Community-acquired pneumonia

• Why it matters: mortality ranges from under 1% in outpatients to over 25% in ICU-managed severe disease.
• Most deterioration happens in the first 48-72 hours — severity assessment at first contact drives outcome.
• Antibiotic timing, oxygenation and fluid/perfusion assessment are the three highest-yield early decisions.

By category

Bacterial (typical)

Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus

Atypical

Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella pneumophila

Viral

Influenza A/B, SARS-CoV-2, RSV, human metapneumovirus, parainfluenza

Aspiration / anaerobes

Oral flora, Prevotella, Fusobacterium — impaired consciousness or dysphagia

Gram negatives

Klebsiella pneumoniae (alcohol use, diabetes), Pseudomonas (bronchiectasis, structural lung disease)

Endemic / geographic

Mycobacterium tuberculosis, Burkholderia pseudomallei, endemic fungi where prevalent

Non-infectious mimics

Drug-induced pneumonitis, organising pneumonia, eosinophilic pneumonia, pulmonary infarction

• Incidence in adults approximately 5-11 per 1000 per year, rising sharply after age 65.
• Bimodal burden: young children and older adults with comorbidity.
• Hospitalisation required in roughly 20-25% of adult cases; 10-20% of admissions need critical care.
• Pneumococcus remains the most frequently identified bacterial pathogen even where a pathogen is found in only 30-50% of cases.

Modifiable risks are highlighted for prevention counselling

• Age ≥ 65 years, frailty, institutional residence
• COPD, asthma, bronchiectasis, interstitial lung disease
• Smoking and harmful alcohol use
• Diabetes, chronic kidney disease, chronic liver disease, heart failure
• Immunosuppression: HIV, chemotherapy, corticosteroids, biologics, asplenia
• Impaired swallow or consciousness (stroke, seizures, sedatives)
• Recent viral respiratory infection, especially influenza
• Proton pump inhibitor use and poor dental hygiene (aspiration risk)

1. 1Pathogen reaches the distal airway by microaspiration of colonised oropharyngeal secretions, inhaled droplets or (rarely) haematogenous spread.
2. 2Mucociliary clearance, cough reflex, surfactant proteins and alveolar macrophages are overwhelmed by inoculum size or virulence.
3. 3Pattern-recognition receptors detect pathogen components and trigger IL-1, IL-6, IL-8 and TNF-α release.
4. 4Neutrophils are recruited into alveoli; capillary permeability increases and alveoli fill with exudate.
5. 5Consolidated alveoli are perfused but not ventilated, producing shunt physiology and hypoxaemia.

Normal physiology → mechanism → tissue change → clinical picture

1. 1Normal physiology: thin alveolar-capillary membrane allows matched ventilation and perfusion with efficient gas exchange.
2. 2Mechanism: alveolar filling with inflammatory exudate abolishes local ventilation while perfusion persists.
3. 3Organ/tissue change: intrapulmonary shunt, reduced compliance, increased work of breathing, regional atelectasis.
4. 4Systemic effect: cytokine spill-over causes fever, vasodilatation, capillary leak and, if severe, organ dysfunction.
5. 5Clinical manifestation: hypoxaemia refractory to modest oxygen, tachypnoea, crackles, bronchial breathing, dullness to percussion.

Gross

Lobar consolidation (firm, airless, grey-red cut surface) or patchy peribronchial bronchopneumonia

Microscopic

Alveoli filled with neutrophils, fibrin and oedema fluid; intact alveolar walls in classic pneumococcal disease

Classic stages

Congestion → red hepatisation → grey hepatisation → resolution over roughly 8-10 days if untreated

Molecular / micro

Gram stain morphology, urinary antigen, multiplex PCR panels for viral and atypical pathogens

Imaging-pathology correlation

Air bronchograms reflect patent bronchi within consolidated alveoli; cavitation suggests S. aureus, Klebsiella, anaerobes or TB

• Cough, initially dry then productive; rust-coloured sputum classically pneumococcal
• Fever, rigors, sweats
• Pleuritic chest pain
• Dyspnoea and exertional limitation
• Malaise, myalgia, anorexia; headache and diarrhoea more common with Legionella

• Tachypnoea (the single most useful early vital sign), tachycardia, fever or hypothermia
• Reduced chest expansion on the affected side, dullness to percussion
• Bronchial breath sounds, coarse crackles, increased vocal resonance, pleural rub
• Hypoxaemia on pulse oximetry; central cyanosis in severe disease
• Confusion (especially in older adults), hypotension, prolonged capillary refill in severe disease

Typical

• Fever, productive cough, pleuritic pain and focal consolidation on examination and chest radiograph.

