Allergic Bronchopulmonary Aspergillosis.Care & specialists in United States

Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease caused by an allergic reaction to Aspergillus fumigatus colonizing the airways of patients with asthma or cystic fibrosis. Symptoms include worsening asthma, mucus plug expectoration, fever, and migratory pulmonary infiltrates.

ABPA affects approximately 2.5% of adults with asthma and 7-9% of patients with cystic fibrosis. Risk is highest in atopic patients with poorly controlled asthma, those with severe asthma, and patients with environmental exposure to Aspergillus spores.

Symptoms include worsening asthma despite inhaled steroids, expectoration of brownish mucus plugs, low-grade fever, haemoptysis, productive cough, and recurrent migratory pulmonary infiltrates on chest imaging. Many patients have years of difficult-to-control asthma before diagnosis.

Diagnosis combines asthma or cystic fibrosis as a host condition, elevated Aspergillus-specific IgE, total serum IgE above 500 IU/mL, plus at least two of positive Aspergillus precipitins, eosinophilia above 500 cells/µL, and CT findings of central bronchiectasis or mucus impaction.

Characteristic CT findings include central bronchiectasis with peripheral sparing, mucus impaction (the finger-in-glove sign), high-attenuation mucus plugs, tree-in-bud opacities, and migratory peripheral consolidation. High-attenuation mucus is highly specific for ABPA.

First-line treatment is oral prednisolone 0.5-0.75 mg/kg/day for 2-4 weeks tapered over 3-6 months, with itraconazole 200 mg twice daily for 16 weeks as steroid-sparing antifungal therapy. Biologics targeting IgE, IL-5, or IL-4/IL-13 are used in steroid-dependent disease.

ABPA is a chronic relapsing condition rather than a curable infection. Most patients achieve remission with treatment, but 30-50% relapse within 5 years. Long-term outcomes depend on early diagnosis, adherence, and lifestyle changes including mould exposure reduction.

No. ABPA is an allergic response to inhaled Aspergillus spores and is not transmitted from person to person. Aspergillus spores are common in the environment, but only susceptible individuals (with asthma or cystic fibrosis) develop the disease.

Total serum IgE is markedly elevated in ABPA, typically above 500 IU/mL and often above 1,000 IU/mL. It is the single best biomarker for diagnosis and monitoring; a 25-50% fall during treatment indicates remission and a 50% rise from baseline often signals relapse.

Antifungals alone are usually insufficient as first-line therapy; oral corticosteroids are the cornerstone for controlling eosinophilic inflammation. Itraconazole or voriconazole is added to reduce exacerbations and lower the steroid dose, especially in patients with frequent relapse.

Yes. Omalizumab (anti-IgE), mepolizumab and benralizumab (anti-IL-5), and dupilumab (anti-IL-4Rα) are increasingly used in steroid-dependent ABPA. Observational evidence shows reduced exacerbations, steroid sparing, and improved lung function. Randomized trials are ongoing.

Long-standing or recurrent ABPA can cause permanent bronchiectasis and, in advanced cases, pulmonary fibrosis. Early diagnosis and adequate treatment slow or prevent structural progression. Patients with high-attenuation mucus or established bronchiectasis at diagnosis have worse long-term outcomes.

Most patients with treated ABPA have near-normal life expectancy. Those with end-stage fibrosis, respiratory failure, or major haemoptysis have higher mortality. Coexisting cystic fibrosis is the main determinant of overall survival in CF patients with ABPA.

A typical course is 3-6 months of prednisolone with progressive tapering. Patients with relapse or steroid dependence may need longer or alternative agents (itraconazole, biologics) to limit cumulative steroid toxicity.

Risk reduction includes optimal asthma or cystic fibrosis control, indoor humidity below 50%, mould remediation in damp homes, HEPA filtration, avoidance of compost and mouldy hay, and respiratory protection in occupational exposure. Annual screening with total IgE in severe asthma helps early diagnosis.

Yes. ABPA can present in adolescents and young adults, especially those with cystic fibrosis. Symptoms include difficult-to-treat asthma, mucus plug expectoration, and recurrent infiltrates. Diagnostic criteria and treatment are similar to adults.

ABPA is an allergic disease driven by hypersensitivity to Aspergillus in the airways of asthma or CF patients. Aspergilloma is a fungal ball that grows in pre-existing lung cavities (e.g., post-TB), causing haemoptysis. Both involve Aspergillus but are pathologically and clinically distinct.

Yes. Regular moderate exercise (walking, swimming, cycling) is encouraged. Pulmonary rehabilitation is beneficial for patients with established bronchiectasis. Avoid mouldy environments and untreated freshwater. Pace activity during exacerbations and resume gradually after recovery.

A Mediterranean-style diet supports overall health; calcium, vitamin D, and protein are important during long-term steroid therapy. Avoid grapefruit juice on itraconazole or voriconazole. Limit alcohol because of antifungal hepatotoxicity risk.

Patients are followed every 6-12 weeks during active treatment with total IgE, lung function, and symptom review. Once in remission, monitoring extends to 3-6 monthly. Total IgE rising more than 50% above baseline often signals relapse.

Routine screening of family members is not recommended unless they have asthma, cystic fibrosis, or recurrent unexplained respiratory disease. Genetic predisposition is modest; environmental exposure is a major contributor.