Community-acquired and hospital-acquired pneumonia

• Pneumonia is infection of the lung tissue distal to the terminal bronchioles, and it is still the single most common serious infection a clinician in general practice and in hospital meets; most cases are treated at home, but hospitalised pneumonia carries significant mortality.
• "Community-acquired" means the infection began outside hospital; "hospital-acquired" begins at least 2 days after admission, "ventilator-associated" begins more than 48 hours after intubation, and aspiration pneumonia follows entry of colonised material into the airway.
• The most common bacterial cause overall remains Streptococcus pneumoniae, with Haemophilus influenzae, atypical organisms such as Mycoplasma, Chlamydophila and Legionella, respiratory viruses, Staphylococcus aureus, gram-negative bacilli, anaerobes and Pneumocystis each dominating in particular settings and hosts.
• Presentation is a triad of cough (often productive), fever and breathlessness plus focal chest signs; the chest radiograph confirms an infiltrate and is required in everyone in whom pneumonia is suspected.
• Severity is best stratified with CURB-65 or the Pneumonia Severity Index to decide place of care, and treatment is empirical because the exact organism is found in fewer than half of cases; in healthy outpatients it is a narrow beta-lactam or macrolide, while in hospital or severe disease it widens to cover atypicals and resistant organisms.
• Complications include parapneumonic effusion, empyema, abscess and sepsis, and two vaccines (pneumococcal and annual influenza) prevent a large share of them.

By the end of this page you should be able to:

1. Define community-acquired, hospital-acquired, ventilator-associated and aspiration pneumonia and give the timing cut-offs that separate them.
2. Name the common pathogens for each age group and setting, and explain why no single organism dominates all of them.
3. Take a history and examination that distinguishes typical from atypical pneumonia and recognises red flags.
4. Read a chest radiograph and the common severity scores (CURB-65, the Pneumonia Severity Index (PSI) and the IDSA/ATS severe criteria) and turn them into a place-of-care decision.
5. Choose empirical treatment, with drug, dose, route and duration, for outpatient, inpatient and intensive-care disease, and for hospital-acquired and ventilator-associated pneumonia.
6. State the indications for cultures, urinary antigens and PCR, and the role of procalcitonin.
7. Describe prevention, especially pneumococcal and influenza vaccines, and manage pneumonia where tests and drugs are limited.
8. Counsel a patient about expected recovery.

Pneumonia is classified first by where it was acquired, because setting predicts the likely pathogen and therefore the empirical treatment.

A distinction that no longer guides treatment is the old "typical versus atypical" split. Clinicians still use the terms informally, but the bacteria called "atypical" are common and cannot be reliably told apart by the bedside picture; the chest radiograph and the symptoms overlap.^[1] What matters is severity and setting.

Pneumonia is common everywhere. In the United States community-acquired pneumonia is estimated to occur in 649 of 100,000 adults each year; for adults older than 65 the incidence is higher and about 967,470 adults aged 65 and over are hospitalised with community-acquired pneumonia annually, with 38 percent one-year mortality.^[1] Rates elsewhere differ markedly: 8.1 per 10,000 in Vietnam and 31.2 per 10,000 in the United Kingdom in older series.^[1] Older adults are hit hardest, with more severe disease, more hospitalisation and higher mortality, and survivors of pneumonia carry an increased risk of cardiovascular events for months afterwards.^[1]

Hospital-acquired pneumonia is the second most common infection in all hospitalised patients and the most common in the intensive care unit, accounting for a quarter of ICU infections and about 22 percent of all hospital-acquired infections in the United States; ventilator-associated pneumonia has an estimated all-cause mortality between 25 and 50 percent.^[3]

The definitive microbiological diagnosis is found in fewer than half of patients with community-acquired pneumonia; with better (molecular) testing, a slightly smaller percentage is now attributed to the old "typical" bacteria and a larger share to viruses and polymicrobial infection.^[1] Two pathogens are identified in over 30 percent of cases in some series, usually a virus plus a bacterium.^[1]

