Allergic Aspergillosis

Allergic aspergillosis” usually means allergic bronchopulmonary aspergillosis (ABPA). It is a strong allergy in the lungs to the mold Aspergillus fumigatus. The mold’s tiny spores are everywhere in the air. Most people clear them. In some people—often those with asthma or cystic fibrosis—the immune system overreacts. The airways become swollen, full of sticky mucus plugs, and can widen and scar (bronchiectasis) if the problem repeats for years. Doctors diagnose ABPA with a mix of symptoms, blood tests (very high IgE and positive Aspergillus-specific IgE/IgG), and chest CT changes. New 2024 international guidelines from ISHAM explain who should be tested, how to classify disease, and how to treat it (steroids or itraconazole first; biologics in selected cases). High-attenuation (“dense”) mucus on CT is especially suggestive. PubMed

ABPA tends to flare and calm. During a flare you may cough, wheeze, feel tight in the chest, and bring up thick brownish plugs. Blood tests show rising total IgE. When treatment works, symptoms improve, chest shadows fade, and IgE usually drops (often by ~25–35% from baseline). Doctors then monitor for months because relapses are common. The 2024 guideline lowered the screening threshold for total IgE ≥500 IU/mL with positive Aspergillus-specific IgE to prompt full evaluation. PubMed+2PMC+2

Allergic aspergillosis means your immune system overreacts to a common mold called Aspergillus (usually A. fumigatus). Instead of ignoring the mold, your body treats it like a dangerous invader. This causes swelling and mucus in the breathing tubes inside your lungs. The reaction looks like severe, hard-to-control asthma. Over time, it can damage the airways and lead to bronchiectasis (widened, scarred airways) if not treated. People with asthma or cystic fibrosis are the ones most at risk of this problem. Doctors most often call this condition “Allergic Bronchopulmonary Aspergillosis,” or ABPA. NCBI+2Cleveland Clinic+2

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Other names

• Allergic bronchopulmonary aspergillosis (ABPA). This is the standard medical name for allergic aspergillosis in the lungs. Older papers may also say “Hinson–Pepys disease.” NCBI+1

• Allergic fungal airway disease / allergic bronchopulmonary mycosis (ABPM). Very similar illness when the allergy is to fungi other than Aspergillus. Many tests and treatments overlap. ERS Publications

• Allergic fungal rhinosinusitis (AFRS). This is a related allergic problem in the nose and sinuses rather than the lungs. Some people can have both sinus and lung disease. PMC+1

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Types

1. ABPA with asthma. The common form. The person has a history of asthma, then develops ABPA on top of it. Asthma symptoms often become difficult to control. PMC

2. ABPA with cystic fibrosis (CF-ABPA). The same allergic process, but in someone with cystic fibrosis. It can be hard to spot because CF alone already causes cough and mucus. PMC

3. Serologic ABPA (ABPA-S). Blood tests show strong allergic signals (very high total IgE and A. fumigatus–specific IgE/IgG), but CT scan does not yet show bronchiectasis. This is an earlier or milder stage. ERS Publications

4. ABPA with central bronchiectasis (ABPA-CB). Allergy has lasted long enough to widen and scar the larger, central airways. People often cough up thick “mucus plugs.” ERS Publications

5. ABPA with high-attenuation mucus. On CT, the mucus looks extra dense (bright) because it is packed with cells and debris. This finding strongly supports ABPA and often signals more severe disease. ERS Publications

6. Allergic bronchopulmonary mycosis (ABPM). Same pattern as ABPA, but due to other molds (for example Candida, Curvularia). Doctors sometimes use the broader term when the exact mold differs. ERS Publications

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Causes

1. Regular exposure to Aspergillus spores. The mold lives in soil, decaying leaves, compost piles, damp buildings, and air vents. Breathing in many spores raises the chance of a reaction. Cleveland Clinic

2. Asthma. ABPA is far more common in people with asthma, especially if asthma is long-standing or poorly controlled. PMC

