Community-acquired pneumonia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The infection-focused CAP sequence is host and exposure assessment, pathogen and resistance hypothesis, proportionate sampling, severity-matched empirical therapy, result interpretation and deliberate de-escalation. Clinical severity remains essential, but the Respiratory CAP chapter owns detailed physiology, oxygen, imaging and ventilatory escalation.

Microbiology has value only when collection and interpretation are disciplined. Prior antibiotics reduce culture yield, salivary sputum obscures lower-airway organisms, colonisation is not automatically causation and a viral PCR result does not by itself exclude clinically important bacterial coinfection.

Every antimicrobial prescription is a provisional decision. At 24–48 hours, integrate trajectory, specimen quality, organism identity, susceptibility, complication imaging and allergy history to continue, narrow, stop or switch route. A named clinician must own results that return after transfer or discharge.

Key points

Begin with host, exposure and resistance risk: recent antibiotics, previous resistant isolates, influenza, aspiration, immune suppression, travel, water-system exposure and clusters can change the pathogen hypothesis.
Do not routinely request microbiology for uncomplicated low-severity adult CAP; in moderate or high severity, choose tests only when the result can refine treatment, detect a complication or trigger public-health action.
When bacteraemia or sepsis is plausible, obtain at least two adult blood-culture sets using two aerobic and two anaerobic bottles, filling each with 8–10 mL and sending them promptly for incubation.
A good lower-respiratory specimen is more useful than salivary sputum. Record previous antibiotics, request the relevant tests and assign a clinician to act on preliminary and post-discharge results.
NICE first-line antibiotic choice follows severity, oral feasibility and allergy phenotype, then recent exposure, previous microbiology and the current local antibiogram modify the empirical plan.
Review treatment and microbiology by 24–48 hours: confirm the diagnosis, narrow spectrum, stop unnecessary agents and switch intravenous therapy to oral when clinical response and absorption allow.
For adults, plan to stop at five days unless a result requires longer treatment or clinical instability persists; write the indication, route, review time and stop rule when prescribing.
Failure to improve is a new diagnostic problem. Look for empyema, abscess, obstruction, resistant or unexpected organisms, ineffective exposure and a non-infectious mimic before simply broadening antibiotics.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Typical respiratory bacteria

Streptococcus pneumoniae remains the principal bacterial hypothesis; Haemophilus influenzae and Moraxella catarrhalis become more plausible with chronic airways disease, smoking and prior airway colonisation.

Context-dependent resistant bacteria

Recent antibiotics, previous resistant isolates, healthcare exposure, structural lung disease or post-influenza deterioration can increase concern for Gram-negative organisms or Staphylococcus aureus without proving either.

Atypical and exposure-linked organisms

Legionella, Mycoplasma, Chlamydia psittaci and Coxiella probabilities depend on water, travel, bird, animal and outbreak histories; clinical features alone are insufficiently specific.

Respiratory viruses and coinfection

Influenza, SARS-CoV-2 and other viruses can cause pneumonitis directly, damage airway defences and permit subsequent bacterial invasion, so viral and bacterial processes may coexist.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Barrier failure and microaspiration
Organisms reach distal airspaces when mucociliary clearance, cough, swallowing or innate immunity fails; microaspiration is common, but invasive infection depends on inoculum and host defence.
2
Alveolar inflammatory response
Innate immune recognition recruits neutrophils and protein-rich exudate into alveoli, producing consolidation while organisms may cross damaged barriers into blood and cause systemic infection.
3
Necrosis and pleural extension
Uncontrolled infection can destroy lung tissue or spread across the pleura, forming abscess, complicated parapneumonic effusion or empyema that requires drainage as well as antimicrobials.
4
Antibiotic selective pressure
Unnecessarily broad or prolonged therapy suppresses susceptible flora, selects resistant organisms and disrupts gut microbiota, increasing toxicity and C. difficile risk without improving source control.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Bacterial syndrome

Purulent sputum, focal consolidation and inflammatory change support bacterial infection but do not identify the organism; severity, host and exposure determine whether microbiological testing will alter care.