The organism changes with the setting because each setting selects for different colonists. S. pneumoniae remains the commonest single bacterial cause of community-acquired pneumonia, accounting for about 5 percent of all cases and 13.5 percent of cases with an identified pathogen in one large United States study, but for about 30 percent in a Norwegian series.^[1] S. aureus causes only about 1.6 percent of hospitalised community-acquired pneumonia and MRSA about 0.7 percent, but MRSA pneumonia after influenza carries inpatient mortality of about 13 percent compared with about 2 percent for non-S. aureus disease.^[1] Klebsiella and Pseudomonas are not typical causes in healthy adults but are expected in alcohol misuse, diabetes, bronchiectasis or cystic fibrosis.^[1]

• Age older than 65 years, and especially older than 85.
• Chronic cardiac or respiratory disease (COPD, bronchiectasis, asthma), diabetes, chronic liver or renal disease, asplenia and hypothyroidism on a broader reading of practice, and immunosuppression (HIV, chemotherapy, long-term corticosteroids, transplantation, biologic therapy).
• Smoking and alcohol misuse.
• Recent influenza.
• Residence in a care home or recent hospitalisation (these now shift the patient away from simple community-acquired pneumonia only when they also carry true MDR risk factors, see the note on healthcare-associated pneumonia in the table above).^[3]

• Acid-suppressive medication: a prospective study found pneumonia in 5 percent of patients taking acid suppressants against 2 percent of those not taking them, with the risk significant for proton-pump inhibitors but not for H2-blockers.^[3]
• Endotracheal intubation (micro-aspiration, biofilm on the tube), prolonged ventilation, malnutrition, and cross-contamination between patients.
• Prior broad-spectrum antibiotics, which select resistant flora.
• Severe underlying illness, because these patients are already critically ill when infection is added.

Understanding the sequence lets you reason rather than memorise.

1. Colonisation. The oropharynx, and at times the stomach, harbour potential pathogens. Aspiration of small amounts of secretions into the lower airway happens even in healthy people during sleep; host defences (cough, mucociliary clearance, alveolar macrophages) usually clear it.
2. Failure of defence. Impaired cough (stroke, sedation), impaired mucociliary clearance (smoking, viral infection, chronic lung disease), or overwhelmed macrophages (large inoculum, particularly virulent organism, immunosuppression) allow bacteria to reach the alveoli.
3. Invasion. Organisms multiply; the innate immune response (neutrophil recruitment, cytokines) causes consolidation, impaired gas exchange and the systemic inflammatory response.
4. Spread. The infection may stay local, or extend to pleural space (parapneumonic effusion, empyema), cause bacteraemia and sepsis, cavitate (abscess), or produce acute respiratory distress.
5. In hospital. The patient's own flora changes to hospital flora and resistant organisms within days; the longer the stay and the more prior antibiotics, the more likely gram-negatives and MRSA become.

S. pneumoniae causes the largest single burden because of its polysaccharide capsule (anti-phagocytic), its ability to spread along alveolar spaces, and its high carriage rate in the community; vaccination against it is therefore the main preventive lever.

Typical bacterial pneumonia classically presents with fever, a productive cough with purulent sputum, dyspnoea and pleuritic chest pain.^[1] Atypical illness tends to be more subacute and indolent, with non-productive cough, headache, myalgia, sore throat, diarrhoea or ear pain, and more subtle pulmonary findings.^[1]

Symptoms that should be noted precisely: onset (abrupt vs gradual), cough and sputum character (rusty sputum in pneumococcus, "currant jelly" in Klebsiella; haemoptysis in severe or necrotising disease), pleuritic pain, breathlessness at rest or on exertion, fever, chills, rigors, and confusion (especially in older adults, where confusion may be the only sign). Recent travel, exposure to birds or animals, water or aerosol exposure, hospitalisation or surgery, and antibiotic or steroid history all matter, as does swallowing difficulty or a recent stroke in the case of aspiration.

