Pneumonia — CAP, HAP, VAP & Aspiration

Overview & definition

Pneumonia is an infection of the lung parenchyma (the alveoli), classified by the setting of acquisition, which drives the likely pathogens and the empirical antibiotics:[1][2]

• CAP — community-acquired, outside hospital or within 48 hours of admission.
• HAP — hospital-acquired, 48 hours or more after admission.
• VAP — ventilator-associated, 48 hours or more after intubation.
• Aspiration — from aspiration of oropharyngeal or gastric contents.

The 48-hour cut-off is the examinable boundary between community and nosocomial pathogens. HAP is sub-classified by onset: early (within 4 days of admission — community-type, usually antibiotic-sensitive organisms) versus late (after 4 days — multidrug-resistant organisms). VAP is a subset of HAP occurring 48 hours or more after intubation.[6]

[3]

CAP — severity and pathogens

Severity scores:[1]

• CURB-65 — Confusion, Urea over 7 mmol/L, Respiratory rate at least 30, Blood pressure (SBP under 90 or DBP 60 or under), age 65 or over. Score 0-1 is outpatient; 2 is ward; 3-5 is ICU.
• PSI/PORT — a more detailed 20-variable score predicting mortality.
• IDSA/ATS severe-CAP criteria — one major (invasive mechanical ventilation, or septic shock needing vasopressors) OR three minor (RR at least 30, PaO2/FiO2 250 or under, multilobar infiltrates, confusion, BUN 20 or over, WBC under 4, hypothermia under 36 degrees Celsius, hypotension needing aggressive fluids). Meets criteria equals ICU admission.[1]

Common CAP pathogens:[1][2]

• Typical — Streptococcus pneumoniae (the commonest), Haemophilus influenzae, Moraxella catarrhalis.
• Atypical — Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumophila.
• Viral — influenza, RSV, SARS-CoV-2.
• Risk factors modify — COPD (Pseudomonas), aspiration (anaerobes, Gram-negatives), immunocompromise (Pneumocystis, fungal).[1]

Pathogens by host profile:[1][2]

• Healthy adult — S. pneumoniae, C. pneumoniae, M. pneumoniae, respiratory viruses.
• COPD / bronchiectasis — add Haemophilus influenzae, Moraxella, and consider Pseudomonas aeruginosa (especially severe COPD on frequent steroids/antibiotics).
• Aspiration risk (stroke, seizure, reduced GCS, dysphagia) — anaerobes plus oral Gram-negatives and streptococci.
• Immunocompromise / HIV — Pneumocystis jirovecii (PJP, if CD4 under 200), fungi (Aspergillus), CMV; plus standard bacterial pathogens which remain commonest.
• Structural lung disease (bronchiectasis, CF) — Pseudomonas aeruginosa (chronic colonisation); Staphylococcus aureus in CF.

[4]

CAP empirical antibiotics

• Outpatient, no comorbidity — amoxicillin, or doxycycline, or a macrolide.[1]
• Outpatient with comorbidity — amoxicillin-clavulanate plus a macrolide, or a respiratory fluoroquinolone.[1]
• Inpatient (non-ICU) — ceftriaxone plus azithromycin, or a respiratory fluoroquinolone.[1]
• ICU — ceftriaxone plus azithromycin (add vancomycin or linezolid if MRSA suspected; add oseltamivir if influenza suspected).[1]
• Duration — 5-7 days (shorter is as effective; guided by clinical stability).[1]

Investigations before antibiotics (do not delay in septic shock):[1]

• Blood cultures x2, sputum for Gram stain and culture, arterial blood gas, full blood count, U&E, LFTs, CRP, lactate.
• Urinary antigens — pneumococcal and Legionella (rapid, high yield in severe CAP).
• Respiratory viral PCR — influenza A/B, SARS-CoV-2, RSV; add oseltamivir empirically if influenza is suspected in season.
• Atypical work-up — Legionella / Mycoplasma serology (paired, fourfold rise) and PCR where available; PJP induced sputum / BAL if immunocompromised.
• Chest X-ray (and CT if complicated: cavitation, effusion, abscess, lymphadenopathy).

