Sinusitis in Patients with ABPA

When to suspect it, when to investigate, and when to refer

Why this matters

Patients with allergic bronchopulmonary aspergillosis (ABPA) are usually managed as having a lung disease. Diagnosis, monitoring, and treatment focus appropriately on the chest, immunology, and asthma control.

However, ABPA occurs within a single continuous airway, extending from the nose and sinuses to the lungs. Disease in the upper airway can coexist with, exacerbate, or complicate lower airway inflammation — yet sinus disease is not routinely assessed in ABPA care pathways.

This article outlines:

  • What is known about sinus disease in this context

  • Which symptoms should raise suspicion

  • When investigation or ENT referral should be considered

  • What GPs and non-specialists can reasonably do

The united airway: a brief reminder

The upper and lower airways share:

  • Type 2 (eosinophilic) inflammation

  • Immunoglobulin E–mediated immune responses

  • Common triggers, including allergens and fungi

Chronic rhinosinusitis is common in asthma and severe asthma, and treatment of sinus disease can improve lower airway outcomes in some patients.
ABPA sits within this same inflammatory spectrum, even though its management is lung-centred.

Sinus disease in ABPA: what is (and isn’t) known

What we know

  • Chronic rhinosinusitis is common in patients with asthma and severe asthma

  • Sinus disease may be symptomatic or relatively silent

  • ABPA guidelines do not mandate routine ENT review or sinus imaging

  • ENT involvement, therefore, varies widely between centres

What we do not know

  • Whether routine ENT assessment improves ABPA outcomes

  • Which ABPA patients benefit most from sinus intervention

  • The optimal timing for ENT referral in ABPA

As a result, clinical judgement remains central.

Symptoms that should prompt consideration of sinus disease

Sinusitis in ABPA patients does not always present with classic “blocked nose and facial pain”.
Key symptoms include:

Common but often overlooked

  • Persistent post-nasal drip

  • Foul, bitter, metallic, or “infected” taste in the mouth

  • Throat clearing, chronic cough

  • Thick or sticky mucus sensation

  • Symptoms are worse on waking or lying flat

More typical sinonasal features

  • Nasal blockage or congestion

  • Facial pressure or fullness

  • Reduced or altered sense of smell

  • Nasal crusting or discharge

Contextual clues

  • Poor durability of response to steroids or antifungals

  • Recurrent “flares” without clear chest triggers

  • Coexisting severe asthma or nasal polyps

  • Symptoms are worse in damp or mould-affected housing

A persistent foul taste in the mouth is a recognised symptom of chronic sinus disease, usually due to post-nasal drainage of inflamed secretions.

Damp homes and sinus disease

Living in damp or mould-affected environments is associated with:

  • Higher rates of chronic rhinosinusitis

  • Upper airway irritation and inflammation

  • Allergic sensitisation to fungal spores

In most cases, this results in inflammatory or allergic sinusitis, not invasive fungal infection.
Fungal involvement may act as an immune trigger, even when not labelled as “fungal sinusitis”.

Fungal sinusitis: rare vs under-recognised

It is important to distinguish between entities:

Type Frequency Key point
Invasive fungal sinusitis Rare Usually immunocompromised; dramatic presentation
Fungal ball (mycetoma) Uncommon Usually obvious on CT
Allergic fungal rhinosinusitis Likely under-recognised Requires active suspicion

Allergic fungal rhinosinusitis overlaps biologically with ABPA:

  • IgE-mediated

  • Eosinophilic inflammation

  • Thick allergic mucin

It is not routinely sought, so it may be under-diagnosed in at-risk groups.

What GPs and non-specialists can reasonably do

1. Take upper airway symptoms seriously

Especially in ABPA or severe asthma patients with:

  • Persistent post-nasal symptoms

  • Foul taste

  • Recurrent unexplained deterioration

2. Examine the nose and throat

  • Look for polyps, discharge, and crusting

  • Note mouth breathing or altered voice quality

  • Check dentition (to exclude dental causes)

3. Consider imaging when symptoms persist

  • CT sinuses (not plain X-ray) is the imaging of choice

  • Particularly appropriate if symptoms last >8–12 weeks or recur

4. Refer to ENT when:

  • Symptoms are persistent or progressive

  • CT shows significant sinus disease

  • There is a poor response to standard medical therapy

  • There is diagnostic uncertainty

Referral does not imply surgery — ENT input may be diagnostic or medical.

What this article is not saying

  • It does not suggest that all ABPA patients need an ENT referral

  • It does not claim that sinus treatment improves ABPA outcomes

  • It does not override existing guidelines

It does suggest that earlier consideration of the upper airway is reasonable in selected patients.

