Community-Acquired Pneumonia

Meet the patient

An 82-year-old care-home resident arrives confused, breathing 30 or more times a minute, with rust-coloured sputum. Her systolic blood pressure is under 90 mmHg with a diastolic of 60 mmHg or less, her urea is over 7 mmol/L, and the chest X-ray shows right lower-lobe consolidation — every CURB-65 feature is positive.^[3]

Two exam questions are now live: what is her CURB-65 score? and which antibiotic, by which hour? Score her first; the rest of the topic is the rationale.^[3]

Overview & Definition

Pneumonia is an acute infection of the lung parenchyma — the alveoli, terminal bronchioles and the adjacent interstitium — that produces exudate and consolidation (usually visible on imaging) and impairs gas exchange.^[2]

Community-acquired pneumonia (CAP) is pneumonia acquired outside hospital or developing within the first 48 hours of admission. The 48-hour rule is the operational boundary between CAP and hospital-acquired (nosocomial) pneumonia (HAP), because organisms causing early-onset inpatient pneumonia reflect the community flora and remain sensitive to standard empirical therapy, whereas pneumonia arising after 48 hours is driven by hospital flora (often multidrug-resistant Gram-negatives and Staphylococcus aureus) that demands broader cover. The distinction matters at the bedside: a patient who arrives at the emergency department septic and is found to have a new infiltrate has CAP and is treated with standard empirical cover, even if the formal microbiological confirmation comes back hours later. ^[1]

Three distinctions an examiner will probe:^[2]

• Pneumonia versus acute bronchitis — bronchitis inflames the large airways, causes a cough (often productive) but produces no consolidation and no new infiltrate on chest X-ray; the patient is usually afebrile and not septic. Acute bronchitis is overwhelmingly viral and does not warrant antibiotics in the absence of specific indications. The chest X-ray is the decisive test.
• Pneumonia versus upper respiratory tract infection (URTI) — a URTI (common cold, pharyngitis) causes coryza, sore throat and malaise without dyspnoea, tachypnoea, focal chest signs or radiographic shadowing. A raised respiratory rate or new oxygen requirement points away from a URTI and towards a lower respiratory tract infection.
• Pneumonia versus atypical "walking pneumonia" — Mycoplasma and other atypicals cause a clinically milder, more insidious illness in which the patient looks better than the radiograph ("walking pneumonia"), but the parenchyma is genuinely infected. ^[1]

The clinical skill in CAP is not making the diagnosis (that is clinical plus chest X-ray) but recognising severity, choosing empirical antibiotics that cover typical AND atypical organisms, and remaining alert to viruses (COVID-19, influenza), aspiration, immunocompromised hosts, and complications (parapneumonic effusion, empyema, lung abscess, sepsis). The single largest process lever is early antibiotics. NICE recommends putting processes in place so that diagnosis (including chest X-ray) and treatment occur within 4 hours of presentation to hospital; if septic shock is present, the observational data below support giving effective antimicrobials within the first hour of documented hypotension.^[15][7][16]

Classification

By place of acquisition (the classification that drives empirical therapy):^[1]

• Community-acquired (CAP) — onset outside hospital or within 48 hours of admission.
• Hospital-acquired (HAP) — onset 48 hours or more after admission, not incubating at admission. Caused by hospital flora (Gram-negative bacilli, S. aureus including MRSA).
• Ventilator-associated (VAP) — arising 48 hours or more after endotracheal intubation.
• (The older healthcare-associated pneumonia, HCAP, category was retired by ATS/IDSA 2019 because it did not reliably predict resistant organisms and led to over-use of broad-spectrum antibiotics.)^[1]

By anatomy / radiology: ^[1]

• Lobar pneumonia — consolidation confined to one lobe or segment; the typical bacterial pattern (S. pneumoniae, K. pneumoniae). Sharp lobar boundary, air bronchogram.
• Bronchopneumonia — patchy, peribronchial consolidation affecting multiple lobes bilaterally; S. aureus, H. influenzae, and terminal events.
• Interstitial pneumonia — inflammation of the interstitium rather than the alveolar space; atypicals and viruses; CXR shows diffuse reticular or reticulonodular shadowing. ^[1]

By aetiology — typical versus atypical (an examiner favourite):^[2]

• Typical: Streptococcus pneumoniae (commonest), Haemophilus influenzae, Moraxella catarrhalis, Klebsiella pneumoniae, Staphylococcus aureus. Lobar consolidation, purulent or rust-coloured sputum, abrupt onset.
• Atypical: Mycoplasma pneumoniae, Chlamydophila pneumoniae/psittaci, Legionella pneumophila, Coxiella burnetii. Insidious, dry cough, prominent systemic features, interstitial CXR. ^[1]

By severity — see Investigations, where every named score (CURB-65, CRB-65, PSI/Pneumonia Severity Index, IDSA/ATS severe-CAP criteria) is reproduced verbatim.^[3][4]