Examine the whole patient, not just the chest. General: fever or hypothermia, tachypnoea, tachycardia, hypotension, cyanosis, confusion. Focal pulmonary signs suggest consolidation: bronchial breath sounds, increased tactile fremitus, egophony and coarse rales over the involved lobe or segment. Decreased tactile fremitus and dullness on percussion suggest parapneumonic effusion or empyema.^[1] In atypical disease, especially Mycoplasma, consolidation may be minimal or absent despite an impressive cough. ^[2]

Extrapulmonary clues point to a cause: relative bradycardia, hyponatraemia, hypophosphataemia, raised creatine phosphokinase and gastrointestinal symptoms in Legionnaires' disease; erythema multiforme, haemolytic anaemia and cold agglutinins in Mycoplasma; severe headache and myalgia in Q fever.^[1]

• Tachypnoea of 30 or more breaths per minute; oxygen saturation below about 90 percent on room air.
• Systolic blood pressure below 90 mmHg or diastolic pressure at or below 60 mmHg.
• New confusion or altered mental status.
• Multilobar or bilateral infiltrates, or a rapidly expanding effusion.
• Immunosuppression, asplenia, or pregnancy with severe illness.
• Recent stroke, depressed consciousness or bulbar weakness with dysphagia (aspiration risk).
• In hospital: fever and infiltrates persisting despite antibiotics for 2 weeks (consider non-bacterial causes and mimics).^[3]

Figure 102-02-Infiltrat seitlich

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Lateral chest radiograph showing an airspace opacity in the lower part of the lung consistent with lobar pneumonia.

Figure 2X-ray of lobar pneumonia

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Frontal chest radiograph of a 67-year-old man with right middle lobe lobar pneumonia

A chest radiograph is required in everyone with suspected pneumonia: to look for an infiltrate and to exclude conditions that mimic pneumonia, such as lung cancer or pulmonary embolism.^[1] Very early infection may be radiographically silent, and chest computed tomography may be needed in immunocompromised patients with negative radiographs but continued suspicion. Repeat imaging is generally not needed if the patient is improving: radiographic improvement lags far behind clinical recovery.^[1][3]

Imaging also reveals complications: pleural effusion, empyema, abscess, cavitation (suggestive of Klebsiella, S. aureus or anaerobes) and lymphadenopathy. Lung ultrasound is increasingly used at the bedside for rapid diagnosis and to detect pleural fluid.^[2]

Pneumonia is a syndromic diagnosis and many conditions mimic it. The differential depends on tempo and comorbidity.

Figure 3Nocardiosis - Gram stain Case 149 (5286067518)

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Microphotograph captioned 'Nocardiosis - Gram stain Case 149' in which numerous long, thin Gram-positive filaments (noted to look like Actinomyces filaments) are present, usually seen within abscesses.

• Chest radiograph (required as above).
• Oxygen saturation (and arterial blood gas if severe, with the PaO2/FiO2 ratio).
• Full blood count, urea or blood urea nitrogen, creatinine, electrolytes. Urea (over 7 mmol per litre in the NICE CURB-65 formulation) and renal function are needed for the severity score. ^[2]
• C-reactive protein (and procalcitonin where it will change management).

Figure 4Gram stain of Streptococcus pneumoniae

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High-power Gram stain showing purple, paired and short-chain gram-positive cocci typical of Streptococcus pneumoniae.

Figure 5Encapsulated strain of Streptococcus pneumoniae in clinical sample sputum Gram staining

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Gram-stained sputum smear under the microscope: pink-stained cells and small organisms in the field, from a sample with Streptococcus pneumoniae.

Blood and sputum cultures should be taken before the first antibiotic dose in patients with severe disease and in all inpatients empirically treated for MRSA or Pseudomonas, and additional testing is warranted in severe disease.^[1] Microbiological testing (blood cultures, sputum cultures, pneumococcal or Legionella urinary antigen) is not needed in low-severity community disease, but should be considered in moderate or severe disease.^[2]

• Sputum Gram stain and culture when Pseudomonas, MRSA or a specific pathogen is suspected.
• Blood cultures in severe disease.
• Urinary antigen tests for S. pneumoniae and Legionella in patients with severe community-acquired pneumonia (pneumococcal antigen supports de-escalation to a narrower antibiotic; Legionella antigen is used when risk factors exist).^[2]
• PCR (multiplex respiratory panel), especially when a viral infection is suspected or in outbreak settings, and for selected fastidious organisms.
• Imaging of complicated disease: ultrasound or computed tomography for parapneumonic effusion or empyema, and diagnostic thoracentesis with fluid analysis (pH, cell count, Gram stain, culture, Light's criteria).

