Understanding an important Aspergillus-related airway disorder
Demystifying Allergic Bronchopulmonary Aspergillosis
Allergic bronchopulmonary aspergillosis, usually shortened to ABPA, is an exaggerated immune response to Aspergillus within susceptible airways. It most often affects people with asthma or cystic fibrosis and can cause worsening wheeze, thick mucus, recurrent lung abnormalities and bronchiectasis.
- Aspergillus allergy
- Asthma
- Thick mucus plugs
- Total IgE
- Eosinophils
- Chest CT
- Antifungal treatment
- Biological therapies
ABPA is not contagious
ABPA develops because of an individual immune response to environmental Aspergillus. It cannot be passed from one person to another.
Sensitisation alone is not ABPA
A positive Aspergillus allergy test is important, but diagnosis also depends on the clinical context and additional immunological or radiological evidence.
What is allergic bronchopulmonary aspergillosis?
ABPA is an Aspergillus-related hypersensitivity disorder in which immune activity against fungus within the airways causes eosinophilic inflammation, increased mucus production and variable lung abnormalities.
Aspergillus is a group of moulds found widely in soil, compost, decaying vegetation, dust and buildings. Everyone inhales fungal spores, usually without developing disease.
In people with susceptible airways, particularly those with asthma or cystic fibrosis, Aspergillus can persist within airway mucus. The immune system may then produce an exaggerated allergic and inflammatory response.
ABPA is not the same as invasive aspergillosis. In ABPA, the main problem is hypersensitivity and airway inflammation rather than fungus invading healthy lung tissue or spreading through the bloodstream.
Aspergillus remains within airway secretions, while the immune response causes inflammation, eosinophil recruitment, mucus plugging and, in some people, permanent bronchial damage.
What happens inside the lungs?
Fungal sensitisation
The immune system produces IgE antibodies against Aspergillus allergens and reacts when those allergens are encountered.
Eosinophilic inflammation
Eosinophils and other inflammatory cells accumulate within the airways and contribute to swelling and tissue injury.
Thick mucus
Inflamed airways produce tenacious mucus that may be difficult to clear and can form plugs or bronchial casts.
Airway obstruction
Bronchospasm, airway-wall swelling and mucus plugging can reduce airflow and worsen asthma symptoms.
Transient lung opacities
Mucus obstruction and inflammation can cause areas of lung collapse or consolidation that change over time.
Bronchiectasis
Repeated inflammation may permanently widen and damage the airways, impairing mucus clearance further.
Who is more likely to develop ABPA?
ABPA most often develops in people with an underlying condition that allows Aspergillus allergens and mucus to remain within the airways.
Asthma
Asthma is the most common underlying respiratory condition associated with ABPA. Risk appears greater in difficult or poorly controlled asthma.
Cystic fibrosis
Thick airway secretions and impaired mucus clearance create an environment in which Aspergillus exposure and sensitisation can become clinically important.
Bronchiectasis
ABPA can cause bronchiectasis, but it may also occur in someone who already has bronchiectasis from another cause.
Aspergillus sensitisation
Demonstrable sensitisation is central to ABPA, although many sensitised patients never develop the full syndrome.
Type 2 inflammation
Raised eosinophils, high IgE and other allergic conditions may reflect an immune phenotype more prone to ABPA.
Environmental exposure
Damp buildings, compost, decaying vegetation and some occupational settings can increase exposure to airborne mould.
People with asthma can read more about specialist asthma diagnosis and treatment .
Fungal sensitisation without ABPA is discussed separately in the guide to asthma with fungal sensitisation .
Symptoms of ABPA
Symptoms overlap substantially with asthma, bronchiectasis and respiratory infection. ABPA should therefore be considered when asthma unexpectedly deteriorates or when mucus and imaging findings are unusual.
Worsening wheeze
Airway inflammation and bronchospasm can increase wheezing and the need for reliever medication.