Key take-home points for clinicians

  • The airway functions as a single inflammatory system

  • Sinus disease may be subtle, under-reported, or atypical

  • A foul taste in the mouth is a meaningful symptom

  • Damp or mould exposure increases sinus disease risk

  • ENT referral is appropriate when symptoms persist or recur

  • Evidence gaps remain — but clinical vigilance is justified

In summary

ABPA is managed as a lung disease, but patients live with a whole airway.
Recognising when sinus disease may be contributing can help explain persistent symptoms and guide appropriate referral — without over-investigation or over-treatment.

by GAtherton

ABPA and Work: What a Patient Poll Tells Us About Employment, Health, and Real-World Impact

An article for patients, GPs, and non-specialist healthcare professionals

Allergic bronchopulmonary aspergillosis (ABPA) is often discussed in terms of lung function, immunology, and imaging. Far less often do we talk about its impact on everyday life, particularly on a person’s ability to work.

A poll run within the National Aspergillosis Centre patient community asked a simple but powerful question:

Who is still able to work while living with ABPA – and who has had to stop or retire?

The responses provide an important insight into the functional and socioeconomic burden of ABPA.

Key findings from the poll (patient-reported)

  • Working full time: 17%

  • Working part time (days or hours): 18% combined

  • Not working: 30%

  • Retirement age: 21%

  • Retired early for health reasons: 12%

  • Currently on sick leave / full-time carer / pre-diagnosis: small but notable groups

Even allowing for the informal nature of a social media poll, the overall pattern is clear.

What this tells us

1. Sustained full-time work is uncommon in ABPA

Fewer than one in five respondents were able to work full time. Even among those still working, many described reduced hours, flexible arrangements, or fragile employment dependent on day-to-day health.

ABPA is often incompatible with predictable, high-demand working patterns.

2. ABPA frequently leads to work loss or early retirement

A substantial proportion of respondents were either:

  • No longer working at all, or

  • Retired earlier than planned specifically because of health

This is particularly striking given that ABPA often affects people during their working years and may coexist with asthma, bronchiectasis, or long-term steroid use.

3. “Retirement age” can hide health-forced exit

Some respondents selected “retirement age,” but accompanying comments revealed that many:

  • Left work earlier than expected

  • Changed careers or reduced responsibilities years before retirement

  • Worked through ill health until they no longer could

This matters when interpreting employment statistics: health-driven work loss may be underestimated.

4. Unpaid work and instability are often overlooked

The poll also highlighted:

  • People currently on prolonged sick leave

  • Full-time unpaid carers

  • Individuals still awaiting diagnosis but already struggling to work

These groups are frequently invisible in employment data, yet represent significant personal and societal impact.

Why ABPA affects the ability to work

For patients and non-specialists, it is important to understand that work difficulties in ABPA are not simply due to “asthma symptoms.”

Common contributors include:

  • Chronic breathlessness and cough

  • Severe fatigue and post-exertional exhaustion

  • Recurrent chest infections

  • Steroid side-effects (muscle weakness, bone disease, mood changes, diabetes risk)

  • Unpredictable flare-ups requiring rest, antibiotics, or hospital care

  • Cognitive and emotional burden of long-term illness

Together, these make consistent attendance, physical work, and high cognitive load difficult to sustain.

Implications for patients

  • Difficulty working is not a personal failure

  • Many others with ABPA face similar challenges

  • Adjustments, reduced hours, or stopping work altogether may be medically appropriate

  • Asking for support is reasonable and justified

Implications for GPs and non-specialist clinicians

  • Employment status should be considered a key outcome of disease control

  • Fit notes, occupational health input, and benefits documentation are part of holistic care

  • ABPA is a fluctuating condition – patients may cope for periods and then deteriorate

  • Statements such as “lung function is stable” do not always reflect real-world functioning

Understanding the work impact helps clinicians better support patients in consultations, reports, and advocacy.

Implications for systems and policy

This poll reinforces that ABPA carries a significant socioeconomic burden, including:

  • Reduced workforce participation

  • Early retirement

  • Increased reliance on health and social support systems

Any assessment of disability, employment capability, or long-term planning must take into account:

  • Variability over time

  • Treatment burden

  • Side-effects of necessary medications

In summary

This patient poll sends a consistent message:

ABPA commonly limits the ability to work, often leading to reduced hours, unstable employment, or early exit from the workforce.

For patients, this experience is shared and valid.
For clinicians, it is a reminder that ABPA is not just a radiological or immunological diagnosis, but a life-limiting condition with real-world consequences.

by GAtherton

Why do some people cough up long, tube-shaped pieces of mucus?

In several chronic lung conditions, the airways can become inflamed and produce thick mucus.
When this mucus sits in the bronchial tubes, it can sometimes harden into a cast shaped exactly like the airway.

