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Pneumonia can be very broadly defined as any infection in the lung. It may present as acute, fulminant clinical disease or as chronic disease with a more protracted course. The histologic spectrum of pneumonia may vary from a fibrinopurulent alveolar exudate seen in acute bacterial pneumonias, to mononuclear interstitial infiltrates in viral and other atypical pneumonias, to granulomas and cavitation seen in many of the chronic pneumonias. Acute bacterial pneumonias can present as one of two anatomic and radiographic patterns, referred to as bronchopneumonia and lobar pneumonia. Bronchopneumonia implies a patchy distribution of inflammation that generally involves more than one lobe. This pattern results from an initial infection of the bronchi and bronchioles with extension into the adjacent alveoli. By contrast, in lobar pneumonia the contiguous airspaces of part or all of a lobe are homogeneously filled with an exudate that can be visualized on radiographs as a lobar or segmental consolidation . Streptococcus pneumoniae is responsible for more than 90% of lobar pneumonias. The anatomic distinction between lobar pneumonia and bronchopneumonia can often become blurry, because
(1) many organisms present with either of the two patterns of distribution and
(2) confluent bronchopneumonia can be hard to distinguish radiologically from lobar pneumonia. Therefore, it is best to classify pneumonias either by the specific etiologic agent or, if no pathogen can be isolated, by the clinical setting in which infection occurs. Classifying pneumonias by the setting in which they arise considerably narrows the list of suspected pathogens for administering empirical antimicrobial therapy. As illustrated in Table 13-7, pneumonia can arise in seven distinct clinical settings (“pneumonia syndromes”), and the implicated pathogens are reasonably specific to each category.

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