Procalcitonin is released in bacterial infection and down-regulated in viral infection, and is used to distinguish bacterial from non-bacterial infection, to assess severity and prognosis, and to guide duration. The 2016 and 2019 IDSA/ATS guidelines advise cautious use of procalcitonin and C-reactive protein, because sensitivity is variable and consistent positive cut-offs do not exist.^[1] Procalcitonin should never override clinical judgement; in hospital, NICE suggests measuring procalcitonin (or CRP) three to four days after starting treatment only if there is clinical concern about treatment failure.^[2]

In HIV, the differential is broader. Pneumocystis jirovecii pneumonia should be suspected with a CD4 count below 200 cells per microlitre (or below 14 percent) and a gradual onset of dyspnoea, non-productive cough, non-focal infiltrates and hypoxaemia.^[1] Pulmonary tuberculosis, bacterial pneumonia and the endemic fungi all need considering. In neutropenic fever with pulmonary infiltrates, think also about invasive aspergillosis and the endemic fungi; escalate early.

The purpose of these tools is to avoid two opposite errors: sending a sick patient home, and keeping a well patient in hospital.

One point each for:

• Confusion (new disorientation in person, place or time, or abbreviated mental test score 8 or less);
• Urea (blood urea nitrogen) over 7 mmol per litre;
• Respiratory rate 30 or more breaths per minute;
• Blood pressure low (systolic below 90 mmHg or diastolic 60 mmHg or less); ^[2]
• Age 65 years or more.^[2]

Interpretation: 0 or 1, low risk (less than 3 percent mortality); 2, intermediate risk (3 to 15 percent); 3 to 5, high risk (more than 15 percent).^[2] NICE suggests considering inpatient care for a score of 3 or more, one of several options (including a virtual ward or hospital-at-home) for a score of 2, and discharge with safety-netting advice for 0 or 1.^[2] A separate CRB-65, omitting the urea and usable in primary care, stratifies as 0 low, 1 or 2 intermediate and 3 or 4 high risk.^[2]

The PSI weighs age, comorbidity and examination and laboratory findings into classes I to V; it was designed to predict mortality and generally recommends outpatient care for classes I to III and inpatient evaluation for IV to V. CURB-65 is simpler and easier to remember; the PSI is more discriminating in older patients with comorbidity. ATS/IDSA 2019 prefers the PSI for deciding outpatient versus inpatient treatment.^[1] Where they disagree, clinical judgement takes precedence, particularly with pregnancy, comorbidity or unsafe home circumstances. ^[2]

Severe community-acquired pneumonia is present with one major criterion or three or more minor criteria.^[1]

• Major criteria: septic shock requiring vasopressors; respiratory failure requiring mechanical ventilation. ^[1]
• Minor criteria: respiratory rate 30 or more per minute; PaO2/FiO2 ratio 250 or less; multilobar infiltrates; confusion; raised urea; leukopenia below 4,000 cells per microlitre; thrombocytopenia below 100,000 per microlitre; hypothermia; hypotension.^[1]

ICU admission is recommended for any patient needing mechanical ventilation or vasopressors, and should be considered with three or more minor criteria.^[1]

A useful companion is SMART-COP, which focuses on the need for ventilatory or vasopressor support and includes systolic blood pressure, multilobar infiltrates, albumin, respiratory rate, tachycardia, confusion, oxygenation and pH. Expanded CURB-65 models and the performance of procalcitonin as an adjunct to these tools are still under study.^[1]

