Community-acquired pneumonia (CAP) is an acute infection of the lung parenchyma acquired outside of hospital or long-term care settings. The pathophysiology involves microbial invasion of the normally sterile lower respiratory tract after failure of host defense mechanisms. Primary defenses include the epiglottic reflex, mucociliary clearance (ciliated pseudostratified columnar epithelium), secretory IgA in airway secretions, and alveolar macrophages. When these defenses are overwhelmed (viral URI damaging ciliated epithelium, aspiration, immunosuppression), pathogens reach the alveoli and trigger an inflammatory cascade. Alveolar macrophages recognize pathogen-associated molecular patterns (PAMPs) via toll-like receptors (TLRs), releasing pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8) that recruit neutrophils from the pulmonary vasculature. Neutrophil migration into alveolar spaces, along with fibrin exudation and edema fluid, fills alveoli and creates consolidation — the hallmark radiographic finding. This alveolar filling impairs gas exchange by creating ventilation-perfusion (V/Q) mismatch and intrapulmonary shunting, producing hypoxemia. Streptococcus pneumoniae, the most common typical CAP pathogen, uses pneumolysin (a pore-forming cytolysin that destroys respiratory epithelium and inhibits neutrophil function), autolysin (releases cell wall components that activate complement and inflammation), and polysaccharide capsule (resists phagocytosis). Atypical pathogens (Mycoplasma...