What is allergic bronchopulmonary aspergillosis?

Allergic bronchopulmonary aspergillosis (ABPA) is a complex condition in which the lungs have an exaggerated immune response to a mould called Aspergillus fumigatus. Aspergillus is widespread in the environment; most people inhale Aspergillus spores frequently without consequence. In susceptible people (most often those with asthma or cystic fibrosis), an exaggerated immune response to Aspergillus in the airways causes recurrent inflammation, mucus impaction, and over time, structural damage to the airways.

Why it is different from typical asthma. Typical asthma is an inflammatory condition of the airways that responds to inhalers and (for severe asthma) to biologics targeting type-2 inflammation. ABPA is also a type-2-driven condition but with the additional feature of allergic response specifically to Aspergillus. Patients with ABPA typically have elevated total IgE, elevated Aspergillus-specific IgE and IgG, eosinophilia, and characteristic CT findings (central bronchiectasis with mucus impaction). The treatment includes asthma-style therapy plus management of the Aspergillus-driven component.

Who gets ABPA. Most patients with ABPA have underlying asthma or cystic fibrosis. ABPA is one of the most common chronic complications of cystic fibrosis. In asthma, ABPA affects roughly 1 to 2 percent of asthmatics overall and a higher percentage of those with severe or difficult-to-control asthma.

The diagnostic pathway. The classic features are recurrent asthma exacerbations, brown sputum plugs (mucus impaction with fungal hyphae), elevated total IgE, elevated Aspergillus-specific IgE and IgG, eosinophilia, and characteristic central bronchiectasis on chest CT. Diagnostic criteria combine these features. Serial IgE monitoring is part of long-term management.

The therapy options.

For acute exacerbation: oral corticosteroids (typically prednisone) over weeks to months, with a tapering schedule.

Antifungal therapy: itraconazole reduces the antigenic load and provides steroid-sparing benefit. Voriconazole and isavuconazole are alternatives for selected patients.

Maintenance therapy: low-dose corticosteroid plus itraconazole has been a traditional approach for recurrent ABPA. The challenge is the long-term side effects of either component.

Biologic therapy: omalizumab (anti-IgE), mepolizumab and benralizumab (anti-IL-5 pathway), and dupilumab (anti-IL-4 and IL-13) are increasingly used in ABPA. They work on the underlying type-2 immune biology and reduce the need for chronic corticosteroid therapy. Patients with cystic fibrosis-associated ABPA particularly benefit.

The diagnostic and monitoring infrastructure. ABPA management benefits from multidisciplinary care: pulmonology working with allergy-immunology, sometimes with infectious diseases for fungal-specific input. Patients with cystic fibrosis benefit from CF specialty centre care that includes ABPA expertise.

What to expect. With modern integrated therapy combining corticosteroid use as needed for exacerbations, antifungal therapy, and biologic therapy as appropriate, most patients with ABPA can achieve substantially better long-term control than the older corticosteroid-and-itraconazole-only approach. The expanded biologic options have made it possible to reduce the chronic corticosteroid burden for many patients, which has implications for long-term bone health, infection risk, and other corticosteroid-related side effects.