceded by pharyngitis.

Radiographic features may be similar to those of Mycoplasma pneumonia. However, more commonly there is a localized area of consolidation in the middle or lower lobes, which may be patchy or homogeneous ( Fig. 3-17 ).

Atypical nonviral pneumonias are rare. They include psittacosis; Q fever, a rickettsial disease; and tularemia.

Chlamydia psittaci is the etiologic agent of psittacosis, which may be transmitted by any avian species, and it is contracted by inhalation of infected aerosol material. The clue to the diagnosis is the history, which should include information about any contact with birds. Psittacosis usually mimics a standard bacterial pneumonia on chest radiography.

Coxiella burnetii is the etiologic agent of Q fever, which is a rickettsial disease. It is most common in the western and southwestern parts of the United States, and it can be transmitted by infected dust from animals. The radiographic features vary, but the most specific pattern simulates mycoplasma or viral pneumonia and usually consists of bilateral, diffuse reticulonodular opacities.

Tularemia, another animal-associated, atypical pneumo nia, is transmitted by ticks in summer and rabbits in winter. There is an ulceroglandular form, which produces a skin papule that eventually ulcerates at the port of entry. Regional lymph nodes may become enlarged and eventually drain and ulcerate. In the typhoidal form, no portal of entry is apparent, but patients are characteristically extremely ill with gastrointestinal symptoms. Pneumonia may occur in patients with either of these presentations.

The most common radiographic feature is that of a localized and homogenous opacity, but lobar consolidation has also been reported. Occasionally, multiple lobes are involved. Bilateral hilar adenopathy may occur.

Primary respiratory viruses (Box 3-14) include the parainfluenza and influenza group of viruses, respiratory syncytial virus (RSV), adenovirus, and picornavirus. The incidence of these infections varies with the age of the patient. For example, in children, RSV is responsible for up to 85% of epidemic lower respiratory tract infections and up to 60% of all pneumonias; in adults, the influenza and parainfluenza groups are responsible for most of the epidemic viral pneumonias. They usually occur during late winter. Adenovirus and picornavirus cause nonepidemic respiratory infections. Other viruses (e.g., cytomegalovirus) produce pneumonia as part of a systemic infection.

In all cases, the infection usually begins in the larger central airways. At this stage, the chest radiograph frequently appears normal. The radiologic correlates of severe inflammation and edema of the bronchial walls include coarse reticular opacities in the form of rings and parallel lines (i.e., tram tracks) due to bronchial wall thickening in the central perihilar lung zones. When the small airways are involved, bronchiolitis develops. Involvement of terminal bronchioles may lead to airway obstruction. This is more likely to occur in infants and young children because the cross-sectional area of the airways is small. Diffuse overinflation and air trapping can be visualized. When the infection spreads to the alveoli, the disease is usually limited to the parenchyma around the terminal airways. The radiographic features in children and adults usually consist of a diffuse reticulonodular pattern, often with focal and patchy areas of consolidation (see Fig. 3 -4). Multiple lobes are usually involved. CT may reveal the anatomic localization of the disease. The bronchiolitis and surrounding inflammation produces nodular opacities, which are located in the center of the lobules. Branching centrilobular opacities represent impaction of small airways, and their appearance has been referred to as the treein-bud pattern ( Fig. 3-18 ). Other common CT findings of viral pneumonia include ground-glass attenuation with a lobular distribution and foci of segmental and subsegmental consolidation.

Influenza is one of the most frequently reported contagious diseases. Symptoms include fever, nonproductive cough, weakness, and myalgias. Most patients who develop severe pneumonia have underlying disease or superinfection with bacterial organisms.

Radiographic features may reflect the complicating bacterial pneumonia. However, a diffuse reticulonodular pattern may be seen in infants and children with the disease.

Adenovirus may occur in epidemic or pandemic proportions. When pneumonia develops, there may be destructive changes involving the peripheral airways, leading to chronic bronchitis, bronchiectasis, and bronchiolitis obliterans. Symptoms tend to persist after resolution of pneumonia. Radiographic features are very similar to pneumococcal pneumonia in pattern and distribution.

RSV, rarely reported in adults, is the most prevalent respiratory viral pathogen in the first 6 months of life. It usually produces focal and diffuse bronchiolitis. If radiographs are abnormal, they usually show increased lung volumes and air trapping, and linear interstitial opacities occasionally may be identified.

Varicella-herpes zoster (i.e., chickenpox) infection may be responsible for severe pneumonia in adults. The radiographic features are fairly characteristic. They consist of nodules ranging from 4 to 6 mm in diameter, with illdefined margins diffusely distributed throughout both lungs (Fig. 3-19) . Radiographic resolution usually occurs over many weeks. One of the interesting sequelae of chickenpox pneumonia is the development of diffuse, discrete pulmonary calcifications that can be identified on routine radiographs obtained after the infection (Fig. 3-20) . Histoplasmosis should be considered in the differential diagnosis of this radiologic appearance.

Cytomegalovirus infection is discussed in Chapter 4.

The Epstein-Barr virus is the presumed etiologic agent for infectious mononucleosis. Although upper respiratory symptoms predominate, patients may develop a nonproductive cough. The chest radiograph is usually normal, but occasionally, pronounced hilar lymph node enlargement with an ill-defined, diffuse reticular pattern in the lungs may be seen.

Mycobacteria are aerobic, nonmotile, non-spore-forming rods that have in common the characteristics of staining bright red with carbol fuchsin and resistance to discoloration by strong acid solutions. The organisms are therefore referred to as acid-fast bacilli (AFB). There are several mycobacterial species, but the most important include Mycobacterium leprae, the cause of leprosy; M. tuberculosis and Mycobacterium bovis, responsible for tuberculosis; and the nontuberculous mycobacteria that are important etiologic agents in the development of pulmonary disease.

