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)

• Novel Diagnostic Criteria Reshape Hypersensitivity Pneumonitis Care

  Hypersensitivity pneumonitis sits at a tricky crossroads in interstitial lung disease. For decades, clinicians across Australia and the wider Asia-Pacific have wrestled with overlapping clinical pictures that look like infection, sarcoidosis, or idiopathic pulmonary fibrosis. The arrival of more structured diagnostic criteria has started to clear some of that fog, offering a way to recognise the condition earlier and treat it before fibrosis becomes entrenched.

  The latest update to the diagnostic framework moves away from the old acute-versus-chronic split. Instead, it leans on exposure history, imaging patterns, and, where available, bronchoalveolar lavage findings. Australian clinicians working in regional centres, where detailed occupational histories can be hard to pin down, have welcomed the move toward more practical, pattern-based reasoning.

  What Changed in the Diagnostic Approach

  Earlier schemes tried to force hypersensitivity pneumonitis into neat buckets: acute, subacute, or chronic. Real patients rarely fit those labels cleanly. The new criteria emphasise a continuous spectrum, recognising that inflammatory and fibrotic features often coexist in the same person. For Australian clinicians whose caseloads stretch from tropical Queensland to cool Tasmania, that flexibility matters.

  Exposure identification remains the cornerstone, but it has been refined. Mould-contaminated homes after summer storms, evaporative air-conditioner units common in suburban Perth, and avid bird-keeping — a fair dinkum Australian pastime — all feature as triggers. The criteria now prompt clinicians to ask about dampness, hobbies, and workplace irritants in a structured way rather than leaving it to memory.

  Imaging and Bronchoalveolar Lavage Patterns

  High-resolution CT remains the workhorse. The updated framework describes three main patterns that help separate hypersensitivity pneumonitis from look-alike conditions.

  • Typical: ground-glass opacities with mosaic attenuation and often air-trapping on expiratory imaging
  • Compatible: many features present but missing one defining component
  • Indeterminate: findings that could sit comfortably in another interstitial lung disease

  Bronchoalveolar lavage helps when imaging is ambiguous. A lymphocytosis above the diagnostic threshold supports hypersensitivity pneumonitis in the right clinical context, although it is not specific. Lung biopsy retains a place for indeterminate cases, with histology showing cellular interstitial pneumonitis, poorly formed granulomas, and airway-centred fibrosis when chronic disease has set in. Multidisciplinary discussion — the backbone of interstitial lung disease review meetings in hospitals like Royal Adelaide or Royal Brisbane and Women's — ties all of this together.

  Distinguishing From Mimics

  Separating hypersensitivity pneumonitis from sarcoidosis, idiopathic pulmonary fibrosis, and connective tissue disease-related interstitial lung disease has always been a hair-splitting exercise. The new criteria lean on antigen exposure assessment as the tiebreaker. Where exposure history is convincing and imaging fits, other labels are deprioritised.

  Smoking-related interstitial lung disease, drug-induced fibrosis, and pneumoconioses from mining exposure — relevant to workers in the Hunter Valley and Pilbara — round out the usual differential. A structured checklist helps clinicians settle on the diagnosis without overshooting toward invasive testing when a careful history would have done the job.

  Clinical Implications for Australian Practice

  For respiratory physicians and generalists across Australia, earlier recognition translates into practical action. Removing the offending antigen — whether that's a budgerigar in the spare room or mould in the ducted system — can halt or slow disease progression. Combined with judicious immunosuppression for inflammatory phases, outcomes improve.

  Patients who present after bushfire smoke exposure or in dusty agricultural regions — common across the wheat belt of Western Australia and the Murray–Darling basin — are now triaged through a more deliberate diagnostic pathway. Rural clinicians who manage initial workups can use the criteria to decide who warrants referral to a tertiary interstitial lung disease clinic rather than waiting for disease to declare itself.

  A few practical steps sit at the core of day-to-day management.

  • Confirm a credible exposure history before accepting the diagnosis, including home, hobby, and workplace triggers
  • Combine HRCT pattern recognition with BAL lymphocytosis where imaging is indeterminate
  • Refer borderline or progressive cases to a multidisciplinary interstitial lung disease meeting
  • Revisit the diagnosis if the patient fails to improve after antigen avoidance and treatment

  What's Worth Watching at Upcoming Meetings

  Recent advances beyond hypersensitivity pneumonitis are also drawing attention at major respiratory congresses, including sessions such as ventilation strategies for ARDS, which explore how evolving evidence reshapes bedside care for acute lung injury. The crossover between interstitial lung disease research and acute respiratory management is tightening, and Australian delegates benefit from hearing about both ends of the spectrum at once.

  TSANZ-endorsed workshops are also embedding the new criteria into continuing education modules, so specialists and trainees gain hands-on familiarity before they sit down with their next complex case. The Lung Foundation Australia has begun circulating patient-friendly summaries that explain exposure assessment and treatment timelines in plain language — a move that has reduced phone calls from anxious patients in the initial workup phase.

  The updated criteria do not promise certainty in every patient. They sharpen the lens. For Australian teams used to managing interstitial lung disease in older, often retired patients — many of whom keep birds, garden extensively, or live in homes with ageing ducted cooling — applying the framework consistently turns up cases that were previously labelled as idiopathic.

  Used well, the new approach shortens time to diagnosis, reduces unnecessary biopsies, and clarifies when immunosuppression is appropriate. Embedding multidisciplinary review into routine workflow, and reaching for patient resources from established Australian bodies, makes the framework stick at the coalface of care across private rooms and public outpatient lists alike.

  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)