[3]

HAP and VAP

Early-onset (within 4 days) — community-type pathogens (S. pneumoniae, H. influenzae, MSSA). Late-onset (after 4 days) — multidrug-resistant (MDR) organisms: Pseudomonas aeruginosa, Acinetobacter, Klebsiella (ESBL), MRSA.[2]

Empirical antibiotics — guided by the local antibiogram and the risk factors for MDR. An anti-pseudomonal beta-lactam (piperacillin-tazobactam, ceftazidime, cefepime, or meropenem) plus vancomycin or linezolid (if MRSA risk) and consider a second anti-pseudomonal agent (an aminoglycoside or a fluoroquinolone) for high-MDR-risk patients.[2]

De-escalation — narrow once the cultures identify the organism and the sensitivities. Treat for 7 days (shorter if the clinical response is good and the organism is not Pseudomonas or non-fermenting Gram-negative).[2]

VAP diagnosis — new or worsening infiltrate on CXR plus fever, leukocytosis, or purulent secretions; confirmed by quantitative cultures (a BAL with 10 to the 4 CFU/mL or more, or a protected specimen brush with 10 to the 3 or more).[2]

MDR organisms in late VAP — the big four:[6]

• Pseudomonas aeruginosa — the archetypal ICU pathogen; produces biofilm on the tube, inherently resistant to many agents, mutates rapidly to resistance under antibiotic pressure. Cover with an anti-pseudomonal beta-lactam (pip-tazo, cefepime, ceftazidime, meropenem); consider dual therapy in septic shock.
• Acinetobacter baumannii — environmental survivor, often extensively drug-resistant; treat with sulbactam combinations, polymyxin/colistin, or tetracyclines (minocycline, eravacycline). High mortality; involve microbiology.
• Enterobacterales with ESBL or carbapenemases (Klebsiella, E. coli) — ESBL: carbapenem (meropenem). Carbapenem-resistant (CRE): ceftazidime-avibactam, meropenem-vaborbactam, colistin, depending on mechanism.
• MRSA — vancomycin (AUC/MIC-guided) or linezolid (better lung penetration, no nephrotoxicity). Cover empirically if MRSA risk or unit prevalence is high.
• Stenotrophomonas maltophilia — inherently carbapenem-resistant; high-dose TMP-SMX (± ticarcillin-clavulanate or levofloxacin). Classic in patients on prolonged carbapenems.

[9]

CPIS — Clinical Pulmonary Infection Score

A bedside score (0-2 each across six domains) used to suspect VAP (CPIS >6) and to support stopping antibiotics if it falls by day 3. Domains: temperature (36-38.9 = 0, >=39 or <36 = 1-2), WBC (4-11 = 0), tracheal secretions (none = 0, purulent = 2), PaO2/FiO2 (>240 = 0, <240 = 2), chest X-ray (none/patchy/consolidation), and semi-quantitative BAL culture (0/<1+ / >1+). Moderate accuracy — an adjunct, not a standalone test.[2]

Aspiration pneumonia

From aspiration of oropharyngeal or gastric contents — typically in the dependent segments (the posterior upper lobe and the apical lower lobe in the supine patient; the basal lower lobes if upright). The organisms are anaerobes plus oral Gram-negatives and streptococci. Treat with amoxicillin-clavulanate or clindamycin (covering anaerobes and oral flora). Not every aspiration needs antibiotics (see the aspiration topic — a witnessed aspiration of sterile gastric contents is a chemical pneumonitis, not an infection).[2]

Complications

• Empyema — pus in the pleural space; drain.
• Lung abscess — a cavitating infection; prolonged antibiotics.
• ARDS — from the severe pneumonia (sepsis-induced permeability oedema).
• Septic shock — the commonest cause of ICU admission and death.
• Metastatic infection — endocarditis, meningitis, septic arthritis.[2]

[4]

Red flags

VAP prevention bundle

Ventilator-associated pneumonia is the second commonest nosocomial infection in ICU and adds roughly 4-9 extra days of mechanical ventilation. Prevention is a bundle of evidence-based measures applied together — the incremental benefit of each element compounds, and the bundle is the single most examinable and cost-effective intervention in ventilated patients.[6][2]

