Fig. 13.28 Lung defense mechanisms. (A) Innate defenses against infection: 1, In the normal lung, removal of microbial organisms depends on entrapment in the mucous blanket and removal by means of the mucociliary elevator; 2, Phagocytosis by alveolar macrophages can kill and degrade organisms and remove them from the air spaces by migrating onto the mucociliary elevator; or 3, phagocytosis and killing by neutrophils recruited by macrophage factors; 4, Complement may enter the alveoli and be activated by the alternative pathway to produce the opsonin C3b, which enhances phagocytosis; 5, Organisms, including those ingested by phagocytes, may reach the draining lymph nodes to initiate immune responses. (B) Additional mechanisms operate after development of adaptive immunity: 1, Secreted IgA can block attachment of the microorganism to epithelium in the upper-respiratory tract; 2, In the lower-respiratory tract, serum antibodies (IgM, IgG) are present in the alveolar lining fluid and activate complement more efficiently by the classic pathway, yielding C3b (not shown); In addition, IgG is an opsonin; 3, The accumulation of immune T cells is important for controlling infections by viruses and other intracellular microorganisms.
PMN, neutrophil.
increased incidence of infections with pyogenic bacteria. For example, patients with mutations in MYD88, an adaptor protein required for signaling by Toll-like receptors, are extremely susceptible to severe necrotizing pneumococcal infections, while patients with congenital defects in IgA production (the major immunoglobulin in airways secretions) are at increased risk for pneumonias caused by encapsulated organisms such as pneumococcus and H. influenzae. On the other hand, defects in TH1 cell–mediated immunity lead mainly to increased infections with intracellular microbes such as atypical mycobacteria. Much more commonly, lifestyle choices interfere with host immune defense mechanisms and facilitate infections. For example, cigarette smoke compromises mucociliary clearance and pulmonary macrophage activity, and alcohol impairs neutrophile function as well as cough and epiglottic reflexes (thereby increasing the risk for aspiration).
Bacterial pneumonias are classified according to the specific etiologic agent or, if no pathogen can be isolated, by the clinical setting in which the infection occurs. Altogether, seven distinct clinical settings are recognized, each associated with a fairly distinct group of pathogens (summarized in
Table 13.5 ). Thus, consideration of the clinical setting can be a helpful guide when anti-microbial therapy has to be given empirically.
Bacterial pneumonias often follow a viral upper-respiratory tract infection. S. pneumoniae (i.e., the pneumococcus) is the most common cause of community-acquired acute pneumonia and is discussed first, followed by other relative common  pathogens.