In the latter part of the 19th century, tuberculosis (Box 3-15) was a leading cause of death in the United States. The advent of drug therapy and improved public health measures led to a steady decline in the incidence of tuberculosis after World War II until 1985. For the next 7 years, a slow but steady increase in the incidence of tuberculosis was observed. This rise was primarily attributed to a large number of cases associated with acquired immunodeficiency syndrome (AIDS). Immigration into the United States of individuals from third world countries also might have contributed to the increased prevalence of tuberculosis.

Since 1993, the rate of tuberculosis has declined considerably. In 2006, the rate of tuberculosis in the United States was the lowest since the beginning of national record keeping in 1953. The tuberculosis rate is continuing to decline, but the rate of decline has recently slowed.

Respiratory or systemic symptoms Patients older than 60 years Diarrhea common Airborne spread through moist air exhaust or cooling towers Diagnosis by serology with indirect fluorescent antibody

Affects upper lobes Rapid spread to other lobes From 1993 to 1997, there was also a decrease in the percentage of multidrug-resistant tuberculosis cases among persons with no prior history of tuberculosis, with a reduction from 2.4% to 1.1%. Since 1997, the rate has remained steady at approximately 1%.

In the United States, tuberculosis case rates vary considerably among different racial and ethnic populations and are lowest among whites. For example, compared with whites, the case rates are nearly 25 times higher for Asians and 10 times higher for blacks and Hispanics. The rate of tuberculosis among foreign-born persons in the United States is nearly 10 times higher than that of persons born in the United States. Other susceptible populations include the aged and the immunocompromised, particularly patients with AIDS.

Infection with tuberculosis occurs as the result of inhalation of airborne droplets containing the tubercle bacilli. The initial infection, referred to as primary tuberculosis, is most common in the lower lobes. The bacteria are ingested by macrophages and initially spread to local lymph nodes at this stage, and they then may disseminate throughout the body. The infection is usually contained if the host is immunocompetent. However, walled-off tubercle bacilli representing a dormant focus of tuberculosis may activate under appropriate conditions. This may occur in the second type of tuberculosis, referred to as reactivation or postprimary tuberculosis.

Reactivation or post primary tuberculosis can occur any time after the primary infection, but the highest rate of reactivation occurs during the first and second years after the initial infection. Reactivation tuberculosis usually involves the lung apex, but a dormant focus of tuberculosis may become active in other organs, such as the bones, kidney, or brain. Clinically active disease may develop at the time of primary tuberculous infection (i.e., primary progressive tuberculosis) or when dissemination occurs (i.e., miliary tuberculosis). Clinical reactivation disease results when there is an ineffective T-cell immune reaction. The typical pathologic feature of tuberculosis is the caseating granuloma.

Chlamydia pneumoniae (TWAR agent) Nonproductive cough Preceding pharyngitis

Localized consolidation in lower lobes Patchy or homogeneous pattern 

Patients with primary tuberculosis are usually asymptomatic but occasionally may have a symptomatic pneumonia. Patients with acute or chronic reactivation tuberculosis usually present with a chronic cough, weight loss, and occasionally with hemoptysis and dyspnea. The symptoms are often insidious. Ninety-five percent of patients with active tuberculosis have a positive tuberculin skin test result. The diagnosis must be made on the basis of culture of the organism, although the presence of AFB on the smear from the sputum is strong presumptive evidence of tuberculosis. Classification of tuberculosis into primary or reactivation phases is based on the radiographic appearance. In third world countries and in the United States during 19th and early 20th centuries, primary tuberculosis was a disease of children, and reactivation tuberculosis was typically a disease of young adults. However, a significant change in the pattern of adult tuberculosis has occurred in the past several decades. Because of diminished exposure of children to tuberculosis, the disease often occurs in the primary form in adults. This has resulted in atypical radiographic manifestations of tuberculosis in adults, attributable to primary infection rather than reactivation of the disease.

The radiographic features of primary tuberculosis are summarized in Box 3-16. Primary tuberculous pneumonia can occur in any lobe of the lung but is more common at the lung bases (Fig. 3-21) . In more than one half of cases, the disease occurs in the lower lobes. Any chronic consolidation, particularly in the bases of the lungs, may suggest tuberculosis. Cavitation, although rare in primary tuberculosis, is more frequently reported in adults than in children with the primary form of disease.

Mediastinal and hilar adenopathy is another feature of primary tuberculosis (Fig. 3-22) . It may occur alone or in association with consolidation in the lung. It tends to be particularly predominant in children. CT may be helpful in identifying and localizing adenopathy. On CT scans, tuberculous adenopathy has a predilection for the right paratracheal, right tracheobronchial, and subcarinal regions. Occasionally, atelectasis may result from extrinsic obstruction of a bronchus by enlarged lymph nodes. On CT scans obtained with intravenously administered contrast material, these nodes often demonstrate low-attenuation necrotic centers.

Pleural effusion due to tuberculous pleurisy, also a feature of primary infection, develops when subpleural foci of tuberculosis rupture into the pleural space. Patients present 3 to 7 months after the initial exposure. Organisms are rarely found in the fluid, and the diagnosis must be confirmed with a pleural biopsy. The Ghon lesion (Fig. 3-23) is a manifestation of primary tuberculosis, which usually occurs in childhood and is selflimited. The host defense mechanisms handle the initial infection, and the area of consolidation in the lung slowly regresses to a well-circumscribed nodule. This nodule then shrinks and may disappear completely or remain as a solitary, calcified granuloma. The adenopathy regresses and may also exhibit calcification (i.e., Rhanke complex).

