Speaker's Highlight

• Don Sin University of British Columbia, St. Paul Hospital (Canada)
  Kenneth R. Chapman Toronto General Hospital Research Institute (Canada)
• Parameswaran Nair McMaster University (Canada)
  Carolyn Calfee UCSF (U.S.A.)
• Gregory P. Downey University of Colorado School of Medicine (U.S.A.)
  David A. Schwartz University of Colorado School of Medicine (U.S.A.)
• Neil Schluger Tuberculosis Control Branch, California Department of Public Health (U.S.A.)
  Nick Kim Critical Care & Sleep Medicine, University of California San Diego (U.S.A.)
• Nicola Hananiah Baylor College of Medicine (U.S.A.)
  Jae-Joon Yim Seoul National University College of Medicine (Republic of Korea)
• Koichiro Asano Tokai University School of Medicine (Japan)
  Diahn-Warng Perng Taipei Veterans General Hospital (Taiwan)
• Konstantinos Kostikas University of Ioannina (Greece)
  Karin Klooster University Medical Center Groningen (Kingdom of the Netherlands)

• Non-cystic fibrosis bronchiectasis: microbiome and clinical phenotypes

  Non-cystic fibrosis bronchiectasis is a chronic lung disorder in which damaged airways widen, leaving people with persistent cough, sputum production, airflow obstruction and recurrent exacerbations. Daily symptom burden is variable, and infection may drive both the structural damage and the decline in lung function.

  The airway microbiome is the community of bacteria, fungi and viruses present in the lungs. Culture remains essential, but it detects only viable organisms that grow in the laboratory; sequencing can reveal a broader community whose relevance must be interpreted alongside symptoms, exacerbations and immune markers.

  Clinical phenotypes describe recurring patterns within that complexity. They can be based on cause, airway infection, inflammation, mucus plugging, structural change or exacerbation frequency. These patterns overlap and may change over time, so a phenotype is a management aid rather than a fixed diagnosis.

  For clinicians attending APSR 2022, in connection with APSR and KATRD, this lens connects laboratory microbiology with the realities of long-term respiratory care. Australian conditions, including bushfire smoke, humid summers, regional access gaps and a mixed public-private health system, shape how bronchiectasis is diagnosed and treated.

  Why airway microbes matter

  Microbes and airway damage reinforce one another. Neutrophil inflammation can damage airway walls, while impaired clearance allows organisms such as Pseudomonas aeruginosa, Haemophilus influenzae and Staphylococcus aureus to persist. Chronic infection and inflammation can then produce bronchiectasis and further compromised mucociliary clearance.

  Sputum culture can guide antibiotic selection, yet a negative sample does not mean the airway is sterile. Low biomass, recent antibiotics, sampling technique and laboratory culture conditions all affect detection. Fungal findings and non-tuberculous mycobacteria require careful interpretation because environmental contamination and airway colonisation are both possible.

  Recognising clinical phenotypes

  Phenotype assessment begins with cause, because bronchiectasis associated with cystic fibrosis, allergic bronchopulmonary aspergillosis, ANCA-associated vasculitis, primary ciliary dyskinesia or immunodeficiency may require additional treatment. Alongside cause, clinicians can identify dominant airway and disease patterns.

  Clinical pattern	Typical clues	Microbial signal	Management emphasis
  Infection-led	Frequent sputum and culture-confirmed bacteria	P. aeruginosa, H. influenzae or S. aureus	Targeted treatment and exacerbation prevention
  Inflammatory or allergic	Eosinophilia, elevated immunoglobulin E and asthma	Aspergillus sensitisation may occur	Treat the underlying inflammation and allergy
  Mucus plugging and remodelling	Persistent obstruction and plugged bronchi on CT	Mixed or low-biomass flora	Airway clearance and mucus-directed treatment
  Mycobacterial	Nodular or branching CT changes with repeated positive cultures	Non-tuberculous mycobacteria	Confirm disease and assess species, disease extent and host factors

  These patterns are not mutually exclusive. A patient may have Pseudomonas colonisation, mucus plugging and frequent exacerbations simultaneously, while immune and structural features may predict relapse and treatment response more reliably than any single microbial result.

  The Australian respiratory environment

  Australian environmental exposures are clinically important. Bushfire smoke episodes affect Sydney, Melbourne and Canberra, while dust, pollen and winter inversions add airway irritation elsewhere. Checking air-quality forecasts and adjusting outdoor exercise can help patients reduce exposure during poor conditions.

  Climatic differences also influence symptoms. Brisbane’s humid summers, Darwin’s tropical conditions and Perth’s dry, pollen-rich environment can change airway symptoms and the organisms recovered from sputum. Air-conditioning may reduce heat exposure but alter indoor humidity, while swimming, hydrotherapy and morning exercise can either aggravate symptoms or support airway clearance.

  Aboriginal and Torres Strait Islander communities experience a disproportionate respiratory burden, shaped by factors including crowded housing, tobacco smoke and delayed access to preventive care. Services are concentrated in metropolitan centres, leaving some regional and remote patients with lengthy waits. Hub-and-spoke care, telehealth and couriered sputum samples can reduce this geographic distance.

  From evidence to everyday care

  Bronchiectasis is confirmed with high-resolution computed tomography and assessed for an underlying cause. Depending on the clinical picture, investigations may include sweat chloride and CFTR testing, immunoglobulin measurement, allergy assessment, ANCA testing or evaluation of ciliary function. Bronchoscopy with lavage remains useful when sputum is unavailable or the cause of obstruction remains uncertain.

  Long-term care combines airway clearance, exercise, smoking cessation, vaccination and prompt treatment of exacerbations. Physiotherapy should be individualised, particularly when bronchiectasis coexists with chronic rhinosinusitis or gastrointestinal disease. Occupational dust, smoke and viral infections should also be addressed, while regular review tracks symptoms, exacerbations, lung function and microbiological changes.

  Antibiotic treatment should be organism-aware and stewardship-led. Long-term inhaled antibiotics may suit selected patients with chronic Pseudomonas, while specialist-directed macrolide therapy can reduce some recurrent exacerbations; both require screening for adverse effects. The Therapeutic Goods Administration regulates medicines under the Therapeutic Goods Act 1989, and the Pharmaceutical Benefits Scheme operates under the National Health Act 1926. Non-PBS products, repeated cultures and some investigations may still create out-of-pocket costs, with private health insurance affecting access for some families.

  A phenotype-guided model for practice

  A phenotype-guided model can be built around four recurring questions: Is a treatable cause present? Which airway pattern dominates? What is driving exacerbations? Can the person clear secretions and access treatment reliably? Each answer should prompt a specific plan, ranging from cystic fibrosis testing and immunoglobulin investigation to airway clearance, inhaled treatment and exacerbation prevention.

  Longitudinal records should connect symptoms, cultures, imaging, medication and admission history. Sequencing and richer microbiome analyses may help selected patients and research programmes, but they should not replace culture or override established clinical evidence. Consent, data governance and careful interpretation remain essential when complex biological data are added to care pathways.

  The practical takeaway is to interpret every sputum result beside symptoms, exacerbation history, imaging and host factors, then target treatment to the dominant treatable pattern rather than to the detected organism alone.

  Richard Russell Nuffield Department of Clinical Medicine, University of Oxford (United Kingdom)
• Mona Bafadhel King’s College London (United Kingdom)
  David Jackson Guy’s and St Thomas’ Hospital, King’s College London (United Kingdom)
• James Chalmers University of Dundee (United Kingdom)
  David Price University of Aberdeen (United Kingdom)