Pseudomonas aeruginosa

The organism

Pseudomonas aeruginosa is a Gram-negative bacterium that lives in soil, water and damp surfaces. It is an opportunist: it rarely troubles a healthy airway, but it establishes readily in one that is already damaged, and it is remarkably difficult to remove once it has.¹

Three features explain almost everything that follows clinically:

• Biofilm. The organism grows as a community embedded in a self-produced matrix rather than as free-floating cells. Biofilm-dwelling bacteria tolerate antibiotic concentrations orders of magnitude above those that eradicate the same organism in a laboratory broth — which is why a sputum sensitivity report and the clinical response can disagree.
• Mucoid conversion. Over months to years, chronic isolates commonly switch to an alginate-overproducing mucoid phenotype. Mucoid growth on a culture plate is a marker that infection is established rather than recent.
• Intrinsic resistance. A low-permeability outer membrane, multiple efflux pumps and an inducible AmpC β-lactamase mean the organism starts resistant to many agents before any acquired resistance appears.

Where it matters

This is not a cystic fibrosis problem alone, and framing it that way causes it to be missed in the much larger group of people with bronchiectasis.

Bronchiectasis

P. aeruginosa is one of the defining pathogens of bronchiectasis, and its presence is one of the strongest single predictors of a poor course. It is a component of the Bronchiectasis Severity Index, which is built from age, BMI, FEV₁, hospital admissions, exacerbation frequency, breathlessness, radiological extent and colonisation status.²

Cystic fibrosis

Historically the dominant pathogen of adult CF, and the organism around which CF antibiotic and segregation practice was built.³ Its epidemiology is now shifting: highly effective CFTR modulator therapy has changed sputum production, exacerbation frequency and the ease of obtaining samples at all.⁴

COPD and other structural lung disease

Increasingly recognised in severe COPD, particularly in frequent exacerbators, those with coexisting bronchiectasis, and after repeated antibiotic and corticosteroid exposure. It is also a leading cause of ventilator-associated pneumonia.

New isolation, intermittent, or chronic?

The distinction drives the treatment decision, and it is a microbiological one rather than a clinical impression. The Leeds criteria, developed in CF and widely applied, classify a patient over the preceding 12 months on at least four samples:

The 2025 European Respiratory Society guideline defines a new isolation pragmatically as either the first time the organism has been grown, or a further isolation after a prolonged period during which it was not detected.⁵

Eradication of a new isolation

The 2025 ERS guideline suggests offering eradication treatment to patients with a new isolation of P. aeruginosa — a conditional recommendation on very low certainty evidence.⁵ That grading is worth stating plainly rather than rounding up: the rationale is strong, the trial evidence is thin.

The guideline is explicit that eradication practice varies among panel members and internationally, and it describes two broad approaches rather than prescribing one:

• A course of systemic antibiotics — commonly two weeks — followed by a repeat sputum culture, stopping if the sample is negative.
• The same, with an inhaled antibiotic added for four weeks to three months, without rechecking cultures in between.

A systematic review and meta-analysis of eradication in adults with bronchiectasis found that eradication is achievable in a substantial proportion of patients, while noting the small number and modest quality of the underlying studies.⁶ The ERASE trial programme is testing inhaled tobramycin for this indication directly.⁷

Managing chronic infection

Once infection is chronic, the goal changes from clearance to reducing bacterial load, exacerbation frequency and symptom burden. The 2025 ERS guideline makes two strong recommendations relevant here, and two recommendations against:⁵

“High risk of exacerbations” is usually taken to mean two or more exacerbations a year, exacerbations severe enough to require hospital treatment, or a high daily symptom burden.

Response to inhaled antibiotics is not uniform. Analysis of the ORBIT 3 and ORBIT 4 trials identified endotypes of P. aeruginosa infection associated with differing response to inhaled antibiotic therapy — an early signal that this will eventually be a stratified rather than a blanket treatment.⁸ Macrolide response is similarly patterned by symptoms and exacerbation risk rather than uniform.⁹

Before starting any inhaled antibiotic, a supervised test dose is standard practice because of the risk of bronchospasm.⁵

Treating an exacerbation

Send sputum before starting antibiotics wherever possible, and let previous culture and sensitivity results guide the empirical choice.¹⁰ A 14-day course has been the convention for Pseudomonas exacerbations; the 2026 CHEST guideline for non-CF bronchiectasis found no clear superiority of longer over shorter courses across the available studies and suggests duration be guided by clinical response rather than a fixed number.¹⁰ Route follows severity, oral tolerance and previous response.