Reactivation tuberculosis usually occurs in the apical and posterior segments of the upper lobes and in the superior segment of the lower lobes. It is characterized by chronic, patchy areas of consolidation (Fig. 3-24) . Cavitation is a hallmark of reactivation tuberculosis (Fig. 3-25) . Cavities result when areas of caseation necrosis erode into the bronchial tree, expelling liquefied debris. CT is more sensitive than plain radiography in the detection of small cavities (Fig. 3-26) . They may have thick or thin walls, which can be smooth or irregular. Bronchogenic spread of tuberculosis occurs when a cavity erodes into an adjacent airway and organisms spread endobronchially to other parts of the lung. The typical radiographic features (Fig. 3-27) consist of ill-defined nodules that usually are 5 to 6 mm in diameter. They are numerous and often bilateral. On CT, the pattern of bronchogenic spread can easily be recognized by a tree-in-bud pattern. This consists of centrilobular, branching, linear opacities with or without the presence of centrilobular nodules within 3 to 5 mm of the pleural surface or interlobular septa. This pattern is best appreciated on high-resolution CT (HRCT). It is not specific for bronchogenic spread of tuberculosis and may occur in other inflammatory diseases involving the peripheral airways.

The chronic lesion of reactivation tuberculosis usually consists of fibronodular opacities in the upper lobes, often with the presence of calcification (Fig. 3-28) . It is usually associated with volume loss and retraction of the hila. Another feature of chronic reactivation tuberculosis is bronchiectasis. Tuberculosis should be considered in the differential diagnosis of upper lobe bronchiectasis. The activity of tuberculous disease cannot be determined by radiographs; it is confirmed only by positive cultures. However, tuberculosis is considered radiographically stable if there has been no change over 6 months.

Unusual patterns of tuberculosis (Box 3-17) may occur in the patient who has altered host resistance to the primary infection. Miliary tuberculosis is a term used to describe diffuse hematogenous dissemination of tuberculosis that has progressed when the host defense system is overwhelmed by massive hematogenous dissemination of organisms. It may occur at any time after the primary infection. The radiographic appearance (Fig. 3-29) is that of multiple, tiny nodules in the interstitium of the lung that are approximately 1 to 2 mm in diameter. CT may allow earlier detection than standard radiography (Fig. 3-30) . Miliary disease takes up to 6 weeks to become apparent on plain radiographs.

Pneumothorax occasionally results from tuberculosis. Tuberculosis may also cause ulceration of the bronchi, and advanced endobronchial tuberculosis may produce lobar atelectasis and strongly simulate a primary carcinoma of the lung. A localized nodular focus of tuberculosis, referred to as a tuberculoma (Fig. 3-31) , occurs in any portion of the lung and may result from primary or reactivation tuberculosis. It is usually solitary, spherical, and smooth. It may contain a central calcification, but tuberculomas occasionally may be multiple and simulate metastatic disease.

Tuberculous empyema and bronchopleural fistula may result from a tuberculous pleural effusion. Such effusions can become loculated and remain dormant for years.

Radiographic patterns of tuberculous disease in patients with acquired immune deficiency syndrome (AIDS) may vary. They are described in Chapter 4. nodule communicating with the right upper lobe posterior segment bronchus (single arrow), with associated centrilobular nodular opacities in the superior segment of the right lower lobe (three arrows). B, CT of another patient shows a typical tree-in-bud pattern. Centrilobular nodules and branching opacities can be identified close to the pleural surface (arrows).

Characteristics Some nontuberculous mycobacteria (Box 3-18) are pathogenic in humans. The most important of these organisms are Mycobacterium avium-intracellulare, often referred to as the MAC complex, and Mycobacterium kansasii. These organisms often exhibit common features. They are usually found in the soil and water. Bronchopulmonary disease is caused by inhalation of the organisms, but no human-tohuman transmission occurs. Unlike tuberculosis, nontuberculous mycobacterial infections do not manifest separate patterns of primary or reactivation disease.

Certain geographic areas have a preponderance of these forms of nontuberculous mycobacterial disease. For example, M. kansasii is more prevalent in the western and southern United States, and MAC is found more often in the southeastern United States.

The three major clinical presentations depend to some degree on the immune status of the host (Chapter 4 describes MAC disease in AIDS patients). In human immunodeficiency virus (HIV)-negative hosts, MAC typically affects male patients who are heavy smokers with underlying COPD. Similar infections may occur in patients with silicosis or bronchiectasis. The radiographic features of M. kansasii and MAC in this group of patients are indistinguishable from tuberculosis. However, MAC lung disease may develop in older women who are considered immunologically competent and who do not have a background of thickening and multiple, calcified nodular and irregular opacities can be seen in the left upper lobe (arrows). Volume loss is not a prominent feature in this case. Although such an appearance suggests inactive disease, serial radiographs are necessary to determine stability. Viable organisms may be present, and the development of clinically active disease may rarely occur.

Hematogenous dissemination Diffuse, 1-to 2-mm nodules Pneumothorax Endobronchial tuberculosis Lobar or segmental atelectasis Tuberculoma Single or multiple Nodules larger than 1 cm Tuberculous empyema Bronchopleural fistula COPD. This disease is usually noncavitary. Many women with this form of nontuberculous mycobacterial infection share similar clinical characteristics and bodily features, including scoliosis and pectus excavatum. It is uncertain whether these skeletal features predispose patients to infection due to poor tracheobronchial secretion drainage and ineffective mucociliary clearance or they are associated with markers for specific genotypes that affect body morphotype and susceptibility to infection.

Because nontuberculous mycobacteria are common contaminants, the identification of invasive disease caused by these infections should be made only when defined clinical, radiographic, and microbiologic criteria have been met as defined by the American Thoracic Society (ATS) and Infectious Disease Society of America (IDSA) guidelines. Radiologic criteria include the presence of nodular or cavitary opacities on the chest radiograph or an HRCT scan that shows multifocal bronchiectasis with multiple small nodules. Establishing a diagnosis of nontuberculous mycobacteria does not necessitate the need for treatment in all cases: rather, the decision to institute multidrug therapy should be based on an assessment of the relative risks and benefits of therapy on an individual patient basis.

