Introduction And Predisposing Factors

  • Complex pulmonary hypersensitivity reaction involving Type I, Type III, and Type IV responses.
  • Triggered by airway colonization by fungus Aspergillus fumigatus.
  • Represents allergic response, not invasive infection.
  • Predisposing conditions include Cystic Fibrosis (prevalence up to 15%) and Asthma (prevalence 1-2%).
  • Rarely occurs in Cystic Fibrosis children under 6 years of age.

Pathophysiology

  • Colonization: Aspergillus fumigatus spores inhaled, trapped in viscid mucus of susceptible hosts.
  • Antigen Release: Fungus germinates, releasing proteolytic enzymes and antigens.
  • Immune Response: Intense T-helper 2 response produces Interleukin-4, Interleukin-5, and Interleukin-13.
  • Massive polyclonal and specific Immunoglobulin E synthesis occurs.
  • Eosinophilic infiltration of bronchial wall develops.
  • Tissue Damage: Immune complexes and inflammatory mediators cause mucus hypersecretion, airway damage, and eventually central bronchiectasis.

Clinical Features

  • Poorly controlled asthma or Cystic Fibrosis despite optimal therapy.
  • Recurrent wheezing exacerbations.
  • Cough productive of brownish-black mucus plugs, golden-brown casts, or rust-colored sputum.
  • Occasional hemoptysis resulting from bronchiectasis.
  • Systemic signs include low-grade fever, malaise, weight loss.
  • Physical signs include polyphonic wheeze, crackles, late-stage clubbing.

Diagnostic Criteria (Isham Working Group 2013)

Predisposing Condition

  • Asthma or Cystic Fibrosis.

Mandatory Criteria

  • Requires both:
    • Positive Type I skin test to Aspergillus or elevated specific Immunoglobulin E against Aspergillus fumigatus.
    • Elevated total serum Immunoglobulin E (>1000 International Units/mL).

Supporting Criteria

  • Requires at least two:
    • Precipitating Immunoglobulin G antibodies to Aspergillus fumigatus.
    • Radiographic pulmonary opacities consistent with Allergic Bronchopulmonary Aspergillosis.
    • Total eosinophil count >500 cells/µL.

Radiological Features

Chest Radiograph

  • Finger-in-glove sign indicating mucoid impaction in dilated bronchi.
  • Tram-track lines representing bronchial wall thickening.
  • Fleeting or transient migratory pulmonary infiltrates.

High-Resolution Computed Tomography

  • Gold standard modality.
  • Central bronchiectasis (pathognomonic finding).
  • High attenuation mucus indicating mucus plugs denser than skeletal muscle (predicts clinical relapse).

Patterson Staging

StageNameClinical FeaturesImmunoglobulin E LevelManagement
IAcuteTypical symptoms, infiltratesVery HighCorticosteroids
IIRemissionAsymptomatic, clear radiographDrops 35-50%Observe
IIIExacerbationRecurrence of symptoms/infiltratesDoublesResume Corticosteroids
IVCorticosteroid-DependentAsthma worsens on weaningPersistently HighCorticosteroids + Antifungals
VFibroticIrreversible fibrosis, respiratory failureVariableSupportive Care

Management

Treatment Goals

  • Control inflammation.
  • Reduce fungal burden.
  • Prevent progression to irreversible fibrosis.

Pharmacotherapy

  • Corticosteroids: Mainstay therapy.
    • Oral Prednisolone 0.5-0.75 mg/kg/day for 2-4 weeks during acute phase.
    • Gradual tapering over 3-6 months based on clinical response.
    • Monitor total serum Immunoglobulin E every 6-8 weeks (>35% decline indicates remission).
  • Antifungal Agents: Adjunct, steroid-sparing therapy.
    • Itraconazole 5 mg/kg/day (maximum 200 mg twice daily) for 4-6 months.
    • Monitor liver enzymes and drug levels.
    • Alternatives include Voriconazole or Posaconazole.
  • Biologics:
    • Omalizumab (Anti-Immunoglobulin E) for refractory Stage IV disease.
    • Mepolizumab (Anti-Interleukin-5) investigational use.

Complications And Prognosis

  • Good prognosis if treated in Stage I or II.
  • Permanent central bronchiectasis.
  • Pulmonary fibrosis and cor pulmonale in Stage V.
  • Side effects of long-term corticosteroids including Cushingoid features and growth failure.