Preparatory Mindset
Pneumonia is the most common infectious cause of death and a guaranteed exam topic in both the theory paper and the clinical (OSCE) setting. The exam skill is a 3-step approach: (1) diagnose pneumonia (clinical syndrome + compatible chest imaging), (2) grade severity to decide outpatient vs inpatient vs ICU (CURB-65/PSI), and (3) choose empiric antibiotics based on where the infection was acquired (community vs hospital) and host risk factors — then de-escalate when the pathogen is known. LMCHK candidates must know the HK-specific empiric regimens and the local antimicrobial-resistance caveats (macrolide resistance in S. pneumoniae, doxycycline preferred for Mycoplasma in Asia). Lung abscess and bronchiectasis are the two classic suppurative complications taught alongside pneumonia.
Core Concepts
Definition & epidemiology
- Pneumonia = acute infection of the lung parenchyma (alveoli/interstitium) caused by bacteria, fungi, viruses, parasites — or by non-infective agents (radiation, chemicals/aspiration, allergens).
- Epidemiology: ~1.1 million hospital admissions/year in the U.S.; 6th leading cause of death overall, 1st leading cause of death from infectious diseases; ~50% of cases have no identified pathogen.
- Mortality: outpatient <1–5%; inpatient ~12%; severe cases 33–50%.
- Risk factors: COPD, CHF, CAD, diabetes, malignancy, extremes of age, aspiration risk.
Classification
1. By aetiology — Infective (viral, bacterial, fungal, mycoplasma/chlamydia/legionella, protozoa) vs non-infective (toxins, chemicals/aspiration, radiation pneumonitis, allergic — e.g., asthmatic bronchopulmonary eosinophilia).
2. By radiological/anatomical pattern:
| Pattern | Typical aetiology | Features |
|---|---|---|
| Lobar | S. pneumoniae (~95%); Klebsiella in aged/DM/alcoholics | Whole-lobe consolidation; high fever, rusty sputum, pleuritic pain; 4 stages — congestion (d1, vasodilatation), red hepatization (d2, exudate+RBC), grey hepatization (d4, neutrophils+macrophages), resolution (d8) |
| Bronchopneumonia (patchy) | Staph, Strep, H. influenzae, Mycoplasma | Patchy consolidation not limited to lobes; suppurative; usually bilateral, lower lobes; extremes of age |
| Interstitial/atypical | Immunocompetent: Mycoplasma, Chlamydia, influenza A, COVID-19; immunocompromised: P. jirovecii, CMV | Ground-glass opacities (GGO) + reticular patterns |
3. By acquired environment (the exam-critical axis):
| Type | Definition |
|---|---|
| CAP | Acquired outside hospital, or diagnosed within 48 h of admission |
| HAP / Nosocomial (NP) | Not present/incubating at admission; develops >48 h after hospitalisation |
| VAP | Develops >48 h after mechanical ventilation |
| HCAP (healthcare-associated) | Nursing home, recent hospitalisation, dialysis, etc. |
Microbiology
- CAP typical bacteria: S. pneumoniae (most common), H. influenzae, M. catarrhalis.
- CAP atypical: Legionella pneumophila, Mycoplasma pneumoniae, Chlamydophila pneumoniae; Klebsiella & other Gram-negatives in diabetics/alcoholics/aspiration risk.
- CAP viruses: influenza (A/B/C), RSV, SARS-CoV-2, adenovirus, measles; emerging — avian influenza (H5N1, H7N9), MERS-CoV.
- HAP/VAP microbiology: Gram-negative pathogens predominate — P. aeruginosa, Klebsiella, E. coli, Acinetobacter, Enterobacter, Stenotrophomonas; Gram-positive — S. aureus (much of it MRSA); anaerobes uncommon in VAP.
- Fungi: Candida, Aspergillus, P. jirovecii (immunocompromised).
Clinical features
- Typical syndrome: fever, chills, cough (with purulent sputum), pleuritic chest pain, dyspnoea + signs of consolidation (rales, increased tactile fremitus, bronchial breath sounds, dullness to percussion).