Breathlessness
Breathlessness may occur during exertion or at rest and may worsen during an ABPA exacerbation.
Persistent cough
Cough may be dry initially but is often associated with thick or difficult-to-clear sputum.
Mucus plugs
Brown, tan, dark or rubbery plugs may occasionally be coughed up, although their absence does not exclude ABPA.
Fever or malaise
Low-grade fever, fatigue and a general feeling of illness can occur, but infection must also be considered.
Chest discomfort
Chest tightness may reflect asthma, while pleuritic or severe pain requires assessment for other causes.
Recurrent “pneumonia”
Migrating or recurrent chest X-ray abnormalities may sometimes represent mucus plugging or inflammatory ABPA changes.
Coughing up blood
Haemoptysis may occur with inflamed or bronchiectatic airways and should be assessed according to its severity.
Symptoms alone cannot diagnose ABPA
Poor asthma control, bacterial infection, viral infection, bronchiectasis, severe asthma with fungal sensitisation and other Aspergillus-related diseases can produce overlapping symptoms.
ABPA compared with other fungal-related conditions
| Condition | Main process | Typical setting | Key distinction |
|---|---|---|---|
| Fungal sensitisation | IgE response to a fungal allergen | Can occur with mild, moderate or severe asthma | Does not by itself establish active ABPA |
| SAFS | Severe asthma accompanied by fungal sensitisation | Asthma remains severe after treatment optimisation | ABPA criteria are not met |
| ABPA | Allergic and eosinophilic response to Aspergillus in the airways | Usually asthma, cystic fibrosis or bronchiectasis | Requires a compatible combination of immunological, clinical and radiological evidence |
| Airway colonisation | Aspergillus grows in airway secretions without necessarily causing active disease | Bronchiectasis or structurally abnormal airways | A positive sputum culture alone does not prove ABPA |
| Chronic pulmonary aspergillosis | Chronic fungal infection of abnormal lung tissue or cavities | Previous TB, emphysema, cavities or other structural disease | Characterised by chronic infection rather than allergic airway disease |
| Invasive aspergillosis | Fungal invasion into lung tissue and sometimes blood vessels | Usually substantial immune suppression or critical illness | A medical emergency requiring urgent antifungal treatment |
How is ABPA diagnosed?
There is no single definitive test. Diagnosis is based on a compatible respiratory condition, evidence of Aspergillus sensitisation and additional immunological or radiological features.
- Review the underlying respiratory condition Asthma, cystic fibrosis, bronchiectasis and the pattern of exacerbations are assessed.
- Test for Aspergillus sensitisation Aspergillus-specific IgE or a skin-prick test assesses immediate allergic sensitisation.
- Measure total IgE Total serum IgE is usually raised in active ABPA and helps with diagnosis and subsequent monitoring.
- Review blood eosinophils Eosinophilia supports type 2 inflammation but may be suppressed by oral or inhaled corticosteroids.
- Measure Aspergillus IgG where appropriate This can provide additional evidence of immune exposure but must be interpreted in context.
- Perform spirometry Lung-function testing may show variable airflow obstruction and helps quantify physiological impact.
- Review chest imaging Chest X-ray and high-resolution CT may identify mucus plugging, bronchiectasis or transient pulmonary opacities.
- Exclude alternatives Infection, chronic pulmonary aspergillosis, severe asthma, eosinophilic disorders and other causes of bronchiectasis may require consideration.