The classic form of atypical mycobacterial infection produces features almost identical to those of reactivation tuberculosis (Fig. 3-32) . Involvement occurs in the apical and posterior segments of the upper lobes and superior segment of the lower lobes. Cavitation is common, and multiple cavities may be observed. The disease tends to be slowly progressive.

MAC lung disease occurring in older women who are usually nonsmokers without evidence of COPD is noncavitary and is associated with bronchiectasis. The classic radiographic features are best appreciated on CT ( Fig. 3-33) . The findings are those of cylindrical bronchiectasis associated with multiple, small, focal lung nodules that are approximately 5 mm in diameter. Any lobe may be involved, but disease in the lingula and middle lobe has the highest prevalence. Occasionally, airspace disease may be delineated. Evidence indicates that patients with these findings are truly infected and not colonized with MAC and that the MAC infection causes the bronchiectasis rather than colonizing preexisting disease.

The wide variety of fungi that may produce lung disease can be divided into two groups. Some are truly pathogenic and can produce pulmonary infection in normal hosts. They include Histoplasma, Coccidioides, Blastomyces, and Cryptococcus. A second group of fungi are secondary invaders or opportunistic organisms, which produce disease in immunosuppressed patients. This group includes Aspergillus, Candida, Cryptococcus, and Mucor. The latter group is discussed in Chapter 4.

Histoplasma capsulatum (Box 3-19) is a dimorphous fungus that gains entry to the lung by inhalation. Distribution is worldwide, and in the United States, it occurs along river valleys, particularly the Ohio, Mississippi, and St. Lawrence. The organism exists in the soil, particularly when it is contaminated by the excrement of birds (e.g., pigeons) or bats. Many epidemics may occur when there is heavy exposure due to demolition or construction in areas containing these droppings, such as bat caves, chicken houses, or attics of old buildings. In endemic areas, up to 80% of the population may be infected, but most individuals are asymptomatic. Inhalation of spores results in a localized infection of the lung, which then migrates to mediastinal and hilar lymph nodes and eventually migrates to the spleen and liver. The organisms usually are destroyed, and there is no residual of the initial infection, although a scar or calcification may occur. If individual foci of infection and necrosis persist, they may enlarge, resulting in a chronic cavitary lesion indistinguishable from that of tuberculosis. Pathologically, well-defined granulomas may be found during the acute phase of disease in the lung, in the mediastinum, and in the various organs to which the organism disseminates. When healed, these granulomas are small and densely calcified. Outbreaks of histoplasmosis are usually associated with constitutional symptoms and nonproductive cough. Many cases never come to medical attention.

The radiographic manifestations of histoplasmosis vary. The acute phase of the disease is characterized by single or multiple areas of consolidation, which are usually segmental or sublobar in distribution. These areas may be accompanied by ipsilateral hilar or mediastinal adenopathy, and occasionally, adenopathy alone may be the only finding. In the epidemic form of the disease, multiple, discrete nodules may be seen throughout both lungs; nodules may occur alone or be associated with hilar adenopathy (Fig. 3-34) . They are usually 1 to 5 mm in diameter, discrete, and poorly marginated. With healing, the nodules may remain visible as multiple, discrete, calcified lesions less than 1 cm in diameter with or without calcified hilar lymph nodes (Fig. 3-35) . A third radiographic pattern consists of a solitary granuloma or histoplasmoma, which is usually well defined and can range in size from several millimeters to 4 cm. It typically contains a central or target type of calcification. These lesions usually occur in the lower lobes, and they may have associated smaller, calcified satellite nodules.

Additional radiographic features may be identified in patients with Histoplasma infection. They include calcifications in the spleen, which often are best detected on CT. Mediastinal lymphadenopathy is common as a sole manifestation of histoplasmosis or accompanying pulmonary consolidation or nodules. Nodes frequently calcify as healing occurs. Calcified lymph nodes may lead to two complications: broncholiths and fibrosing mediastinitis. Calcified lymph nodes may over time erode into a bronchus, producing broncholithiasis and its resulting symptom complex. Patients may have unexplained chronic cough and hemoptysis. CT can best identify the intrabronchial calcification that may be associated with distal atelectasis of a segment or lobe (Fig. 3-36) A rare chronic form of histoplasmosis can simulate tuberculosis. It usually consists of thin-or thick-walled cavities with patchy areas of consolidation, particularly involving the upper lobes with fibrosis and retraction. Disseminated histoplasmosis, which may occur in normal individuals, is much more common in immunosuppressed patients. Radiographically, the appearance is identical to that of miliary tuberculosis.

Coccidioides immitis infection (Box 3-20) follows inhalation of infected spores in endemic areas such as desert areas of the southwestern United States and Central and South America. Clinical manifestations vary. Most individuals are asymptomatic, or they may experience a mild flulike illness of the lower respiratory system. Acute, severe disease may be associated with fever, cough, and pleuritic chest pain.

With the initial inhalation of the spores, a local response or pneumonitis occurs. The immune system eventually destroys the organism, with resolution of the pneumonia. About 5% of individuals may have a chronic, often asymptomatic pulmonary lesion, such as a pulmonary nodule or cavity. Similar to tuberculosis, reactivation of the initial focus can occur. Dissemination of the organism to hilar and mediastinal nodes is common, and diffuse dissemination is rare but almost universally fatal.

The initial pneumonic form of the disease is characterized by an area of consolidation anywhere in the lung but most commonly in the lower lobes. It is usually sublobar, segmental, or patchy. It may be bilateral. Hilar and mediastinal lymph node involvement occurs in about 20% of cases, and rarely, it can be seen in the absence of the parenchymal consolidation. Most of these lesions resolve spontaneously without therapy.

