Internal Diseases and Therapy · MU Sofia

6. Hospital – acquired pneumonia and pneumonia in immunocompromised patients

Covers hospital-acquired and ventilator-associated pneumonia, from definitions and likely pathogens through risk factors, diagnosis and empirical antibiotic regimens by severity, to prevention. Also explains pneumonia in immunocompromised patients, organised by the type of immune defect, with separate sections on Pneumocystis, invasive aspergillosis, CMV pneumonia and other infections. Tables compare risk factors, empirical regimens and immune defects.

Inside: 2 sections · 1 labelled picture · 3 tables · 14 flashcards · 8 min

Topic 6 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 2 sections, about 945 words (8 min of reading), with 14 flashcards.

In this note

  1. Hospital-acquired (nosocomial) pneumonia
  2. Pneumonia in immunocompromised patients

Hospital-acquired (nosocomial) pneumonia

Definitions

  • Hospital-acquired pneumonia (HAP): pneumonia that develops ≥ 48 hours after admission and was not incubating at the time of admission.
  • Ventilator-associated pneumonia (VAP): a subtype that develops ≥ 48 hours after endotracheal intubation.
  • Early-onset (< 5 days in hospital): usually community-type organisms with a better prognosis; late-onset (≥ 5 days): multidrug-resistant (MDR) organisms, higher mortality.
  • HAP is the second most common hospital infection and the leading infectious cause of death in hospital; VAP occurs in about 10–25% of ventilated patients, mortality 20–50%.

Pathogens

  • Gram-negative bacilli (about 60%): Pseudomonas aeruginosa, Enterobacteriaceae (Klebsiella, E. coli, Enterobacter, Serratia — often ESBL or carbapenemase producers), Acinetobacter baumannii, Stenotrophomonas.
  • Staphylococcus aureus, including MRSA.
  • Early-onset: S. pneumoniae, H. influenzae, MSSA, sensitive Enterobacteriaceae.
  • Rarely: Legionella (contaminated hospital water), anaerobes (aspiration), fungi (Candida in sputum is usually colonisation, not pneumonia), viruses (influenza, RSV, SARS-CoV-2 outbreaks).

Risk factors

Mechanism: the oropharynx and stomach become colonised by hospital Gram-negatives within days → microaspiration of secretions (in VAP, leaking around the endotracheal tube cuff and from the biofilm on the tube) → pneumonia when host defences are weak.

Risk factors for MDR pathogens

  • IV antibiotics in the previous 90 days (the most important).
  • Septic shock or need for ventilation at the time of HAP; ARDS before VAP; ≥ 5 days in hospital before VAP; acute renal replacement therapy.
  • High local prevalence of resistant organisms (unit > 10–20% MRSA or resistant Gram-negatives); known colonisation.

Clinical features and diagnosis

  • Diagnosis: new or progressive infiltrate on chest imaging + at least two of: fever > 38 °C (or hypothermia), leukocytosis or leukopenia, purulent secretions, worsening oxygenation.
  • In the ventilated patient: more and purulent tracheal secretions, rising oxygen requirement or PEEP, fever, haemodynamic instability.
  • Differential diagnosis: atelectasis, pulmonary oedema, ARDS, PE, aspiration pneumonitis, drug reaction, pulmonary haemorrhage.
  • Before antibiotics: lower respiratory tract samples for Gram stain and (semi)quantitative culture — sputum, endotracheal aspirate, or bronchoscopic/blind BAL or protected brush; blood cultures (2 sets); pleural fluid if effusion; MRSA nasal swab (a negative result helps stop anti-MRSA treatment); Legionella and pneumococcal urinary antigen in selected cases.
  • Procalcitonin and CPIS (Clinical Pulmonary Infection Score) help, but the decision is clinical.

Empirical treatment (ERS/ESICM/ESCMID/ALAT algorithm)

  • Always follow the local antibiogram of the hospital or ICU.
  • De-escalate within 48–72 h to a narrow agent according to cultures, or stop if pneumonia is excluded.

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