3. Cystic fibrosis. Thick airway secretions trap spores and make it easier for allergy to grow. PMC

4. Atopy (general allergy tendency). People with eczema, allergic rhinitis, or multiple environmental allergies have a more reactive immune system. PMC

5. High mold burden at home or work. Damp homes, water damage, and poor ventilation increase airborne spores. Cleveland Clinic

6. Warm, humid climate. These conditions favor mold growth outdoors and indoors. Cleveland Clinic

7. Chronic airway inflammation. Any long-term airway swelling can make the lining “stickier,” helping spores settle. (This is an inference from pathophysiology described in reviews.) ERS Publications

8. Genetic susceptibility. Certain immune system patterns (HLA types and other variants) are linked to stronger responses to Aspergillus. (Observational associations reported in reviews.) ERS Publications

9. Frequent corticosteroid bursts for asthma. Steroids help asthma but may also change local immunity and mucus flow, which can complicate fungal colonization/allergy patterns. (Review-level inference.) ERS Publications

10. Airway colonization by Aspergillus. The fungus can live on airway mucus without “invading,” constantly presenting allergens to the immune system. NCBI

11. Viral respiratory infections. Recent colds or flu can flare asthma and open the door to worse allergy symptoms. (Common clinical observation discussed in ABPA care reviews.) PMC

12. Exposure during yard work, farming, or composting. Turning soil or compost releases many spores at once. Cleveland Clinic

13. Indoor hobbies with plant material. Gardening indoors, keeping potted plants, or storing damp organic matter raises indoor spores. Cleveland Clinic

14. Occupational exposure. Sawmills, grain storage, greenhouses, and demolition sites can carry heavy spore loads. Cleveland Clinic

15. Poorly maintained HVAC systems. Filters and ducts can harbor mold if not serviced. Cleveland Clinic

16. Smoking and second-hand smoke. Smoke irritates airways, thickens mucus, and impairs clearance. (General airway-health inference supported across pulmonary reviews.) ERS Publications

17. Air pollution. Particles irritate and inflame the bronchial lining, making reactions stronger. (Review-level inference.) ERS Publications

18. Use of hot tubs/steam rooms with poor disinfection. Warm, damp environments can aerosolize spores. Cleveland Clinic

19. Home renovation or water damage. Disturbs hidden mold and spreads spores into rooms. Cleveland Clinic

20. Family history of severe allergy or asthma. A general inherited tendency to atopy can make ABPA more likely. PMC

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Symptoms

1. Worsening wheeze and breathlessness. Asthma feels harder to control, with more frequent attacks. Mayo Clinic

2. Chronic cough. Often daily, often worse at night or in the early morning. Mayo Clinic

3. Coughing up thick “mucus plugs.” Plugs can look like brownish strings or casts. This is very typical of ABPA. NCBI

4. Fever and malaise during flares. A sign of active airway inflammation. Mayo Clinic

5. Chest tightness or pressure. Comes with airway narrowing and mucus buildup. Cleveland Clinic

6. Occasional coughing of blood. Blood-streaked sputum can appear when inflamed airways are friable. Mayo Clinic

7. Reduced exercise tolerance. Shortness of breath limits activity. Wikipedia

8. Worsening need for rescue inhaler. More puffs per day than usual. PMC

9. Recurrent “pneumonia-like” episodes that clear and recur. Chest X-ray spots that move around are a classic clue. Wikipedia

10. Noisy breathing (rhonchi) from mucus. Heard by the patient and on exam. Cleveland Clinic

11. Sinus congestion and polyps in some people. Upper-airway allergy can coexist. PMC

12. Nighttime cough and sleep disturbance. A sign of poor asthma control with allergic triggers. Cleveland Clinic

13. Unintended weight loss in advanced disease. If bronchiectasis becomes severe or infection complicates the course. (General bronchiectasis association.) Wikipedia

