💡 Note: Treat with systemic steroids + antifungal therapy (e.g., Itraconazole).
🔬 Monitor progress with **serial total serum IgE** levels.
📖 About
- Allergic Bronchopulmonary Aspergillosis (ABPA) is a hypersensitivity reaction to the fungus Aspergillus fumigatus.
- 🚫 It is not an invasive infection — rather, it’s an exaggerated allergic immune response.
- 🧪 The immune mechanism involves:
- Type I (IgE-mediated immediate hypersensitivity)
- Type III (immune complex–mediated inflammation)
🧬 Aetiology & Pathophysiology
- Aspergillus spores are widespread in the environment (soil, compost, decaying vegetation).
- 🌬️ About 10% of asthmatics (especially steroid-dependent) may develop ABPA.
- Immune cascade:
- CD4+ Th2 cells release IL-4/IL-5 → ⬆ IgE + eosinophilia 🧾
- IL-8 recruits neutrophils → airway inflammation + tissue injury
- Patients with cystic fibrosis (CF) are particularly prone due to mucus stasis and chronic colonisation.
🩺 Clinical Features
- Asthma-like symptoms: wheeze, breathlessness, chronic cough 😮💨
- Systemic: malaise, fever during exacerbations 🌡️
- Recurrent exacerbations with **thick mucus plugging** (sometimes expectorated).
- ⚠️ Poor asthma control → frequent steroid dependency.
🔍 Investigations
- Bloods:
- ⬆ Total serum IgE (often >1000 IU/mL)
- ⬆ Eosinophils
- Specific IgE to A. fumigatus
- Sputum: May show Aspergillus hyphae.
- Skin-prick test: Positive to A. fumigatus.
- CXR/HRCT: Transient opacities, central bronchiectasis, upper-lobe fibrosis, mucus impaction (“finger-in-glove” sign 🖐️).
💊 Management
- Asthma optimisation: Continue bronchodilators + inhaled corticosteroids.
- Systemic steroids: Prednisolone 40–50 mg/day tapered over weeks → improves symptoms + lung function.
- Mucus clearance: Steroid therapy often leads to expectoration. Bronchoscopy may occasionally be required.
- Antifungal therapy: Itraconazole (200 mg BD) may reduce fungal burden + steroid dependence.
- Monitoring: Regular serum IgE tracking – rising levels suggest relapse 🔄.
⚠️ Teaching Pearls / Pitfalls
- Distinguish ABPA from invasive aspergillosis (ABPA is immune-mediated, not infective).
- Bronchiectasis is usually **central** rather than peripheral in ABPA – a key imaging clue 🔎.
- Relapses are common → requires long-term follow-up with both respiratory + immunology input.
📚 References
3 Clinical Cases — Allergic Bronchopulmonary Aspergillosis (ABPA) 🍄🫁
- Case 1 — Asthmatic with recurrent flares 🫁: A 29-year-old woman with long-standing asthma presents with worsening wheeze, cough productive of brown mucus plugs, and fleeting pulmonary infiltrates on CXR. Bloods: eosinophilia, total IgE markedly raised. Teaching: ABPA occurs in asthmatics sensitised to Aspergillus. Clues = poorly controlled asthma, mucus plugs, transient CXR changes. Treatment = oral corticosteroids ± antifungals (itraconazole).
- Case 2 — Cystic Fibrosis patient 💨: A 23-year-old man with CF has recurrent chest infections, increased sputum volume, and declining lung function despite standard CF therapy. HRCT: central bronchiectasis. Bloods: raised IgE, Aspergillus-specific IgE positive. Teaching: ABPA is a recognised complication of CF, worsening bronchiectasis and lung decline. Early recognition is vital. Management = steroids and antifungal therapy, alongside CF airway clearance.
- Case 3 — Recurrent “pneumonia” misdiagnosis 🦠: A 41-year-old man presents with multiple admissions for “atypical pneumonia” with migratory opacities. He has poorly controlled asthma. CXR: patchy upper-lobe infiltrates that resolve then reappear elsewhere. Serum precipitins to Aspergillus positive. Teaching: ABPA often masquerades as recurrent pneumonia but imaging shows migratory infiltrates. Key differentiators: asthma background, eosinophilia, IgE rise, and positive Aspergillus testing.