People often describe these casts as:

  • long, ribbon-like or “snakeskin” pieces

  • rubbery or stretchy

  • white, yellow, or green

  • shaped like the inside of a tube

Coughing one up can feel dramatic but is usually a sign that your lungs are finally able to clear a blockage.

What does it mean if a cast has black flecks or dark spots?

This can look alarming, but several common, mostly harmless explanations exist.

1. Old or dried blood

Tiny amounts of bleeding from irritated airways can dry and turn:

red → brown → black

This often appears as tiny black dots or threads.

2. Inhaled particles

Dust, soot, pollution, or smoke can get trapped in mucus deeper in the lungs and show up as dark specks.

3. Debris from infection or inflammation

Long-standing inflammation can cause:

  • darkened mucus fragments

  • tiny bits of fungal, bacterial or biofilm material

  • oxidised (darkened) mucus layers

These often look like pepper-like flecks and are not dangerous on their own.

4. Oxidation or ageing of thick mucus

When mucus sits for a long time before it is coughed out, it can become darker in spots.

When this is usually not worrying

Black flecks are often harmless when:

  • the amount is small

  • the colour change is occasional

  • you feel better after coughing the cast out

  • there is no new increase in blood, fever, or breathlessness

  • this fits your usual pattern of mucus plugging

Most people with chronic airway disease experience occasional colour changes in mucus.

When to mention it to your doctor

You should let your team know if:

  • black flecks keep appearing repeatedly

  • you cough up more blood than usual

  • your breathing worsens suddenly

  • your sputum smells different

  • you have fever or chest pain

  • casts become bigger, more frequent, or harder to clear

These changes do not always mean something serious, but they are worth checking.

Why do casts form in the first place?

Conditions that can cause airway casts include:

  • Bronchiectasis

  • ABPA (Allergic Bronchopulmonary Aspergillosis)

  • Severe or eosinophilic asthma

  • Chronic infections, including fungal or bacterial

  • COPD with mucus hypersecretion

Inflammation makes mucus thicker, and narrowed airways make it harder to clear.
Over time, mucus can mould itself into the shape of the airway — becoming a cast.

What to do if you cough one up

  1. Stay calm — this often brings relief.

  2. Take note of its colour and size.

  3. Hydrate well to thin mucus.

  4. Continue your usual airway-clearance technique (physio, nebulisers, saline, etc.)

  5. Let your team know if it is unusual for you.

Final reassurance

Coughing up a long, tube-like piece of mucus can feel shocking, but in most cases it simply means your lungs are clearing a blocked area.
Black flecks are usually:

  • old blood

  • trapped dust or soot

  • dried mucus debris

Most of the time, these findings are not dangerous, but they can give useful clues about airway inflammation.

by GAtherton

⭐ Allergic Bronchopulmonary Aspergillosis (ABPA): Why Diagnosis Is Missed and Who Needs to Be More Aware

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.

⭐ How Common Is ABPA?

ABPA is more common than most clinicians realise:

Population Estimated prevalence
General asthma 1–2%
Severe asthma clinics 3–10%
Cystic fibrosis 5–15%
Bronchiectasis (non-CF) 1–4%

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.

⭐ 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.

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.

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.

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

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.

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.

⭐ 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

2. Severe asthma clinic patients

Prevalence is up to 10%, especially those with:

  • high IgE

  • eosinophilia

  • sensitisation to multiple allergens

  • steroid dependence

3. Bronchiectasis patients

Bronchiectasis often coexists with ABPA and can worsen flares.

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

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

5. People with CF (Cystic Fibrosis)

5–15% develop ABPA at some stage.

⭐ 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.

⭐ 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

⭐ 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.

⭐ 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.

by GAtherton

🌿 Biologics when ABPA and CPA overlap: What Patients Need to Know

Understanding how they work, when they’re helpful, and when extra care is needed

Biologic medicines (such as omalizumab, mepolizumab, benralizumab, dupilumab and newer options like tezepelumab) are increasingly used to treat Allergic Bronchopulmonary Aspergillosis (ABPA) and severe asthma. They can be life-changing for some people.

However, their place in Chronic Pulmonary Aspergillosis (CPA) — especially in people who have both ABPA and CPA together — is more complicated and needs careful specialist supervision.

This article explains what we know so far.

🌟 1. ABPA and CPA are different conditions — but some people have both

  • ABPA is mainly an allergic reaction to Aspergillus in the airways.

  • CPA is a chronic fungal infection that causes cavities, scarring, and long-term lung damage.

  • Some people start with ABPA and later develop CPA, or the two conditions overlap.

  • The 2024 international ABPA guidelines now recognise this overlap as real and important.

Because biologics target allergy pathways rather than fungal infection, treatment decisions must look at both sides of the disease.