14. Chest pain with deep breathing or coughing. From irritated airways and chest wall strain. Cleveland Clinic

15. Fatigue. Ongoing inflammation and poor sleep are common reasons. Cleveland Clinic

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Diagnostic tests

Doctors do not rely on one test. They put together the story: risk (asthma/CF), symptoms, and a pattern across blood tests, allergy tests, breathing tests, and imaging. International guidelines updated in 2024 describe structured criteria using clinical features, very high IgE, positive Aspergillus–specific IgE, supportive IgG (precipitins), and typical CT findings such as central bronchiectasis or high-attenuation mucus. Below are common tests, grouped to match how a clinic visit usually proceeds. ERS Publications+1

A) Physical examination (what the clinician checks)

1. General assessment and vital signs. Fever during flares and rapid breathing can point to active inflammation. Oxygen level may be checked at the same time. Mayo Clinic

2. Auscultation of the chest. Wheezes, rhonchi, and coarse crackles suggest narrowed, mucus-filled airways that are typical in ABPA. Cleveland Clinic

3. Inspection for increased work of breathing. Use of accessory muscles and prolonged exhalation suggest airway obstruction. Cleveland Clinic

4. Clubbing or chest wall changes (in advanced cases). Rare in early ABPA but can appear with long-standing bronchiectasis. Wikipedia

5. Nasal and sinus exam. Polyps and allergic mucin suggest associated allergic fungal rhinosinusitis. PMC

B) “Manual” office tests and bedside procedures

6. Peak expiratory flow (PEF). A simple handheld test showing day-to-day variation; big swings fit an allergic/asthma-driven process like ABPA. Cleveland Clinic

7. Spirometry (pre- and post-bronchodilator). Shows airflow obstruction that improves after inhaled bronchodilator; this supports asthma with allergic triggers. Cleveland Clinic

8. Bronchodilator reversibility test. A quantified improvement in FEV₁ after albuterol strengthens the asthma component of ABPA. Cleveland Clinic

9. Induced sputum collection. Hypertonic saline can help collect mucus plugs for lab analysis and culture. NCBI

10. Skin prick testing to Aspergillus antigen. A quick in-clinic allergy test; immediate wheal-and-flare shows IgE-mediated sensitization, which is central in ABPA. NCBI

C) Laboratory and pathological tests

11. Total serum IgE. This is usually very high in ABPA. Traditional cutoffs were ≥1,000 IU/mL, but newer work and the 2024 international guidance allow lower thresholds in context (for example ≥500 IU/mL) with the right combination of other findings. Levels help both diagnosis and follow-up. Dove Medical Press+3ATS Journals+3JAci Online+3

12. Aspergillus fumigatus–specific IgE. A positive, elevated result is essential because ABPA is an IgE-driven allergy to Aspergillus. NCBI

13. Aspergillus-specific IgG (precipitins). Shows immune exposure and helps confirm the diagnosis, especially when combined with IgE and imaging. JAci Online

14. Peripheral eosinophil count. Many patients have eosinophilia (classically >1,000 cells/µL), which reflects allergic inflammation. ScienceDirect

15. Sputum culture and microscopy. May show Aspergillus species or brownish mucus plugs packed with eosinophils; culture supports the picture but is not required alone. NCBI

16. Exhaled nitric oxide (FeNO). High values suggest allergic airway inflammation; helpful to track inflammation in asthma overlapping with ABPA. (Physiology tool used in asthma clinics.) Cleveland Clinic

D) Electro-physiologic/monitoring tests

17. Pulse oximetry. Quick, noninvasive check of oxygen saturation at rest and with walking; lower values during flares suggest significant airway blockage. Cleveland Clinic

18. Impulse oscillometry or body plethysmography (advanced lung mechanics). These device-based tests show small-airway dysfunction that can persist even when basic spirometry looks near normal. (Used in specialized labs for difficult asthma/ABPA.) Cleveland Clinic

19. Bronchial challenge (methacholine or mannitol). A controlled test that shows “twitchy” airways typical of strong allergy/asthma; it supports the ABPA picture when needed. Cleveland Clinic

