With estimated prevalence of 1–2% in asthma clinics and up to 10% in severe asthma services.

Allergic Bronchopulmonary Aspergillosis (ABPA) is a chronic immune reaction to Aspergillus that affects people with asthma or cystic fibrosis. It causes airway inflammation, mucus plugging, recurrent exacerbations, and bronchiectasis if untreated.

Despite being treatable, ABPA remains heavily underdiagnosed, even in countries with advanced respiratory services. Many people are told for years that they have “difficult asthma” or “recurrent chest infections,” only for ABPA to be diagnosed much later, often with significant lung damage already present.

The UK National Aspergillosis Centre (NAC) provides specialist expertise, yet only a small proportion of expected ABPA cases reach specialist review.

This article explains why ABPA is missed, which patients are at risk, which specialities need to be more alert, and the red flags that should prompt testing or referral.

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⭐ How Common Is ABPA?

ABPA is more common than most clinicians realise:

Across the UK, this equates to an estimated 15,000–25,000 people living with ABPA — but only a small minority ever receive the correct diagnosis.

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⭐ Why ABPA Is Often Missed

1. ABPA looks like “difficult asthma”

Typical symptoms — wheeze, cough, mucus, breathlessness — mimic:

• severe asthma

• eosinophilic asthma

• uncontrolled asthma despite treatment

Patients may be repeatedly stepped up through inhalers, oral steroids, and biologics before ABPA is even considered.

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2. Exacerbations are mistaken for infections

Many ABPA flare-ups are treated as:

• pneumonia

• viral infection

• “chest infection”

• post-viral asthma worsening

Without fungal-specific thinking, the diagnosis is rarely made.

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3. IgE and eosinophils fluctuate

IgE is a cornerstone of ABPA diagnosis, but:

• systemic steroids suppress IgE

• biologics (benralizumab, mepolizumab, dupilumab) reduce eosinophils

• flare-ups produce temporary spikes

• baseline ranges vary between labs

Clinicians often overlook ABPA in patients on biologics because eosinophils are normal — despite the underlying fungal allergy still being active.

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4. Radiology findings get mislabelled

ABPA causes:

• mucus plugging

• “tram lines” and bronchial thickening

• fleeting infiltrates

• upper lobe bronchiectasis

These are often:

• labelled “infection”

• attributed to asthma airway remodelling

• not compared across time

• missed on CT unless specifically looked for

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5. Inconsistent awareness across specialities

Some clinicians are unfamiliar with:

• ISHAM diagnostic criteria

• interpreting IgE/IgG results

• the relationship between asthma and fungal allergy

• the overlap between ABPA and bronchiectasis

This leads to diagnostic delay or misdiagnosis.

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6. ABPA evolves into chronic disease if untreated

Repeated inflammation → mucus plugging → bronchiectasis → fibrosis.
By the time a diagnosis is made, airway damage can be permanent.

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⭐ Who Is at Highest Risk?

1. Asthma patients with repeated exacerbations

Especially those who:

• fail maximal inhaler therapy

• require multiple steroid courses

• have sudden, dramatic mucus plugging events

• experience episodic “flares” with no clear cause

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2. Severe asthma clinic patients

Prevalence is up to 10%, especially those with:

• high IgE

• eosinophilia

• sensitisation to multiple allergens

• steroid dependence

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3. Bronchiectasis patients

Bronchiectasis often coexists with ABPA and can worsen flares.

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4. Patients with mucus plugging (“finger-in-glove” signs)

These striking CT appearances strongly suggest ABPA but are often misattributed to infection.

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5. People with CF (Cystic Fibrosis)

5–15% develop ABPA at some stage.

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⭐ Which Specialities Need Greater Awareness?

• Severe asthma services & biologics clinics
  (highest yield group for ABPA detection)

• Respiratory medicine
  (diagnosis often falls here but is highly variable)

• General practice
  (sees frequent “exacerbations”)

• Emergency departments & acute medical units
  (manage acute mucus plugging, chest tightness)

• Paediatric respiratory medicine
  (early recognition prevents chronic damage)

• Cystic Fibrosis services

• Radiology
  (fleeting infiltrates and mucus plugging often give the earliest clues)

The National Aspergillosis Centre should be the referral point for complex or uncertain cases.

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⭐ Red Flags Suggesting ABPA

1. Asthma with repeated, unexplained exacerbations

Especially if poorly responsive to normal treatment.

2. High total IgE (>500–1000 IU/mL)

Or rising IgE over time.

3. Eosinophilia (unless suppressed by treatment)

4. Positive Aspergillus sensitisation

(Skin prick test or specific IgE)

5. Bronchiectasis, particularly central or upper lobe

6. Fleeting pulmonary infiltrates

7. Mucus plugging on CT (“finger-in-glove” appearance)

8. ABPA flare triggered by stopping antifungals

9. Asthma + Aspergillus in sputum

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⭐ The Cost of Missed ABPA Diagnosis

Failure to diagnose ABPA leads to:

• progressive airway damage

• permanent bronchiectasis

• steroid dependence

• hospital admissions

• repeated infections

• respiratory failure in advanced stages

• reduced quality of life

• avoidable healthcare expenditure

Delayed diagnosis increases the risk of progression to CPA, a far more serious chronic fungal infection requiring long-term antifungal therapy.

Early recognition, correct treatment, and referral to specialist centres like the National Aspergillosis Centre dramatically improve long-term outcomes.

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⭐ Conclusion

ABPA is not rare — especially within severe asthma clinics, bronchiectasis services, and CF units. Yet it remains significantly underdiagnosed because its symptoms mirror those of common respiratory conditions, and because key investigations like IgE, IgG, and CT interpretation are inconsistently used.

A structured approach — recognising red flags, performing appropriate testing, and referring complex cases to the National Aspergillosis Centre — can reduce the burden of avoidable airway damage and improve the lives of thousands of patients.

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