🌿 2. Biologics in ABPA: the evidence is strong and growing

Biologics can help patients with ABPA or severe asthma by:

  • reducing steroid use

  • improving breathing

  • decreasing mucus plugging

  • lowering flare-ups

  • improving quality of life

Biologics most commonly used in ABPA include:

Biologic Target Notes
Omalizumab IgE Well established, helps many ABPA patients
Mepolizumab IL-5 Helps eosinophilic inflammation
Benralizumab IL-5Rα Similar to mepolizumab; long-acting
Dupilumab IL-4Rα Very promising for allergic disease; growing evidence for ABPA
Tezepelumab TSLP Very new; limited ABPA data so far

For many people with ABPA, biologics are safe and effective when monitored.

⚠️ 3. Biologics and CPA: much less evidence

  • CPA is caused by persistent fungal infection and structural lung damage.

  • Biologics do not treat fungal infection, and they do not prevent cavities.

  • In CPA, the mainstay of treatment is still:

    • antifungal medication (usually itraconazole, voriconazole or posaconazole)

    • careful imaging (CT scans)

    • airway clearance

    • sometimes surgery or bronchoscopy

There is no strong evidence that biologics help CPA itself.

🔄 4. What about patients who have both ABPA and CPA?

This is where things become more complex.

Biologics may help the allergic part (ABPA), but:

  • they do not treat fungal infection

  • they do not stop fungal cavities from progressing

  • they may reduce inflammation that normally helps the body contain infection

If antifungal treatment is interrupted or not strong enough, fungal activity may increase while the allergic symptoms improve — so regular monitoring is essential.

Specialist centres (like the NAC) now emphasise:

✔️ Continue antifungals if CPA is active
✔️ Watch cavities with regular CT scans
✔️ Monitor Aspergillus IgG/IgE and fungal cultures
✔️ Check whether symptoms are from allergy, infection, or both
✔️ Make joint plans between asthma/airway doctors and mycology specialists

❓ 5. Are some biologics better than others for ABPA/CPA overlap?

There is no official guidance yet, but early observations suggest:

⭐ Most promising for ABPA:

  • Dupilumab seems particularly effective for allergic disease (IgE, mucus, airflow), though still off-label for ABPA.

⭐ Increasing interest:

  • Tezepelumab works outside the eosinophil pathway and may be useful in some asthma types, but research in ABPA is only just starting.

⭐ Useful in selected cases:

  • Anti-IL-5 biologics (mepolizumab, benralizumab) help airway eosinophils but may not help every ABPA patient.

⚠️ Uncertain in CPA:

  • None of the biologics treat fungal infection or cavities directly.

  • Their role in active CPA remains unclear and requires careful oversight.

🧭 6. What this means for patients

If you have ABPA only, biologics may be an excellent option — especially if:

  • steroids cause side-effects

  • your asthma is uncontrolled

  • you have frequent flare-ups

  • your IgE levels are very high

  • mucus plugging or wheezing continues despite treatment

If you have CPA or cavities, treatment needs to be more cautious:

  • antifungal medication usually needs to continue

  • biologics may still help if the allergic component is significant

  • CT scans must be repeated to make sure cavities are not progressing

  • specialists must weigh benefits vs. risk for each patient individually

💬 7. Summary

  • Biologics can be extremely helpful for ABPA.

  • They do not treat CPA, and cannot replace antifungal medicines.

  • In patients with both ABPA and CPA, the approach must be personalised.

  • Dupilumab and (possibly) tezepelumab are emerging biologics with promise, but evidence is still developing.

  • Decisions should always be made with a specialist centre such as the National Aspergillosis Centre (NAC).

by GAtherton

Understanding Mucous Casts in Allergic Bronchopulmonary Aspergillosis (ABPA)

People living with Allergic Bronchopulmonary Aspergillosis (ABPA) often notice thick, unusual mucus coming up during a flare. Some of this mucus can look very different from “normal” sputum and may be described as mucous casts. This leaflet explains what they are, why they happen, and what they mean for your ABPA.

⭐ What are mucous casts?

A mucous cast is a thick, sticky plug of mucus that forms inside your airways.
It takes on the exact shape of the airway or branch it was sitting in – a bit like a soft mould of the inside of your lungs.

When coughed up, casts may look:

  • long and tube-shaped

  • soft and rubbery

  • curled or C-shaped

  • occasionally branching, like a twig

  • pale yellow/cream with darker specks

These darker flecks can include dead inflammatory cells, airway debris, and sometimes tiny amounts of fungal material trapped inside.

⭐ Why do they happen in ABPA?

ABPA is not an infection, but an allergic over-reaction to the Aspergillus fungus.
This allergic inflammation causes:

1. Excess mucus production

Your airways create far more mucus than usual.

2. Thicker, stickier mucus

Inflammation changes the chemistry of the mucus, making it harder to clear.