1. Diagnose and treat promptly (within 4 hours of presentation in hospital).^[2]
2. Take cultures and antigens before antibiotics when disease is severe or resistant pathogens are suspected, and never delay antibiotics for a sick patient.
3. Give the narrowest agent that covers the likely organism for the setting, because broader agents select resistance and Clostridioides difficile infection.
4. Stop the inciting antibiotic (if any) that precipitated the infection, and review sedatives, proton-pump inhibitors and other drugs.
5. Optimise oxygenation, fluids and nutrition; thromboprophylaxis and early mobilisation; avoid unhelpful antitussives and sedatives.
6. Escalate early if the patient worsens on the first 2 to 3 days of treatment.
7. Review at 48 hours and switch from intravenous to oral therapy when stable.^[2]

For previously healthy adults with no comorbidities and no risk factors for resistant S. pneumoniae, the 2019 ATS/IDSA summary (as set out in reference 1) gives:

• Amoxicillin 1 g by mouth three times a day, or
• a macrolide (azithromycin 500 mg once then 250 mg daily; azithromycin 500 mg daily for three days; or clarithromycin 500 mg twice daily), or ^[1]
• doxycycline 100 mg twice a day.^[1]

Macrolide monotherapy should be used only in areas where pneumococcal resistance is below 25 percent.^[1]

NICE's 2025 guidance uses a 500 mg three-times-a-day dose of amoxicillin and doxycycline or clarithromycin for penicillin-allergic or atypical cover.^[2] The adult dose variation (1 g vs 500 mg three times daily) reflects regional formularies; check your local guidance and the drug monograph.

For adults with comorbidities (chronic heart, lung, liver or renal disease; diabetes; alcohol misuse; malignancy; asplenia; immunosuppression; recent antibiotics; or other MDR risk) use a beta-lactam plus macrolide or doxycycline, or a respiratory fluoroquinolone:^[1]

• Beta-lactam: amoxicillin-clavulanate 2 g/125 mg twice daily, 875 mg/125 mg twice daily or 500 mg/125 mg three times daily; or cefpodoxime 200 mg twice daily; or cefuroxime 500 mg twice daily; and a macrolide or doxycycline; or
• respiratory fluoroquinolone (moxifloxacin 400 mg daily, or levofloxacin 750 mg daily). ^[1]

• A beta-lactam: ampicillin-sulbactam 1.5 to 3 g every 6 hours; or ceftriaxone 1 to 2 g daily; or cefotaxime 1 to 2 g every 8 hours; or ceftaroline 600 mg every 12 hours; and a macrolide; or ^[1]
• a respiratory fluoroquinolone; or
• if macrolides and fluoroquinolones are contraindicated, the beta-lactam plus doxycycline.^[1]

In penicillin allergy, aztreonam may be substituted for the beta-lactam; the likelihood of true cross-reactivity with cephalosporins is small.^[1]

• A beta-lactam (as above) and a macrolide or a respiratory fluoroquinolone.^[1]
• If MRSA is suspected: vancomycin 15 mg per kg every 12 hours (adjusted by levels), or linezolid 600 mg every 12 hours.^{[1] [2]}
• If Pseudomonas is suspected: piperacillin-tazobactam 4.5 g every 6 hours, cefepime 2 g every 8 hours, ceftazidime 2 g every 8 hours, meropenem 1 g every 8 hours or imipenem 500 mg every 6 hours (monotherapy normally adequate; double cover only in suspected resistant Pseudomonas or very high mortality risk), or aztreonam 2 g every 8 hours.^[1][3] During co-endemic influenza, start an antiviral (oseltamivir in hospitalised patients) for any patient with influenza-like illness and pneumonia.^[1]

Corticosteroids are considered in adults with high-severity community-acquired pneumonia in hospital, for 4 to 7 days or until discharge, with intravenous hydrocortisone or dexamethasone as the alternative.^[2]