E) Imaging tests

20. Chest radiograph and high-resolution CT (HRCT). X-rays may show fleeting (“transient”) opacities that move around. HRCT is the key test: it can show central bronchiectasis, mucus plugging, “finger-in-glove” mucus impaction, and sometimes dense (high-attenuation) mucus—features that strongly support ABPA in the right clinical setting. Wikipedia+1

Non-pharmacological treatments (therapies & other measures)

Each item includes Description – Purpose – Mechanism (how it helps)

1. Education and action plan – Your team teaches you what ABPA is, how to spot flares, and when to adjust medicines. Purpose: early control. Mechanism: reduces delays to steroids/antifungals and prevents lung damage by acting fast when IgE rises or symptoms recur (per ISHAM monitoring). PubMed

2. Allergen-minimized home – Keep indoor humidity <60% (ideally 30–50%), fix leaks, ventilate kitchens/baths, clean visible mold safely. Purpose: cut daily mold load. Mechanism: low humidity and moisture deprive mold of what it needs to grow. CDC+2US EPA+2

3. HEPA filtration – Use a true-HEPA room purifier in the bedroom/living area. Purpose: reduce airborne spores/particles. Mechanism: HEPA traps particles down to ~0.3 µm, lowering inhaled triggers. (Environmental infection-control sources support humidity/air quality targets.) CDC

4. Dehumidifiers & HVAC care – Run a dehumidifier during humid months; change HVAC filters on schedule; ensure AC drip pans drain. Purpose: stable indoor humidity. Mechanism: less moisture → less mold. US EPA

5. Targeted remediation – For persistent mold, hire trained remediators; avoid DIY if you have asthma/ABPA. Purpose: safe removal. Mechanism: proper containment prevents spore bursts that can trigger flares; CDC advises high-risk people avoid staying in moldy homes during cleanup. CDC

6. Personal protection during exposure – If you must enter dusty/moldy places (gardening, compost, old buildings), use a well-fitting N95 and limit time. Purpose: reduce spore inhalation. Mechanism: filtration barrier lowers airway antigen exposure. (Aligned with general mold-exposure harm reduction.) CDC

7. Asthma breathing techniques – Pursed-lip breathing, diaphragmatic breathing. Purpose: ease breathlessness. Mechanism: reduces dynamic airway collapse and improves ventilation.

8. Airway clearance routines – Hydration, warm steam from a clean humidifier (used intermittently and kept meticulously clean), controlled coughing, oscillatory PEP devices if prescribed. Purpose: mobilize mucus plugs. Mechanism: mechanical shear thins/clears mucus; prevents atelectasis. (Humidifiers must be maintained; poorly cleaned cool-mist devices can aerosolize allergens.) CDC

9. Pulmonary rehabilitation – Supervised exercise with education. Purpose: improve stamina and quality of life. Mechanism: conditioning lowers dyspnea and anxiety.

10. Vaccinations – Annual influenza and age-appropriate pneumococcal vaccines. Purpose: prevent infections that can trigger ABPA flares. Mechanism: fewer viral/bacterial exacerbations → fewer steroid bursts.

11. Smoking cessation & smoke avoidance – Purpose: protect airways. Mechanism: smoke worsens inflammation and mucus.

12. Allergen skin-prick testing (with counseling) – Purpose: identify co-sensitizations (dust mite, cockroach, pollens) that also worsen asthma. Mechanism: targeted avoidance reduces overall Th2 load and exacerbations.

13. Written medication calendar & IgE tracking – Purpose: adherence and early relapse detection. Mechanism: structured monitoring of total IgE trends as recommended by ISHAM. PubMed

14. Nasal care for coexisting AFRS/rhinitis – Daily saline rinses; steroid nasal sprays as directed. Purpose: cut post-nasal drip and sinus triggers. Mechanism: reduces upper-airway fungal/allergic burden; cornerstone after AFRS surgery. Ann Allergy

15. Occupational/environmental adjustments – Rotate away from high-mold tasks (grain storage, composting) if possible. Purpose: minimize daily exposure. Mechanism: less antigen → fewer flares.