The radiographic features of chronic coccidioidomycosis include solitary or multiple nodules. These tend to cavitate rapidly, and the cavities typically have very thin walls ( Fig. 3-37) . The thin-walled cavity is the classic lesion of coccidioidomycosis, but it occurs in only 10% to 15% of cases. Disseminated coccidioidomycosis is rare and is characterized radiographically by nodules ranging from 5 mm to 1 cm in diameter. A classic miliary pattern can also be observed. (Box 3-21) is a dimorphic fungus that grows in a mycelial form in the soil. Infection can occur by inoculation of the skin or by inhalation of organisms into the lungs. The organism is endemic in North America, occurring mostly in the same areas where histoplasmosis occurs but also in the southeastern United States. Blastomycosis is an infection associated with hunters because the organisms are prevalent in wooded areas.

The organism is usually inhaled from the soil, and if the initial port of entry is the lung, a focal pneumonic process will occur. The disease can be self-limited, or a disseminated form can occur.

The radiographic findings are nonspecific but consist of areas of inhomogeneous consolidation in a segmental or nonsegmental distribution in any area of the lung. The next most common manifestation is that of solitary and multiple pulmonary nodules. The solitary nodules may simulate lung carcinoma. These nodules are 3 to 6 mm in diameter. A third pattern results from disseminated disease and consists of a diffuse nodular or micronodular pattern.

Cryptococcus neoformans (Box 3-22) is an encapsulated, yeastlike fungus that exists in the soil and in the yeast form in humans. The soil may be contaminated by pigeon or chicken excreta. Seventy percent of individuals who have clinical disease are immunocompromised (see Chapter 4). The central nervous system is the most frequently affected site.

In the normal host, the most common finding is that of single or multiple pulmonary nodules that are approximately 1 to 5 cm in diameter and that usually occur in the lower lobes (Fig. 3-38) . Cavitation, lymph node enlargement, and pleural effusion are uncommon. Adenopathy is rarely identified. Characteristically, the single or multiple nodules tend to abut the pleura.

Characteristics Candidiasis (Box 3-23) may be caused by a group of various organisms in the Candida genus, of which Candida albicans is the most important species. C. albicans lives in human and animal sources and may be a normal inhabitant of the 

Spores in soil contaminated with pigeon and chicken excreta Of patients with clinical disease, 70% are immunocompromised Central nervous system involvement

Single or multiple nodules larger than 1 cm Affects lower lobes oral pharynx. As a result, short of an open lung biopsy, the true invasiveness or pathogenicity of this organism when recovered from the sputum is difficult to determine. It is an unusual infection found in immunocompromised individuals.

The most common sites of infection are the mucous membranes and skin. Pulmonary candidiasis is unusual but may occur as a primary infection of the lungs, presumably resulting from aspiration of the organisms from the oral cavity. In most immunocompromised patients, pulmonary infection accompanies a diffuse, widespread fungemia.

The radiographic findings are usually nonspecific. Although most fungal diseases, particularly in immunocompromised hosts, are characterized by multiple nodules with cavitation, Candida pneumonia is more likely to produce areas of consolidation that are multiple and patchy and involve both lungs. Cavitation and hilar adenopathy are rare, and pleural effusion occurs in approximately 25% of cases.

Characteristics Actinomyces (Box 3-24) is a rod-shaped bacterium rather than a fungus, but it is often considered a fungus because of its clinical presentation and radiographic findings. The organism is found in the mouth, and pulmonary infection usually occurs in people with extensive dental caries and poor oral hygiene. Involvement results from aspiration of these organisms.

There are three forms of actinomycosis: cervicofacial, gastrointestinal, and thoracic. The hallmark of the pulmonary disease is a focal abscess with extension to the chest wall, with secondary complications such as osteomyelitis, bronchopleural fistula, and pericarditis. The organism is an anaerobe, and anaerobic cultures must be obtained to confirm the diagnosis. Typical sulfur granules may be identified on pathologic specimens.

The radiographic features initially consist of an area of consolidation in the lung. This area may become rounded and suggest an abscess. Classic signs include extension of the disease process into the chest wall with bone destruction and osteomyelitis (Fig. 3-39) . Chest wall invasion is best appreciated on CT. Pleural effusions are moderately common. Invasion of the ribs or vertebral bodies characteristically causes bone destruction and fairly extensive reactive periostitis. Notice the erosion of the cortex of the overlying rib (arrows).

Characteristics Nocardia (Box 3-25) is a gram-positive organism, and although it is classified as a bacterium, it shares many features with fungal disease. It is weakly acid fast and can be confused with mycobacteria or Legionella. It is similar to Actinomyces, but the disease usually occurs in immunocompromised patients rather than in normal hosts (see Chapter 4).

Focal consolidation is the most common finding, although the disease can appear as single or multiple nodules with cavitation. Unlike aspergillosis, progression of disease usually is rather slow. Chest wall involvement may occur but is rare.

Aspergillus (Table 3 -3) is a dimorphic fungus. The most common of the many species is Aspergillus fumigatus. Aspergillus grows widely in soil and water, in decaying vegetation, and in animal material. Aspergillosis occurs in several different forms in the lung, including noninvasive (mycetoma) and semi-invasive aspergillosis, invasive aspergillosis, and allergic bronchopul-monary aspergillosis. The type of involvement depends on the immune status of the host. Infection is initiated by the inhalation route, and Aspergillus spores may exist in the mouth and airways of normal hosts. Immunocompetent or mildly immunosuppressed patients may acquire mycetomas or semi-invasive aspergillosis, whereas those who are severely immunosuppressed develop invasive aspergillosis. Allergic bronchopulmonary aspergillosis usually occurs in asthmatic patients.

The most common radiographic form of aspergillosis is the mycetoma or fungus ball. The fungus ball consists of aspergillus hyphae, mucus, and cellular debris developing within a preexisting cyst, cavity, bulla, or area of bronchiectasis. It grows as a saprophytic organism and usually is noninvasive. A high prevalence of mycetoma has been found among patients with sarcoidosis or cystic fibrosis. Symptoms usually include hemoptysis, which may be life threatening.