• Five days for uncomplicated community-acquired pneumonia, stopping once the patient is clinically stable.^[1][2]
• Clinically stable means no fever for 48 hours and not more than one of the instability criteria: systolic pressure below 90 mmHg, heart rate above 100, respiratory rate above 24, oxygen saturation below 90 percent on room air, or abnormal mental status.^[2]
• Seven days for suspected or proven Pseudomonas or MRSA, ceasing after the patient has been afebrile for 48 to 72 hours and shows no instability.^[1]
• Longer (community-acquired) if the pathogen identified is not covered by the initial agent, or if there is complicated disease (empyema, abscess), or an immunocompromised host.^[1]

For pneumonia beginning within 48 hours of admission, treat as community-acquired pneumonia.^[2]

For non-severe late (5 days or more, or high-risk) hospital-acquired pneumonia without resistance risk factors:

• Co-amoxiclav 500/125 mg by mouth three times a day for 5 days, then review; or alternative oral agents for penicillin allergy based on local resistance data (doxycycline, cefalexin, co-trimoxazole, or levofloxacin if switching from intravenous therapy).^[2]

For severe disease or risk factor for resistance (recent antibiotics, comorbidity, colonisation with multidrug-resistant organisms, recent healthcare contact):

• Intravenous options include piperacillin-tazobactam 4.5 g three times daily (four times if severe), ceftazidime 2 g three times daily, ceftriaxone 2 g once daily, cefuroxime, meropenem 0.5 to 1 g three times daily, ceftazidime-avibactam, and, when other agents are unsuitable, levofloxacin.^[2]
• For suspected or confirmed MRSA, add vancomycin (15 to 20 mg per kg intravenously twice or three times daily, with a loading dose of 25 to 30 mg per kg in seriously ill patients, maximum 2 g per dose) or teicoplanin (6 mg per kg every 12 hours for three doses then 6 mg per kg daily); linezolid 600 mg twice daily if vancomycin cannot be used.^[2]
• A simpler first-line regimen for early or low-risk HAP is ceftriaxone 2 g daily, or levofloxacin 750 mg daily, or ampicillin-sulbactam 3 g every 6 hours, or ertapenem 1 g daily, or aztreonam 2 g every 8 hours.^[3]

For ventilator-associated pneumonia, empirically cover S. aureus and Pseudomonas plus other gram-negative bacilli. Cover MRSA in units with a high prevalence of MRSA or where prevalence is unknown, with vancomycin or linezolid; cover MSSA preferentially with piperacillin-tazobactam, cefepime, levofloxacin, imipenem or meropenem. Single antipseudomonal cover is enough unless risk factors for multidrug-resistant organisms are present (recent intravenous antibiotics, septic shock or ARDS before VAP, 5 or more days of hospitalisation before onset, acute renal replacement therapy, high local resistance), when combine an antipseudomonal beta-lactam or ceftolozane-tazobactam or ceftazidime-avibactam with a fluoroquinolone or (in selected cases) aminoglycoside.^[3] Aminoglycosides in general should be avoided for VAP because of poor lung penetration and nephrotoxicity; Pseudomonas VAP fails in up to 40 percent regardless of regimen.^{[3] [1]}

Duration for hospital-acquired and ventilator-associated pneumonia is generally 7 days of appropriate therapy, with review at 5 days and tailoring to the culture result; ventilator-associated pneumonia (other than non-fermenting gram-negatives such as Pseudomonas) can be treated in 7 days.^{[3] [1]}

Aspiration pneumonia is usually a mixed infection dominated by aerobes; anaerobes are not important pathogens in hospital-acquired disease and need covering only in specific circumstances. The focus is on protecting the airway, swallowing assessment and treating the likely aerobes (often a third-generation cephalosporin or beta-lactam, with anaerobic cover if there is abscess or putrid sputum). Seek speech and language therapy assessment before oral intake resumes.

High-flow nasal oxygen is considered when standard oxygen fails to meet saturation targets, with senior review. In high-severity community disease NICE now considers a 4 to 7 day course of corticosteroids.^[2] Follow-up chest radiography at 6 weeks is reasonable in high-risk patients to confirm resolution, or sooner if not improving (a non-resolving opacity needs investigation for tuberculosis or malignancy). Patient-facing teaching: fever usually resolves within a week, chest pain and sputum by 4 weeks, cough and breathlessness by 6 weeks, most symptoms by 3 months, but fatigue can last 6 months.^[2]

Pneumonia can extend well beyond the lobe.