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Epidemiology & Risk Factors

CAP is among the leading causes of infectious death worldwide, with the highest burden in the very young, the elderly, and the immunocompromised. A 2015 Lancet seminar estimated incidence at 1.5 to 14.0 cases per 1000 person-years, varying by region, season and population; the age pattern is U-shaped (children under 5 and adults over 65). In England and Wales, NICE reported that 0.5 to 1 percent of adults have CAP each year, that it is diagnosed in 5 to 12 percent of adults presenting to GPs with lower-respiratory symptoms, that 22 to 42 percent of those diagnosed are admitted, and that hospital mortality is 5 to 14 percent (over 30 percent among the 1.2 to 10 percent of admissions managed in ICU). There is a winter peak that overlaps with influenza, when secondary bacterial pneumonia (classically S. pneumoniae and S. aureus) follows viral infection.^[2][15]

Streptococcus pneumoniae remains the main identifiable pathogen worldwide. In Europe it accounts for about 35 percent of aetiologically labelled cases (range 12 to 68) and about 27 percent worldwide; H. influenzae and the atypicals (Mycoplasma, Chlamydia, Legionella) follow. Even with improved testing, the pathogen is not detected in nearly half of pneumonia episodes — which is why empirical therapy for hospitalised CAP must cover typical and atypical organisms.^[2]

Host and environmental risk factors: extremes of age, cigarette smoking (impairs mucociliary clearance and alveolar macrophage function), chronic lung disease (COPD, bronchiectasis, asthma), alcohol misuse (depresses macrophage function and raises aspiration risk), diabetes mellitus, chronic cardiac, renal or liver disease, immunocompromise (HIV, chemotherapy, splenectomy, hypogammaglobulinaemia, immunosuppressants including anti-TNF and corticosteroids), aspiration risk (stroke, dysphagia, reduced conscious level, seizures, anaesthesia, reflux), and — important in the developing world — malnutrition and indoor biomass-fuel smoke.^[2]

Risk-factor to organism associations (high-yield for viva and MCQ): ^[1]

Pathophysiology

The lung distal to the vocal cords is normally sterile, defended by three layered mechanisms: the cough reflex (large-particle clearance), mucociliary clearance (the ascending mucus escalator of the airway epithelium, destroyed by smoking and viral injury), and alveolar macrophages (the final phagocytic sentinel). Pneumonia occurs when these defences are overwhelmed or bypassed.^[2]

Routes by which pathogens reach the alveoli: ^[1]

• Microaspiration of oropharyngeal flora — the commonest mechanism in typical bacterial CAP. Even healthy people microaspirate during sleep; disease occurs when the inoculum is large or defences are impaired.
• Macroaspiration of gastric or oropharyngeal contents — stroke, reduced conscious level, seizures, anaesthesia, severe reflux.
• Inhalation of aerosolised droplets — Mycobacterium tuberculosis, Legionella, influenza, SARS-CoV-2, Histoplasma.
• Haematogenous spread — S. aureus from tricuspid endocarditis in injecting drug users; septic emboli.
• Direct extension — rarely, from a contiguous infection (empyema, mediastinitis) or following chest trauma. ^[1]

Once in the terminal airway, organisms multiply, triggering alveolar macrophage cytokine release (interleukin-1, tumour necrosis factor-alpha, interleukin-6). These cytokines recruit neutrophils and a protein-rich exudate into the alveolar space — producing consolidation. The exudate collapses alveolar units and floods gas-exchange surfaces, generating ventilation-perfusion mismatch and intrapulmonary shunt (perfused but unventilated alveoli) — the mechanism of hypoxaemia that does not correct with supplemental oxygen as readily as hypoxaemia from pure V/Q mismatch. The same cytokines spill into the systemic circulation, producing fever, tachycardia, tachypnoea and the systemic inflammatory response. Resolution follows as macrophages clear the exudate and type II pneumocytes regenerate surfactant.^[2]

Why the hypoxaemia of consolidation is partly a shunt (examiner point): consolidated alveoli are perfused but not ventilated — blood traverses them without being oxygenated, a true right-to-left intrapulmonary shunt. Because shunted blood bypasses the gas-exchange surface entirely, raising the inspired oxygen only marginally improves arterial oxygenation (the oxygenated blood cannot "carry" the shunted blood's deficit). This contrasts with pure V/Q mismatch (e.g. mild COPD), which corrects well with supplemental oxygen. The widened alveolar-arterial (A-a) oxygen gradient is the bedside signature of shunt and pneumonia. ^[1]

Why "typical" and "atypical" differ mechanistically: typical organisms multiply extracellularly in the alveolar space (the pneumococcal polysaccharide capsule resists phagocytosis), generating a dense neutrophil-rich lobar exudate and a productive cough. Atypicals proliferate intracellularly or along the respiratory epithelium and interstitium — Mycoplasma adheres via the P1 adhesin to respiratory epithelium, Legionella multiplies inside alveolar macrophages (inhibiting phagolysosome fusion) and Chlamydophila replicates inside epithelial cells. The result is a less exudative, more interstitial process with disproportionate systemic upset and a non-productive cough. Because atypicals lack a cell wall (Mycoplasma) or hide inside cells (Legionella, Chlamydophila), beta-lactams are ineffective — a macrolide, tetracycline or respiratory fluoroquinolone is required. ^[1]