16. Sleep optimization & reflux control – Head-of-bed elevation; treat GERD if present. Purpose: reduce nighttime cough/wheeze. Mechanism: less microaspiration and vagal bronchospasm.

17. Weight management & graded activity – Purpose: improve breathing efficiency. Mechanism: lower metabolic load reduces dyspnea at exertion.

18. Psychological support – Anxiety strategies, CBT if needed. Purpose: reduce symptom amplification; support adherence. Mechanism: lowers stress-mediated bronchospasm.

19. Sick-day rules – Pre-agreed plan for quick access to oral steroids/antifungals at flare onset. Purpose: shorten relapse. Mechanism: prompt anti-inflammatory action follows guideline logic. PubMed

20. Travel prep – Carry action plan, inhalers, spacer, and recent IgE/medication list. Purpose: safe travel. Mechanism: prevents treatment gaps.

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Drug treatments

Doses are common starting points for adults; always individualize & check local product labels, renal/hepatic function, interactions, and pregnancy status.

1. Prednisolone (systemic corticosteroid) • 0.5 mg/kg/day for ~2 weeks, then taper over 2–3 months (typical initial regimen; tailor per response). Purpose: first-line for acute ABPA or exacerbations. Mechanism: broad anti-inflammatory; rapidly reduces airway swelling and IgE. Side effects: hyperglycemia, mood changes, infection risk, bone loss. 2024 ISHAM recommends oral prednisolone monotherapy (or itraconazole) for acute ABPA. PubMed

2. Itraconazole (oral azole antifungal) • 200 mg twice daily with food for 16 weeks (classic RCT); therapeutic drug monitoring often used. Purpose: reduce fungal burden and steroid need; alternative to initial steroids or add-on in relapses. Mechanism: inhibits ergosterol synthesis in Aspergillus, lowering antigen stimulus to the immune system. Side effects: liver enzyme rise, GI upset, drug interactions (CYP3A4); absorption reduced by PPIs (capsules). RCT showed less steroid need and lower IgE vs. placebo. 2024 ISHAM allows prednisolone or itraconazole as initial monotherapy. PubMed+1

3. Voriconazole (azole) • 200 mg twice daily (after 400 mg BID day 1 in some protocols). Purpose: second-line azole if itraconazole fails/intolerant. Mechanism: antifungal burden reduction. Side effects: photosensitivity, visual disturbances, liver enzyme rise, QT prolongation; check levels.

4. Posaconazole (azole; delayed-release) • 300 mg twice on day 1, then 300 mg daily; monitor levels. Purpose: alternative azole for refractory disease or when other azoles not tolerated. Mechanism/side effects: similar antifungal; hepatotoxicity/QT risk, drug interactions.

5. Omalizumab (anti-IgE biologic) • SC every 2–4 weeks per weight & baseline IgE. Purpose: steroid-sparing in ABPA with allergic asthma phenotype. Mechanism: binds free IgE → down-regulates FcεRI on mast cells/basophils → fewer allergic flares. Side effects: injection-site reactions, rare anaphylaxis; first dose separated from vaccines per GINA advice. Meta-analysis shows reduced exacerbations, OCS dose, total IgE, and improved FEV₁ in ABPA. PubMed+1

6. Mepolizumab (anti-IL-5) • 100 mg SC every 4 weeks. Purpose: for eosinophilic phenotype with ABPA flares. Mechanism: reduces eosinophils → less mucus plugging/inflammation. Side effects: headache, injection reactions; steroid-sparing benefits shown for severe asthma and supportive evidence in ABPA. PubMed+1

7. Benralizumab (anti-IL-5 receptor) • 30 mg SC q4 weeks ×3 then q8 weeks. Purpose: similar to mepolizumab; case-series data in ABPA. Mechanism: depletes eosinophils via ADCC. Side effects: similar class profile; real-world ABPA data emerging. PubMed