Cross-infection and segregation

Molecular typing in the 1990s and 2000s showed that some P. aeruginosa strains spread between people with CF — the Liverpool and Manchester epidemic strains being the best characterised. That finding is what produced modern CF segregation: cohort separation, single rooms, no shared waiting areas, and strict equipment decontamination.^3,11

What has changed since the older guidance

Much of the segregation and infection-control architecture in current use descends from the UK CF Trust's 2004 Pseudomonas aeruginosa infection-control document, and that document remains the clearest statement of why segregation exists.¹¹ Four points have moved since:

• The consolidated infection-control standard is now the 2013 CF Foundation guideline, which superseded the earlier organism-by-organism documents.³
• Eradication moved from an idea to a recommendation, and then to a graded conditional recommendation with its uncertainty stated.^5,6
• Bronchiectasis acquired its own evidence base, rather than borrowing from CF — ERS in 2017 and 2025, BTS in 2019, CHEST in 2026.^2,5,10
• CFTR modulators changed CF epidemiology after all the older documents were written, reducing exacerbations and altering the sputum on which all of this surveillance depends.⁴

Role of the physiotherapist

• Order of treatment matters. Bronchodilator, then airway clearance, then the nebulised antibiotic — clearing secretions first improves deposition of the drug where it is needed.
• Daily airway clearance is the intervention that addresses the biofilm's habitat. Antibiotics act on the organism; clearance reduces the retained secretion in which it lives.
• Watch for the bronchospasm that follows a first inhaled antibiotic dose, and make sure the supervised test dose actually happened.
• Device hygiene is a clinical intervention, not housekeeping. Nebulisers, PEP and oscillating PEP devices are all documented reservoirs.
• A change in sputum volume, colour or viscosity is often the earliest sign of a new isolate or an exacerbation. Teach patients to notice and report it, and send a sample.
• Exercise and pulmonary rehabilitation carry a strong recommendation in their own right, and both are unaffected by colonisation status.⁵

References & evidence base

1. LiPuma JJ. The changing microbial epidemiology in cystic fibrosis. Clin Microbiol Rev 2010;23(2):299–323.
2. Chalmers JD, Goeminne P, Aliberti S, et al. The bronchiectasis severity index: an international derivation and validation study. Am J Respir Crit Care Med 2014;189(5):576–585.
3. Saiman L, Siegel JD, LiPuma JJ, et al. Infection prevention and control guideline for cystic fibrosis: 2013 update. Infect Control Hosp Epidemiol 2014;35(S1):S1–S67.
4. Middleton PG, Mall MA, Dřevínek P, et al. Elexacaftor–tezacaftor–ivacaftor for cystic fibrosis with a single Phe508del allele. N Engl J Med 2019;381(19):1809–1819.
5. Chalmers JD, Haworth CS, Flume P, et al. European Respiratory Society clinical practice guideline for the management of adult bronchiectasis. Eur Respir J 2025;66:2501126.
6. Conceição M, Shteinberg M, Goeminne PC, et al. Eradication treatment for Pseudomonas aeruginosa infection in adults with bronchiectasis: a systematic review and meta-analysis. Eur Respir Rev 2024;33.
7. A phase 4 multicentre, 2×2 factorial randomised, double-blind, placebo-controlled trial of tobramycin inhalation solution for Pseudomonas aeruginosa eradication in bronchiectasis: ERASE. ERJ Open Res 2024;10(1):00938-2023.
8. Hull RC, Stobo J, Abo-Leyah H, et al. Endotypes of Pseudomonas aeruginosa infection in bronchiectasis are associated with inhaled antibiotic response: results from ORBIT 3 and ORBIT 4. Am J Respir Crit Care Med 2025;211:1397–1408.
9. Sibila O, Stobo J, Perea L, et al. Symptoms, risk of future exacerbations, and response to long-term macrolide treatment in bronchiectasis: an observational study. Lancet Respir Med 2025;13:911–920.
10. Management of adults with non-cystic fibrosis bronchiectasis: CHEST clinical practice guideline. Chest 2026.
11. UK Cystic Fibrosis Trust Infection Control Group. Pseudomonas aeruginosa infection in people with cystic fibrosis: suggestions for prevention and infection control. 2nd ed. Bromley: Cystic Fibrosis Trust; November 2004.

References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.