The four classic stages of lobar pneumonia (histological, now largely of historical/exam interest): (1) Congestion (first 24 hours) — vascular engorgement and intra-alveolar oedema; (2) Red hepatization (days 2 to 3) — exudate rich in erythrocytes and fibrin, lung resembles liver; (3) Grey hepatization (days 4 to 6) — fibrin and neutrophils dominate, grey-brown solid lung; (4) Resolution (after day 7) — enzymatic digestion of fibrin, macrophage clearance, restoration of normal architecture (no scar, unless necrosis occurred). Incomplete resolution may progress to organisation (fibroblast ingrowth) or suppuration (abscess formation).^[2]

A normal blood pressure does not exclude severe illness or early sepsis — compensatory vasoconstriction maintains the pressure until late. Assess perfusion (capillary refill, lactate, urine output, conscious level), not the pressure alone.^[2]

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Clinical Presentation

Typical (bacterial) CAP — abrupt onset: fever with rigors, purulent or rust-coloured sputum (pneumococcus), dyspnoea and pleuritic chest pain (from pleural inflammation), tachypnoea. Examination reveals signs of consolidation (see below).^[2]

Atypical CAP — insidious onset over days: dry cough, prominent headache, myalgia, fatigue, sore throat and gastrointestinal symptoms, low-grade fever, and few chest signs despite a symptomatic patient. The chest X-ray frequently looks worse than the patient (or, less often, the patient worse than the X-ray). ^[1]

Symptom-by-symptom, with the mechanism an examiner wants: the cough is the host attempt to clear the exudate; rust-coloured sputum is pneumococcal haemorrhagic exudate; pleuritic pain reflects inflammation of the parietal pleura (the visceral pleura has no pain fibres); dyspnoea and tachypnoea arise from hypoxaemia (shunt), stimulation of juxtacapillary (J) receptors by interstitial inflammation, and the metabolic acidosis of sepsis; rigors mark the abrupt cytokine-driven upward reset of the hypothalamic temperature set-point; confusion in the elderly reflects hypoxaemia, dehydration, sepsis-related delirium, or a combination. A raised respiratory rate is the single most sensitive sign of a lower respiratory tract infection and is the first to climb and the last to normalise.^[2]

Organism-specific pointers (examiner favourites): ^[1]

• Legionella pneumophila — diarrhoea, abdominal pain, hyponatraemia, confusion, severe presentation; source is water systems, cooling towers, air-conditioning, spa pools; diagnose with urinary antigen (detects serogroup 1); also causes a mild Pontiac fever.
• Mycoplasma pneumoniae — young adults, dry cough, headache; extrapulmonary features are the exam twist — erythema multiforme / Stevens-Johnson syndrome, cold-agglutinin autoimmune haemolytic anaemia, Guillain-Barre syndrome, myocarditis, arthralgia, rash.
• Klebsiella pneumoniae (Friedlander) — alcoholics and diabetics; thick red-currant-jelly sputum; upper-lobe predilection with a bulging fissure; cavitates.
• Staphylococcus aureus — post-influenza (rapidly progressive, bilateral), injecting drug users (septic emboli from tricuspid endocarditis); causes cavitation and, in children, pneumatoceles.
• Chlamydia psittaci — psittacosis from bird (parrot, pigeon) exposure; splenomegaly, relative bradycardia.
• Coxiella burnetii — Q fever from farm animals; hepatitis and endocarditis.
• Viral — influenza, COVID-19 (often with anosmia/ageusia, bilateral ground-glass), RSV (elderly, infants).
• Pneumocystis jirovecii — HIV with CD4 under 200 cells/microL; insidious dyspnoea, dry cough, marked exertional desaturation, bilateral perihilar interstitial infiltrates, raised serum LDH. ^[1]

Which organism — rusty sputum, post-influenza, red-currant-jelly, bird exposure, CD4 under 200?ShowHide

Rust-coloured / blood-tinged sputum = S. pneumoniae (the classic). Red-currant-jelly = Klebsiella pneumoniae (alcoholic, diabetic). Post-influenza, rapidly progressive, cavitation = Staphylococcus aureus. Bird exposure, splenomegaly, relative bradycardia = Chlamydia psittaci (psittacosis). HIV, CD4 under 200, raised LDH, exertional desaturation = Pneumocystis jirovecii. Cooling tower, diarrhoea, hyponatraemia = Legionella.

^[1]

Atypical presentation in the elderly: confusion, falls, functional decline, anorexia, new incontinence — fever and cough may be absent. A lower threshold to admit, investigate and treat is essential. New-onset atrial fibrillation in an older patient with breathlessness is a classic CAP presentation. The immunocompromised may present with subtle dyspnoea and a normal examination but extensive radiographic disease — Pneumocystis classically causes marked exertional desaturation disproportionate to resting findings. ^[1]

Differential Diagnosis

An acute febrile illness with lung shadowing is not always CAP. Work through each with its distinguishing features:^[2]