• Semirecumbent positioning 30-45 degrees — supine positioning is an independent risk factor for VAP; the supine patient aspirates oropharyngeal secretions around the cuff. Drakulovic showed semirecumbent (45 degrees) reduced VAP from 34% (supine) to 8%.[7] Target 30-45 degrees head-up whenever there is no contraindication (spinal instability, severe hypotension, prone).
• Daily spontaneous awakening trials (SAT) + spontaneous breathing trials (SBT) — paired sedation interruption and weaning reduces days of mechanical ventilation (and therefore VAP risk). The ABC trial (Awakening and Breathing Controlled) paired a daily SAT with a daily SBT and increased ventilator-free days.[8]
• Oral hygiene with chlorhexidine 0.12-0.2% — oropharyngeal colonisation with Gram-negatives precedes VAP; chlorhexidine mouthwash reduces this. Note the 2020 IDSA update advised against chlorhexidine in some populations (possible mortality signal in cardiac surgical patients at higher concentration) — routine oral care with tooth brushing plus chlorhexidine remains standard in general ICU.[6]
• Subglottic secretion drainage (SSD) — using an endotracheal tube with a dedicated suction port above the cuff removes the pooled, colonised secretions that leak past the cuff. Use in patients expected to be intubated over 48-72 hours.[2]
• Hand hygiene and strict aseptic suction technique — the foundation of all infection prevention.
• Peptic ulcer prophylaxis and DVT prophylaxis (stress ulcer + VTE prophylaxis) — part of the original "ventilator bundle"; they reduce stress-related mucosal disease and thromboembolism rather than VAP directly, but are bundled with the VAP measures.
• Avoid unnecessary intubation / use NIV where possible; minimise sedation; early mobilisation; tight glucose control — adjuncts that shorten ventilator days.[2][6]

[8]

Diagnosis of VAP — the diagnostic dilemma

VAP is suspected when a ventilated patient develops a new or progressive infiltrate on chest X-ray plus at least two of: fever over 38 degrees Celsius, leukocytosis or leukopenia, purulent tracheal secretions. The diagnosis is, however, notoriously unreliable on imaging alone — atelectasis, pulmonary oedema, ARDS, and contusion all mimic it. Two philosophies exist:[2][6]

• Clinical (non-invasive) — start antibiotics on clinical grounds, sample tracheal aspirate, and re-evaluate at 48-72 hours; stop antibiotics if cultures are unconvincing and the patient improves. Simpler, but over-treats.
• Invasive / quantitative — bronchoalveolar lavage (BAL) or protected specimen brush (PSB) with quantitative culture thresholds: BAL 10^4 CFU/mL or more, PSB 10^3 CFU/mL or more. More specific; reduces antibiotic exposure. Either strategy is acceptable provided there is a consistent local protocol.[6]

Clinical Pulmonary Infection Score (CPIS)

The CPIS combines six domains (temperature, WBC, tracheal secretions, oxygenation PaO2/FiO2, chest X-ray infiltrate, and semi-quantitative BAL culture) scored 0-2 each. A CPIS over 6 supports VAP; it can also be followed over time — a falling CPIS at day 3 supports stopping antibiotics at 5-7 days. CPIS has only moderate accuracy and should not be the sole basis for the decision.[2]

Antibiotic duration and de-escalation

The modern mantra is shorter is better — once the patient is clinically responding, prolonged courses do not improve outcomes and drive resistance, Clostridioides difficile, and AKI. The pivotal evidence:[1][3][9]

• CAP — 5 days (minimum) and stop once the patient is clinically stable for 48-72 hours and afebrile. Up to 7 days if slower to resolve (typical CAP: 5-7 days). Atypical pathogens (Legionella, mycoplasma) are covered by the macrolide; Legionella may warrant 7-14 days.[1]
• VAP — 7 days for uncomplicated VAP. The PNEUMA trial randomised VAP to 8 vs 15 days and found no difference in mortality, recurrence, or MDR organisms, but 15-day patients had more antibiotic-free days wasted. Exception: if the organism is non-fermenting Gram-negative (Pseudomonas, Acinetobaster, Stenotrophomonas) or there is bacteraemia, extend to 7-8 days and reassess.[3]
• Procalcitonin-guided — the PRORATA trial showed that a procalcitonin algorithm (stop when procalcitonin falls >80% from peak or below 0.5 ng/mL) reduced antibiotic days in ICU without increasing mortality; the Schuetz meta-analysis confirms safety across lower respiratory tract infections. Useful as a decision aid to stop antibiotics, not to start them.[9][10]