8. Dupilumab (anti-IL-4Rα) • 200–300 mg SC every 2 weeks (per label for asthma). Purpose: steroid-sparing in ABPA with Type-2 inflammation; helpful with comorbid nasal polyps/AFRS. Mechanism: blocks IL-4/IL-13 signaling. Side effects: conjunctivitis, transient eosinophilia; ABPA meta-analysis supports benefit. PubMed

9. Tezepelumab (anti-TSLP) • 210 mg SC every 4 weeks. Purpose: add-on in severe asthma when Type-2 markers are variable; ABPA evidence is weaker but evolving. Mechanism: upstream epithelial cytokine blockade. Side effects: injection reactions; limited ABPA data. PubMed

10. High-dose inhaled corticosteroid (ICS) (e.g., budesonide, fluticasone) • dose per guideline. Purpose: treat the asthma foundation. Mechanism: airway anti-inflammatory; reduces day-to-day triggers. Side effects: oral thrush, dysphonia; rinse mouth. Global Initiative for Asthma – GINA

11. ICS/LABA combinations (e.g., budesonide/formoterol). Purpose: better symptom control and exacerbation reduction in asthma component. Mechanism: anti-inflammatory + bronchodilation. Side effects: tremor, palpitations (LABA). Global Initiative for Asthma – GINA

12. Short-acting β₂-agonist (SABA) (e.g., salbutamol) as reliever. Purpose: quick relief of bronchospasm. Mechanism: smooth-muscle relaxation. Side effects: tremor, tachycardia.

13. LAMA (e.g., tiotropium) in severe asthma. Purpose: extra bronchodilation. Mechanism: blocks M3 receptors; reduces bronchoconstriction. Side effects: dry mouth. Global Initiative for Asthma – GINA

14. Leukotriene receptor antagonist (montelukast). Purpose: adjunct for allergic asthma; evidence in ABPA limited. Mechanism: blocks CysLT1 pathway. Side effects: rare neuropsychiatric events; discuss risks. Ann Allergy

15. Azithromycin (anti-inflammatory dosing, e.g., 250–500 mg 3×/week) where appropriate after QT and resistance review. Purpose: reduce steroid bursts in severe asthma phenotypes. Mechanism: immunomodulation, biofilm effects. Side effects: QT prolongation, GI upset.

16. Nebulized hypertonic saline if prescribed in mucus-plugging phenotypes. Purpose: thin mucus. Mechanism: osmotic water draw into airway lumen. Side effects: bronchospasm—pre-treat with bronchodilator.

17. Nebulized amphotericin B (specialist-guided). Purpose: occasionally used in refractory AFRS/airway colonization; evidence limited. Mechanism: topical antifungal. Side effects: cough/bronchospasm; mixed data. Ann Allergy

18. Proton-pump inhibitor or alginate for GERD when reflux worsens cough. Purpose: reduce cough/asthma triggers. Mechanism: less microaspiration.

19. Antihistamines for upper-airway allergy (non-sedating). Purpose: help rhinitis that aggravates asthma. Mechanism: H1 blockade.

20. Calcium + vitamin D & bone protection during repeated steroid use (± bisphosphonate if indicated). Purpose: prevent osteoporosis. Mechanism: supports bone remodeling; steroid stewardship per asthma guidelines. Global Initiative for Asthma – GINA

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Dietary molecular supplements

Use only as add-ons to prescribed treatment; discuss interactions (especially with azoles).

1. Vitamin D₃ (e.g., 1000–2000 IU/day if deficient) – immune modulation; low vitamin D associates with worse asthma control. Mechanism: shifts toward regulated T-cell responses.