• Pulmonary embolism (PE) — pleuritic pain and dyspnoea out of proportion to signs; risk factors (immobility, malignancy, recent surgery, pregnancy); usually no fever or septic picture; wedge-shaped peripheral infarct or normal CXR; confirmed by CT pulmonary angiogram and raised D-dimer. CAP and PE co-exist more often than chance — keep both on the list.
• Pulmonary oedema (cardiogenic) — bilateral peri-hilar bat-wing shadowing, Kerley B lines, cardiomegaly, history of cardiac disease, elevated NT-proBNP, rapid response to diuretics; fever absent.
• Tuberculosis — subacute or chronic course, night sweats, weight loss, haemoptysis; upper-lobe infiltrate with cavitation; sputum acid-fast bacilli / GeneXpert / mantoux / IGRA positive; high-risk epidemiology.
• Lung cancer — post-obstructive pneumonia that is slow to resolve or recurs in the same lobe; weight loss, smoker over 50; bronchoscopy and follow-up imaging.
• Atelectasis / lobar collapse — volume loss signs (shifted trachea/mediastinum toward the lesion, raised hemidiaphragm); no fever.
• Acute bronchitis — cough with no consolidation and a normal chest X-ray; usually viral; no antibiotics unless specific indication.
• Viral pneumonitis / COVID-19 — bilateral ground-glass opacities, lymphopenia, viral prodrome; isolate and test.
• Interstitial lung disease acute exacerbation or organising pneumonia — subacute, characteristic HRCT pattern, sterile cultures.
• Pulmonary vasculitis (e.g., granulomatosis with polyangiitis) — cavitating nodules, haemoptysis, sinusitis, renal involvement.
• Aspiration pneumonitis (Mendelson) — chemical injury from sterile gastric contents, often follows anaesthesia or reduced consciousness; resolves over 24 to 48 hours unless secondarily infected. ^[1]

Always specifically consider TB and PE when the presentation, epidemiology or radiology is not a straightforward CAP.^[2]

Clinical & Bedside Assessment

Vital signs drive severity — measure and record respiratory rate, oxygen saturation, blood pressure, temperature, heart rate, conscious level (GCS or confusion screen) and urine output. The single most sensitive marker of a lower respiratory tract infection is a raised respiratory rate, and it is the first to climb and the last to normalise — yet it is the vital sign most often omitted or guessed.^[2]

Signs of consolidation on focused respiratory examination: reduced chest expansion on the affected side, dullness to percussion over solidified lung, bronchial (tubular) breath sounds, fine inspiratory crackles, increased vocal resonance and tactile fremitus, and a possible pleural rub. A silent hemithorax with dullness suggests a pleural effusion or complete collapse. ^[1]

Always assess for sepsis at the bedside (respiratory rate, mentation, blood pressure, lactate and urine output). Examine for complications — a parapneumonic effusion (stony dull, absent breath sounds), empyema (swinging fever with a dull effusion), and perioral cyanosis indicating hypoxaemia. Check for appendix-signs of metastatic infection (new murmur in endocarditis, neck stiffness, joint swelling) when bacteraemia is suspected. ^[1]

Investigations

First-line investigations in admitted CAP:^[1]

• Chest X-ray — NICE defines CAP clinically as symptoms and signs of an acute lower respiratory tract infection confirmed by a chest X-ray showing new shadowing not due to another cause (for example pulmonary oedema or infarction).^[15]
• Full blood count, urea and electrolytes, liver function, glucose — organ function and severity assessment; urea over 7 mmol/L is a CURB-65 point.^[3]
• Procalcitonin — ATS/IDSA 2019 recommends starting empiric antibiotics in radiographically confirmed CAP regardless of the initial procalcitonin; reported sensitivity for bacterial infection ranges from 38 to 91 percent, so a low value must not be used to withhold the first dose.^[1]
• Arterial or venous blood gas — assess hypoxaemia, hypercapnia and acid-base.
• Blood cultures — ATS/IDSA 2019 recommends not obtaining blood cultures in outpatients and not routinely in hospitalised non-severe CAP; obtain pretreatment cultures in severe CAP or when covering MRSA or P. aeruginosa. In one prospective hospitalised cohort the yield was 12.6 percent, with S. pneumoniae in 69 of 76 positives, and the result changed initial treatment in one case (0.2 percent).^[1][11]
• Targeted microbiological testing — urinary antigens, sputum studies and respiratory viral PCR where the clinical picture demands: the ATS/IDSA 2019 guideline expanded microbiological testing for patients suspected of drug-resistant infections, with stewardship according to the microbiological results.^[5][2]
• HIV test and ECG — tuberculosis and Pneumocystis are AIDS-defining; arrhythmia (new atrial fibrillation) is common in the elderly. ^[1]

Chest X-ray patterns and what they imply: ^[1]

When and why each microbiological test: blood cultures and sputum are reserved for severe CAP or specific risk factors (ATS/IDSA 2019), not mild disease. The Legionella urinary antigen detects serogroup 1. Procalcitonin cannot replace the decision to start antibiotics in confirmed CAP; it may later support shortening duration only where length of stay already exceeds usual 5-to-7-day practice.^[1]

Severity scores — reproduced verbatim

CURB-65 (one point each, maximum 5):^[3][6]