Post-influenza deteriorationRed flag

New fever, shock, haemoptysis, cavitation or rapid decline after apparent influenza improvement raises concern for bacterial coinfection, including Staphylococcus aureus, and needs urgent reassessment.

Legionella or cluster clueRed flag

Travel accommodation, healthcare or workplace water exposure, hyponatraemia, diarrhoea, confusion or linked cases should prompt Legionella testing and early health-protection discussion rather than bedside diagnosis alone.

Aspiration context

Reduced consciousness, dysphagia, vomiting or poor dentition establishes aspiration risk; abrupt chemical pneumonitis and established bacterial aspiration infection require different antibiotic decisions.

Immunocompromised presentationRed flag

Neutropenia, transplantation, advanced HIV or substantial immunosuppression may blunt fever and expand the differential beyond routine CAP organisms, requiring early specialist sampling and treatment design.

Microbiological treatment failureRed flag

Persistent fever, bacteraemia or deterioration despite therapy suggests inadequate exposure, resistance, an uncovered pathogen, infected pleural fluid, abscess or another source requiring investigation and control.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Microbiology triage by severityFirst step
Why
Avoid low-yield testing while identifying patients whose results could change treatment.
Interpretation and limitations
NICE advises no routine microbiological tests for low-severity adult CAP. In moderate or high severity, select cultures, urinary antigens or molecular tests from sepsis features, sample quality, prior therapy, comorbidity and exposure.
02
Correctly filled adult blood-culture sets
Why
Detect bacteraemia and enable susceptibility-guided narrowing when bloodstream infection is clinically plausible.
Interpretation and limitations
Before antibiotics when this causes no harmful delay, collect at least two sets: two aerobic and two anaerobic bottles, 8–10 mL per bottle. Send immediately for incubation and document collection sites and prior doses.
03
Lower-respiratory culture
Why
Recover a bacterial pathogen in selected moderate, high-severity, complicated or non-responding disease.
Interpretation and limitations
Assess whether sputum is genuinely lower respiratory and send it promptly. Salivary contamination, recent antibiotics and airway colonisation reduce confidence; interpret microscopy, culture abundance and host context together.
04
Respiratory viral PCR
Why
Detect influenza, SARS-CoV-2 or another relevant virus and support infection-control or antiviral decisions.
Interpretation and limitations
Use according to circulating infections, exposure and local policy. Detection can coexist with bacterial pneumonia, while prolonged shedding or an upper-airway result may not explain every lower-airway abnormality.
05
Pneumococcal and Legionella urinary antigens
Why
Support targeted narrowing or identify Legionella when adult disease severity and risk factors justify testing.
Interpretation and limitations
NICE supports pneumococcal antigen for de-escalation and Legionella antigen when risk factors exist. A positive result needs clinical correlation; a negative Legionella urine test does not exclude every species or serogroup.
06
Pleural-fluid sampling
Why
Diagnose infected pleural fluid and obtain material for culture when an effusion complicates pneumonia.
Interpretation and limitations
Use ultrasound-guided aspiration and send pH promptly in a blood-gas syringe alongside cell count, Gram stain and culture. Purulence, organisms, low pH or loculation drives the pleural source-control pathway.
07
Expanded failure investigation
Why
Find a missed organism, host defect, anatomical obstruction or uncontrolled focus when improvement is absent.
Interpretation and limitations
Recheck specimen quality and exposure history, then use CT, repeat or invasive respiratory sampling, HIV testing or targeted mycobacterial, fungal and atypical assays with respiratory and infection specialists.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Tuberculosis

Subacute symptoms, weight loss, cavitation, exposure or epidemiological risk requires immediate infection-control assessment and mycobacterial sampling rather than repeated routine CAP courses.

Opportunistic lung infection

PJP, invasive fungi and other immune-dependent pathogens become plausible with HIV, transplantation, neutropenia or immunosuppressive therapy and require different specimens and treatment pathways.

Aspiration pneumonitis

An abrupt inflammatory syndrome after witnessed large-volume aspiration may be chemical rather than established bacterial infection; trajectory and secondary infection determine whether antibiotics are needed.