- Systemic: myalgia, malaise, fatigue; elderly may present atypically (confusion, falls, no fever).
- Classic vignettes: young adult (e.g., 20 y/o female) with dry cough + patchy LUL infiltrate → atypical (Mycoplasma); elderly smoker (75 y/o male) with rigors, purulent sputum, RLL consolidation → S. pneumoniae.
Diagnosis
Diagnostic triad for CAP (per Chinese textbook): ① community-acquired; ② pneumonia-related manifestations — new respiratory symptoms (cough, purulent sputum, chest pain, dyspnoea), consolidation signs/rales, WBC >10×10⁹/L or <4×10⁹/L; ③ chest radiography (new infiltrate). Diagnosis = ① + ③ + one of ②, after excluding TB, tumour, interstitial lung disease, pulmonary oedema, atelectasis, PE.
Investigations:
- CBC: leukocytosis with left shift (PMN).
- Sputum gram stain & culture: quality criteria — PMN >25/LPF, epithelial cells <10/LPF, single predominant organism; yields variable.
- Blood culture: yield 5–15%; stronger indication in severe CAP or host risk factors (cirrhosis, asplenia, complement deficiency, leukopenia).
- Urinary antigen: S. pneumoniae & Legionella serogroup 1 — 50–80% sensitive, >90% specific; rapid (15 min), detects Pneumococcus after antibiotics started; no susceptibility data.
- Serology: C. pneumoniae, Mycoplasma, Legionella (slow turnaround); influenza NP swab (rapid flu test, 50–70% sensitive); molecular — mNGS/tNGS.
- CXR: infiltrates, air bronchogram, consolidation; establishes complications (effusion, multilobar).
- Severity scores: CURB-65 (Confusion, Urea >7 mmol/L, RR ≥30, BP <90/60, age ≥65) and PSI (Pneumonia Severity Index) → site-of-care decisions.
- Severe CAP criteria (IDSA/ATS + HK handbook): 1 of 3 major (mechanical ventilation, septic shock, acute renal failure) OR 2 of 6 minor (multi-lobar involvement, confusion, RR >30, PaO₂/FiO₂ <250, SBP <90/DBP <60 mmHg, urea >7 mmol/L).
Management
Principles: empiric antibiotics guided by severity + local resistance patterns (CHINET in China); appropriate (matches sensitivities) + adequate (correct route/penetration, combination if needed); de-escalate when pathogen known; supportive care (O₂, fluids/electrolytes/nutrition, bronchodilators); prevention (influenza + pneumococcal vaccines, aspiration precautions).
Empiric therapy by severity (teacher PPT / IDSA-ATS 2007 + HK handbook):
- Outpatient, healthy, no antibiotics in past 3 months: macrolide (azithromycin); 2nd choice doxycycline. In China: penicillin or 1st/2nd-gen cephalosporin ± macrolide.
- Outpatient with comorbidities/recent antibiotics: respiratory fluoroquinolone (moxifloxacin, levofloxacin 750 mg) OR beta-lactam + macrolide.
- Inpatient ward: respiratory fluoroquinolone OR beta-lactam (ceftriaxone/cefotaxime) + macrolide.
- ICU, no Pseudomonas risk: IV beta-lactam + IV macrolide or IV fluoroquinolone.
- ICU, Pseudomonas risk: IV anti-pseudomonal beta-lactam (cefepime, imipenem, meropenem, piperacillin-tazobactam) + anti-pseudomonal quinolone (double), or + aminoglycoside + macrolide/quinolone (triple); CA-MRSA → add vancomycin or linezolid; PCN-allergic → aztreonam.
- Switch IV→PO when: improved cough/dyspnoea, afebrile ×2 (8 h apart), functioning GI tract with oral intake.
- Duration: minimum 5 days + afebrile 48–72 h + ≤1 sign of clinical instability; longer if initial therapy inactive against the pathogen or extrapulmonary complication. "Hit hard early, short duration, de-escalate."