| Investigation | Possible contribution | Important limitation |
|---|---|---|
| Aspergillus-specific IgE | Demonstrates sensitisation to Aspergillus | Sensitisation alone does not diagnose ABPA |
| Total serum IgE | Supports diagnosis and provides a baseline for monitoring | It is non-specific and may be affected by treatment |
| Blood eosinophils | Supports an eosinophilic inflammatory phenotype | Corticosteroids can substantially lower the count |
| Aspergillus IgG | May support evidence of immune exposure | Can also be raised in other Aspergillus-related conditions |
| Skin-prick test | Identifies immediate hypersensitivity | Antihistamines and variable extracts can affect results |
| Sputum fungal culture | May identify Aspergillus growing in airway secretions | A negative culture does not exclude ABPA, and a positive culture does not confirm it |
| FeNO | May identify type 2 airway inflammation | Does not specifically diagnose ABPA |
| Chest CT | May show bronchiectasis, mucus impaction and characteristic high-attenuation mucus | Normal imaging does not necessarily exclude early or serological ABPA |
The role of airway nitric-oxide testing is explained in the FeNO testing guide .
Spirometry, gas-transfer testing and additional respiratory physiology are described on the lung-function testing page .
Previous treatment can alter the test results
Oral corticosteroids may reduce eosinophils, IgE and radiological inflammation. A specialist may need to review older blood tests, previous imaging and the timing of treatment before interpreting current results.
What can chest imaging show?
Mucus plugging
What it is
Thick allergic mucus may obstruct individual bronchi.
Possible appearance
Branching, tubular or finger-like opacities may appear on imaging.
Clinical effect
Obstruction can cause wheeze, collapse of lung segments and sudden deterioration.
Bronchiectasis
What it is
Permanent abnormal widening and distortion of the bronchi.
ABPA pattern
Proximal or central airways may be prominently involved, although distribution varies.
Long-term effect
Impaired mucus clearance can increase bacterial infection and exacerbation risk.
High-attenuation mucus
What it means
Impacted mucus appears denser than ordinary airway secretions on CT.
Diagnostic value
This is a particularly supportive finding when present.
Limitation
Many people with ABPA do not have this feature.
Read more about chest X-ray and CT imaging .
How is ABPA treated?
Treatment aims to suppress damaging allergic inflammation, reduce the fungal burden within airway mucus, restore asthma control, clear retained secretions and prevent permanent lung damage.
Oral corticosteroids
Prednisolone can reduce eosinophilic inflammation rapidly and may be used for clinically active or acute ABPA.
Triazole antifungals
Itraconazole or another appropriate triazole may reduce airway Aspergillus burden and can be used in selected treatment strategies.
Asthma treatment
Corticosteroid-containing inhalers, bronchodilators and a written asthma action plan remain important.
Airway clearance
Respiratory physiotherapy may help mobilise thick mucus, particularly when bronchiectasis or mucus plugging is present.
Antibiotics
Antibiotics do not treat ABPA itself but may be required for a coexisting bacterial bronchiectasis exacerbation.
Biological treatment
A biologic may be considered in selected recurrent, treatment-dependent or severe-asthma-associated disease.
Exposure reduction
Significant indoor damp, visible mould or intense occupational exposure should be addressed where practicable.
Vaccination and prevention
Influenza, COVID-19 and indicated pneumococcal vaccination may reduce additional respiratory illness.
Treatment depends on disease activity
An isolated positive blood test in a clinically stable person does not automatically require systemic corticosteroids or antifungal treatment. Symptoms, lung function, IgE change and imaging should be considered together.
Oral corticosteroid treatment
Systemic corticosteroids suppress the immune inflammation driving active ABPA. They can improve symptoms, airflow and radiological abnormalities, but the potential benefit must be balanced against toxicity.
Potential benefits
Reduced wheeze, improved breathing, resolution of infiltrates and a fall in total IgE may occur.
Infection risk
Steroids can increase susceptibility to bacterial, viral, fungal and opportunistic infection.
Metabolic effects
Blood glucose, appetite, weight, blood pressure and mood may be affected.
Long-term toxicity
Osteoporosis, cataracts, muscle weakness and adrenal suppression become more important with repeated or prolonged treatment.
Do not stop prolonged corticosteroid treatment suddenly
Longer courses can suppress natural adrenal hormone production. Dose reduction should follow the plan provided by the treating clinician.
