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)

• Update on Diagnosis and Treatment of Allergic Bronchopulmonary Aspergillosis

  Allergic bronchopulmonary aspergillosis (ABPA) is an immune-mediated reaction to Aspergillus fumigatus, usually affecting people with asthma or cystic fibrosis. The condition can resemble an asthma flare, bacterial pneumonia, fungal infection or unexplained bronchiectasis, so timely recognition depends on combining symptoms, blood tests and chest imaging.

  Current practice places greater emphasis on early diagnosis, objective evidence of fungal sensitisation and prevention of permanent airway damage. For clinicians in Australia, this also means adapting international criteria to local access to respiratory specialists, pathology services, PBS-listed medicines and the needs of patients living far from major centres.

  Recognising the Clinical Pattern

  ABPA should be considered when asthma becomes difficult to control or when recurrent “chest infections” occur alongside fleeting pulmonary infiltrates, brownish sputum plugs, wheeze or worsening breathlessness. Fatigue and productive cough are common, although fever is less typical unless another infection is present. People with cystic fibrosis may have overlapping symptoms, making a change from their usual respiratory pattern particularly important.

  The diagnosis can be missed when symptoms are attributed solely to poor inhaler technique, smoking, viral illness or chronic rhinosinusitis. A careful history should cover exacerbation frequency, corticosteroid exposure, occupational mould, damp housing and previous imaging. Guidance on chronic cough management is also relevant because persistent cough may be the first reason a patient enters a broader respiratory assessment.

  Confirming the Diagnosis

  The central laboratory finding is evidence of sensitisation to A. fumigatus, generally through a positive fungal-specific IgE test or skin-prick testing. Total serum IgE is often markedly raised, and peripheral eosinophilia supports the diagnosis, although eosinophil counts can be suppressed by oral corticosteroids. Aspergillus-specific IgG may strengthen the case, particularly where imaging shows bronchiectasis or mucus plugging.

  Current diagnostic frameworks commonly require a compatible underlying condition, fungal sensitisation, an elevated total IgE level and additional features such as eosinophilia, characteristic imaging or raised fungus-specific IgG. Thresholds and criteria have evolved, and clinicians should use the most current specialist guidance rather than treating any single result as definitive. A high total IgE alone is not specific: it may occur in atopy, parasitic disease and other inflammatory disorders.

  Reading Imaging and Laboratory Results

  High-resolution CT is more informative than a plain chest X-ray when ABPA is suspected. Findings can include central bronchiectasis, bronchial wall thickening, mucus impaction and areas of consolidation. High-attenuation mucus is particularly suggestive, but its absence does not exclude disease. Imaging also helps identify established bronchiectasis and assess complications such as lobar collapse or fibrotic change.

  Sputum culture may detect Aspergillus, but isolation does not by itself distinguish colonisation from ABPA. Conversely, a negative culture cannot rule out an allergic response. Clinicians should consider allergic fungal airway disease, chronic pulmonary aspergillosis, eosinophilic lung disease, tuberculosis, non-tuberculous mycobacterial infection and severe asthma with fungal sensitisation when the clinical picture is incomplete or atypical.

  Choosing Initial Treatment

  For an acute or newly diagnosed flare, systemic corticosteroids remain a standard treatment because they rapidly suppress airway inflammation. The exact dose and duration should be individualised according to disease severity, comorbidities, blood glucose, bone health and relapse risk. A written monitoring plan is important, especially for patients who have received repeated courses of prednisolone.

  An oral triazole, most often itraconazole, may be used as a steroid-sparing option or when disease responds incompletely to corticosteroids. Drug interactions, liver toxicity, absorption and serum concentrations require attention. Acid-suppressing medicines can reduce itraconazole absorption, while interactions with inhaled or systemic corticosteroids may increase adverse effects. Voriconazole or posaconazole may be considered in selected cases under specialist supervision, particularly where intolerance or treatment failure complicates management.

  Asthma therapy should continue in parallel. This includes checking inhaler technique, adherence, trigger exposure and the suitability of inhaled corticosteroid and long-acting bronchodilator therapy. Antifungal treatment is not a substitute for well-managed asthma, and routine antifungal use is not appropriate for every patient with fungal sensitisation.

  Managing Relapse and Resistant Disease

  Relapse may present with renewed wheeze, cough, mucus plugging, falling lung function, new infiltrates or a substantial rise in total IgE from the patient’s post-treatment baseline. Total IgE is useful for monitoring trends, but it should not be interpreted in isolation. Symptoms, eosinophils, spirometry and imaging provide necessary context, particularly when infection or another asthma trigger is also possible.

  Repeated steroid exposure creates risks including osteoporosis, hypertension, diabetes, cataracts and infection. For recurrent or treatment-dependent disease, a respiratory physician may consider biologic therapy such as omalizumab, mepolizumab, benralizumab or dupilumab. Evidence is evolving, and choice depends on asthma phenotype, eosinophil levels, IgE range, previous therapy, comorbid nasal disease and local funding arrangements. Specialist review is essential before changing treatment.

  Practical Points for Australian Care

  In Australia, care may involve a general practitioner, respiratory physician, cystic fibrosis service, pharmacist and radiology team across different locations. A patient in regional Queensland or Western Australia may need coordinated pathology and imaging appointments, while people in Sydney, Melbourne or Brisbane may have easier access to tertiary bronchiectasis clinics. Clear documentation of baseline IgE, lung function and CT findings helps maintain continuity when care is shared.

  Useful assessment points include:

  • Asthma or cystic fibrosis with recurrent exacerbations
  • Total IgE, eosinophils and Aspergillus-specific IgE
  • High-resolution CT findings and prior imaging
  • Medication interactions, steroid toxicity and adherence

  Treatment planning should reflect Australia’s healthcare environment. PBS availability, Therapeutic Goods Administration approvals, private prescribing costs and specialist referral pathways can affect access to azoles and biologic medicines. Remote patients may benefit from telehealth follow-up, local spirometry and pathology collection, provided urgent review is available for hypoxaemia, severe breathlessness or rapidly worsening symptoms.

  Practical treatment safeguards include:

  • Confirming inhaler technique at every major review
  • Checking liver function and interacting medicines with azoles
  • Recording an individual post-treatment IgE baseline
  • Reviewing vaccination, bone protection and metabolic health

  Environmental advice should be realistic rather than alarmist. Dampness and visible mould should be addressed, and smoke exposure reduced during Australian bushfire periods, but patients should not assume that every outdoor fungal exposure causes ABPA. The key principle is to connect compatible symptoms with objective evidence, treat active inflammation promptly and monitor for structural airway disease. ABPA is best remembered as a treatable allergic airway disorder in which accurate diagnosis and careful long-term follow-up protect lung function.

  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)