• Parapneumonic effusion: any pleural fluid accompanying pneumonia; small and free-flowing effusions often resolve with antibiotics alone.
• Empyema: infected, purulent pleural fluid, requiring drainage (chest tube), sometimes surgical debridement or decortication.
• Pulmonary abscess and necrotising pneumonia: cavities within the lung, classically with Klebsiella, S. aureus or anaerobes; prolonged antibiotics and drainage of the abscess if it fails to resolve.
• Respiratory failure, including acute respiratory distress syndrome in severe infection.
• Sepsis and septic shock, with multi-organ dysfunction.
• Cardiovascular complications: up to about a third of patients with community-acquired pneumonia have an acute cardiovascular event (myocardial infarction, heart failure) precipitated by the infection, which raises mortality and re-admission.^[1]
• Post-infective bronchiectasis and organising pneumonia, if inflammation fails to resolve.
• Death: overall mortality of non-severe community pneumonia managed as an outpatient is very low; hospitalised disease in older adults is much more dangerous (about 38 percent one-year mortality in adults 65 and over with community-acquired pneumonia in the United States).^[1]
• Persistent fatigue and slow recovery are expected and are not by themselves complications; they settle over weeks to months.^[2]

Most uncomplicated disease responds quickly to the correct antibiotic and resolves within 7 to 10 days, though the chest radiograph and the patient's stamina recover more slowly. Age, comorbidity, multilobar disease, confusion, serious initial vital signs and raised urea predict worse outcome, which is exactly what CURB-65 and the PSI quantify. The commonest long-term problem after a hospital admission is recurrence and readmission, so addressing smoking, alcohol intake, swallowing safety and vaccination before discharge pays off.

Prevention works at four levels: vaccination, risk-factor management, infection control in hospital, and early, accurate treatment.

Vaccination. Two vaccines matter most for pneumonia prevention.

• Pneumococcal vaccines. Routine pneumococcal vaccination is recommended for all children younger than 5 years with a 4-dose conjugate series (PCV15 or PCV20) at 2, 4, 6 and 12 to 15 months. All adults aged 50 and over should receive a conjugate vaccine (PCV15, PCV20 or PCV21); if PCV15 is used, give a dose of the polysaccharide vaccine PPSV23 one year later, while PCV20 and PCV21 complete the course. Vaccination is also recommended for children and adults at increased risk (chronic heart, lung, liver or kidney disease; diabetes; asplenia; immunocompromise; smoking; and several other indications).^[4]
• Influenza vaccine. Everyone aged 6 months and over should have it every season, and it is particularly important for those at higher risk of complications. Annual vaccination reduces both influenza itself and the bacterial pneumonia that follows it.^[5]

Risk-factor management includes smoking cessation, good dental care, careful use of opioids and sedatives, screening for and treating dysphagia and (after a stroke or in neurodegenerative disease) modifying food texture and using thickened liquids with speech and language therapy, and avoiding unnecessary acid suppression. Avoiding unnecessary antibiotics protects the patient's own flora.

Hospital prevention includes hand hygiene, elevation of the head of the bed, oropharyngeal care, staff training, antibiotic stewardship and, where possible, removing the ventilator at the earliest safe opportunity; none of these need expensive technology.

Children. Non-severe disease is increasingly treated with shorter courses; other points are as in the paediatric formularies (check local guidance). RSV and influenza vaccines are now available for specific high-risk infants and older adults.

Pregnancy. Empirical choice is usually a beta-lactam (amoxicillin or an oral cephalosporin) with macrolide cover where atypicals are suspected; avoid fluoroquinolones and tetracyclines. Erythromycin rather than other macrolides is preferred in pregnancy when needed. Seek obstetric advice for significant or severe disease.^[2]

Older adults. Atypical presentations (confusion, functional decline) are common and pneumonia may be the final common path of several conditions; the mortality is high, so treat early and review daily.

