Allergic Bronchopulmonary Aspergillosis (ABPA) for Expert Patients and non-Specialist Clinicians

Expert Information for Patients, GPs, and Specialist Nurses


🔎 What Is ABPA?

ABPA is a complex hypersensitivity reaction to Aspergillus fumigatus colonising the airways. It is not a fungal infection in the classic sense, but rather an exaggerated immune response — particularly involving IgE and eosinophils — seen in people with asthma or cystic fibrosis (CF).

It leads to recurrent inflammation, mucus plugging, and bronchial damage (including central bronchiectasis) if untreated.


🧬 Disease Mechanism

  • Type I and III hypersensitivity to A. fumigatus

  • Chronic airway inflammation causes mucus impaction and permanent lung damage

  • Associated with elevated total and specific IgE, eosinophilia, and recurrent flares


👥 Who Is at Risk?

  • Moderate to severe asthma

  • Cystic fibrosis

  • Rarely, patients with bronchiectasis or other chronic airway disease

ABPA is often underdiagnosed, especially in adults with difficult-to-control asthma.


⚠️ Common Symptoms

  • Worsening asthma control

  • Wheeze and chest tightness

  • Cough with thick mucus plugs

  • Shortness of breath

  • Intermittent low-grade fever

  • Haemoptysis (less common, usually mild)

  • Fatigue and poor response to inhaled steroids alone


🧪 Diagnosis

Diagnosis is based on a combination of clinical, radiological, and immunological features.

Core Investigations:

  1. Total IgE ≥1000 IU/mL (or >500 in treated patients)

  2. Aspergillus-specific IgE positive

  3. Aspergillus-specific IgG (or precipitating antibodies)

  4. Blood eosinophilia (>0.5 x10⁹/L typically)

  5. Chest CT: central bronchiectasis, mucus plugging (“finger-in-glove”), fleeting infiltrates

  6. Sputum culture or PCR positive for A. fumigatus

Diagnostic Criteria:

Use updated ISHAM criteria (2024 version preferred) combining major and minor features.


💊 Treatment

First-Line:

  • Oral corticosteroids (e.g. prednisolone) – cornerstone of flare management

    • Typically tapered over 3–6 months

Adjunct:

  • Itraconazole or posaconazole – reduces antigen burden and steroid need

    • 3–6 months or longer; monitor liver function and drug levels

Steroid-Sparing Options:

  • Biologics (increasingly used, especially in steroid-dependent or relapsing patients):

    • Omalizumab (anti-IgE)

    • Mepolizumab, Benralizumab (anti-IL-5)

    • Dupilumab, Tezepelumab (emerging options)


🧾 Monitoring

  • Total IgE every 1–3 months (a 25–50% rise may indicate relapse)

  • Pulmonary function tests (FEV1, peak flow)

  • Repeat CT if clinical deterioration or poor steroid response

  • Sputum cultures in persistent symptoms (to exclude Aspergillus bronchitis)


⚠️ Complications

  • Progression to bronchiectasis

  • CPA (if antifungals are stopped prematurely in chronic cases)

  • Recurrent flares leading to irreversible damage

  • Steroid side effects (weight gain, osteoporosis, adrenal suppression)


📚 More Information

  • Specialist referral: patients should be considered for referral to the National Aspergillosis Centre (NAC) or local respiratory immunology team for persistent/recurrent ABPA.

  • Patient support: aspergillosis.org, CF Trust, Asthma + Lung UK

  • Key guidelines: Guidance


Aspergillus Tracheobronchitis (ATB) for Expert patients and non-Specialist Clinicians

Expert Information for Patients, GPs, and Specialist Nurses


🔎 What Is Aspergillus Tracheobronchitis?

Aspergillus tracheobronchitis (ATB) is a rare but serious form of airway-invasive aspergillosis that primarily affects the trachea and large bronchi, rather than the lung parenchyma. It occurs predominantly in immunocompromised patients and may present with obstructive airway symptoms or respiratory failure.