Septic pulmonary emboli

Multiple peripheral nodules, cavitation, bacteraemia, intravenous access or endocarditis features suggest haematogenous infection and require blood cultures, echocardiographic assessment and source management.

Non-infectious airspace disease

Pulmonary oedema, embolism, malignancy, haemorrhage and organising pneumonia can mimic infection; atypical imaging or treatment failure should trigger targeted reconsideration rather than automatic antibiotic escalation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Sample, isolate and notifySecure actionable evidence without delaying treatmentFirst stepCAP severity, sepsis physiology, host factors or an epidemiological clue makes microbiology or public-health action useful.

1Before antimicrobials when safe, collect only specimens that answer a defined question; record prior exposure, anatomical source, collection time and the clinician who owns each result.
2Institute pathogen-appropriate respiratory precautions immediately when influenza, COVID-19, measles, tuberculosis or another transmissible infection is plausible; do not wait for laboratory confirmation to protect others.
3For suspected Legionnaires’ disease, a linked cluster or another notifiable infection, contact the relevant UK health-protection route promptly and preserve travel, accommodation, workplace and water-exposure details.

02First-line empirical therapyMatch initial spectrum to severity and resistance riskFirst lineDefinitiveA clinical diagnosis of CAP has been established and treatment must begin before definitive microbiology.

1Apply the current NICE adult severity table, using oral treatment first when feasible; clarify the allergy phenotype, pregnancy, renal and hepatic function, interactions and ability to absorb before selecting a regimen.
2Modify the national option only for documented recent antibiotics, previous resistant isolates or colonisation, immunosuppression, a specific exposure, a suspected complication or current local resistance guidance.
3Start promptly within the relevant pneumonia or sepsis timeframe, documenting indication, spectrum rationale, route, specimen status, 24–48-hour review and an expected five-day adult stop point.

0324–48-hour reviewNarrow, stop or switch using results and responsePreliminary microbiology, clinical trajectory and medicine-safety information are available.

1Confirm that bacterial pneumonia remains the best diagnosis, inspect specimen quality and reconcile organism identity with the syndrome rather than treating colonisation or contamination automatically.
2If a reliable susceptibility result supports it, select the narrowest effective agent; stop redundant combination therapy and review allergy, renal function, QT risk, diarrhoea and other toxicity.
3Switch intravenous treatment to oral when improving, haemodynamically stable and able to absorb. Stop after five days in clinically stable adults unless microbiology or a complication supplies a documented longer-course indication.

04Non-response and source controlRebuild the diagnosis before broadeningFever, organ dysfunction, bacteraemia or respiratory illness fails to improve or worsens after initial treatment.

1Reassess dosing, adherence, absorption, renal clearance, prior antibiotics, resistance history and whether the recovered organism is causal; repeat cultures only when they answer a clearance or new-sepsis question.
2Use imaging and pleural assessment to find empyema, abscess, necrosis or obstruction and arrange drainage, surgery or bronchoscopy when control of the focus—not more spectrum—is the missing treatment.
3EscalationExpand testing with infection and respiratory specialists for tuberculosis, PJP, fungi, viral pneumonitis, septic emboli or immune defects, and escalate any cluster or unusual exposure to health protection.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Provides focused beta-lactam treatment for likely pneumococcal and other susceptible typical bacterial infection when low-severity CAP is treated empirically.

Amoxicillin

NICE first-line treatment for low-severity adult CAP is 500 mg orally three times daily for 5 days; higher doses may be selected from the BNF for severe infection.

Verify the reaction rather than recording an imprecise penicillin allergy. Review renal function, pregnancy, rash, diarrhoea and prior resistant isolates; it does not treat atypical organisms.

Offers an oral alternative with atypical-pathogen activity when the documented allergy or clinical context makes amoxicillin unsuitable.

Doxycycline

When amoxicillin is unsuitable in low or moderate severity, NICE lists 200 mg orally on day 1 followed by 100 mg once daily for 4 further days.

Avoid during pregnancy. Prevent oesophageal injury by taking with water while upright, separate it from polyvalent cations and review photosensitivity and important interactions.

Adds or supplies atypical-pathogen coverage when disease severity, penicillin suitability and the national treatment table support its use.

