INFECTIOUS SYNDROMES

Pneumonia

Classification: Infection of lung parenchyma producing inflammatory alveolar/interstitial injury and impaired gas exchange (Fiske & Bloch, 2019; Norris, 2020).

Key diagnostic discriminator: An acute compatible respiratory syndrome plus a new pulmonary infiltrate supports pneumonia. Acquisition setting, aspiration risk, immune status, and severity determine likely organisms and management (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).

Clinical priority: Escalate for rising oxygen need, exhaustion, inability to protect the airway, multilobar disease, empyema, shock, acute kidney injury, or altered consciousness (Fiske & Bloch, 2019; Ma & Lucey, 2012).

Etiology and risk factors

  • Pathogens include bacteria, viruses, fungi, and atypical organisms. Organism probability varies among community-acquired, hospital-acquired, ventilator-associated, aspiration-associated, and immunocompromised-host pneumonia (Fiske & Bloch, 2019; Norris, 2020).
  • Risk factors include age extremes, smoking, chronic lung/heart disease, dysphagia or impaired consciousness, poor cough/ciliary clearance, recent healthcare/antibiotic exposure, and immune compromise (Fiske & Bloch, 2019; Norris, 2020).

Pathophysiology

  • Microaspiration/inhalation, macroaspiration, hematogenous spread, or contiguous extension overwhelms mechanical and immune defenses (Fiske & Bloch, 2019; Norris, 2020).
  • Inflammatory cells and protein-rich exudate fill alveoli or injure interstitium. Consolidation, shunt and ventilation-perfusion mismatch reduce oxygenation; systemic inflammation can progress to sepsis and organ dysfunction (Fiske & Bloch, 2019; Norris, 2020).

Clinical manifestations

  • Fever or hypothermia, cough with or without sputum, dyspnea, pleuritic pain, tachypnea, tachycardia, crackles, bronchial breath sounds, dullness, hypoxemia, or focal consolidation findings (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).
  • Older adults may present with confusion, falls, anorexia, or functional decline. Viral disease may include upper-respiratory symptoms and myalgias. Severe disease causes respiratory failure, hypotension, or altered mentation (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).

Findings that argue against or redirect

  • Acute bronchitis usually lacks a new infiltrate. A normal early chest radiograph does not fully exclude pneumonia in dehydration, neutropenia, or early disease; reassess if suspicion remains high (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).
  • Sudden pleuritic pain, disproportionate hypoxemia, and thromboembolic risk redirect toward pulmonary embolism. Bilateral edema pattern, jugular venous pressure, and cardiac congestion favor heart failure (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).
  • An immediate event after aspiration with rapid improvement may be chemical pneumonitis rather than bacterial aspiration pneumonia (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).

Diagnostic evaluation

  • Assess oxygen saturation, respiratory effort, perfusion, mental status, and illness severity. In adults with suspected community-acquired pneumonia, establish a compatible clinical syndrome and confirm pulmonary infiltrate with chest radiography or, where appropriate expertise exists, lung ultrasound. Use computed tomography selectively when initial imaging is nondiagnostic or a complication is suspected (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).
  • Do not obtain routine sputum or blood cultures for uncomplicated outpatient community-acquired pneumonia. Obtain pretreatment respiratory and blood cultures for severe disease and when empiric coverage for methicillin-resistant Staphylococcus aureus or Pseudomonas aeruginosa is used or supported by validated risk factors (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).
  • Use molecular influenza testing when influenza is circulating. Do not use an initial procalcitonin result to withhold empiric antibiotics in radiographically confirmed community-acquired pneumonia (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).
  • Use the Pneumonia Severity Index with clinical judgment to guide site-of-care decisions in immunocompetent adults. Hospital-acquired, ventilator-associated, aspiration-related, and immunocompromised-host pneumonia require setting-specific evaluation (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).

Expected diagnostic and laboratory findings

  • Supportive: new infiltrate/consolidation with a compatible clinical syndrome. Leukocytosis, leukopenia, elevated inflammatory markers, and hypoxemia indicate response/severity but are nonspecific (Fiske & Bloch, 2019; Seller & Symons, 2018).
  • Definitive etiology requires a credible lower-respiratory, blood, antigen, or molecular result interpreted against colonization and specimen quality. Many cases remain without an identified pathogen (Fiske & Bloch, 2019; Seller & Symons, 2018).

Differential diagnosis

  • Acute bronchitis/COPD or asthma exacerbation: wheeze/cough without new parenchymal infiltrate (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).
  • Heart failure: vascular congestion, edema/orthopnea, and cardiac evidence (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).
  • Pulmonary embolism: sudden symptoms, thromboembolic risk, and confirmatory vascular imaging (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).
  • Tuberculosis, malignancy, organizing pneumonia, or eosinophilic disease: chronic/recurrent course, characteristic exposure/imaging, and targeted testing (Ma & Lucey, 2012; Maselli & Anzueto, 2012; Seller & Symons, 2018).

Treatment and management

  • Support oxygenation, ventilation, hydration, perfusion, and secretion clearance. Select empiric antimicrobials according to acquisition setting, severity, comorbidities, local resistance, recent microbiology, and validated risk for resistant organisms, then narrow or stop therapy as data permit (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).
  • For adult outpatients and inpatients with nonsevere community-acquired pneumonia who reach clinical stability, a course shorter than five days, with a minimum of three days, may be appropriate. Treat severe community-acquired pneumonia for at least five days and use longer courses for complications, deep infection, or pathogens that require extended therapy (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).
  • When respiratory viral testing is positive, base empiric antibacterial treatment on comorbidity, care setting, severity, imaging, and the probability of bacterial coinfection. The 2026 ATS guideline suggests no empiric antibacterials for otherwise healthy outpatients with low concern for bacterial coinfection and conditionally favors empiric coverage for comorbid outpatients and hospitalized adults, with reassessment as data evolve and local stewardship guidance applied (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).
  • Do not use systemic corticosteroids for nonsevere community-acquired pneumonia. Consider them for selected adults hospitalized with severe community-acquired pneumonia after evaluating contraindications, influenza status, timing, and local protocol (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).
  • Drain a complicated parapneumonic effusion or empyema. Vaccination, smoking cessation, oral care, mobility, and dysphagia management reduce selected future risk (Fiske & Bloch, 2019; Jones et al., 2026; Metlay et al., 2019).

Additional complications and red flags

  • Pneumonia in a profoundly immunocompromised host requires a broader, specialist-guided differential and diagnostic strategy (Fiske & Bloch, 2019; Ma & Lucey, 2012).

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References

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Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Seller, R. H., & Symons, A. B. (2018). Differential diagnosis of common complaints (7th ed.). Elsevier.