ATB can exist on a spectrum from superficial colonisation to ulcerative or pseudomembranous invasion of the bronchial wall.


🧬 Pathophysiology

  • Inhaled Aspergillus spores adhere to and invade damaged airway mucosa.

  • Occurs more commonly when local airway immunity is impaired (e.g. in transplant recipients or critical illness).

  • May co-exist with invasive pulmonary aspergillosis (IPA) or appear in isolation.


👥 Who Is at Risk?

High-risk groups include:

  • Lung transplant recipients

  • Hematopoietic stem cell transplant patients

  • Severe COPD or structural airway disease

  • Patients with prolonged corticosteroid use

  • Critically ill or mechanically ventilated patients

  • COVID-19 or influenza patients (sometimes overlapping with CAPA/IAPA)


⚠️ Clinical Presentation

Symptoms depend on the degree of airway obstruction and depth of invasion:

  • Cough (dry or productive)

  • Worsening breathlessness

  • Stridor or wheeze

  • Hoarseness or vocal changes

  • Fever unresponsive to antibiotics

  • Haemoptysis (may be life-threatening)

  • Airway obstruction or collapse in advanced cases

ATB may be mistaken for tracheobronchial malignancy, infection, or stenosis.


🧪 Diagnosis

Bronchoscopy is essential for diagnosis:

  • Direct visualisation of:

    • Ulceration

    • Pseudomembranes

    • Plaques

    • Necrotic debris

  • Biopsies may reveal fungal hyphae invading mucosa.

Microbiological Investigations:

  • Culture and PCR for Aspergillus from BAL or brushings

  • BAL galactomannan

  • Serum galactomannan or β-D-glucan may be supportive

  • CT chest may be normal or show airway thickening, bronchial wall invasion, or tree-in-bud opacities


💊 Treatment

Systemic Antifungals:

  • Voriconazole is first-line

  • Isavuconazole or liposomal amphotericin B if azole intolerant or resistant

Airway Management:

  • Debridement or bronchoscopic removal of pseudomembranes in severe obstruction

  • Airway stenting in refractory strictures

  • Nebulised antifungals (e.g. amphotericin B) may be used as adjunct in selected cases

Prompt initiation of antifungal therapy is vital. Delays can lead to respiratory failure or death.


🧾 Monitoring

  • Clinical response: breathlessness, cough, fever

  • Repeat bronchoscopy in some cases

  • CT imaging of airways

  • Antifungal drug levels

  • Liver and renal function


📚 More Information

  • ATB is under-recognised, especially in non-neutropenic or critically ill patients.

  • Should be considered in transplant recipients or ICU patients with persistent respiratory symptoms and negative bacterial cultures.

  • Referral to respiratory, infectious diseases, and ICU teams is essential.

  • Resources: aspergillosis.org ; BTS Statement on  aspergillosis


Aspergillus Bronchitis for Expert Patients and non-Specialist Clinicians

Expert Information for Patients, GPs, and Specialist Nurses


🔎 What Is Aspergillus Bronchitis?

Aspergillus bronchitis is a chronic fungal infection of the airways by Aspergillus fumigatus (or rarely other Aspergillus species), seen in individuals with structural lung disease or impaired mucociliary clearance. Unlike ABPA, it is not allergic in origin and does not involve systemic invasion, but is characterised by persistent fungal colonisation with active infection.


🧬 Pathophysiology

  • Chronic colonisation of the conducting airways by Aspergillus

  • Local immune dysfunction (but not systemic immunosuppression)

  • Low-grade inflammation and increased mucus production

  • Often coexists with bronchiectasis, COPD, or CF


👥 Who Is at Risk?

Most commonly seen in patients with:

  • Bronchiectasis (non-ABPA)

  • Cystic fibrosis

  • COPD or asthma with sputum production

  • Post-viral or structural airway damage

  • Chronic antibiotic or corticosteroid use

Not typically seen in severely immunocompromised hosts (in whom invasive aspergillosis is more likely).