2. Omega-3 (fish oil, EPA/DHA 1–2 g/day) – anti-inflammatory lipid mediators; may modestly reduce airway inflammation.

3. N-acetylcysteine (600 mg 1–2×/day) – mucolytic; replenishes glutathione; may help mucus clearance.

4. Magnesium (dietary or 200–400 mg/day) – smooth-muscle support; avoid in renal failure.

5. Quercetin (food-based flavonoid) – antioxidant/anti-allergic properties (limited human airway data).

6. Probiotics (selected strains) – gut–lung axis support; evidence in ABPA is limited; avoid in immunocompromised hosts.

7. Curcumin (500–1000 mg/day with pepper/bioperine) – anti-inflammatory; monitor for interactions.

8. Honey/ginger as symptomatic soothers – cough relief; not disease-modifying.

9. Sodium alginate before bed if reflux – reduces nighttime microaspiration.

10. Electrolyte-rich hydration – thins mucus; supports airway clearance.

Evidence for supplements in ABPA specifically is limited; they do not replace steroids/azoles/biologics backed by trials and guidelines. PubMed+2PubMed+2

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Regenerative / stem-cell drugs

There are no approved stem-cell or regenerative drugs for ABPA. Using such products outside trials can be dangerous. Instead, clinicians use targeted immune-modulating biologics with real-world and meta-analytic support in ABPA or strong evidence in severe asthma. Below are the evidence-based immune modulators sometimes used for ABPA management:

1. Omalizumab – see above; dosing by weight/IgE every 2–4 weeks; mechanism: anti-IgE; effects: fewer exacerbations and lower OCS needs in ABPA series/meta-analysis. PubMed

2. Mepolizumab – 100 mg SC q4w; anti-IL-5; reduces eosinophils, mucus plugging; supportive ABPA evidence. PubMed

3. Benralizumab – 30 mg SC q4w×3 then q8w; anti-IL-5R; eosinophil depletion; case series in ABPA. PubMed

4. Dupilumab – 200–300 mg SC q2w; anti-IL-4Rα; decreases Type-2 signaling; helpful with nasal polyps/AFRS overlap. PubMed

5. Tezepelumab – 210 mg SC q4w; anti-TSLP; emerging/weak ABPA evidence; option when biomarkers are mixed. PubMed

6. Vaccination program (influenza, pneumococcal) – not a “drug” in the narrow sense, but a proven immune intervention that reduces infection-triggered flares and steroid exposure.

If you see “stem-cell therapy for ABPA” advertised, ask for peer-reviewed, guideline-endorsed evidence; the ISHAM 2024 guideline and current asthma strategies do not recommend stem-cell drugs for ABPA. PubMed

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Procedures / surgeries

1. Flexible bronchoscopy for mucus-plug extraction – Why: severe plugging with lobar collapse or refractory hypoxemia. What: bronchoscopic suction/cryo-extraction of thick mucus to reopen airways. Goal: immediate ventilation improvement.

2. Endoscopic sinus surgery (AFRS) – Why: remove allergic mucin and open sinus drainage in patients with AFRS causing recurrent disease. Goal: restore ventilation and allow topical steroids to work. Post-op: daily saline and steroid sprays are key. Ann Allergy

3. Bronchial artery embolization – Why: control massive hemoptysis from bronchiectatic vessels. Goal: stop life-threatening bleeding.

4. Lobectomy/segmentectomy (rare) – Why: localized destroyed lung or coexisting aspergilloma with repeated bleeding/infection unresponsive to other care. Goal: remove a non-functioning, complication-prone segment.

5. Image-guided drainage of complicated pleural collections – Why: if secondary infections/effusions complicate advanced disease. Goal: source control.

Surgery is not routine ABPA care; it is for complications or AFRS. Medical therapy and prevention remain central. PubMed+1

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 Prevention tips

1. Keep indoor humidity <60% (ideally 30–50%).

2. Fix leaks fast; dry wet areas within 24–48 hours.

3. Vent bathrooms/kitchens; use exhaust fans.

4. Change HVAC filters on schedule; maintain AC drip pans & drains.

5. Use HEPA air cleaners in key rooms.

6. Avoid compost piles, decaying leaves, grain storage dust, and construction dust when possible; wear N95 if exposure is unavoidable.

7. Do not keep heavily mold-prone items (damp carpets, wet cardboard) indoors.

8. Follow your asthma/ABPA action plan; don’t skip controller medicines.

9. Get flu and pneumococcal vaccines as advised.

10. Don’t stay in a moldy space during cleanup if you have asthma/ABPA. US EPA+1

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When to see a doctor

• Urgent / emergency now: severe breathlessness, lips or fingers turning blue, coughing large amounts of blood, fainting, or peak flow <50% of your usual best despite rescue treatment.