Clarithromycin

NICE lists 500 mg orally twice daily for 5 days as an alternative where appropriate, or as added atypical cover in specified moderate- and high-severity regimens.

Check QT prolongation, electrolyte disturbance, hepatic function and CYP3A4 interactions, including interacting statins. Use a pregnancy-appropriate alternative and renal adjustment where indicated.

This is the national first-line high-severity combination when beta-lactam treatment is suitable; clinical instability also requires respiratory, sepsis and critical-care management.

Co-amoxiclav plus a macrolide

For high-severity adult CAP, NICE lists co-amoxiclav 500/125 mg orally or 1.2 g intravenously three times daily plus clarithromycin 500 mg twice daily for 5 days.

Follow the current local severe-CAP policy, renal and hepatic adjustment and allergy assessment. Review intravenous need and combination spectrum by 48 hours; monitor C. difficile and macrolide toxicity.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Bacteraemia and sepsis

Invasion beyond lung tissue can produce bloodstream infection, shock and metastatic foci; organism identity determines whether clearance cultures and endovascular investigation are required.

Empyema and abscess

Pleural or parenchymal suppuration causes persistent fever and treatment failure because infected material may need image-guided drainage, surgery or a longer organism-directed course.

Antimicrobial toxicity

Allergy, kidney or liver injury, QT prolongation, interactions and C. difficile infection may complicate treatment, particularly when combinations remain broad after microbiology becomes available.

Persistent or recurrent infection

Resistance, inadequate exposure, obstruction, aspiration or an unrecognised immune defect can prevent clearance and should be identified before repeating the same empirical regimen.

Outbreak transmission

A shared environmental or transmissible cause can expose others beyond the patient, making rapid notification, case linkage and infection-control action part of clinical management.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record a named owner and expected reporting time for every culture, antigen or molecular test, including results likely to return after transfer or discharge.
At 24–48 hours review clinical response, specimen quality, organism identity, susceptibilities, allergy history, route, interactions, renal and hepatic function and the planned stop date.
Track antibiotic-associated diarrhoea, rash, cytopenia, kidney or liver injury and QT risk; investigate suspected C. difficile infection rather than merely adding another antimicrobial.
For an organism that can persist in blood, repeat cultures only according to organism- and source-specific clearance guidance and investigate an endovascular or uncontrolled focus when positivity continues.
Confirm that pleural drainage, abscess management, device action or other source control has occurred and is functioning; persistent infection cannot be solved by spectrum alone.
After recovery address influenza, pneumococcal and other indicated vaccination, smoking cessation, aspiration prevention and any newly recognised immune or structural predisposition.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Specimen quality outranks quantity

A well-filled blood-culture set or representative lower-airway specimen can change treatment; multiple contaminated or salivary samples mainly create diagnostic noise.

A virus does not close the case

Influenza and other respiratory viruses may be the primary cause or precede bacterial coinfection, so PCR and the evolving clinical phenotype must be interpreted together.

Colonisation is not causation

Airway organisms, especially in structural lung disease, require correlation with specimen quality, abundance, previous cultures, radiology and response before they justify broader treatment.

Urinary antigen has boundaries

Pneumococcal antigen can support narrowing and Legionella antigen can identify important disease, but persistence and incomplete species or serogroup coverage limit binary interpretation.

Source control can be first-line

When pleural pus, an abscess or obstruction sustains infection, timely drainage or procedural management may matter more than choosing a broader antibiotic.

11Common pitfallsFrequent interpretation and management errors.

01
Sending blood cultures and sputum routinely for every uncomplicated low-severity outpatient.
02
Delaying life-saving treatment while pursuing an ideal specimen in an unstable patient.
03
Equating a positive airway result with invasive disease without assessing sample quality and colonisation.
04
Stopping antibacterial therapy solely because a respiratory virus is detected despite evidence of coinfection.
05
Continuing broad intravenous combination treatment without a documented 24–48-hour review and oral-switch decision.
06
Responding to deterioration only by adding antibiotics while missing empyema, abscess, obstruction or another diagnosis.
07
Allowing an important culture or public-health result to return without a named clinician responsible for action.