Antifungal treatment
Triazole antifungals reduce Aspergillus growth within airway secretions. They may be used when corticosteroids should be avoided, when the response is inadequate, when disease recurs during steroid reduction or as part of an agreed specialist regimen.
| Medicine | Possible role | Important considerations |
|---|---|---|
| Itraconazole | Common oral triazole option in ABPA | Absorption, liver tests, drug levels and numerous medicine interactions require attention |
| Voriconazole | Alternative when itraconazole is unsuitable or ineffective | Visual effects, photosensitivity, liver toxicity, QT effects and interactions may occur |
| Posaconazole | Alternative specialist option in selected cases | Formulation, absorption, liver monitoring, interactions and cost must be considered |
| Isavuconazole | May be considered in selected Aspergillus-related disease | Not a routine first choice for every ABPA patient |
Triazoles can interact with asthma medicines
Triazoles can markedly increase exposure to some inhaled or nasal corticosteroids, increasing the risk of adrenal suppression and Cushing-like effects. Every prescribed, over-the-counter and herbal medicine should be reviewed before treatment.
Monitoring may include:
- baseline and repeat liver-function tests;
- review of medicine interactions;
- pregnancy and contraception advice;
- ECG assessment where clinically relevant;
- antifungal drug-level monitoring;
- review of adherence and absorption;
- assessment for antifungal resistance.
Omalizumab, mepolizumab and other biological therapies
Biological therapies target selected immune pathways involved in allergic or eosinophilic inflammation. Evidence in ABPA is growing, but these treatments are generally reserved for selected patients rather than used routinely at first diagnosis.
Omalizumab
Target
Omalizumab binds free IgE and reduces allergic signalling.
Possible benefit
Observational evidence suggests fewer exacerbations and reduced corticosteroid exposure in selected patients.
Limitation
ABPA can produce very high IgE levels, and eligibility or dosing requires specialist interpretation.
Mepolizumab and benralizumab
Target
These therapies target IL-5 or its receptor and reduce eosinophilic inflammation.
Possible benefit
Case series and observational studies suggest a corticosteroid-sparing effect in some recurrent cases.
Clinical selection
Blood eosinophils, severe-asthma phenotype, treatment history and attack frequency influence selection.
Dupilumab and other options
Target
Dupilumab inhibits IL-4 and IL-13 signalling involved in type 2 inflammation.
Evidence
Evidence is mainly from reports, small series and extrapolation from severe-asthma treatment.
Place in care
Use should follow specialist assessment of ABPA activity, asthma phenotype and previous treatment.
Biological therapies are not antifungals
Biologics modify the immune response. They do not directly kill Aspergillus and do not replace antifungal treatment when reducing fungal burden is an important part of the treatment strategy.
ABPA and bronchiectasis
Bronchiectasis can be both a complication of ABPA and a coexisting condition. Once structural airway damage is established, management needs to address mucus retention and bacterial infection as well as allergic inflammation.
Airway clearance
A respiratory physiotherapist can teach techniques to mobilise thick sputum and reduce mucus retention.
Sputum culture
Bacterial and mycobacterial cultures can guide treatment and help distinguish infection from allergic inflammation.
Exacerbation treatment
A bacterial exacerbation may require antibiotics even when the ABPA itself is being treated successfully.
Haemoptysis assessment
Inflamed bronchiectatic airways may bleed. The volume and clinical stability determine urgency.
Read more about bronchiectasis diagnosis and treatment .
The interaction between ABPA, asthma, bronchiectasis and infection is covered in the article on living with bronchiectasis and co-morbidities .
Monitoring treatment response and recurrence
ABPA can relapse after an initial response. Monitoring therefore considers symptoms, asthma control, serum IgE, eosinophils, lung function and imaging rather than relying on one measurement.
Symptoms
Wheeze, cough, sputum, exercise tolerance and night symptoms are compared with the patient’s baseline.