• C — Confusion at initial hospital assessment (new disorientation in time, place or person).
• U — Blood urea over 7 mmol/L.
• R — Respiratory rate 30 breaths/min or more.
• B — Blood pressure: systolic under 90 mmHg OR diastolic 60 mmHg or less.
• 65 — age 65 years or over. ^[3]

Lim 2003 derivation cohort (1,068 adults) — 30-day mortality by exact score, which is not the same as the NICE risk-band percentages:^[3]

(Where urea is unavailable, CRB-65 uses the same four clinical variables and adds nothing for urea — a CRB-65 of 0 may be suitable for home treatment, while a score of 1 or more warrants hospital assessment.)^[3]

Pneumonia Severity Index (PSI / PORT)^[4] — a 20-variable model (demographics, comorbidity, examination and laboratory findings) that stratifies patients into classes I to V. It is more accurate than CURB-65 at identifying low-risk patients safe for outpatient care, but it is slower and harder to use at the bedside because it requires laboratory results and arithmetic. Use PSI to confirm low risk; use CURB-65 for rapid bedside triage and to trigger the sepsis pathway.

IDSA/ATS severe-CAP criteria (2007 definition, restated in the 2019 guideline) — one major criterion (septic shock needing vasopressors, or respiratory failure needing mechanical ventilation) or three or more of nine minor criteria: respiratory rate 30 or more, PaO2/FiO2 250 or less, multilobar infiltrates, confusion, BUN 20 mg/dL or more, WBC under 4,000/µL, platelets under 100,000/µL, hypothermia under 36 °C, and hypotension needing aggressive fluids. No score replaces clinical judgement.^[1]

^{[7] [3] [8] [11] [10]}

Management — Resuscitation

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ABCDE assessment first. Give oxygen for hypoxaemia; in COPD or other patients at risk of hypercapnic respiratory failure, avoid uncontrolled high-concentration oxygen because it can precipitate CO2 retention. Escalate the delivery device by need (nasal cannula, face mask, reservoir mask, high-flow nasal cannula or CPAP) and re-check a blood gas after a change.^[1]

In septic CAP, speed of antibiotics is the single strongest lever. In 2,154 adults with septic shock who received effective antimicrobials only after hypotension began, therapy within the first hour of documented hypotension was associated with 79.9 percent survival to discharge, and each further hour of delay over the next 6 hours cost an average of 7.6 percent survival. NICE additionally requires hospital processes that allow diagnosis and treatment of CAP within 4 hours of presentation.^[7][15]

Do not delay antibiotics for investigations. A sample drawn moments before the first dose is ideal, but in the septic patient treatment comes first.^[7]

^{[3] [16] [4] [7]}

Management — Definitive & Stepwise

Empirical antibiotics are severity- and setting-driven and must cover both typical and atypical organisms in every hospitalised patient.^[1][5]

^{[5] [2] [15] [16] [2] [5]}

Duration of therapy: hospitalised patients can safely stop after a minimum of 5 days once afebrile for 48 hours with no more than one sign of clinical instability — duration based on clinical stability criteria was validated in a multicentre randomised trial of 312 inpatients.^[8]

IV-to-oral switch (step-down): once the patient is haemodynamically stable, improving clinically, afebrile, and able to swallow and absorb oral medication — typically within 2 to 4 days. Switch to the oral equivalent of the IV agent or a bioequivalent oral agent (e.g., IV amoxicillin to oral amoxicillin, IV clarithromycin to oral clarithromycin).^[1]

Discharge criteria: the patient is clinically stable, tolerating oral intake and oral antibiotics, with a safe social situation, and a safety-net if not improving. ATS/IDSA 2019 suggests not routinely obtaining follow-up chest imaging in adults whose symptoms have resolved within 5 to 7 days. Persistently unresolved symptoms still need a structured re-think (wrong diagnosis, resistant organism, complication, or obstructing lesion).^[1]

Adjunctive corticosteroids: in a Cochrane review of 17 RCTs (2,264 participants), systemic corticosteroids reduced mortality in adults with severe pneumonia (RR 0.58, 95% CI 0.40 to 0.84); NNT 18 (95% CI 12 to 49) to prevent one death; hyperglycaemia was more common (RR 1.72, 95% CI 1.38 to 2.14). A later ICU-versus-non-ICU meta-analysis of 18 RCTs (4,472 participants) reported mortality RR 0.66. ATS/IDSA 2019 nevertheless recommends not routinely using corticosteroids in non-severe CAP and suggests not routinely using them in severe CAP, while endorsing Surviving Sepsis recommendations when refractory septic shock is present.^[9][18][1]

Supportive care: venous thromboembolism prophylaxis (low-molecular-weight heparin) for immobile hospitalised patients; physiotherapy and mucolytics have limited evidence but assisted sputum clearance helps the weak or post-operative patient; glycaemic control (insulin sliding scale if needed); nutritional support; review of chronic medications; and reduction of aspiration risk (head-up positioning, swallow assessment) in the vulnerable elderly. ^[1]

