Chapter 3 Pulmonary Infections in the Normal Host
Pneumonia ranks sixth among the causes of death in the United States and is the leading cause of death due to infection. The factors responsible for this high mortality rate include an increasing elderly population, immunocompromised hosts in greater numbers, new etiologic agents of pneumonia, antibiotic-resistant organisms, and unusual organisms acquired from international travel. The etiologic agent can reach the lungs by several routes. The most common is inhalation of airborne droplets, followed by aspiration of nasopharyngeal organisms, hematogenous spread to the lungs from other extrathoracic sources of infection, direct extension from a localized site of infection, and infection from penetrating wounds.
Clinical features are important in the determination of the etiologic agent of pneumonia (Table 3-1). Community-acquired pneumonias occurring in previously healthy individuals are caused by Streptococcus pneumoniae in 50% to 75% of cases and by Mycoplasma pneumoniae, viral organisms, or Legionella pneumophila. Nosocomial pneumonias (i.e., acquired in the hospital by patients who are already ill) typically are caused by gram-negative organisms or Staphylococcus aureus. Certain preexisting conditions are associated with pneumonias due to specific organisms. For example, patients with altered states of consciousness or those in coma are more likely to develop aspiration and subsequently develop infections due to mouth organisms (i.e., gram-negative organisms and anaerobes). S. aureus infection can occur after influenza pneumonia; in patients with chronic obstructive pulmonary disease (COPD), Haemophilus influenzae infection is common. S. aureus and Pseudomonas aeruginosa organisms are common superinfectants in patients with cystic fibrosis.
|Clinical Circumstance||Likely Causative Organisms|
|Previously well, community-acquired||50% to 75% due to Streptococcus pneumoniae (pneumococcus), Mycoplasma pneumoniae, virus, or Legionella pneumophila|
|Hospital-acquired, otherwise ill||Gram-negative organisms, including Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli, and Enterobacter species; Staphylococcus aureus; less commonly, S. pneumoniae and Legionella|
|Alcoholism||S. pneumoniae most common; gram-negative organisms, anaerobes, and S. aureus frequent causes|
|Diabetes mellitus||Suspect gram-negative organisms and S. aureus|
|Altered consciousness, coma||Gram-negative organisms and anaerobes|
|Drug addiction||If not an AIDS patient, suspect Staphylococcus and gram-negative organisms|
|After influenza||S. aureus|
|Chronic bronchitis with exacerbation||Haemophilus influenzae (common)|
|Cystic fibrosis||Mucoid, P. aeruginosa|
From Woodring JH: Pulmonary bacterial and viral infections. In Freundlich IM, Bragg DG (eds): A radiologic approach to diseases of the chest. Baltimore, Williams & Wilkins, 1992.
The pathologic classification of pneumonia is based on the anatomic localization of the disease process. Categories include lobar pneumonia, bronchopneumonia or lobular pneumonia, hematogenous bacterial infection, and acute interstitial pneumonia.
Lobar pneumonia results when inhaled organisms reach the subpleural zone of the lung and produce alveolar wall injury with severe hemorrhagic edema. This is followed by a rapid multiplication of organisms and invasion of the infected edema fluid by polymorphonuclear leukocytes. Rapid spread occurs through the terminal airways and pores of Kohn, and consolidation of an entire lobe or segment may occur. This process is frequently aborted by administration of antibiotic therapy. The pattern commonly is seen in pneumonias due to S. pneumoniae. Klebsiella pneumoniae, L. pneumophila, and M. pneumoniae can also produce lobar consolidation.
This type of pneumonia produces a pattern of confluent opacification, often with air bronchograms (Fig. 3-1). The entire lobe may be involved, but more frequently because of early use of antibiotics, the pneumonia involves only one or more segments within a lobe (i.e., sublobar form). A lobar pneumonia may result in expansion of the lobe due to voluminous edema, which is usually caused by infection with K. pneumoniae (Fig. 3-2). The enlargement of the lobe can be recognized radiographically by bulging of the interlobar fissures. Necrosis, cavitation, and development of a unique complication, pulmonary gangrene, may ensue.
Figure 3-1 Posteroanterior (A) and lateral (B) views of lobar consolidation involving the middle lobe supported the diagnosis of Streptococcus pneumoniae (pneumococcus) infection.
Figure 3-2 Anteroposterior view of a patient with Klebsiella pneumonia shows homogeneous opacity of the right upper lobe with slight bulging of the minor fissure (arrow).
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.