3. Swollen, narrowed airways

This makes it easy for mucus to get stuck and form plugs.

4. Trapped material

Casts can contain:

  • fungal spores

  • inflammatory cells

  • dust or other inhaled particles

  • old blood or tissue debris

All of this can glue together into a cast.

⭐ Are mucous casts harmful?

They are not dangerous on their own, but they can cause problems:

  • Airway blockage → breathlessness, wheeze, sudden tightness

  • Chest infections → trapped mucus is an ideal place for bacteria

  • ABPA flare-ups → casts often appear during periods of high inflammation

  • Reduced airflow on CT scans → seen as “bronchial impaction”

Telling your clinical team when you notice casts helps them judge how active your ABPA is.

⭐ What do mucous casts look like in ABPA?

Patients often describe:

  • “noodles”

  • “worms”

  • “rubbery plugs”

  • “little branches”

  • “specks of brown/black” within pale mucus

These appearances are normal in ABPA and do not mean your lungs are permanently worsening.

⭐ How are mucous casts managed?

1. Airway clearance

This is the most important step. Techniques include:

  • huff-coughing

  • active cycle of breathing

  • nebulised saline (hypertonic or isotonic)

  • flutter/PEP devices (Acapella, Aerobika)

  • chest physiotherapy

These help loosen and move mucus from deeper airways.

2. Medication

Depending on your treatment plan:

  • inhalers (bronchodilator + inhaled steroids)

  • biologics (e.g., mepolizumab, dupilumab, omalizumab)

  • antifungal medication if prescribed as part of your ABPA care

  • oral steroids if medically appropriate

Biologics can reduce the inflammation that causes casts, so many patients notice fewer plugs over time.

3. Monitoring

Your team may keep an eye on:

  • sputum samples

  • IgE levels

  • CT scan changes

  • symptom patterns

⭐ When should I tell my team?

Contact your clinical team if you notice:

  • more frequent mucous casts

  • sudden breathlessness or chest tightness

  • a drop in your usual oxygen saturation

  • fever or signs of infection

  • coughing up blood

  • a change in colour or smell of mucus

⭐ Reassurance

Mucous casts are very common in ABPA.
They can look alarming, but they are simply a sign that your airways are inflamed and producing thick mucus.

Coughing them out is helpful, not harmful.
It allows the affected airway to reopen and can rapidly improve breathing.

✅ Further Reading

For more patient-oriented information, you can visit the AFIT website where the term “casts” is discussed in the context of aspergillosis: Aspergillus.org.uk – search “casts”.

by GAtherton

🌿 ABPA: Infection, Allergy, Biologics, and What It All Means for You

A calm, supportive guide for patients living with Allergic Bronchopulmonary Aspergillosis (ABPA)

Allergic Bronchopulmonary Aspergillosis (ABPA) can be confusing.
Some people hear “fungus” and think it is a dangerous infection.
Others hear “allergy” and think it has nothing to do with fungi at all.

The truth is somewhere in the middle — and understanding this can make your treatment feel much clearer and less frightening.

This article explains:

  • Whether ABPA is an infection, an allergy, or both

  • How the fungus Aspergillus fumigatus fits into the picture

  • Why biologics help — and whether they allow the fungus to grow

  • Why your future with ABPA is more hopeful than ever

🌼 1. Is ABPA an infection or an allergic over-reaction?

The simplest explanation is:

ABPA happens when Aspergillus lives in mucus in the airways, and the immune system overreacts. It’s driven by allergy, not by fungal invasion.

In ABPA:

  • Aspergillus fumigatus sits in mucus, especially in asthma, bronchiectasis or cystic fibrosis

  • It does not invade or damage lung tissue

  • The immune system becomes over-sensitised and reacts too strongly

This allergic reaction triggers:

  • Very high IgE

  • High eosinophils

  • Swelling, tightness, wheeze

  • Thick “stringy” mucus or plugs

  • Repeated flare-ups that feel like chest infections

The inflammation — not the fungus — is what damages the lungs over time.

🌻 2. If it’s not a typical infection, why treat the fungus?

Even though ABPA is allergic, reducing fungal load can still help.

Here’s why:

  • Less fungus in mucus → less allergen

  • Less allergen → less immune reaction

  • Less reaction → fewer flare-ups, better breathing

This is why some people take antifungals.
But antifungals are not always necessary, especially today with the arrival of biologics.

🌈 3. Do biologics weaken the immune system and let the fungus grow?

No.
This is a very common worry — but the biologics used for ABPA do not suppress the parts of the immune system that keep you safe from fungi.

Biologics such as:

  • Omalizumab (anti-IgE)

  • Mepolizumab / Benralizumab (anti-IL-5)

  • Dupilumab (anti-IL-4/IL-13)

  • Tezepelumab (anti-TSLP)

target overactive allergic pathways, not antifungal defences.