Specific Subtypes & Scenarios

• Aspiration pneumonia — occurs in patients with dysphagia (stroke, reduced conscious level, debility) and usually presents as a community-acquired pneumonia with a focal infiltrate in a dependent bronchopulmonary segment; treatment is broad-spectrum antibiotics plus management of the underlying dysphagia. Distinguish it from aspiration pneumonitis (sterile gastric contents in a patient with markedly reduced consciousness), which is treated essentially supportively.^[13]
• Atypical pneumonias — Legionella pneumophila causes severe pneumonia with extrapulmonary features (gastrointestinal symptoms, hyponatraemia, confusion). Recommended treatment is a macrolide or a fluoroquinolone; in a prospective series of 113 adults, 52 received clarithromycin, 43 azithromycin and 18 levofloxacin.^[14]

Complications & Pitfalls

Local: parapneumonic effusion, empyema (pus in the pleural space), lung abscess, necrotising pneumonia, pneumatocele (especially children with S. aureus), bronchopleural fistula.^[2]

Systemic: sepsis and septic shock, acute respiratory distress syndrome (ARDS), acute kidney injury, metastatic infection (endocarditis, meningitis, septic arthritis, pericarditis), new atrial fibrillation (elderly), hyponatraemia (SIADH or adrenal in severe disease), disseminated intravascular coagulation, and multi-organ failure. The acute respiratory distress syndrome is graded by the Berlin Definition on the PaO2/FiO2 ratio: mild 200 mmHg < PaO2/FiO2 ≤ 300, moderate 100 < PaO2/FiO2 ≤ 200, and severe PaO2/FiO2 ≤ 100 mmHg, with stepwise higher mortality (27, 32 and 45 percent in the validating datasets).^[12]

Parapneumonic effusion — a pleural effusion accompanies about 20 percent of hospitalised bacterial pneumonia. Aspirate every effusion for diagnosis (pleural fluid pH, glucose, lactate dehydrogenase, Gram stain and culture), using image guidance if the collection is small or loculated. Insert a chest tube when any one of the following is present: effusion half a hemithorax or more in size, loculations, pleural fluid pH under 7.20 (or glucose under 60 mg/dL), positive Gram stain or culture, or purulent appearance. Drainage options include therapeutic thoracentesis, tube thoracostomy, intrapleural fibrinolytics, thoracoscopy with breakdown of adhesions, or thoracotomy with decortication.^[10]

Classic pitfalls: under-treating severe CAP (missed ICU need or missed atypical cover); not covering atypicals in hospitalised patients; failing to consider TB or PE in the atypical case; delaying antibiotics for tests; over-investigating mild disease; missing bacteraemia (no repeat blood cultures); forgetting the follow-up CXR that unmasks an underlying lung cancer; and giving uncontrolled oxygen to a COPD patient precipitating CO2 narcosis. ^[1]

Approach to non-resolving (slowly resolving) pneumonia — a common and examiner-tested scenario. Pneumonia is expected to show radiographic improvement within 4 weeks and complete resolution by 8 to 12 weeks; failure to improve demands a structured re-think. Work through five questions:^[2]

• Wrong diagnosis — is it TB, fungal infection, PE with infarct, organising pneumonia, vasculitis, or pulmonary oedema masquerading as CAP? Re-image with HRCT and re-sample.
• Wrong organism / wrong antibiotic — atypical not covered (no macrolide), Legionella, Mycoplasma, TB, or a resistant organism (MRSA, Pseudomonas); obtain sputum AFB / GeneXpert, atypical serology, and review the antibiogram.
• Impaired host defence — undiagnosed HIV, immunosuppression, diabetes, malignancy; test HIV and check immunoglobulins.
• Complication — parapneumonic effusion, empyema, lung abscess, bronchopleural fistula, ARDS; ultrasound and sample any pleural collection.
• Underlying structural lesion — post-obstructive lung cancer, inhaled foreign body, bronchiectasis; arrange bronchoscopy and further imaging for any non-resolving opacity to exclude malignancy. ^[1]

The single highest-yield action in the older smoker with non-resolving pneumonia is bronchoscopy to exclude an obstructing lung cancer. ^[1]

Prognosis & Disposition

CURB-65 correlates with 30-day mortality. NICE bands are 0 or 1 low (under 3 percent), 2 intermediate (3 to 15 percent), 3 to 5 high (over 15 percent) and should be combined with clinical judgement for site of care. Lim's derivation mortalities by exact score are 0.7, 3.2, 3, 17, 41.5 and 57 percent. NICE hospitalised-CAP mortality overall is 5 to 14 percent. Lim also found albumin under 30 g/dL independently associated with death.^[3][15]

The PSI is better than CURB-65 at identifying genuinely low-risk patients safe for outpatient care (classes I and II), whereas CURB-65 is the better bedside triage tool for spotting severe disease and triggering the sepsis pathway. No score replaces clinical judgement — a socially isolated or frail patient, or one unable to take oral medication, may warrant admission even with a low score. ^[1]

If symptoms have resolved within 5 to 7 days, ATS/IDSA 2019 does not recommend routine follow-up chest imaging. Non-resolving or recurrent same-lobe pneumonia still warrants a hunt for obstructing lung cancer, TB, or a complication — that is a clinical indication, not a routine film in the well patient.^[1]