⚠️ Common Symptoms

  • Persistent productive cough

  • Thick sputum often yellow or green

  • Worsening breathlessness or wheeze

  • Chronic sputum positivity for Aspergillus

  • Mild fever or malaise (but often afebrile)

  • Poor response to antibiotics alone

Symptoms may resemble chronic bacterial bronchitis or overlap with infective exacerbations of bronchiectasis.


🧪 Diagnosis

Diagnosis requires a combination of clinical and microbiological evidence, with exclusion of ABPA and CPA.

Diagnostic Features:

  1. Chronic productive cough (>4 weeks)

  2. Repeated isolation of Aspergillus from sputum or BAL

  3. Elevated Aspergillus IgG (typically present)

  4. Normal or mildly elevated total IgE (typically <1000 IU/mL)

  5. Absence of cavitary lesions or ABPA features on CT

  6. Response to antifungal treatment supports diagnosis

🛑 Exclude:

  • ABPA (IgE >1000, eosinophilia, central bronchiectasis)

  • CPA (cavities, weight loss, radiological progression)


💊 Treatment

First-Line:

  • Oral antifungals (usually for 3–6 months)

    • Itraconazole (first choice)

    • Voriconazole or posaconazole (if resistant/intolerant)

  • Monitor drug levels and LFTs

Adjuncts:

  • Physiotherapy and airway clearance techniques

  • Nebulised saline or mucolytics

  • Treat co-infections (e.g. Pseudomonas) where relevant

In patients with CF, consider co-management with a specialist CF team.


🧾 Monitoring

  • Sputum cultures to monitor persistence or clearance

  • Aspergillus IgG levels

  • Symptoms (sputum, breathlessness)

  • Liver function and drug monitoring

  • Periodic CT imaging if symptoms worsen or haemoptysis occurs


📚 More Information


⚠️ Warning Signs for Possible Aspergillosis in Primary Care

We often state that a GP does not need to know all the details of what aspergillosis is, they just need to know what the warning signs might be so that they know when they should refer the patient to their local hospital specialist. What are those warning signs?

🟠 1. Asthma Not Responding to Guidelines-Based Treatment

  • Poor control despite high-dose inhaled steroids or long-acting bronchodilators

  • Frequent oral steroid bursts (>2 in a year)

  • Persistent cough or breathlessness between attacks

  • Thick or brown mucus plugs coughed up

🟢 Ask: “Are you still having symptoms even though you’re taking all your preventers?”


🟠 2. Recurrent Chest Infections

  • Multiple antibiotic courses (especially in bronchiectasis or COPD patients)

  • Sputum samples that repeatedly show Aspergillus or colonising fungi

  • Chest x-rays showing cavities, nodules, or persistent infiltrates

🟢 Ask: “Have you had several chest infections this year that needed antibiotics or steroids?”


🟠 3. Unexplained Fatigue, Weight Loss, or Night Sweats

  • Especially if imaging shows lung abnormalities or patient is immunocompromised

  • May indicate CPA, not just asthma

🟢 Ask: “Have you lost weight without trying, or felt unusually tired for weeks?”


🟠 4. Pre-existing Lung Conditions with New or Worsening Symptoms

  • Especially in patients with:

    • Bronchiectasis

    • COPD/emphysema

    • Old TB

    • Sarcoidosis

  • These conditions increase risk of CPA or colonisation becoming invasive


🟠 5. High Total IgE or Eosinophils

  • Total IgE > 1000 IU/mL with asthma + mucus plugs = strong ABPA clue

  • Blood eosinophils persistently >0.5 (especially off steroids)

  • Aspergillus-specific IgE or IgG positive

🟢 Flag: “Could this patient have allergic fungal disease or ABPA?”