Atypical

• Older adults: falls, delirium, functional decline or isolated tachypnoea without fever.
• Diabetes/immunosuppression: minimal cough, blunted fever, rapid deterioration.
• Atypical pathogens: prolonged dry cough, headache, extrapulmonary features, patchy interstitial radiographic changes.
• Post-influenza S. aureus: biphasic illness with sudden worsening and cavitation.

1. 1Confirm the syndrome: acute respiratory symptoms plus fever or abnormal vitals plus focal chest findings.
2. 2Assess oxygenation and perfusion immediately; treat hypoxaemia and hypotension before completing work-up.
3. 3Obtain a chest radiograph (or lung ultrasound/CT when radiograph is equivocal) to confirm a new infiltrate.
4. 4Score severity (CURB-65 or CRB-65, plus qSOFA/NEWS2) to choose care setting.
5. 5Take microbiological samples proportionate to severity — sputum and blood cultures, urinary antigens, viral PCR.
6. 6Start empirical antimicrobials guided by severity, comorbidity and local resistance; do not delay for investigations.
7. 7Reassess at 48-72 hours: clinical response, de-escalation and search for complications if not improving.

• Clinical: at least two of cough, purulent sputum, dyspnoea, pleuritic pain, fever > 38 °C, focal chest signs.
• Radiographic: new infiltrate or consolidation not explained by another cause.
• Diagnosis is clinical-radiographic; microbiology supports and refines but is not required to start treatment.

Initial

• Pulse oximetry, chest radiograph, FBC, urea/electrolytes, CRP, capillary or arterial blood gas if SpO2 < 92%.

Confirmatory

• Sputum Gram stain and culture, blood cultures ×2, pneumococcal and Legionella urinary antigen, respiratory viral PCR, HIV testing where relevant.

Severity

• Lactate, procalcitonin trend (where used), renal and hepatic panel, coagulation screen.

Complication assessment

• Pleural fluid analysis if effusion > 1 cm: pH, glucose, LDH, protein, Gram stain, culture — pH < 7.2 indicates drainage.

Monitoring

• CRP or procalcitonin trend, oxygen requirement, repeat imaging only if failure to improve or clinical deterioration.

Acute heart failure

Rule in: orthopnoea, raised JVP, S3, bilateral basal crackles, elevated BNP. Rule out: fever, focal consolidation, purulent sputum.

Pulmonary embolism

Rule in: sudden pleuritic pain, hypoxaemia with clear lung fields, risk factors, raised D-dimer. Rule out: lobar consolidation with fever.

Pulmonary tuberculosis

Rule in: weeks of cough, weight loss, night sweats, upper-lobe cavitation. Rule out: hyperacute onset over 48 h.

COPD/asthma exacerbation

Rule in: wheeze, known obstruction, no new infiltrate. Rule out: consolidation, high fever.

Lung cancer with obstruction

Rule in: smoker, weight loss, non-resolving consolidation, volume loss. Rule out: complete radiographic resolution.

Organising / eosinophilic pneumonia

Rule in: antibiotic non-response, migratory opacities, peripheral eosinophilia. Rule out: rapid antibiotic response.

CURB-65

CURB-65

Confusion, Urea > 7 mmol/L, RR ≥ 30, BP < 90/60, age ≥ 65 — 1 point each

0-1

Low severity — usually outpatient management

2

Moderate — consider short-stay or hospital admission

≥ 3

High severity — admit, assess for critical care

• qSOFA ≥ 2 or NEWS2 ≥ 5 identifies patients needing urgent senior review.
• Scores support but never override clinical judgement, social circumstances and oxygen requirement.

Immediate

• Oxygen to target SpO2 88-92% if at risk of hypercapnia, otherwise 94-98%; fluid resuscitation if hypoperfused; analgesia and antipyretics.

Antimicrobial (first-line)

• Low severity: amoxicillin orally (or doxycycline/macrolide if penicillin allergy).
• Moderate: amoxicillin plus a macrolide, or respiratory fluoroquinolone where appropriate.
• Severe: IV beta-lactam (co-amoxiclav or ceftriaxone) plus macrolide; add MRSA or Pseudomonas cover only when risk factors are present.
• Aspiration risk: agent with anaerobic activity (co-amoxiclav; add metronidazole if using a cephalosporin).
• Follow local antimicrobial policy and susceptibility data — regimens vary substantially by country.