• Prompt appointment (24–72 h): new or worsening cough/wheeze, fever with chest symptoms, brown/green plugs, rising home peak-flow variability, need for reliever more than every 4 hours, or a sudden rise in total IgE on routine monitoring.

• Routine follow-up: every 1–3 months during the first year after diagnosis, then individualized; repeat IgE and imaging as your clinician advises (per guideline stage-wise management). PubMed

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What to eat and what to avoid

• Eat: a balanced anti-inflammatory pattern—plenty of fruits, vegetables, whole grains, legumes, nuts, seeds, fish (omega-3s), lean proteins; drink enough water to keep mucus thinner.

• If on itraconazole capsules: take with food; avoid medications that cut stomach acid unless your doctor approves (they can reduce absorption).

• Limit or avoid: alcohol (worsens liver risk with azoles), grapefruit (raises levels of several drugs including some azoles), smoke exposure, and heavily mold-contaminated foods (do not eat any food that looks or smells moldy).

• Reflux-friendly habits: smaller evening meals, head-of-bed elevation to reduce nighttime cough.

• Supplements: only what your clinician agrees with, because azoles and biologics can interact with other products. PubMed

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Frequently asked questions

1. Is ABPA an infection?
   Not exactly. It’s mainly an allergic reaction to Aspergillus in the airways. Antifungals help by lowering the antigen load, but ABPA is not the same as invasive aspergillosis. PubMed

2. Can I catch it from someone?
   No. ABPA is not contagious. It is your immune system’s overreaction to common spores. PubMed

3. Who is at risk?
   People with asthma or cystic fibrosis are most at risk. Screening may start with Aspergillus-specific IgE and total IgE. PubMed

4. What blood tests matter?
   Total IgE (often ≥500 IU/mL in ABPA), Aspergillus-specific IgE/IgG, and sometimes eosinophils. IgE helps track flares and response. PubMed+1

5. What scans are used?
   Chest CT looks for central bronchiectasis, mucus plugging, and high-attenuation mucus. Chest X-ray may show fleeting shadows. PubMed

6. What is the first treatment during a flare?
   Guidelines suggest oral prednisolone or itraconazole monotherapy, chosen by your clinician; both are evidence-based for acute ABPA. PubMed

7. Why antifungals if it’s an allergy?
   Fewer fungi → less allergen → fewer immune flares. An RCT proved itraconazole reduces steroid needs and IgE. PubMed

8. Where do biologics fit?
   If disease keeps relapsing or steroids cause side effects, biologics such as omalizumab, mepolizumab, or dupilumab may help. Evidence shows fewer exacerbations and lower steroid use in ABPA cohorts. PubMed

9. How do we track improvement?
   Symptoms and lung function improve; chest shadows fade; total IgE falls (often ≥25–35%). Your team sets your personal target and schedule. PubMed

10. Can ABPA be cured?
    It can go into long remissions, but relapses are common. Care aims to prevent damage and keep control. PubMed

11. Is sinus surgery part of ABPA care?
    Not for lungs. But if you also have AFRS, endoscopic sinus surgery plus topical steroids is standard. Ann Allergy

12. Do humidifiers help or hurt?
    Humidified air can soothe, but poorly cleaned cool-mist units can aerosolize microbes. Keep indoor RH <60% and clean devices perfectly. CDC+1

13. Are “stem-cell treatments” real for ABPA?
    No approved stem-cell drugs for ABPA. Use guideline-endorsed therapies instead. PubMed

14. Can I exercise?
    Yes—once symptoms are controlled. Use your reliever as instructed before activity; pulmonary rehab is helpful.

15. What about pregnancy?
    Discuss all medicines with your specialist; plans often favor the lowest effective steroid dose, careful azole consideration, and control of asthma to protect mother and baby.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 12, 2025.

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