Total IgE
A fall after treatment helps establish a new baseline. A substantial rise may support recurrence when accompanied by clinical deterioration.
Blood eosinophils
Eosinophils may help assess inflammation but are strongly influenced by corticosteroid treatment.
Lung function
Spirometry can document changes in airflow obstruction and help assess response.
Chest imaging
Chest X-rays often suffice for monitoring changing opacities, while CT is used when additional structural detail is needed.
Treatment toxicity
Steroid effects, antifungal interactions, liver function and biologic response should be reviewed.
Total IgE does not need to become normal
Treatment response is assessed against the patient’s own post-treatment baseline. Persistently raised IgE does not by itself mean that treatment has failed.
Can Aspergillus exposure be reduced?
It is impossible to avoid Aspergillus completely because spores are widespread outdoors and indoors. It is nevertheless reasonable to reduce unusually intense exposure.
Correct damp and leaks
Repair water ingress, leaking pipes and persistent condensation rather than repeatedly cleaning visible mould alone.
Improve ventilation
Use appropriate extraction when cooking or bathing and maintain adequate ventilation without excessive indoor cold.
Compost and decaying leaves
These can release large concentrations of fungal spores when disturbed.
Occupational exposure
Gardening, farming, waste management and work in water-damaged buildings may require individual risk assessment.
Environmental control does not replace medical treatment
Avoidance measures may reduce exposure but cannot reliably suppress active ABPA without appropriate investigation and treatment.
Living with ABPA
- Know your usual symptoms Recognising a meaningful change in cough, sputum, wheeze or exercise tolerance can support earlier assessment.
- Follow the asthma action plan Continue prescribed inhalers and understand when additional treatment or urgent help is required.
- Clear mucus regularly Use the airway-clearance technique agreed with the respiratory physiotherapist when bronchiectasis or retained mucus is present.
- Attend monitoring Blood tests, lung function and imaging help distinguish stable disease from recurrence.
- Report treatment side effects Steroid and antifungal adverse effects should be addressed early rather than tolerated silently.
- Check medicine interactions Consult the treatment team before starting new prescribed, over-the-counter or herbal medicines.
- Remain physically active Appropriate regular activity supports cardiovascular fitness, respiratory muscle function and wellbeing.
- Avoid smoking Smoking and vaping add further airway injury and complicate asthma and bronchiectasis management.
When should medical help be sought?
Arrange prompt clinical review for:
- worsening wheeze or increasing reliever use;
- new or increasing thick sputum;
- mucus plugs or bronchial casts;
- a persistent fall in peak flow or exercise tolerance;
- fever or symptoms suggesting infection;
- new chest X-ray abnormalities;
- increasing blood IgE after previous treatment;
- possible steroid or antifungal side effects.
Seek urgent or emergency help for:
- severe or rapidly worsening breathlessness;
- inability to speak in complete sentences;
- blue or grey lips or skin;
- collapse, fainting, exhaustion or new confusion;
- significant coughing of fresh blood;
- severe chest pain;
- very low or rapidly falling oxygen saturation;
- a severe allergic reaction or facial swelling.
Call 999 for immediately life-threatening symptoms.
Conclusion
Allergic bronchopulmonary aspergillosis is an exaggerated immune response to Aspergillus within susceptible airways, most often in people with asthma or cystic fibrosis.
The condition can cause wheeze, breathlessness, thick mucus, recurrent pulmonary opacities, mucus plugging and bronchiectasis.
A positive Aspergillus allergy result alone does not establish ABPA. Diagnosis requires a compatible combination of respiratory history, Aspergillus sensitisation, total IgE and additional immunological or imaging findings.
Treatment may involve oral corticosteroids, triazole antifungal therapy, optimised asthma treatment, airway clearance and management of coexisting bronchiectasis or infection.
Omalizumab, mepolizumab and other biological therapies may help selected patients with recurrent, treatment-dependent or severe-asthma-associated disease, but treatment decisions require specialist review.
