Pneumonia

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Pneumonia - Medical Student Exam Overview

Sources: Harrison's Principles of Internal Medicine 22E (2025), Fishman's Pulmonary Diseases, Grainger & Allison's Diagnostic Radiology

Definition

Pneumonia is an infection of the pulmonary parenchyma. It is frequently misdiagnosed, mistreated, and underestimated despite carrying significant morbidity and mortality. - Harrison's Principles of Internal Medicine 22E, p. 1066

Classification by Acquisition Setting

TypeDefinitionKey Features
CAP (Community-Acquired)Acquired outside hospital or healthcare settingsMost common; S. pneumoniae is the leading cause
HAP (Hospital-Acquired)Develops ≥48 h after admissionGram-negatives, S. aureus dominate
VAP (Ventilator-Associated)Develops ≥48-72 h after endotracheal intubationHigh mortality; bronchopneumonia pattern typical
Aspiration PneumoniaMacroaspiration of oropharyngeal/gastric contentsAccounts for 5-15% of CAP; gravity-dependent lung zones
The older category "healthcare-associated pneumonia (HCAP)" has been discontinued - it did not reliably predict resistant organisms and led to overuse of broad-spectrum antibiotics. - Harrison's 22E

Pathophysiology

Route of Entry

Microorganisms reach the lower respiratory tract by:
  1. Microaspiration of oropharyngeal organisms (most common)
  2. Inhalation of airborne droplets
  3. Hematogenous spread from a distant focus
  4. Direct mucosal dispersion

Positive Feedback Loop Model (Modern Concept)

The lung is not a sterile environment - it has its own microbiota. Pneumonia is not simply "invasion of a sterile space" but an emergent phenomenon:
  • Inflammatory event → epithelial/endothelial injury → cytokine/chemokine/catecholamine release
  • Some catecholamines selectively promote growth of S. pneumoniae and P. aeruginosa
  • This creates a self-accelerating loop: more inflammation → more nutrients for bacteria → more bacterial growth → dominant pathogen emerges
  • In CAP/HAP, the trigger is often a viral infection + microaspiration

Host Defense Mechanisms (that can be overcome)

  • Nasal hairs, turbinates, branching airways
  • Mucociliary clearance
  • Gag and cough reflexes
  • Alveolar macrophages, neutrophils, secretory IgA

Mediators of Damage

  • IL-6, TNF → fever
  • IL-8, G-CSF → neutrophil recruitment
  • Neutrophil/macrophage mediators → alveolar capillary leak → impaired oxygenation, hypoxemia, infiltrates
  • Some bacteria interfere with hypoxic vasoconstriction → severe hypoxemia

Pathology - Classic Stages (Lobar Pneumococcal Pneumonia)

These four stages are a high-yield exam topic:
StageHistologyKey Feature
1. EdemaProteinaceous exudate + bacteria in alveoliVascular engorgement; serous fluid
2. Red HepatizationRBCs fill alveoli; neutrophils appearLung = liver-like consistency; red-red color
3. Gray HepatizationRBCs lysed; neutrophils + fibrin dominate; bacteria disappearInfection being contained; gas exchange improves
4. ResolutionMacrophages clear debris (neutrophils, bacteria, fibrin)Return to normal
This staging best applies to lobar pneumococcal pneumonia; VAP typically shows a bronchopneumonia pattern instead. - Harrison's 22E, p. 1067

Types by Radiographic Pattern

This is a high-yield classification for matching pathogen to X-ray appearance:
Radiographic PatternCharacteristicCommon Organisms
Lobar consolidationEntire lobe opacified; air bronchograms; no volume lossS. pneumoniae, Klebsiella pneumoniae
BronchopneumoniaPatchy, multifocal infiltrates; peribronchial distributionS. aureus, Gram-negative bacilli, anaerobes, S. pneumoniae
Interstitial pneumoniaReticular/reticulonodular pattern; peribronchovascular infiltrateViruses, Mycoplasma pneumoniae
CavitationAir-fluid level within opacityS. aureus (pneumatoceles), M. tuberculosis, Gram-negatives, anaerobes
MiliaryDiffuse tiny nodulesM. tuberculosis, endemic fungi, viruses
Important caveat: No radiographic pattern is specific for any one organism. Overlap is common and differentiation based solely on CXR is unreliable. - Grainger & Allison's Diagnostic Radiology
Lobar Pneumonia mechanism: Organisms induce alveolar inflammatory edema. When consolidation fills an entire lobe, an air bronchogram appears (airway outlined by surrounding fluid-filled alveoli). Volume loss is absent or minimal in early consolidation. - Fishman's Pulmonary Diseases

Typical vs. Atypical Pneumonia

FeatureTypicalAtypical
OnsetAcute (hours)Subacute (days)
PresentationProductive cough, rigors, pleuritic chest pain, high feverDry cough, headache, myalgias, low-grade fever
PathogensS. pneumoniae, H. influenzae, KlebsiellaMycoplasma, Chlamydophila pneumoniae, Legionella, viruses
CXRLobar consolidationInterstitial/patchy bilateral infiltrates
SputumPurulent, productiveScant or absent
Response to beta-lactamsYesNo (need macrolide/fluoroquinolone)