Special Populations

• Elderly and debilitated — aspiration pneumonia and diffuse aspiration bronchiolitis occur mainly in elderly, debilitated patients with dysphagia and often masquerade as community-acquired pneumonia (sometimes recurrent); treating the pneumonia means treating the swallow too.^[13]
• Pregnancy — do not delay effective therapy; choose agents with established safety in pregnancy per current national guidance, and treat promptly and fully.
• Immunocompromised (HIV, transplant, chemotherapy, neutropenia) — the ATS/IDSA 2019 guideline expanded microbiological testing for patients suspected of drug-resistant infections; involve microbiology and infectious diseases early.^[5]
• Asplenic or hyposplenic — risk of overwhelming infection with encapsulated organisms; empirical cover and vaccination are the priorities, per standing national immunisation schedules.
• COPD — monitor for oxygen-related carbon dioxide retention; individualise empiric cover to prior isolates and local resistance patterns.
• Children — severity scoring, hydration and rapid escalation drive outcomes; drug and dose selection is weight-based and guideline-driven. ^[2]

Evidence, Guidelines & Regional Differences

Key changes in the ATS/IDSA 2019 guideline:^[1][5]

• Empirical therapy must cover atypical organisms in all hospitalised CAP (beta-lactam plus macrolide, OR a respiratory fluoroquinolone).
• HCAP was retired — do not automatically broaden therapy for "healthcare-associated" exposure; instead use validated risk factors for resistant pathogens (prior respiratory isolation of Pseudomonas, recent IV antibiotics, recent hospitalisation) to decide.
• Routine blood cultures and sputum culture are reserved for severe CAP or specific risk factors (not mild disease).
• Corticosteroids are NOT recommended routinely.
• Do not withhold initial antibiotics because of a low procalcitonin in radiographically confirmed CAP.
• Follow-up chest imaging is not routine if symptoms resolve within 5 to 7 days.^[1]

^{[9] [18] [1] [1]}

Prevention — vaccination (the intervention examiners reward):^[1]

• Pneumococcal vaccination — conjugate vaccines (PCV13, PCV15, PCV20) and/or polysaccharide vaccine (PPSV23) per the age- and risk-based schedule; PCV20 simplifies the schedule.
• Annual influenza vaccination — reduces influenza and secondary bacterial pneumonia.
• COVID-19 vaccination — reduces severe COVID-19 pneumonitis.
• Smoking cessation, optimisation of chronic disease, oral hygiene (reduces aspiration pneumonia in care-home residents), and Hib and pertussis immunisation in children. ^[1]

Which vaccine schedule for a 70-year-old with COPD?ShowHide

Give pneumococcal vaccination (PCV15 or PCV20, with PPSV23 a year later if PCV15 is used and not previously given), annual influenza vaccine, and COVID-19 vaccination as the core preventive bundle. Smoking cessation is the single most modifiable host risk factor.

^[1]

Exam Pearls

• CURB-65: Confusion, Urea over 7 mmol/L, RR 30 or more, systolic BP under 90 or diastolic 60 or less, age 65 or more — Lim 2003 30-day mortality 0.7, 3.2, 3, 17, 41.5 and 57 percent at scores 0 to 5. NICE uses bands (0–1 low, 2 intermediate, 3–5 high) plus judgement for site of care.^[3][15]
• S. pneumoniae is the commonest blood-culture isolate in hospitalised CAP (69 of 76 positives in a prospective cohort).^[11]
• Legionella: extrapulmonary features (GI symptoms, hyponatraemia, confusion) — treat with a macrolide or fluoroquinolone.^[14]
• Give effective antimicrobials within 1 hour of documented hypotension in septic shock — each further hour of delay over 6 hours costs an average of 7.6 percent survival (Kumar). NICE: diagnose and treat CAP within 4 hours of hospital presentation.^[7][15]
• Stop antibiotics at a minimum of 5 days once afebrile for 48 hours and clinically stable.^[8]
• Drain a parapneumonic effusion if loculated, purulent, pH under 7.20, glucose under 60 mg/dL, culture- or Gram-stain-positive, or half a hemithorax or more.^[10]
• Aspiration pneumonia means dysphagia: broad-spectrum antibiotics PLUS swallow management.^[13]
• PSI accurately identifies low-risk patients; CURB-65 is the simpler bedside stratification tool.^[4]
• Do not withhold the first antibiotic dose because of a low procalcitonin in confirmed CAP.^[1]
• Corticosteroids cut mortality in severe CAP (RR 0.58) but ATS/IDSA 2019 does NOT recommend them routinely.^[9][5]

Exam application bank (NEET-PG / INICET)

One-line answer

Community-acquired pneumonia (CAP) is an acute infection of the lung parenchyma acquired outside hospital (or within the first 48 hours of admission). The commonest pathogen is Streptococcus pneumoniae; atypicals (Mycoplasma pneumoniae, Chlamydophila pneumoniae/psittaci, Legionella pneumophila), respiratory viruses (influenza, SARS-CoV-2, RSV), Haemophilus influenzae, Moraxella catarrhalis, and in selected hosts Staphylococcus aureus, Klebsiella pneumoniae and anaerobes. Typical CAP presents abruptly with fever, productive or rust-coloured sputum, dyspnoea, pleuritic chest pain and signs of consolidation; atypical CAP is insidious with a dry cough and prominent systemic features. Diagnosis is clinical plus chest X-ray; severity is graded with CURB-65 (Confusion, Urea over 7, RR 30 or more, systolic BP under 90 or diastolic 60 or less, age 65 or more). Treat with empirical antibiotics wit

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. ^[1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. ^[1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. ^[1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. ^[1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. ^[1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Community-Acquired Pneumonia.