People with difficult asthma, Aspergillus sensitisation, mucus plugging, recurrent lung opacities or unexplained bronchiectasis can arrange a specialist respiratory assessment.
Frequently asked questions
Is ABPA a fungal infection?
ABPA is primarily an allergic and eosinophilic response to Aspergillus growing or persisting within airway mucus. It is different from invasive fungal infection.
Is ABPA contagious?
No. ABPA is caused by an individual immune response to environmental Aspergillus and cannot be transmitted between people.
Does everyone with asthma and Aspergillus allergy have ABPA?
No. Many people have fungal sensitisation without meeting the broader diagnostic criteria for ABPA.
Can ABPA occur without asthma?
Asthma is the most common setting, but ABPA can also occur with cystic fibrosis, bronchiectasis and occasionally other susceptible airway conditions.
Can ABPA be cured?
Treatment can control active disease and prevent progression, but recurrence is possible. Long-term monitoring is therefore important.
What blood tests are used?
Testing commonly includes Aspergillus-specific IgE, total IgE, eosinophils and sometimes Aspergillus IgG, interpreted with clinical and radiological information.
Does a high total IgE confirm ABPA?
No. Total IgE is non-specific and can rise in many allergic, inflammatory and infectious conditions.
Can a normal eosinophil count exclude ABPA?
No. Corticosteroids and other treatments may suppress eosinophils, so previous results and treatment timing are important.
Does every patient need a CT scan?
CT is valuable for identifying bronchiectasis and mucus impaction, but the need and timing depend on previous imaging and the clinical question.
Why are oral corticosteroids used?
They suppress the allergic and eosinophilic inflammation responsible for active disease.
Why are antifungals used if ABPA is an allergy?
Reducing Aspergillus growth within airway mucus may reduce the allergen burden that is driving inflammation.
Can itraconazole interact with inhalers?
Yes. It can increase exposure to some inhaled corticosteroids and may cause clinically important adrenal and systemic steroid effects.
Can omalizumab treat ABPA?
Omalizumab may reduce exacerbations and steroid requirements in selected patients, but it is not routine first-line treatment for every case.
Can mepolizumab treat ABPA?
Mepolizumab may be considered in selected eosinophilic or treatment-dependent cases. Evidence is less extensive than for its established role in severe eosinophilic asthma.
Does ABPA always cause bronchiectasis?
No. ABPA can be identified before permanent bronchial damage is visible, although recurrent or prolonged disease increases bronchiectasis risk.
Can ABPA look like pneumonia?
Yes. Mucus plugging, collapse and inflammatory infiltrates may create recurrent or migrating opacities that resemble infection.
Should all mould be avoided?
Complete avoidance is impossible. Significant damp, visible mould and unusually intense exposure should be reduced where practicable.
References and further information
- British Thoracic Society. British Thoracic Society Clinical Statement on Aspergillus-related chronic lung disease. Published May 2025. View the BTS clinical statement
- International Society for Human and Animal Mycology. Revised clinical practice guidelines for diagnosing, classifying and treating allergic bronchopulmonary aspergillosis. View the revised ISHAM guidance
- National Institute for Health and Care Excellence. Asthma: diagnosis, monitoring and chronic asthma management. NICE guideline NG245. View the NICE asthma guideline
- London Chest Specialist. Asthma diagnosis and treatment. Read about specialist asthma care
- London Chest Specialist. Asthma with fungal sensitisation. Read about fungal sensitisation and SAFS
- London Chest Specialist. Bronchiectasis diagnosis and treatment. Read about bronchiectasis care
- London Chest Specialist. Living with bronchiectasis and co-morbidities. Read about ABPA and overlapping respiratory conditions
- London Chest Specialist. Fractional exhaled nitric oxide: a quick guide. Read the FeNO testing guide
- London Chest Specialist. Lung-function tests. Read about respiratory physiological testing
