As summarized in Chap. 10, the respiratory system has many defenses against infectious disease. The vibrissae in the nose and the mucociliary covering of the mucosa in the conducting portion of the respiratory system trap particles and micro-organisms, moving them cephalad to the pharynx to be expectorated or swallowed. Macrophages within the respiratory parenchyma phagocytize small particles and microorganisms and, if overwhelmed, recruit neutrophils from alveolar septal capillaries. Finally, immunoglobulin A in the mucosal secretions supports humoral immunity. In general, suboptimal humoral immunity and/or suboptimal nonimmune defense systems increase the risk for pyogenic bacterial infection, whereas suboptimal cell-mediated immunity increases the risk of infection by intracellular and low-virulence organisms, typically viruses and some bacteria. Other risk factors for the development of respiratory tract infection include decreased/absent cough reflex, reduced phagocytic/bactericidal activity of alveolar macrophages (eg, by alcohol, smoking, anoxia, oxygen intoxication), pulmonary congestion/edema, accumulation of airway secretions (eg, cystic fibrosis or distal to an obstruction), and mucociliary dysfunction, both congenital (eg, immotile cilia syndrome, Kartagener syndrome) and acquired (eg, viral illness, toxic effects of inhaled smoke).

This chapter will focus on the pathology of infectious disease and is organized by general morphologic similarities. There are three major morphologic patterns in infections of the respiratory tract: intra-alveolar accumulation of neutrophils, with or without abscess formation; interstitial expansion by mononuclear inflammatory cells; and granulomatous inflammation. Lung infections can also be organized based on their clinical settings rather than by their morphologic patterns (Table 34.1).

In suppurative bacterial pneumonia, there is consolidation (ie, solidification) of lung parenchyma due to the accumulation of neutrophil-rich intra-alveolar exudate (Fig. 34.1). The consolidation of bacterial pneumonia is classically subclassified into two patterns: lobar pneumonia and bronchopneumonia (or lobular pneumonia).

In lobar pneumonia, there is consolidation of contiguous airspaces, typically an entire lobe (Fig. 34.2). Lobar pneumonia is identifiable on an x-ray by a well-circumscribed radiopacity correlating to the affected lobe. Lobar pneumonia evolves through phases of congestion, red hepatization, gray hepatization, and resolution (Fig. 34.3).

During the congestion phase, the affected lobe is heavy, red, and boggy; histologically, there is vascular congestion, accumulation of intra-alveolar neutrophils, and pulmonary edema. Eventually, the lungs develop the consistency of liver (hepatization). Early in hepatization, the gross appearance is red, and the microscopic morphology comprises alveoli packed with neutrophils, erythrocytes, and fibrin; fibrous or fibrinopurulent pleural exudates are common in this phase. Later in the hepatization phase, the color of the lobe becomes gray as the fibrinous inflammatory exudate persists but becomes devoid of erythrocytes. As the inflammatory reaction resolves, the consolidated exudate is digested, leaving a granular semi-solid fluid to be resorbed. Due to the availability and efficacy of antibiotic therapy, lobar pneumonia is now rare.

In bronchopneumonia, the pattern of consolidation is of noncontiguous airspaces and typically involves more than one lobe with a bronchiolocentric distribution. Grossly, the patches of consolidation are gray-red to yellow with a surrounding rim of hyperemia and edema (Fig. 34.4). Histologically, bronchopneumonia progresses through stages similar to lobar pneumonia (Fig. 34.3). Pleural involvement in bronchopneumonia is less common than in lobar pneumonia. Radiographically, bronchopneumonia is typified by multiple foci of radiopacity.

The clinical presentation of lobar pneumonia and of bronchopneumonia includes malaise, fever, and a productive cough, occasionally with pleurisy and pleural friction rub. Appropriate antibiotic therapy (Chap. 35) usually results in restoration of lung structure and function. Complications include abscess formation (see below) due to tissue destruction and necrosis, empyema (Chaps. 26 and 29), organization of the intra-alveolar exudate into solid fibrous tissue [Fig. 34.3(c)], and dissemination of the infectious organism, possibly leading to meningitis, arthritis, endocarditis, or sepsis. The mortality of patients hospitalized for bacterial pneumonia is less than 10%, with death typically related to the development of one of the aforementioned complications or due to the presence of a significant predisposition like debilitation or chronic alcoholism. There are numerous etiologies for suppurative bacterial pneumonia, many of which are briefly discussed below.

Streptococcus pneumoniae (previously Pneumococcus pneumoniae) is a gram-positive coccus; its cocci are typically paired. It is the most common cause of lobar pneumonia (>90% of cases) and is the most common cause of community-acquired acute pneumonia (15%-25% of cases). The most common microbiologic isolates are types 1, 2, 3, and 7. Of note, S. pneumoniae type 7 also causes lung abscess (see below). Staphylococcus aureus is another gram-positive coccus, but in contrast to the paired cocci of S. pneumoniae, the cocci of S. aureus are typically in “grapelike” clusters (Fig. 34.5). S. aureus typically causes bronchopneumonia with multiple abscesses (see below) but can cause lobar pneumonia. Risk factors for S. aureus pneumonia include recent measles infection in children, recent influenza infection in adults, and intravenous drug abuse.

Haemophilus influenzae is a gram-negative coccobacillus that generally causes bronchopneumonia that notably in children can be complicated by empyema (Chaps. 26 and 29) and extrapulmonary infection. Risk factors for H. influenzae pneumonia include recent viral infection, cystic fibrosis, chronic bronchitis, and bronchiectasis (Chaps. 20, 22, and 38). Moraxella catarrhalis is another gram-negative coccobacillus that generally causes bronchopneumonia. Risk factors for M. catarrhalis pneumonia include old age and chronic obstructive pulmonary disease (Chaps. 20 and 22).

Klebsiella pneumoniae is the most common gram-negative bacillus (rod) causing bacterial pneumonia. The morphology is that of bronchopneumonia or lobar pneumonia as well as lung abscess formation (see below). Clinically, K. pneumoniae pneumonia has an abrupt onset with a cough productive of gelatinous sputum. Risk factors for K. pneumoniae pneumonia include debilitation, malnourishment, and alcoholism. Recovery is often complicated by abscess formation, fibrosis, and/or bronchiectasis (Chap. 20), and K. pneumoniae pneumonia has a significant mortality rate, even with therapy. Pseudomonas aeruginosa

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