They do not affect:

  • Neutrophils

  • Macrophages

  • Dectin-1

  • TLR antifungal pathways

  • Complement

These are the real fungus-clearing systems — and biologics leave them intact.

🍃 4. Do biologics actually help clear fungus? Surprisingly, sometimes yes.

Many patients on biologics show:

  • Fewer mucus plugs

  • Better airflow

  • Fewer positive sputum cultures

  • Reduced symptoms

  • Lower exacerbation rates

  • Less need for steroids or antifungals

When mucus plugs shrink, fungus loses its hiding place.
Your natural defences can finally clear it.

So biologics do not encourage growth — they may even help reduce fungal load.

🌺 5. Why are outcomes improving so much?

ABPA used to be a condition dominated by:

  • frequent flare-ups

  • repeated steroids

  • fear of lung damage

  • long periods of being unwell

Today, with biologics:

  • far fewer flare-ups

  • easier breathing

  • more stable lung function

  • much less steroid use

  • better quality of life

  • higher confidence and control

For many patients, biologics are transforming ABPA from a cycle of crises into a more manageable long-term condition.

🌼 6. Key reassurance

If you remember only one sentence, let it be this:

Biologics calm the allergic response that causes ABPA, without weakening your natural ability to clear fungus — and many patients do better than ever on them.

🌟 7. Moving forward with confidence

ABPA is complex, but it is treatable, manageable, and increasingly well-understood.
You are not dealing with a dangerous lung infection — you are dealing with an over-active immune response that modern treatments can control.

With the right support, airway clearance, the best inhalers, and (where needed) biologics or antifungals, most people:

  • stabilise

  • breathe more easily

  • reduce flare-ups

  • protect their lungs

  • live full, active lives

You’re not alone — and the future for ABPA care has never looked brighter.

by GAtherton

Inhaled Steroids and ABPA: Do They Help or Should They Be Avoided?

Many people living with allergic bronchopulmonary aspergillosis (ABPA) also use inhaled steroid inhalers such as Symbicort, Fostair, Seretide or Clenil. It’s common to feel confused about whether these inhalers help, whether they should be continued, or whether they could cause harm.

This guide explains what inhaled steroids do, what they don’t do, and how they fit into the treatment of ABPA, asthma, and bronchiectasis.

1. Understanding the basics

What are inhaled steroids?

Inhaled corticosteroids (ICS) are medications breathed directly into the lungs to reduce airway inflammation, especially in asthma. Combination inhalers (e.g., Symbicort, Fostair) contain a steroid + a long-acting bronchodilator.

What they don’t do

Inhaled steroids do not treat ABPA itself.
ABPA is caused by an immune over-reaction to Aspergillus in the lungs. This reaction sits too deep in the airways for inhaled steroids to reach, and the inflammation is too strong for inhaled doses to control.

This is why ABPA flares are treated with:

  • Oral steroids, or

  • Biologics, such as mepolizumab, benralizumab, dupilumab or omalizumab.

2. Why inhaled steroids are still useful for many ABPA patients

Although inhaled steroids don’t treat ABPA directly, most people with ABPA also have asthma.
In asthma:

  • the airways are twitchy

  • inflamed

  • narrow easily

  • and respond well to inhaled steroids

If your symptoms include wheeze, chest tightness, breathlessness that varies from day to day, or a good response to your reliever inhaler, there is a strong chance that asthma is part of your condition.

In those cases, inhaled steroids can be very helpful in keeping the asthma component under control.

3. When inhaled steroids may offer little benefit

Some patients with ABPA have:

  • minimal asthma

  • mainly bronchiectasis

  • or are fully controlled on a biologic

In these situations, inhaled steroids might not provide much additional benefit and occasionally can increase the risk of airway infections, especially in people with significant bronchiectasis.

This is why doctors sometimes sound vague: the answer genuinely depends on your individual mix of ABPA, asthma, and bronchiectasis.

4. How biologics change the picture

Biologics used for ABPA and asthma (e.g., benralizumab, mepolizumab, dupilumab) reduce airway inflammation far more effectively than inhaled steroids. Once a patient is stable on a biologic, many specialists will slowly reduce the inhaled steroid dose if asthma symptoms remain well-controlled.

This does not happen quickly — it is done gradually and only if your breathing tests and symptoms stay stable.

5. Why there is no simple “yes” or “no” answer

Doctors often hesitate to give a straight answer because inhaled steroids can be:

  • Essential for asthma

  • Optional for mild asthma

  • Less useful if ABPA is the main issue

  • Potentially overused in some bronchiectasis patients

  • Safely reduced in people doing well on biologics

Your treatment has to sit in the right place on that spectrum.

6. Questions that can help you get a clear answer from your own team

Many patients say they receive vague responses. These direct questions can help:

✔ “Am I using this inhaler for my asthma, or for my ABPA?”