Specific pneumonias
| Type | Key features | Treatment |
|---|---|---|
| Pneumococcal (most common) | Post-viral onset; high fever (up to 39.5 °C); pleuritic pain; rusty sputum; labial herpes simplex; consolidation signs; lancet-shaped Gram-positive diplococci | PCN-sensitive (MIC <0.1): amoxicillin/doxycycline/macrolide; intermediate (0.1–1.0): cefotaxime/clindamycin/FQ; highly resistant (>2): vancomycin |
| Mycoplasma | Children >3 y & young adults; gradual prodrome (malaise, headache, fever); harsh dry hacking cough; extra-pulmonary (rash, arthralgia, serous otitis); patchy interstitial/perihilar infiltrates, tree-in-bud; cold agglutinins; organism lacks cell wall | Doxycycline or macrolide (HK: doxycycline preferred — high macrolide resistance in Asia); fluoroquinolone alternative |
| S. aureus | Debilitated/chronically ill; similar to pneumococcal but more complications: necrosis, cavitation, empyema, effusion, pneumothorax; Gram-positive cocci in leukocytes | MSSA: ampicillin/amoxicillin; MRSA: vancomycin |
| Viral (influenza A) | Winter/spring; fever, chills, headache, myalgia, fatigue, cough, dyspnoea; CXR GGO/multiple patchy infiltrates; secondary bacterial infection (Staph, Strep, H. influenzae) | Supportive; oseltamivir (esp. influenza season); treat secondary bacterial infection; COVID-19: per current protocols |
Lung abscess
- Definition: severe localised suppuration in the lung with cavity formation ± air-fluid level on CXR — a product of lung necrosis, often surrounded by infection.
- Classification: aspirated (primary — commonly affected positions, R > L), secondary (pulmonary infection, bronchial obstruction, neighbouring-organ infection), haematogenous (extrapulmonary infection/sepsis).
- Aetiology: mixed infection — anaerobic bacilli predominant; aerobic: S. aureus, P. aeruginosa, Klebsiella, Legionella.
- Clinical: foul sputum (layers on standing), fever/chills/night sweats, weight loss, clubbing, localized dullness, bronchial/absent breath sounds; differentials — aspiration of foreign body, pulmonary infarction, cavitating tumour.
- Management: antibiotics 6–8 weeks (e.g., clindamycin 600 mg IV q8h; cefuroxime + metronidazole then oral; penicillin G effective) ± surgical/percutaneous drainage.
Bronchiectasis
- Definition: abnormal, irreversible dilatation of proximal subsegmental bronchi — end stage of processes destroying the bronchial wall and supporting tissue.
- Causes: infection (Pseudomonas, H. influenzae, Aspergillus, TB, viruses); immune dysfunction (hypogammaglobulinaemia, immunosuppressants, HIV, ABPA, RA); congenital (α1-AT deficiency, PCD, Kartagener syndrome); airway obstruction, toxic inhalation, IBD.
- Clinical: chronic cough, copious purulent foul sputum (200–500 mL/day), recurrent hemoptysis, dyspnoea, fatigue, weight loss, finger clubbing, coarse/moist crackles, rhonchi.
- HRCT findings: bronchoarterial ratio >1 (internal bronchial diameter > adjacent artery), lack of bronchial tapering (>2 cm), bronchi within 1 cm of costal pleura, bronchial wall thickening (68%), ring sign / double-track sign, cystic expansion.
- Management: airway clearance; antibiotics (Pseudomonas-directed if colonised); anti-inflammatory/immunomodulators (macrolides); bronchodilators (reversible obstruction); control underlying disease; surgery (focal resection) or transplant; O₂ for hypoxaemia/cor pulmonale; hemoptysis management.
HKHA Handbook (LMCHK) — Key Points
- Outpatient stable: PO amoxicillin-clavulanate ± macrolide OR doxycycline. - Hospitalised mild-moderate: PO/IV amoxicillin-clavulanate ± macrolide OR doxycycline; alternatives IV ceftriaxone/cefotaxime ± macrolide/doxycycline; anti-pseudomonal (piperacillin-tazobactam, cefepime) ± macrolide/doxy for chronic lung disease (e.g., bronchiectasis); consider oseltamivir in influenza season. - Severe (1 of 3 major OR 2 of 6 minor criteria — see above): IV piperacillin-tazobactam / ceftriaxone / cefepime ± macrolide OR doxycycline.