The mantra

Cover typical AND atypical; let CURB-65 choose the door; antibiotics inside four hours.^[1][3]

Ward-round test — three stems, thirty seconds each

Stem 1 — the 82-year-old at the top (answer)ShowHide

Score the patient from the vignette: confusion, RR 32, urea 11, BP 88/50, age 82. What is the score, the disposition, and the antibiotic clock? Model: CURB-65 is 5 (all five positive) — severe CAP, ICU. Give high-flow oxygen, fluids and empirical IV antibiotics within 1 hour if there is septic shock, otherwise within 4 hours: a beta-lactam (e.g. co-amoxiclav or ceftriaxone) plus a macrolide (clarithromycin or azithromycin), covering typical and atypical organisms. Send blood cultures and a urinary antigen panel first, but do not delay antibiotics for them.^[1][3]

Stem 2 — the student with a dry cough and cold agglutinins (answer)ShowHide

A 19-year-old university student has a week of dry cough, headache and myalgia; CXR shows patchy interstitial shadowing that looks worse than he is. Cold agglutinins are positive. Organism and drug? Model: Mycoplasma pneumoniae — an atypical, walking pneumonia, classically in young adults in outbreaks. It lacks a cell wall, so beta-lactams fail: use a macrolide (clarithromycin or azithromycin), doxycycline, or a respiratory fluoroquinolone. Watch for extrapulmonary features — erythema multiforme and cold-agglutinin haemolytic anaemia.^[1]

Stem 3 — cavitating pneumonia after influenza (answer)ShowHide

A 55-year-old smoker develops rapidly progressive, bilateral pneumonia with cavitation one week after a flu-like illness. Which organism, and what does it change? Model: Staphylococcus aureus — post-influenza, often necrotising with cavitation and (in children) pneumatoceles. Add anti-staphylococcal cover (flucloxacillin or vancomycin if MRSA is possible) to the standard regime, consider ICU early, and isolate or test for influenza with the option of antivirals. Post-viral bacterial pneumonia is a classic, lethal stem.^[1]

References17ShowHide

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 Am J Respir Crit Care Med, 2019.PMID 31573350
2. [2]Prina E, Ranzani OT, Torres A. Community-acquired pneumonia Lancet, 2015.PMID 26277247
3. [3]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 Thorax, 2003.PMID 12728155
4. [4]Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients with community-acquired pneumonia N Engl J Med, 1997.PMID 8995086
5. [5]Metlay JP, Waterer GW. Update in adult community-acquired pneumonia: key points from the new American Thoracic Society/Infectious Diseases Society of America 2019 guideline Curr Opin Pulm Med, 2020.PMID 32084039
6. [6]Patel S. Calculated decisions: CURB-65 score for pneumonia severity Emerg Med Pract, 2021.PMID 33529515
7. [7]Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock Crit Care Med, 2006.PMID 16625125
8. [8]Uranga A, España PP, Bilbao A, et al. Duration of Antibiotic Treatment in Community-Acquired Pneumonia: A Multicenter Randomized Clinical Trial JAMA Intern Med, 2016.PMID 27455166
9. [9]Stern A, Skalsky K, Avni T, et al. Corticosteroids for pneumonia Cochrane Database Syst Rev, 2017.PMID 29236286
10. [10]Porcel JM, Light RW Parapneumonic pleural effusions and empyema in adults: current practice Rev Clin Esp, 2009.PMID 19889319
11. [11]Saldías PF, Reyes BT, Sáez BJ, et al. Clinical predictors of bacteremia in immunocompetent adult patients hospitalized for community-acquired pneumonia Rev Med Chil, 2015.PMID 26203565
12. [12]Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute respiratory distress syndrome: the Berlin Definition JAMA, 2012.PMID 22797452
13. [13]Marik PE Aspiration syndromes: aspiration pneumonia and pneumonitis Hosp Pract (1995), 2010.PMID 20469622
14. [14]Falcó V, Molina I, Juste C, et al. Treatment for Legionnaires' disease. Macrolides or quinolones? Enferm Infecc Microbiol Clin, 2006.PMID 16792936
15. [15]National Institute for Health and Care Excellence Pneumonia in adults: diagnosis and management (CG191) NICE, 2014.Source
16. [16]Lim WS, Smith DL, Wise MP British Thoracic Society community acquired pneumonia guideline and the NICE pneumonia guideline: how they fit together Thorax, 2015.PMID 25977290
17. [18]Diaz Caballero LA, Aijaz A, Saleem Paryani N, et al. Comparing the efficacy of corticosteroids among patients with community-acquired pneumonia in the ICU versus non-ICU settings: A systematic review and meta-analysis Steroids, 2024.PMID 38354995