Figure 3-3 CT of a pneumococcal left upper lobar consolidation shows clearly defined air bronchograms and evidence of cavitation.
|Radiographic Finding||Likely Causative Organisms|
|Round pneumonia||Suspect Streptococcus pneumoniae (pneumococcus)|
|Complete lobar consolidation||S. pneumoniae, Klebsiella pneumoniae, and other gram-negative bacilli; Legionella pneumophila and occasionally Mycoplasma pneumoniae|
|Lobar enlargement||K. pneumoniae, pneumococcus, Staphylococcus aureus, Haemophilus influenzae|
|Bilateral pneumonia (bronchopneumonia)||S. pneumoniae still common, but suspect others, including S. aureus, streptococci, gram-negative bacilli, anaerobes, L. pneumophila, virus, and aspiration syndromes|
|Interstitial pneumonia||Virus, M. pneumoniae, and occasionally H. influenzae, S. pneumoniae, and other bacteria|
|Septic emboli||Usually S. aureus; occasionally gram-negative bacilli, anaerobes, and streptococci|
|Empyema or bronchopleural fistula||S. aureus, gram-negative bacilli, anaerobes, and occasionally, pneumococcus; mixed bacterial infections common|
|Contiguous spread to chest wall||Actinomycosis; occasionally other bacteria or fungi|
|Cavitation||S. aureus, gram-negative bacilli, anaerobic bacteria, and streptococci; cavitation uncommon with S. pneumoniae or L. pneumophila|
|Pulmonary gangrene||K. pneumoniae, Escherichia coli, H. influenzae, Mycobacterium tuberculosis, S. pneumoniae, anaerobes, or fungi|
|Pneumatoceles||S. aureus, gram-negative bacilli, H. influenzae, M. tuberculosis, and measles; S. pneumoniae rare|
|Lymphadenopathy||M. tuberculosis, fungi, virus, M. pneumoniae, common bacterial lung abscess, and rarely plague, tularemia, and anthrax|
|Fulminant course with acute respiratory distress syndrome (ARDS)||Virus, S. aureus, streptococci, M. tuberculosis, and L. pneumophila|
From Woodring JH: Pulmonary bacterial and viral infections. In Freundlich IM, Bragg DG (eds): A Radiologic Approach to Diseases of the Chest. Baltimore, Williams & Wilkins, 1992.
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 opacities 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.
Acute Interstitial Pneumonia
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 (Fig. 3-5). 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 of Infection
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 long-standing 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.
Figure 3-6 Septic infarcts in an intravenous drug abuser. A, The posteroanterior chest radiograph shows multiple, bilateral cavitary nodules. B and C, CT examination demonstrates that most of the infarcts are peripheral in location; some abut the pleura and occasionally are wedge shaped. True and pseudocavities (curved arrow) are present.
COMPLICATIONS OF PNEUMONIA
Box 3-1 outlines the complications of pneumonia.
Box 3-1 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.
Figure 3-7 Cavitary pneumonia due to gram-negative organisms. CT shows two areas of cavitation with an air-fluid level in the more posterior area, indicating bronchial communication.
Figure 3-8 Primary lung abscess due to aspiration. The posteroanterior (A) and lateral (B) views show a well-defined, masslike opacity in the superior segment of the right lower lobe. There is cavitation with an air-fluid level and a thick wall.
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.
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.
Hilar and Mediastinal Adenopathy
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 Effusions and Empyema
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/mm3, 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.
Figure 3-11 Parapneumonic effusion (pneumococcal pneumonia). A, The posteroanterior view shows a right upper lobe consolidation. B, An oblique view 2 days later demonstrates a right effusion.
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.
PNEUMONIAS CAUSED BY GRAM-POSITIVE BACTERIA
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.
Box 3-2 Streptococcus pneumoniae
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.
Figure 3-12 Rounded pneumonia. The lateral (A) and posteroanterior (B) chest radiographs and CT (C) of an adult patient shows an ill-defined, rounded opacity in the left upper lobe due to rounded pneumonia caused by pneumococcus. The opacity simulated a lung neoplasm radiographically, but it completely resolved after antibiotic therapy.
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 bilateral consolidation involving the lower lungs is the most frequent radiographic presentation. Pneumatoceles, thin-walled 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.
Box 3-3 Staphylococcus aureus
Figure 3-13 Staphylococcus aureus abscess. In the composite of four CT images of a patient with a left lower lobe staphylococcal abscess, notice the thick walls of the cavity (closed arrows) and the retained thick exudate in the center. Pockets of air in the peripheral regions of the cavity probably represent small pneumatoceles (open arrows).
(Courtesy of Dorothy L. McCauley, MD. New York University Medical Center, New York, NY.)
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).
Box 3-4 Streptococcus pyogenes
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 AEROBIC ORGANISMS
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 overgrowth of resistant organisms because of widespread use of broad-spectrum antibiotics.
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.
ASPIRATION PNEUMONITIS AND ANAEROBIC PNEUMONIA
Pulmonary aspiration (Box 3-9) is a common clinical problem. Many conditions predispose persons to aspiration, including reduced levels of consciousness, alcoholism, drug addiction, esophageal disease, periodontal and gingival disease, seizure disorders, and nasogastric tubes.
Box 3-9 Aspiration Pneumonitis and Anaerobic Pneumonia
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).
Figure 3-14 Aspiration pneumonia in a patient with a history of seizures. The posteroanterior (A) and lateral (B) chest radiographs demonstrate consolidation in the superior segment of the right lower lobe.
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
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 community-acquired 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.
Box 3-10 Atypical Pneumonia Syndrome
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.
Box 3-11 Mycoplasma pneumoniae
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).
Box 3-12 Legionnaires’ Disease