Common Causative Pathogens

CAP Pathogens (most to least common):
  • Streptococcus pneumoniae (most common overall)
  • Mycoplasma pneumoniae (most common atypical; young adults)
  • Haemophilus influenzae (COPD patients)
  • Legionella pneumophila (atypical; hyponatremia, GI symptoms, Pontiac fever)
  • Chlamydophila pneumoniae
  • Respiratory viruses (influenza, RSV, SARS-CoV-2, metapneumovirus)
  • Staphylococcus aureus (post-influenza; cavitation/pneumatoceles)
  • Klebsiella pneumoniae (alcoholics; "currant jelly sputum"; upper lobe)

Clinical Features

Symptoms:
  • Fever, chills, sweats, tachycardia
  • Cough (non-productive or productive - mucoid, purulent, blood-tinged)
  • Gross hemoptysis → suggests necrotizing pneumonia (think CA-MRSA)
  • Dyspnea, pleuritic chest pain
  • GI symptoms (nausea, vomiting, diarrhea) in up to 20% of patients
  • Fatigue, headache, myalgias, arthralgias
Signs on examination:
  • Tachypnea; accessory muscle use
  • Dullness to percussion (consolidation/effusion)
  • Increased tactile fremitus (consolidation)
  • Crackles (crepitations), bronchial breath sounds, pleural friction rub
  • Elderly: may present with new-onset confusion or worsening of chronic illness with few respiratory symptoms

Diagnosis

Clinical Diagnosis

Requires: compatible history (cough, fever, dyspnea, sputum) + new infiltrate on chest radiography
The sensitivity/specificity of physical examination alone is only 58% and 67% respectively.

Imaging

ModalityRole
CXR (PA + lateral)First-line; determines extent, detects complications (cavitation, effusion, pneumothorax)
CT chest (HRCT)More sensitive; detects infiltrates up to 5 days earlier than CXR; used if CXR normal but clinical suspicion high, or to rule out alternative diagnoses
False-negative CXR occurs in: early disease, neutropenia, hypovolemia, PCP (Pneumocystis jirovecii)

CT Images of Viral Pneumonia

CT - Influenza pneumonia (peripheral ground-glass opacities):
CT chest showing peripheral ground-glass opacities in influenza pneumonia
CT - COVID-19 pneumonia (bilateral ground-glass opacities + consolidation):
CT chest showing bilateral ground-glass opacities and consolidation in COVID-19 pneumonia

Laboratory (for hospitalized patients)

  • Blood cultures (before antibiotics) - low yield (~14%) but important
  • Sputum Gram stain + culture (if quality sputum obtainable)
  • Urine antigen tests: S. pneumoniae antigen (high sensitivity/specificity), Legionella antigen
  • Nasopharyngeal swab/PCR: influenza, SARS-CoV-2, RSV
  • Inflammatory markers: CRP and procalcitonin (PCT) - PCT is insufficiently accurate alone and should NOT be used to withhold antibiotics

Microbiological gram stain (microscopy):

Sputum gram stain showing lancet-shaped diplococci (pneumococcal) and polymorphonuclear leukocytes
Sputum from pneumococcal lobar pneumonia - Gram-positive lancet-shaped diplococci with polymorphonuclear leukocytes.

Severity Scoring (Site-of-Care Decision)

CURB-65 (simpler, bedside)

LetterCriterion
CConfusion (new onset)
UUrea >7 mmol/L (BUN >19 mg/dL)
RRespiratory rate ≥30/min
BBlood pressure: systolic ≤90 or diastolic ≤60 mmHg
65Age ≥65 years
  • Score 0 → outpatient (30-day mortality ~1.5%)
  • Score 1-2 → hospitalize (unless solely due to age ≥65)
  • Score ≥3 → consider ICU (mortality ~22%)

PSI (Pneumonia Severity Index)

  • More validated and accurate than CURB-65 but complex (20 variables)
  • Classes I-V; Class V mortality = 29.2%

Direct ICU admission criteria

  • Septic shock requiring vasopressors
  • Acute respiratory failure requiring mechanical ventilation
  • Or ≥3 of 9 minor criteria (tachypnea, hypoxemia, multilobar infiltrates, confusion, uremia, leukopenia, thrombocytopenia, hypothermia, hypotension)

Complications (High-Yield)

ComplicationNotes
Parapneumonic effusion / EmpyemaMost common with S. pyogenes, S. aureus
Lung abscessCavitation with air-fluid level; anaerobes, S. aureus, Klebsiella
BacteremiaOccurs in ~25-30% of pneumococcal CAP
ARDSBilateral infiltrates; PaO2/FiO2 <300
Respiratory failureMay require mechanical ventilation
Septic shockEnd-organ failure

High-Yield Exam Mnemonics

CURB-65 = severity scoring for CAP
Classic pathogens by setting:
  • Young, healthy, walking pneumonia → Mycoplasma
  • Elderly, community → S. pneumoniae
  • Post-influenza, cavitation → S. aureus
  • Alcoholic, upper lobe, "currant jelly" sputum → Klebsiella
  • Nosocomial/ventilated → Pseudomonas, Acinetobacter, MRSA
  • Hyponatremia + GI symptoms → Legionella
  • Immunocompromised (HIV, CD4 <200) → Pneumocystis jirovecii
Stages of lobar pneumonia: Congestion → Red hepatization → Gray hepatization → Resolution (Come Right Go Rest)

Sources: Harrison's Principles of Internal Medicine 22E (2025) Ch. 131 | Fishman's Pulmonary Diseases and Disorders Ch. 122 | Grainger & Allison's Diagnostic Radiology Ch. 5
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