Adjuncts

• Oseltamivir if influenza confirmed or strongly suspected within the treatment window.
• Corticosteroids only where an evidence-based indication exists (e.g. severe CAP protocols, COVID-19 with hypoxaemia).

Procedural / severe disease

• Chest drain for complicated effusion/empyema; intrapleural fibrinolysis or surgical decortication if loculated.
• Non-invasive ventilation or high-flow nasal oxygen for selected respiratory failure; intubation for refractory hypoxaemia or exhaustion.

Supportive

• Early mobilisation, VTE prophylaxis, nutrition, swallow assessment where aspiration is suspected, smoking cessation.

Monitoring

• Vitals and oxygen requirement 4-hourly initially; review antibiotics at 48-72 h; step down IV to oral once stable and afebrile.

Linked drug entities

• amoxicillin — first-line oral therapy for low-severity CAP in most settings
• azithromycin — atypical cover, added in moderate-to-severe disease
• ceftriaxone — IV beta-lactam for hospitalised or severe disease
• paracetamol — antipyresis and pleuritic pain

Early

• Hypoxaemic respiratory failure, sepsis and septic shock, acute kidney injury, hyponatraemia.

Intermediate

• Parapneumonic effusion, empyema, lung abscess, atrial fibrillation, myocardial infarction, delirium.

Late

• Persistent breathlessness and fatigue, bronchiectasis, pulmonary fibrosis (rare), functional decline in older adults.

• Natural history: fever settles in 2-4 days with effective therapy; cough and fatigue may persist for weeks; radiographic clearance lags by 4-6 weeks.
• Mortality: under 1-2% in outpatients, roughly 5-15% in hospitalised patients, over 25% with septic shock or ICU admission.
• Prognostic factors: age, comorbidity burden, hypotension, hypoxaemia, multilobar involvement, raised urea and lactate, bacteraemia.
• Recurrence should prompt evaluation for structural lung disease, aspiration, immunodeficiency or malignancy.
• Longer term: hospitalised CAP is associated with excess cardiovascular events and mortality in the following year.

• Pneumococcal vaccination per national schedule for older adults and at-risk groups
• Annual influenza vaccination; COVID-19 vaccination per local policy
• Smoking cessation and alcohol reduction
• Optimise diabetes, heart failure and COPD control
• Oral hygiene and dysphagia management to reduce aspiration

• Clinical review at 48-72 hours for outpatients; earlier if deteriorating.
• Repeat chest radiograph at approximately 6 weeks if persistent symptoms, age > 50 or smoker — to exclude underlying malignancy.
• Confirm vaccination, smoking cessation and comorbidity optimisation before discharge.
• Pulmonary rehabilitation or graded activity advice for prolonged deconditioning.

Pregnancy

Target SpO2 ≥ 94-95%; beta-lactams and macrolides generally used; avoid fluoroquinolones and tetracyclines

Lactation

Penicillins and macrolides compatible with breastfeeding

Paediatrics

Weight-based amoxicillin; assess work of breathing, feeding and hydration; viral aetiology predominates in infants

Elderly

Atypical presentation; screen for delirium, dehydration, aspiration and functional decline

CKD

Adjust beta-lactam and fluoroquinolone dosing to eGFR; avoid nephrotoxin stacking

Liver disease

Caution with macrolides and co-amoxiclav; monitor liver enzymes

Immunocompromised

Broaden differential to Pneumocystis, fungi, Nocardia, TB; obtain early specialist input and CT

• WHO clinical management of severe acute respiratory infection (2023)
• Surviving Sepsis Campaign (2021) for the sepsis overlap
• Always cross-check with the national antimicrobial policy that applies to your practice setting

• Trials of shortened antibiotic courses (3-5 days) support early stop rules in responding, non-severe patients.
• Corticosteroid use in severe CAP remains an area of active investigation and guideline divergence.
• Procalcitonin-guided stopping reduces antibiotic exposure without harm in selected populations.

• WHO — Clinical management of severe acute respiratory infection, 2023 (guideline, global).
• Surviving Sepsis Campaign international guidelines, 2021 (guideline, global).
• DrZep editorial summary, demo dataset v0.1, retrieved 2026-09-01.