[3]

Empiric therapy at a glance

[3]

MDR risk factors (modify empiric cover)

For VAP, risk factors for multidrug-resistant pathogens that mandate broadened cover are:[6]

• Prior intravenous antibiotics within 90 days.
• Septic shock at VAP onset or ARDS accompanying VAP.
• Five or more days in hospital prior to VAP onset (i.e. late-onset).
• Acute renal replacement therapy prior to VAP onset.

MRSA-specific risk factors (warrant empiric vancomycin/linezolid): prior IV antibiotics, known MRSA colonisation, hospital unit with high MRSA prevalence, and (for CAP) post-influenza or cavitary picture.[7]

Pseudomonas-specific risk factors for CAP (rare — structural lung disease, bronchiectasis, frequent steroids/antibiotics in severe COPD): warrant an anti-pseudomonal beta-lactam in the CAP regimen.[1]

[7]

CURB-65 and severity — the exam decision tool

CURB-65 (Lim 2003, Thorax) stratifies CAP into mortality risk and disposition:[4]

• Confusion (disorientation in time/place/person).
• Urea > 7 mmol/L.
• Respiratory rate >= 30/min.
• Blood pressure — SBP < 90 or DBP <= 60 mmHg.
• 65 — age 65 years or older.[4]

The PSI/PORT (Fine 1997, NEJM) is a more granular 20-variable model that is more sensitive for identifying low-risk patients but is more cumbersome; IDSA/ATS minor criteria (three or more) or one major criterion (need for invasive ventilation or septic shock needing vasopressors) is the trigger for ICU admission.[5][1]

[4]

Exam practice

[4] [3]

Clinical pearls — high-yield for the exam

Red flags — don't miss these

References

1. [1]Metlay JP, Waterer GW, Long AC, et al. Diagnosis and treatment of adults with community-acquired pneumonia. An official clinical practice guideline of the American Thoracic Society and Infectious Diseases Society of America. American Journal of Respiratory and Critical Care Medicine, 2019.PMID 31573350
2. [2]Karnad DR, Nor MBM, Richards GA, et al. Intensive care in severe malaria: Report from the task force on tropical diseases by the World Federation of Societies of Intensive and Critical Care Medicine. Journal of critical care, 2018.PMID 29132978
3. [3]Chastre J, Wolff M, Fagon JY, Chevret S, et al. Comparison of 8 vs 15 days of antibiotic therapy for ventilator-associated pneumonia in adults: a randomized trial (PNEUMA). JAMA, 2003.PMID 14625336
4. [4]Lim WS, van der Eerden MM, Laing R, et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study (CURB-65). Thorax, 2003.PMID 12728155
5. [5]Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients with community-acquired pneumonia (Pneumonia Severity Index / PORT). New England Journal of Medicine, 1997.PMID 8995086
6. [6]Kalil AC, Metersky ML, Klompas M, et al. Executive Summary: Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the IDSA and ATS. Clinical Infectious Diseases, 2016.PMID 27521441
7. [7]Drakulovic MB, Torres A, Bauer TT, et al. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients. Lancet, 1999.PMID 10584721
8. [8]Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial). Lancet, 2008.PMID 18191684
9. [9]Bouadma L, Luyt CE, Tubach F, et al. Use of procalcitonin to reduce patients' exposure to antibiotics in intensive care units (PRORATA trial). Lancet, 2010.PMID 20097417
10. [10]Schuetz P, Wirz Y, Sager R, et al. Procalcitonin guidance in patients with lower respiratory tract infections: a systematic review and meta-analysis. Clinical Chemistry and Laboratory Medicine, 2018.PMID 29715176