Immunocompromised adults. Broader testing (urine antigens, PCR, fungal markers, Aspergillus galactomannan depending on risk), broader cover (including Pneumocystis, fungi, mycobacteria) and lower thresholds for ICU referral.

Where computed tomography, echocardiography, PCR and broad-spectrum intravenous agents are limited, the honest approach is clinical and empirical, with the cheapest effective agents used carefully.

• Diagnose on clinical grounds supported by a chest radiograph if possible, and by sputum in selected cases. Where only a plain radiograph is available, a new lobar infiltrate with fever and tachypnoea is enough to start treatment.
• Use cheap, effective first-line drugs. Amoxicillin (for non-severe disease), benzylpenicillin or ceftriaxone intravenously for inpatients, and oral or intravenous clarithromycin for atypical cover where available; erythromycin is a cheaper atypical alternative. Metronidazole can be added for severe aspiration.
• Oxygen is the priority. Pulse oximetry, low-flow oxygen, simple positioning, humidification and (where available) continuous positive airway pressure; early referral or transfer for mechanical ventilation.
• Parapneumonic effusion and empyema can be diagnosed with ultrasound and drained with a needle or tube; drainage improves outcome more than any antibiotic upgrade.
• Intravenous-to-oral switch as soon as stable conserves cost and lines.
• Vaccination programmes (including pneumococcal and influenza where they exist) and smoke-reduction programmes give the best return.
• Severe or complicated disease should be referred early; telemedicine support is useful where specialist advice is distant.

Throughout, the guidance used here is guideline-based where possible (ATS/IDSA 2019, NICE 2025, and local formularies), but individual doses, routes and durations must be checked against the formulary in force in the place you work.

• Pulmonary chapter (cross-check for oxygen transport, gas exchange and imaging).
• Clinical examination of the respiratory system.
• Tuberculosis and non-tuberculous mycobacterial disease.
• Sepsis, including quick assessment and early antibiotics.
• Pleural effusion and empyema diagnosis and drainage.
• Acute respiratory distress syndrome.
• Immunisation schedules: pneumococcal and influenza.
• Antimicrobial resistance and antibiotic stewardship.
• Dysphagia and aspiration risk after stroke.
• HIV: primary care and opportunistic infections.

• Pneumonia is infection of the lung parenchyma, defined by clinical infection plus new radiographic infiltrates; timing of acquisition (community, hospital at 2 or more days, ventilator at more than 48 hours, aspiration) predicts the likely pathogen.
• S. pneumoniae is the commonest single bacterial cause of community-acquired pneumonia but a smaller share of late and hospital-acquired disease, which is dominated by gram-negatives and S. aureus (including MRSA).
• Clinical signs of consolidation (bronchial breath sounds, increased fremitus, egophony) are present in typical disease; atypical disease may have few chest signs.
• A chest radiograph is mandatory, confirms the diagnosis and excludes mimics; repeat imaging is not routine if the patient is improving.
• CURB-65 (or CRB-65 in primary care) and the PSI guide the place of care; one major or three minor IDSA/ATS severe criteria flag ICU admission.
• Treatment is empirical by severity and setting; non-severe disease is usually 5 days, and MRSA or Pseudomonas disease 7 days, stopping when the patient is stable.
• Severe community-acquired disease uses a broad beta-lactam plus macrolide or fluoroquinolone, with MRSA and Pseudomonas cover by risk, and a 5 to 7 day course of corticosteroids is now considered.
• Hospital-acquired and ventilator-associated disease need risk-stratified MRSA and antipseudomonal cover, generally for 7 days.
• Complications are parapneumonic effusion, empyema, abscess, sepsis and acute cardiovascular events; drainage rather than drugs alone treats empyema.
• Prevention rests on pneumococcal vaccination (4-dose childhood series; a conjugate vaccine for adults 50 and over, with PPSV23 a year later if PCV15) and annual influenza vaccination, plus smoke reduction and swallowing safety.