Internal Diseases and Therapy · MU Sofia

4. Bacterial community –acquired pneumonia

Covers the definition of community-acquired pneumonia, its bacterial causes with a table of pathogens and their typical settings, and the main risk factors and routes of infection. It then describes the pathogenesis, the lobar and bronchopneumonia patterns, and the stages of lobar pneumonia in a table. Clinical signs, imaging, laboratory and microbiology tests, severity scores such as CURB-65, treatment overview, complications and prevention close the note.

Inside: 10 sections · 2 labelled pictures · 4 tables · 15 flashcards · 10 min

Topic 4 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 10 sections, about 1,122 words (10 min of reading), with 15 flashcards.

In this note

  1. Definition
  2. Etiology
  3. Risk factors
  4. Pathogenesis
  5. Clinical presentation
  6. Diagnosis
  7. Assessment of severity
  8. Treatment (overview — details in "Treatment of pneumonias")
  9. Complications
  10. Prevention

Definition

  • Pneumonia: an acute infection of the lung parenchyma (alveolar spaces and/or interstitium) with a new infiltrate on chest imaging and clinical signs of lower respiratory tract infection.
  • Community-acquired pneumonia (CAP): acquired outside hospital, or diagnosed within 48 h of admission, in a patient who has not been in a healthcare institution recently.
  • One of the leading infectious causes of death, especially in the elderly and in patients with comorbidities.

Etiology

In about half of cases no pathogen is found. Among identified bacteria:

Risk factors

  • Age > 65 and immobility; smoking; alcohol abuse.
  • Chronic disease: COPD, asthma, bronchiectasis, cystic fibrosis, heart failure, diabetes, chronic kidney or liver disease.
  • Immunosuppression: HIV, asplenia, malnutrition, chemotherapy, corticosteroids and other immunosuppressants.
  • Impaired airway protection → aspiration: stroke, seizures, anaesthesia, sedatives, intoxication, dysphagia, oesophageal disease.
  • Preceding viral infection (influenza), crowded living conditions (prisons, shelters), toxins; drugs that reduce gastric acid (PPIs).

Pathogenesis

  • Routes: microaspiration of oropharyngeal secretions (the most common), inhalation of airborne droplets, aspiration of gastric contents, food or liquids; rarely haematogenous spread (S. aureus from endocarditis or catheters).
  • Pneumonia develops when the pathogen overcomes the defences: cough reflex, mucociliary clearance, secretory IgA, surfactant, alveolar macrophages.
  • Bacteria multiply in the alveoli → inflammatory exudate (neutrophils, fibrin, red cells) fills the alveoli = consolidation.
  • Consolidated alveoli are perfused but not ventilated → V/Q mismatch and intrapulmonary right-to-left shunt → hypoxaemia with ↑ A–a gradient. Hypoxaemia worsens when the patient lies on the affected side (better perfusion of the dependent lung).

Patterns of involvement

  • Lobar pneumonia: a whole lobe (or lung) uniformly consolidated; classically S. pneumoniae (also Klebsiella).
  • Bronchopneumonia (lobular): patchy consolidation around bronchioles, often bilateral and basal; S. aureus, H. influenzae, Gram-negatives, anaerobes; infants, the elderly, bedridden patients.
  • Interstitial pneumonia: inflammation of the alveolar walls; viruses, Mycoplasma (atypical picture).
  • Miliary: haematogenous spread (tuberculosis, fungi).

Drawing of both lungs contrasting lobar pneumonia (one whole lobe consolidated, left of image) with bronchopneumonia (scattered patchy foci around the bronchi, right of image).

Image: “Lobar Pneumonia and bronchopneumonia illustrated” by Suraj at Malayalam Wikipedia, Public domain, via Wikimedia Commons.

Stages of lobar pneumonia

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