🟠 6. Radiology That Doesn’t Match the Diagnosis

  • If the patient is being treated as asthma or pneumonia but:

    • HRCT shows bronchiectasis with mucus plugging

    • X-rays don’t improve despite treatment

    • Old TB scar now shows a cavity

🟢 Flag: “Does this imaging suggest something more than asthma or infection?”


🧭 What Should GPs and Nurses Do Next?

✅ Request:

  • Blood tests: Total IgE, eosinophils, Aspergillus-specific IgE/IgG

  • Sputum for fungal culture if available

  • CXR or HRCT if not done recently

✅ Refer:

  • Respiratory specialist or Advice & Guidance

  • National Aspergillosis Centre (NAC) in Manchester is a national specialist (tertiary) NHS centre, so does not accept referrals directly from GP's, instead GP's should refer to their local respiratory specialist team at a hospital nearby. NHS referral structure


📋 Clinical Triggers for Flagging Aspergillosis

Trigger Possible Condition
Uncontrolled asthma + high IgE + mucus ABPA
Chronic cough + weight loss + cavity on CT CPA
Asthma + sensitisation to fungi + frequent steroids SAFS

Waiting for Microbiological results after bronchoscopy or sputum?

Here’s a detailed overview of culture times for respiratory samples, including sputum, bronchoalveolar lavage (BAL), bronchial washings, and tissue biopsies. The times can vary slightly depending on the lab's protocols, but the ranges below are generally reliable.


🦠 Bacterial Cultures

Organism Type Culture Time Notes
Common respiratory bacteria 1–3 days Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis — fast growers.
Gram-negative bacilli 2–4 days Pseudomonas, Klebsiella, E. coli — often from hospital-acquired infections.
Anaerobic bacteria 5–7 days Require special culture conditions; longer if from lung abscess.
Atypical bacteria (e.g., Legionella) 5–7 days or longer Special media (e.g., BCYE); PCR is faster.
Nocardia 7–14 days (up to 21) Slow-growing, weakly acid-fast; resembles TB.

🌿 Fungal Cultures

Fungus Type Culture Time Notes
Aspergillus species 5–14 days (held up to 6 weeks) Colonies may appear within 5–10 days; full ID and sensitivity takes longer.
Candida species 1–3 days Grows quickly, but needs correlation with clinical signs (often coloniser).
Cryptococcus neoformans 3–7 days Faster than most moulds; may require specific media.
Dimorphic fungi (e.g., Histoplasma) 2–6 weeks Very slow-growing; incubation up to 6 weeks needed.
Zygomycetes/Mucorales 2–5 days Grow rapidly but fragile; easily missed if lab isn't alerted.

🧫 Mycobacterial Cultures

Mycobacteria Type Culture Time Notes
Mycobacterium tuberculosis 2–8 weeks Liquid cultures (e.g., MGIT) reduce time to ~10–21 days, but solid media held longer.
NTM (Non-tuberculous mycobacteria) 2–8 weeks (some longer) M. avium, M. kansasii, M. abscessus, etc.; slow or rapid growers.

🧪 Other Tests on Respiratory Samples (Non-culture)

Test Time Use
Gram stain / KOH prep Minutes to 1 day Rapid preliminary information.
Fungal PCR (e.g., Aspergillus) 1–3 days Can be used on BAL, biopsy; fast but not always standard.
Galactomannan (BAL) 1–3 days Indicates Aspergillus antigen; useful in early detection.
Cytology/Histopathology 3–7 days Can reveal fungi, TB, malignancy.

🔁 Summary: Longest-held Cultures

Held Up to Organism
6–8 weeks Mycobacteria (TB, NTM), dimorphic fungi (Histoplasma, Blastomyces)
3–6 weeks Moulds (Aspergillus, Scedosporium, Fusarium)
2–3 weeks Nocardia, anaerobes

If you're awaiting results after a bronchoscopy, most bacterial and yeast results return within the first 3–5 days, whereas fungal or TB/mycobacterial cultures may take weeks — especially if slow-growing pathogens are suspected.