(If it’s for ABPA, that usually signals a misunderstanding.)

✔ “Do you think my asthma is active, and is the dose of inhaled steroid still appropriate?”

This invites your clinician to be specific.

✔ “If I stay stable on my biologic, could we review the inhaled steroid dose in the future?”

This aligns with typical specialist practice.

7. The bottom line

  • Inhaled steroids do not treat ABPA itself.

  • They are helpful if you also have asthma — which many ABPA patients do.

  • They may be less useful if asthma is mild or absent, especially in pure bronchiectasis.

  • When patients stabilise on biologics, inhaled steroid doses are often reviewed and sometimes reduced.

  • The best approach is individual: the right treatment mix varies from patient to patient.

If you’re unsure what role your inhaler is playing, it’s absolutely reasonable to ask your specialist to explain exactly why you’re on it and whether the dose is still right for you.

by GAtherton

ABPA or Bronchiectasis? A Detailed Guide to Understanding Flare-Ups

Many people with allergic bronchopulmonary aspergillosis (ABPA) also live with bronchiectasis, and the symptoms can overlap so much that it’s difficult to know what’s flaring. This guide explains what is happening inside the lungs, the typical signs of each condition, and how to judge when to seek help.

1. What exactly happens during an ABPA flare?

ABPA is an allergic immune reaction to Aspergillus in the airways.
The fungus is usually present in tiny amounts, but the immune system over-reacts to it.

During a flare:

  • The immune system releases large amounts of inflammatory chemicals (especially IgE and eosinophils).

  • Airways become swollen, narrow and sticky.

  • Thick, glue-like mucus forms and can block off airway sections.

Typical symptoms of an ABPA flare

  • Increased wheeze, chest tightness or asthma-like symptoms

  • Shortness of breath, sometimes sudden

  • Very thick, sticky, tenacious sputum

  • Mucus plugs — sometimes shaped like soft tubes or “casts” of an airway

  • Drop in peak flow or lung function

  • IgE levels rising (but this may lag behind symptoms by days or weeks)

Colour of mucus in ABPA

  • Often golden-brown

  • Can be brown or even dark brown if old mucus is clearing

  • May contain small black dots (fungal elements) but this can also appear in bronchiectasis

2. What happens during a bronchiectasis flare?

Bronchiectasis is a structural lung condition. The airways are wider and more damaged, meaning mucus gets trapped more easily.

During a flare:

  • The airway lining becomes irritated or infected.

  • Mucus production increases.

  • Trapped mucus becomes a breeding ground for bacteria.

  • Breathing may be heavier simply because of mucus load.

Typical symptoms of a bronchiectasis flare

  • Increase in sputum volume

  • Change in sputum colour (yellow, green, brown)

  • Worsening cough

  • Feeling more tired, feverish, or run down

  • Chest tightness from mucus but not usually dramatic wheeze

  • No immediate change in IgE levels

Bronchiectasis and brown sputum

  • Brown sputum is common when old blood, dried mucus or debris is being cleared.

  • After a lung bleed, blood changes colour as it ages:

    • Fresh = bright red

    • 24–48 hours = dark red

    • After a few days = brown, tar-like, sticky

This often appears suddenly after you think everything has settled.

3. Comparing the two conditions side-by-side

Feature ABPA Flare Bronchiectasis Flare
Main cause Immune/allergic reaction to Aspergillus Infection, inflammation, mucus trapping
Breathing Sudden ↑ wheeze + breathlessness Heavy/chesty breathing, fatigue
Mucus amount Normal amount but very thick or plug-like More mucus than usual
Mucus colour Golden-brown, brown, plug-like Yellow, green, brown
Mucus plugs Common Possible but less typical
IgE Often rises (but may lag) Stable
Peak flow Drops significantly Mild change or no change
General wellbeing Often feel “inflamed” without infection symptoms More infection-like tiredness/malaise

4. Understanding brown sputum properly

Brown sputum doesn’t always mean ABPA.

It can be:

  • Old blood breaking loose

  • Dried mucus from bronchiectasis

  • A mixture of dried secretions and oxidised blood proteins

  • Debris from a recently cleared airway infection

This is why a single brown plug — especially after a bleed — is rarely a sign of ABPA on its own.

5. When you should ask for help

Contact your specialist if you notice any of these:

  • Several days of brown plugs or repeated mucus casts

  • Dramatically increased wheeze

  • Peak flow drop >20% from your baseline

  • Fever, chills, or sudden tiredness

  • Breathlessness that feels “different” from normal

  • A major change in your usual bronchiectasis pattern

  • New chest pain

Seek urgent help if:

  • You cough up fresh bright red blood

  • You feel suddenly very breathless

  • You cough up a large amount of blood-stained sputum

  • You have signs of severe infection (rigors, high fever, confusion)

6. And what about IgE?

IgE is helpful, but has limitations:

  • It rises slowly — sometimes days or weeks after symptoms appear.