The radiographic appearance of a fungus ball or mycetoma can be quite characteristic (Fig. 3-40) . Typically, there is a solid, round opacity within a cavity or thin-walled cyst. Air may dissect into the solid mass, creating the appearance of an air crescent. In most cases, the fungus ball is mobile, and changes in position occur with changes in body posture. Extensive pleural thickening at the apex of the thorax frequently accompanies the development of a mycetoma. In making the differential diagnosis, necrotizing squamous cell carcinoma and an intrapulmonary abscess should be considered.

No treatment is necessary for asymptomatic individuals, but for those who develop severe hemoptysis, there

Gram-positive, acid-fast bacilli Immunocompromised hosts

Single or multiple nodules with or without cavitation Slow progression Focal consolidation are several therapeutic options. One is an interventional radiologic technique that consists of embolization of bronchial arteries that supply the cavity. Direct installation of amphotericin B in the form of a paste inserted through a percutaneous catheter into the cavity has been successful in some cases.

Semi-invasive aspergillosis occurs in mildly immunosuppressed patients, such as those with alcoholism, chronic debilitating illness, or advanced malignancy. The lesion usually begins as a focal consolidation in the apex of one or both lungs that progresses over a period of months to become cavitary. It may form a crescent of air (i.e., air crescent sign) similar to that seen in a mycetoma. A thick-walled cavity, which later becomes thin walled and contains a fungus ball, is then formed.

The appearance may be identical to that of a mycetoma. It consists of a cavity with or without a fungus ball and air crescent, or it may be a localized area of consolidation. Extensive pleural thickening can be identified.

The features of invasive aspergillosis are described in Chapter 4, which discusses pulmonary infections in the immunocompromised patient.

Characteristics Allergic bronchopulmonary aspergillosis (see Chapter 13) occurs almost exclusively in asthmatic individuals. Aspergillus spores contained within mucous plugs in the tracheobronchial tree incite an allergic reaction. The syndrome consists of blood eosinophilia with positive precipitins and marked elevation of IgE antibodies. Large masses of mucus and Aspergillus hyphae can become trapped in the airways, producing mucoid impaction of the bronchi.

The most characteristic pattern is that of mucoid impaction of the bronchus. Central branching opacities, which sometimes are referred to as a finger-in-glove or V pattern, are identified. A more extensive description is provided in Chapter 13. Atelectasis distal to the areas of mucoid impaction usually does not occur because of collateral air drift. Air trapping may be identified, and lobar consolidation may be present. As the mucous plugs are expectorated, areas of central bronchiectasis can be identified, particularly on CT scans. Patients usually respond to steroids, but in the chronic form of the disease, scarring and upper lobe bronchiectasis are prominent features.

Mucormycosis, almost exclusively a disease in immunocompromised patients, is discussed in Chapter 4.

Pneumocystis jiroveci (formerly called Pneumocystis carinii) is discussed in Chapter 4.

In the United States, parasitic infection of the lung is rare. Pneumonia is caused by a hypersensitivity reaction to the organisms, or it results from systemic invasion of the lungs and pleura. 

Toxoplasma gondii pulmonary involvement usually develops as part of a more generalized disease. The congenital variety is the most common, and it results from transmission of the organism from mother to fetus. It is associated with a consolidative and hemorrhagic pneumonia in neonates. In adults, toxoplasmosis, like pneumocystosis, occurs in patients who are immunocompromised. The radiographic appearance is that of fairly diffuse reticulonodular opacities.

Echinococcus granulosus (Box 3-26), the cause of most cases of human hydatid disease, occurs in two forms: pastoral and sylvatic, which differ in definitive and intermediate hosts and in geographic distribution. The pastoral variety is more common and occurs in sheep, cows, or pigs as the intermediate hosts, and in dogs as the definitive host. It is particularly common in sheep-raising areas. The sylvatic variety has as the definitive host the dog, wolf, or arctic fox.

Approximately 65% to 70% of Echinococcus cysts occur in the liver, and 15% to 30% occur in the lungs. The hydatid cyst is composed of two layers, an exocyst and an endocyst. Daughter cysts may be formed within the endocyst. Cysts may rupture in the lung parenchyma, with resulting intense inflammation. Rupture into the bronchus may result in severe hypotensive shock.

Echinococcal cysts are usually well-circumscribed, spherical or oval masses that may be single or multiple (Fig. 3-41) .

They are usually located in the lower lobes. If communication develops between the cysts and the bronchial tree, air may enter between the pericyst and exocyst, producing the appearance of a thin crescent of air around the periphery of the cyst, sometimes called the meniscus or crescent sign. Bronchial communication occurs directly into the endocyst. Occasionally, an air crescent sign and air-fluid level can be identified. The membrane of the cyst, which has ruptured into the bronchial tree, may float on the fluid within the cyst, giving rise to the classic water lily sign. CT can differentiate cystic from solid lesions and may identify the pathognomonic features in ruptured or complicated hydatid cysts, such as the presence of daughter cysts and endocyst membranes. Calcification of a pulmonary hydatid cyst is rare.

Pulmonary amebiasis is rare and is usually a sequela of hepatic or gastrointestinal involvement. Amebiasis is caused by the protozoan Entamoeba histolytica. This organism causes dysentery and has a worldwide distribution. Pleuropulmonary complications usually occur when the liver is involved. Patients present with right upper quadrant and right-sided pleuritic chest pain.

The common radiographic features are right-sided pleural effusion with basal consolidation. Involvement of the lung may result from rupture of an amebic abscess in the liver. Occasionally, areas of consolidation in the right lower lobe may progress to abscess formation with cavitation.