- Onset <4 days, no prior antibiotics: S. pneumoniae/H. influenzae/M. catarrhalis/S. aureus → IV/PO amoxicillin-clavulanate OR IV ceftriaxone. - Onset ≥4 days + recent antibiotics, OR onset ≥5 days, OR mechanical ventilation/septic shock: MRSA/P. aeruginosa/Acinetobacter/Klebsiella/Enterobacter → IV piperacillin-tazobactam / cefepime / meropenem-imipenem ± vancomycin if MRSA risk.
- Clinical definition: pneumonia = (1) syndrome of fever, chills, SOB, cough, pleuritic chest pain, sputum + (2) compatible consolidation on chest imaging.
- Initial assessment: consider TB endemicity, immunocompromised status, atypical/emerging pathogens (FTOCC: Fever, Travel, Occupation, Cluster, Contact), influenza/COVID-19; early isolation if airborne pathogen suspected.
- CAP empiric treatment (HK standard):
- HK resistance warnings (IMPACT): high prevalence of reduced penicillin susceptibility and macrolide resistance in S. pneumoniae → macrolide/azalide, tetracycline or co-trimoxazole must NOT be used alone for empiric CAP; emerging fluoroquinolone resistance (elderly, chronic lung disease); doxycycline preferable to macrolide when Mycoplasma suspected (high macrolide resistance in Asia).
- HAP (≥48 h after admission) — two principles: regimen based on local pathogens + de-escalation when pathogen known:
- NHAP (nursing home-acquired pneumonia) — covered under Geriatrics (Gr 28-29); treat as severe CAP/HAP with broader cover; remember elderly often present atypically.
- Most CAP improves within 72 hours; consult infectious-disease specialists if in doubt.
High-Yield Points
- Pneumonia = clinical syndrome + compatible consolidation on imaging (both needed).
- Lobar (S. pneumoniae, rusty sputum, 4 stages) vs bronchopneumonia (patchy, bilateral, lower lobes) vs interstitial/atypical (GGO, Mycoplasma/viral).
- CAP = <48 h of admission; HAP = >48 h; VAP = >48 h of ventilation.
- Severity: CURB-65 and PSI decide site of care; severe = 1 major (ventilation/shock/ARF) or 2 minor (multilobar, confusion, RR>30, P/F<250, hypotension, urea>7).
- Empiric therapy is driven by where the pneumonia was acquired + severity + host risk.
- HK: never use macrolide alone for CAP (resistance); doxycycline preferred for Mycoplasma.
- Lung abscess: anaerobic-predominant mixed infection; clindamycin; treat 6–8 weeks.
- Bronchiectasis: irreversible proximal airway dilatation; HRCT — bronchoarterial ratio >1, double-track sign; Pseudomonas colonisation drives antibiotic choice.
- Switch IV→PO when improving/afebrile; minimum 5 days total.
Topic Summary
Pneumonia is diagnosed by clinical syndrome plus chest imaging, then risk-stratified (CURB-65/PSI/severe criteria) to choose the site of care and empiric antibiotics based on the acquisition setting (CAP vs HAP vs VAP). S. pneumoniae dominates CAP; Gram-negatives and MRSA dominate HAP; Mycoplasma and viruses cause the interstitial/atypical picture. HK-specific empiric regimens (amoxicillin-clavulanate ± macrolide/doxycycline; anti-pseudomonal cover for severe disease) and local resistance rules (no macrolide monotherapy; doxycycline for Mycoplasma) are LMCHK must-knows. Lung abscess (cavity ± air-fluid level, anaerobes, 6–8 weeks of clindamycin-based therapy) and bronchiectasis (irreversible proximal dilatation, HRCT signs, Pseudomonas-directed management) round out the suppurative complications.