  • It can stay stable at your “baseline” even when mild inflammation is happening.

  • A stable IgE level is reassuring, but it does not rule out a flare.

Think of IgE as a trend, not an immediate alarm light.

7. The real-world takeaway

  • Bronchiectasis = more mucus, infected/inflamed feeling, colour change.

  • ABPA = allergic response, wheeze, plugs, sudden breathing changes.

  • Brown sputum alone is not enough to diagnose either way.

  • After a bleed, brown sputum is expected for days as the airway clears.

Learning your own pattern takes time. Even experienced patients still contact their team if something feels wrong — and that’s always the safest approach.

by GAtherton

🌲 Why Rough-Cut Wood Arrives Mouldy — and How to Reduce the Risk (Important for Aspergillosis Patients)

For anyone living with aspergillosis, ABPA, bronchiectasis or asthma, mould exposure can trigger symptoms or flares. Recently, several patients have reported that rough-cut timber is arriving mouldy from DIY suppliers, sawmills, or timber merchants.

Here’s why this happens — and what suppliers should be doing to prevent it.

⭐ Why rough-cut wood gets mouldy (especially in the UK)

Mould grows on timber whenever three conditions are present:

  1. Moisture

  2. Poor airflow

  3. Warm or humid air

Rough-cut timber is especially vulnerable because:

  • its uneven surface holds moisture,

  • it is often stacked tightly,

  • it may not be dried properly,

  • and UK weather (rain + high humidity) encourages mould.

Many suppliers wrap wood in plastic, which traps condensation during transport. This can create a humid “greenhouse” around the timber — perfect for mould growth in only 24–48 hours.

⭐ What UK suppliers should be doing (even for low-cost timber)

These are standard industry practices in UK timber yards and sawmills. None of them require wood to be kiln-dried (which is more expensive).

✔ 1. Air-dry properly (“sticker stacking”)

Boards must be stacked with spacers (“stickers”) between them so air can circulate.
No airflow = mould.

✔ 2. Store under cover, not outside in the rain

A simple open-sided shelter is enough.
Rain-soaked timber nearly always grows mould in transit.

✔ 3. Use breathable wrapping — NOT plastic sheeting

Plastic traps moisture.
Breathable paper wrap or perforated cover prevents condensation build-up.

✔ 4. Apply anti-fungal dip (borate)

Most UK sawmills use anti-mould dips to prevent blue-stain and mould during storage.
This costs pennies per board.

✔ 5. Moisture-test before delivery

A good supplier will check wood is below 20–22% moisture before dispatch.
Wet wood + UK weather = guaranteed mould.

⭐ Kiln drying is not essential

Kiln-dried timber is more expensive because it uses energy, equipment, and time to force-dry the wood.

But you do not need kiln-dried timber to avoid mould.

You simply need a supplier who:

  • stores the timber properly,

  • allows airflow,

  • avoids plastic,

  • and checks moisture before delivery.

If rough-cut wood is arriving mouldy, it usually means these steps were not followed.

⭐ What you can do to protect yourself (aspergillosis patients)

If you receive wood that:

  • smells musty,

  • has surface mould,

  • or shows green/black spots,

…it is best not to bring it indoors until cleaned.

✔ Immediately unwrap outdoors

Plastic wrapping traps mould spores.

✔ Keep well away from ventilation intakes, windows, or living areas

This avoids airborne spores entering the home.

✔ If mould is visible — return it

You have the right to reject mouldy timber.

✔ If keeping it, clean outdoors with PPE

Use:

  • gloves

  • FFP3 mask

  • borax solution (borax + hot water)
    to remove early surface mould.

Never sand mould indoors — sanding releases spores.

⭐ Simple Diagram: Correct Way to Store Wood to Prevent Mould

Correct storage includes:

  • boards stacked with spacers between them (“sticker stacked”),

  • raised on bearers above the ground,

  • stored under a roof with airflow on all sides,

  • NEVER wrapped in sealed plastic,

  • ends exposed to allow moisture to escape.

This method is cheap, simple, and prevents mould without needing expensive kiln drying.

⭐ Summary for Aspergillosis Patients

Rough-cut wood should not arrive mouldy.
Mould growth usually means it was:

  • stacked badly,

  • stored wet,

  • wrapped in plastic,

  • or shipped before drying.

For people with aspergillosis, ABPA, bronchiectasis or severe asthma, mould spores can trigger symptoms — so it’s completely reasonable to:

  • refuse mouldy timber,

  • request proper handling,

  • or ask the supplier to follow UK best practice.

by GAtherton

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