Schistosomiasis is a common disease in many areas of the world, including Central and South America, the Middle East, and the Far East. The intermediate host of this parasite is the snail. Humans contact the parasites in water. The parasites penetrate the skin, reach the circulation, and eventually grow in the mesenteric or pelvic venous plexus, where they mature into adult worms and lay eggs. Pulmonary symptoms may occur during the larval migration phase in the lungs due to a hypersensitivity reaction. A progressive diffuse endarteritis and thrombosis may result from impaction of ova in the pulmonary circulation, with the eventual development of pulmonary arterial hypertension.

Pathologic changes in the lungs result from deposition of eggs or ova, which are released directly into the systemic venous blood or occasionally into the portal system, where eggs can reach the lungs through anastomotic channels as the liver becomes cirrhotic. The embolized ova become impacted in pulmonary arterioles and then extruded into the surrounding tissue. This causes an obliterative arteriolitis, which can result in increased pulmonary artery pressure. The ova may mature into adult worms in the lungs and can cause lung damage. 

Pulmonary arterial hypertension is the most common finding in patients with pulmonary schistosomiasis (Fig. 3-42) . The appearance consists of dilation of the central pulmonary arteries with rapid tapering. The passage of larva through the pulmonary capillaries can cause a transitory eosinophilic pneumonia, simulating Loeffler's syndrome. This is characterized by the presence of peripheral areas of consolidation.

The lungs may be infected by a number of worms, causing ascariasis, strongyloidiasis, trichinosis, ancylostomiasis (i.e., hookworm disease), and filariasis (i.e., tropical eosinophilia). Most of these organisms produce hypersensitivity reactions in the lungs, similar to Loeffler's syndrome (see Chapter 9).

Outbreaks of several newly recognized viral infections, including avian influenza, severe acute respiratory syndrome-associated coronavirus, and hantavirus, have been associated with high mortality rates. These infections have presented challenges to clinicians, radiologists, scientists, and public health officials.

Avian influenza is caused by the H5N1 subtype of the influenza A virus. Human transmission occurs through close contact with infected birds, usually from ingestion of infected poultry. The first documented case occurred in 1997 in Hong Kong. In 2003, the virus resurfaced in Vietnam. Approximately 180 people throughout Southeast Asia have been infected, with a nearly 50% mortality rate. Affected patients present with a rapidly progressive pneumonia that may lead to respiratory failure and ARDS. Chest radiographs usually show abnormalities at the time of presentation. The most common finding is multifocal consolidation (Fig 3-43) , which is bilateral in 80% of cases. Consolidation may infrequently be complicated by areas of cavitation. Bilateral pleural effusions occur in about one third of cases.

Severe acute respiratory syndrome (SARS) is caused by the SARS-associated coronavirus. It results in a systemic infection that is manifested clinically as a progressive pneumonia. The first reported case in humans occurred in China in 2002. In 2003, SARS spread to Hong Kong and subsequently to Canada, Singapore, and Vietnam. Before the infection could be contained by vigorous public health measures, more than 8000 persons were infected, with a nearly 10% fatality rate. No additional human infections have been reported since 2003. After an initial incubation period of 2 to 10 days (mean, 6 days), affected patients typically present with headache, malaise, fever, and nonproductive cough.

Chest radiographs show abnormalities at the time of clinical presentation in about 80% of cases. The most common radiographic finding is poorly defined airspace consolidation. Although about one half of cases appear to have a focal distribution at the time of presentation, progression to multifocal involvement is common. Areas of consolidation have a predilection for the lower lobes and lung periphery. CT shows abnormalities at the time of clinical presentation, even when chest radiographs do not. The most common CT finding is ground-glass opacification (Fig 3-44) , which is often accompanied by small foci of consolidation and interlobular and intralobular thickening. Severe SARS may progress to diffuse alveolar damage.

Overall, 20% of patients with SARS require mechanical ventilation, and 10% of patients do not survive the infection. Survivors often have residual abnormalities seen on CT, reflecting interstitial fibrosis and small airways disease.

Hantaviruses are carried by rodent vectors. Human infection occurs after inhalation of aerosolized rodent feces or urine. The Sin Nombre hantavirus (translated as "the nameless virus") was initially discovered in the southwestern United States in 1993 as a cause of pulmonary edema and respiratory failure accompanied by hematologic abnormalities. This clinical entity is referred to as the hantavirus pulmonary syndrome (HPS).

HPS is caused by endothelial damage to the lung. The initial interstitial edema manifests radiographically as Kerley lines, bronchial wall thickening, and subpleural edema. Although some patients recover fully from the initial stage of infection, many progress to diffuse alveolar edema, which is manifested by symmetric perihilar and basilar airspace consolidation (Fig 3-45 ). This phase of illness requires mechanical ventilation and is associated with a high mortality rate. As the disease progresses, it may be accompanied by myocardial depression, which worsens tissue hypoxia and contributes to the high mortality rate associated with this syndrome.

The Centers for Disease Control and Prevention (CDC) lists several infectious agents as a category A threats, denoting the highest potential for public health impact. These agents include inhalational anthrax (Bacillus anthracis), plague (Y. pestis), smallpox (variola major), botulism (Clostridium, botulinum), tularemia (Francisella tularensis), and hemorrhagic fever (Ebola and Marburg filoviruses). Among these infections, anthrax has the unique distinction that imaging studies may allow prompt diagnosis and institution of life-saving therapy before organ damage is irreversible. For this reason, the discussion focuses on anthrax. 

Anthrax has been used as a biologic weapon since World War II. The most recent episode occurred in 2001, when highly refined anthrax spores were placed in envelopes and mailed through the United States postal system. This act of bioterrorism resulted in 22 diagnosed cases of anthrax, which were evenly split between inhalational and cutaneous forms. Almost one half of those with the inhalational form died. B. anthracis is a sporulating, gram-positive bacterium that may result in cutaneous, gastrointestinal, or pulmonary infection. The latter, which is also referred to as inhalational anthrax, is the deadliest form. The spores are 2 to 6 μm, an ideal size for deposition in the distal respiratory tract after inhalation. Once inhaled, the spores are ingested by macrophages. Surviving spores are transported to mediastinal lymph nodes, where they germinate for 2 to 30 days (mean, 1 week).

Radiologic findings have not been identified before germination. After germination, the organisms synthesize a toxin, resulting in the prodromal phase of the disease. This is manifested by flulike symptoms of fever, chills, fatigue, and cough. The prodromal phase lasts about 4 days and is rapidly followed by the second phase of the illness, which is characterized by stridor, respiratory failure, and shock. In many cases, death occurs despite antibiotic therapy.

Imaging findings for anthrax reflect hemorrhagic lymphadenitis and mediastinitis caused by the release of anthrax toxin within the mediastinum. In the prodromal phase of the illness, the chest radiograph typically demonstrates mediastinal widening and unilateral or bilateral hilar enlargement. These findings are frequently accompanied by pleural effusions. Although limited peribronchovascular airspace opacities may be present, extensive consolidation is uncommon. Imaging findings of mediastinal widening and pleural effusions are helpful for differentiating inhalational anthrax from a community-acquired respiratory infection.

CT may provide convincing evidence of inhalational anthrax before confirmatory laboratory tests have returned (Fig 3-46 ). Unenhanced CT may show high-attenuation (46 to 62 Hounsfield units) mediastinal and hilar lymph nodes, which may rapidly enlarge over a period of days. These findings reflect the presence of hemorrhage and edema within lymph nodes. Because of this characteristic appearance, unenhanced CT is considered the imaging modality of choice for the diagnosis of inhalational anthrax.

After contrast administration, rim enhancement and central low attenuation of lymph nodes may be seen. Rapidly enlarging pleural effusions are commonly identified by CT, and they may contain dependently layering, highattenuation fluid, reflecting serosanguineous exudates. Peribronchovascular thickening correlates with the presence of edema, hemorrhage, and necrosis of the airways and adjacent lymphatics. The constellation of these CT findings is almost pathognomonic for inhalational anthrax, but a variety of other causes of mediastinitis may produce similar findings in the appropriate clinical setting.

Inhalational anthrax is treated with an antibiotic regimen that includes ciprofloxacin or doxycycline combined with two other agents, usually rifampin and clindamycin. Early recognition of anthrax and prompt administration of antibiotics before the onset of fulminant illness can dramatically improve patient survival. 

Tree-in-bud pattern: frequency and significance on thin section CT

Aspiration and inhalation pneumonias

Pulmonary coccidioidomycosis

Reported Tuberculosis in the United States. Department of Health and Human Services, CDC

Pulmonary manifestations of Mycobacterium intracellulare

Epidemiology of tuberculosis

Chlamydia pneumoniae pneumonia in hospitalized patients

An overview of pulmonary fungal infections

Mycobacterium tuberculosis

Coccidioidal pneumonia

Legionella pneumonias

Gram-negative bacillary pneumonias

Tuberculous pleural effusions

The chest radiograph in Legionnaires' disease: further observations

Aspiration pneumonia, lung abscess, and empyema

The roentgen manifestations of thoracic actinomycosis

Fraser and Pare's Diagnosis of diseases of the chest

Inhalational anthrax

Semi-invasive pulmonary aspergillosis: a new look at the spectrum of aspergillus infections of the lung

The spectrum of pulmonary aspergillosis

The acute bacterial pneumonias

Histoplasma capsulatum

The varied roentgen manifestations of primary coccidioidomycosis

An official ATS/ IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases

Pulmonary blastomycosis: radiologic manifestations

Mycobacterium aviumintracellulare complex: evaluation with CT

Mycoplasmal, viral, and rickettsial pneumonias

Viral pneumonia

Radiology of severe acute respiratory syndrome (SARS): the emerging pathologic-radiologic correlates of an emerging disease

Radiology of bacterial weapons-old and the new?

Hantavirus pulmonary syndrome: radiologic findings in 16 patients

Thoracic cryptococcosis: immunologic competence and radiologic appearance

Viral pneumonia in adults: radiologic and pathologic findings

Clinicoradiographic correlation with the extent of Legionnaire disease

CT features of thoracic mycobacterial disease

Pulmonary septic emboli: changes with CT

Anaerobic pleural and pulmonary infections

Pneumonia caused by Mycoplasma pneumoniae infection

CT features of pulmonary Mycobacterium avium complex infection

Studies in chronic allergic bronchopulmonary aspergillosis. I. Clinical and physiological findings

Thoracic manifestations of tropical parasitic infections: a pictorial review

Pneumatocele formation in adult pneumonia

Tuberculosis: frequency of unusual radiographic findings

Pulmonary infections

Granulomatous infections of the lung

Tuberculosis in the normal host: radiological findings

Spectrum of pulmonary non-tuberculous mycobacterial infection

Atypical mycobacterial infection in the lung: CT appearance

Pulmonary aspiration complexes in adults

Guidelines for the management of adults with community-acquired pneumonia: diagnosis, assessment of severity, antimicrobial therapy, and prevention

Pneumococcal pneumonia in hospitalized patients' clinical and radiological presentations

Pulmonary cryptococcosis

Adult respiratory distress syndrome

Infectious pneumonias-including aspiration states

The radiologic manifestations of H5N1 avian influenza

Hilar and mediastinal adenopathy caused by bacterial abscess of the lung

Viral pneumonitis

Thoracic histoplasmosis

Other mycobacterium species

Tuberculosis among elderly persons: an outbreak in a nursing home

Imaging of bacterial pulmonary infection in the immunocompetent patient

Severe acute respiratory syndrome: radiographic appearance and pattern of progression in 138 patients

Pulmonary aspiration of gastric contents

Update: the radiographic features of pulmonary tuberculosis

Pulmonary bacterial and viral infections